Chad 20091214 en

COMMUNICABLE DISEASE
EPIDEMIOLOGICAL PROFILE
Central African Republic and Chad
Disease Control in Humanitarian Emergencies (DCE)

Global Alert and Response Department (GAR)
The Communicable Disease Epidemiological Country Pro-
file series was conceived and developed by the WHO team
for Disease Control in Humanitarian Emergencies (DCE), to
provide up-to-date information on the major communi-
cable disease threats faced by the resident and displaced
populations in emergency affected countries.
The information provided aims to assist with the public

health strategy, prioritization and coordination of com-
municable disease control activities between all agencies
working in such countries.
Diseases have been included if they fulfil one or more of the

following criteria: have a high burden or epidemic poten-
tial, are (re) emerging diseases, important but neglected
tropical diseases, or diseases subject to global elimination
or eradication programmes.
World Health Organization

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WHO/HSE/GAR/DCE/2009.2
COMMUNICABLE DISEASE
EPIDEMIOLOGICAL PROFILE
Central African Republic and Chad

ii
CENTRAL AFRICAN REPUBLIC AND CHAD
World Health Organization 2009
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Communicable disease epidemiological profile

iii
Contents
Acknowledgements ................................................................................................................................................................ v
Part I
Introduction .................................................................................................................................................................................. 1
Purpose ...................................................................................................................................................................................... 3
Target audience .................................................................................................................................................................. 3
Document rationale ...................................................................................................................................................... 3
Background to the humanitarian crisis ................................................................................................... 3
Priority high-burden communicable diseases in CAR and Chad ............................... 6
Part II
CONTENTS
Summary of recent communicable disease outbreaks,
Central African Republic and Chad .................................................................................................................. 7
Part III
Country-specific disease information and technical
guidance for high-burden communicable diseases ...................................................................... 11
Acute lower respiratory infections (ALRI) ........................................................................................ 13
African trypanosomiasis (sleeping sickness) .................................................................................. 17
Bacillary dysentery (shigellosis) .................................................................................................................... 24
Cholera .................................................................................................................................................................................... 29
Diarrhoeal diseases (others) .............................................................................................................................. 35
Diphtheria ............................................................................................................................................................................ 39
Hepatitis E ........................................................................................................................................................................... 45
HIV/AIDS ............................................................................................................................................................................. 49
Influenza (seasonal) ................................................................................................................................................... 69
Influenza (avian) ........................................................................................................................................................... 77
Influenza (human A(H5N1) infection) ................................................................................................. 79

iv
Leishmaniasis (cutaneous and mucosal) ............................................................................................. 90

Leishmaniasis (visceral) ........................................................................................................................................ 94
Leprosy .................................................................................................................................................................................... 98
Lymphatic filariasis ................................................................................................................................................. 103
Malaria ................................................................................................................................................................................. 109
Measles .................................................................................................................................................................................. 117
Meningococcal disease (meningitis and
meningococcal septicaemia) ......................................................................................................................... 127
Onchocerciasis (river blindness) ............................................................................................................... 134
Pertussis (whooping cough) ........................................................................................................................... 139

Poliomyelitis ................................................................................................................................................................... 145
Rabies ..................................................................................................................................................................................... 153
Rift Valley fever (RVF) ........................................................................................................................................ 158
Schistosomiasis (bilharziasis) ...................................................................................................................... 168
Soil-transmitted helminthiases (ascariasis,
hookworm infection, trichuriasis) ........................................................................................................... 174
Tetanus ................................................................................................................................................................................. 179
Tuberculosis .................................................................................................................................................................... 182
Yellow fever ...................................................................................................................................................................... 196
Part IV
Annexes ....................................................................................................................................................................................... 203
Annex 1 ............................................................................................................................................................................... 205
Annex 2 ................................................................................................................................................................................ 218
Annex 3 ................................................................................................................................................................................ 219
Annex 4 ............................................................................................................................................................................... 229
Annex 5 ................................................................................................................................................................................ 231

v
Acknowledgements
This document was edited by the unit on Disease Control in Humanitarian

Emergencies (DCE), part of the Global Alert and Response Department (GAR)
in the Health Security and Environment Cluster (HSE) of the World Health
Organization (WHO).
This communicable disease profile was produced by the Communicable Diseases
Working Group on Emergencies (CD-WGE) at WHO headquarters, the Division
of Communicable Disease Prevention and Control (DCD) at the WHO Regional
Office for Africa (AFRO), the country office of the WHO representative for the
Central African Republic and Chad. The CD-WGE provides technical and opera-
ACKNOWLEDGEMENTS
tional support on communicable disease issues to WHO regional and country
offices, ministries of health, other United Nations agencies and nongovernmental
and international organizations. The Working Group includes the departments of
Epidemic and Pandemic Alert and Response (EPR), the Special Programme for
Research and Training in Tropical Diseases (TDR), Food Safety, Zoonoses and
Foodborne Diseases (FOS), Public Health and Environment (PHE) in the Health
Security and Environment (HSE) cluster; the Global Malaria Programme (GMP),
Stop TB (STB), HIV/AIDS and Control of Neglected Tropical Diseases in the HTM
cluster; the departments of Child and Adolescent Health and Development (CAH),
Immunizations, Vaccines and Biologicals (IVB) in the Family and Community
Health (FCH) cluster; Injuries and Violence Prevention (VIP) and Nutrition for
Health and Development (NHD) in the Noncommunicable Diseases and Mental
Health (NMH) cluster; the department of Essential Health Technologies (EHT)
in the Health Systems and Services (HSS) cluster; Security and Staff Services (SES)
in the General Management (GMG) cluster; and the cluster of Health Action in
Crises (HAC) and the Polio Eradication Initiative (POL).
The following were involved in the development and review of this document
and their contribution is gratefully acknowledged:
Bernadette Abela-Ridder, Giuseppe Annunziata, Harveen Bal, James Bartram,
Eric Bertherat, Gautam Biswas, Jan Brouwer, Yves Chartier, Claire Chauvin, Meena
Cherian, Lester Chitsulo, Renu Dayal-Drager, Ousmane Diouf, Albis Gabrielli,
Walter Kazadi, Mona Lacoul, Christine Lamoureux, Casimir Manengu, David

vi
Meddings, Elizabeth Mumford, Zinga Jose Nkuni, Salah Ottmani, Shamim Ahmad
Qazi, Xavier de Radiques, Aafje Rietveld, Nikki Shindo, Peter Strebel, Jos Vandelaer,
Kaat Vandemaele, Zita Weise-Prinzo, Sergio Yactayo, Ahmed Zouiten.
Editorial support was provided by Mary Roll-Vallanjon. Maps were provided by
Mona Lacoul.
Contributions to previous risk assessments from the following focal points have
also been incorporated:
Jorge Alvar, Andrea Bosman , Claire-Lise Chaignat, Alice Croisier, Alya Dabbagh,
Katya Fernandez-Vegas, Olivier Fontaine, Pierre Formenty, Antonio Gerbase,
Pascale Gilbert-Miguet, Alexandra Hill, Angela Merianos, Franois-Xavier Meslin,
Michael Nathan, Benjamin Nkowane, Asiya Odugleh-Kolev, William Perea, Cathy

Roth, Johannes Schnitzler, Pere-P. Simarro.
We would like to thank the Office of Foreign Disaster Assistance (OFDA) of the
United States Agency for International Development for their support in develop
ment of this document.

PART I
Introduction
3
Purpose
The purpose of this communicable disease profile for the Central African Republic
(CAR) and Chad is to provide up-to-date information on the major communicable
disease threats faced by the resident and displaced populations in these two coun-
tries. The purpose of the information given herein is to assist with the strategy for,
and the prioritization and coordination of, communicable disease control activi-
ties between all agencies working in these countries.
Target audience
The information in this document is essentially addressed to public health pro-
fessionals working for the population in the Central African Republic and Chad.
Document rationale
The epidemic-prone and endemic infectious diseases have been selected in order to
INTRODUCTION
outline the burden of priority communicable diseases. Where available, data and
disease-specific guidelines for their prevention and control are given. Information
is also included on recent outbreaks. The quantity and quality of data are com-
promised by the duration, nature and severity of the humanitarian crisis in these
countries that has severely affected health systems and programmes.
I
Background to the humanitarian crisis
The humanitarian crisis affecting CAR and Chad is multifactorial (see Annex 1
for a chronology of events).
II
Since becoming independent, both countries have been afflicted by political insta-
bility and violence that has been exacerbated by their proximity to Sudan.1
The humanitarian crises in CAR and western Chad should be seen, therefore, in
the context of a subregional situation that involves the southern part of Sudan. III
Cross-border hostilities have resulted in the displacement of populations, either
as internally displaced persons (IDP) or refugees. The political boundaries of the
Central African Republic, Chad and Sudan are shown in the map below.
IV
1 Please refer to the Sudan communicable disease epidemiological profile in this series at http://www.who.int/
diseasecontrol_emergencies/toolkits/en/.

4
Political boundaries of the Central African Republic, Chad and Sudan

5
There are internally displaced persons (IDPs) and refugees in camp settings both
in CAR and Chad. These populations live in emergency settings, and the epidemio-
logical problems connected with their presence are specific. Current estimates
indicate that around 100000 refugees and 200000 IDPs are in CAR, and 300000
refugees and 180000 IDPs in Chad (further information may be found in the
resource documents listed in Annex 2). The effects also have repercussions on
otherwise unaffected bordering states such as Cameroon and Nigeria.
The political instability amplifies background problems related to climate and
development that have traditionally caused a high burden of morbidity and mor-
tality, e.g. recurrent natural disasters (floods and drought), infectious diseases
(malaria, meningitis, HIV/AIDS), and malnutrition.
CAR and Chad have suffered decades of political instability and armed conflict,
the consequences of which are reflected in their deteriorating ranking in the
UNDP Human Poverty Index (HPI) and Human Development Index (HDI):
CAR HPI = 98/108, HDI = 171/177; Chad HPI = 108/108, HDI = 170/177.
INTRODUCTION
The HPI particularly reflects hardship in the health area as it measures the pro-
portion of the population not expected to survive beyond the age of 40.
At a systemic level, the chronic nature of the crisis has resulted in the destruction
of much of the basic infrastructure (e.g. drinking-water and sanitation) and over-
loaded the few remaining services. Health systems and programmes are mostly
suboptimal, damaged, looted or destroyed and have not received any investment
for several years. The cumulative effects on the population are evident in the key I
national health indicators and other statistics (Annex1). In the case of < 5 mor-
tality per 1000 live births, figures have increased since 1990: for CAR, from 173 to
175; for Chad, from 201 to 209. The crisis is compounded by attacks that increas-
ingly target humanitarian workers. II
Given the continued political instability and hostile cross-border activity, further
influxes of refugees and IDPs may be anticipated. On the other hand, the repatria-
tion of currently displaced populations remains unlikely.
III
The precarious state of the health infrastructure means that the threat and poten-
tial impact of an infectious disease event (export, reintroduction, amplification)
or natural disaster (floods, drought) are genuine.
Disease surveillance and notification at national and international levels are severely IV

6
compromised. This is reflected as a lack of epidemiological information for some

of the diseases covered in this document. However, an emergency surveillance
system has been set up in eastern Chad that is to produce a weekly epidemiologi-
cal bulletin.2
Priority high-burden communicable diseases in CAR

and Chad
1. Acute lower respiratory tract infections
2. Diarrhoeal diseases (cholera, bacillary dysentery (Shigella, Salmonella))
3. Hepatitis E
4. Measles
5. Meningitis
6. Malaria
7. Poliomyelitis
8. HIV/AIDS
9. Tuberculosis.
For the vaccine-preventable, high-burden communicable diseases, routine immuni-

zation is insufficient to prevent outbreaks and when it does take place, it is further
compromised by vaccine-supply disruption. Vaccination campaigns should be
planned and implemented in accordance with WHO recommendations.
Although the specific context in each country varies, the issues are comparable,
with similar characteristics and requiring similar interventions to reduce morbid-
ity and mortality. The health strategy (for the general population or concentrations
of refugees or IDPs) should focus on a coordinated approach to public health
measures and disease prevention, detection, response and control for both the
priority communicable diseases with outbreak potential and the endemic com-
municable diseases with potential for amplification.
2 http://www.who.int/hac/crises/tcd/en/.

PART II
Summary of recent communicable disease

outbreaks, Central African Republic and Chad
9
Central African Republic: communicable disease outbreaks, as reported

to WHO from January 2000 to August 2008
Month/year Diseasea Cases Deaths Case-fatality ratio (%)
April 2008 Yellow fever 2 1 50
April 2008 Polio (imported WPV1) 1 0 0
SUMMARY OF RECENT COMMUNICABLE DISEASE OUTBREAKS

December 2007 Measles 116 1 0.9
January 2008
November 2007 Meningococcal disease 45 5 11.1

February 2008 (NmA)
November 2006 Yellow fever 1 0 0
JanuaryJune 2005 Measles 195 18 9.2
December 2003 Measles 225 36 16.0

May 2004
MarchApril 2004 Meningococcal disease 43 7 16.2

(NmA)
JuneOctober 2003 Shigellosis 379 23 6.1
JanuaryMay 2003 Measles 443 86 19.4
2002 Yellow fever 1 0 0
JanuaryApril 2002 Measles 287 19 6.6

I
FebruaryJune 2001 Meningococcal disease 1816 343 18.8

(NmA + W135)
II
February 2000 Meningococcal disease 86 14 16.2
Source: http://www.who.int/csr/don/archive/country/en/index.html.
a Where possible, outbreak location is given in Part III for each specific disease under Country-specific
disease burden. III
IV

10
Chad: communicable disease outbreaks, as reported to WHO from

December 2000 to August 2008
Month/year Diseasea Cases Deaths Case-fatality ratio (%)
MarchApril 2007 Meningococcal disease 350 17 5.1

(NmA predominant, some
W135)
MarchMay 2007 Meningococcal disease 31 3 9.7

(NmA)
FebruaryJune 2007 Measles 147 1 0.7
JuneDecember 2006 Cholera 1633 68 4.1

MarchApril 2006 Meningococcal disease 200 16 8

(NmA)
JanuaryMarch 2005 Menigococcal disease 387 53 13.7

(NmA)
January 2005 Meningococcal disease 8 0 0

Refugee camps (Nm W135)
JanuaryMay 2005 Measles 20278 516 2.5
September 2004 Hepatitis E 1442 46 3.2

Refugee camps
JuneSeptember 2004 Cholera 3910 164 4.2
April 2004 Meningococcal disease 19 4 21

(NmA)
2003present Poliomyelitis (WPV1 and 86 0 0

WPV3)
JulyAugust 2001 Cholera 3557 113 3.2
December 2000 Menigococcal disease 3579 401 11.2

February 2001 (NmA)
Source: http://www.who.int/csr/don/archive/country/en/index.html.
a Where possible, outbreak location is given in Part III for each specific disease under Country-specific
disease burden.

PART III
Country-specific disease information and

technical guidance for high-burden
communicable diseases
13
ACUTE LOWER RESPIRATORY INFECTIONS (ALRI)
Country-specific disease burden

Central African Republic
The under-five mortality rate is 175 per 1000 live births.3 Approximately 19% of
these deaths are attributed to pneumonia.4
Chad

The under-five mortality rate is 209 per 1000 live births.3 Approximately 23% of
these deaths are attributed to pneumonia.4
Description
Infectious agent
Bacteria: the most common are likely to be Streptococcus pneumoniae and
Haemophilus influenzae type b (and Staphylococcus aureus to a lesser extent).
Several respiratory viruses, notably respiratory syncitial virus (RSV).
Case definition
Clinical description
I
ALRI include bronchitis, bronchiolitis and pneumonia (bronchopneumonia and
lobar pneumonia). Pneumonia is the most severe and is fatal in 1020% of cases
if inappropriately treated.
Pneumonia. Cough or difficult breathing and breathing 50 times or more per minute II
for infants aged 211months; breathing 40 times or more per minute for children
aged 1259 months and no chest indrawing, no stridor nor general danger signs.*
Severe pneumonia. Cough or difficult breathing and any general danger sign* or
chest indrawing or stridor in a calm child. III
In infants aged less than 2 months, the presence of any of the following indicates
severe pneumonia: cough or difficult breathing and breathing 60 times or more
3 UNICEF/WHO, 2006. See: State of the worlds children. New York, UNICEF, 2008 (www.unicef.org/sowc08/ IV
statistics/tables.php).
4 UNICEF/WHO, 2004.

14
per minute or grunting, or nasal flaring, or fever, or low body temperature, or

any general danger sign.*
* General danger signs: for children aged 2 months to 5 years: inability to drink or breastfeed; persistent
vomiting; convulsions; lethargy or unconsciousness.
Mode of transmission
Airborne, through droplets.
Incubation period
Depends on the infective agent. Usually 25 days.
Communicability period
Depends on the infective agent. Usually during the symptomatic phase.
Epidemiology
General
In developing countries, for the under-five age group, the estimated disease burden
is 151 million new episodes of pneumonia per year, of which 1120 million episodes
require hospital admission. This represents an estimated 0.29 episodes/child year
(e/cy) until the age of 5.
ALRI are likely to be a major cause of disease and death in children under five
years of age given the presence of major risk factors for ALRI transmission and
development. Indoor air pollution and low temperatures may increase the relative
risk of children acquiring pneumonia.
Geographical distribution
Worldwide.
Seasonality
In tropical settings, incidence is highest in the rainy season (and among children
aged under5 years).
Alert threshold
An increase in the number of cases above the expected number for that time of
the year in a defined area.

15
Risk factors for increased burden

Population movement allows contact between non-immune and infected indi-
viduals and increases transmission of the pathogen.
Overcrowding increases the risk of transmission which is spread by droplets and
compounded by poor ventilation.
Poor access to health services. Prompt identification and treatment of cases are
the most important control measures. Poor access to health services may delay or
prevent adequate treatment, without which the case-fatality ratio can be very

high (20% or more in emergency situations).
Food shortages. Malnutrition, vitamin A deficiency, low birth weight and poor
breastfeeding practices are important risk factors for development of the disease
and increase its severity.
Lack of safe water and poor sanitation. Unsafe water, poor personal hygiene,
insufficient hand-washing and inadequate ventilation increase the risk of spread
of respiratory infections.
Prevention and control measures

Case management
The priority is the early recognition of symptoms in the community diagnosis by
health-care workers and initiation of appropriate treatment of cases. Integrated man- I
agement of illness should be practised for any sick child seen by a provider trained
in the WHO and UNICEF Integrated Management of Childhood Illnesses (IMCI).
Non-severe pneumonia
II
In countries with low HIV prevalence, 3 days of antibiotic therapy (oral
amoxicillin and co-trimoxazole) should be used in children aged from
2 months to 5 years.
Where antimicrobial resistance to co-trimoxazole is high, oral amoxicillin is III
the best choice.
Oral amoxicillin should be used twice daily at a dose of 25 mg/kg per dose.
Severe pneumonia
IV
For management of HIV-infected children, newly developed WHO treatment
guidelines should be used.

16
Children with wheeze and fast breathing and/or lower chest indrawing should
be given a trial of rapid-acting inhaled bronchodilator before they are classi-
fied as having pneumonia and prescribed antibiotics.
Where referral is difficult and injection is not available, oral amoxicillin may
be given to children with severe pneumonia.
Very severe pneumonia

Injectable ampicillin plus injection gentamicin is a better choice than injectable
chloramphenicol for very severe pneumonia in children aged 259 months.
Supportive measures such as continued feeding to avoid malnutrition, vitamin A

if indicated, antipyretics to reduce high fever, and protection from cold (especially
keeping young infants warm) are part of integrated case management. Prevention
of low blood glucose is necessary for severe cases.
Proper advice should be given to carers of non-severe cases on home-based care,
including compliance with antibiotic treatment instructions.
Signs of malnutrition should be assessed, as this increases the risk of death due
to pneumonia. Severely malnourished children (weight-for-height index <3 Z
Score, or bilateral pitting oedema or MUAC (mid-upper-arm circumference)
<11 cm) should be referred to hospital. It is important to note that the diagnosis
of pneumonia for children with severe malnutrition may be difficult with X-rays.
See Child health in emergencies in Annex 3.
Prevention
Efforts should be made to improve early diagnosis and treatment with effective
antibiotics, particularly through raising community awareness, developing
mobile clinics and training health-care workers. Immunization against diph-
theria, pertussis and measles reduces the impact and severity of disease.
Health education should be carried out on early danger signs for prompt care-
seeking.
Immunization coverage should be improved.
Adequate nutrition, including exclusive breastfeeding and appropriate comple-
mentary feeding, should be ensured to avoid malnutrition.
Immunization
Hib, measles, pertussis and pneumococcal conjugate immunization are effective
in reducing the impact of ALRI. Immunization coverage is generally suboptimal.

17
African trypanosomiasis (sleeping sickness)

CAR has four foci of transmission: Ouham (Ouham prefecture), a continuation
of the Mandul focus in Chad; Haut Mbomou (Haut-Mbomou prefecture), continu-
ing the Tambura focus in southern Sudan; Nola-Bilolo (Sanga-Mbar prefecture),
AFRICAN TRYPANOSOMIASIS (SLEEPING SICKNESS)

continuing the Yokadouma focus in Cameroon and Lobaye (Lobaye Prefecture)
continuing the northern Equateur focus in the Democratic Republic of the Congo
(see map of CAR prefectures in Annex 1).
African trypanosomiasis is a rural and chronic disease, and hence mobile teams
are the most effective response. However in the Ouham focus, this is not possible
as a result of the current situation, and the vast majority of cases are detected
passively, in health facilities, during the late stages of disease.
As a consequence, those infected act as a reservoir in the villages for the vectors
and this in turn creates the potential for further human transmission. During
2002, the number of new cases reported in the Ouham focus was 137; however in
2007 it was 610, 70% of which were detected by passive screening.
As indicated above, there are many disease foci in countries bordering on CAR.
The disease evolution in CAR depends in many ways on the epidemiological
development of these bordering foci. Such epidemiological interdependence I
occurred during the Sudanese and Congolese crises in the case of the border
regions of Haut Mbomou and Lobaye.
Chad
II
Areas of transmission are specifically in the southern border areas as indicated
above, which are continuations of the northern focus of Ouham in CAR.
As a result of insecurity, refugee populations originating from rural areas of CAR
have settled in southern Chad. III
Description
Infectious agent
IV
Protozoan: Trypanosoma brucei gambiense (chronic disease) and T. b. rhodesiense
(acute disease). In both cases, the outcome is death if the disease is undiagnosed

18
and untreated. T. b. gambiense (chronic disease) is generally found in the western,

central and south-western parts of Africa. T. b. rhodesiense (acute form) is gener-
ally found in the eastern and south-eastern areas of the continent.
Case definition
First stage (haemolymphatic involvement). There is a painful chancre (papular or
nodular) at the primary site of the tsetse fly bite (rare in T. b. gambiense infection).
There may be fever, intense headache, insomnia, painless lymphadenopathy,
anaemia, local oedema and rash.
Second stage (neurological involvement). Parasites cross the bloodbrain barrier
and attack the central nervous system. Cachexia, somnolence and signs of central
nervous system involvement are apparent.
The disease may last for several months or even years. The natural progression of
the disease (when not treated) leads to body wasting, somnolence, coma and death.
The disease is always fatal without treatment.
Laboratory tests
Serological (for screening). Card agglutination trypanosomiasis test (CATT) (for
T.b. gambiense only). A negative CATT result indicates that there is no disease; a
positive result must be confirmed by microscopy. Immunofluorescent assay: for
T. b. rhodesiense mainly and possibly for T. b. gambiense.
Parasitological (for diagnosis). Visualization (by microscopy) of trypanosomes in
blood, lymph node aspirates or cerebrospinal fluid (CSF).
Case classification
Suspected: any case without direct demonstration of the parasite that is com-
patible with the clinical description and/or with positive serology. In the first
stage or early in the second stage of the disease, there are often no clinical
signs or symptoms classically associated with the disease. Suspicion is then
based on local risk of contracting the disease and on local disease historical
background.
Confirmed: a case with direct demonstration of the parasite, whether or not
compatible with the clinical description.
First stage: parasite seen in blood and/or lymph nodes, with CSF containing
no detectable trypanosomes and a leukocyte count 5/l.

19
Second stage: parasite seen in blood and/or lymph nodes, with CSF
containing trypanosomes and/or a leukocyte count > 5/l.
The disease is transmitted primarily by the bites of infected tsetse flies (Glossina
spp.). Transmission is also possible through contamination with infected blood
or through the placenta (congenital).
Incubation period

T. b. gambiense infection has a long incubation period that may last several months
or even years. T. b. rhodesiense infections progress rapidly and are more virulent,
with a short incubation period lasting from 3 days to a few weeks.
The disease is communicable to the tsetse fly as long as the parasite is present in the
blood of the infected person or animal reservoir (521 days after the infective bite).
Parasitaemia occurs in waves of varying intensity in untreated cases during all stages
of the disease. Once infected, the tsetse fly remains infective for life (16 months).
Epidemiology
General
T. b. gambiense, human African trypanosomiasis, which causes the chronic form I
of this disease, is endemic in CAR and Chad and is a neglected tropical disease.
An important feature of African trypanosomiasis is its focal nature: it tends to
occur in circumscribed zones, and observed prevalence levels vary greatly from
one geographical area to another, and even between one village and another II
within the same area.
African trypanosomiasis also affects cattle. Expansion of animal trypanosomiasis
into new areas may lead to massive outmigrations and abandonment of settlements.
Long-distance migration increases periods of stress resulting from trekking, which III
render cattle more susceptible to infection.
In general, countries are placed in four categories in terms of prevalence; those
that report no cases, <50 cases, 50 to 1000 cases, >1000cases. Both Chad and CAR
are classed by WHO as being countries which report 501000 cases per year. in IV
each country, the spatial distribution of the diseases is very diverse; it is found in
both macro- and micro- foci.

20
When encountering patients with chronic neurological symptoms, medical officers

in charge of IDPs or refugee populations coming from rural areas where there are
known disease foci should strongly suspect this disease.
The disease is confined to tropical Africa between 15 N and 20 S. Sleeping sick-
ness threatens >60 million people in 36 countries of sub-Saharan Africa, of which
only 34 million are under surveillance, with regular examination or access to a
health centre that can provide screening.
The animal form of the disease threatens an estimated 50 million cattle in 37
African countries. The risk is most serious in the sub-humid zone and wetter parts
of the semi-arid zone, which holds the continents greatest potential for agricul-
tural expansion. The disease reduces the availability and efficiency of draught
animals used for preparing land for crops.
Seasonality
The disease has no clearly obvious seasonal pattern. Seasonal fluctuations in the
density of tsetse flies have implications for grazing patterns and this may result
in conflict with sedentary farmers.
Reservoirs
Humans are the major reservoir of T. b. gambiense infection. Domestic cattle and
wild animals, especially bushbucks and antelopes, are the main reservoirs of T. b.
rhodesiense.
Epidemics
Outbreaks occur when humanfly contact is intensified, when reservoir hosts
introduce virulent strains into a tsetse-infested area or when populations are dis-
placed into endemic areas.
Overcrowding. An increased density of the human population destroys tsetse habi-
tat, thereby reducing fly density and subsequently reducing the risk of transmission.

Population movement. Risk is associated with settlement in a high-transmission area.
Poor access to health services. Systematic population screening is necessary, par-
ticularly for gambiense sleeping sickness which has a very long asymptomatic

21
period. The complex nature of the disease and inadequate control tools require
efficient health structures and trained personnel for diagnosis and treatment.
Food shortages. These result in people entering the forest and rivers for food,
fishing and hunting, thereby increasing humanfly contact and the risk of con-
tracting the infection.
Lack of safe water and poor sanitation. The tsetse fly is not attracted by dirty
water. However, lack of water supply in villages forces people to search for water
in tsetse habitats, increasing the risk of infection.

Case management
Early screening and diagnosis are essential, as treatment is easier during the first
stage of the disease (the patient does not present with psychiatric symptoms, fewer
injections are required, and treatment poses less risk to the patient and may be
given on an outpatient basis).
Diagnosis and treatment require trained personnel; self-treatment is not possible.
All confirmed cases must be treated as soon as possible. Most available drugs
have been in use for many years, are difficult to administer in poor conditions,
and frequently unsuccessful.
T. b. gambiense infection: I
First stage: pentamidine 4 mg/kg per day intramuscularly (IM) for 7 consecu-
tive days on an outpatient basis.
Second stage: II
eflornithine: hospitalization, with 400 mg/kg administered in slow infu-
sions (lasting approximately 2 hours) four times a day. Infusions of 100mg/kg
are given every 6 hours for 14 days.
melarsoprol hospitalization, with injections of 2.2 mg/kg/day adminis- III
tered intravenously (IV) for 10 consecutive days.
In case of treatment failure with one drug, the other should be used.
T. b. rhodesiense infection: IV
First stage (early stages of the disease): suramin IM, 20mg/kg per week for 5 weeks.

22
Second stage: melarsoprol hospitalization, with injections of 2.2 mg/kg per

day administered IV for 10 consecutive days.
General comments. Melarsoprol causes reactive encephalopathy in 510% of patients,

with a fatal outcome in about half of the cases. Increasing rates of resistance to
melarsoprol (as high as 25%) have been reported in some areas in T.b.gambiense
foci in southern Sudan, Kasai and Equateur provinces in the Democratic Republic
of the Congo and foci in northern Uganda and northern Angola. The drug must
be administered in hospital settings and in intensive care units if possible.
Eflornithine (slow IV 100mg/kg every 6 hours) is difficult to administer under
field conditions.
WHO has established a human African trypanosomiasis treatment and drug

resistance network. Four working groups deal with: (1) drug availability and
accessibility; (2) coordination of drug development and clinical trials; (3) research
on resistance and treatment schedules; and (4) surveillance of resistance.
Drug procurement. Since 2001, a publicprivate partnership signed by WHO has
made all drugs widely available. The drugs are donated to WHO. Requests for
supplies are made to WHO by governments of disease-endemic countries and
organizations working in association with these governments. Mdecins sans
frontires undertakes stock control and delivery of the drugs in accordance with
WHO guidelines. All the drugs are provided free of charge: recipient countries
pay, when possible, only the transport costs and customs charges. Drug donations
to WHO of pentamidine, suramin, melarsoprol and eflornithine are sufficient to
meet global needs until 2011.
Prevention
Routine preventive measures through public education on the following should
be encouraged:
avoidance of known foci of sleeping sickness and/or tsetse infestation;

wearing suitable clothing (including long sleeves and long trousers) in endemic
areas;
routine use of insect repellents and mosquito nets.
Case detection and containment of the human reservoirs through periodical

population screening and chemotherapy of cases remain the cornerstone of dis-
ease control for T. b. gambiense sleeping sickness. Active periodical screening

23
(active case-finding) of the population of endemic foci by mobile screening teams

is the best option, since infected subjects may remain asymptomatic and conta-
gious for months or years before developing overt symptoms. Screening usually
comprises CATTs of the entire population visited by teams.
Vector control through tsetse-fly control programmes:
application of insecticides or aerosol insecticides;

use of insecticide-impregnated traps and screens.

Destruction of tsetse habitats by selective clearing of vegetation: clearing bushes
and tall grasses around villages is useful when peridomestic transmission occurs.
Indiscriminate destruction of vegetation is not recommended.
Epidemic control
T.b.gambiense. see Prevention above.
T. b. rhodesiense. Where epidemics are caused by T.b. rhodesiense, active screening
using parasitological methods and vector-control measures is appropriate. Mass
treatment of cattle provides an additional benefit for effective control. All identified
cases must be promptly treated. Tsetse-fly control measures (e.g. aerosol insecticides
sprayed by helicopter and fixed-wing aircraft) should be implemented urgently.
II
III
IV

24
Bacillary dysentery (shigellosis)

Outbreaks of Shigella dysenteriae type 1 sensitive to ciprofloxacin occurred during
JuneOctober 2003 in Ouham-Pend prefecture (379 cases, CFR 6.9%).
Chad
No information available.
Description
Infectious agent
The infectious agent is a bacterium of the genus Shigella which includes four species
(S. dysenteriae , S. flexneri, S. boydii and S. Sonnei), also designated as serogroups
A, B, C and D respectively. Each serogroup is further subdivided into serotypes.
S. sonnei and S. boydii usually cause relatively mild illness. Although S. flexneri is
the chief cause of endemic shigellosis in developing countries, Shigella dysenteriae
serotype 1 (Sd1) causes the most severe disease and is usually responsible for epi-
demics that are often significant and may even be at a regional level.
Case definition
Case classification
Suspected case: diarrhoea with visible blood in the stools.
Confirmed case: a case corresponding to the suspected case definition, with
isolation of Shigella from stools.
It is transmitted through the faecaloral route, particularly through contaminated
water and food. The infectious dose of microbes in humans is very low (10100
organisms). Flies may also transmit the organism. Food stalls are a common source
of contaminated meals.
Incubation period
The incubation period is usually 13 days, and may be up to one week for Sd1.

25
During acute infection and up to four weeks after illness (without treatment);
23 days with appropriate treatment. Asymptomatic carriers exist.
Epidemiology
General
Globally, shigellosis is estimated to cause 80 million cases of bloody diarrhoea and
700 000 deaths per year. 99% of cases occur in developing countries; 70% of cases
and 60% of deaths occur in children under 5 years of age. Illness in infants under
6 months is unusual. In endemic areas, the disease is more severe in young children
BACILLARY DYSENTERY (SHIGELLOSIS)

than in adults, among whom many infections may be asymptomatic. The elderly, the
weak and the malnourished of all ages are particularly susceptible to severe disease
and death. Early detection of cases and use of antibiotic therapy are essential.
Worldwide, shigellosis is endemic in both temperate and tropical climates.
Multidrug-resistant Shigella with considerable geographical variations have
appeared worldwide in relation to the widespread use of antimicrobial agents.
Seasonality
No data available.
I
Alert threshold
In the absence of a clear epidemic threshold, an epidemic should be suspected if:
there is an unusual and sudden rise in the number of new cases or deaths due II
to bloody diarrhoea reported weekly;
there is an increase in the proportion of bloody diarrhoea among diarrhoeal cases;
there are five or more linked cases of bloody diarrhoea.
III
Any of the above scenarios should lead to investigation of the disease agent by
laboratory testing.
Epidemics
IV
Susceptibility is general. Secondary attack rates in households can be as high as
40%. Outbreaks may occur in crowded conditions where sanitation facilities are

26
lacking and personal hygiene is poor, such as in refugee camps, institutions for
children, day-care centres, psychiatric hospitals and prisons. This increases the
risk of faecal pathogens contaminating food.
Case fatality is estimated to be < 1% among those whose illness is insufficient to
require treatment in hospital. However, case fatality may be as high as 15%. More
severe disease and greater risk of death are likely to be seen in infants and in
adults > 50 years, children not breastfed, children recovering from measles, the
malnourished or any patient who develops dehydration, unconsciousness, hypo-
or hyperthermia, or presents with a history of convulsions.

Population movement increases transmission of the infectious agent.

Overcrowding increases the risk of infection. The risk of epidemics of Sd1 is high
in camp settings (up to one third of the population at risk may be affected).
Poor access to health services. Early detection and containment of cases are para-
mount to reduce transmission.
Food shortages. Malnutrition increases gastrointestinal tract susceptibility to inva-
siveness of the organism and severity of disease. Breastfeeding protects infants
and young children, and it is therefore important to continue breastfeeding infants
and children during illness.
Lack of safe water and poor sanitation. These represent a highly significant risk
factor. The risk of epidemics of Sd1 is high in camp settings (up to one third of
the population at risk may be affected).
Other risk factors. Poor hygiene and lack of soap may lead to contaminated food,
especially at food stalls.

Case management
Early and appropriate therapy is very important; treatment with an effective anti-
microbial may reduce the severity and duration of shigellosis. Selection depends
on resistance patterns of the bacteria and on drug availability.
Rapid acquisition of antimicrobial resistance is a problem in the treatment Sd1
in Africa. It is therefore important to confirm the antibiotic susceptibility of

27
S. dysenteriae not only in the early stages of an outbreak but also to confirm the
resistance patterns during the course of an outbreak, through the taking of regu-
lar stool samples, as patterns may vary.
Ciprofloxacin is the current first-line antibiotic of choice recommended for treat-
ment of Sd1. There is no available antibiotic resistance data for CAR or Chad.
Recommendations for treatment of Shigella dysenteriae type 1a
Patient group/ Dose Dosing frequency Duration of treatment

treatment
Adults: ciprofloxacin 500 mg Twice a day 3 days
BACILLARY DYSENTERY (SHIGELLOSIS)

Children: ciprofloxacin 250 mg/15 kg body weight Twice a day 3 days
For children aged less than 10 mg Daily 2 weeks

6 months: add zinc
For children aged 6 months 20 mg Daily 2 weeks

to 3 years: add zinc
a Rapidly-evolving antimicrobial resistance is a serious problem. Sd1 is usually resistant to ampicillin and
trimethoprimsulfamethoxazole (TMPSMX).
Supportive treatment using oral rehydration salts (ORS), continued feeding (fre-
quent small meals) and antipyretics to reduce high fever are also essential.
More detailed advice on how to rehydrate and how to feed a child during a diarrhoeal
disease episode is given in The treatment of diarrhoea, A manual for physicians and
I
other senior health workers. Details of this and other sources of further informa-
tion are given in the reference list below, and under Child health in emergencies
in Annex 3.
II
Sd1 is often more severe or fatal in young children, the elderly and malnourished
individuals; prompt treatment with antibiotics is essential. If in short supply, anti-
biotics should be reserved for such high-risk groups.
Breastfeeding is protective to infants and young children. It is therefore important III
to continue breastfeeding infants and children during the illness.
Prevention
Information may be found in the section on Diarrhoeal diseases in this document, IV
under Prevention; in Annex 4 under Water, sanitation and health, and in references
(2) and (3) under Further reading.

28
Epidemic control
Health authorities should be informed if one or more suspected cases are identified.
Early detection and notification of epidemic dysentery, especially among adults,
allow timely mobilization of resources needed for appropriate case management
and control. The outbreak should be confirmed following WHO guidelines.
Rectal swabs from suspected cases should be collected and immediately shipped
in a cold chain (04 C) to a laboratory in an appropriate medium (e.g. Cary-Blair)
for culture to confirm the diagnosis of Sd1. Ideally, the specimen should be ana-
lysed within 2 hours. The viability of bacteria in this medium when refrigerated
for between 13 days is very variable and laboratory analysis findings unreliable.
It is therefore recommended that 1020 samples are used to confirm the outbreak,
the pathogen strain and antibiotic susceptibility. Fresh stool samples may be sent
if Cary-Blair medium is not available, but the sample must reach the laboratory
and be processed within 6 hours. Once the outbreak is confirmed, it is not neces-
sary to obtain laboratory confirmation for every patient.
Testing of Sd1 isolates for antimicrobial susceptibility should be done at regular
intervals to determine whether treatment guidelines remain appropriate. Interna-
tional referral laboratories are available to assist in the identification of the organism
and confirmation of the antimicrobial resistance pattern.
Do not wait for laboratory results before starting treatment/control activities.
Patients with known Shigella infections should not be employed to handle food
or to provide child or patient care. Patients must be told the importance and
effectiveness of hand-washing with soap and water after defecation as a means of
curtailing transmission.
Further reading
1. The treatment of diarrhoea: a manual for physicians and other senior health workers. Geneva,
World Health Organization, 2005 (www.who.int/entity/child_adolescent_health/documents/
9241593180/en/).
2. Guidelines for the control of shigellosis, including epidemics due to Shigella dysenteriae type 1.
Geneva, World Health Organization, 2005 (www.who.int/topics/cholera/publications/shigellosis/
en/index.html).
3. Acute diarrhoeal diseases in complex emergencies: critical steps. Geneva, World Health
Organization, 2004 (www.who.int/topics/cholera/publications/critical_steps/en/index.html).
4. First steps for managing an outbreak of acute diarrhoea. Geneva, World Health Organization, 2003
(WHO/CDS/CSR/NCS/2003.7 Rev 1; www.who.int/cholera/publications/first_steps/en/index.html).
5. Emerging issues in water and infectious disease (www.who.int/water_sanitation_health/emerging/en/).

29
CHOLERA

No information available.
Chad
Recent outbreaks:
JuneDecember 2006 (1633 cases, 68 deaths, CFR 4.1%). Areas affected:

Karassoua Moussari (Hadjer Lamis), Bol district (islands of Lake Chad),
NDjamena and Kanem regions.
JuneSeptember 2004 (3910 cases, CFR 4.2%). Areas affected: Bousso,
Massaguet (Hadjar Lamine), Lac, Kanem, NDjamena, Mongo and Ati.
JulySeptember 2001 (3557 cases, CFR 3.2%,). Areas affected: south-western
CHOLERA
part of the country (NDjamena, Massakory, Bongo, Bol).
Description
Infectious agent
I
The bacterium Vibrio cholerae O1 and O139.
Case definition
Clinical case : a person aged > 5 years that develops severe dehydration or dies II
from acute watery diarrhoea.
Suspected case: that corresponds to the clinical case definition.
Confirmed case: isolation of Vibrio cholerae O1 or O139 from stools in any patient
with diarrhoea.
III
Mainly faecaloral route:
IV
drinking contaminated water, including accidental ingestion of contami-
nated surface water;

30
eating food (fruits and vegetables) contaminated through water, soil, dirty
hands or during preparation (rice, millet, food from street vendors), or
contaminated seafood.
Person to person:
when taking care of cholera patients;
through direct contact with bodies from deceased cholera patients (e.g.
washing the body for funeral ceremonies);
some cultural practices, such as placing bodies of the deceased in a river,
may play a major role in the spread of epidemics.
Indirect contamination (hands): poor hygiene and lack of soap.
Wound infections may arise from environmental exposure, especially in

brackish water as a result of occupational accidents among fishermen.
Incubation period
The incubation period is usually a few hours to 5 days.
During the symptomatic phase until 23 days after recovery. Very rarely, for
months. Asymptomatic carriers are common.
Epidemiology
General
Cholera is a significant public health problem in the subregion and outbreaks
have occurred annually. Typical settings for cholera are peri-urban slums where
there is no basic health infrastructure and where access to safe drinking-water
and adequate sanitation cannot be assured.
Cholera treatment units should be prepared before the emergence of an outbreak
in high-risk areas (see below Interagency diarrhoeal disease kits). When the disease
is properly managed, cholera case-fatality rates should be < 1% during outbreaks.
As the risk of cholera outbreaks is high in overcrowded settings, preparedness is
the key factor for successfully reducing associated mortality. Disease surveillance
systems should be strengthened in order to be sensitive enough to detect major
outbreaks.

31
Cholera is endemic in CAR and Chad.
Seasonality
Cases are distributed mainly during the wet season starting in JulyAugust. Climate
fluctuations related to warming of oceans, such as El Nio, may be associated with
an increase in cholera cases.
Alert threshold
Any suspected case must be investigated.
A cholera outbreak should be suspected if: a person aged > 5 years develops severe
dehydration or dies from acute watery diarrhoea (clinical case definition); or there
is a sudden increase in the daily number of patients with acute watery diarrhoea,
especially patients who pass the rice water stools typical of cholera.
CHOLERA
Population movement plays an important role in the transmission of the infec-
tious agent.
Overcrowding increases the risk of contact with the bacterium contained in vomitus,
excreta and contaminated water or food.
Poor access to health services. Early detection and containment of cases (isolation
I
facilities) are paramount in reducing transmission.
Food shortages. In the context of food shortage, nutritional status is a determinant
of the severity of diarrhoea in patients with cholera. Malnutrition enhances the
II
risk of diarrhoeal illness, which in turn produces more profound malnutrition.
Prolonged diarrhoea in malnourished patients may result in a significant increase
in the need for fluids, electrolytes and nursing capacity.
Lack of safe water and poor sanitation are the main risk factors. III

Case management
IV
The mainstay of the case management of cholera is the treatment of dehydration using
ORS or IV fluids (Ringers lactate). IV rehydration should be used for severe cases only.

32
Use of antibiotics (doxycycline/tetracycline) is not essential for disease treatment

but may be used in severe cases to reduce the volume of diarrhoea (and of the
rehydration solutions required), and to shorten its duration and the period of
Vibrio cholerae excretion. The antimicrobial susceptibility pattern should be
assessed in order to select the appropriate antibiotic.
The patient should be continuously fed to prevent malnutrition. Recommendations
on how to feed a child during treatment of diarrhoea are given in The treatment of
diarrhoea, a manual for physicians and other senior health workers (see reference (4)
below). See also Child health in emergencies in Annex 3.
The CFR can be extremely high (540%) without proper treatment. With appro-
priate case management, the CFR should be <1%. (See Interagency diarrhoeal
disease kits below.)
Epidemic control
Health authorities should be informed immediately if one or more suspected cases
are identified. The outbreak should be confirmed following WHO guidelines on
prevention and control of cholera outbreaks.5
Stool samples should be taken with a rectal swab and transported in Cary-Blair
medium. If a transport medium is not available, a cotton-tipped rectal swab may
be soaked in the liquid stool, placed in a sterile plastic bag, tightly sealed and sent
to the laboratory.
It is recommended that at least 10 cases are used to confirm the outbreak and
identify antibiotic susceptibility. Once confirmed, it is not necessary to obtain
laboratory confirmation for every patient.
Do not wait for laboratory results before starting case management and control
activities.
Ensure prompt case management and confirm the diagnosis.

Isolate severe cases in cholera treatment centres.
Provide adequate health education.
Set up ORS corners to increase the populations access to oral rehydration.
5 Available at www.who.int/cholera/publications/cholera_outbreak/en/index.html; www.emro.who.int/CSR/

Media/PDF/cholera_whopolicy.pdf.

33
Ensure access to safe water and proper sanitation.

Ensure hand-washing with soap.
Ensure safe food handling.
Interagency diarrhoeal disease kits (which contain four separate modules) may be
obtained for preparedness or response. It is advisable to have complete kits for
preparedness, but each module may be ordered separately according to the avail-
ability of components locally. Information regarding the content of these kits may
be found below in the reference list.
The shelf-life of all components of the kit is a minimum of three years. No cold
chain is required.6
Prevention
Information may be found in the section on Diarrhoeal diseases below, under
Prevention; in Annex 4 under Water, sanitation and health, and in references (2)
and (7) below.
CHOLERA
Immunization
Implementation of normal prevention and control measures, including the improve-
ment of water and sanitation, remains the foundation of outbreak prevention and
response. The use of oral cholera vaccine (OCV) is considered to be a public health
tool additional to the normal recommended cholera prevention and control meas- I
ures, especially when given pre-emptively if the population at risk can be accurately
identified. Currently there is only one WHO prequalified oral cholera vaccine,
killed whole-cell V. cholerae O1 recombinant B-subunit of cholera toxoid (WC/rBS),
available for use in public health. II
The relevance of OCVs should be assessed by using the WHO decision-making
tool on a case-by-case basis (see reference (3) below). Earlier parenteral cholera
vaccine should not be used and has never been recommended by WHO.
For more specific information on cholera vaccines and their use, please contact
III
the Global Task Force on Cholera Control at WHO headquarters.7
6 These kits or modules may be purchased by non-WHO agencies through MEG, the Medical Export Group
BV, Gorinchem, Netherlands (info@meg.nl and www.meg.nl) or by WHO through a usual requisition IV
(product kit and modules are available in the WHO catalogues under kits).
7 cholera@who.int.

34
References
1. Cholera annual report 2007. Weekly Epidemiological Record, 2008, 83(31):269284 (http://www.
who.int/wer/2008/wer8331.pdf).
2. Interagency diarrhoeal disease kits - information note. Geneva, World Health Organization,
2006 (http://www.who.int/topics/cholera/materials/en/; http://www.who.int/cholera/technical/
DiarrhoealDiseaseKits/en/index.html).
3. Oral cholera vaccine use in complex emergencies: what next? Cairo, December 2005. Geneva,
World Health Organization, 2006 (WHO/CDS/NTD/IDM/2006.2; http://www.who.int/topics/
cholera/publications/cholera_vaccines_emergencies_2005.pdf).
4. The treatment of diarrhoea: a manual for physicians and other senior health workers. Geneva,
World Health Organization, 2005 (http://www.who.int/entity/child_adolescent_health/
documents/9241593180/en/).
5. First steps for managing an outbreak of acute diarrhoea. Geneva, World Health Organization,
2004 (WHO/CDS/CSR/NCS/2003.7 Rev1; http://www.who.int/topics/cholera/publications/
first_steps/en/index.html).
6. Cholera outbreak: assessing the outbreak response and improving preparedness. Geneva,
World Health Organization, 2004 (WHO/CDS/CPE/ZFK/2004.4; http://www.who.int/topics/
cholera/publications/cholera_outbreak/en/index.html).
7. Acute diarrhoeal diseases in complex emergencies: critical steps. Geneva, World Health Organiza
tion, 2004 (WHO/CDS/CPE/ZFK/2004.6; http://www.who.int/topics/cholera/publications/
critical_steps/en/)
8. Laboratory methods for the diagnosis of epidemic dysentery and cholera. Geneva, World Health
Organization, 1999 (WHO/CDS/CSR/EDC/99.8; http://www.cdc.gov/ncidod/dbmd/diseaseinfo/
cholera/complete.pdf).
9. Prevention and control of cholera outbreaks WHO policy and recommendations (http://www.
emro.who.int/CSR/Media/PDF/cholera_whopolicy.pdf).

35
DIARRHOEAL DISEASES (OTHERS)

Country-specific data are not available.
Chad
Country-specific data are not available.
Description
Infectious agent

Bacteria: the bacteria that cause the most severe outbreaks are Shigella
dysenteriae type 1 and Vibrio cholerae (see Bacillary dysentery and Cholera
above). Salmonella spp. (commonly S. enteritidis, S. typhimurium) and a small
number of strains of Escherichia coli may also cause disease.
Protozoa: e.g. Entamoeba histolytica, Giardia lamblia and Cryptosporidium
parvum.
Viruses: e.g. rotavirus and Norwalk virus.
Case definition
Three or more abnormally loose or fluid stools over a period of 24 hours. I
Faecaloral route, particularly contaminated water and food.
Incubation period
II
Salmonella generally require an 848 hour incubation period, whereas E. coli
typically require longer, with 28 days (median 34 days). The duration of the
disease in both cases is usually 25 days. The average incubation period is 24
weeks for E. histolytica, 710 days for G. lamblia and 7 days for C. parvum. The III
incubation period for rotavirus is about 48 hours; it mainly affects children aged
< 5 years and symptoms may last for up to 1 week.
IV
During the acute stage of the disease and for the duration of faecal excretion.
Temporary Salmonella carriers may continue to exist for several months.

36
Epidemiology
General
In camp situations, diarrhoeal diseases have accounted for between 25% and 40%
of deaths in the acute phase of the emergency. More than 80% of deaths are among
children aged < 2 years.
No data available, but endemic.
Seasonality
Year-round exposure and risk.
Alert threshold
An increase in the number of cases above the expected number compared with
the same period in previous years in a defined area.

Population movement may facilitate transmission of the pathogen and importations.
Overcrowding facilitates transmission.
Poor access to health services. Early detection and containment of cases are para-
mount in reducing transmission.
Food shortages. Malnutrition increases gastrointestinal tract susceptibility to invasive-
ness of some organisms and severity of disease. Persistent diarrhoea lasting 14 days
or longer may in turn result in malnutrition and cause serious extra-intestinal infection.
Lack of safe water and poor sanitation are the most important risk factors.
Prevention of diarrhoeal diseases depends on the provision and use of safe water,
adequate sanitation and health education for proper hygiene and food safety. The
supply of adequate quantities of water to the population should be one of the high-
est priorities. The minimal emergency requirement is 20 litres/person per day.
Common sources of infection in emergency situations are:
contaminated water sources (e.g. by faecally-contaminated surface water enter-

ing an incompletely sealed well) or water contaminated during storage (e.g. by
contact with hands soiled by faeces);
shared water containers and cooking pots.

37

Case management
Reduction of mortality caused by diarrhoeal disease is primarily related to effec-
tive management of dehydration, particularly in children.
Prevention: give recommended home fluid and ORS.

Treatment of dehydration with ORS for mild to moderate dehydration, or
with IV fluids (Ringers lactate) for severe dehydration is the mainstay of
the management of diarrhoeal illness.
Use of antibiotics depends on the infectious agent.
Resume feeding with a normal diet when vomiting has stopped. It is important
to separate those who are eating from those who are not. Food should be cooked

on site. Continue breastfeeding of infants and young children.
Epidemic control
Health authorities should be informed immediately if an increase in the number
of cases above the expected number is identified. The outbreak should be confirmed
following WHO guidelines. Proper case management and epidemic control activi-
ties should be ensured.
Prevention
The prevention of diarrhoeal diseases depends on the provision and use of safe
water, adequate sanitation and health education.
I
Safe drinking-water
Provision of an adequate and safe supply, collection and storage system.
Provision of information on the importance of clean water and appropriate
household storage of water (see Water, sanitation and health in Annex 4). II
Safe disposal of human excreta
Provision of adequate facilities for the disposal of human waste.
Provision of information on the importance of human waste disposal, use of III
sanitation covers and correct maintenance of sanitation facilities.
Food safety
Provision of adequate food storage facilities (for both uncooked and cooked IV
food), cooking utensils, adequate quantities of water and fuel to allow for
cooking and reheating.

38
Health education on the importance of food safety and safe food-handling.
Hand-washing with soap

Provision of soap in sufficient quantities for hand-washing, bathing and laun-
dry needs.
Health education on the relationship between disease spread and lack of or
poor hand-washing before eating, after toileting, before food preparation and
after cleaning/changing children.
Breastfeeding
Provision of information on the protective qualities of breastfeeding and the
importance of breastfeeding ill children.

Practical support for breastfeeding ill children.
References
1. The treatment of diarrhoea: a manual for physicians and other senior health workers. Fourth
rev. Geneva, World Health Organization, 2005 (www.who.int/child-adolescent- health/New_
Publications/CHILD_HEALTH/ISBN_92_4_159318_0.pdf).
2. Acute diarrhoeal diseases in complex emergencies: critical steps. Geneva, World Health Organiza
tion, 2004 (WHO/CDS/CPE/ZFK/2004.6; www.who.int/topics/cholera/publications/critical_
steps/en/index.html).
3. First steps for managing an outbreak of acute diarrhoea. Geneva, World Health Organization,
2003 (WHO/CDS/CSR/NCS/2003.7 Rev1; www.who.int/topics/cholera/publications/first_
steps/en/index.html).
4. Laboratory methods for the diagnosis of epidemic dysentery and cholera. Geneva, World Health
Organization, 1999 (WHO/CDS/CSR/EDC/99.8; www.cdc.gov/ncidod/dbmd/diseaseinfo/
cholera/complete.pdf).

39
DIPHTHERIA

Zero cases were reported to WHO for 2007, as of 1 July 2008.8
Chad
No report was made to WHO for 19992007, as of 1 July 2008.
Description
Infectious agent
The bacterium Corynebacterium diphtheriae.
Case definition
DIPHTHERIA
Upper respiratory tract illness with laryngitis or pharyngitis or tonsillitis plus
adherent greyish membranes on tonsils and/or nasopharynx.
Diphtheria is an acute toxin-mediated disease caused by toxigenic strains of
Corynebacterium diphtheriae. The disease affects the mucous membranes of the I
respiratory tract (respiratory diphtheria), the skin (cutaneous diphtheria), and
occasionally mucous membranes at other sites (eyes, ears or vagina). Cutaneous
and nasal diphtheria are localized infections that are rarely associated with sys-
temic toxicity. II
Symptoms of respiratory diphtheria have a gradual onset and include malaise,
sore throat, difficulty swallowing, loss of appetite and a mild fever (rarely >38 C),
with laryngeal involvement and hoarseness. Within 23 days, a firmly adherent,
grey membrane forms over the mucous membrane of the tonsils, pharynx or both. III
In severe cases, cervical lymphadenopathy and soft tissue swelling in the neck
give rise to a bull-neck appearance. Extensive membrane formation may result
in life-threatening or fatal airway obstruction. Diphtheria toxin may cause serious
life-threatening systemic complications, including myocarditis and neuropathies.
IV
8 www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencedip.htm.

40
Respiratory diphtheria, particularly in unimmunized persons, is a medical emer-

gency with a case-fatality rate of 510%, even with treatment.
Laboratory confirmation
Isolation of C. diphtheriae from a clinical specimen.
Case classification
Probable case: a case that meets the clinical description.
Confirmed case: a probable case confirmed by laboratory or epidemiologically
linked to a laboratory-confirmed case.
Carrier: presence of C. diphtheriae in nasopharynx, without symptoms.
Note. People with positive C. diphtheriae identification who do not meet the clin-
ical description (i.e. asymptomatic carriers) should not be reported as probable
or confirmed cases.
Contact (usually direct, rarely indirect) with the respiratory droplets from a case
or carrier, discharge from skin lesions, and fomites (uncommon). In rare cases, the
disease may be transmitted through foodstuffs (raw milk has served as a vehicle).
Incubation period
Usually 25 days, occasionally longer.
Until viable C. diphtheriae have disappeared from discharges and lesions; usually
2 weeks or less and seldom more than 4 weeks. The rare chronic carrier may shed
C. diphtheriae for 6 months or more. The disease is usually not contagious 48 hours
after antibiotics are given.
Epidemiology
General
DPT3 coverage is reported as 20% in CAR and 40% in Chad, and global coverage
is estimated at 79%. Low vaccination coverage (<80%) for routine Expanded
Programme on Immunization (EPI) diseases increases the risk of outbreaks.9
9 http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencedip.htm.

41
Outbreaks may occur when toxigenic C. diphtheriae is introduced into populations

with low herd immunity (poor DTP3 coverage in children; low natural boosting or
diphtheria toxoid booster coverage in adolescents and adults), especially when social
or natural conditions lead to overcrowding of susceptible groups. This frequently
occurs when there are large-scale movements of non-immunized populations.
Throughout CAR and Chad.
Alert threshold
Any probable case must be investigated.
Recent epidemics
None recorded.
DIPHTHERIA
Population movement allows importation and facilitates transmission.
Overcrowding facilitates transmission.
Poor access to health services prevents access to routine immunization services
resulting in low herd immunity. Early detection and containment of cases reduce
transmission.
I
Lack of safe water and poor sanitation promote cutaneous diphtheria spread (in
conjunction with crowding).
Prevention and control measures II

The control of diphtheria is based on three measures:
ensuring high population immunity through vaccination (primary prevention);

rapid investigation and treatment of contacts (secondary prevention of spread); III
early diagnosis and proper case management (tertiary prevention of compli-
cations and deaths).
Case management
IV
Diphtheria antitoxin is the cornerstone of therapy for respiratory diphtheria. The
antitoxin neutralizes the diphtheria toxin only before its entry into cells. It is

42
therefore critical that diphtheria antitoxin be administered as soon as a presump-

tive diagnosis has been made.
Note. Diphtheria antitoxin is not indicated for cutaneous disease.
Diphtheria antitoxin is an equine serum preparation. Testing for patient hypersen-
sitivity is mandatory before administration to avoid potentially fatal anaphylactic
reactions.10
In addition, antibiotic therapy, by killing the organism, has three benefits:
termination of toxin production;

improvement of local infection;
prevention of spread of the organism to uninfected people.
Do not wait for laboratory results before starting treatment/control activities.
Patients
Diphtheria antitoxin IM (20 000100 000 units) in a single dose, immediately
after throat swabs have been taken and sensitivity-testing performed (dosing
depends on the extent of disease);11
plus:
procaine penicillin IM (25 00050 000 units/kg/day for children; 1.2 million
units/day for adults in two divided doses) or parenteral erythromycin (4050
mg/kg per day to a maximum of 2 g/day) until the patient can swallow;
then oral penicillin V (125250 mg four times a day) or oral erythromycin
(4050 mg/kg per day with a maximum of 2 g/day) in four divided doses.
Antibiotic treatment should be continued for a total period of 14 days.
Isolation
Pharyngeal diphtheria: strict isolation is necessary.
Cutaneous diphtheria: strict isolation is not necessary. However, barrier pre-
cautions must be observed in order to prevent contact with cutaneous lesions.
10 The protocol for sensitivity testing may be found at: www.hpa.org.uk/cdph/issues/CDPHvol2/no4/

guidelines.pdf or www.cdc.gov/vaccines/vpd-vac/diphtheria/dat/downloads/protocol_032504.pdf.
11 Dosing guidelines may be found at: www.hpa.org.uk/cdph/issues/CDPHvol2/no4/guidelines.pdf.

43
Note. Clinical diphtheria does not necessarily confer natural immunity, and patients
should therefore be vaccinated before discharge from a health facility.
Close contacts
Surveillance for 7 days for all people with close contact, regardless of vaccination
status, and throat culture. All must receive: a dose of age-appropriate diphtheria
toxoid-containing vaccine, unless a dose has been received within the previous
12 months; a single dose of benzathine penicillin G IM (600 000 units for children
aged <6 years; 1.2 million units for children aged 6 years). Alternatively, a 7-day
course of oral erythromycin may be used. If culture is positive, antibiotics should
be given as mentioned above under Patients.
Carriers
All must receive a single dose of benzathine penicillin G IM (600 000 units for
children aged <6 years; 1.2 million units for children aged 6).
Immunization
DIPHTHERIA
During an epidemic, the population at risk should be immunized as soon as pos-
sible. In an epidemic involving adults, groups that are most affected and at highest
risk should be immunized. Immunization procedures should be repeated 12
months later to provide at least two doses to recipients. A third dose should be
provided after 612 months to those without a known history of previous primary
immunization. I
Diphtheria and tetanustoxoid-containing vaccine should be given. DT should be
used for children <7 years; alternatively, DTP may be used in populations with
poor DTP3 coverage. For older children and adults, Td is preferred (a combination
of diphtheria toxoid of reduced content and tetanus toxoid). If Td is unavailable,
II
DT may be used in the setting of epidemic control.
In non-epidemic situations, the approach to a previously unvaccinated population
is to provide a full 3-dose primary series (the first 2 doses separated by 12 months III
and the third given 612 months after the second) using:
7years: DTP;
7years and adults: Td (combination reduced diphtheria and tetanus toxoid);
IV
routine EPI should include DTP1 (6 weeks), DTP2 (10 weeks), DTP3 (14 weeks)
and if resources and circumstances permit, DTP4 (2 years).

44
Epidemic control
Inform the health authorities if one or more probable cases are identified.
Confirm the suspected outbreak, following WHO guidelines.
Investigate any probable case; check whether it fulfils the case definition,
record date of onset, age and vaccination status.
Confirm the diagnosis; collect both nasal and pharyngeal swabs for culture
and swabs from any wounds or skin lesions. If appropriate facilities are avail-
able, determine the biotype and toxigenicity of C. diphtheriae.
Identify close contacts and define population groups at high risk. Adult con-
tacts must avoid contact with children and must not be allowed to undertake
food handling until proved not to be carriers.

Implement outbreak response measures; give priority to case management
and immunization of the population in areas not yet affected but to which
the outbreak is likely to spread.
Immunize the population at risk as soon as possible, especially children. In
an epidemic involving adults, immunize groups that are most affected and at
highest risk. Repeat immunization procedures one month later to provide at
least two doses to recipients.
In endemic situations, DT or DTP should be given for children <7 years, and Td
for children > 7 years, adolescents and adults (age-appropriate combination of
diphtheria and tetanus toxoids). Preferably Td vaccine should be given (combina-
tion of reduced diphtheria content and tetanus toxoids).
To ensure injection safety during immunization, autodisable syringes and safety
boxes are recommended. Safe disposal of used sharp instruments should be ensured.

45
HEPATITIS E

Outbreaks took place: in April 2008, with 40 cases and no reported deaths, affect-
ing the districts of Ombella Mpoko, Lobaye and Basse Kotto; and in JulyOctober
2002. Further details are not available.
Chad
The following outbreaks were reported: starting January 2008 and still ongoing
as of end August 2008, with 934 cases and 9 deaths (CFR 0.96%) in the IDP camp
Dog Dor and in Goz Amir refugee camp (health district of Goz Beida); and in
JuneSeptember 2004, with 1 442 cases and 46 deaths (CFR 3.2%) in the refugee
camps of Goz Amer, Goz Abal and neighbouring villages in the south-eastern area.
HEPATITIS E
Description
Infectious agent
Single-stranded RNA virus. Man is the natural host, although antibodies have
been detected in primates and other animal species such as pigs and rodents.
Case definition I
In general, hepatitis E is a self limiting-illness followed by recovery. Prolonged
viraemia or faecal shedding are unusual and chronic infection does not generally
occur, but has been described in persons who have received organ transplants.
II
Fulminant forms of hepatitis may occasionally occur, with case-fatality ratios
ranging from 0.54%. The fulminant form of the disease occurs more frequently
during pregnancy and regularly induces a case-fatality ratio of 20% in the third
trimester.12
III
It is an acute illness typically including acute jaundice, dark urine, anorexia,
malaise, extreme fatigue and right upper quadrant tenderness. Biological signs
include increased urine urobilonogen and >2.5 times the upper limit of serum
IV
12 http://www.who.int/topics/hepatitis/en/.

46
alanine aminotransferase. Hepatitis E virus (HEV) cannot be distinguished reli-

ably from other forms of acute viral hepatitis except by specific serological testing.
Case classification
Suspected case: a case that is compatible with the clinical description.
Confirmed case: a suspected case that is laboratory-confirmed.
Laboratory-confirmed case: positive for IgM anti-HEV.13
Primarily faecaloral. Transmission is associated primarily with ingestion of
faecally-contaminated drinking-water. The potential for HEV transmission from
contaminated food is still under investigation, and there is no evidence of trans-

mission by percutaneous or sexual exposures.
Incubation period
The mean period has varied from 26 to 42 days in various epidemics (range 1564 days).
Unknown. HEV has been detected in stools 14 days after onset of jaundice, and
approximately four weeks after ingestion.
Epidemiology
General
Epidemic and sporadic cases of hepatitis E suggest a global distribution of multi-
ple strains of hepatitis E of varying pathogenicity. The global and national burden
are unknown.
Outbreaks and sporadic cases occur over a wide geographical area. Epidemics have
been reported in central and south-eastern Asia, northern and western Africa, and
in Mexico, especially where faecal contamination of drinking-water is common.
Seasonality
Perennial.
13 http://www.who.int/immunization_monitoring/diseases/hepatitis_surveillance/en/index.html.

47
Alert threshold
In the absence of a clear epidemic threshold, an epidemic should be suspected if:
multiple cases of confirmed disease are seen in a single geographical area;

deaths of pregnant women are reported with fever/jaundice syndrome.
Epidemics
The highest rates of infection occur in regions where low standards of sanitation
promote transmission.

Population movement increases the likelihood of contaminated water and low hygiene.
Overcrowding is highly significant, as it facilitates transmission.
Poor access to health services is also a risk factor.
Food shortages. Although they do not represent a direct risk factor, malnutrition
HEPATITIS E
increases gastrointestinal tract susceptibility to invasiveness of the organism and
the severity of disease.
Lack of safe water and poor sanitation. Overcrowding, lack of safe water, poor
hygiene and inadequate sanitation increase the risk of infection. The risk of epi-
demics of hepatitis E is high in camp settings. In endemic areas, the highest rates of
clinically evident disease occur in young to middle-aged adults. Lower disease rates I
in younger age groups may be the result of anicteric and/or subclinical infection.

Epidemic control II
Prevention and detection are the key, given that there is no known therapy to alter
the course of the disease and that it is spread by the faecaloral route. The mode
of transmission should be determined, the water supply investigated, populations
at increased risk should be identified, and sanitary and hygiene practices improved III
to eliminate contamination of food and water.
Prevention
Public water supplies should be protected, purified and chlorinated. Education IV
should be given to promote household-water treatment, sanitary disposal of faeces
and hand-washing after defecation and before handling.

48
Vaccines to prevent hepatitis E are under development, but none are yet com-
mercially available. Immune globulin prepared from plasma collected in HEV-
endemic areas has not been effective in preventing clinical disease during HEV
outbreaks. IG prepared from plasma collected from parts of the world where
HEV is not an endemic disease such as the United States of America is unlikely
to be effective.

49
HIV/AIDS

The prevalence of HIV in adults in CAR is among the highest in all of western
and central Africa, and is estimated by UNAIDS to be 6.3%, with large regional
variations. The prevalence has been as high as 11% in Bamingui-Bangoran (in
the north) and 14% in Haut-Mbomou (in the east), while it is about 3% or lower
in Basse-Kotto (in the south) Nana-Mambr and Ouham-Pend (both in the
west).14 The epidemic is becoming increasingly feminized with prevalence among
women almost double that of men (7.8% versus 4.3%). Information on prevalence
among at-risk populations such as injecting drug users or men having sex with
men is not available.
HIV and AIDS estimates, Central African Republic
HIV/AIDS
Adult (1549) HIV prevalence rate 6.3% (range: 5.96.7%)
Adults (15+) living with HIV 140 000 (range: 130 000150 000)
Adults (15+) and children living with HIV 160 000 (range: 150 000170 000)
Women (15+) living with HIV 91 000 (range: 85 00097 000)

I
AIDS deaths (adults and children) 11 000 (range: 950012 000)
Children aged 014 living with HIV 14 000 (range: 12 00016 000)
Source: Report on the global AIDS epidemic. Geneva, UNAIDS, 2008.
See also: UNAIDS epidemiological fact sheet: Central African Republic, 2008 update; http://www.who.int/global II
atlas/predefinedReports/EFS2008/full/EFS2008_CF.pdf; http://www.unaids.org/en/KnowledgeCentre/HIV
Data/Epidemiology/epifactsheets.asp.
Chad
III
The most recent estimated prevalence in the adult population is 3.5% with large
regional variations, generally higher in urban areas and lower in rural areas
(N'Djamena, 8%; eastern Logone, 9.8%). There is no information on prevalence
among injecting drug users or men having sex with men.
IV
14 Ministre de lconomie, du plan et de la coopration internationale de la Rpublique centrafricaine, 2007.

50
HIV and AIDS estimates, Chad
Adult (1549) HIV prevalence 3.5% (range: 2.44.3 %)
Adults (15+) living with HIV 180 000 (range: 110 000 - 220 000)
Adults (15+) and children living with HIV 200 000 (range: 130 000 - 240 000)
Women (15+) living with HIV 110 000 (range: 66 000 -130 000)
AIDS deaths (adults and children) 14 000 (range: 11 000 - 20 000)
Children aged 014 living with HIV 19 000 (range: 14 00 - 27 000)
Source: Report on the global AIDS epidemic. Geneva, UNAIDS, 2008.

See also: UNAIDS Epidemiological fact sheet: Chad, 2008 update; http://www.who.int/globalatlas/predefined
Reports/EFS2008/full/EFS2008_TD.pdf; http://www.unaids.org/en/KnowledgeCentre/HIVData/Epidemiology/
epifactsheets.asp; http://www.theglobalfund.org/programs/grantdetails.aspx?compid=614&grantid=249&lang
=en&CountryId=TCD; http://www.who.int/hiv/countries/en/index.html.
Description
Infectious agent
Human immunodeficiency virus (HIV). Two types have been identified: HIV-1
and HIV-2, with similar epidemiological characteristics. HIV-2 is less pathogenic
than HIV-1.
Case definition
Acquired immunodeficiency syndrome (AIDS) is the late clinical stage of HIV
infection, defined as an illness characterized by one or more indicator diseases.
WHO revised the staging system for HIV infection in 2006.15 The revised staging
system for adults and adolescents, and for children, is outlined below.
Revised WHO clinical staging of HIV/AIDS for adults and adolescents

Primary HIV infection
Asymptomatic infection;
acute retroviral syndrome.
15 WHO case definitions of HIV for surveillance and revised clinical staging and immunological classification of
HIV-related disease in adults and children, available at http://www.who.int/hiv/pub/guidelines/hivstaging/
en/index.html.

51
Clinical stage 1
Asymptomatic;
persistent generalized lymphadenopathy (PGL).
Clinical stage 2
Moderate unexplained weight loss (<10% of presumed or measured body
weight), recurrent respiratory tract infections (sinusitis, bronchitis, otitis media,
pharyngitis);
herpes zoster;
angular cheilitis;
recurrent oral ulcerations;
papular pruritus eruptions;
seborrheic dermatitis;
fungal nail infections of fingers.
Clinical stage 3
HIV/AIDS
Unexplained severe weight loss (>10% of presumed or measured body weight);
unexplained chronic diarrhoea for longer than one month;
unexplained persistent fever (> 37.6 C intermittent or constant, for longer
than one month);
I
persistent oral candidiasis;
oral hairy leukoplakia;
pulmonary tuberculosis (current);
severe bacterial infections (such as pneumonia, empyema, pyomyositis, bone II
or joint infection, meningitis or bacteraemia);
acute necrotizing ulcerative stomatitis, gingivitis or periodontitis;
unexplained anaemia (< 8 g/dl), neutropaenia (<0.5 109 per litre) or chronic
thrombocytopaenia (< 50 109 per litre).
III
Clinical stage 4
HIV wasting syndrome;
pneumocystis pneumonia;
IV
recurrent severe bacterial pneumonia;

52
chronic herpes simplex infection (orolabial, genital or anorectal of more than

one months duration or visceral at any site);
oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs);
extrapulmonary tuberculosis;
Kaposi sarcoma;
cytomegalovirus infection (retinitis or infection of other organs);
central nervous system toxoplasmosis;
HIV encephalopathy;
extrapulmonary cryptococcosis including meningitis;
disseminated non-tuberculous mycobacterial infection;
progressive multifocal leukoencephalopathy;

chronic cryptosporidiosis (with diarrhoea);
chronic isosporiasis;
disseminated mycosis (coccidiomycosis or histoplasmosis);
recurrent non-typhoidal Salmonella bacteraemia;
lymphoma (cerebral or B-cell non-Hodgkin) or other solid HIV-associated
tumours;
invasive cervical carcinoma;
atypical disseminated leishmaniasis;
symptomatic HIV-associated nephropathy or symptomatic HIV-associated
cardiomyopathy.
Revised WHO clinical staging of HIV/AIDS for children

Clinical stage 1
Asymptomatic;
persistent generalized lymphadenopathy (PGL).
Clinical stage 2
Unexplained persistent hepatosplenomegaly;
papular pruritic eruptions;
fungal nail infection;
angular cheilitis;
lineal gingival erythema;

53
extensive wart virus infection;

extensive molluscum contagiosum;
recurrent oral ulcerations;
unexplained persistent parotid enlargement;
herpes zoster;
recurrent or chronic upper respiratory tract infections (otitis media, otorrhoea,
sinusitis or tonsillitis).
Clinical stage 3
Unexplained moderate malnutrition or wasting not adequately responding to
standard therapy;
unexplained persistent diarrhoea (14 days or more);
unexplained persistent fever (above 37.5 C intermittent or constant for longer
than one month);
persistent oral candidiasis (after first 68 weeks of life);
oral hairy leukoplakia;
HIV/AIDS
acute necrotizing ulcerative gingivitis or periodontitis;
lymph node tuberculosis;
pulmonary tuberculosis;
severe recurrent bacterial pneumonia;
symptomatic lymphoid interstitial pneumonitis;
I
chronic HIV-associated lung disease including brochiectasis;
unexplained anaemia (< 8 g/dl), neutropaenia (< 0.5 109 per litre) and or
chronic thrombocytopaenia (< 50 109 per litre).
II
Clinical stage 4
Unexplained severe wasting, stunting or severe malnutrition not responding
to standard therapy;
pneumocystis pneumonia;
III
recurrent severe bacterial infections (such as empyema, pyomyositis, bone or
joint infection or meningitis but excluding pneumonia);
chronic herpes simplex infection (orolabial or cutaneous of more than one
months duration or visceral at any site);
IV
oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs);

54
extrapulmonary tuberculosis;
Kaposi sarcoma;
cytomegalovirus infection: retinitis or cytomegalovirus infection affecting
another organ,with onset at age older than 1 month;
central nervous system toxoplasmosis (after 1 month of life);
extrapulmonary cryptococcosis (including meningitis);
HIV encephalopathy;
disseminated endemic mycosis (coccidiomycosis or histoplasmosis);
disseminated non-tuberculous mycobacterial infection;
chronic cryptosporidiosis (with diarrhoea);
chronic isosporiasis;
cerebral or B-cell non-Hodgkin lymphoma;
progressive multifocal leukoencephalopathy;
symptomatic HIV-associated nephropathy or HIV-associated cardiomyopathy.
Laboratory evidence of HIV

HIV testing is most commonly done by detecting HIV antibody in serum samples
using enzyme-linked immunosorbent assay (ELISA, or enzyme immuneassay,
EIA). After infection, there is a period called the window period during which
the body starts to produce antibodies, but the levels are too low to be detected by
current HIV tests. However, during this time the virus replicates actively and
HIV infection can be transmitted. This window period lasts about 3 months.
When the HIV antibody test is positive by ELISA or EIA, it must be confirmed with
another test of higher specificity such as the Western blot, the indirect fluorescent
antibody (IFA) test or a second ELISA test that is methodologically and/or anti-
genically independent of the first.
The rapid tests that are recommended by WHO have been evaluated at WHO
collaborating centres and have levels of sensitivity and specificity comparable to
those of WHO-recommended ELISA tests. The use of rapid HIV tests affords
several advantages in emergency and disaster settings including:
Rapid tests that do not require refrigeration will be more suitable for remote
and rural areas and sites without a guaranteed electricity supply. Long shelf-
life is also important, especially for remote areas and sites where relatively few
tests are performed.

55
Many rapid tests require no laboratory equipment and can be performed in

settings where electrical and water supplies need not be guaranteed.
Some rapid tests can detect HIV antibodies in whole blood (finger-prick
samples) as well as serum/plasma, and testing may therefore be performed
by non-laboratory personnel with adequate training and supervision.
Sexual intercourse (vaginal or anal) with an infected partner, especially in
presence of a concurrent ulcerative or non-ulcerative sexually transmitted
infection (STI). The primary route of HIV infection is heterosexual.
Infected mother to her child during pregnancy, labour and delivery or
through breastfeeding.
Transfusion of infected blood or blood products.
Contaminated needles, syringes, other injecting equipment and injecting
solutions (contamination often occurs when drug solutions are mixed or when
multiple users draw up solutions from a single container), through accidental
injury of patients or service providers in occupational health, or those who
are injecting drug users.
HIV/AIDS
Incubation
Variable. On average, the time from HIV infection to clinical AIDS is 810 years,
although AIDS may be manifested in less than 2 years or be delayed in onset beyond
10 years. Incubation times are shortened in resource-poor settings and in older patients. I
Any person who is infected with HIV, even when asymptomatic, may transmit
the infection to another person through the routes of transmission described
above. Infectiousness is observed to be high during the initial period after infec-
II
tion. Studies suggest infectiousness increases with the viral load (number of viral
elements in the blood), which is high during the initial stage of contamination
and also later when AIDS develops, with increasing immune deficiency, clinical
symptoms and presence of opportunistic infections. III
Epidemiology
General
IV
Sub-Saharan Africa remains the worst-affected region in the world. With just over
10% of the worlds population, it is home to more than 60% of all people living

56
with HIV. At the end of 2006, 25.8 million people in sub-Saharan Africa were
living with HIV. In 2005, an estimated 3.2 million people in the region became
newly infected, while 2.4 million adults and children died of AIDS.16 Around 59%
of all adults living with HIV in sub-Saharan Africa are women (13.2 million).
Sexual violence. Displaced persons are often physically and socially powerless,
with women and children at particular risk of sexual coercion, abuse or rape.
Sexual violence carries a higher risk of infection because those violated cannot
protect themselves from unsafe sex, and because the virus can be transmitted
more easily if body tissues are torn during violent sex.
Sex work. The need to exchange sexual favours for survival and ensuring basic
needs, such as money, shelter, security, etc., is common in or around refugee camps
and inevitably involves both the refugee and host communities. Both sex workers
and clients are at risk of HIV infection if unprotected sex is practised.
Injecting drug use. In the typical conditions of an emergency, it is highly likely
that drug injectors will be sharing needles, a practice that carries a very high risk
of HIV transmission if one of the people sharing is infected.
Unsafe blood transfusions. Transfusion with HIV-infected blood carries an almost
100% risk of transmitting the virus. In emergency situations, when regular trans-
fusion services have broken down, it is particularly difficult to ensure blood safety.
It is important to avoid unnecessary blood transfusions and to ensure that blood
is tested for HIV and other bloodborne pathogens.
Adolescent health. Children in camp settings may have few occupations, below-
average schooling and education opportunities, and are thus more exposed than
children in other situations.
Global.
Seasonality
Not applicable.
Alert threshold
One suspected case must be investigated.
16 UNAIDS estimates available at: http://www.unaids.org/en/Regions_Countries/default.asp).

57

Population movement
In emergency situations, population movement often causes a breakdown in
family and social ties and erodes traditional values and coping strategies. It may
result in lack of privacy and high-risk sexual behaviour, but may also increase
sexual violence. Lack of information and education, and shortages of basic com-
modities for preventing HIV such as condoms in such settings, may also increase
the risk of HIV transmission.
Overcrowding
Groups with differing levels of HIV awareness and of HIV prevalence are often
placed together in temporary and sometimes overcrowded locations, or are in
contact with surrounding populations such as in refugee camps, where there is
greater potential for sexual contact. Overcrowding may also influence patterns of
injecting drug use and result in an increased risk of contaminated injection equip-
ment being shared (this has been noted in refugee camps).
HIV/AIDS
Poor access to health services
People already infected with HIV are at greater risk of physical deterioration
during an emergency because:
the health-care system may break down (attacks on health centres, inability
to provide supplies, flight of health-care staff);
I
caregivers may be killed or injured during an emergency, leaving behind chil-
dren already made vulnerable by infection with HIV/AIDS or loss of parents
to AIDS;
populations have limited physical access to health facilities owing to roads
II
being blocked;
the financial resources required to maintain basic services are more limited
than usual;
III
they are more likely to suffer from disease and death as a consequence of
limited access to food, clean water and good hygiene as a result of weakened
immune systems;
there may be stigma and discrimination towards AIDS patients;
IV
basic commodities and HIV services, condoms, education and communica-
tion, testing and counselling services are lacking;

58
accessing ARV drugs is difficult as separate procurement systems are needed,

ART drugs needs and regimen may vary, and their shelf-life is limited.
Without adequate medical services, STIs, if left untreated in either partner, greatly
increase the risk of acquiring HIV. Important materials for HIV prevention, par-
ticularly condoms, are likely to be lacking in an emergency situation. In emergency
situations, services for drug-dependence treatment usually do not exist, and access
to sterile injection equipment will be less likely.
Food shortages
The need for food is paramount in emergency situations, so that exchanging
sex for money to buy food and other essentials may occur. HIV/AIDS patients
have greater nutritional requirements and will suffer the consequences of food
shortages more rapidly and severely.
People living with HIV/AIDS are in need of a balanced diet with extra energy
compared to the needs of a person who is not infected.
Energy requirements are likely to increase by 10% to maintain body weight
and physical activity in asymptomatic HIV-infected adults, and growth in
asymptomatic children.
During symptomatic HIV, and subsequently during AIDS, energy require-
ments increase by approximately 2030% to maintain adult body weight.
Energy intakes need to be increased by 50100% above normal requirements
in children experiencing weight loss.
The quality of the diet plays a key role in alleviating the side-effects of HIV
(e.g. diarrhoea, nausea, sore mouth, etc.) as well as the side-effects of ARTs
(metabolic side-effects such as insulin resistance, hyperlipidaemia, etc.).

Prevention
Reduce sexual transmission
Awareness and life-skills education, especially for young people, to ensure
that everyone is well informed: of what does, and does not, constitute a mode
of transmission; of how and where to acquire condoms free of charge and
medical attention if necessary; and of basic hygiene principles.
Condom promotion to ensure that good quality condoms are freely available to
those who need them, using culturally sensitive instructions and distribution.

59
STI management, including for sex workers, using the syndromic STI man-
agement approach, with partner notification and promotion of safer sex.
Reduce mother-to-child transmission of HIV

Most children living with HIV acquire the infection through mother-to-child
transmission (MTCT), which may occur during pregnancy, labour, delivery
or during breastfeeding.
The risk of MTCT may be reduced to under 2% by interventions that include:
antiretroviral (ARV) prophylaxis given to women during pregnancy and
labour and to the infant in the first weeks of life;
obstetric interventions including elective caesarean delivery (prior to the
onset of labour and rupture of membranes), and complete avoidance of
breastfeeding;
where elective caesarean delivery is not possible, avoidance of unnecessary
obstetrically invasive procedures, such as artificial rupture of membranes
or episiotomy.
HIV/AIDS
In the absence of any intervention, the risk of MTCT is 1530% in non-
breastfeeding populations. Breastfeeding by an infected mother increases the
risk by 520% to a total of 2045%.
In many resource-constrained and emergency settings, elective caesarean
delivery is seldom feasible and it is often neither acceptable nor safe for mothers I
to refrain from breastfeeding. In these settings, the efforts to prevent HIV infec-
tion in infants initially focused on reducing MTCT around the time of labour
and delivery, which accounts for between one third and two thirds of overall
transmission.
II
Many countries with a heavy burden of HIV have recently adopted more effec-
tive ARV regimens, beginning in the third trimester of pregnancy, which may
reduce the risk of transmission during pregnancy and childbirth to 24%.
Even when these regimens are used, however, infants remain at substantial III
risk of acquiring infection during breastfeeding. Where feasible, acceptable,
affordable, sustainable and safe methods are available, infant-feeding practices
should be modified. Otherwise, exclusive breastfeeding for the first months
of life is recommended.
IV
The primary prevention of HIV among women, especially young women,
should be emphasized.

60
Unintended pregnancies among HIV-infected women should be avoided, and

family planning methods promoted, particularly in women who are infected
with HIV.
Blood safety
HIV testing of all transfused blood.
Avoid non-essential blood transfusion.
Recruitment of safe blood-donor pool.
Prevention among injecting drug users

Ready access to sterile needles, syringes and other injection equipment (and
disposal of used equipment).

HIV risk-reduction education and counselling for injecting drug users (includ-
ing peer outreach when possible).
Drug-dependence treatment services, including substitution treatment (e.g.
methadone) where possible.
Access to STI and HIV/AIDS treatment for injecting drug users.
Universal precautions
Washing hands thoroughly with soap and water, especially after contact with
body fluids or wounds.
Using protective gloves and clothing when there is risk of contact with blood
or other potentially infected body fluids.
Safe handling and disposal of waste material, needles and other sharp instru-
ments. Proper cleaning and disinfection of medical instruments between patients.
Physical protection
The protection of the most vulnerable, especially women and children, from vio-
lence and abuse is not only an important principle of human rights but is also
essential for reducing the risk of HIV infection.
Protecting health-care workers

In order to reduce nosocomial transmission, health workers should strictly adhere
to universal precautions with all patients and laboratory samples whether or not
they are known to be infected with HIV. Health-care workers should have access
to voluntary counselling, testing and care. Often, health workers deployed in com-

61
plex emergencies experience significant occupational stress and those tested, as

part of the management of occupational exposures, will require additional support.
Voluntary counselling and testing programmes

The establishment of voluntary counselling and testing services to help individuals
make informed decisions about HIV testing should be considered when relative
stability is restored. At times, people are coerced into testing or are required to
make decisions about testing when they are suffering acute or post-traumatic
stress disorders.
As displaced persons are often tested before resettlement in other countries, it is
critical that they receive counselling on the legal and social implications of the
test. Often, migration or temporary residency status is contingent on the appli-
cant having HIV-antibody seronegative status.
Post-test counselling is essential for people with both seronegative and seropositive
results. Displaced persons and conflict survivors who are already traumatized
will require additional psychosocial support if they test seropositive. Typically,
the support networks of displaced persons are disrupted, and suicide risk assess-
HIV/AIDS
ment therefore forms an important part of post-test counselling in a refugee or
conflict context.
Testing of orphaned minors should be carried out with the consent of their official
guardians, only where there is an immediate health concern or benefit to the child.
There should be no mandatory screening before admittance to substitute care. I
Immunization
Asymptomatic HIV-infected children should be immunized with the Expanded
Programme on Immunization (EPI) vaccines. II
Symptomatic HIV-infected children should not receive either BCG or yellow
fever vaccine.
Case management
III
The three main interventions are:
1. post-exposure prophylaxis (PEP) and prevention of mother-to-child trans-

mission (PMTCT);
2. antiretroviral therapy (ART);
IV
3. nutritional care.

62
(1) Provision of antiretrovirals (ARVs) for prevention

ARVs can prevent HIV infection in exposed individuals. Prophylactic interven-
tions include the prevention of mother-to-child transmission (PMTCT) and
post-exposure prophylaxis (PEP).
When conditions allow provision of ARV for prevention, the minimum criteria
for eligibility for PMTCT and PEP are based on a defined risk of exposure to
HIV.17
(2) Antiretroviral therapy (ART)

ART programmes in resource-poor settings have efficacy rates similar to those
reported for developed countries. Country-specific national guidelines on use of

ART should be implemented if they exist.
Efforts to increase nationwide coverage of voluntary counselling and testing, pre-

and post-test counselling, prevention of STIs and reproductive health services
should be intensified.
ART results in improvement in clinical status and brings about effective reversal
of the clinical stage in patients with symptomatic disease.
1. When should ART be started?

The WHO classification of HIV-associated clinical disease has recently been re-
vised in order to provide greater consistency between the adult and paediatric
classification systems. Clinical staging is intended for use in emergency and
crisis situations after HIV infection has been confirmed by HIV-antibody test-
ing. It should form part of the baseline assessment (first visit) on entry into a care
and treatment programme and is used to guide decisions on when to start co-
trimoxazole prophylaxis and when to start and switch to ART in situations where
CD4 testing is not available. The following table provides recommendations for
initiating ART.
17 Please refer to: Mother-to-child transmission of HIV (http://www.who.int/hiv/topics/mtct/en/index.html);

Post-exposure prophylaxis to prevent HIV infection: joint WHO/ILO guidelines for the use of occupational
and non-occupational post-exposure prophylaxis (PEP) to prevent human immunodeficiency virus (HIV)
infection (http://www.who.int/hiv/pub/guidelines/PEP/en/index.html); Summary report of the joint ILO/
WHO technical meeting for the development of policy and guidelines on occupational and non-occupational
post-exposure prophylaxis for HIV infection (HIV-PEP); Occupational post-exposure prophylaxis for HIV:
a discussion paper; Post-exposure prophylaxis following non-occupational exposures.

63
Recommendations for initiating ART in adults and adolescents according

to clinical stages and the availability of immunological markers
WHO clinical Classification CD4 testing not available CD4 testing available
staging
1 Asymptomatic Do not treat Start treatment if CD4 count

< 200 cells/mm3
2 Mild Do not treat Start treatment if CD4 count

< 200 cells/mm3
3 Advanced Treat Consider treatment if CD4 < 350

cells/mm3 and initiate ART before
CD4 count drops below 200
cells/mm3
4 Severe Treat Treat irrespective of CD4 cell count
After a patient has been tested HIV-positive and shows symptoms of AIDS (see
Case definition/clinical staging above), the process of initiating ART involves
HIV/AIDS
assessing patient readiness to commence therapy and understanding its implications
(lifelong therapy, adherence, toxicities). Support from family and peer support
from individuals (treatment buddy) groups is critical when ART is initiated, as
adherence to treatment is difficult but essential to the treatment efficacy, but also
to prevent drug resistance. I
High-quality care and support to all people living with HIV/AIDS (PLWHA)
includes counselling, psychosocial and nutritional support, treatment for oppor-
tunistic infections (e.g. TB) and palliative care. Importantly, PLWHA should be
supported to live normal and productive lives that are free of stigmatization and II
discrimination.
Current WHO recommendations require that the first-line regimen for adults
and adolescents contain two nucleoside reverse transcriptase inhibitors (NRTIs) III
plus one non-nucleoside reverse transcriptase inhibitor (NNRTI) (see the figure
below). This first-line regimen, based on a combination of two NRTIs plus one
NNRTI, is efficacious, generally less expensive than other regimens, has generic
formulations, is often available as fixed-dose combinations (FDCs) and does not
IV
require a cold chain. In addition, it preserves a potent new class of drugs (protease
inhibitors) for second-line treatments.

64
First-line ARV drugs for adults and adolescentsa
Preferential two NRTIs/NNRTI approachb
AZT c or d4T EFV

3TC ou FTC
TDF c or ABC NVP
Triple NRTI approachd
AZT: zidovudine, D4T: stavudine; TDF: tenofovir; ABC: abacavir; 3TC: lamivudine; FTC: emtricitabine;
EFV: efavirenz; NVP: nevirapine
a These recommendations should be used with consideration of any country-specific national guidelines for
ARV treatment that have been developed.

b Preferential two NRTIs/NNRTI approach is based upon a combination of three drugs: two NRTIs combined
with either NVP or EFV as the NNRTI.
c Preferred NRTI to be combined with 3TC or FTC in standard first-line regimens.
d Triple NRTI approach (i.e. three NRTI drugs selected only from the options shown within the dotted circle)
may be considered as an alternative for first-line regimens in situations where NNRTI options provide
additional complications (e.g. women who have CD4 counts between 250 and 350 cells/mm3, viral hepatitis
coinfection, TB coinfection, severe reactions to NVP or EFV, and HIV-2 infection).
There are various precautions that must be observed:
Monotherapy or dual therapy should not be used to treat chronic HIV infection;
they may be used only in the setting of PMTCT and post-exposure prophylaxis.
Certain dual NRTI backbone combinations should not be used within three-
drug therapy. These are d4T + AZT (proven antagonism), d4T + didanosine
(overlapping toxicities) and 3TC + FTC (interchangeable, but should not be
used together).
The combinations of TDF + 3TC + ABC and TDF + 3TC + didanosine select
for the K65R mutation and are associated with high incidences of early viro-
logical failure.
The combinations of TDF + didanosine + any NNRTI are also associated with
high rates of early virological failure.
The use of didanosine should be reserved for second-line treatment, in which
situation it is possible to consider TDF + didanosine with boosted protease
inhibitor (PI), provided that caution and close monitoring are practised.
2. When should a first-line regimen drug be replaced by another?

Patients may experience toxic side effects or intolerance and be prescribed another
drug from the first-line regimen. The toxicities of first-line ARVs and recommended

65
drug substitutions are provided in the table below. Another example would be the
need to substitute Efavirenz for pregnant women.
Toxicities of first-line ARVs and recommended drug substitutions
ARV drug Common associated toxicity Suggested substitute
ABC Hypersensitivity reaction AZT or TDF or d4T
AZT Severe anaemiaa or neutropeniab TDF or d4T or ABC

Severe gastrointestinal intolerancec
Lactic acidosis TDF or ABCd
d4T Lactic acidosis TDF or ABCd

Lipoatrophy/metabolic syndromee
Peripheral neuropathy AZT or TDF or ABC
TDF Renal toxicity AZT or ABC or d4T

(renal tubular dysfunction)
EFV Persistent and severe central nervous NVP or TDF or ABC (or any PI)h
system toxicityf
HIV/AIDS
Potential teratogenicity (first trimester of NVP or ABC (or any PI)h
pregnancy or women not using adequate
contraception)
NVP Hepatitis EFV or TDF or ABC (or any PI)h
Hypersensitivity reaction TDF or ABC (or any PI)h I

Severe or life-threatening rash
(Stevens-Johnson syndrome)g
a Exclude malaria in areas of stable malaria; severe anaemia (grade 4) is defined as Hb < 6.5 g/dl.
b Defined as neutrophil cell count < 500/mm 3 (grade 4).
II
c Defined as severe, refractory gastrointestinal intolerance that prevents ingestion of ARV drug regimen
(e.g. persistent nausea and vomiting).
d Reinitiation of ART should not include d4T or AZT in this situation. TDF or ABC is preferred.
e Substitution of d4T may not reverse lipoatrophy.
f E.g. persistent hallucinations or psychosis. III
g Severe rash is defined as extensive rash with desquamation, angioedema, or a reaction resembling serum
sickness; or a rash with constitutional findings such as fever, oral lesions, blistering, facial oedema or
conjunctivitis; Stevens-Johnson syndrome can be life-threatening. For life-threatening rash, substitution
with EFV is not recommended, although this approach has been reported in a small number of patients in
Thailand without recurrence of rash. IV
h PI class should be preferentially reserved for second-line therapy as no potent regimens have been identi-
fied for recommendation following initial PI failure.

66
3. When should a first-line regimen be replaced by a second-line regimen?

A change from a first- to a second-line regimen should be made when there is
treatment failure and symptoms of AIDS develop while the patient has been taking
ART first-line medicines consistently.
Detailed recommendations for switching to second-line ARV regimens are given
the table below, indicating the second-line strategies to be considered in adoles-
cents and adults who experience failure of the first-line regimens described above.
The availability of second-line ARV drugs is a challenge as these drugs are more
expensive, most need refrigeration and the procurement process is difficult. In
emergency settings, second-line regimens may not be available.
Detailed recommendations for switching to second-line ARV regimens in

adults and adolescents
First-line regimen Second-line regimen
RTI component PI componenta
Standard strategy AZT or d4T + 3TCb + NVP or EFV ddI + ABC or

TDF + ABC or
TDF + 3TC ( AZT)c
TDF + 3TCb + NVP or EFV ddI + ABC or

ddI + 3TC ( AZT)c PI/rd
ABC + 3TCb + NVP or EFV ddI + 3TC ( AZT)c or

TDF + 3TC ( AZT)c
Alternative strategy AZT or d4T + 3TCb + TDF or ABC EFV or NVP ddI
a NFV does not need refrigeration and may be used as a PI alternative in settings without a cold chain.
b 3TC and FTC are considered interchangeable because they are structurally related and share pharmaco-
logical properties and resistance profiles.
c 3TC may be considered to be maintained in second-line regimens to potentially reduce viral fitness, confer
residual antiviral activity and maintain pressure on the M184V mutation to improve viral sensitivity to AZT
or TDF. AZT may prevent or delay the emergence of the K65R mutation.
d There are insufficient data to detect differences among currently available RTV-boosted PIs (ATV/r, FPV/r,
IDV/r, LPV/r and SQV/r) and the choice should be based on individual programme priorities. In the
absence of a cold chain, NFV may be employed as the PI component but it is considered less potent than an
RTV-boosted PI.
(3) Nutritional care for people living with HIV/AIDS

Nutritional care plays a key role in the care of people living with HIV. Nutritional
care should include support to the patient and care providers to obtain the correct

67
quantities of food, and individual nutrition counselling should be given to patients

and their caregivers in order to improve the quality of feeds. Nutritional care and
support is important to alleviate the side-effects of HIV/AIDS as well as the side-
effects of ARTs.
4. When and how should ART be stopped?

If a patient has exhausted all available antiretroviral and opportunistic treatment
options and is clearly in a terminal condition because of advanced HIV infection
or has distressing or intolerable side-effects of therapy, it is reasonable to stop giving
ARVs and institute an active palliative and end-of-life care plan.
In case of an emergency or disaster where drug shortages are likely, patients
should be given strategies to help manage a treatment disruption. It is important
through education and adherence counselling to prevent alterations in the drug
regime such as change in dosages, irregular treatment, or drug sharing.
If ARV supplies are running out, the treatment should be stopped completely.
Patients should be informed not to conserve medications, change dosing regimens,
and to avoid acquiring ARVs from unofficial sources, as the quality of the drugs
HIV/AIDS
cannot be guaranteed.
In case of treatment disruption of a treatment regimen including nevirapine or
efavirenz experts recommend to supply patients with an additional supply of seven
days of the two other drugs of the treatment, nucleoside reverse transcriptase
inhibitor (NRTI) drugs, e.g. lamivudine (3TC) and stavudine (D4T) or 3TC and I
zidovudine (ZDV). This wash-out treatment period with two NRTI drugs is
intended to cover the time it takes for the non-nucleoside reverse transcriptase
inhibitors (NNRTIs) to be eliminated from the system, as NNRTIs last longer in
the bloodstream. For other regimens, should the treatment be discontinued, it
II
should be stopped as soon as any drug is missing and patients should be trained
not to take the remaining doses of incomplete treatment.
References III
1. WHO HIV/AIDS guidelines (http://www.who.int/hiv/pub/en/index.html http://www.who.int/
hiv/pub/guidelines/en/).
2. Antiretroviral therapy for HIV infection in adults and adolescents in resource-limited settings:
towards universal access recommendations for a public health approach. Geneva, World Health IV
Organization, 2006 (http://www.who.int/hiv/pub/guidelines/WHO%20Adult%20ART%20
Guidelines.pdf).

68
3. Antiretroviral drugs for treating pregnant women and preventing HIV infection in infants in
resource-limited settings: towards universal access recommendations for a public health
approach. Geneva, World Health Organization, 2006 (http://www.who.int/hiv/pub/guidelines/
WHOPMTCT.pdf).
4. Integrated Management of Adolescent and Adult Illness (IMAI) modules. Geneva, World Health
Organization, 2006 (http://www.who.int/3by5/publications/documents/imai/en/index.html).
5. Policy and programming guide for HIV/AIDS prevention and care among injecting drug users.
Geneva, World Health Organization, 2005 (http://www.who.int/hiv/pub/prev_care/policy
programmingguide.pdf).
6. On-line toolkit for HIV testing and counselling. Geneva, World Health Organization, 2004
(http://who.arvkit.net/tc/en/index.jsp).
7. HIV and infant feeding: a framework for priority action. Geneva, World Health Organization,
2003 (http://www.who.int/hiv/pub/mtct/en/HIVandInfantFeeding.pdf).
8. Living well with HIV/AIDS. A manual on nutritional care and support for people living with
HIV and AIDS. FAO/WHO, 2002 (http://www.fao.org/docrep/005/y4168e/y4168e00.htm).
9. The public health approach to STD control: technical update. Geneva, UNAIDS, 1998
(http://www.who.int/hiv/pub/sti/en/stdcontrol_en.pdf).

69
INFLUENZA (SEASONAL)

No country data are available for the Central African Republic and Chad.
Description
Infectious agent
Influenza viruses A, B and C: influenza virus A that has multiple subtypes, of
which two (H1N1 and H3N2) are currently circulating widely among humans;
other influenza A subtypes of animal origin (16 HA and 9 NA subtypes), of which
several (H5, H7 and H9) have caused sporadic human infections in some countries.
Case definition
Clinical case definition
A person with rapid onset of fever of >38 C and cough or sore throat in the ab-
sence of other diagnoses. Diagnosis can be made on the basis of epidemiological
characteristics: cases with similar clinical presentation usually cluster or form an
epidemic typically with short intervals between case onset (14 days). The positive
predictive value of this case definition is highest when influenza is circulating in
the community (and is higher in adults or adolescents than in young children). I
Case classification
Suspected: a case that meets the clinical case definition.
Confirmed: a case that meets the clinical case definition and is laboratory- II
confirmed.
Laboratory criteria for diagnosis

Laboratory confirmation of influenza infection may be done by isolation of viruses III
from throat, nasal or nasopharyngeal secretions or tracheal aspirate of washings
using cell culture or in embryonated eggs; direct identification of viral antigens in
nasopharyngeal cells and fluids (FA test or ELISA); rapid diagnostic test; or viral
RNA amplification. Demonstration of a 4-fold or greater rise in specific antibody IV
titre between acute and convalescent sera may also be used to confirm acute infec-
tion. Ideally, respiratory specimens should be collected as early in the illness as

70
possible. Virus shedding starts to wane by the third day of symptoms, and in most
cases the virus is not detected after 5 days in adults, although virus shedding may
occur for a longer period in children.
Antigen detection in respiratory specimens

(1) Rapid diagnostic tests (for A and B seasonal influenza). Near-patient tests, or
point-of-care rapid testing (enzyme immunoassays or neuraminidase assay) are
commercially available. In general, the sensitivity of rapid tests is variable (median
7075%) and lower than that of cell culture, while their specificity is high (median
9095%). Because of the low sensitivity, false-negative results are a major concern
with these tests. Results are available within 1530 minutes.
(2) Polymerase chain reaction (PCR). RT-PCR assays detect both viable and non-
viable influenza virus RNA and are in general more sensitive than culture. Results
can be available within a few hours.
(3) Virus culture. This is considered as the gold standard. WHO provides stand-
ardized reagents to test the viruses. It is critical to provide information regarding
circulating influenza subtypes and strains. This is needed to guide decisions re-
garding influenza treatment and chemoprophylaxis and to formulate vaccine for
the coming year. It takes 210 days.
Antibody detection in serum specimens is rarely useful in immediate clinical
management and is used rather for retrospective diagnosis. It may be used for
epidemiological purposes (detection of start of seasonal outbreak, studies). An
antibodies titre 4-fold rise between an acute and a convalescent serum suggests
a recent infection (paired samples collected at least two weeks apart).
Influenza may be diagnosed clinically by typical symptoms during a recognized
seasonal epidemic period when reliable surveillance data are available.
The transmission of human influenza viruses occurs through exposure to large
particle (>5 m) respiratory droplets at distances closer than 1 m and through
direct, and perhaps indirect, contact (e.g. fomites, with hand contamination and
self-inoculation into nose or eye). Some evidence indicates that airborne trans-
mission over 1 m is possible. The relative contributions and clinical importance of
the different modes of influenza transmission are currently unknown. Incubation
takes between 17 days (usually 2 days) for a person to develop symptoms.

71
The patient may have detectable virus and possibly be infectious from 12 days
before onset of symptoms. Infectiousness may last for up to 7 days after onset of
illness in adults (perhaps longer if infection is caused by a novel virus subtype),
and for up to 21 days after onset in children aged < 12 years.
Epidemiology
The influenza virus circulates globally.
Seasonality
In some tropical countries, viral circulation occurs year-round with peaks during
rainy seasons. In temperate countries, influenza epidemics peak during winter
months. High attack rates (47.4%) with a case-fatality rate of 1.5% were reported
during seasonal influenza epidemics in the Democratic Republic of the Congo
and Madagascar in 2002. In Madagascar, despite rapid intervention within three
months, more than 27 000 cases and 800 deaths were reported.18
Alert threshold
An increase in the number of cases above what is expected for a certain period of
the year or any increase in cases of fever of unknown origin should be investigated,
after eliminating other causes. Accumulated surveillance data are required to
I
determine the threshold. Currently, no such data are available for CAR and Chad.
Risk factors for increased burden II

Population movement is a risk factor, because of the influx of non-immune pop-
ulations into areas where the virus is circulating, or of infected individuals into
areas with immunologically naive population.
Overcrowding with poor ventilation facilitates transmission and rapid spread. III
Poor access to health services. Prompt identification, isolation and treatment of
the cases (especially treatment of secondary bacterial pneumonia by antimicrobials)
are the most important control measures (see section on Case management).
IV
18 See: http://www.who.int/docstore/wer/pdf/2003/wer7813.pdf.

72
Without proper treatment, the case-fatality rate of complicated infection in people

with chronic underlying conditions can be high. Most vulnerable populations
are infants and young children, the elderly (65 years and above) and those who
are chronically immunocompromised, including the malnourished.
Food shortages. Low birth weight, malnutrition, vitamin A deficiency and poor
breastfeeding practices are likely to be important risk factors for infection and
development of the disease, and complications may prolong the duration of illness.
Lack of safe water and poor sanitation may reduce hand-washing practices and
facilitate spread.
Other factors. Lower temperatures and dry conditions contribute to longer virus
survival in the environment. Low temperatures may also lead to crowded living
conditions that may result in increased transmission (home confinement, increased

proximity of individuals indoors, with insufficient ventilation of living spaces).
Smoking is a risk factor for complications and prolonged illness.
Immunocompromised individuals. Depending on how severely the individual is
affected, viral replication could be protracted (weeks to, rarely, months). Complica-
tions are more frequent, and the likelihood of increased risk of antiviral resistance
emergence during, and potentially enduring after, drug administration is higher.
Influenza infection itself may transiently depress cellular immune function, so
that there is a potential risk for increased activity of HIV and possibly of reacti-
vation of latent infections (such as tuberculosis).
Risk assessment conclusions. Little is known about the burden of human influenza
in Africa, and it may vary depending on the country and its geographical situation.
There could be severe health consequences in poorly nourished, densely crowded
populations with limited access to adequate health care.

Case management
Early recognition, isolation of symptomatic patients and appropriate treatment
of complicated cases are important.
For most people, influenza is a self-limiting illness that does not require specific
treatment. Aspirin and other salicylate-containing medications should be avoided
in children and adolescents aged < 18 years in order to avoid the risk of a severe
complication known as Reye syndrome. Paracetamol may be used for management
of fever as clinically indicated.

73
Antiviral drugs may be used for specific and early treatment. M2 inhibitors
(amantadine or rimantadine for influenza A only if the circulating virus is proven
to be susceptible by local surveillance) and neuraminidase inhibitors (oseltamivir
or zanamivir for influenza A and B) given within the first 48 hours, may reduce
symptoms and virus shedding. Neuraminidase inhibitors also reduce complica-
tions that need antibiotics and lead to hospitalization.
Antiviral resistance to treatment is more likely to develop with the use of M2

inhibitors. Therefore, where possible, neuraminidase inhibitors should be selected
for treatment provided that they are registered for use in the country. If supplies
are limited, antiviral treatment should be reserved for patients at high risk of
complication (e.g. the elderly or those with underlying chronic conditions).
Neuraminidase inhibitors seem to have less frequent and less severe side-effects,
and are generally better tolerated than M2 inhibitors.
Patients should be monitored for the development of bacterial complications. Only
then should antibiotics be administered accordingly. Other supportive therapies
such as rehydration may be needed.
Isolation is impractical in most circumstances because of the highly transmissible

nature of the virus and the delay in diagnosis. However, ideally all persons admitted
to a hospital with a respiratory illness, including suspected influenza, should be
placed in single-patient rooms or, if not available, placed in a room with patients
who have a similar illness (cohorting). When cohorting is used, adequate spacing
I
between beds should be provided for droplet precautions. For influenza, isolation
should continue for the initial 57 days of illness, and possibly longer for patients
who are severely immunocompromised and who may be infectious for longer
periods. Both standard and droplet precautions are recommended.
II
There is no need to adapt dosages for the elderly for the neuraminidase inhibitor
oseltamivir. However, dosage should be adapted for people suffering moderate renal
failure (creatinine clearance <30 ml/min). Oseltamivir should not be adminis- III
tered to any person who has experienced an allergic reaction to the drug in the
past or to pregnant women unless clinical circumstances indicate necessity (note
lack of data on safety in this population). Nursing mothers are advised to refrain
from breastfeeding during treatment. IV

74
Neuraminidase inhibitor
Oseltamivira treatment schedules
Age Dosage Duration
Adults 75 mg twice a day 5 days
Childrenb
15 kg 30 mg twice a day 5 days
> 15 kg to 23 kg 45 mg twice a day 5 days
> 23 kg to 40 kg 60 mg twice a day 5 days

> 40 kg 75 mg twice a day 5 days
Doses should be reduced for individuals with decreased renal function.
a Use in children < 1 year of age has not been approved.

b Children 1 year of age or older require weight-adjusted doses.
M2 inhibitors: amantadine and ramantadine

Amantadine treatment schedules
Weight and/or age Dosage Duration
19 years (up to 45 kg) 5 mg/kg/day in two divided doses up 5 days

to a maximum of 150 mg/day
1065 yearsa (over 45 kg) 100 mg twice a day 5 days
> 65 years 100 mg once a day 5 days
a In some jurisdictions, a once-daily dose of 100 mg is recommended, e.g. the recommended regimen in the
British National Formulary (BNF) and in Japan is 100 mg for patients > 10 years. Doses should be reduced
for individuals with decreased renal function as shown below.
Creatinine clearance (ml/min/1.73m 2) Dose

3050 200 mg first day and 100 mg each day thereafter
1529 200 mg first day and 100 mg on alternate days
< 15 200 mg every 7 days
The recommended dosage for patients on haemodialysis is 200 mg every 7 days.
Amantadine should be used with caution in patients receiving treatment with neuropsychiatric drugs and
patients with seizure disorders, where the potential risks outweigh the benefits. This drug should not be used
by women who are breastfeeding.

75
Rimantadine treatment schedules
Age Dosage Duration
112 yearsa 5 mg/kg/day in two divided doses up 5 days

to a maximum of 150 mg/day
1364 years 100 mg twice daily 5 days
65 years and over 100 mg once a day 5 days
Doses should be reduced for individuals with decreased renal function. Use with caution in patients with hepatic
dysfunction.
a Use in children < 13 years of age has not been approved in some countries.
Prevention
Nonpharmaceutical public health measures: respiratory etiquette (covering coughs
and sneezes) and hand-hygiene are the most feasible measures to prevent the spread
of seasonal influenza infection during epidemics.
Vaccination
Immunization with influenza vaccine is the primary measure to control seasonal
influenza epidemics. The objective of influenza vaccination is to reduce disease
morbidity and mortality in groups at risk for severe illness and death (mainly the
elderly, infants and young children, and persons with chronic underlying condi-
tions). This may be done through vaccination of at-risk individuals before the I
season (if the burden of disease is known), and vaccination of caregivers (to pre-
vent them from becoming the source of infection).
Immunization with available inactivated virus vaccines can provide 7090%
protection against illness in healthy young adults when the vaccine antigen closely II
matches the circulating strains of virus.
A single dose suffices for those with prior exposure to influenza A and B viruses;
2 doses at least 4 weeks apart are essential for children < 9 years old who have not
previously been vaccinated against influenza. Routine immunization programmes
III
should focus efforts on vaccinating those at greatest risk of serious complications
or death from influenza and those who might spread influenza (health-care per-
sonnel and household contacts of high-risk persons) to high-risk persons.
IV
Proper health education and planning of yearly vaccination campaigns is
recommended.

76
The recommended composition of seasonal influenza vaccines is reviewed twice

a year by WHO.19
Surveillance
Influenza is a disease under international surveillance. Countries are encouraged
to report the disease activity and virus isolation to WHO through FLUNET.
Currently there is no official FLUNET laboratory point of contact in CAR and
Chad, and assistance may be best obtained through the WHO Regional Office
for Africa (see Annex 3 for contact details).
Surveillance of influenza is essential for:
characterization of the epidemic influenza pattern in terms of seasonality

and identification of risk groups, and to estimate the burden of disease and
its impact, in order to allow for yearly planning of prevention (vaccination)
and response activities (medical and nonmedical interventions);
identification of changes in the epidemiological pattern over the year to allow
timely implementation of planned medical and nonmedical preparedness
and response measures;
characterization of circulating influenza virus strains to support updating of
the composition of the annual seasonal influenza vaccine for the northern
and southern hemispheres and allow early detection of new influenza A virus
subtypes;
monitoring the emergence of viruses resistant to recommended antiviral
treatments.
19 The following related WHO recommendations are available: Update on the recommended composition of
vaccine against seasonal influenza (http://www.who.int/csr/disease/influenza/vaccinerecommendations/
en/index.html); WHO position paper on influenza vaccines (http://www.who.int/wer/2005/wer8033/en/
index.html); Recommendations for the use of inactivated vaccines (http://www.who.int/docstore/wer/
pdf/2000/wer7535.pdf).

77
INFLUENZA (AVIAN)

As of August 2008, no outbreaks of highly pathogenic avian influenza A (H5N1)
virus infection in poultry or other animals and associated human cases had been
reported in the Central African Republic or Chad. Avian influenza A(H5N1) out-
breaks in poultry and/or wild birds have been reported in neighbouring countries
(Cameroon, Niger, Nigeria and Sudan). One human case of influenza H5N1 has
been reported in Nigeria.20
Description
Avian influenza or bird flu is a contagious disease of animals caused by viruses
that normally infect birds. Avian influenza viruses may be transported from farm
to farm by the movement of live birds, carcasses, poultry equipment and products,
INFLUENZA (AVIAN)
people (contaminated shoes, clothing) and other items contaminated by infected
birds or poultry products (vehicles, equipment, feed and cages).
Several of the avian influenza viruses have been able to cross the species barrier
to infect humans and lead to illness. These are the highly pathogenic avian influ-
enza (HPAI) A(H5N1), A(H7N3) and A(H7N7) viruses; and the low pathogenic
avian influenza (LPAI) A(H7N2) and A(H9N2) viruses (referring to pathogenicity
in chickens). I
The low pathogenic forms of avian influenza commonly cause mild symptoms in
poultry and may easily go undetected. The highly pathogenic form spreads rapidly
through poultry flocks, causing disease affecting multiple internal organs, and
has a mortality that may approach 100%, often within 48 hours. Pathogenicity II
may differ among different poultry species.
Only A(H5N1) and A(H7N7) have been reported to cause human death. However,
these and other avian influenza viruses are a cause of concern to human health
because of the possibility that they might mutate into a form that spreads easily III
among humans, which could lead to an influenza pandemic.
The circulation of H5N1 in avian populations and subsequent human infection
has led to the declaration of a state of pandemic alert by WHO since 2004.
IV
20 Further updates on the animal situation may be obtained from OIE (World Organisation for Animal Health)
at: http://www.oie.int/wahid-prod/public.php?page=weekly_report_index&admin=0

78
The first laboratory-confirmed human case of infection with HPAI A(H5N1) was
reported in Hong Kong Special Administrative Region of China in 1997 (18 cases
including 6 deaths), during a period of outbreaks in poultry. Outbreaks occurred
again in South-East Asia in 2003, followed by concurrent human infections at the
end of 2003 in several countries (China, Thailand, Viet Nam).
Since then, HPAI A(H5N1) has spread to wild birds and to poultry in central Asia,
Europe and Africa. The first animal outbreak of HPAI A(H5N1) in Africa was
confirmed in poultry farms in northern Nigeria in early February 2006. HPAI
A(H5N1) was also confirmed in poultry and/or wild birds in Egypt and Niger in
February 2006, Cameroon in March 2006, and Sudan and Cte dIvoire in April
2006, Benin 2007, Burkina Faso 2006, Djibouti 2006 (plus 1 human case), Ghana
2007 and Togo 2007.

In poultry, HPAI A(H5N1) virus can spread rapidly within a flock. Chickens may
experience disease affecting multiple internal organs, with a mortality that may
approach 100%, often within 48 hours. Ducks may be infected and contagious
but remain asymptomatic.
HPAI A(H5N1) may also infect several mammalian species besides humans, and
the Food and Agriculture Organization of the United Nations (FAO) produces a
regular information bulletin on the spread of HPAI A(H5N1) in animal populations.21
21 Further information may be obtained from the EMPRES AI page at http://www.fao.org/ag/againfo/

programmes/en/empres/home.asp. See also: H5N1 avian influenza: timeline of major events (http://www.
who.int/csr/disease/avian_influenza/ai_timeline/en/index.html); Avian influenza situation in Asia:
altered role of domestic ducks (http://www.who.int/csr/don/2004_10_29/en/index.html); Laboratory study
of H5N1 viruses in domestic ducks: main findings (http://www.who.int/csr/disease/avian_influenza/labstudy_
2004_10_29/en/); Pro-poor highly pathogenic avian influenza risk reduction (HPAI) http://www.fao.org/
ag/againfo/subjects/en/health/diseases-cards/avian_update.html).

79
INFLUENZA (HUMAN A(H5N1) INFECTION)

No cases have been reported in Central African Republic and Chad to date.
Description
Case definition
Clinical description22

Common initial symptoms are fever (usually > 38 C) and cough, plus signs and
symptoms of lower respiratory tract involvement including dyspnoea. Upper res-
piratory tract symptoms such as sore throat and coryza are present only sometimes.
Gastrointestinal symptoms were frequently reported in cases in Thailand and
Viet Nam in 2004 but less frequently since 2005. Lower respiratory tract mani-
festations often develop early in the course of illness and clinically apparent
pneumonia with radiological changes has usually been found at presentation.
The disease usually progresses rapidly and often progresses to an acute respiratory
distress syndrome. Median times of 4 days from the onset of illness to presentation
at a health-care facility and 910 days until death in fatal cases has been reported.
Atypical presentations have included fever and diarrhoea without pneumonia,
and fever with diarrhoea and seizures progressing to coma. Common laboratory I
findings include leukopenia, lymphopenia, mild-to-moderate thorombocytopenia,
and elevated levels of aminotransferases. Lymphopenia and increased levels of
lactate dehydrogenase at presentation have been associated with a poor prognosis.
Of 6 infected pregnant women, 4 have died, and the 2 survivors had a spontaneous
abortion. Mild illnesses such as upper respiratory illness without clinical or II
radiological signs of pneumonia have recently been reported more frequently in
children. Limited seroepidemiological studies conducted since 2004 suggest that
subclinical infection appears uncommon. The overall case-fatality ratio is high
(63% as of July 2008). III
22 Updated WHO guidelines on the clinical management of human infections due to avian A(H5N1) virus
were published in August 2007. Subsequently, a review article on human infection with avian influenza
A(H5N1), that contains additional information, was published in January 2008 by the Writing Committee
of the Second World Health Organization Consultation, on Clinical aspects of human infection with avian IV
influenza A(H5N1) virus (Update on avian influenza A(H5N1) virus infection in humans. New England
Journal of Medicine, 2008, 358:261273).

80
Case classification
Person under investigation: a person whom public health authorities have
decided to investigate for possible H5N1 infection.
Suspected H5N1 case: a person presenting with unexplained acute lower respi-
ratory illness with fever (> 38 C ) and cough, shortness of breath or difficulty
breathing and one or more of the following exposures in the 7 days prior to
symptom onset:
close contact (within 1 m) with a person (e.g. caring for, speaking with, or
touching) who is a suspected, probable, or confirmed H5N1 case;
exposure (e.g. handling, slaughtering, plucking, butchering, preparation
for consumption) to poultry or wild birds or their remains or to environ-

ments contaminated by their faeces in an area where H5N1 infections in
animals or humans have been suspected or confirmed in the last month;
consumption of raw or undercooked poultry products in an area where
H5N1 infections in animals or humans have been suspected or confirmed
in the last month;
close contact with a confirmed H5N1 infected animal other than poultry
or wild birds (e.g. cat or pig);
handling samples (animal or human) suspected of containing H5N1 virus
in a laboratory or other setting.
Probable H5N1 case (notify WHO):
Probable H5N1 case definition 1: a person meeting the criteria for a sus-
pected case and one of the following additional criteria: (a) infiltrates or
evidence of an acute pneumonia on chest radiograph plus evidence of res-
piratory failure (hypoxemia, severe tachypnea); or (b) positive laboratory
confirmation of an influenza A infection but insufficient laboratory evi-
dence for H5N1 infection.
Probable H5N1 case definition 2: a person dying of an unexplained acute
respiratory illness who is considered to be epidemiologically linked by time,
place, and exposure to a probable or confirmed H5N1 case.
Confirmed H5N1 case (notify WHO): a person meeting the criteria for a sus-
pected or probable case AND one of the following positive results conducted
in a national, regional or international influenza laboratory whose H5N1 test
results are accepted by WHO as confirmatory:

81
Isolation of an H5N1 virus.

Positive H5 PCR results from tests using two different PCR targets, e.g.
primers specific for influenza A and H5 HA.
A four-fold or greater rise in neutralization antibody titre for H5N1 based
on testing of an acute serum specimen (collected 7 days or less after
symptom onset) and a convalescent serum specimen. The convalescent
neutralizing antibody titre must also be 1:80 or higher.
A microneutralization antibody titre for H5N1 of 1:80 or greater in a single
serum specimen collected at day 14 or later after symptom onset and a
positive result using a different serological assay, for example, a horse red
blood cell haemagglutination inhibition titre of 1:160 or greater or an H5-

specific western blot positive result.
Application of the H5N1 case definitions

The case definitions apply to the current phase of pandemic alert (phase 3) for
H5 N1 and may change as new information about the disease or its epidemiology
becomes available. National authorities should formally notify only probable and
confirmed H5N1 cases to WHO. The case definitions for persons under investi-
gation and suspected cases have been developed to help national authorities in
classifying and tracking cases. The case definitions are not intended to provide
complete descriptions of disease in patients but rather to standardize reporting
of cases.
In clinical situations, decisions concerning treatment, care or triage of persons
I
who may have H5N1 infection should be based on clinical judgment and epide-
miological evidence, and not on adherence to case definitions. While most patients
with H5N1 infection have presented with fever and lower respiratory complaints,
the clinical spectrum is broad.23 II
A case of human influenza caused by a new subtype should be immediately noti-
fied to WHO under the International Health Regulation (IHR). For human infec-
tion with HPAI A(H5N1) virus, WHO has developed standardized case definitions
to facilitate: III
1. reporting and classification of human cases of H5N1 infection by national
and international health authorities;
IV
23 See: WHO case definitions for human infections with influenza A(H5N1) virus (http://www.who.int/csr/
disease/avian_influenza/guidelines/case_definition2006_08_29/en/index.html).

82
2. standardization of language for communication purposes;

3. comparability of data across time and geographical areas.
Most human infection is reported to be after exposure to infected birds. Infected
birds also shed the virus in large quantities in their respiratory secretions and in
their faeces. All parts of the animal and its blood may contain the virus. Human
infection may occur through touching, slaughtering, plucking and butchering of
infected birds and probably contact with contaminated environments. Unprotected
manipulation or consumption of raw meat and eggs of infected birds should also
be considered risk factors for possible infection, especially if there are poor hygiene
practices (hands, tools, environment, etc.). In some cases, infected birds (especially
ducks) may not appear to be ill. Freezing does not kill the virus. Cooking thor-
oughly will kill the virus.24
Human-to-human transmission was suspected in several clusters (cases related
in time and place and documented as probable in Thailand in 2004, Indonesia in
2006, Pakistan and China in 2007). Human-to-human transmission, when sus-
pected, is likely to have occurred in the context of intimate unprotected prolonged
contact between a severely ill patient and the contact(s) to whom he/she transmitted
the infection (for example when taking care of the patient or sharing a bedroom
with them).
Incubation period
After exposure to infected poultry, the incubation period generally appears to be
7 days or less, in many cases 25 days. In clusters in which limited human-to-
human transmission has probably occurred, the incubation period appears to be
approximately 35 days.
Limited data suggest that patients may remain infectious for as long as 3 weeks,
perhaps even longer in immunosuppressed patients (i.e. corticosteroid use). The
longest documented period has been 27 days after the onset of illness based upon
detection of virus antigen in a patients respiratory specimens.
24 See Prevention of foodborne disease: five keys to safer food (http://www.who.int/foodsafety/consumer/

5keys/en/index.html).

83
Epidemiology
General
As of 19 June 2008, a total of 385 laboratory confirmed cases (243 fatal) had been
reported from 15 countries since November 2003, including Djibouti, Egypt and
Nigeria.25

No predisposing factors for infection have been identified that can explain the
low incidence of H5N1 observed in humans to date, despite extensive exposure.
However, the risk for infection through inappropriate handling of sick birds

remains. So far, no domestic mammals have been identified as a source of infec-
tion. However, cats and dogs can become infected.
Population movement increases the risk of importation from neighbouring
countries. Concern that additional human cases may occur in affected parts of
Africa is high given the close contact between people and poultry (estimated 1.1
billion chickens on the African continent, mostly in backyard farming systems).
Poor access to health services. Throughout much of Africa, rapid detection and
investigation of outbreaks is hampered by the absence of an early warning system
for avian influenza in animals or humans, inadequate diagnostic capacity, and
difficulties in shipping specimens, both locally and internationally, for diagnostic
confirmation. I
Food shortages increase the risk of importation from neighbouring countries.

II
Case management
The patient should be isolated and strict infection control measures applied.
Standard and droplet precautions should be the minimum level of precautions to
be used in all health-care facilities when providing care for patients with acute III
febrile respiratory illness, regardless of whether AI infection is suspected. The
most critical elements of these precautions include facial protection (nose, mouth
and eyes if sprays/splashes of secretions are anticipated) and hand-hygiene.
IV
25 Cumulative number of confirmed human cases of avian influenza a/(h5n1) reported to WHO (http://www.
who.int/csr/disease/avian_influenza/en/).

84
Therefore standard plus droplet precautions should be applied for routine patient
care of suspected or confirmed AI-infected patients, which comprise adequate
hand-hygiene, use of gowns, clean gloves, medical masks and eye protection if
splashes are anticipated. If aerosol-generating procedures are performed, personal
protective equipment ( PPE ) should include a particulate respirator instead of a
medical mask.26
Treatment with antivirals should be administrated in case of suspected infection
(clinical presentation and notion of exposure) in the absence of an alternative
diagnosis.
Oseltamivir is the primary recommended antiviral treatment. Observational data
on treatment with oseltamivir in the early stages of the disease suggest its useful-
ness in reducing A(H5N1) virus infection-associated mortality. Furthermore,

evidence that the A(H5N1) virus continues to replicate for a prolonged period
indicates that treatment with oseltamivir is also warranted when the patient
presents to clinical care at a later stage of illness.
Modified regimens of oseltamivir treatment, including twofold higher dosage (i.e.
150 mg twice daily for adults), longer duration and possibly combination therapy
with amantadine or rimantadine (in countries where A(H5N1) viruses are likely
to be susceptible to adamantanes) may be considered on a case-by-case basis,
especially in patients with pneumonia or progressive disease.
Additional supportive therapy

Corticosteroids should not be used routinely, but may be considered for septic
shock with suspected adrenal insufficiency requiring vasopressors (the agent that
causes vasoconstriction and maintains or increases blood pressure, e.g. norepine
phrine, epinephrine or dopamine). Prolonged or high-dose corticosteroids may
result in serious adverse events in A(H5N1) virus-infected patients, including
opportunistic infection.
Antibiotic chemoprophylaxis should not be used. However, when pneumonia is
present, antibiotic treatment is appropriate initially for community-acquired
pneumonia according to published evidence-based guidelines. When available,
the results of microbiological studies should be used to guide antibiotic usage for
suspected bacterial coinfection in patients with A(H5N1) virus infection.
26 See: Avian influenza, including influenza A(H5N1), in humans: WHO interim infection control guideline
for health-care facilities (http://www.who.int/csr/disease/avian_influenza/guidelines/infectioncontrol1/
en/index.html).

85
Monitoring of oxygen saturation should be performed whenever possible at pres-

entation and routinely during subsequent care (e.g. pulse oximetry, arterial blood
gases), and supplemental oxygen should be provided to correct hypoxemia.
Therapy for A(H5N1) virus-associated ARDS should be based on published
evidence-based guidelines for sepsis-associated ARDS, specifically including
lung protective mechanical ventilation strategies.27
Management of contacts
Chemoprophylaxis: antiviral chemoprophylaxis should generally be considered
according to the risk stratification:

High-risk exposure groups are currently defined as household or close family
contacts of a strongly suspected or confirmed H5N1 patient, because of poten-
tial exposure to a common environmental or poultry source as well as exposure
to the index case.
Moderate-risk exposure groups are currently defined as personnel involved in
handling sick animals or decontaminating affected environments (including
animal disposal) if personal protective equipment may not have been used
properly.
Individuals with unprotected and very close direct exposure to sick or dead
animals infected with the H5N1 virus or to particular birds that have been
directly implicated in human cases.
Health-care personnel in close contact with strongly suspected or confirmed
I
H5N1 patients, for example during intubation or performing tracheal suction-
ing, or delivering nebulized drugs, or handling inadequately screened/sealed
body fluids without any or with insufficient personal protective equipment.
This group also includes laboratory personnel who might have unprotected II
exposure to virus-containing samples.
Low-risk exposure groups are currently defined as health-care workers not in
close contact (distance greater than 1 m) with a strongly suspected or confirmed
H5N1 patient and having no direct contact with infectious material from that III
patient; health-care workers who used appropriate personal protective equipment
during exposure to H5N1 patients; personnel involved in culling non-infected
or likely non-infected animal populations as a control measure; personnel
IV
27 See: Clinical management of human infection with avian influenza A(H5N1) virus (http://www.who.int/csr/
disease/avian_influenza/guidelines/clinicalmanage07/en/index.html).

86
involved in handling sick animals or decontaminating affected environments

(including animal disposal), who used proper personal protective equipment.
To assist countries in prioritizing the use of antiviral drugs for chemoprophylaxis,

particularly where their availability is limited, a three-tier-risk categorization for
exposure was developed.
Where neuraminidase inhibitors are available:
In high-risk exposure groups , including pregnant women, oseltamivir should

be administered as chemoprophylaxis, continuing for 710 days after the last
exposure (strong recommendation); zanamivir could be used in the same
way (strong recommendation) as an alternative.

In moderate-risk exposure groups, including pregnant women, oseltamivir
might be administered as chemoprophylaxis, continuing for 710 days after
the last exposure (weak recommendation); zanamivir might be used in the
same way (weak recommendation).
In low-risk exposure groups, oseltamivir or zanamivir should probably not
be administered for chemoprophylaxis (weak recommendation). Pregnant
women in the low-risk group should not receive oseltamivir or zanamivir for
chemoprophylaxis (strong recommendation).
Amantadine or rimantadine should not be administered as chemoprophylaxis
(strong recommendation).
Where neuraminidase inhibitors are not available:
In high- or moderate-risk exposure groups, amantadine or rimantadine might

be administered for chemoprophylaxis if local surveillance data show that the
virus is known or likely to be susceptible to these drugs (weak recommendation).
In low-risk exposure groups, amantadine and rimantadine should not be
administered for chemoprophylaxis (weak recommendation).
In pregnant women, amantadine and rimantadine should not be administered
for chemoprophylaxis (strong recommendation).
In the elderly, people with impaired renal function and individuals receiving
neuropsychiatric medication or with neuropsychiatric or seizure disorders,
amantadine should not be administered for chemoprophylaxis (strong recom-
mendation). Health monitoring is recommended for close contacts of cases
up to 7 days after the last exposure and consists of monitoring temperature

87
and symptoms such as cough. It is also required of health-care professionals

who have had contact with patients, their body fluids and secretions, their
room or potentially contaminated equipment. Quarantine of close contacts of
suspected cases during the health-monitoring period is not necessary unless
there is suspicion of human-to-human transmission.28
Prevention
Reduce human exposure to H5N1. For individuals, the risk of bird-to-human
transmission of avian influenzas can be reduced through proper precautions;
hand-hygiene, hygiene precautions when handling birds (especially when sick or
dead) or their products for consumption or when in environments that may be

contaminated with faeces of sick birds. In communities, the risk may be reduced
by control of spread of the infection in the animal population, and reduction of
human contact with infected birds. Human-to-human transmission of H5N1 may
be prevented through early detection and isolation of suspected and confirmed cases
in a dedicated health-care facility and application of infection-control measures.
Food safety precautions29

Humanitarian agencies may:
Contribute to reducing human exposure to avian influenza A(H5N1) by inform-

ing communities affected by AI in birds of risks of exposure to sick or dead
animals (particularly poultry/birds) and of strategies for risk avoidance includ-
ing avoiding close contact with sick/dead animals and their remains, or with I
environments contaminated by their faeces, avoiding consumption of raw or
undercooked poultry products, and performance of hand-hygiene after han-
dling, slaughtering, plucking, butchering or preparing poultry/wild birds.
Ensure that information is provided in close coordination with the animal II
and public health authorities to prevent discrepancies in preventive messages.
Promote immediate reporting to relevant local and national animal health
authorities of unexpected illness/deaths in birds/animals.
Investigate people developing unexplained acute respiratory illness after ex- III
posure to ill/dead birds for H5N1 infection.
28 See: WHO Rapid advice guidelines on pharmacological management of humans infected with avian influenza
A(H5N1) virus (http://www.who.int/csr/disease/avian_influenza/guidelines/pharmamanagement/en/
index.html); WHO guidelines for investigation of human cases of avian influenza A(H5N1) (http://www. IV
who.int/csr/resources/publications/influenza/WHO_CDS_EPR_GIP_2006_4/en/index.html).
29 http://www.who.int/foodsafety/fs_management/No_07_AI_Nov05_en.pdf.

88
Agencies might support such efforts through integration of these activities into other
field programs such as agriculture, livelihoods, food security, water and sanitation.
Surveillance
The early-warning system should be strengthened. Humanitarian agencies should
facilitate the early detection, notification and early response to initial suspected
cases/clusters in humans of H5N1 avian influenza or a novel pandemic influenza
virus.
It is important that relevant authorities are notified immediately in case of any sus-
pect die-off or severe unexplained illness in animals, especially if affecting birds.
Relevant authorities and WHO should also be informed immediately upon suspi-
cion of human infection with an avian influenza virus so as to ensure rapid and
adequate case management, and relevant further planning and action as necessary.
References
1. Infection-control recommendations for avian influenza in health-care facilities. Aide-memoire,
April 2008 (http://www.who.int/csr/disease/avian_influenza/guidelines/aidememoireinfcont/
en/index.html).
2. Protection of individuals with high poultry contact in areas affected by avian influenza H5N1:
consolidation of pre-existing guidance, February 2008 (http://www.who.int/csr/disease/avian_
influenza/guidelines/high_contact_protection/en/index.html).
3. Infection prevention and control of epidemic- and pandemic-prone acute respiratory diseases in
health care. WHO interim guidelines, June 2007 (http://www.who.int/csr/resources/publications/
WHO_CD_EPR_2007_6/en/index.html).
4. Collecting, preserving and shipping specimens for the diagnosis of avian influenza A(H5N1)
virus infection. Guide for field operations, October 2006 (http://www.who.int/csr/resources/
publications/surveillance/WHO_CDS_EPR_ARO_2006_1/en/index.html).
5. International Food Safety Authorities Network. Highly pathogenic H5N1 avian influenza
outbreaks in poultry and in humans: food safety implications, November 2005 (http://www.
who.int/foodsafety/fs_management/No_07_AI_Nov05_en.pdf ).
6. Avian influenza A(H5) in rural areas in Asia: food safety considerations (http://www.who.int/
foodsafety/micro/avian2/en/index.html).
7. WHO recommendations relating to travellers coming from and going to countries experiencing
outbreaks of highly pathogenic H5N1 avian influenza (http://www.who.int/csr/disease/avian_
influenza/travel2005_11_3/en/print.html).

89
8. Questions and answers on potential transmission of avian influenza (H5N1) through water,
sanitation and hygiene and ways to reduce the risks to human health (http://www.who.int/water_
sanitation_health/emerging/en/).
9. Review of latest available evidence on risks to human health through potential transmission of
avian influenza (H5N1) through water and sewage (http://www.who.int/water_sanitation_
health/emerging/avianflu/en/index.html; http://www.who.int/water_sanitation_health/
emerging/en/).

I
II
III
IV

90
LEISHMANIASIS (CUTANEOUS AND MUCOSAL)

There is no recent epidemiological information available from CAR on cutaneous
leishmaniasis.
Chad
In OctoberNovember 2007, WHO assisted Chad in an outbreak of about 200
cases at the Teguine camp on the eastern border close to Sudan.
In Chad, cutaneous leishmaniasis is more frequent than previously thought,

although recent data are minimal. Reported cases include 121 in 1968, 836 in
1975 and 164 cases in 1976. There are several foci in the north and north-east of
the country (subdesert and desert zones), in the NDjamena area and in south-
central Chad along the Chari river.
Description
Infectious agent
Protozoan disease caused by several species of the genus Leishmania.
The presence of the insect vector Phlebotomus duboscqi has been recorded in the
Abch (Chad) focus in the subdesert zone.
Case definition
Appearance of one or more skin lesions, typically on uncovered parts of the body.
The face, neck, arms and legs are the most common sites. A nodule may appear at
the site of inoculation and may enlarge to become an indolent ulcer. The sore may
remain in this stage for a variable time before healing it typically leaves a depressed
scar. Other atypical forms may occur; some strains can disseminate and cause mucosal
lesions. Sequelae may involve nasopharyngeal tissues and can be very disfiguring.
Laboratory criteria
positive parasitology (stained smear or culture from the lesion); very scarce
parasites in the case of mucosal leishmaniasis;

91
positive PCR;
mucosal leishmaniasis only: positive serology (immunofluorescent assay,
ELISA)
WHO operational definition. A case of cutaneous leishmaniasis can be defined

as a person showing clinical signs (skin or mucosal lesions) with parasitological
confirmation of the diagnosis (positive smear or culture) and/or positive PCR
and/or, for mucosal leishmaniasis only, serological diagnosis.

From the animal reservoir (in some cases from humans) through the bite of infec-
tive female sandflies (phlebotomines).
There are two modes of transmission: (1) anthroponotic where the vector feeds on
an infected person and then feeds on an uninfected individual, with a cluster effect
in transmission; (2) zoonotic, when the vector feeds on an infected animal and
subsequently feeds on another potential host, eventually a human. Overcrowding
and inadequate sanitation increase the risk of infection. The risk of anthroponotic
cutaneous leishmaniasis epidemics is higher in camp settings.
Incubation period
At least one week but up to many months.
Communicability period I
Not directly transmitted from person to person, but infectious to sandflies as long
as parasites remain in lesions of untreated cases, which usually lasts from a few
months up to two years.
II
Epidemiology
General
Leishmaniasis is a neglected tropical disease that has demonstrated that refugee III
camps may act as amplification sites, firstly in the camp populations and then,
once they have repatriated, in their country of origin. For example in 1992, an
outbreak of anthroponotic cutaneous leishmaniasis occurred in refugee camps in
the North West Frontier province of Pakistan. When the refugees were repatriated, IV
the disease was imported into Afghanistan resulting in 1.5 million cases (70 000
cases annually).

92
Leishmaniasis is associated with IDPs, refugees, malnutrition, HIV/AIDS, poor

sanitation and poverty. Of the two forms of the disease, cutaneous and visceral,
the former is far more common and the latter is not often associated with out-
breaks in camps.
In endemic areas, the disease is more severe in young children than in adults,
among whom many infections may be asymptomatic. Early detection of cases
and institution of specific therapy are essential.
There are 82 endemic countries with a huge variety of eco-epidemiological set-
tings, including rural and, less frequently, urban areas.
Seasonality
Seasonal depending on the geography and sandfly species.
Alert threshold
In the absence of a clear epidemic threshold, an epidemic should be suspected when
there is an unusual and sudden rise in the number of people suffering ulcers in
exposed areas. Investigation of the disease agent by laboratory testing should be
performed in all cases.

Population movement increases the risk of exposure to sandflies.
Overcrowding facilitates transmission. The vector has a short flight range, and
humans act as the reservoir.
Poor access to health services is also a risk factor, as early detection and contain-
ment of cases are paramount to reduce transmission.
Food shortages. Malnutrition may increase susceptibility to cutaneous disease as
a result of immunosuppression.
Lack of safe water and poor sanitation are a risk factor for vector-breeding sites.

Case management
Early detection and appropriate, rapid therapy prevents development of invasive
cutaneous lesions (e.g. mucocutaneous leishmaniasis in the Americas).

93
Epidemic control
In areas of high incidence, intensive efforts should be made to control the disease
by providing diagnostic and drug facilities and through appropriate measures
directed against phlebotamine sandflies and the mammalian reservoir hosts.
Prevention
The main measures are case management, environmental management and vec-
tor control.30

I
II
III
IV
30 See: http://www.who.int/leishmaniasis/en/.

94
LEISHMANIASIS (VISCERAL)

There is no recent epidemiological information available from CAR on visceral
leishmaniasis.
Chad
The disease is endemic. Epidemiological knowledge is fragmentary, and no recent
data are available. Between 1966 and 1973, 64 human cases were reported from
the NDjamena central hospital.
Description
Infectious agent
Intracellular Protozoa genus Leishmania. The parasite has not been identified, but
is most likely to be L. donovani. P. orientalis is the suspected vector.
Case definition
An illness with prolonged irregular fever of unknown origin, splenomegaly and
weight loss as main symptoms.
Laboratory criteria
Positive parasitology, Giemsa-stained smears from bone marrow, lymph node,
blood or culture of the organism from biopsy or aspirated material. Spleen or
liver biopsies, too dangerous, should not normally be taken.
Positive serology (immunofluorescent assay, ELISA, direct agglutination test,
immunocromatography dip sticks).
Positive PCR.
WHO operational definition. A case of visceral leishmaniasis (VL) is a person

showing clinical signs (prolonged irregular fever, splenomegaly and weight loss)
with serological (at peripheral geographical level) and/or (when feasible at central
level) parasitological confirmation of the diagnosis. In endemic malarious areas,

95
visceral leishmaniasis to be suspected when fever lasts for more than two weeks and
no response has been achieved with antimalarial drugs (assuming drug-resistant
malaria has also been considered).
There are two modes of transmission:
1. Anthroponotic where the vector feeds on an infected person and then feeds
on an uninfected individual. If a case is living in close proximity to others,
the risk of catching the disease is 26 times higher than normal. People living
just 50 m from a case have only a three times risk of infection, hence there is
a significant cluster effect. In the 1990s, the Nuer tribe in Sudan was decimated,
and 30% of its population (100000) died. Overcrowding and inadequate sani-
tation increase the risk of infection. The risk of epidemics of leishmaniasis is
high among immunodepressed groups.
2. Zoonotic transmission takes place when the vector feeds on an infected animal
(normally a canid) and subsequently feeds on another potential host.
In anthroponotic foci of visceral leishmaniasis, humans are the sole reservoir and
transmission occurs from person to person through the sandfly bite. Anthroponotic
visceral leishmaniasis is the main cycle recognized in East Africa and, by extension,
the focus in Chad could be similar. Chacals, vervets, dogs and other mammals
have been identified as secondary reservoirs in Sudan. In zoonotic visceral leish-
maniasis foci, such as in northern Africa, the cycle is from the animal reservoir I
through the bite of infected sandflies, with dogs being the main reservoir.
Incubation period
Generally 26 months. Range: 10 days to several years. II
Not transmitted from person to person but infectious to sandflies as long as par-
asites persist in the circulating blood or skin of the mammalian reservoir host. III
Epidemiology
General
IV
Leishmaniasis is a neglected tropical disease which has demonstrated that poor
housing, poverty, IDPs, refugees, displaced populations, malnutrition and immuno-

96
suppression are increasing risk factors. Refugee camps could play a role as ampli-
fication sites considering the cluster effect in leishmaniasis transmission, firstly
in the camp populations and then, once repatriated, in their country of origin,
although cutaneous leishmaniasis outbreaks occur more frequently in refugee camps.
In endemic areas, the disease is more severe in young children than in adults,
among whom many infections may be asymptomatic. The elderly, the weak and the
malnourished of all ages are particularly susceptible to severe disease and death.
Visceral leishmaniasis is present in 64 countries. Sudan, Ethiopia, Kenya, Uganda
and Somalia are the countries most affected in eastern Africa. In Chad, only spo-
radic visceral leishmaniasis cases have been described. The main affected groups
are children, seasonal workers, malnourished and displaced persons, and HIV
coinfected patients.
Seasonality
Seasonal according to the sandfly species.
Alert threshold
In the absence of a clear epidemic threshold, an epidemic should be suspected if
there is an unusual and sudden rise in the number of new cases or deaths caused
by high non-malarial fever, splenomegaly and wasting syndrome. Any of the above
scenarios should lead to investigation of the disease agent by laboratory testing.

Population movement increases the risk of exposure to sandflies.
Overcrowding facilitates transmission. The vector has a short flight range, and
humans act as the reservoir in anthroponotic foci.
Poor access to health services is a risk factor, as early detection and containment
of cases are paramount to reduce transmission.
Food shortages. Malnutrition increases the risk of contracting leishmaniasis as a
result of immunosuppression. More severe forms of leishmaniasis are observed
in malnourished patients.
Lack of safe water and poor sanitation are a risk factor for vector breeding sites.

97

Case management
Early detection and appropriate, rapid therapy prevents development of visceral
severe forms and eventual death.31
Epidemic control
In areas of high incidence, intensive efforts should be made to control the disease
by providing rapid diagnostic tests and chemotherapy, and through appropriate
measures directed against phlebotamine sandflies and the mammalian reservoir
hosts if appropriate.
Prevention
The main measures are case management, environmental management and vec-
tor control.32
II
III
IV
31 See: http://www.who.int/leishmaniasis/resources/documents/VL_NMR_1107_ok.pdf.
32 See: http://www.who.int/leishmaniasis/en/.

98
LEPROSY

Pockets of endemicity still remain in some areas of the country. Prevalence as of
2005 was 1.11.5 per 10 000 population. Globally, six countries have yet to reach
an elimination target of 1 case per 10 000 population at the national level. CAR is
not one of these six remaining countries, but the Democratic Republic of the Congo
that borders CAR to the south is one of them (with prevalence rates of 22.5 per
10000 population).33
Chad
As of 2005, prevalence for Chad was estimated at 1 or less per 10 000 population.
Data are scarce. Chad is not one of the six countries that have not yet reached the
elimination target of 1 case per 10 000 population at the national level.
Description
Infectious agent
Bacterium: Mycobacterium leprae.
Case definition
WHO operational definition: a case of leprosy is defined as a person showing
hypopigmented or reddish skin lesion(s) with definite loss of sensation. The opera-
tional case definition includes:
retrieved defaulters with signs of active disease;

relapsed cases who have previously completed a full course of treatment.
Case classification (clinical)

Paucibacillary leprosy (PB): 15 patches or lesions on the skin.
Multibacillary leprosy (MB): more than 5 patches or lesions on the skin.
33 http://www.who.int/lep/situation/BurdenEnd2005.pdf; http://www.who.int/lep/situation/PrateEnd2005v2-
WM2.pdf; http://www.who.int/lep/situation/prevalence/en/index.html.

99
Laboratory criteria for confirmation: in practice, laboratories are not essential for
the diagnosis of leprosy.
Not clearly established: organisms probably enter the human body through the
mucous membranes of the upper respiratory tract and possibly through broken
skin, during close and frequent contact with untreated infected people.
Incubation period
Nine months to 40 years (average 57 years).
If not treated: transmission is possible, the risk being higher for contacts of
MB cases than of PB cases;
Treated: infectivity disappears after a few doses of treatment with multidrug
therapy (MDT).
LEPROSY
Epidemiology
General
During the 1980s, most African countries were highly endemic for leprosy, with
an average national prevalence exceeding 2% (leprosy is considered a public health
problem when the prevalence is higher than 1case per 10 000 population). Global I
annual new case detection continues to show a sharp decline, falling by over 40 000
cases (13.4%) during 2006 compared with the new cases reported during 2005. The
burden of the disease for the four most endemic countries (Brazil, Democratic
Republic of the Congo, Mozambique and Nepal) represents about 23% of annual II
global new case detection and 34% of global registered cases end 2006/early 2007.
The WHO African Region made substantial progress towards the elimination of
leprosy during the 1990s. These efforts are still ongoing in order that the elimi-
nation of leprosy may be achieved in each country. The elimination of leprosy is III
a key component of poverty alleviation, and all countries show strong political
commitment and give high importance and priority to the elimination of this
secular and stigmatizing disease.
The diagnosis and treatment of leprosy are easy, and most endemic countries are IV
striving to fully integrate leprosy services into existing general health services.
This is especially important for those underserved and marginalized communi-

100
ties that are the most at risk from leprosy. Previously highly endemic countries
have now achieved elimination, and the few countries that remain are close to
eliminating the disease.
Leprosy situation, end 2006
WHO region Registered prevalence Number of new cases detected in

(excluding Europe) per 10 000 population 2004 (per 100 000 population
Africa 29 548 (0.55) 27 902 (5.15)
Americas 64 715 (0.76) 47 612 (5.58)
Eastern Mediterranean 3 986 (0.09) 3 261 (0.71)

South-East Asia 116 663 (0.7) 174 118 (10.51)
Western Pacific 9 805 (0.06) 6 124 (0.35)
Global total 224 717 259 017
Source: Weekly Epidemiological Record, 2007, 82(25):225-232; http://www.who.int/wer/2007/wer8225.pdf.
In Africa, Madagascar and Mozambique have prevalence rates of 22.5 cases per
10 000 population; the Democratic Republic of the Congo has rates of 1.52; and
Central African Republic and the United Republic of Tanzania have rates of 1.11.5.
Rates in all other African countries are below 1.
Seasonality
No seasonality has been registered.
Recent epidemics
The disease has no epidemic potential.

Population movement potentially increases the risk of contact with cases.
Overcrowding increases the risk of contact.
Poor access to health services. Prompt identification and treatment of cases are the
most important control measures. Lack of early diagnosis and treatment caused by
difficulties in diagnostic methodology and accessing health services (geographical,
financial, security) increases the burden of disease and the risk of transmission.

101

Case management
Treatment by MDT should be given according to the case classification, as shown
below.
MB leprosy (the standard regimen is a combination of the following drugs for

12 months):
Adults
rifampicin: 600 mg once a month;
dapsone: 100 mg once a day;
clofazimine: 50 mg once a day and 300 mg once a month.
Children should receive appropriately scaled-down doses (in child blister-
packs).
PB leprosy (the standard regimen is a combination of the following drugs for
6 months):
Adults
LEPROSY
rifampicin: 600 mg once a month;
dapsone: 100 mg once a day.
Children should receive appropriately scaled-down doses (in child blister-
packs).
I
A core element of the elimination strategy is to make diagnosis and MDT available
at all health centres, to all existing leprosy patients. MDT is provided free of charge
by WHO. Any interruption of treatment schedules has serious implications for
treatment outcome. II
Prevention and control
The following actions are essential for prevention of leprosy and maintaining the
ongoing elimination campaign: III
ensuring that accessible and uninterrupted MDT services are available to all
patients through flexible and patient-friendly drug delivery systems;
guaranteeing that MDT services are sustainable by integrating leprosy serv- IV
ices into the general health services and building the ability of general health
workers to treat leprosy;

102
encouraging self-reporting and early treatment by promoting community

awareness and changing the image of leprosy;
monitoring performance of MDT services, quality of patient care and progress
made towards elimination through national disease surveillance systems.
The age-old stigma associated with the disease remains an obstacle to self-reporting
and early treatment. The image of leprosy has to be changed at the global, national
and local levels. Reducing contact with known leprosy patients is of dubious value
and can lead to stigmatization. It is important that environments in which patients
will not hesitate to come forward for diagnosis and treatment at any health facility
are created.
Immunization
BCG vaccination may induce protection against the disease; this is part of the
control method against TB and therefore need not be undertaken specifically
against leprosy.

103
LYMPHATIC FILARIASIS

Lymphatic filariasis (LF) is endemic in both Central African Republic and Chad.
Description
Infectious agent
Helminth: Wuchereria bancrofti, a filarial worm belonging to the class Nematoda.
Case definition
Hydrocele or lymphoedema in a resident of an endemic area for which other
causes of these findings have been excluded.
Laboratory criteria
Positive parasite identification by:
direct blood examination; or

ultrasound; or
positive antigen detection test. I
Case classification
Suspected: not applicable.
Probable: a case that meets the clinical case definition. II
Confirmed: a person with positive laboratory tests even if he/she does not meet
the clinical case definition.
The burden of lymphatic filariasis, as measured in disability-adjusted life years III

(DALYs), is the highest of all tropical diseases after malaria.
The bite of infected blood-feeding female mosquitoes (mainly Anopheles spp., also IV
Culex spp.) that transmit immature larval forms of the parasitic worms from human
to human.

104
Incubation period
612 months for the microfilariae to appear in blood (the prepatent period)
with signs of lymphatic damage. Repeated attacks of filarial fever occur (pain
and inflammation of lymph nodes and ducts, often accompanied by fever,
nausea and vomiting).
520 years: manifestations of chronic illness may include elephantiasis (swell-
ing of limbs), hydrocele (swelling of the scrotum), enlarged breasts in females
and chyluria (cloudy/milky urine).
As long as microfilariae are present in the peripheral blood (from 612 months to
510 years after the infective bite).
Epidemiology
Chad and CAR are both endemic countries. Countries are categorized as endemic
where prevalence is > 1% microfilaraemia or antigenaemia. To date, some 30%
(382 million) of the global at-risk population is estimated to be in the LF-endemic
countries of the WHO African Region. Where endemic, LF is distributed in con-
tiguous zones. However, prevalence rates vary greatly from one geographical area
to another, and even between one village and another within the same district.
Seasonality. Even if data on the seasonality of vectoral density are not available,
the rainy season is likely to be associated with a higher risk of transmission (north
of the equator: AprilSeptember). The frequency of acute adenolymphangitis (ADL)
attacks also increases during the wet season.
Recent epidemics
The disease is not outbreak-prone.

Population movement. Disease-free populations may be displaced into endemic
areas or vice versa.
Overcrowding. Living in crowded conditions increases the risk of transmission.

105
Poor access to health services. Lack of early diagnosis and treatment as a result
of difficulties in diagnostic methodology and accessing health services (geograph-
ical, financial, security) increases the risk of transmission.
Lack of safe water and poor sanitation. Hygienic measures for the affected body
parts are essential to prevent ADL attacks secondary to lymphoedema. Poor san-
itation may contribute to creating breeding sites for mosquito vectors (especially
Culex spp.).
Other factors
Economic and social impact: filariasis is closely associated with the economies and
infrastructure of endemic communities. There is an established link between the
prevalence of LF, reduced productivity and poverty. LF exerts a heavy social burden
that is especially severe because of the specific attributes of the disease, particularly
since chronic complications are often hidden and considered shameful. For men,
genital damage is a severe handicap, leading to physical limitations and social stig-
matization. For women, shame and taboos are also associated with the disease.
The introduction of a Programme to Eliminate Lymphatic Filariasis (PELF) in the
countries brings beyond filariasis benefits, since albendazole is also an effective
and safe drug for treating soil-transmitted helminths; ivermectin is effective against
many intestinal parasites, scabies and lice.
Health programmes coupled with development projects addressing the key com-
ponents that contribute to LF can improve the chances of success. Specifically,
projects that would reduce mosquito breeding sites, improve housing and sanita- I
tion facilities, and stimulate economic development should be considered.
Additionally, because of the industry-wide impact of LF in some regions, there is
great potential for a strong private-sector role in the elimination of this disease
as a public health problem. II
However, owing to financial constraints and inadequate staffing, less than 10% of
the at-risk population are covered by mass drug administration (MDA) so far. In
addition, the implementation of other programme components, such as vector
control and disability management and prevention, are consequently delayed. III

Case management
IV
Hygiene measures for the affected body parts (and, when necessary, antibiotics
and antifungal agents) can reduce the risk of ADL:

106
wash the affected parts twice daily with soap and clean water, and keep the
affected part dry;
raise the affected limb at night;
exercise to promote lymph flow;
keep nails short and clean;
wear comfortable footwear;
use antiseptic, antibiotic or antifungal creams to treat small wounds or
abrasions;
in severe cases, systemic antibiotics may be necessary.
Drug regimen for individual microfilarial-positive patients:
Diethylcarbamazine citrate (DEC) 6 mg/kg single dose for 12 days, repeated

at 16 month intervals if necessary. However, a single 6 mg/kg dose is equally
effective in killing the adult worm and in reducing the number of microfilaria.
Since the use of DEC in patients with either onchocerciasis or loasis (disease
caused by the nematode worm Loa loa) may be unsafe, it is important that
patients with Bancroftian filariasis who live in areas endemic for these other
infections be examined for coinfection with these parasites before being treated
with DEC.
Alternatively, ivermectin and albendazole may be used. Ivermectin, although
very effective in decreasing microfilaraemia, appears not to kill adult worms
(i.e. it is not macrofilaricidal) and thus does not cure infection completely.
Albendazole can be macrofilaricidal for W. bancrofti, but optimization of its
usage has not been attempted and is not recommended to be given alone.
Control is based on community interventions that require the mapping of LF and

Loa loa distribution. Such mapping is important as ivermectin is often used with
albendazole as dual therapy for LF treatment. However, those suffering from Loa
loa coinfection should not be exposed to ivermectin as it promotes a massive
destruction of microfilariae that may cause an allergic reaction and in individuals
with high Loa loa burden may cause encephalopathy.34 It is therefore important
to be aware of the geographical distribution of LF and Loa loa. Mapping has not
been completed in CAR or Chad.
34 Please refer to WHO Guidelines on preventive chemotherapy in human helminthiasis (http://whqlibdoc.

who.int/publications/2006/9241547103_eng.pdf).

107

Prevention of infection may be achieved only by either reducing contact between
humans and vectors or reducing the amount of infection the vector can acquire,
by treating the human host.
Population level
Mass chemotherapy with safe drugs given once a year to the entire population at
risk is a safe and feasible approach to reducing transmission. This may be imple-
mented by community volunteers.
The recent advent of the extremely effective single-dose, once-yearly drug regimen
has permitted an alternative approach and the launch of the Global Programme
to Eliminate Lymphatic Filariasis (GPELF) in 2000. GPELF has two main goals:
to interrupt transmission of infection; and
to prevent disability caused by the disease.
In order to interrupt transmission, the entire at-risk population must be treated

for a period long enough to ensure that levels of microfilariae in the blood remain
below those necessary to sustain transmission. Therefore, a yearly 1-dose MDA of
the following drugs must be given:
As CAR and Chad are also coendemic with concurrent onchocerciasis, the
recommended drugs are: albendazole 400 mg + ivermectin 150 g/kg body I
weight, once a year for at least 5 years or until the microfilaraemia prevalence
is brought below 1% in most areas and less than 1 in 1000 school entry children
show infection, whichever occurs later.
In areas with concurrent loasis: mass interventions cannot be envisaged sys- II
tematically because of the risk of severe adverse reactions in patients with
high-density Loa loa infections (about 1 in 10 000 treatments). Currently, MDA
with ivermectin cannot be implemented in areas coendemic for Loa loa.
To alleviate and prevent suffering and disability: III

increase lymph flow through elevation and exercise of the swollen limb;
reduce secondary bacterial and fungal infections of limbs or genitals where
the lymphatic function has already been compromised by filarial infection. IV
Secondary infection is the primary determinant of the worsening of lymphoedema
and elephantiasis.

108
Scrupulous hygiene and local care are very effective in preventing painful, debili-
tating and damaging episodes of lymphangitis. Measures consist of regular washing
with soap and clean water, daily exercising of the limbs, and wearing of comfort-
able footwear.
Whereas MDA may generally be expected to reduce or interrupt LF transmission,
the goal of GPELF could be achieved more rapidly through additional vector con-
trol in some situations. The large-scale use of long-lasting insecticidal nets (LLINs),
already encouraged for malaria control, will also have a benefit in reducing trans-
mission of LF.
Individual level
LF vectors usually bite between the hours of dusk and dawn. Contacts with infected
mosquitoes may be decreased through the use of repellents, LLINs or insecticide-
impregnated materials.
Epidemic control
Because of relatively low infectivity and long incubation, outbreaks of LF are unlikely.

109
MALARIA

In both CAR and Chad, malaria risk exists throughout the country. Both coun-
tries face major challenges with regard to malaria control.

Few data are available, but WHO has estimated the total number of malaria cases
at 1 600000. A Malaria Strategic Plan was introduced in 2007.35
Chad
In Chad, malaria is one of the most important public health problems. At health-
facility level it represents 30% of consultations and 15% of reported deaths. It is
the major cause of morbidity and mortality especially in pregnant women and
children < 5 years. The 410 649 malaria cases reported in 2005 may represent a
considerable underestimation of the true burden of disease.
MALARIA
WHO-estimated burden of malaria
Estimated cases
Age group Numbers Lower range Upper range
Fever suspected of All ages 7 095 000 3 965 000 10 400 000 I
being malaria < 5 years 4 301 000 760 000 8 250 000
Malaria cases All ages 4 179 000 2 335 000 6126 000
< 5 years 2 533 000 447 000 4 859 000
Malaria deaths All ages 18 000 8 900 30 000 II

< 5 years 17 000 8 300 28 000
Malaria case-fatality All ages 0.43

rate (%) < 5 years 0.67
Source: World Malaria Report 2008. Geneva, World Health Organization, 2008. III
The three climatic divisions of the country (northern desert, central Sahelian
transition zone and southern tropical) determine the epidemiological profiles of
malaria. Most of the cases occur in the hyperendemic southern tropical part of
IV
35 Source: World Malaria Report 2008. Geneva, World Health Organization, 2008.

110
the country (bordering CAR) which houses 70% of the population, whereas the
dry desert north is an area of no- and low- endemicity (1% of the population).
The transition zone (29% of the population) experiences an inconsistent burden
of disease given the seasonal variation in rainfall and short transmission period,
and is at risk of epidemics.
The Ministry of Health has recently revised the National Malaria Strategic Plan,
which is in the process of validation, to cover the period 20082012.
Description
Infectious agent
Plasmodium falciparum, which causes the most life-threatening form of the dis-
ease, causes over 90% of all malaria deaths.
Case definition
Probable case
Uncomplicated malaria: patient with fever or history of fever within the
past 48 hours (with or without other symptoms such as nausea, vomiting
and diarrhoea, headache, back pain, chills, muscle pains and fatigue).
Severe malaria: patient with fever or a recent history of fever, plus drowsi-
ness with extreme weakness and associated signs and symptoms related
to organ failure (e.g. disorientation, loss of consciousness, convulsions,
severe anaemia, jaundice, haemoglobinuria, spontaneous bleeding, acute
respiratory distress, pulmonary oedema and shock).
Confirmed case (uncomplicated or severe): patient with uncomplicated or
severe malaria with laboratory confirmation of diagnosis of malaria infection
by microscopy or rapid diagnostic tests (RDT) detecting antigen.
In sub-Saharan African countries with stable high-transmission settings, such as

CAR and Chad, it is recommended that all fever cases in children < 5 years be
treated as malaria. Treatment for malaria based on clinical diagnosis alone is jus-
tified given the high prevalence of infection and high malaria risk in this age
group, which is most vulnerable to lethal outcome from the malarial infection.
The risk of comorbidity requires a high index of clinical suspicion and close moni-
toring which may be aided by Integrated Management of Childhood Illnesses
(IMCI) algorithms for diagnosis and treatment.

111
Vector-borne, through the bite of certain species of Anopheles mosquitoes that
bite mainly between dusk and dawn.
Malaria may also be transmitted through transfusion by injection of infected blood.
Rarely, infants may contract malaria in utero (through transplacental transfer of
parasites) or during delivery.
Transmission is related to the presence of infective female Anopheles mosquitoes
and of infective gametocytes in the blood of patients. Untreated or insufficiently
treated patients may be a source of mosquito infection for up to 40 years in
P. malariae malaria and 5 years in P. vivax and P. ovale malaria.
Significant biological features of some major malaria vectors in Africa
Anopheles Resting Feeding time Host Breeding sites Insecticide

species location and location preferences susceptibility
A. gambiae Mainly indoors Mainly late Mainly humans Sunlit temporary Resistance to
pools, rice fields DDT, HCH,a
Indoors
MALARIA
recently to
pyrethroids in
west Africa
A. arabiensis Indoors and Mainly late Humans and Temporary Resistance to

outdoors animals pools, rice fields DDT, and to
Indoors and
outdoors
malathion in I
Sudan
A. funestus Mainly indoors Mainly late Mainly humans Semi-permanent Resistance to

and permanent DDT, recently to
Indoors
water, especially
with vegetation,
pyrethroids in
southern Africa.
II
swamps, slow
streams, ditch
edges
Source: Malaria control in complex emergencies. An inter-agency field handbook. Geneva, World Health III
Organization, 2005 (www.who.int/malaria/interagencyfieldhandbook.html).
a Hexachlorocyclohexane
Incubation period
IV
Average incubation periods for mosquito-transmitted P. falciparum is 914 days,
P. vivax and P. ovale 1218 days and P. malariae 1840 days.

112
Malaria should be considered in all cases of unexplained fever that starts at any
time between one week after the first possible exposure to malaria risk and two
months (or even later in rare cases) after the last possible exposure.
Factors which influence transmission include: altitude, rainfall, humidity, tem-
perature, surface water distribution and vegetation. The highest transmission
occurs during and just after the period of the rainy season.
Epidemiology
General
Africa has the highest burden of malaria cases and deaths globally. In most coun-
tries, reported cases underrepresent the actual total number of malaria cases, since
many cases are not reported to the national health information systems nor cap-
tured by public health services as they go to private pharmacies or traditional
healers. 30% of malarial deaths in Africa occur in the wake of war, local violence and
emergencies. These malaria deaths often exceed those caused by the conflict itself.
Temperatures within the range 1832 C are considered suitable climatic conditions
for complete vector development and malaria parasite transmission. In highlands
above 2000 m, temperatures may fall below 18 C, which decreases parasite devel-
opment and malaria transmission significantly. In semi-arid and desert areas,
temperatures are often above 32C and mosquito survival is compromised.
The Sahelian zone in Africa is the boundary zone between the Sahara to the north
and more fertile regions to the south, extending from the Atlantic coast to the
Horn of Africa and running through Senegal, Mauritania, Mali, Burkina Faso,
Niger, Nigeria, Chad, Sudan and Eritrea.
Seasonality
Central African Republic: malaria transmission predominantly caused by
P. falciparum occurs throughout the year in the whole country.
Chad: transmission risk exists year-round throughout the country. The peak
transmission season is expected from May to December, during and just after
the rainy season.

113
Alert threshold
Any increase in the number of cases above what is expected for that time of the
year in a defined area. For emergencies and for settings where no historical data
are available for comparison, a clustering of severe cases and deaths should
raise an alarm. Another method suggested for defining a threshold is a doubling
of cases compared with the baseline (average weekly number of cases compared
to the weekly average over the previous 23 weeks), adjusted for fluctuations in
clinic attendance resulting from external factors such as a sudden influx of a
migrant population. Other features of epidemic malaria are an increase in the
incidence of severe cases and an increase in the incidence in children > 5 years
and adults.

Population movement. The potential for epidemics may increase because of the
influx of less-immune populations moving from areas of no or low malaria
transmission to highly endemic areas. The movement of populations from, into
MALARIA
and within the region is likely to affect the malaria situation. Displaced people
move between regions of a range of endemicities. Although malaria transmission
occurs throughout the year in most of the subregion, not all of the population
have protective levels of acquired immunity.
I
Overcrowding. As a result of increased population density, exposure to mosquito
bites in temporary shelters increases.
Poor access to health services. Delay in access to effective treatment increases

the likelihood of severe disease and death. This delay also increases the pool of II
malaria gametocyte carriers (the mature sexual stage of the parasite in humans
that, once picked up in the blood-meal of a mosquito, develops into the infective
stage for transmission to another human).
Food shortages. Malnutrition increases vulnerability to severe malaria once III

infection has occurred. Severe malnutrition often masks symptoms and signs of
infectious diseases, making prompt clinical diagnosis and early treatment very
difficult. This may result in increased mortality.
IV
Lack of safe water and poor sanitation. Temporary stagnant water bodies may
increase malaria-vector breeding opportunities, especially in arid environments.

114

National malaria treatment protocol, Central African Republic
Species Uncomplicated Treatment Severe Pregnancy

failure malaria
Unconfirmed Laboratory- Treatment Prevention
confirmed
P. falciparum AL* AL* QN (7days) QN (7days) QN (7days) SP (IPTp)
Source: Source: WHO Global Malaria Programme, Global AMDP database AFRO, May 2008
(http://apps.who.int/malaria/amdp/amdp_afro.htm)
National malaria treatment protocol, Chad

Species Uncomplicated Treatment Severe Pregnancy

failure malaria
Unconfirmed Laboratory- Treatment Prevention
confirmed
P. falciparum AS+AQ* AS+AQ* QN (7 days) QN (7 days) QN SP (IPTp)

or AL* or AL*
Source: WHO Global Malaria Programme, Global AMDP database AFRO, May 2008
(http://apps.who.int/malaria/amdp/amdp_afro.htm)
AS = artesunate, AQ = amodiaquine, AL = artemether-lumefantrine, QN = quinine, SP = sulfadoxine-

pyrimethamine; IPTp = intermittent preventive treatment during pregnancy.
* Policy adopted, not currently being deployed, implementation process ongoing
Laboratory diagnostic (microscopy) services are available at regional and district

hospitals, other district health facilities and private laboratories. Malaria diagnosis
is done by rapid diagnostic tests (RDTs) in some clinics. RDTs that detect histidine-
rich protein-II (HRP-II) may continue to produce positive test results for up to
14 days after effective treatment of a malaria infection, even when patients no
longer have detectable parasites on microscopy. RDTs should therefore not be
used to assess parasite clearance or for rescreening treated patients.
RDTs may lose their sensitivity when stored in hot and humid conditions and
usually should be stored at < 30C. It is recommended that heat-stability data
should be requested from the manufacturer before purchase.36
36 For more information on RDTs, please refer to: http://www.who.int/malaria/rdt.html and http://www.
wpro.who.int/sites/rdt.

115
Key strategies for malaria control include:
capacity-building of the national malaria control programme in management

and coordination;
case management;
vector control;
epidemic preparedness and response in epidemic-prone districts;
information, education and communication materials for malaria control and
community mobilization;
community-based malaria control;
operational research;
strengthening of monitoring and evaluation.
Both countries have a five-year strategic plan for malaria control (CAR, 20072011;
Chad, 20082012). Intermittent preventive treatment (IPTp) with sulfadoxine-
pyrimethamine at least twice during pregnancy (during the second and third tri-
mesters) is recommended for pregnant women living in areas where transmission
is high and where SP is > 80% effective. It is best implemented through antenatal care.
MALARIA
Long-lasting insecticidal nets (LLINs) provide personal protection for all those who
sleep under the net. They also have the potential to significantly reduce the adult
mosquito population when coverage is above 80% (community impact), thereby reduc-
ing transmission and subsequently morbidity and mortality. LLINs may be distrib-
uted with integrated mass vaccination campaigns or as stand-alone distributions.
Health education on proper use and care is vital for the success of LLIN programmes.
I
Periodic indoor spraying of shelters with residual insecticide (IRS) may reduce
transmission when applied according to WHO recommendations and when the
following conditions are met:
II
a high percentage of the structures in an operational area have adequate
sprayable surfaces, and can be expected to be well sprayed;
the majority of the vector population is endophilic, i.e. rests indoors;
the vector is susceptible to the insecticide in use. III
The main purpose of IRS is to reduce transmission by reducing the survival of malaria
vectors entering houses or sleeping units. IRS is not applicable during acute phases
of emergencies. It may be useful in well-organized temporary settlements/camps.37
IV
37 http://www.who.int/malaria/indoorresidualspraying.html.

116
Environmental control may be difficult during the acute phase of an emergency

except on a local scale, and impact is often limited. To reduce the number of vector
breeding sites:
drain clean water around water-tap stands and rainwater drains;

use larvicides in vector breeding sites if these are limited in number (seek
expert advice);
drain ponds (although this may not be acceptable if ponds are used for wash-
ing and/or for animals).
Vigorous health education at community level is important to improve rapid

treatment-seeking behaviour for fever cases, for effective LLIN use and improving
indoor residual spraying (IRS) acceptability.

International travellers should use chemoprophylaxis and use personal protection
to prevent mosquito bites between dusk and dawn, and immediately seek diagnosis
and treatment for any fever occurring a week or more after entering the country.
The recommended chemoprophylaxis options for international travellers to CAR
and Chad are: atovaquone-proguanil, doxycycline or mefloquine.38
38 More information for international travellers is available at http://www.who.int/ith.

117
MEASLES

Reported cases, Central African Republic, by year
Year 2007 2006 2005 2004 2003 2002 2001 2000
49 3 471 2 013 652 938 2 837 3 207
Source: Data provided by the Ministry of Health through the WHO/UNICEF joint reporting form
(http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencemea.htm).
Outbreaks:
December 2007 January 2008: 116 cases; 1 death; CFR 0.9%; Ouham.
JanuaryJune 2005: 195 cases; 18 deaths; CFR 9.2%; Lobaye.
DecemberMay 2004: 225 cases; 36 deaths; CFR 16%; Nana-Mambre.
MEASLES
JanuaryJune 2004: 1040 cases; 80 deaths; CFR 13%; Basse-Kotto.
JanuaryMay 2003: 443 cases; 86 deaths; CFR 19.4%; Ouham.
JanuaryApril 2002: 287 cases; 19 deaths; CFR 6.6%; Kemo.
JanuaryJune 2002: 495 cases; 11 deaths; CFR 2.2%; Nana-Mambre. I
Differences between reported measles cases in the WHO/UNICEF joint report-
ing form (JRF) and the outbreak data above are probably due to underreporting
of cases in the JRF. In the joint global plan for reducing measles mortality, 2006 II
2010, WHO and UNICEF have identified 47 priority countries to be targeted. These
countries account for more than 95% of global measles deaths and include CAR.
Measles morbidity and mortality has decreased over the past few years. This is
attributable to increasing routine measles vaccine (MV) coverage as well as the III
implementation of a nationwide catch-up vaccination campaign (20052006).
Because of human and cold-chain resource constraints, the nationwide catch-up

campaign was conducted in two phases, October 2005 and January 2006, target-
IV
ing 1 838 877 children aged 6 months to 14 years. Overall campaign coverage
was 92% and administrative coverage results are shown in the map below.

118
Measles vaccine coverage in the campaign targeting children aged 6 months to 14 years, by prefecture,
Central African Republic, 20052006

119
In 2006, CAR also initiated national child survival days (journes nationales de
survie de lenfant) as an additional strategy to improve routine vaccination cover-
age. Three rounds were conducted in 2006, in August, September and October. The
result of these activities was that only 3 laboratory-confirmed cases of measles were
detected in 2006 and no outbreaks reported. The outbreak in Ouham province (2007
2008) is the first reported and confirmed outbreak since the catch-up campaign.
The presence of the Pasteur Institute in Bangui (Institut Pasteur de Bangui) and
its close collaboration with the Ministry of Health and WHO, have greatly facili-
tated the implementation of measles (and yellow fever) case-based surveillance.
Case-based measles surveillance performance is among the best in the central
African subregion. The non-measles febrile and rash investigation rate was 5.6
per 100 000 population and 22 of 24 districts (sous-prefectures) investigated at
least one suspected measles case with a blood specimen in 2007.
A nationwide follow-up campaign is planned for October or November 2008. This
campaign will target children aged 659 months and will integrate the distribu-
tion of treated bednets, deworming and vitamin A supplementation. Providing
an additional dose of oral polio vaccine (OPV) is also under discussion.
MEASLES
Chad
Reported cases, Chad, by year
Year 2007 2006 2005 2004 2003 2002 2001 2000
441 1 594 2 10 324 15 801 7 277 27 908 3 546 I

Source: Data provided by the Ministry of Health through the WHO/UNICEF joint reporting form and WHO
regional offices (http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencemea.htm).
Outbreaks: II
FebruaryJune 2007: 147 cases; 1 death; CFR 0.7%; Ndjamena.
JanuaryMay 2005: 20 278 cases; 516 deaths; CFR 2.5%.
Province, cases, deaths. Batha, 750, 31; Chari Baguima, 8 039, 164; Kanem, III
516, 2; Lac, 225, 2; Logone occidental, 375, 5; Logone oriental, 725, 33;
Mayo-Kebi, 1 008, 24; Moyen Chari, 5 589, 169; Quaddai, 1 050, 11; Salamat,
1 460, 34; Tandjile, 280, 5.
Differences between reported measles cases in the WHO/UNICEF joint reporting IV
form (JRF) and the outbreak data above are probably due to underreporting of
cases in the JRF.

120
Because of persistently low routine measles immunization coverage (23% report-

ed in 2006), between 1990 and 2004, an average of over 14000 cases were report-
ed annually. Case-fatality ratios varied between 1% and 5% (Ministry of Health,
Integrated Disease Surveillance and Response). The number of reported cases
has dramatically decreased since the nationwide catch-up vaccination campaign
Catch-up measles vaccine coverage by region, Chad, 20052006


121
conducted between March 2005 and January 2006. Overall, 5 060 371 children
aged 9 months to 14 years were targeted for MV during three campaign rounds.
During these rounds, national vaccination administrative coverage was reported
as being 92% with variation at the provincial and district levels.
Administrative vaccination coverage, catch-up supplemental

immunization activity (SIA)
Campaign Dates Target No. districts reporting Coverage

phase population administrative coverage (n = 54)
< 90% 9094% 95%
Phase 1 1424 March 303 062 2 2 97%

2005
Phase 2 26 Sept5 Oct 2 045 298 7 5 6 80%

2005
Phase 3 1625 January 2 712 011 1 31 101%*

2006
* Total population was underestimated
MEASLES
Despite high administrative vaccination coverage levels attained by the majority
of districts, laboratory-confirmed cases were detected in several districts in the
months following the campaign and an outbreak occurred in Ndjamena approxi-
mately 14 months after the catch-up supplemental immunization activity (SIA) I
(albeit with far fewer cases and deaths than during the 2005 outbreak).
The sub-optimal quality of the catch-up SIA and continued poor routine vaccina-
tion coverage (~20%) results in an ever-growing susceptible population. A follow-
up campaign in Chad is tentatively scheduled to occur in the last quarter of 2008 II
following the rainy season and should target approximately 1.6 million children
aged 659 months. Unfortunately, politicomilitary events as well as the spread of
a current polio epidemic may defer this campaign.
Measles case-based surveillance with laboratory-confirmation of suspected cases III
was initiated subregionally in 2006. Prior to this, laboratory confirmation of sus-
pected measles outbreaks was undertaken at the national reference laboratory on
an ad hoc basis starting in 2004. Although cascade training for measles and yellow
fever case-based surveillance of regional and district surveillance focal points IV
was completed in May 2007, case-based measles surveillance performance con-
tinues to be poor. The non-measles febrile and rash investigation rate of 0.80 per

122
100 000 population is well below the objective of 2.0 per 100000 population, and
only 50% of districts investigated at least one suspected case with a blood specimen.
Description
Infectious agent
Measles virus (genus Morbillivirus, family Paramyxoviridae).
Case definition
Any person with:
fever; and
maculopapular (i.e. non vesicular) rash; and
cough or coryza (i.e. runny nose) or conjunctivitis (i.e. red eyes);
or any person in whom a clinical health worker suspects measles infection.
Laboratory criteria
Presence of measles-specific IgM antibodies.
Case classification
Suspect: a case that meets the clinical case definition or any person in whom
a clinical health worker suspects measles infection.
Laboratory-confirmed: a case that meets the clinical case definition and is
laboratory-confirmed;
Confirmed through epidemiological linkage: a case that meets the clinical
case definition and is from the same district or zone where an outbreak has
been laboratory-confirmed during the previous 30 days.
Cases may be clinically further classified as uncomplicated (simple) or complicated

by the presence or absence of medical complications (pneumonia, diarrhoea, stomatitis,
malnutrition, encephalitis, otitis media, croup, subacute sclerosing panencephalitis).
Airborne by droplet spread; or direct contact with the nasal and throat secretions
of infected people or via an object (e.g. toys) that has been in close contact with
an infected person.

123
Incubation period
After infection, there is an asymptomatic incubation period of 1012 days, with a
range from 7 to 18 days from exposure to the onset of fever.
Measles is most infectious from 4 days before the rash until 12 days after rash onset.
Epidemiology
General
In 2005, the World Health Assembly adopted an ambitious global goal for measles
control, as part of the Global Immunization Vision and Strategy document, that
aims to achieve a 90% reduction in measles mortality by 2010 compared with 2000.
Measles is one of the most contagious diseases known and remains a leading cause
of death among children worldwide. Most children will have uncomplicated measles
and require supportive care as outpatients. The overwhelming number of measles
deaths occur in countries with a low GNP, weak health infrastructure, or experi-
MEASLES
encing or recovering from war, civil strife or natural disaster. Infection rates soar
because of the deterioration of routine immunization and increased transmission
among refugees and IDPs as a result of crowded living conditions.
Measles is still widely distributed and reported from various parts of Chad and CAR.
I
Seasonality
The highest incidence of cases is usually observed between the end of the dry season
and the beginning of the rainy season (north of the equator: FebruaryMarch). II
Alert threshold
One case must lead to an alert. Laboratory-confirmation of all cases is not required;
only a few cases from each outbreak need to be laboratory-confirmed. III

Population movement. Influx of non-immune populations into areas where the IV
pathogen is circulating or of infected individuals into areas where the population
is not immunized.

124
Overcrowding. Crowded conditions and poor indoor ventilation facilitate rapid

transmission.
Poor access to health services. Case-fatality ratios may be reduced by effective
case management, including the administration of vitamin A supplements.
Food shortages. Disease is more severe among children with malnutrition and
vitamin A deficiency. Malnourished children are at particularly high risk of
complications and death following an attack of measles. The disease may trigger
acute proteinenergy malnutrition and worsen vitamin A deficiency.

Measles control measures in emergency settings have two major components:

measles prevention through mass vaccination campaigns/routine immunization;
and measles outbreak response.
Immunization in emergency and post-emergency phases

In an acute emergency, the population at risk should be immunized as soon as
possible if vaccination coverage is < 8090% or unknown. The priority is to immu-
nize children aged 6 months to 15 years, regardless of vaccination status or disease
history. Expansion to older age groups is of lower priority and should be based
on evidence of high susceptibility among the age group. The age range may be
reduced if resources are limited, e.g. 6 months to 12 years or 6 months to 5 years.
Children who are vaccinated against measles < 9 months of age should receive a
second measles vaccination. This should be given as soon as possible after reach-
ing 9 months of age, with an interval of at least 1 month between doses.
Measles morbidity and mortality in malnourished populations are preventable
with vaccination targeting those aged 6 months to 15 years. Vitamin A supple-
mentation is necessary with measles vaccination in all those aged <5 years, as it
minimizes the complications of the disease. If there is evidence of clinical vitamin A
deficiency in older age groups, treatment with vitamin A should be initiated as
per WHO guidelines.
To ensure injection safety during immunization, autodisable syringes and safety
boxes are recommended. Safe disposal of used sharps should be ensured.
Outbreak response
Inform the health authorities if one or more suspected cases are identified.

125
Confirm the suspected outbreak, following WHO guidelines.

Investigate suspected case: check whether case fulfils the case definition,
record date of onset, age and vaccination status.
Confirm the diagnosis: collect blood specimens from 35 initial reported cases.
Assess the extent of the outbreak and the population at risk.
Implement outbreak response measures as follows:
Give priority to proper case management and immunization of groups at
highest risk (e.g. children aged 6 months 15 years) as soon as possible
even in areas not yet affected where the outbreak is likely to spread. This
range may be reduced if resources are limited, e.g. 6 months to 12 years or
6 months to 5 years.
Through social mobilization ensure parents bring previously unvaccinated
children for immunization.
The presence of several cases of measles in an emergency setting is an indi-
cation for a measles immunization campaign. Even among individuals who
have already been exposed, and are incubating the natural virus, measles
MEASLES
vaccine, if given within 3 days of exposure, may provide protection or
modify the clinical severity of the illness.
Isolation is not indicated and children should not be withdrawn from feed
ing programmes.
Case management I
For uncomplicated cases:
Give vitamin A immediately upon diagnosis and ensure that the child receives
a second dose the next day (may be given to parent to administer at home). II
Advise the parent to treat the child at home (control fever and provide nutri-
tional feeding).
For cases with non-severe eye, mouth or ear complications: III

Children may be treated at home.
Give vitamin A immediately upon diagnosis and ensure that the child receives
a second dose the next day (may be given to parent to administer at home).
IV
If pus is draining from the eyes, clean eyes and treat with 1% tetracycline eye
ointment.

126
If there are mouth ulcers, treat with gentian violet.

If pus is draining from the ear, clean ear discharge and treat with antibiotics
for 5 days (amoxicillin first-line, or co-trimoxazole second-line), as per
national ARI policy and IMCI guidelines currently under development.
Treat malnutrition and diarrhoea, if present, with sufficient fluids and high-
quality diet.
For cases with severe, complicated measles (any general danger signs, clouding of
cornea, deep or extensive mouth ulcers, pneumonia):
Refer urgently to hospital.

Treat pneumonia with an appropriate antibiotic.

If there is clouding of the cornea or pus draining from the eye, clean eyes and
apply 1% tetracycline eye ointment.
If the child has any eye signs indicating vitamin A deficiency (i.e. night blind-
ness, Bitt spots, conjunctival and corneal dryness, corneal clouding or corneal
ulceration), then he or she should receive vitamin A immediately, a second
dose the next day and third dose 24 weeks later.
Note
General danger signs: inability to drink or breastfeed, repeated vomiting,
convulsions, lethargy or unconsciousness.
Vitamin A should not be given to women who may be pregnant.
Dosages of vitamin A in measles-treatment regimens
Age Immediately on diagnosis Following day
Infants < 6 months 50 000 IU 50 000 IU
Infants 611 months 100 000 IU 100 000 IU
Children > 11 months 200 000 IU 200 000 IU

127
MENINGOCOCCAL DISEASE (MENINGITIS AND

MENINGOCOCCAL SEPTICAEMIA)
MENINGOCOCCAL DISEASE (MENINGITIS AND MENINGOCOCCAL SEPTICAEMIA)

Outbreaks:
November 2007 February 2008: 45 cases; 5 deaths; CFR 11.1%; NmA, Kaga-
Bandoro, Nana-Grbizi).
April 2004: 43 cases; 7 deaths; CFR 16.27%; NmA, Nana Bougila, Zere, Ouham.
FebruaryJune 2001: 1816 cases; 343 deaths; CFR 18.8%; Paoua, Ouham-Pend
in the north-western part of the country bordering on Chad and Cameroon
(including 3 Haj pilgrims N. meningitidis serogroup W135).
February 2000: 86 cases; 14 deaths; CFR 16.2%; Bamingui-Bangoran, Haute
Kotto, Ouham-Pend and Vakaga).
Chad
Outbreaks:
MarchApril 2007: 350 cases; 17 deaths; CFR 5.1%; predominantly NmA but I
some W135, Tandjile region, Bere district.
MarchMay 2007: 31 cases; 3 deaths; CFR 9.7%; NmA, Salamat region, Am
Tinman district.
MarchApril 2006: 152 cases; 9 deaths; CFR 5.9%; NmA, Mayo-Kebbi-East II
and Logone oriental regions, Fianga and Doba districts.
JanuaryMarch 2005: 293 cases; 29 deaths; CFR 9.8%; Nm A, Mayo-Kebbi-East
and Mandoul regions, Bongor and Moissal districts.
January 2005: 9 cases; no deaths; Nm W135, Ouaddai region, refugee camps III
in Brejing, Farchana and Treguine, Adre district.
April 2004: 19 cases; 4 deaths; CFR 21%; NmA, Wadi Fira region, Iriba
district.
IV
Dec 2000 March 2001: 3579 cases; 401 deaths; CFR 11.2%; NmA, Moyen
Chari, Mayo Kebb, Logone oriental and Logone occidental.

128
Description
Infectious agent
Bacterium: Neisseria meningitidis serogroups A, B, C, Y, W135.
Case definition
An illness with sudden onset of fever (> 38.5 C rectal, > 38.0 C axillary) and one
or more of the following:
neck stiffness;
altered consciousness;
other meningeal sign or petechial or purpural rash.
In patients aged < 1 year, suspect meningitis when fever is accompanied by a

bulging fontanelle.
Laboratory criteria
Positive cerebrospinal fluid (CSF) antigen detection; or
positive bacterial culture.
Case classification
Suspected: a case that meets the clinical case definition above.
Probable: a suspected case as defined above; and
turbid CSF (with or without positive Gram stain); or
continuing epidemic.
Confirmed: a suspected or probable case with laboratory-confirmation.
Direct contact with respiratory droplets.
Incubation period
The incubation period varies between 2 and 10 days (most commonly 4 days).
From the onset of symptoms until 24 hours after the institution of therapy, but
asymptomatic carriers are the most important source of infection.

129
Epidemiology
General
The highest burden of meningococcal disease occurs in sub-Saharan Africa in an

area known as the meningitis belt that lies between Senegal and Ethiopia and
includes all, or part of, at least 15 countries of which CAR and Chad.
Twelve subtypes or serogroups of Neisseria meningitidis have been identified and
four (N. meningitidis A, B, C and W135) are recognized as causing epidemics.
The pathogenicity, immunogenicity, epidemic capabilities and vaccines differ
according to the serogroup. Thus the identification of the serogroup responsible
for a sporadic case is crucial for epidemic containment.
In 1996, Africa experienced the largest recorded outbreak of epidemic meningitis
in history, with over 250 000 cases and 25 000 deaths registered. Between 1996
and 2002, a further 223000 new cases of meningococcal meningitis were reported
to WHO. The countries most affected were Burkina Faso, Chad, Ethiopia and
Niger. The meningitis belt also appears to be extending further south. In 2002,
the Great Lakes region was affected by outbreaks in villages and refugee camps
that caused over 2200 cases, including 200 deaths.
In major African epidemics, attack rates range from 100 to 800 per 100 000 popu-
lation, but individual communities have reported rates as high as 1000 per 100 000.
While in endemic disease the highest attack rates are observed in young children,
during epidemics, older children, teenagers and young adults are also affected.
Geographical distribution I
Chad and CAR are in the African meningitis belt, an area that experiences repeated
epidemics of meningococcal disease, in addition to the substantial number of
endemic cases.
II
Seasonality
Epidemics of meningococcal disease occur in seasonal cycles between the end of
November and the end of June. Dry, windy and dusty seasons increase transmis-
sion of the disease. Conversely rains decrease transmission. III
Alert threshold
Population > 30 000: 5 cases per 100 000 inhabitants per week or a cluster of
cases in an area.
IV
Population < 30 000: 2 cases in 1 week or an increase in the number of cases
compared with previous non-epidemic years.

130
Intervention:
1. Inform authorities
2. Investigate
3. Confirm
4. Treat cases
5. Strengthen surveillance
6. Prepare.
Epidemic threshold
Population > 30 000: 10 cases per 100 000 inhabitants per week if
no epidemic for 3 years and vaccination coverage < 80%;
alert threshold crossed early in the dry season.
15 cases per 100 000 inhabitants per week in other situations.
Population < 30 000: 5 cases occur in 1 week, or

doubling of the weekly number of cases in a 3-week period; or
for mass gatherings, refugees and displaced persons, 2 confirmed cases in
1 week are enough to initiate vaccination of the population.
Other situations should be studied on a case-by-case basis.
Intervention:
Mass vaccination
Distribute treatment to health centres
Treat according to epidemic protocol
Inform the public.

Population movement. Travel, migration and displacement facilitate the circula-
tion of virulent strains within a country, or from country to country.
Overcrowding. Crowding of susceptible people and poor indoor ventilation are
important risk factors for outbreaks. Crowding during emergencies, or because

131
of cattle or fishing-related activities, or in military camps and schools, facilitates

spread of the disease.
Poor access to health services. Case identification is crucial for rapid implemen-

tation of control measures. The case-fatality ratio in the absence of treatment can
be very high (50%).

Enhanced epidemiological surveillance and prompt case management with oily
chloramphenicol and reactive mass vaccination campaigns are used to control
epidemics. Routine immunization is not possible with currently available vaccines,
as polysaccharide vaccines only provide protection for 35 years and cannot be
used in children aged < 2 years since current meningococcal vaccines are not
immunogenic in this age group (i.e. no antibodies are produced). Even large-scale
coverage with current vaccines does not provide sufficient herd immunity.
Concurrent infections: upper respiratory tract infections may increase transmis-
sion of meningitis.
Low vaccination coverage (< 80%) increases the number of susceptible people in
the population.
Consequently, the current WHO recommendation for outbreak control is mass
vaccination in every district that is in an epidemic phase, as well as those contigu-
I
ous districts that are in the alert phase. It is estimated that a mass immunization
campaign, promptly implemented, can avoid 70% of cases.
Case management
Meningococcal disease (either meningitis or septicaemia) is potentially fatal and
II
should always be considered a medical emergency.
Non-epidemic conditions
Admission to a hospital or health centre is necessary for diagnosis (lumbar
III
puncture and CSF examination).
Lumbar puncture must be done as soon as meningitis is suspected, before
starting antimicrobials.
IV
As infectivity of patients is moderate and disappears quickly following anti-
microbial treatment, isolation of the patient is not necessary.

132
Antimicrobial therapy must be instituted as soon as possible after lumbar

puncture (without waiting for laboratory results) and should be combined
with supportive treatment.
Initial antimicrobial therapy should be effective against the three major causes of
bacterial meningitis (N. meningitidis, Streptococcus pneumoniae and Haemophilus
influenzae) until bacteriological results are available (see below).
Initial empirical antimicrobial therapy for presumed bacterial meningitis
Age group Probable pathogens Antimicrobial therapy
First choice Alternative

Epidemic situations
All age groups N. meningitidis Benzylpenicillin or Ampicillin or

oily chloramphenicol ceftriaxone or
cefotaxime or
co-trimoxazole
Non-epidemic situations
Adults and children N. meningitidis Benzylpenicillin or Ampicillin or

> 5 years S. pneumoniae oily chloramphenicol ceftriaxone or
cefotaxime or
co-trimoxazole
Children H. influenzae Ampicilin or Ceftriaxone or

1 month to 5 years S. pneumoniae amoxycilin or cefotaxime
N. meningitidis chloramphenicol
Neonates Gram-negative bacteria Ampicillin and gentamicin Ceftriaxone or

Group B streptococci cefotaxime or
Listeria spp. chloramphenicol
Once diagnosis of meningococcal disease has been established:
The drugs of choice include benzylpenicillin, ampicillin or chloramphenicol

injection or other antibiotics based on antimicrobial susceptibility tests.
The third-generation cefalosporins, ceftriaxone and cefotaxime, are excellent
alternatives but are a little more expensive.
A 7-day course is the general rule for treatment of meningococcal disease beyond
the neonatal period.
The long-acting (oily) form of chloramphenicol has also been shown to be effec-
tive and is preferred for mass interventions during epidemics.

133
Epidemic conditions
During epidemics of confirmed meningococcal disease, case management needs
to be simplified to permit the health system to respond to rapidly increasing

numbers of cases.
Diagnosis: as the flood of patients could make the routine use of lumbar
puncture to confirm meningitis impossible, every suspected case of meningitis
should be considered and treated as having meningococcal meningitis.
Treatment: long-acting oily chloramphenicol (100 mg/kg up to 3 g in a single
dose) given intramuscularly, is the drug of choice for all age groups, particu-
larly in areas with limited health facilities. For those who do not improve
rapidly, an additional dose of the same antimicrobial 48 hours after the first
dose is recommended.
Reactive vaccination
A mass vaccination campaign may halt an epidemic of meningococcal disease if
carried out appropriately. Laboratory diagnosis and confirmation of epidemic sero-
groups will guide the type of vaccine needed, either meningococcal polysaccharide
bivalent A/C (if serogroup A or C is confirmed as the epidemic serogroup), menin-
gococcal polysaccharide trivalent A/C/W135 (if serogroup W135 is confirmed) or
tetravalent vaccine A/C/Y/W135 (if serogroup Y or W135 is confirmed). Vaccination
should be concentrated in the area where the epidemic is maximal.
I
Camp settings: following confirmation (serogroup identified) of two cases,
mass vaccination is recommended if the serogroup(s) identified is(are) included
in either the bivalent (A/C) or tetravalent (A/C/Y/W135) vaccine. At-risk popu-
lations (e.g. 230 years of age) should be given priority.
II
General population: if an outbreak is suspected, vaccination should be consid-
ered only after careful investigation (including confirmation and serogroup
identification) and assessment of the population group at highest risk.
Chemoprophylaxis of contacts of meningitis patients is not warranted during an III

epidemic. In small clusters or outbreaks among closed populations (e.g. extended
household, boarding schools), chemoprophylaxis may still be appropriate.
IV

134
ONCHOCERCIASIS (RIVER BLINDNESS)

Approximately 1.5 million people are at risk. Since 2007 a technical adviser has
been placed by the African Programme for Onchocerciasis Control (APOC) in
the office of the WHO representative to support the country relaunch of mass
ivermectin distribution activities after a 5-year interruption owing to civil unrest.
Although further mapping still needs to be done to update the number of villages
affected, onchocerciasis is known to be endemic in 11 of the 16 regions. Control

operations first sponsored by an NGO (the Christoffel-Blindenmission) began in
1993 but were interrupted in1996 as a result of civil unrest. The African Programme
for Onchocerciasis Control (APOC) commenced in 1997 as part of an Africa-wide
control initiative. With WHO support, the country has recently developed a stra-
tegic plan for integrated control of helminth infections, including onchocerciasis.
Chad
The disease is endemic in 7 of 18 regions (17 districts) in the southern part of the
country. Approximately 1.6 million people are targeted annually for mass drug
treatment, mainly under the auspices of APOC. Treatment coverage has averaged
75% over the past 7 years.
Description
Infectious agent
Onchocerca volvulus, a filarial worm belonging to the class Nematoda.
Case definition
In an endemic area, a person with fibrous nodules in subcutaneous tissues. These
must be distinguished from lymph nodes or ganglia. People suffering from onchocer-
ciasis may experience:
Skin lesions: dermal changes are secondary to tissue reaction to the motile
larvae as they migrate subcutaneously or to their destruction in the skin.

135
Itching: the pruritus of onchocerciasis is the most severe and intractable that is
known. In lightly-infected individuals, this may persist as the only symptom.
Rashes: the rash usually consists of many raised papules, which are caused by
microabscess formation, and may disappear within a few days or may spread.
Sowda, from the Arabic for black or dark, is an intensely pruritic eruption
usually limited to one limb and including oedema, hyperpigmented papules
and regional lymphadenopathy.
Depigmentation of the skin: areas of depigmentation over the anterior shin,
with islands of normally pigmented skin, commonly called leopard skin,
are found in advanced dermatitis.
Subcutaneous nodules: these are asymptomatic subcutaneous granulomas,
0.53.0 cm, resulting from a tissue reaction around adult worms. They occur

most frequently over bony prominences: in Africa, the nodules are often located
over the hips and lower limbs.
Lymphadenopathy: frequently found in inguinal and femoral areas, lymphad-
enopathy can result in hanging groin (especially when associated with skin
atrophy and loss of elasticity) and elephantiasis of the genitalia.
Eye lesions: ocular onchocerciasis is related to the presence of live or dead micro-
filariae. Involvement of all tissues of the eye has been described, and many changes
in both anterior and posterior segments of the eye may occur. The more serious
lesions lead to serious visual impairment including blindness.
General debilitation: onchocerciasis has also been associated with weight loss and I
musculoskeletal pain.
Laboratory criteria
Presence of one or more of the following: II
microfilariae in skin snips taken from the iliac crest (Africa) or scapula (Americas);
adult worms in excised nodules;
typical ocular manifestations, such as slit-lamp observations of microfilariae
in the cornea, the anterior chamber or the vitreous body;
III
serology (especially for non-indigenous people).
Case classification
IV
Confirmed: a suspected case that is laboratory-confirmed.

136
Onchocercal microfilariae produced in one person are carried to another by
the bite of infected female blackflies belonging to the genus Simulium (mainly
S. damnosum but in some foci S. neavei). The blackfly lays its eggs in the water of
fast-flowing rivers thus the name river blindness. Adult blackflies emerge after
812 days and live for up to 4 weeks, during which time they may cover hundreds
of kilometres in flight.
Microfilariae are ingested by a blackfly feeding on an infected person; these
microfilariae then penetrate the thoracic muscles of the fly. Here, a few of them
develop into infective larvae and after several days migrate to the cephalic cap-
sule to be liberated into human skin during the bite wound of a subsequent
blood meal.
Infective larvae develop into adult parasites in the human body where adult forms
of O. volvulus may live for up to 1415 years and are often found encased in fibrous
subcutaneous nodules. Each adult female produces millions of microfilariae that
migrate under the skin and through the eyes, producing a variety of dermal and
ocular symptoms (see above).
Humans are the only reservoir. Other Onchocerca species found in animals cannot
infect humans but may occur together with O. volvulus in the insect vector.
Incubation. Larvae take at least 612 months to mature. Adult worms are usually
innocuous, apart from the production of the subcutaneous nodules (these can
develop as early as 1 year after infection). The main pathological sequelae of
O. volvulus infection are caused by the death of microfilariae in skin and ocular
tissue, where they may be found after a period of 734 months. Microfilariae
are found in the skin usually after only 1 year or more from the time of the
infective bite.
Human to blackfly: infected individuals may infect blackflies as long as living
microfilariae occur in their skin. Microfilariae are continuously produced by
adult female worms (about 700 per day), and may be found in the skin after a
prepatent period of 734 months following introduction of infective larvae.
They may persist for up to 2 years after the death of the adult worms.
Blackfly to human: blackfly vectors become infective (i.e. able to transmit
infective larvae) 79 days after the blood meal.

137

Population movement. Migration of infected people from areas where transmis-
sion is still ongoing could result in resurgence of onchocerciasis in areas previously
free of the disease.
Overcrowding increases the risk of infectious bites.
Other factors
The great majority (99%) of the 37 million people thought to be infected live in
30 countries in sub-Saharan Africa.
Onchocerciasis is not a fatal disease, but its consequences may be severe if it is
left untreated. These include disfigurement, severe itching, skin depigmentation

(which may hinder social integration) and, most devastatingly, vision impairment
and eventual blindness.
Onchocerciasis also has important socioeconomic consequences. Fear of blindness
has led to depopulation of fertile river valleys of the western African savannah,
greatly diminishing agricultural production and increasing poverty and famine.
The dramatic consequences of onchocerciasis in western Africa led WHO, in collabo-
ration with other agencies including the World Bank, the United Nations Development
Programme (UNDP) and the Food and Agriculture Organization of the United
Nations (FAO) to launch the Onchocerciasis Control Programme (OCP) in 1974.
The programme operated over 1 200 000 km and worked to protect 30 million
people in 11 countries from the debilitating effects of river blindness. OCP was I
officially closed in December 2002 after virtually stopping transmission of the
disease in all the participating countries except Sierra Leone, where operations
were interrupted by a decade-long civil war.
Currently, there is little risk of infection, however disease surveillance needs to II
continue with focus on those areas into which migration is occurring.39

III
Case management
Administration of ivermectin once a year over a period of at least 1520 years
will reduce infection to insignificant levels and prevent the appearance of clinical
IV
39 Guidelines for rapid assessment of Loa loa. Geneva, WHO, 2002 (TDR/IDE/RAPLOA/02.1; http://www.
who.int/tdr/publications/publications/pdf/loaguidelines.pdf).

138
manifestations. The recommended dosage is equivalent to 150 g/kg body weight

(in practice, dosage is according to height, using 14 tablets of 3 mg formulation).
Established clinical manifestations are also treated by ivermectin.
Treatment with ivermectin is contraindicated in:
children < 5 years (age), less than 15 kg (weight), or less than 90 cm (height);
pregnant women;
lactating mothers of infants less than 1 week old;
severely ill people.
Epidemic control
Recrudescence of transmission may occur and can be managed by ivermectin

administration if mass treatment programmes maintain good treatment coverage.
Prevention
The two main strategies for prevention and control of onchocerciasis in Africa are:
(1) Vector control

Destruction of Simulium larvae by application of insecticides such as temephos
(Abate) through aerial spraying to breeding sites in fast-flowing rivers, in order
to interrupt the cycle of disease transmission. Once the cycle has been interrupted
for 1415 years, the reservoir of adult worms dies out in the human population,
thus eliminating the source of the disease. This was the basic strategy of the OCP.
(2) Community-directed treatment with ivermectin (CDTI)

CDTI involves the once-yearly administration of ivermectin (150 g/kg body weight).
The introduction of ivermectin in 1987 provided a feasible chemotherapeutic
regimen for large-scale treatment of onchocerciasis for the first time. Ivermectin
is an effective microfilaricide that greatly reduces the numbers of skin micro-
filariae for up to a year. For example, in 2005, more than 3 million people were
treated with ivermectin in Ethiopia with a therapeutic coverage of 75%. Efforts to
prevent resurgence should focus on areas into which migration occurs and could
include ivermectin treatment programmes.

139
PERTUSSIS (WHOOPING COUGH)

Reported cases, Central African Republic, by year
Year 2007 2006 2005 2004 2003 2002 2001
02 65 87 561 80 10 1 358
Source: WHO vaccine-preventable diseases monitoring system, 2008 global summary (as of 1 August 2008)
(http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidenceper.htm).

Chad
No data are available.
Description
Infectious agent
Bordetella pertussis, the pertussis bacillus.
Case definition
I
The initial stage the catarrhal stage is characterized by coryza (runny nose),
sneezing, low-grade fever and a mild, occasional cough, similar to the common
cold. It has an insidious onset, with an irritating cough that gradually becomes
paroxysmal, usually within 12 weeks, and lasts for 12 months or longer.
II
The patient has bursts, or paroxysms, of numerous rapid coughs, apparently
caused by difficulty in expelling thick mucus from the tracheobronchial tree. At
the end of the paroxysm, a long inspiratory effort is usually accompanied by a III
characteristic whoop. In younger infants, periods of apnoea (cessation in breathing)
may follow the coughing spasms, and the patient may become cyanotic (turn blue).
The disease lasts 48 weeks. In the convalescent stage, recovery is gradual. The
cough becomes less paroxysmal. However, paroxysms often recur with subsequent IV
respiratory infections for many months after the onset of pertussis. Fever is gen-
erally minimal throughout the course of pertussis.

140
Complications most commonly include pneumonia. Otitis, haemorrhages (sub-

conjunctival petechiae and epistaxis), convulsions, encephalopathies and death
occur more rarely.
Complications are more frequent and severe in younger infants. In developing
countries, case-fatality rates are estimated at 3.7% for children aged < 1 year and
1% for children aged 14 years. Older individuals (i.e. adolescents and adults), and
those partially protected by the vaccine, may become infected with B. pertussis,
but usually have milder disease.

A case diagnosed as pertussis by a physician; or
a person with a cough lasting at least 2 weeks with at least one of the following
symptoms:
paroxysms (i.e. fits) of coughing;
inspiratory whooping;
post-tussive vomiting (i.e. vomiting immediately after coughing) without
other apparent cause.
Laboratory criteria
Isolation of B. pertussis;
Detection of genomic sequences by polymerase chain reaction (PCR);
Positive paired serology.
Case classification
Suspect case: a case that meets the clinical case definition.
Confirmed case: a clinical case that is laboratory-confirmed.
Primarily by direct contact with discharges from respiratory mucous membranes
of infected people via the airborne route. Humans are the only hosts. Although
the disease may be milder in older individuals, these infected people may transmit
the disease to other susceptible individuals, including non-immunized or under-
immunized infants. Adults are often found to be the first case in a household
with multiple pertussis cases.

141
Incubation period
The incubation period usually lasts 710 days and rarely more than 14 days.
Pertussis is highly communicable in the early, catarrhal stage (90%). Communi-
cability gradually decreases after the onset of the paroxysmal cough. Patients may
be contagious for up to 3 weeks after the onset of paroxysmal cough in the absence
of treatment, or up to 5 days after onset of treatment.
Epidemiology
General

Outbreaks of Bordetella pertussis are common in settings of population displace-
ment, but definitive laboratory evidence is rare. This may be because of the difficulty
of obtaining laboratory-confirmation from suspected cases. Risk factors for
transmission in settings such as those found in CAR include low levels of routine
immunization (2005 estimates of DTP3 coverage < 40%), crowding, malnutrition,
and coinfection with other illnesses (HIV, malaria, tuberculosis, etc.). Fluctuations
in the number of reported cases reflect a weak surveillance system and may mask
the actual number of cases.
Examples of outbreaks that have occurred in humanitarian settings are:
I
1. Democratic Republic of the Congo, January 1999 February 2000: 1136 cases,
including 23 (2%) deaths. Vaccination coverage (DTP1) of infants < 12 months
in the affected area was estimated to be 32%. Response activities consisted of
case-management support with provision of erythromycin, active surveillance, II
and strengthening of routine EPI services. A vaccination campaign following
the outbreak was not well accepted by the population, owing to fears of second-
ary effects.
2. Democratic Republic of the Congo, 2001: 2633 cases, including 17 (0.6%) III
deaths. 89% of the cases were 5 years of age. Cases were defined as having
the characteristic coughing fits, whooping, and vomiting after coughing
for 2 weeks (suspect case) or longer than 2 weeks (probable case). Suspect
cases were treated with erythromycin for 2 weeks. A vaccination campaign IV
in one village targeted children 672 months old and covered 81% of the tar-
geted population.

142
3. Afghanistan, 2003: 115 cases, including 17 (14.8%) deaths in an isolated border

population with estimated vaccination coverage of < 40%. A 10-day treatment
regimen of erythromycin was given to all children (regardless of immuniza-
tion status, contact with cases, or presence of symptoms) under 15 years of age
in 5 affected subdistricts, involving 189 villages.
4. Sudan, 2004: the number of cases is unknown, including 300 deaths, no defini-
tive laboratory diagnosis but clinically diagnosed as pertussis. The affected
populations lived in two remote counties not covered by health services.
Outbreak-control measures included door-to-door mass treatment of cases
and all children and contacts in the affected families using erythromycin.
5. Sudan, 2005: 419 cases, including 13 (3.1%) deaths. Response activities included
mass treatment of cases and contacts with erythromycin. Routine vaccination

of children <5 years of age was accelerated in the affected areas.
The case-fatality ratio of pertussis in industrialized countries is very low (0.1%),

however in developing countries the average CFR is 3.9% in infants and 1% in
114 year-olds. Severe disease and death is mainly reported in very young non-
immune infants.
However in malnourished unvaccinated populations with high prevalence of coin-
fections, the CFR may reach 15%. Complications, most notably bronchopneumonia,
occur most frequently in those aged < 6 months. The incidence of pertussis-associated
encephalopathy is 0.9 per 100000.
Except for cases where prior pertussis vaccination resulted in anaphylactic reac-
tion, there are no strict contraindications to this vaccine. All infants, including
HIV-positive individuals, should be immunized against pertussis. There are no
data to support the perception that previous encephalitis may be a contraindica-
tion for pertussis vaccination.
Despite its efficient prevention of clinical disease, the vaccine has a limited impact
on the circulation of B. pertussis, even in countries with high vaccination coverage.
Remaining non-immunized children and older individuals with waning immunity
may serve as reservoirs for the infection and transmit B. pertussis to non-immunized
young infants. Susceptible adolescents and adults allow the occurrence of pertussis
outbreaks, although high vaccination coverage may prolong the interepidemic intervals.
No details of the geographical distribution of cases reported are available.

143
Seasonality
Pertussis has no distinct seasonal pattern, but activity may increase in the summer
and autumn.
Alert threshold
One case is sufficient for an alert and must be investigated, especially if the case
occurs in high-risk areas (i.e. with low vaccination coverage).

Population movement facilitates the spread of B. pertussis.
Overcrowding. Crowded conditions facilitate transmission. The disease is usually

introduced into a household by an older sibling or a parent.
Poor access to health services may also mean no access to routine immunization
services. Susceptibility of non-immunized individuals is universal, and vaccina-
tion is the mainstay of pertussis control. Low vaccination coverage is a major risk
factor for increased transmission (diphtheriatetanuspertussis vaccine (DTP3)
coverage is < 40% in Chad and < 20% in CAR).

Case management I
The drug of choice for the treatment of pertussis is erythromycin or erythromycin
estolate, which should be administered for 7 days to all cases and close contacts
of people with pertussis, regardless of age and vaccination status, and for all
those living in households where there is an infant aged < 1 year. Clarithromycin II
and azithromycin are also effective.
Drug administration both modifies the course of illness (if initiated early) and
eradicates the organism from secretions, thereby reducing communicability, but
does not reduce symptoms except when given during the catarrhal stage or early III
in the paroxysmal stage. Symptomatic treatment and supportive case management
are important.
Immunization
IV
Vaccination is the most effective way to control pertussis. Active primary immuni-
zation against B. pertussis infection with the whole-cell vaccine (wP) is recommended

144
in association with the administration of diphtheria and tetanus toxoids (DTP)

at 6, 10 and 14 weeks of age, and a fourth dose at the age of 2 years if resources
are available. No single-antigen pertussis vaccine is available.
Although the use of acellular vaccines (aP) is less commonly associated with
adverse reactions, price considerations affect their use, and wP vaccines are the
vaccines of choice for some countries.
In general, pertussis vaccine (wP) is not given to individuals aged 7 years or older,
since local reactions may be increased in older children and adults and the disease
is less severe in older children.
The efficacy of the vaccine in children who have received at least 3 doses is esti-
mated to exceed 80%. Protection is greater against severe disease and begins to
wane after about 3 years.
Epidemic control
The highly contagious nature of the disease leads to large numbers of secondary
cases among non-immune contacts. Prophylactic antibiotic treatment (erythromycin)
in the early incubation period may prevent disease, but difficulties of early diag-
nosis, costs involved and concerns related to the occurrence of drug resistance all
limit prophylactic treatment to selected individual cases. Priority should be given to:
protecting children under 1 year of age and pregnant females in the final
3 weeks of pregnancy because of the risk of transmission to the newborn; and
stopping infection among household members, particularly if these include
children under 1 year of age and pregnant women in the final 3 weeks of
pregnancy.
The strategy relies on chemoprophylaxis of contacts within a maximum of 14 days

following the first contact with the index case.
Index cases must avoid contact with day-care centres, schools and other places
where susceptible individuals are grouped, for up to 5 days after commencing
treatment or for up to 3 weeks after onset of paroxysmal cough, or until the end
of cough, whichever comes first.
All cases and contacts must have their immunization status verified and brought
up to date.

145
POLIOMYELITIS
Country-specific information
The last polio case was reported in April 2008.
Polio cases reported nationally, Central African Republic, 20012008
Year 2008 2007 2006 2005 2004 2003 2002
3 0 0 0 30 1 0
Source: Polio Eradication Initiative, data as of 23 July 2008 (http://www.polioeradication.org/http://www.who.

int/immunization_monitoring/en/globalsummary/timeseries/tsincidencepol.htm).
Since 2001, CAR has been free of indigenous poliovirus but has experienced succes-
sive importations of wild poliovirus (WPV) type 1 from Chad during 20032004,
leading to an outbreak that was successfully stopped. In April 2008, CAR experi-
POLIOMYELITIS
enced further importation of WPV-1 from the Democratic Republic of the Congo
(Bangui commune). As of 11 August 2008, there has been no further evidence of
virus circulation in CAR.
Surveillance indicators are of certification quality at national level. However at
provincial level quality began to deteriorate in the north and west of the country
from mid-2007. The non-polio acute flaccid paralysis (AFP) rate was suboptimal
in the western and northern parts of the country for the 6 months prior to and I
including December 2007. For the period JanuaryJuly 2008, the non-polio AFP
rate for the western part of the country remained suboptimal. The current situa-
tion contributes to weakened surveillance and routine immunization activities.
In response to this concern and the recent importation of WPV-1 in Bangui, the
polio eradication programme has planned national immunization days (NIDs)
II
in 2008 using trivalent oral polio vaccine (OPV) and monovalent OPV. These
activities may be limited as a result of security issues.
Chad III
Polio cases reported nationally, Chad, 20012008
Year 2008 2007 2006 2005 2004 2003 2002 2001
37 21 1 2 24 25 0 0
IV
Source: Polio Eradication Initiative, data as of 23 July 2008 (http://www.polioeradication.org/http://www.who.
int/immunization_monitoring/en/globalsummary/timeseries/tsincidencepol.htm).

146
In 2008, Chad experienced a major polio outbreak following successive importa-

tions, notably from Nigeria. As of 19 August 2008, Chad had reported 12 (WPV-3)
cases from 6 regions (Hadjer-Lamis, Kanem, Logone occidental, NDjamena,
Ouaddai, Wadi Fira). The last WPV type 1 case had onset in November 2007.
However, owing to the suboptimal quality of surveillance, ongoing circulation of
WPV1 cannot be excluded. In late 2007, Chad exported WPV type 1 to neigh-
bouring Sudan. The situation is of particular concern given that Chad was a key
link in 20042005 when WPV spread from Nigeria to the Horn of Africa and the
Middle East.
Chad has reached certification-standard surveillance at national level. However,
subnational surveillance gaps exist and may be exacerbated by the current con-
flict. From July 2007 to June 2008, data indicate good surveillance performance
in Kanem, Moyen Chari, Ouaddai and Wadi-Fira, but suboptimal indicators in
Chari-Baguirmi, Hadjer-Lamis, Lac and NDjamena (a total of 2.23 million people,
25% of the total population).
The persistent transmission in Chad may be due to suboptimal quality of supple-
mentary immunization activities (SIAs) with many missed children, caused by
weakened subnational health systems, poor campaign management, population
movements and insecurity in some areas. Current circumstances will further con-
tribute to such shortfalls and may even precipitate cancellation of planned activities.
Chad is planning some staggered SIA activity during 2008 using mOPV1 and
mOPV3 in November and mOPV1 and tOPV in December. These activities will
be security- and access-dependent.
Description
Infectious agent
Poliovirus (Enterovirus group): types 1, 2, 3.
Case definition
All three types of wild poliovirus may cause paralysis, although most infections
(at least 95%) remain asymptomatic.
Most symptomatic cases report a nonspecific febrile illness lasting a few days,
corresponding to the viraemic phase of the disease. In a few cases, fever may be
followed by the abrupt onset of meningitic and neuromuscular symptoms, such

147
as stiffness in the neck and pain in the limbs. Initial symptoms may also include
fatigue, headaches, vomiting and constipation (or, less commonly, diarrhoea).
In a very small percentage of cases ( 1% of infected susceptible individuals), the
gradual onset (24 days) of flaccid paralysis may then follow. Paralytic disease
usually affects the lower limbs and is typically asymmetric and more severe
proximally (at the tops of the legs). Bulbar (brainstem) paralysis may also occasion-
ally occur, leading to respiratory muscle involvement and death unless artificial
respiration is used. Mortality from paralytic poliomyelitis is between 2% and 10%,
mainly as a result of bulbar involvement and/or respiratory failure.
Risk factors for paralytic disease are a large inoculum of virus, increasing age,
pregnancy, recent tonsillectomy, strenuous exercise and intramuscular injections
during the incubation period. After the acute illness, there is often a degree of
recovery of muscle function; 80% of eventual recovery is attained within 6 months,
although recovery of muscle function may continue for up to 2 years. After many
years of stable neurological impairment, new neuromuscular symptoms develop
(weakness, pain and fatigue, post-polio syndrome) in 2540% of patients.
POLIOMYELITIS
Acute flaccid paralysis (AFP) in a child aged < 15 years, including Guillain
Barr syndrome;* or
any paralytic illness in a person of any age when polio is suspected.
* For practical reasons, GuillainBarr syndrome is considered as poliomyelitis until proven otherwise.
I
Laboratory criteria
Isolation of wild poliovirus in stool sample.
II
Case classification
Confirmed: AFP with laboratory-confirmed wild poliovirus in stool sample.
III
Polio-compatible: AFP clinically compatible with poliomyelitis, but without
adequate virological investigation.
IV
Poliovirus is highly communicable. Transmission is primarily person to person
via the faecaloral route.

148
Incubation period
The time between infection and onset of paralysis is 430 days.
From 36 hours after infection, for 46 weeks.
Epidemiology
General
Weak infrastructure and competing priorities represent considerable challenges
to polio eradication strategies. All countries remain at risk of importations, regard-

less of their geographical proximity to polio-endemic countries. It is therefore
important that certification standard surveillance is widely maintained in order
to avoid late detection of any wild poliovirus importation.
Priorities include:
reaching previously non-immunized children and gaining access to all areas,

including those that are inaccessible as a result of conflict;
sustaining high-quality AFP surveillance to improve targeting of supplemen-
tary immunization activities (SIAs);
improving basic infrastructure for the Expanded Programme on Immunization.
All countries are required to conduct a number of activities to minimize the risk
of a wild poliovirus escaping into the environment, either from a research labo-
ratory or a vaccine manufacturing site.
These include the following:
appointment of a national containment coordinator;

compilation of a list of all biomedical facilities which could hold wild polio
virus stock;
surveying of all identified biomedical facilities to determine with certainty
which hold wild polioviruses;
submission of finalized biomedical survey report to WHO;
completion of containment process with the wild poliovirus stocks secured
under appropriate biosafety conditions, or being destroyed.

149
This stage is to be commenced 1 year after the global interruption of wild polio-
virus transmission.40 With transborder population movements, there is a risk of
the poliovirus being exported to CAR which has remained polio-free since 2004,
as well as other neighbouring countries. It is likely that the current outbreak in
Chad implies that circulation of the virus has not been completely arrested since
20032005 in spite of 14 national immunization days and 8 subnational immuni-
zation days.
Chad has attained the certification standard for AFP surveillance indicators since
2005, with non-polio AFP rates of 2 per 100000 in the < 15 population and of
80% stool samples taken within 14 days of paralysis onset.
Nevertheless, subnational surveillance gaps exist and may be exacerbated by cur-
rent conflict: 2007 data indicates good surveillance performance in Kanem, Ouaddai,
Moyen Chari and Wadi-Fira, but suboptimal indicators in NDjamena, Chari-
Baguirmi, Lac and Hadjer-Lamis (2.23 million people, i.e. 25% of the total population).
While the majority of WPV isolates were type 1, 2 cases (1 in 2006 and 1 in 2007)
POLIOMYELITIS
were type 3. The former was determined to have been a direct importation from
Nigeria, while the latter may have circulated in Chad or elsewhere for some time.
In September 2007, a case of WPV genetically linked to circulating viruses in
Abeche was detected in the South Darfur region of Sudan, further highlighting
the risk that the ongoing outbreak in Chad represents for neighbouring countries.
The observed persistent transmission in Chad may be due to suboptimal quality
of SIAs with many missed children occasioned by weakened subnational health
I
systems, poor campaign management, population movements and insecurity in
some areas. Current circumstances will further contribute to such shortfalls and
may even precipitate cancellation of planned activities.
II
After the November 2007 NIDs, 18 of 55 districts were surveyed for coverage. On
average, 14% of the children were found to have been missed, with 12 out of 18
districts having over 10% missed children. Similarly, as an indication of population
immunity, less than 50% of non-polio AFP cases had 4 doses of OPV in 2007.
III
Since August 2007, WHO has added 11 international consultants to assist with
the planning, preparation and supervision of SIAs. In November of that year, a
joint mission of the WHO Regional Office for Africa, the Regional Office for the
Eastern Mediterranean and headquarters was undertaken to work with the country
IV
40 For details on containment or certification issues, see www.polioeradication.org.

150
to define a 6-month plan covering key interventions to improve SIA quality and
surveillance.
Furthermore, the Regional Director of the African Region wrote to the President
urging his personal involvement. For 2008, it is envisaged that Chad will conduct
at least five rounds of high-quality SIAs with enhanced technical support and
monitoring. Current circumstances may reduce the quality of polio surveillance
and routine immunization. Planned NIDs and SNIDs may be compromised as a
result of evacuation of international staff, lack of security and difficulty of access.
Substantial progress has been made towards eradicating poliomyelitis from the
region. However, outbreaks of polio follow importation of wild poliovirus into

polio-free areas. Despite progress in controlling outbreaks in polio-free areas
following importation, ongoing transmission of wild poliovirus in endemic areas
poses a constant risk to the achievement of polio eradication globally.
The Advisory Committee for Polio Eradication has advised that global success in
eradicating polio now depends on four countries Afghanistan, India, Nigeria
and Pakistan. International concern is very high regarding the pace of eradica-
tion in the remaining endemic areas in Afghanistan, India, Nigeria and Pakistan.
The longer it takes to interrupt transmission in these countries, the greater the
danger of wild poliovirus being exported to areas in the region.
Seasonality
The intensity of transmission increases during the rainy season.
Alert threshold
Any AFP case must be notified and investigated. An outbreak may be suspected
when a rapid increase in the reported number of new AFP cases within a district
or in adjacent districts occurs within a 2-month period.

Population movement facilitates transmission from infected to non-immune
population.
Overcrowding is important in promoting transmission.
Poor access to health services results in limited access to routine immunization
services, and the risk of undetected poliovirus circulation.

151
Lack of safe water and poor sanitation. As the disease is spread by the faecal
oral route, lack of water, and poor hygiene and sanitation promote transmission.

Case management
Management of the acute phase of paralytic poliomyelitis is supportive and
symptomatic:
bed rest;
close monitoring of respiration; respiratory support in case of respiratory
failure or pooling of pharyngeal secretions;
moist hot-packs for muscle pain and spasms;
passive physical therapy to stimulate muscles and prevent contractures;
antispasmodic drugs;
frequent turning to prevent bedsores.
POLIOMYELITIS
If hospitalization is required, the patient should be isolated, particularly avoiding
contact with children. Safe disposal of discharge and faeces, disinfection of any
soiled articles and immediate reporting of further cases are essential.
Two types of poliovirus vaccine are available:
I
1. Oral poliovirus vaccine (OPV): OPV is an oral vaccine based on live attenuated
strains of all three virus types (tOPV) or one specific virus type (mOPV). It is
easily administered by health workers or volunteers, induces a good humoral
(antibody) and mucosal (intestinal) immune response and is considerably
cheaper than inactivated poliovirus vaccine (IPV). OPV is the only vaccine of II
choice for poliomyelitis eradication because it achieves much better mucosal
immunity than IPV while limiting dissemination of wild poliovirus in the
community. Polio supplementary immunization activities were planned in
CAR and Chad during 2008. III
2. Inactivated poliovirus vaccine (IPV): IPV may be given only by intramuscular
injection and requires trained health workers. It elicits an excellent antibody
response but only minimal intestinal mucosal response; it is much more expen-
sive than OPV. All countries in the subregion have a routine immunization IV
policy that requires three doses of OPV. However, supplementary immunization
activities are also conducted in the country in order to increase immunization

152
coverage as much as possible: these consist of national immunization days

(NIDs), sub-NIDs (SNIDs campaigns similar to NIDs but covering smaller
areas) and mop-up campaigns, during which two OPV doses are given to all
children aged < 5 years, preferably during the season of low transmission for
enteroviruses (cooler season). The interval between the two doses depends on
the type of vaccine used. In camp settings, all children aged 059 months should
be vaccinated on arrival. Every AFP case must be notified and investigated.
Epidemic control
Every country should have standard operating procedures in place to rapidly mount
mop-up campaigns upon confirmation of a polio case. Such plans are also a pre-
requisite for polio-free certification. In case of a suspected outbreak, undertake:
Investigation
Clinical and epidemiological investigation.
Rapid virological investigation (2 stool samples within 14 days of onset of
symptoms must be sent to a WHO-accredited laboratory).
Outbreak confirmation will be based on the isolation of wild poliovirus from
a stool specimen obtained from an AFP case.
Intervention
House-to-house mop-up campaigns with OPV covering a wide geographical
area (at least the province involved and relevant neighbours) should be con-
ducted within 4 weeks after confirmation of the wild poliovirus case if no
NIDs or SNIDs are planned to cover the area within the next three months.
Mop-up campaigns target a minimum of 500 0001 million children.
If NIDs/SNIDs were already planned, a major focus on quality of the SIA should
be made for the area of the outbreak and adjacent districts. Surveillance should
be enhanced through intensive monitoring of all reporting units to ensure active
surveillance and zero reporting, extensive retrospective record reviews and active
case-finding in surrounding areas.

153
RABIES

No outbreaks have been reported to WHO from Central African Republic and Chad.
Description
Infectious agent
Rabies virus, a Rhabdovirus of the genus Lyssavirus.
Case definition
Paresis or paralysis, delirium, convulsions. Without medical attention, death in
about 6 days, usually due to respiratory paralysis.
RABIES
An acute neurological syndrome (encephalitis) dominated by forms of hyperactivity
(furious rabies) or paralytic syndrome (dumb rabies) that progresses towards coma
and death, usually by respiratory failure, within 710 days after the first symptom.
Bites or scratches from a suspected animal can usually be traced in the patients
medical history.
I
Laboratory criteria
One or more of the following:
II
detection of rabies viral antigens by direct fluorescent antibody (FA) or by
ELISA in clinical specimens, preferably brain tissue (collected post mortem);
detection by FA on skin biopsy (collected ante mortem);
FA positive after inoculation of brain tissue, saliva or CSF in cell culture, or
III
after intracerebral inoculation in mice or in suckling mice;
detectable rabies-neutralizing antibody titre in the serum or the CSF of an
unvaccinated person;
IV
detection of viral nucleic acids by PCR on tissue collected post mortem or in
a clinical specimen (brain tissue or skin, cornea, urine or saliva).

154
Case classification
Human rabies:
Suspected: a case that is compatible with the clinical case definition.

Probable: a suspected case plus history of contact with a suspected rabid animal.
Confirmed: a suspected case that is laboratory-confirmed.
Human exposure to rabies:
Possibly exposed: a person who had close contact (usually a bite or a scratch)
with a rabies-susceptible animal in (or originating from) a rabies-infected area.
Exposed: a person who had close contact (usually a bite or a scratch) with a
laboratory-confirmed rabid animal.
Usually by the bite of an infected mammalian species (dog, cat, fox, bat): bites or
scratches introduce virus-laden saliva into the human body. No human-to-human
transmission has been documented.
Incubation period
The incubation period usually ranges from 2 to 10 days but may be as long as 7 years.
In dogs and cats, usually for 37 days before onset of clinical signs (rarely over
4 days) and throughout the course of the disease. Longer periods of excretion
before onset of clinical signs have been observed in other animal species.
Epidemiology
General
Reliable data on rabies are scarce in many areas of the globe, making it difficult
to assess its full impact on human and animal health. WHO commissioned a
reassessment of the burden of rabies in 2004. According to this study, the annual
number of deaths worldwide caused by rabies is estimated to be 55 000, mostly in
rural areas of Africa and Asia. An estimated 10 million people receive postexposure
treatments each year after being exposed to rabies-suspect animals.

155
In the WHO African and South-East Asia regions, human mortality from endemic
canine rabies was estimated to be 55 000 per year (90% confidence interval: 21 500
90 800), with 44% of these deaths occurring in Africa. The number of deaths
officially reported in most developing countries greatly underestimates the true
incidence of the disease.
The subregion is considered endemic for rabies. Risk of cases in humans is sig-
nificant if individual cases or outbreaks of rabies are reported in dogs or other
susceptible animals in the same zone. Availability of food sources for dogs and
susceptible wild animals in close proximity to human populations increases the
risk. Children aged 515 years are the group at major risk.
More than 99% of all human rabies deaths occur in the developing world;
although effective and economical control measures are available, the disease
has not been brought under control throughout most of the affected countries.
The application of effective and economical control measures is hampered by a
range of economic, social and political factors. Lack of accurate data on the true
public health impact of the disease is a major factor contributing to the low com-
mitment to rabies control.
RABIES
The majority of rabies deaths generally occur in rural areas.
Seasonality I
No seasonality reported.
Alert threshold
One case in a susceptible animal species and/or human must lead to an alert. II

Population movement is a risk factor. III
Overcrowding. An infected animal has the opportunity to bite more people; dog-
population density parallels human-population density.
Poor access to health services. Prompt administration of vaccine post exposure IV
(plus immunoglobulin if heavy exposure) is the only way to prevent death of an
infected person.

156

Case management
There is no specific treatment for rabies once the symptoms have started. Rabies
is an almost invariably fatal disease. The most effective way to prevent rabies is to
wash and flush the wound or point of contact with soap and water, detergent or
plain water, and then apply ethanol or tincture or aqueous solution of iodine.
Antirabies vaccine should be given as soon as possible for Category II and III
exposures, according to WHO-recognized regimens (see below). Antirabies immu-
noglobulin should be applied for Category III (severe) exposures only.
Suturing should be postponed; if it is necessary, immunoglobulin (in severe expo-
sure) must first be applied before instillation at the periphery of the wound. Where
indicated, antitetanus treatment, antimicrobials and drugs should be administered
to control infections other than rabies.
Recommended treatments according to type of contact with suspect animal
Category Type of contact with a suspect or Type of Recommended treatment

confirmed rabid domestic or wild exposure
animal, or animal unavailable for
testing
I Licks on intact skin None None, if reliable case history is

available.
II Nibbling of uncovered skin Minor exposure Administer vaccine immediately.

Minor scratches or abrasions without Stop treatment if animal remains
bleeding healthy throughout an observation
period of 10 days or if animal is
humanely killed and proven to be
negative for rabies by a reliable
laboratory using appropriate
diagnostic techniques.
III Single or multiple transdermal bites or Severe exposure Administer rabies immunoglobulin
scratches, licks on broken skin and vaccine immediately. Stop
Contamination of mucous membrane treatment if animal remains healthy
with saliva (i.e. licks) throughout an observation period of
Exposures to bats 10 days or if animal is humanely
killed and found to be negative for
rabies using appropriate diagnostic
techniques.
If a person develops the disease, death is inevitable. Universal barrier nursing

practices are necessary for patients.

157
Epidemic control
Immediate notification if one or more suspected cases are identified.
Confirm the outbreak, following WHO guidelines.
Confirm diagnosis and ensure prompt management.
Prevention
WHO promotes human rabies prevention through:
well-targeted postexposure treatment using modern vaccine types and, when

appropriate, antirabies immunoglobulin;
increased availability of safe and effective rabies vaccine;
elimination of dog rabies through mass vaccination of dogs, and dog-population
management.
Immunization
Mass preventive vaccination in humans is generally not recommended but may
be considered under certain circumstances for the age group 515 years.
RABIES
I
II
III
IV

158
RIFT VALLEY FEVER (RVF)

There has been positive animal serology in the Central African Republic and Chad,
but no reported animal or human outbreaks. Health workers should retain a high
index of suspicion for patients presenting with haemorrhagic symptoms (e.g. obstet-
rics and bloody diarrhoea) or while investigating an outbreak of unknown cause.
Description
Infectious agent
Rift Valley fever (RVF) virus is a member of the Phlebovirus genus, one of the five
genera in the family Bunyaviridae causing zoonosis (a disease which primarily
affects animals, but occasionally causes disease in humans).
Case definition
98% of cases are unnoticed and characterized by a feverish syndrome with sudden
onset, flu-like fever, myalgia, arthralgia and headaches. The fever may or may not
be biphasic. Hyperleucocytosis is followed by a leucopenia. Some patients may
develop a stiffness of the neck, photophobia, anorexia, nausea and vomiting and
therefore in its first stages, RVF may be confused with meningitis. These symp-
toms last in general from 4 to 7 days, after which the antibodies can be detected
(IgM and IgG) as well as the disappearance of the virus in the blood.
2 % of cases have serious complications:
1. Ocular form (most frequent, around 1% of RVF cases): chorioretinitis, tem-

porary blindness. Chorioretinitis appears 13 weeks after the first symptoms.
Patients report blurred or decreased vision. Symptoms resolve spontaneously
within 1012 weeks from the onset of systemic symptoms. Macular retinitis,
paramacular retinitis and optic atrophy are the most frequent causes of visual
loss in RVF. When the optic disc is affected, there is a permanent fall of vision
(50% of cases). Deaths are rare.
2. Meningoencephalic form: intense cephalgias and meningitides. Loss of mem-
ory, hallucinations, vertigo, coma. Appears 13 weeks after the first symptoms.
Deaths are rare. Neurological complications may appear later.

159
3. Haemorrhagic icterus form: 2-4 days after the beginning of the disease, the
patient presents the signs of a severe hepatitis, including jaundice and haem-
orrhages that may be fatal (vomiting blood, blood in the stools, purpura an
area of bleeding within the skin) or bleeding from the gums. The case-fatality
ratio may be as high as 50%. Death may occur between day 3 and 6 post onset.
The viraemia may last for up to 10 days.
Laboratory criteria
The virus may be detected by reverse transcriptase polymerase chain reaction
(RT-PCR) in the patients blood from day 1 to day 5, and later if the immune
response is not activated. Serological tests differentiate other fevers of viral or
unknown origin, and the diagnosis is facilitated by RNA analysis. The immune
response to infection becomes detectable after 47 days, with the appearance of
IgM and IgG antibodies and the disappearance of circulating virus from the

bloodstream. Enzyme-linked immunosorbent assay (the ELISA or EIA methods)
may demonstrate the presence of specific IgM antibodies to the virus. The virus
itself or the viral genome revealed by RT-PCR may be detected in blood during
the viraemia phase of illness. The virus may also be detected in postmortem tis-
sues by a variety of techniques, including virus propagation (in cell cultures or
inoculated animals), antigen detection tests and RT-PCR.
Community diagnosis
RVF should be suspected when abnormally heavy rains are followed by the wide- I
spread occurrence of abortions and mortality among newborn animals, charac-
terized by necrotic hepatitis, and when haemorrhages and influenza-like disease
are seen in people handling animals or their products.
II
The vast majority of human infections (90%) are caused by direct or indirect
contact with infected animal blood or organs (e.g. liver, spleen). These human
infections are associated with handling of animal tissues during butchering or
autopsy (performed by farmers, slaughtering houses, veterinarians, etc.). The virus
III
may also infect humans through inoculation (e.g. if the skin is broken, or through
a wound from an infected knife).
Some human infections are caused by mosquito bites, mainly by the bite of infected IV
Aedes mosquitoes. A. mcintoshi may be infected transovarially (transmission of
the virus from infected female mosquitoes to offspring via eggs) and account for

160
maintenance of RVF virus in enzootic foci. Many different species of mosquitoes

are vectors for the RVF virus. Other arthropods such as C. pipens have also been
linked to RVF in epidemics. Mechanical transmission of RVF virus by haematopha-
gous flies is also possible. The aerosol mode of transmission has also led to infection
in laboratory workers. No person-to-person transmission has been documented.
Incubation period
The incubation period varies from 2 to 12 days.
There is no direct person-to-person transmission. Infected mosquitoes probably
transmit the virus throughout life. Viraemia is essential for vector infection and
often occurs during early clinical infection in humans.
Epidemiology
General
Rift Valley fever was identified in 1931.The virus (RVFV) was first isolated during
the investigation of an epidemic among sheep on a farm north of Lake Naivasha
in the Rift Valley of Kenya. Outbreaks of RVF have occurred in sub-Saharan and
northern Africa. A major outbreak occurred in Kenya and Somalia in 19971998.
In September 2000, RVF was reported for the first time outside the African con-
tinent in neighbouring countries (Saudi Arabia and Yemen). The expansion to the
Arabian Peninsula raises the threat of expansion into other parts of Asia and Europe.
RVF is a viral zoonosis that primarily effects animals but has the capacity to in-
fect humans.
Many types of animals may be infected with RVF (cattle, sheep, camels and goats).
Sheep appear to be more susceptible than cattle, while goats are less susceptible
than sheep or cattle.
An epizootic (animal disease epidemic) of RVF is usually first manifested as a
wave of unexplained abortions among livestock:
the abortion rate among pregnant, infected ewes is almost 100%;

animals of different ages also differ in their susceptibility to severe illness:
over 90% of lambs infected with RVF die, whereas mortality among adult
sheep may be as low as 10%.

161
An epizootic may signal the start of a human epidemic:
The vast majority of human infections result from direct or indirect contact
with the blood or organs of infected animals. The virus may be transmitted to
humans through the handling of animal tissue during slaughtering or butch-
ering, assisting with animal births, conducting veterinary procedures, or
from the disposal of carcasses or fetuses. Certain occupational groups such
as herders, farmers, slaughterhouse workers and veterinarians are therefore at
higher risk of infection. The virus infects humans through inoculation, for
example via a wound from an infected knife or through contact with broken
skin, or through inhalation of aerosols produced during the slaughter of in-
fected animals. The aerosol mode of transmission has also led to infection in
laboratory workers.
There is some evidence that humans may also become infected with RVF by

ingesting the unpasteurized or uncooked milk of infected animals.
Human infections have also resulted from the bites of infected mosquitoes,
most commonly the Aedes mosquito.
Transmission of RVF virus by hematophagous (blood-feeding) flies is also
possible.
To date, no human-to-human transmission of RVF has been documented,
and no transmission of RVF to health-care workers has been reported when
standard infection-control precautions have been put in place. I
There has been no evidence of outbreaks of RVF in urban areas.
Seasonality
In warmer climates where insect vectors are present continuously, seasonality
II
is usually not seen. However, epidemics may occur following exceptionally
heavy rains as a result of an increase in the number of vector breeding sites and
conditions. New systems that monitor variations in climatic conditions are being
applied to give advance warning of impending outbreaks by signalling events III
that may lead to increases in mosquito numbers. Such warnings allow authori-
ties to implement pre-emptive public health measures to avert an impending
epidemic.
IV
Susceptibility appears to be general in both sexes at all ages. Since infection leads
to immunity, susceptible individuals in endemic areas are mainly children.

162

Population movement. During outbreaks, livestock movement may contribute to
the expansion and spread of infection to non-affected areas.
Overcrowding. Conditions favouring close contact with infected animals and
exposure to vectors constitute a risk factor for increased transmission.
Poor access to health services. Prompt access to medical services is essential for
appropriate case management and implementation of outbreak control measures.
Food shortages. The malnourished are more likely to die of the disease.

Case management
Disease among humans is usually characterized as a mild febrile illness. Most
human cases of RVF are relatively mild febrile illness of short duration, and so
will not require any specific treatment. However, 1% or less of RVF infections may
result in a fatal haemorrhagic fever. Two to four days after the onset of illness,
the patient shows evidence of severe liver disease, with jaundice, petechiae and
haemorrhagic phenomena, vomiting blood, passing blood in the faeces, developing
a purpuric rash and bleeding from the gums. Patients with the RVF haemorrhagic
fever syndrome may remain viraemic for up to 10 days. The case-fatality ratio for
patients developing haemorrhagic disease is high at approximately 50%.
Less than 1% of RVF infections result in meningoencephalitis. The onset of this
syndrome is also usually 13 weeks after the first symptoms appear. Death in
patients with only meningoencephalitis is uncommon. A higher proportion
(0.52%) develop vascular retinitis with permanent loss of vision if the lesions
are in the macula. The onset of eye disease is usually 13 weeks after the first
symptoms appear. Death in patients with only ocular disease is uncommon.
Currently, there is no specific treatment for the disease. Ribavirin was employed
in the treatment of confirmed cases of RVF during the 2000 outbreak in Saudi
Arabia without success. Other treatments under consideration include interferon,
immune modulators and convalescent-phase plasma. Supportive treatment for
the more severe cases is the mainstay:
replacement of the blood volume and components, red cells, platelets;

rehydration, electrolytic balance, intensive care;

163
use of antibiotics drugs (to avoid secondary infections);

use of antimalarial drugs if needed (coinfections);
analgesic drugs.
Although person-to-person transmission has not been documented, standard

infection-control practices should be implemented to avoid possible secondary
infections when managing patients with the haemorrhagic form of the disease.
RVF virus should be considered as a bloodborne pathogen. Contact with the
patients lesions and body fluids should be minimized using standard infection-
control practices including:
restriction of access to patient wards;

use of personal protective equipment;
safe disposal of waste;

disinfection of all non-disposable supplies and equipment;
safe burial practices.
Immunization
A formalin-inactivated vaccine named TSI-GSD-200 (3 injections) has been
developed by the Salk Institute for human use. It is shown to be safe and immuno-
genic in human studies. Testing of this vaccine in 598 at-risk laboratory personnel
in 19861997 showed only minor side-effects and good long-term immunity at I
12-year follow-up. However, this vaccine is not licensed and is not commercially
available.
A single-dose human live attenuated vaccine, named MP-12, is currently under-
going trials. An open-label, single-dose, phase II study is ongoing to assess the II
safety, immunogenicity, and genetic stability of RVF MP-12 vaccine in humans,
but it is not approved for human use. Other candidate vaccines are under investi-
gation. Killed RVF virus (RVFV) vaccines and live-attenuated RVFV vaccines
for animals (veterinary use) are available, but they may cause birth defects and
abortions in pregnant animals (see below under Prevention and control for use).
III

Controlling RVF in animals
IV
Outbreaks of RVF in animals may be prevented by a sustained programme of
animal vaccination. Both modified live attenuated virus and inactivated virus

164
vaccines have been developed for veterinary use. Only one dose of the live
vaccine is required to provide long-term immunity, but the vaccine that is
currently in use may result in spontaneous abortion if given to pregnant animals.
The inactivated virus vaccine does not have this side-effect, but multiple doses
are required in order to provide protection which may prove problematic in
endemic areas.
Animal immunization must be implemented prior to an outbreak if an epiz-
ootic is to be prevented. Once an outbreak has occurred, animal vaccination
should not be implemented because there is a high risk of intensifying the
outbreak. During mass animal-vaccination campaigns, animal-health work-
ers may, inadvertently, transmit the virus through the use of multidose vials
and the reuse of needles and syringes. If some of the animals in the herd are
already infected and viraemic (although not yet displaying obvious signs of
illness), the virus will be transmitted among the herd, and the outbreak will
be amplified.
Restricting or banning the movement of livestock may be effective in slowing
the expansion of the virus from infected to uninfected areas.
As outbreaks of RVF in animals precede human cases, the establishment of
an active animal health surveillance system to detect new cases is essential in
providing early warning for veterinary and human public health authorities.
Public health education and risk reduction

During an outbreak of RVF, close contact with animals, particularly with
their body fluids, either directly or via aerosols, has been identified as the
most significant risk factor for RVF virus infection. In the absence of specific
treatment and an effective human vaccine, raising awareness of the risk factors
of RVF infection as well as the protective measures individuals can take to
prevent mosquito bites, is the only way to reduce human infection and deaths.
Public health messages for risk reduction should focus on:
Reducing the risk of animal-to-human transmission as a result of unsafe
animal husbandry and slaughtering practices. Gloves and other appro-
priate protective clothing should be worn and care taken when handling
sick animals or their tissues or when slaughtering animals.
Reducing the risk of animal-to-human transmission arising from the un-
safe consumption of fresh blood, raw milk or animal tissue. In epizootic
regions, all animal products (blood, meat and milk) should be thoroughly
cooked before eating.

165
The importance of personal and community protection against mosquito

bites through the use of impregnated mosquito nets, personal insect
repellent if available, wearing light-coloured clothing (long-sleeved shirts
and trousers) and avoiding outdoor activity at peak biting times of the
vector species.
Infection control in health-care settings

Although no human-to-human transmission of RVF has been demonstrated,
there is still a theoretical risk of transmission of the virus from infected patients
to health-care workers through contact with infected blood or tissues. Health-
care workers caring for patients with suspected or confirmed RVF should
implement standard precautions when handling specimens from patients.
Standard precautions define the work practices that are required to ensure a
basic level of infection control. Standard precautions are recommended in the

care and treatment of all patients regardless of their perceived or confirmed
infectious status. They cover the handling of blood (including dried blood),
all other body fluids, secretions and excretions (excluding sweat), regardless
of whether they contain visible blood, and contact with non-intact skin and
mucous membranes.41
As noted above, laboratory workers are also at risk. Samples taken from sus-
pected human and animal cases of RVF for diagnosis should be handled by
trained staff and processed in suitably equipped laboratories. I
Vector control
Other ways in which to control the spread of RVF involve control of the vector
and protection against bites. II
Larviciding measures at mosquito breeding sites are the most effective form
of vector control if breeding sites can be clearly identified and are limited in
size and extent. During periods of flooding, however, the number and extent
of breeding sites is usually too high for larviciding measures to be feasible. III
The risk of transmission from infected blood or tissues exists for people working
with infected animals or for individuals during an outbreak:
IV
41 A WHO aidememoire on standard precautions in health care is available at http://www.who.int/csr/
resources/publications/standardprecautions/en/index.html.

166
gloves, goggles, surgical masks, boots, gowns, aprons and other appropriate
protective clothing should be worn, and care taken when handling sick ani-
mals or their tissues;
health-care workers looking after patients with suspected or confirmed RVF
should employ standard precautions when taking and processing specimens
from patients;
laboratory workers and those collecting samples are at risk, so samples taken
for diagnosis from suspected human and animal cases of RVF should be han-
dled by trained staff and processed in suitably equipped laboratories.
Importantly, suspect cases/epidemics in humans and animals must be notified to

local authorities, WHO, the Food and Agriculture Organization of the United
Nations (FAO) and the World Animal Health Organisation, also known as Office
international des pizooties (OIE).
Epidemic control
The following key elements are essential in the control of RVF epidemics:
1. A coordination mechanism for outbreak response that is recognized by all

partners involved in outbreak control operations.
2. Effective and efficient coordination on interventions between animal and
human health authorities.
3. Social mobilization and health education programmes to inform the public
and restrict practices that promote transmission in the community such as:
avoiding direct contact with animal body fluids of sick or dead animals;
avoiding slaughtering or manipulating animals (and their fetuses) suspected
of infection with RVF without appropriate protection;
wearing gloves and masks (or any other device to avoid direct contact, e.g.
plastic bags) when handling sick or dead animals, particularly when assis-
ting birth (fetus and placenta), slaughtering, burying dead animals or fetuses;
washing hands with disinfectant or soap immediately after contact with
any animal fluids;
ensuring safe animal husbandry and slaughter practices and hand-hygiene,
especially in the lead-up to community festive seasons;
avoiding consumption of dead animal meats;
controlling animal slaughtering activities at home and in facilities;

167
early reporting of suspected cases in humans and animals;

using personal protective equipment when handling patients and articles
belonging to patients with RVF;
seeking early treatment for human infections;
avoiding risky funeral practices.
4. Safe and humane case management, including standard infection control
practices and appropriate funeral practices.
5. Vigilant surveillance, standardized epidemiological practices (serological
surveys to identify infected animals and affected districts) and appropriate
laboratory services.
6. Health and veterinary workers in RVF-prone areas should receive advance
training in the use of standard infection-control precautions for avoidance of
mechanical infections.

7. Animal health measures to limit the epizootic:
restrict movement of animals from enzootic areas to clean areas;
do not vaccinate in epizootic areas;
if climatic conditions are signalling a high risk for an RVF epidemic, vete-
rinary services might vaccinate in at-risk zones to avert an impending
epidemic.
8. Implement international administrative measures, as required:
I
enforce international agreements designed to prevent transfer of mosqui-
toes by ships, airplanes and land transport;
OIE and FAO may restrict the trade of animals from an affected country
to an RVF-free country.
II
9. Provision of good logistics and security.
III
IV

168
SCHISTOSOMIASIS (BILHARZIASIS)

Both types of schistosomiasis, urinary (S. haematobium) and intestinal (S. mansoni,
S. intercalatum), are endemic in the Central African Republic and Chad.

Intestinal schistosomiasis is reported throughout the country. Urinary schisto-
somiasis is less widespread and is found on the banks of the Oubangui river and
its affluents, as well as in the upper basin of the Chari river (along the Bahr Oulou,
Manovo, Gribingui, Ouham and Nana Barya rivers).

Transmission of S. haematobium is particularly intense in the marshy plains along
the Chad border, where stagnant or slow-flowing waters represent an environment
favourable to the snail hosts. Transmission of S. mansoni is widespread through-
out the country.
Chad
Urinary schistosomiasis is present throughout the country (with the exception of
the northern part that is sparsely populated); prevalence and intensity of infection
are highest in the Sahelian zone and in the Logone and Chari river basins, the most
densely-populated region, in the west of the country. Intestinal schistosomiasis
occurs mainly in the Logone and Chari river basins; prevalence and intensity are
usually lower than for urinary schistosomiasis.
Transmission of S. haematobium occurs in all temporary or permanent water-
bodies in the southern half of the country, while transmission of S. mansoni is
limited to permanent watercourses of the south-west and to the springs of the
Ouadda massif. While snail hosts are not found in the main channel of the Logone
and Chari rivers, transmission is high in their minor branches, in tributaries, and
in the pools which remain in their annual flood-plain.
Description
Infectious agent
Helminths: Schistosoma haematobium (agent of urinary schistosomiasis); Schis-
tosoma mansoni (agent of intestinal schistosomiasis). All are blood fluke worms

169
belonging to the class Trematoda. Intestinal schistosomiasis caused by Schistosoma

intercalatum may be endemic in the tropical rain forest areas of DRC and Chad.42
Case definition
Urinary schistosomiasis
Endemic areas (moderate or high prevalence):
Suspected: not applicable.
Probable: not applicable.
Confirmed: a person with visible haematuria; or positive reagent strip for
haematuria; or S. haematobium eggs in urine (microscopy).
Non-endemic areas and areas of low prevalence:
Suspected: a person with visible haematuria; or positive reagent strip for
haematuria; and possible contact with infective water.
Confirmed: a person with S. haematobium eggs in urine (microscopy).
Intestinal schistosomiasis
Endemic areas (moderate or high prevalence):
Suspected: a person with nonspecific abdominal symptoms, blood in stool,
hepato(spleno)megaly.
Probable: a person who meets the criteria for presumptive treatment, accor- I
ding to the locally-applicable diagnostic algorithms.
Confirmed: a person with eggs of S. mansoni in stools (microscopy).
Non-endemic areas and areas of low prevalence:

II
Suspected: a person with nonspecific abdominal symptoms, blood in stools,
hepatosplenomegaly and possible contact with infective water.
Confirmed: a person with eggs of S. mansoni in stools (microscopy). III
The disease is water-related, and occurs when the human skin is penetrated by
the schistosome larvae (cercariae). Patients with schistosomiasis discharge the
IV
42 http://www.who.int/wormcontrol/databank/Chad_ncp2.pdf .

170
schistosome eggs in their urine (S. haematobium) or faeces (S. mansoni, occasion-
ally S. haematobium). When the eggs reach a body of fresh water, they liberate
first-stage larvae (miracidia) that penetrate suitable snail hosts (Bulinus spp. and
Biomphalaria spp.) and develop into final-stage larvae (cercariae). The cercariae
emerge from the snail and penetrate human skin, usually while the person is
swimming, working or wading in water (mainly among people engaged in agri-
culture and fishing). Construction of irrigation and dam projects in endemic areas
may result in increased local schistosomiasis transmission.
Incubation period
Within 4 days: localized dermatitis at the site of cercarial penetration.
Within 28 weeks: acute febrile reaction (Katayama fever; almost completely

absent in S. haematobium infection).
From 3 months to several years: chronic illness manifestations.
As long as eggs are discharged by patients. This may be from 1012 weeks to more
than 10 years after infection.
Epidemiology
General
The most intense transmission occurs where populations concentrate around
water sources. Such patterns of disease may be mirrored and amplified in IDP and
refugee populations who also congregate around water sources, as demonstrated
in 2007 when infected Somali populations moved to Kenya. As schistosomiasis
may be coendemic with soil-transmitted helminthiasis, coordinated treatment
for both may be appropriate. The mapping of pathogen distribution is therefore
fundamental.
In general, cases tend to occur:
along major river valleys;

in settlements in irrigated areas;
in recurrent lake formations caused by seasonal changes;
in settlements near perennial or semi-permanent ponds or lakes.

171
Seasonality
Overall, transmission of schistosomiasis occurs throughout the year. Transmission
in semi-permanent ponds or lakes is linked to the rainy season (JuneSeptember).
In certain conditions, dry periods tend to increase transmission of the disease as
a result of higher cercarial densities in bodies of water and of drying of wells, with
consequent increased use of unsafe water.

Population movement may lead to the introduction of S. mansoni and/or S. haema-
tobium in areas previously free or endemic for only one of the species.
Overcrowding. Higher human densities lead to increased discharge of schistosome
eggs in bodies of water and therefore to an increased chance of snails being pen-
etrated and colonized by miracidia.
Poor access to health services. Regular treatment of cases and preventive chemo-
therapy have been proven effective in reducing egg discharge, thus limiting intro-
duction of Schistosoma spp. into schistosome-free areas. Reduced egg discharge
also prevents late-stage complications of schistosomiasis in infected individuals.
Food shortages. Malnutrition and schistosomiasis have a synergic role in causing
iron-deficiency anaemia.
Lack of safe water and poor sanitation. The use of surface water infested by cer-
cariae and contamination of water by urination/defecation are prerequisites for
I
the transmission of schistosomiasis.
Prevention and control measures II

Case management
Praziquantel is the drug of choice against all schistosome parasites. A single oral
dose of 40 mg/kg is generally sufficient to produce cure rates of 8090% and dra-
matic reductions in the average number of eggs excreted. Praziquantel treatment III
for one person requires, on average, 3 tablets of 600 mg in one dose. The cost of a
tablet is now less than US$ 0.10, bringing the total drug cost of a treatment to
about US$ 0.30. Drug costs decrease when the entire population is included in
prevention programmes. A dose pole (for calculating dosage according to height) IV
is available to facilitate the delivery of praziquantel in schools or in community-
based programmes.

172
Prevention
Control of helminths occurs as coordinated mass drug administration, generally
for children and women of childbearing age. Case management and control of
schistosomiasis are priority interventions given the effect of this disease on the
general health status of infected individuals as well as the role it plays in increas-
ing the severity of concomitant infections.
Programme work should be concerned with the distribution of praziquantel by
community health workers, cooperatives and school health workers. Community
treatment was initially implemented in a limited number of localities. The United
Nations World Food Programme is expanding its country food distribution pro-
grammes to include school-deworming with praziquantel a pilot programme
was successfully completed in 2004. Praziquantel may be available on the local

market; if so, the quality of the drug should be tested before it is used in control
programmes. In addition to preventive chemotherapy, other recommended inter-
ventions are:43
Community diagnosis (through primary school surveys) and regular treat-

ment of endemic populations according to community prevalence categories
(see below).
Creation of alternative, safe water sources to reduce contact with infective
water.
Proper disposal of faeces and urine to prevent viable eggs from reaching bodies
of water containing snail hosts.
Health education to promote early care-seeking behaviour, use of safe water
and proper disposal of excreta.
Reduction of snail habitats and snail contact (through irrigation and agricul-
tural practices, and environmental management).
Treatment of snail-breeding sites with molluscicide
43 For documents and publications on schistosomiasis, see http://www.who.int/wormcontrol/en/.

173
Recommended treatment strategy for schistosomiasis in preventive

chemotherapy
Category Prevalence among Action to be taken

school-age children
High-risk community > 50% by parasitological Treat all school-age Also treat adults
methods (intestinal and children (enrolled and not considered to be at risk
urinary tract schisto enrolled) once a year (from special groups to
somiasis); or > 30% by entire communities living
questionnaire for visible in endemic areas).
haematuria (urinary
schistosomiasis)
Moderate-risk community > 10% but < 50% by Treat all school-age Also treat adults
parasitological methods children (enrolled and not considered to be at risk
(intestinal and urinary enrolled) once every 2 years (special risk groups only).
schistosomiasis); or < 30%
by questionnaire for visible
haematuria (urinary
schistosomiasis)
Low-risk community < 10% by parasitological Treat all school-age Praziquantel should be
methods (intestinal and children (enrolled and not available in dispensaries
urinary schistosomiasis) enrolled) twice during and clinics for treatment of
their primary schooling suspected cases.
(e.g. once on entry and
once on exit)
Source: Preventive chemotherapy in human helminthiasis: coordinated use of anthelminthic drugs in control inter-
ventions. A manual for health professionals and programme managers. Geneva, World Health Organization, 2006. I
II
III
IV

174
SOIL-TRANSMITTED HELMINTHIASES (ASCARIASIS,

HOOKWORM INFECTION, TRICHURIASIS)

Data are sparse, but infection may be expected to show marked geographical dis-
tribution in the north and north-west of the country in the tropical zones.
Chad
Infection shows a marked geographical distribution in the east and south-east
(the Sudanian and tropical zones of the country). A nationwide survey of school-
children was completed in 2002.44 Hookworm (Necator americanus) was found
to have a prevalence of 32.7% in the south and east of the country. The extreme
temperatures experienced in the north and west are unfavourable to the ova of
A. lumbricoides or T. trichiura.
Description
Infectious agent
Helminths: Ascaris lumbricoides, hookworm (Necator americanus), Trichuris
trichiura.
Case definition
Ascariasis
Suspected: abdominal or respiratory symptoms and history of passing worms.
Confirmed: suspected case and passage of A. lumbricoides (anus, mouth and
nose), or presence of A. lumbricoides eggs in stools (microscopic examination).
Hookworm infection
Suspected: severe anaemia for which there is no other obvious cause.
Confirmed: suspected case and presence of hookworm eggs in stools (micro-
scopic examination).
44 Beasley M et al. Health of schoolchildren in Chad. Tropical Medicine and International Health, 2002, 7(7):
625-630.

175
Trichuriasis
SOIL-TRANSMITTED HELMINTHIASES (ASCARIASIS, HOOKWORM INFECTION, TRICHURIASIS)

Suspected: bloody, mucoid stools.
Confirmed: suspected case and presence of T. trichiura eggs in stools.
Ingestion of eggs, mainly as a contaminant of food: A. lumbricoides and T. trichiura.
Active penetration of the skin by larvae in the soil (hookworm).
Incubation period
48 weeks for A. lumbricoides.
From a few weeks to many months for hookworm disease.
Unspecified for T. trichiura.
A. lumbricoides eggs appear in the faeces 4575 days after ingestion and become
infective in soil after 1421 days. They may remain viable in soil for years.
Infected people may contaminate soil as long as mature fertilized female worms
live in the intestine (lifespan of adult worms can be 1224 months).
Hookworm eggs appear in the faeces 67 weeks after infection. As larvae, they
become infective in soil after 710 days and may remain infective for several
weeks. Infected people may contaminate soil for several years.
T. trichiura eggs appear in the faeces 7090 days after ingestion and become infec- I
tive in soil after 1014 days. Infected people may contaminate soil for several years.
Epidemiology
II
General
STH infection is usually endemic, with little likelihood of rapid changes in incidence.
Surveys identify areas of particularly high endemicity where mass treatment is
warranted. Soil-transmitted helminthiasis may be coendemic with schistosomiasis, III
so that coordinated treatment for both may be appropriate. STH infections can
be controlled with low-cost, highly effective interventions that markedly improve
the quality of life of affected populations.45
IV
45 http://www.who.int/wormcontrol/databank/en/; http://www.who.int/wormcontrol/documents/maps/en/
car.pdf; http://www.who.int/wormcontrol/documents/maps/en/chad.pdf.

176
Epidemiological data on geographical distribution remain scarce for these countries.
Seasonality
Distribution is influenced by environmental parameters, with extreme tempera-
tures being unfavourable to the ova of A. lumbricoides or T. trichiura. The peak of
transmission is usually at the end of the rainy season (SeptemberOctober). The
lowest transmission rate is at the end of the dry season (AprilMay).

Population movement. Risk is exclusively linked to insufficient sanitation. It is

not a risk factor if people remain in the same place for a period of time shorter
than that needed for eggs to be discharged by an infected patient and become
infective themselves (at least 4550 days).
Overcrowding. Risk is exclusively linked to the number of people defecating and
of unsafe disposal of faeces.
Poor access to health services. Regular treatment of entire endemic communities
has a limited effect on breaking the transmission cycle and reducing overall trans-
mission rates. However, regular treatment has been shown to be highly effective
in preventing development of morbidity due to STH infections in infected indi-
viduals (preventive chemotherapy).
Food shortages. Malnutrition and STH infections have a synergic role in causing
iron-deficiency anaemia and vitamin A deficiency.
Lack of safe water and poor sanitation. The proportion of people effectively using
sanitation facilities is the most important factor.

Prevention
As control of helminthiasis occurs as coordinated mass drug administration, the
mapping of pathogen distribution is fundamental.
Control
Highly-endemic areas would call for annual deworming of school-age children and
other high-risk groups according to WHO guidelines on preventive chemotherapy.

177
Control of STH infections can play a major role in reducing the burden of commu-
SOIL-TRANSMITTED HELMINTHIASES (ASCARIASIS, HOOKWORM INFECTION, TRICHURIASIS)

nicable disease borne by populations in emergency situations. Moreover, given its
simplicity and feasibility, control of STH infections may represent a starting point
for the reconstruction of health-care systems in countries affected by emergencies.
Case management
All STH compete with the host for nutrients, causing malabsorption of fats, pro-
teins, carbohydrates and vitamins, and directly contributing to malnutrition.
They may also cause growth retardation. A. lumbricoides infestation exacerbates
vitamin A deficiency. Elimination of ascarids may result in rapid clinical improve-
ment in night blindness and dryness around the eye.
Hookworm infestation is strongly associated with chronic anaemia. Significant
inverse correlations between intensity of worm infestation and haemoglobin level
have been demonstrated. Heavy T. trichiura infestation may cause diarrhoea and
severe malabsorption.
STH may be controlled with very cheap interventions. The average cost in a school
distribution campaign (including drugs, distribution and monitoring activities)
is approximately US$ 0.100.15 per child.
For treatment, the following four drugs are recommended by WHO and may be
safely administered to children past the first year of life:
Albendazole 400 mg single dose (200 mg in children

aged 12 years); or I
Mebendazole 500 mg single dose; or
Levamisole 2.5 mg/kg single dose; or
Pyrantel 10 mg/kg single dose.
II
Levamisole and pyrantel are less commonly used because they are more difficult
to administer.
Notes
III
1. These drugs must not be given during the first trimester of pregnancy.
2. Where mass treatment with albendazole for filariasis is envisaged, chemotherapy
of intestinal helminths will take place as part of antifilarial chemoprophylaxis.
3. Iron supplementation is also recommended in communities with high preva- IV
lence of iron-deficiency anaemia (such as those where hookworm disease is
highly endemic).

178
Recommended treatment strategy for soil-transmitted helminthiases
Category Prevalence of any STH Action to be taken Also treat:

infection among
school-age childrena
High-risk community > 50% Treat all school-age Preschool children;

children (enrolled and not women of childbearing
enrolled) twice each yearb age, including pregnant
women in the 2nd and 3rd
trimesters and lactating
mothers;
adults at high risk in
certain occupations (e.g.
tea-pickers and miners).
Low-risk community > 20% and < 50% Treat all school-age Preschool children;
children (enrolled and not women of childbearing
enrolled) once each year age, including pregnant
women in the 2nd and 3rd
trimesters and lactating
mothers;
adults at high risk in
certain occupations (e.g.
tea-pickers and miners).
Source: Preventive chemotherapy in human helminthiasis: coordinated use of anthelminthic drugs in control inter-
ventions. A manual for health professionals and programme managers. Geneva, World Health Organization, 2006.
a When prevalence of any STH is less than 20%, large-scale preventive chemotherapy interventions are not
recommended. Affected individuals should be dealt with on a case-by-case basis.
b If resources are available, a third drug distribution intervention might be added. In this case, the appropriate
frequency of treatment would be every 4 months.

179
TETANUS

Central African Republic and Chad are among the countries where MNT is still
a public health problem and they are also among 16 countries where less than 50%
of districts have eliminated MNT. Elimination is defined by WHO as fewer than
1 case of neonatal tetanus per 1000 live births in all districts.

A total of 68 cases of tetanus was reported for 2007, all of which were reported as
neonatal.46
Chad
A total of 100 cases of tetanus was reported for 2007, all of which were reported
as neonatal.47
TETANUS
Description
Infectious agent
The bacterium Clostridium tetani.
Case definition48
I
Suspected case of neonatal tetanus:
any neonatal death between 3 and 28 days of age in which the cause of
death is unknown; or II
any neonate reported as having suffered from neonatal tetanus between
3 and 28 days of age and not investigated
Confirmed case of neonatal tetanus: any neonate with normal ability to suck III
and cry during the first 2 days of life; and who
46 http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencette.htm.
47 http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencette.htm.
48 Source; WHO-recommended standards for surveillance of selected vaccine preventable diseases. IV
(WHO/V&B/03.01) (http://www.who.int/immunization/documents/WHO_VB_03.01/en/index.html;
http://www.who.int/immunization/documents/WHO_VB_03.01/en/index.html)

180
between 3 and 28 days of age, cannot suck normally; and

becomes stiff or has spasms (i.e. jerking of the muscles).
Note. The basis for case classification is entirely clinical and does not depend on
laboratory-confirmation. NT cases reported by physicians are considered to be
confirmed.
C. tetani spores occur worldwide as constituents of soil and in the gastrointestinal
tracts of animals (including humans). Infection occurs when the spores are intro-
duced into the body through a puncture wound with spore-contaminated faeces,
dust or soil-damaged tissue. Or after surgical procedures that include abortions

and circumcision. Cases have followed wounds considered too trivial for medical
attention. Neonatal tetanus usually occurs through the introduction of spores via
the umbilical cord (e.g. through the use of an unclean instrument to cut the cord
during delivery, or through the application of contaminated materials on the
umbilical stump after delivery).
Incubation period
321 days, range one day to several months, average 10 days.
No direct person-to-person transmission.
Epidemiology
General
Globally:49
The annual reported incidence of tetanus has declined as coverage of DTP3

has risen.
Cases of maternal and neonatal tetanus (MNT) are vastly underreported
including in the African region.
All countries aim at eliminating MNT as a public health problem.
49 http://www.who.int/immunization_monitoring/diseases/Tetanus_coverage.jpg .

181
WHO estimates that globally about 160 000 deaths occur every year as a result of
tetanus, of which 128 000 were newborns (2004 estimates). Most of these neonatal
tetanus (NT) deaths occur in less than 50 countries in Asia and Africa.
Worldwide.
Seasonality
Universal.

Poor access to health services means:
increased likelihood for poor wound management and treatment;

decreased likelihood for protection through immunization;
increased possibility of risk-prone behaviour surrounding childbirth (thus
increasing risk for neonatal tetanus).
TETANUS
Case management
See Annex 3, Wounds and injuries. I
Epidemic control
Outbreaks are rare, but when they occur a thorough case-investigation and search
should be undertaken for a common source, e.g. repeated use of needles for injec- II
tions, unhygienic medical and/or delivery procedures, low vaccination coverage.
Prevention
Education of the public on the necessity of immunization. III
Universal active immunization.
Prophylactic wound management.
Prevention of maternal and neonatal tetanus requires maternal immunization with IV

tetanus toxoid vaccine, and use of hygienic delivery practices (e.g. assistance by a
trained attendant, delivery in a health facility, change of harmful traditional practices).

182
TUBERCULOSIS

Although not listed among the 22 highest-burden countries globally, TB represents
a significant burden of disease for CAR. The disease affects the entire population,
with extreme vulnerability among the impoverished (67%) and/or those with HIV.
TB burden, Central African Republic, 2006 estimates

Prevalence (all cases per 100 000 population per year) 528
Incidence (new cases per 100 000 population per year), male > female 345
Trend in incidence rate (per year, 20042005) -0.1%
Mortality (deaths per 100 000 population per year) 80
Prevalence of HIV in adult TB patients (1549 years) No data
New TB cases with MDR 1.1%
Source: Global tuberculosis control: surveillance, planning, financing. Geneva, World Health Organization, 2008
(WHO/HTM/TB/2008.393).
Chad
TB burden, Chad, 2005 estimates
Prevalence (all cases per 100 000 population) 570
Incidence (new cases per 100 000 population per year, male > female 299
Trend in incidence rate (per year) -0.1%
Mortality (deaths per 100 000 population per year) 76
Prevalence of HIV in adult TB patients (1549 years) 18%
Proportion of new TB cases that are multidrug-resistant (2004) 1.6%
Source: Global tuberculosis control: surveillance, planning, financing. Geneva, World Health Organization, 2008
(WHO/HTM/TB/2008.393).

183
Description
Infectious agent
The bacterium Mycobacterium tuberculosis. This complex includes M. tuberculosis
and M. africanum primarily from humans, and M. bovis primarily from cattle. More
recently, M. canettii and M. microti have been incorporated in this complex.
Case definition
The most important symptom in the selection of a tuberculosis (TB) suspect is
productive cough of long duration (> 2 weeks or in accordance with current
national tuberculosis control programme (NTCP) directives).
Patients with TB often have other symptoms such as:
haemoptysis
significant weight loss
chest pain
TUBERCULOSIS
breathlessness
fever/night sweats
tiredness
loss of appetite.
In camp settings, it is the priority of the health services to detect the sources of I
infection by sputum microscopy, and to cure them. Pulmonary TB patients with
sputum-positive microscopy are the main source of TB infection.
Case classification II
Suspect: any person who presents with symptoms or signs suggestive of TB,
in particular cough of long duration (> 2 weeks or in accordance with current
NTCP directives).
Case:* a patient in whom TB has been bacteriologically confirmed or diagnosed III
by a clinician. Note. Any person given anti-TB treatment should be recorded
as a case. A trial TB treatment should not be given as a method for diagnosis.
Definite case:* a patient who is culture-positive for the M. tuberculosis complex.
In countries where culture is not routinely available, a patient with one or IV
more sputum smears positive for acid-fast bacilli (AFB) is also considered a
definite case.

184
* This new definition of a sputum-smear TB case is recommended by WHO and was endorsed by the Strategic
Technical and Advisory Group for Tuberculosis in June 2007.
Laboratory criteria for diagnosis

Each TB suspect should have two (formerly three) sputum samples examined by
light binocular microscopy for AFB. Secretions build up in the airways overnight;
an early morning sputum sample is therefore more likely to contain TB organisms
than a sample later in the day. In practice, a TB suspect should provide two spu-
tum samples, with at least one obtained from an early-morning collection.
If at least one sputum smear is positive. Smears should be stained using the Ziehl
Neelsen method. Any TB suspect with at least one positive smear is a smear-
positive TB patient, who must then be registered and started on anti-TB treatment.
When the two sputum smears are negative. If the initial two smears are negative,
but pulmonary TB is still suspected because of persistent symptoms, the TB sus-
pect should be treated for acute respiratory infection with broad-spectrum anti-
biotics for at least 1 week (e.g. amoxicillin or co-trimoxazole, but not anti-TB drugs
or any fluoroquinolone). If there is no improvement, the patients sputum should
be re-examined 2 weeks after the first sputum examination.
At least 65% of all pulmonary TB cases are expected to be confirmed by positive
sputum-smear examination. X-ray lesions compatible with active TB should
encourage further sputum examination if the two sputum-smear examinations
were negative. X-ray itself is not a diagnostic tool for pulmonary TB.
In some circumstances, a compatible X-ray together with symptoms consistent
with TB will lead to the diagnosis of pulmonary TB in smear-negative cases. Thus,
if the two samples are again negative after the trial of antibiotics, either a com-
patible X-ray interpreted by an experienced physician or, in the absence of X-ray
facilities, the experienced physicians judgement alone will decide whether some-
one is categorized as having smear-negative pulmonary TB.
Additional cases of TB may be found among close contacts of known smear-
positive cases, either family members or individuals sleeping in the same shelter.
Close TB contacts with suggestive symptoms for TB suspicion (e.g. productive
cough of long duration) should be screened for TB, using the procedures described
above. Among TB contacts, the priority for TB screening should be given to chil-
dren and people with underlying conditions such as HIV-positive persons. If the
screening of TB contacts aged < 5 years shows that there is no active TB, insoniazid
preventive therapy (IPT) should be provided to them (5mg/kg/day for 6 months).

185
TB in HIV-positive patients
HIV-positive patients with TB infection have a much higher risk of developing
active TB than HIV-negative patients. Pulmonary TB is still the commonest
form of TB in HIV-infected patients. The clinical presentation of TB depends on
the degree of immunosuppression. The principles of TB control are the same even
when there are many HIV-infected TB patients. It is important to look systemati-
cally for symptoms or signs of TB in HIV-positive patients and to start treatment
without delay based on bacteriological, radiological and clinical evidence.
HIV testing should be promoted among TB patients. HIV-positive TB patients should
be provided with co-trimoxazole preventive therapy (CPT). Whenever possible, eli-
gible HIV-positive TB patients should be provided with antiretroviral (ARV) therapy.
Diagnostic criteria for classification of TB in adults

WHO has recently revised recommendations to diagnose and treat tuberculosis in
HIV-prevalent and resource-constrained settings.
Pulmonary tuberculosis (pulmonary TB). Pulmonary TB refers to disease involving
TUBERCULOSIS
the lung parenchyma. Tuberculous intrathoracic lymphadenopathy (mediastinal
and/or hilar) or tuberculous pleural effusion without lung involvement is a case
of extrapulmonary TB. A patient with both pulmonary and extrapulmonary TB
should be classified as a case of pulmonary TB.
Smear-positive pulmonary TB. The revised case definition of smear-positive pul-
monary tuberculosis is the same for HIV-positive and HIV-negative patients, i.e. I
requiring at least one positive smear in settings with a functional system of external
quality assurance for smear microscopy.
Smear-negative pulmonary TB. The revised case definition of smear-negative pul-
monary tuberculosis includes: II
at least two sputum specimens negative for AFB; and
radiographical abnormalities consistent with active tuberculosis; and
laboratory-confirmation of HIV infection; or III
strong clinical evidence of HIV infection; and
decision by a clinician to treat with a full course of antituberculosis chemotherapy.
If there is no laboratory-confirmation of HIV infection or if the patient has no IV

strong clinical evidence of HIV infection, the following criteria should be used to
establish the diagnosis of smear-negative pulmonary TB:

186
at least two sputum specimens negative for AFB; and

no clinical response to a course of broad-spectrum antibiotics; and
radiographic abnormalities consistent with active pulmonary TB; and
decision by a clinician to treat with a full course of antituberculosis chemotherapy.
This group also includes cases without smear result, which should be exceptional
in adults but relatively more frequent in children. A patient whose initial sputum
smears were negative and whose subsequent sputum culture result is positive is a
smear-negative pulmonary TB case whether or not there is a laboratory HIV con-
firmation and whether or not there is strong clinical evidence of HIV infection.
Extrapulmonary tuberculosis. This refers to tuberculosis of organs other than the
lungs, e.g. pleura, lymph nodes, abdomen, genitourinary tract, skin, joints and
bones, meninges. Diagnosis should be based on culture-positive specimens, or
histological or strong clinical evidence consistent with active EPTB, followed by
a medical decision by a clinician to treat with a full course of antituberculosis
chemotherapy. Some cases will be easy to diagnose such as peripheral lymphad-
enitis, with swelling of cervical or axial lymph nodes, chronic evolution and/or
production of caseous discharge. Other cases, such as severe life-threatening
forms (e.g. miliary TB, TB meningitis), TB of bone or joints, TB peritonitis, TB
laryngitis) will be suspected but should be referred to a hospital for assessment.
This definition is used whether the patient has laboratory-confirmation of HIV
infection or not, as well as whether the patient presents with strong clinical evi-
dence of HIV infection or not.50
Airborne transmission of tubercle bacilli that are included in droplets nuclei.
The droplets nuclei are produced when patients with active pulmonary or laryn-
geal TB cough or sneeze. Bovine TB results from exposure to tuberculous cattle,
usually by ingestion of unpasteurized milk or dairy products.
Progression to active disease

Progression from TB infection to active TB disease may take from weeks to years;
latent infections may persist throughout life. The risk of TB occurrence is relatively
50 For further information on the revised recommendations on the diagnosis and treatment of TB in HIV
prevalent settings, please see: Improving the diagnosis and treatment of smear-negative pulmonary and
extra-pulmonary tuberculosis among adults and adolescents (http://www.who.int/entity/tb/publications/
2006/tbhiv_recommendations.pdf).

187
high during the first year following TB infection then progressively decreases by
half within the following 45 years. Only 10% of infected people with a normal
immune system will develop active TB at some point in life.
As long as viable tubercle bacilli are being discharged in the sputum. Effective
treatment usually eliminates communicability within 8 weeks.
Epidemiology
General
Various factors present challenges for successful TB control in the subregion.
HIV is the most powerful factor known to increase the risk of developing active
TB among people infected with tubercle bacilli. Low BCG vaccination coverage
among children < 1 year of age and poor nutritional status increase vulnerability
to development of active disease.
TUBERCULOSIS
Cases are reported from all subnational levels in the region.
Seasonality
No specific seasonality is reported. I
Alert threshold
Not applicable.
II
Population movement. Population displacement disrupts existing TB control
activities. This leads to an increased risk of transmission since TB cases with the
potential to spread the disease will be identified and treated after a long delay or
III
not at all. The proportion of interruptions of TB therapy, TB relapses and treatment
failure is also likely to increase. This contributes to the emergence of drug-resistant
strains and increasing deaths from TB.
IV
Overcrowding and poor indoor ventilation are recognized as the important factors
leading to increased risk of transmission.

188
Poor access to health services. People affected by TB who cannot access health
services for diagnosis and treatment remain infectious for a longer period. The case-
fatality rate is high without proper treatment. The iterative interruption of treat-
ment is one of the most important causes of development of multidrug-resistant
TB (MDR-TB).
Food shortages. TB, often in combination with HIV/AIDS, is common in mal-
nourished populations. The consequent immune system dysfunction increases
the risk of TB occurrence. Malnourished populations, especially malnourished
children of all ages, are considered to be at particular risk of developing severe
active TB.

Case management
Following the diagnosis of TB, and before treatment starts, all patients should be
questioned carefully as to whether or not they have ever taken anti-TB drugs.
Patients should be classified according to the following criteria:
site of disease;
severity of disease;
bacteriological status (assessed by sputum microscopy);
history of anti-TB treatment (new or previously treated).
New case
A patient who has never had treatment for TB or who has taken anti-TB drugs for
less than 4 weeks and has:
sputum smear-positive pulmonary TB; or

sputum smear-negative pulmonary TB; or
extrapulmonary TB.
Previously-treated case
A patient who has at any time received anti-TB treatment for more than 1 month.
This group of patients comprises:
Return after interruption: patient who returns to treatment with positive bac-
teriology (e.g. sputum smear-positive microscopy), following interruption of

189
treatment for 2 months or more. This could be common among recent refugees
or internally displaced persons.
Failure: a patient who remained, or became again, smear-positive, 5 months
or later during treatment; also, a patient who was smear-negative before
starting treatment and became smear-positive after the second month of
treatment. Therefore, these patients after having failed a previous treatment
are started on a re-treatment regimen.
Relapse: a patient previously treated for TB who has been declared cured or
treatment completed, and is diagnosed with bacteriologically-confirmed (smear
or culture-positive) tuberculosis.
Chronic: a patient who remained, or became again, smear-positive at the end
of a fully supervised, standardized re-treatment regimen.
Good case management includes directly observed therapy during the intensive
phase for all new sputum smear-positive cases, the continuation phase of rifampicin-
containing regimens and the entire re-treatment regimen.
TUBERCULOSIS
There are three main types of treatment regimens: Category I for new smear-
positive pulmonary cases, and severely ill TB patients; Category II for re-treatment
cases; and Category III for smear-negative pulmonary or extrapulmonary cases
(not severely ill patients) (see Treatment categories below).
The chemotherapeutic regimens are based on standardized combinations of five
essential anti-TB drugs:
I
1. rifampicin (R)
2. isoniazid (H)
3. pyrazinamide (Z)
4. ethambutol (E) II
5. streptomycin (S).
TB drugs should be given to TB patients in fixed-dose combination forms. Each

of the standardized chemotherapeutic regimens consists of two phases: III
1. Initial (intensive) phase
23 months, with 35 drugs given daily under direct observation, for maximum
reduction in the number of TB organisms.
IV
The number of drugs used relates to the risk of failure of treatment due to
possible bacterial resistance.

190
2. Continuation phase
46 months, with 23 drugs (including rifampicin) given 3 times a week under
direct observation or, in some cases (e.g. during repatriation of refugees), 2 drugs
(ethambutol and isoniazid) for 6 months given daily unsupervised, but in a
fixed-dose combination form.*
All doses of rifampicin-containing regimens should be given by staff.
Actual swallowing of medication must be checked by a health worker or treat-
ment supporter.
Hospitalized patients should be kept in a separate ward for the first 2 weeks
of treatment.
* Regimens are written in short form with the number of months the medication is to be given in front of
the letter and the doses per week written after the letter. If there is no number after the letter, a daily dos-
age is given. The symbol / separates the different phases of the therapy, e.g. 2 RHZE/4H3R3 means that
for the first 2 months of treatment, rifampicin, isoniazid, pyrazinamide and ethambutol are given daily. This
is followed by 4 months of rifampicin and isoniazid given regularly but each given only 3 times per week.
HIV-positive patients51
1. Anti-TB drug treatment is the same for HIV-positive and HIV-negative patients.
However: (i) thioacetazone should not be administered to HIV-positive TB
patients as there is an increased risk of severe and sometimes fatal skin reac-
tions; and (ii) HIV-positive TB patients should be prescribed a rifampicin-
containing regimen throughout the 6-month course of the treatment.
2. Controlled clinical trial studies have shown that isoniazid preventive treatment
(IPT) reduces the risk of TB disease in HIV-positive individuals with latent
TB infection (shown by a positive tuberculin skin test).
3. The decision to use IPT should be carefully evaluated, and firstly requires
exclusion of active TB in the patient.
4. To manage effectively the problem of HIV-TB co-infection, TB and HIV pro-
grammes should coordinate activities through a TB/HIV coordinating body.
Treatment categories52
Standardized short-course chemotherapy using regimens of 68 months:
51 See: WHO/TB-HIV interim policy on collaborative TB/HIV activities. Geneva, World Health Organization,
2004 (WHO/HTM/TB/2004.330, WHO/HTM/HIV/2004.1; http://whqlibdoc.who.int/hq/2004/WHO_
HTM_TB_2004.330.pdf). Additionally, please consult NTCP guidelines.
52 See: Treatment of tuberculosis: guidelines for national programmes, 3rd ed. Geneva, World Health Organiza-
tion, 2003 (WHO/TB/2003.313); Tuberculosis control in refugee situations: an inter-agency field manual.
Geneva, World Health Organization, 1997 (WHO/TB/97.221, under revision); An expanded DOTS frame-
work for effective tuberculosis control. Geneva, World Health Organization, 2002 (WHO/CDS/TB/2002.297).
Additionally, please see NTCP guidelines.

191
Category I (EHRZ/RH)
These patients are:
new smear-positive TB cases; and
severely ill patients with other forms of TB (new smear-negative pulmo-
nary TB with extensive parenchymal involvement, and new cases of severe
forms of extrapulmonary TB).
The recommended regimen is for 6 months. The initial (or intensive) phase of
treatment lasts for 2 months, with rifampicin, isoniazid, pyrazinamide and
ethambutol given daily or 3 times a week, under direct supervision.
At the end of the second month, most patients will have a negative result on
sputum microscopy; they may then progress to the second stage of treatment
the continuation phase. This phase lasts for 4 months, with rifampicin and
isoniazid given 3 times per week, under direct supervision.
If the sputum-smear examination is positive at the end of the second month,
the initial phase is prolonged for a third month. The patient then starts the
TUBERCULOSIS
continuation phase irrespective of the results of the sputum examination at
the end of the third month.
In the continuation of the treatment, if the smears are still positive at the end
of the fifth month or at the end of the treatment regimen, the patient is classi-
fied a treatment failure case. The patient is re-registered, and commences a
full course of the re-treatment regimen as a Category II patient. I
The drug dose is adjusted for weight gain at the end of the initial phase (second
or third month).
This category includes patients with TB meningitis, disseminated TB, peri-
carditis, peritonitis, bilateral or extensive pleurisy, vertebral disease with II
neurological complications, and intestinal and genitourinary disease.
Daily self-administered ethambutol and isoniazid may be used in the continua-
tion phase for 6 months, so this treatment regimen takes a total of 8 months.
However, note that there is a higher rate of treatment failure and relapse III
associated with this regimen using ethambutol and isoniazid in the continua-
tion phase.
Category II (2SHRZE/1HRZE/5HRE)
IV
This category should be used for patients who were previously treated and are
now sputum smear-positive. This includes:

192
treatment after interruption;

treatment failure; and
relapse after treatment.
These patients should receive a standardized re-treatment regimen, fully super-
vised throughout both phases of treatment.
The initial phase of treatment lasts for 3 months, where isoniazid, rifampicin,
pyrazinamide and ethambutol are given daily. This regimen is supplemented
by streptomycin daily for the first 2 months.
The initial phase of this regimen is followed by a continuation phase of 5 months
treatment with isoniazid, rifampicin and ethambutol given 3 times per week.
Sputum-smear examination is performed at the end of the initial phase of

treatment (at the end of the third month), during the continuation phase of
treatment (at the end of the fifth month) and at the end of treatment (at the
end of the eighth month). If the patient is sputum smear-positive at the end
of the third month, the initial phase of treatment is extended with isoniazid,
rifampicin, pyrazinamide and ethambutol for 1 more month. Patients who
are still positive at the end of the fourth month progress to the continuation
phase, regardless of the results of the sputum examination.
Category III
The Category III regimen is indicated in:
patients with smear-negative pulmonary TB (with limited parenchymal

involvement);
adults and children with non-serious extrapulmonary TB (including sympto-
matic primary TB usually observed in children).
These patients receive the same treatment regimen as Category I patients.
However, ethambutol may be omitted in the initial phase of treatment in
patients with limited parenchymal involvement, non cavitary smear-negative
pulmonary TB who are known to be HIV-negative and in children with pri-
mary TB.
When the continuation phase cannot be carried out under direct observation,
daily ethambutol and isoniazid should be used in the continuation phase for
6 months. All doses of rifampicin-containing regimens should be directly
observed by staff or a treatment supporter. Actual swallowing of medication
should be checked.

193
Health education
Key elements of community education emphasize:
destigmatization of TB patients;
curability of TB disease;
early (self) referral of TB suspects;
the importance of adherence to treatment;
contact-tracing and investigation.
The most important messages to teach are:
TB in adults should be suspected when the person has a productive cough of

long duration (> 2weeks) or in accordance with the directives of the NTCP,
and/or blood in sputum, with significant weight loss.
Cover the mouth whenever coughing or sneezing to prevent the spread of
TUBERCULOSIS
microorganisms.
Anyone may contract TB.
TB is curable.
Early treatment is important for best results and to prevent spread, especially
to family members.
Children are especially at risk if not treated and may develop severe, even fatal I
forms of TB.
Identification of TB and appropriate treatment constitute the best prevention.
All TB patients must take the full course of treatment prescribed.
Treatment makes patients non-infectious in 8 weeks, but cure takes 68
II
months.
Treatment must be completed even though the patient may feel better sooner.
Interruption of treatment may result in a recurrence of TB, which may be diffi III
cult or impossible to treat and spread TB bacilli to others, especially to children.
All patients should be treated sympathetically and with respect.
Controlling TB is a community responsibility.
IV
Note. Diagrams should be used as much as possible: a high literacy should not be
assumed. Cured patients are often helpful teachers and supporters of new patients.

194
Prevention
Detection and treatment of smear-positive (infectious) TB cases are the most effective
interventions to prevent the transmission of TB. Complementary control strategies:
Health education to improve and strengthen adherence to treatment.

Good ventilation and reduction of overcrowding in health clinics, and sepa-
ration of hospitalized patients in a dedicated ward for at least the first 2 weeks
of treatment.
Particular care to separate infectious TB patients from HIV-positive individuals.
BCG to prevent severe forms of TB in children (see Immunization below).
Children < 5 years of age who are close contacts of smear-positive pulmonary
TB patients and who, after investigation, have no active TB, should receive
isoniazid prophylaxis as follows: 5mg/kg/day for 6 months with a steady follow-
up (e.g. every 2 months). This will significantly reduce the likelihood of TB
disease occurrence. Breastfeeding children of sputum smear-positive mothers
are the most important group for isoniazid prophylaxis. If the child is well,
BCG vaccination may be carried out after the isoniazid prophylaxis course; in
the event of a sudden disruption in the programme, isoniazid may be stopped,
and BCG should be given before the child leaves the programme (preferably
after a 1-week interval). Children aged 5 years and over who are well do not
require prophylaxis, but only clinical follow-up.
Immunization
BCG has been shown to be effective in preventing severe forms of disease such as
TB meningitis and miliary TB in children. As overcrowding and malnutrition
are common in many refugee and displaced populations, the risk of TB trans-
mission to children is increased. BCG is strongly recommended for all newborn
children and any children up to the age of 5 years who have not already received
it. The vaccination of newborns should be incorporated into routine immuniza-
tion programmes for all children. Revaccination with BCG is not recommended.
Management of TB in displaced populations

Diagnosis of TB in children
TB in children is a general disease, which may affect any part of the body. Children
rarely have smear-positive pulmonary TB, so they are rarely infectious. In com-
plex emergency situations with a large number of children, extrapulmonary forms

195
of TB should be suspected, diagnosed and treated appropriately. Often, this requires

referral to a hospital for X-ray and special examinations (e.g. lumbar puncture in
case of meningitis TB suspicion).
Children with headache, change of temperament, recent squint or ocular muscle
paralysis should be suspected of meningitis. TB is one, albeit rare, cause of men-
ingitis (meningococcal meningitis is a more common cause in complex emergency
settings).
Definitive diagnosis requires hospital referral. Children with high fever, dyspnoea,
gastrointestinal symptoms, confusion (i.e. those in whom acute miliary TB is
suspected) must also be referred to hospital for assessment and diagnosis.
Suspected TB of the bone, tuberculous arthritis or pleural effusions also require
referral.
Commoner forms of extrapulmonary disease (e.g. cervical or axillary lymphad-
enitis, peritonitis with ascites) can be diagnosed and treated in a camp situation.
The diagnosis of TB in children should be considered in a child if there is:
TUBERCULOSIS
an illness lasting for more than 10 days;
a history of close contact with a TB patient;
a poor response to antibiotic therapy;
a poor response to one month of nutritional rehabilitation;
weight loss or abnormally slow growth; I
loss of energy; or
increasing irritability and drowsiness.
Note. The same considerations explained above for adults apply to children for II
the diagnosis of TB in HIV-positive patients.
III
IV

196
YELLOW FEVER

Outbreaks:
April 2008: Ouham-Pend prefecture; 2 suspected cases (one was laboratory-

confirmed); 1 death; CFR 50%. A reactive mass vaccination campaign was
organized in June 2008 in five communes (Birvan Bol, Bozoum, Danaynin,
Dan Gbabiri and Kouazo); 56 519 people were vaccinated, with a reported
administrative coverage of 98.7 %.
November 2006: a laboratory-confirmed case of fever and jaundice was re-
ported from the Bossembele prefecture, in a village in the Boyali II locality.
No additional cases were found on investigation. Aedes mosquitoes were not
detected by entomological investigation. A mass vaccination campaign was
completed. 6000 people were vaccinated, with a reported administrative cov-
erage of 105% in the target population of 10 000 inhabitants.
Case-based yellow fever surveillance has been operational since mid-2006 and
has also attained surveillance performance objectives (investigation rate 2.0
per 100000 population and 80% districts investigating at 1 suspected case with
a blood specimen.53
Chad
No cases have been reported since 2006.54
Description
Infectious agent
Yellow fever virus, belonging to the Flavivirus group.
53 http://www.who.int/immunization_monitoring/en/globalsummary/timeseries/tsincidencemea.htm.
54 http://whqlibdoc.who.int/hq/2007/WHO_IVB_2007_eng.pdf; http://www.who.int/immunization_
monitoring/en/globalsummary/timeseries/tsincidencemea.htm.

197
Case definition
Characterized by acute onset of fever followed by jaundice within 2 weeks of onset
of first symptoms. Haemorrhagic manifestations and signs of renal failure may
occur. There are two disease phases of yellow fever:
Acute phase. While some infected people have no symptoms at all, this first
phase is normally characterized by fever, muscle pain (with prominent back-
ache), headache, shivers, loss of appetite, nausea and/or vomiting. Often, the
high fever is paradoxically associated with a slow pulse (Fagets sign). Most
patients improve after 34 days and their symptoms disappear, but 15% enter
the toxic phase.
Toxic phase. Fever reappears, the patient rapidly develops jaundice and com-
plains of abdominal pain with vomiting. Bleeding may occur from the mouth,
nose, eyes and/or stomach. Once this happens, blood appears in the vomit
YELLOW FEVER
and faeces. Kidney function deteriorates; this may range from abnormal pro-
tein levels in the urine (albuminuria) to complete renal failure with no urine
production (anuria). Half the patients in the toxic phase die within 710 days
after onset. The remainder recover without significant organ damage.
Laboratory criteria
Isolation of yellow fever virus; or
I
presence of yellow fever-specific IgM or a fourfold or greater rise in serum
IgG levels in paired sera (acute and convalescent); or
positive postmortem liver histopathology; or II
detection of yellow fever antigen in tissues by immunohistochemistry; or
detection of yellow fever virus genomic sequences in blood or organs by
polymerase chain reaction (PCR).
III
Case classification
Suspected: a case that is compatible with the clinical description.
IV
Confirmed: a suspected case that is laboratory-confirmed (national reference
laboratory) or epidemiologically-linked to a confirmed case or outbreak.

198
The bite of infective mosquitoes. The vectors of yellow fever in forest areas in Africa
are mosquitoes from the Aedes species: A. africanus, A. simpsoni, A. furcifer. In
urban areas, the vector is A. aegypti (all-day biting species).
Incubation period
From 3 to 6 days.
The blood of patients is infective for mosquitoes shortly before onset of fever and
for the first 35 days of illness. The disease is highly communicable where many
susceptible people and abundant vector mosquitoes coexist. Once infected, mos-
quitoes remain so for life.
Epidemiology
General
Globally, yellow fever epidemics have been on the rise over the past 20 years.
Mosquitoes, mosquito habitats and susceptible populations are increasing. The
precise extent of illness and death caused by yellow fever is not known. Disease
surveillance is not adequate to detect cases of sylvatic yellow fever that may occur in
remote areas. Moreover, an outbreak of yellow fever may go undetected because the
signs and symptoms have a wide spectrum and overlap with those of many other
diseases; it is therefore difficult for health workers to make a definitive diagnosis
based on the signs and symptoms alone. Mild cases may go undetected because
the patient is likely to be treated at home and does not seek care in a health facility.
Thirty-three countries in Africa are at risk from yellow fever. These countries,
which include CAR and southern Chad, lie within a band from 15 N to 10 S.
The virus is constantly present with low levels of infection (i.e. endemic).
The viral presence may amplify into regular epidemics especially as surveillance
is suboptimal, and the disease is difficult to recognize during the early stages and
easily confused with other more common diseases (e.g. malaria, typhoid, dengue,
poisoning).
All three types of transmission cycle for yellow fever occur in Africa. Sylvatic,
intermediate and urban:

199
Sylvatic yellow fever generally results in sporadic cases most commonly among
young men working in the forest.
Intermediate yellow fever results in small-scale epidemics and occurs in humid
or semi-humid savannah. Separate villages in an area suffer simultaneous cases.
Urban yellow fever results in large epidemics that tend to spread outwards
from one source to cover a wide area.
Seasonality
In forested areas where the yellow fever virus circulates between mosquitoes and
monkeys, the disease is continuously present throughout the year. In field or
savannah areas outside the forest areas, transovarian transmission may contribute
to maintenance of the virus even during the dry season.
Alert threshold
One confirmed case should be considered as an epidemic and lead to the rapid
implementation of control measures. Yellow fever is a significant public health
problem in the subregion, where cases have been periodically reported for several
YELLOW FEVER
decades. The risk of resurgence of major epidemics of yellow fever, particularly in
heavily populated urban settings, is increasing for many reasons, including low
immunization coverage, the invasion of urban settings by A. aegypti and the change
in the demographic balance in most countries, shifting populations from being
mostly rural to mostly urban.
I
Population movement. Unvaccinated people moving to areas of endemicity are
at risk. Changes in land use constitute a risk factor. The movement of people from
rural to urban areas during emergencies may result in large numbers of people II
living in conditions of poverty, crowded housing and poor sanitation, all of which
are conditions that amplify the risk of transmission.
Overcrowding. As a result of increased population density and increased exposure
to mosquito bites in temporary shelters.
III
Poor access to health services
Collapse of vaccination programmes.

Increased death rates due to lack of appropriate case management.
IV
Weak mosquito control programmes and persistent low vaccination coverage
rates for yellow fever exacerbate the risk.

200

Case management
No specific treatment for yellow fever is available.
Dehydration and fever may be corrected with oral rehydration salts.
Intensive supportive care may improve the outcome but is rarely available.
Epidemic control
An infected mosquito spreads yellow fever when it bites non-infected humans.
When indirect human-to-human transmission is established, the conditions for
an epidemic are in place. Depending on the travel patterns of infected humans or
infected mosquitoes, the epidemic spreads from village to village and into cities.
Under epidemic conditions, the following must be implemented:
Mass vaccination with yellow fever vaccine.

Emergency mosquito-control measures:
eliminating potential mosquito breeding sites (the most important mos-
quito control measure for yellow fever control);
spraying to kill adult mosquitoes (less important because of small impact);
use of insecticide-treated bednets for hospitalized cases.
Prevention
Vaccination is the single most important measure for preventing yellow fever. In
endemic areas, vaccination must be given routinely through the incorporation of
yellow fever vaccine in routine child immunization programmes and mass preven-
tive campaigns. Yellow fever vaccine is not recommended for symptomatic HIV-
infected persons or other immunosuppressed individuals; for theoretical reasons,
it is not recommended for pregnant women.
The following strategies are recommended for yellow fever control programmes:
1. Vaccinating the population aged over 9 months in districts where coverage is

less than 80%; if funds are limited, a lower-cost intervention would be to vac-
cinate children aged between 9 months and 14 years to reach at least 50% of the
population; yellow fever vaccination should be integrated in routine activities
of the Expanded Programme on Immunization in at-risk areas. In 1989, CAR
introduced yellow fever vaccine in routine immunization.

201
2. Where necessary, mass vaccination campaigns to prevent epidemics.

3. Improved disease surveillance to enable early outbreak detection and rapid
response.
4. Implementation of effective vector control measures for A. aegypti in urban
centres.
Yellow fever surveillance is critical for monitoring the incidence of the disease
and allowing the prediction and early detection of outbreaks and the monitoring
of control measures. Case-reporting of yellow fever is universally required by the
International Health Regulations (IHR).
YELLOW FEVER
I
II
III
IV

202

PART IV
Annexes
205
ANNEX 1
Key national indicators and general information

A. Central African Republic
1. Main indicators, Central African Republic
Indicator Value Source
Most recent population census December 2003 UN statistics, August 2008
Estimated population 3 151 072, 62% rural UN statistics, August 2008
Life expectancy at birth 44 UN Population Division, 2006
Neonatal mortality rate per 1000 live births 48 UNICEF, 2000
Infant mortality rate (< 1 year) per 1000 live births 115 UNICEF, 2006
< 5 mortality rate per 1000 live births 175 UNICEF, 2006
< 5 mortality ranking 15/189 UNICEF, 2006
ANNEXES
Low-birth-weight infants 13% UNICEF, 19992006
< 5 wasting 10.5% Multiple indicator cluster

including 4.7% severe cases survey, 2000
< 5 underweight, moderate and severe 29% UNICEF, 19962006

I
< 5 severely underweight 8% UNICEF, 20002006
< 5 with stunting, moderate and severe 38% UNICEF, 20002006
Births attended by skilled personnel 53% UNICEF, 20002006
Maternal mortality ratio (adjusted) per 100 000 980 UNICEF, 2005
II
Nurses/midwives per 10 000 1.4 WHO, 1995
Physicians per 10 000 0.4 WHO, 1995
Population using improved drinking-water sources 75% UNICEF, 2004 III

Population living on < 1 US$ per day 66% UNDP, 2006
Adult literacy 48.6% WHO, 2004
Human development ranking 171/177 UNDP, 2005 IV

Human Poverty Index 98/108 UNDP, 2005

206
http://unstats.un.org/unsd/demographic/products/vitstats/serATab2.pdf
http://www.who.int/hac/crises/en/
http://www.who.int/hac/crises/caf/sitreps/car_jan2007.pdf
http://www.unicef.org/infobycountry/index.html
http://www.unicef.org/infobycountry/car_statistics.html
http://hdr.undp.org/en/statistics/

2. Administrative information, Central African Republic
Prefectures: 14, including 2 economic prefectures

Sub-prefectures: 71
Prefectures, Central African Republic

I
II ANNEXES
III
IV
207
208
3. History of natural disasters, Central African Republic

Year Type of disaster
2007 (September) Floods
2005 (August) Floods
2004 (November) Floods
2000 (January) Floods
1996 (October) Floods


209
4. Chronology of humanitarian emergencies, Central African Republic

1958 Self-government within French Equatorial Africa
1960 Central African Republic becomes independent
1965 Military coup (army commander Jean-Bedel Bokassa)
1979 Bokassa ousted in coup by Dacko
1981 Dacko deposed by Kolingba
1993 Patasse beats Kolingba and Dacko in elections, ending 12 years of
military rule
1996 Soldiers mutiny
1997 African peacekeepers replace French troops
1999 Patasse re-elected
2001 Patasse, assisted by Libyan, Chadian and Congolese troops, suppresses
Kolingba coup
Government troops clash with forces of army chief of staff General Bozize
ANNEXES
2002 Libyan-backed forces again help subdue a further attempt by General
Bozize to overthrow Patasse
2003 Bozize successfully deposes Patasse
2005 Flooding of capital Bangui I
Thousands flee lawless north-western region for Chad
2006 Rebels seize town in north-east; French air support helps regain control
2007 Rebel People's Democratic Front signs peace accord with Bozize II
UN peacekeeping force authorized to protect civilians from Darfur
crossing border
2008 Civil servants strike; prime minister and cabinet resign III
http://news.bbc.co.uk/2/hi/africa/country_profiles/1067615.stm
http://www.reliefweb.int/rw/RWB.NSF/db900SID/LSGZ-7AWJYR?OpenDocument
IV

210
5. Internally displaced persons, Central African Republic

According to the United Nations Office for the Coordination of Humanitarian
Affairs (OCHA)/Relief web site as of 28 March 2008: 197 000.
http://www.reliefweb.int/rw/rwb.nsf/db900sid/EGUA-7DBL2F?OpenDocument&query=UNICEF%20
Humanitarian%20Action%20Update%20Central%20African%20Republic
http://www.wfp.org/operations/current_operations/project_docs/101892.pdf
6. Refugees from Central African Republic

According to the OCHA/Relief web site as of 28 March 2008: 98 000 CAR citi-
zens residing in Cameroon, Chad and Sudan.
http://www.reliefweb.int/rw/RWB.NSF/db900SID/LSGZ-7AWJYR?OpenDocument
http://www.wfp.org/operations/current_operations/project_docs/101892.pdf

211
7. National immunization schedule, Central African Republic

Vaccine Schedule
BCG Bacille CalmetteGurin vaccine Birth
DTwP Diphtheria and tetanus toxoid with 6, 10, 14 weeks

whole cell pertussis
Measles Measles vaccine 9 months
OPV Oral polio vaccine Birth; 6, 10, 14 weeks
TT Tetanus toxoid Pregnant women
+ 1 month, + 6 months;
+ 1 year and + 1 year
YF Yellow fever 9 months
Source: WHO-IVB/UNICEF, 2008.
http://www.unicef.org/publications/files/Immunization_Summary_2007.pdf
http://whqlibdoc.who.int/hq/2007/WHO_IVB_2007_eng.pdf
ANNEXES
http://www.who.int/immunization_monitoring/en/globalsummary/ScheduleResult.cfm
http://www.who.int/immunization_monitoring/routine/en/
8. Immunization coverage, Central African Republic

Antigen Coverage (%) for 2006
I
BCG 70
DPT 3 40
Measles 35
II
Polio 3 36
TT2 + PAB 56
http://www.unicef.org/publications/files/Immunization_Summary_2007.pdf III
IV

212
B. Chad
1. Main indicators, Chad
Indicator Value Source
Most recent population census April 1993 UN statistics, April 2008
Estimated population 6 279 931, 75% rural UN statistics, August 2008
Life expectancy at birth (M/F) 44/47 WHO, 2003
Neonatal mortality rate per 1000 live births 45 UNICEF
Infant mortality rate (< 1 year) per 1000 live births 124 UNDP, 2004
< 5 mortality rate per 1000 live births 209 UNICEF, 2006
< 5 mortality ranking 7/189 UNICEF, 2006
Low-birth-weight infants 22% UNICEF, 19992006
< 5 underweight, moderate and severe 37% UNICEF, 19962006
< 5 suffering from wasting, moderate and severe 14% UNICEF, 20002006
< 5 severely underweight 14% UNICEF, 20002006
< 5 with stunting, moderate and severe 41% UNICEF, 19962006
Births attended by skilled personnel 16% WHO, 2000
Maternal mortality ratio (adjusted) per 100 000 1500 UNICEF, 20002006
Nurses/midwives per 10 000 1.7 WHO, 2001
Physicians per 10 000 0.3 WHO, 2001
Population using improved drinking-water sources 42% UNICEF, 2004
Population living below national poverty line 64% UNDP, 2006
Adult literacy 48.6% WHO, 2004
Human development ranking 170/177 UNDP, 20072008
Human Poverty Index 108/108 UNDP, 2004
http://unstats.un.org/unsd/demographic/products/vitstats/serATab2.pdf
http://www.who.int/hac/crises/tcd/sitreps/chad_jan2007.pdf
http://www.who.int/hac/crises/en/
http://www.unicef.org/infobycountry/index.html
http://www.unicef.org/infobycountry/chad_statistics.html
http://hdr.undp.org/en/statistics/

213
2. Administrative information, Chad
Regions/provinces: 18
Departments: 54
http://www.theglobalfund.org/search/docs/7TCDM_1488_0_full.pdf
Administrative divisions, Chad
ANNEXES
I
II
III
IV

214
3. History of natural disasters, Chad

Year Type of disaster
2004 (August) Locusts
1985 (July) Floods
1984 (November) Drought

1981 (November) Drought

215
4. Chronology of humanitarian emergencies, Chad

1913 French conquest of Chad complete
1960 Independence: Chad's post-independence history is marked by instability
and violence largely stemming from interethnic tension between the mainly
Arab-Muslim north and predominantly Christian and animist south
1963 Violence triggered in Muslim north by banning of political parties that
escalates into a guerrilla war
1975 President deposed and killed in a coup
1977 Libya assists north
1987 Chadian government with French and US assistance force Libya from
the north
1990 President toppled by Libyan-backed rebels based in Sudan led by a former
presidential ally, and current president, Idriss Deby
1998 Movement for Democracy and Justice in Chad (MDJT) begins armed
rebellion
ANNEXES
2003 Chad becomes an oil exporter (pipeline to Cameroon)
2004 Darfur impact; arrival of Sudanese refugees to escape Darfur; fighting
spills over border to Chad
2006 State of emergency declared in eastern areas bordering Sudan I
2007 UN Security Council authorizes UN/European peacekeeping force
2008 Rebel offensive reaches capital N'Djamena; EU approves peacekeeping
force to protect Darfur refugees from violence in Chad; peace accord
signed in March in Senegal between Chad and Sudan; in May, Chadian
II
and Sudanese militia violence; Sudan breaks off diplomatic relations
http://news.bbc.co.uk/2/hi/africa/1068745.stm
III
IV

216
5. Internally displaced persons, Chad

According to the United Nations Office for the Coordination of Humanitarian
Affairs (OCHA)/Relief web site as of 16 January 2008: 180 000.
http://www.reliefweb.int/rw/RWB.NSF/db900SID/EGUA-7AWQRT?OpenDocument
http://www.wfp.org/country_brief/indexcountry.asp?country=148
6. Refugees in Chad
According to the OCHA/Relief web site as of 9 June 2008: from Sudan, 250 000;
from Central African Republic, 57 000.
http://www.reliefweb.int/rw/rwb.nsf/db900sid/EDIS-7FFRGV?OpenDocument&query=Humanitarian%20
action%20in%20Chad:%20Facts%20and%20figures%20snapshot%20report
http://www.wfp.org/country_brief/indexcountry.asp?country=148

217
7. National immunization schedule, Chad

Vaccine Time of administration
BCG Bacille Calmette-Gurin vaccine Birth
DTwP Diphtheria and tetanus toxoid with 6, 10, 14 weeks

acellular pertussis vaccine
Measles Measles vaccine 9 months
OPV Oral polio vaccine Birth; 6, 10, 14 weeks
TT Tetanus toxoid 1st contact pregnancy;

+ 1, + 2 + 6 months;
+ 1 year and + 1 year
YF Yellow fever 9 months
http://www.who.int/immunization_monitoring/en/globalsummary/ScheduleResult.cfm
ANNEXES
8. Immunization coverage, Chad
Vaccine Coverage (%) for 2006
BCG 40
DPT 3 20 I
Measles 23
Polio 3 36
TT2 + PAB 39 II
III
IV

218
ANNEX 2
Map resources
Registered refugee camp populations: age and sex breakdown
(as of 29 February 2008)
http://www.reliefweb.int/rw/fullMaps_Af.nsf/luFullMap/1D54E6D8C36FCB798525741A005BC96A/$File/
unhcr_RFG_tcd080328-d.pdf?OpenElement
Eastern Chad: IDP figures (as of May 2008)

http://www.reliefweb.int/rw/rwb.nsf/db900SID/LPAA-7FNM54?OpenDocument&rc=1&emid=SKAR-6JKEX4
Central African Republic: refugee and IDP movements (as of 2008)

http://www.reliefweb.int/rw/rwb.nsf/db900sid/LPAA-7HNQZ3?OpenDocument&rc=1&cc=caf
IDPs in the Central African Republic (as of December 2007)

http://www.reliefweb.int/rw/rwb.nsf/db900sid/LRAY-7BRKFM?OpenDocument&rc=1&cc=caf
https://www.cia.gov/library/publications/the-world-factbook/geos/cd.html
http://www.reliefweb.int/rw/RWB.nsf/doc404?OpenForm&cc=caf&rc=1
http://ochaonline.un.org/chad/MapCentre/tabid/3640/Default.aspx
http://www.usaid.gov/locations/sub-saharan_africa/sudan/images/satellite/index.html
http://www.usaid.gov/locations/sub-saharan_africa/countries/sudan/
http://www.reliefweb.int/rw/rwb.nsf/db900sid/PANA-79NHB7?OpenDocument&rc=1&cc=caf

219
ANNEX 3
WHO information sources

World Health Organization
Regional Office for Africa
Division of Communicable Disease Prevention and Control (DDC)
http://afro.who.int/ddc/index.html
Headquarters
Global Alert and Response (GAR)
http://www.who.int/csr/en/
Disease Control in Humanitarian Emergencies (DCE)

http://www.who.int/diseasecontrol_emergencies/en/cdemergencies@who.int
Health Action in Crises (HAC)

http://www.who.int/hac/en/
ANNEXES
Acute lower respiratory tract infections
Acute respiratory tract infections in children
http://www.who.int/fch/depts/cah/resp_infections/en/
African trypanosomiasis I
Human African trypanosomiasis (sleeping sickness)
http://www.who.int/trypanosomiasis_african/en/
Child health in emergencies II

Emergencies documents
http://www.who.int/child_adolescent_health/documents/emergencies/en/index.html
Pocket book of hospital care for children

http://www.who.int/child_adolescent_health/documents/9241546700/en/index.html
III
Acute respiratory tract infections in children
http://www.who.int/fch/depts/cah/resp_infections/en/
The treatment of diarrhoea; a manual for physicians and other senior health IV
workers (2005)
http://www.who.int/entity/child_adolescent_health/documents/9241593180/en/

220
Technical updates of the guidelines on the integrated management of childhood

illness (2005)
http://www.emro.who.int/cah/pdf/imci_technical_updates.pdf
IMCI chart booklet (WHO/UNICEF, 2006)

http://www.who.int/child_adolescent_health/documents/IMCI_chartbooklet/en/index.html
IMCI for high HIV settings

http://whqlibdoc.who.int/publications/2006/9789241594370.cb_eng.pdf
Home treatment for children with severe pneumonia just as effective as hospital
http://www.who.int/child_adolescent_health/news/2008/09_01/en/index.html
Pocket book of hospital care for children: guidelines for the management of
common illnesses with limited resources (2005)

http://www.who.int/child-adolescent- health/New_Publications/CHILD_HEALTH/PB/00.PB_full_low.pdf
Paediatric HIV and treatment of children living with HIV

http://www.who.int/hiv/topics/paediatric/en/index.html
Operational guidance on infant feeding in emergencies

http://www.ennonline.net/ife/view.aspx?resid=6
Cholera (see also diarrhoeal diseases)

Cholera and other epidemic diarrhoeal diseases control: technical cards on environ-
mental sanitation (1997)
http://www.who.int/csr/resources/publications/cholera/WHO_EMC_DIS_97_6/en/
Joint WHO/UNICEF statement for cholera vaccine use in tsunami-affected areas

http://www.who.int/cholera/tsunami_choleravaccine/en/index.html
Laboratory methods for the diagnosis of epidemic dysentery and cholera (1999)
http://www.cdc.gov/ncidod/dbmd/diseaseinfo/cholera/top.pdf
Cholera: prevention and control

http://www.who.int/topics/cholera/control/en/index.html
Interagency diarrhoeal disease kits: information note (2006)

http://www.who.int/cholera/technical/DiarrhoealDiseaseKits/en/index.html
Communicable disease control in emergencies

Communicable disease control in emergencies: a field manual (2005)
http://whqlibdoc.who.int/publications/2005/9241546166_eng.pdf

221
Diarrhoeal diseases (see also cholera)

Acute diarrhoeal diseases in complex emergencies: critical steps
http://www.who.int/cholera/publications/critical_steps/
Cholera outbreak: assessing the outbreak response and improving preparedness

http://www.who.int/cholera/publications/cholera_outbreak/
First steps for managing an outbreak of acute diarrhoea

http://www.who.int/cholera/publications/first_steps/
Guidelines for the control of shigellosis, including epidemics due to Shigella

dysenteriae type 1
http://www.who.int/topics/cholera/publications/shigellosis/
Oral cholera vaccine use in complex emergencies: what next? Report of a WHO
meeting (Cairo, Egypt, 1416 December 2005)
http://www.who.int/cholera/publications/cholera_vaccines_emergencies_2005.pdf
Background document: the diagnosis, treatment and prevention of typhoid

fever (2003)
http://whqlibdoc.who.int/hq/2003/WHO_V&B_03.07.pdf
ANNEXES
Diphtheria
WHO position paper on diphtheria vaccine
http://www.who.int/immunization/wer8103Diphtheria_Jan06_position_paper.pdf
I
Drug donations
Guidelines for drug donations
http://whqlibdoc.who.int/hq/1999/WHO_EDM_PAR_99.4.pdf
II
Environmental health in emergencies
Guidelines for drinking-water quality (3rd ed., incorporating 1st addendum)
http://www.who.int/water_sanitation_health/dwq/gdwq3rev/en/index.html
Environmental health in emergencies and disasters: a practical guide III

http://www.who.int/water_sanitation_health/emergencies/emergencies2002/en/index.html
WHO technical notes for emergencies

http://www.who.int/water_sanitation_health/hygiene/envsan/technotes/en/index.html
IV
Frequently asked questions in case of emergencies
http://www.who.int/water_sanitation_health/emergencies/qa/en/index.html

222
Four steps for the sound management of health-care waste in emergencies

http://www.healthcarewaste.org/en/documents.html?id=184&suivant=25
Food safety/Foodborne disease outbreaks

Ensuring food safety in the aftermath of natural disasters
http://www.who.int/foodsafety/foodborne_disease/emergency/en/
Five keys to safer food: simple advice to consumers and food handlers
http://www.who.int/foodsafety/consumer/5keys/en/index.html
Guideline for the safe preparation, storage and handling of powdered infant
formula (WHO, 2007)
http://www.who.int/foodsafety/publications/micro/pif2007/en/index.html
Foodborne disease outbreaks: Guidelines for investigation and control

http://www.who.int/foodsafety/publications/foodborne_disease/fdbmanual/en/
Gender and gender-based violence

IASC guidelines for gender-based violence interventions in humanitarian
settings (2005)
http://www.humanitarianinfo.org/iasc/content/products/docs/tfgender_GBVGuidelines2005.pdf
IASC gender handbook in humanitarian action: women, girls, boys and men
different needs equal opportunities (2006)
http://www.humanitarianinfo.org/iasc/content/documents/subsidi/tf_gender/IASC%20Gender%20Handbook
%20(Feb%202007).pdf
Clinical management of rape survivors: developing protocols for use with refugees
and internally displaced persons (WHO/UNHCR, 2004, revised ed.)
http://www.who.int/reproductive-health/publications/clinical_mngt_rapesurvivors/
Hepatitis
Hepatitis A
http://www.who.int/csr/disease/hepatitis/whocdscsredc2007/en/
Hepatitis E
http://www.who.int/csr/disease/hepatitis/whocdscsredc200112/en/
http://www.who.int/mediacentre/factsheets/fs280/en/
HIV/AIDS
Guidelines for HIV/AIDS interventions in emergency settings: Interagency
Standing Committee guidelines
http://www.who.int/3by5/publications/documents/iasc/en/

223
IMCI for high HIV settings

http://whqlibdoc.who.int/publications/2006/9789241594370.cb_eng.pdf
Guidance on provider-initiated HIV testing and counselling in health facilities

Influenza
Avian influenza
http://www.who.int/topics/avian_influenza/en/
Pandemic influenza preparedness and mitigation in refugee and displaced

populations (2nd ed., May 2008)
http://www.who.int/diseasecontrol_emergencies/WHO_HSE_EPR_DCE_2008_3web.pdf
Pandemic influenza preparedness and response .WHO guidance document

(April 2009)
http://www.who.int/csr/disease/influenza/pipguidance2009/en/index.html

populations: WHO guidelines for humanitarian agencies (revised 2008)
(WHO/HSE/EPR/DCE/2008.3) (A training manual designed for delivery by
agency health coordinators to all essential staff, complementing these guidelines,
ANNEXES
has also been developed and field-tested in refugee and displaced settings.)
http://www.who.int/diseasecontrol_emergencies/HSE_EPR_DCE_2008_3rweb.pdf

populations: WHO training modules for humanitarian agencies (2006)
(WHO/CDS/NTD/DCE/2006.2) I
http://www.who.int/diseasecontrol_emergencies/training/influenza/en/index.html
Laboratory-specimen collection
Guidelines for the collection of clinical specimens during field investigation of
outbreaks (2002) II
http://www.who.int/csr/resources/publications/surveillance/WHO_CDS_CSR_EDC_2000_4/en/
Leishmaniasis
The disease and its epidemiology III
http://www.who.int/leishmaniasis/disease_epidemiology/en/index.html
http://www.who.int/leishmaniasis/en/
Malaria
IV
Guidelines for the treatment of malaria
http://www.who.int/malaria/docs/TreatmentGuidelines2006.pdf

224
Malaria control in complex emergencies. An inter-agency field handbook (2005)

http://www.who.int/malaria/docs/ce_interagencyfhbook.pdf
Malnutrition
Nutrition in emergencies publications
http://www.who.int/nutrition/publications/nut_emergencies/en/
Communicable diseases and severe food shortage situations (2005)

http://www.who.int/diseasecontrol_emergencies/guidelines/Severe_food_shortages.pdf
The management of nutrition in major emergencies (2000)

http://whqlibdoc.who.int/publications/2000/9241545208.pdf
Infant feeding in emergencies: guidance for relief workers in Myanmar and China
http://www.who.int/child_adolescent_health/news/2008/13_05/en/index.html
Guidelines for the inpatient treatment of severely malnourished children (2003)

http://www.who.int/nutrition/publications/guide_inpatient_text.pdf
Community-based management of severe malnutrition

http://www.who.int/nutrition/topics/comm_based_malnutrition/en/index.html
Management of the child with a serious infection or severe malnutrition:

guidelines at first referral level in developing countries
http://www.who.int/child_adolescent_health/documents/fch_cah_00_1/en/index.html
Guiding principles for feeding infants and young children during emergencies (2004)
http://www.who.int/nutrition/publications/guiding_principles_feedchildren_emergencies.pdf
Infant and young child feeding in emergencies: operational guidance for emer-
gency relief staff and programme managers (IFE, 2007)
http://www.ennonline.net/pool/files/ife/ops-guidance-2-1-english-010307.pdf
Management of dead bodies

Management of dead bodies after disasters: a field manual for first responders (2006)
http://www.paho.org/english/dd/ped/DeadBodiesFieldManual.pdf
Management of dead bodies in disaster situations (2004)

http://www.paho.org/english/DD/PED/DeadBodiesBook.pdf
Measles
Joint statement on reducing measles mortality in emergencies (WHO/UNICEF)
http://whqlibdoc.who.int/hq/2004/WHO_V&B_04.03.pdf

225
Information on measles
http://www.who.int/immunization/topics/measles/en/index.html
Measles fact sheet

Measles vaccine position paper

http://www.who.int/immunization/wer7914measles_April2004_position_paper.pdf
Medical waste in emergencies

Water, sanitation and health
http://www.who.int/water_sanitation_health/medicalwaste/emergmedwaste/en/
Guidelines for safe disposal of unwanted pharmaceuticals in and after emer

gencies (1999)
Four steps for the sound management of health-care waste in emergencies (2005)
ANNEXES
Meningitis
Control of epidemic meningococcal disease: WHO practical guidelines (2nd ed., 1998)
http://www.who.int/csr/resources/publications/meningitis/whoemcbac983.pdf
Mental health in emergencies

I
Mental health in emergencies
http://www.who.int/mental_health/resources/emergencies/en/index.html
IASC guidelines on mental health and psychosocial support in emergency

settings (2007) II
http://www.humanitarianinfo.org/iasc/content/products/docs/Guidelines%20IASC%20Mental%20Health%20
Psychosocial.pdf
Outbreak communications
III
Outbreak communication guidelines
http://www.who.int/csr/resources/publications/WHO_CDS_2005_28/en/index.html
Poliomyelitis
WHO-recommended surveillance standards for poliomyelitis
IV
http://www.who.int/immunization_monitoring/diseases/poliomyelitis_surveillance/en/index.html

226
Polio vaccine position paper

http://www.who.int/immunization/wer7828polio_Jul03_position_paper.pdf
Pertussis
Pertussis vaccine position paper
http://www.who.int/immunization/topics/wer8004pertussis_Jan_2005.pdf
Shigella (see also other diarrhoeal diseases)

Guidelines for the control of epidemics due to Shigella dysenteriae type 1
http://whqlibdoc.who.int/publications/2005/9241592330.pdf
Soil-transmitted helminths
Preventive chemotherapy in human helminthiasis
Surgery/emergency surgical care

Integrated management of essential and emergency surgical care (IMEESC) tool kit
http://www.who.int/surgery/publications/imeesc/en/index.html
Surveillance
Protocol for the assessment of national communicable disease surveillance and
response systems: guidelines for assessment teams (2001)
http://www.who.int/csr/resources/publications/surveillance/whocdscsrisr20012.pdf
WHO report on global surveillance of epidemic-prone infectious diseases (2000)

http://www.who.int/csr/resources/publications/surveillance/WHO_CDS_CSR_ISR_2000_1/en/
Tetanus/maternal and neonatal tetanus

Maternal and neonatal tetanus elimination
http://www.who.int/immunization_monitoring/diseases/MNTE_initiative/en/index.html
Immunological basis of immunization: tetanus

http://www.who.int/immunization/documents/ISBN9789241595551/en/index.html
Position paper on tetanus immunization

http://www.who.int/immunization/wer8120tetanus_May06_position_paper.pdf
Maternal and neonatal tetanus (published in The Lancet, December 2007)

http://www.who.int/hpvcentre/Maternal_and_neonatal_tetanus_Seminar.pdf

227
Travel advice
Guide on safe food for travellers
http://www.who.int/foodsafety/publications/consumer/travellers/en/index.html
International travel and health (2008)

http://www.who.int/ith/en/
Vaccines
Vaccines and biologicals
http://www.who.int/immunization/en/
Vaccine-preventable diseases: monitoring system (2007, global summary)

http://www.who.int/immunization/documents/WHO_IVB_2007/en/index.html
Immunization against diseases of public health importance

http://www.who.int/immunization_delivery/en/index.html
Linking vaccines with other interventions

http://www.who.int/immunization_delivery/interventions/en/index.html
Standards for surveillance of selected vaccine-preventable diseases: position papers
ANNEXES
on vaccines
http://www.who.int/immunization/documents/positionpapers/en/index.html
Documents on vaccines and immunization

http://www.who.int/immunization/documents/en/
http://www.who.int/vaccines-documents/ I
Immunological basis of immunization series
http://www.who.int/immunization/documents/general/en/index.html
WHO-recommended standards for surveillance of selected vaccine-preventable

diseases II
http://www.who.int/immunization/documents/WHO_VB_03.01/en/index.html
Vector control
Integrated vector management III
http://www.who.int/malaria/integratedvectormanagement.html
Malaria vector control

http://www.who.int/malaria/vectorcontrol.html
Pesticides and their application for the control of vectors and pests of public IV
health importance (2006)
http://whqlibdoc.who.int/hq/2006/WHO_CDS_NTD_WHOPES_GCDPP_2006.1_eng.pdf

228
Wounds and injuries

Prevention and management of wound infections
http://www.who.int/hac/techguidance/tools/Prevention%20and%20management%20of%20wound%20
infection.pdf
Integrated management of essential and emergency surgical care (IMEESC) tool kit
http://www.who.int/surgery/publications/imeesc/en/index.html
Best practice guidelines on emergency surgical care in disaster situations

http://www.who.int/surgery/publications/BestPracticeGuidelinesonESCinDisasters.pdf
WHO generic essential emergency equipment list

http://www.who.int/surgery/publications/EEEGenericListFormatted%2006.pdf
Yellow fever
Yellow fever disease
http://www.who.int/vaccines-documents/DocsPDF/www9842.pdf
District guidelines for yellow fever surveillance

http://www.who.int/csr/resources/publications/yellowfev/whoepigen9809.pdf
Manual for the monitoring of yellow fever virus infection

http://whqlibdoc.who.int/hq/2004/WHO_IVB_04.08.pdf
Zoonoses
Zoonoses and veterinary public health
http://www.who.int/zoonoses/resources/en/

229
ANNEX 4
WHO fact sheets on communicable diseases

Title Fact sheet No./Publication date/URL
African trypanosomiasis (sleeping sickness) 259, revised August 2006

Anthrax 264, October 2001

Cholera 107, revised September 2007

http://www.who.int/mediacentre/factsheets/fs107/en
Dengue 117, revised April 2002

Diphtheria 89, revised December 2000

Ebola 103, revised September 2007

ANNEXES
Food safety and foodborne illness 237, revised March 2007
Food safety in emergencies http://www.who.int/foodsafety/foodborne_disease/

emergency/en/
Hepatitis B 204, revised October 2000

I
Hepatitis C 164, revised October 2000
Hepatitis E 280, revised January 2005

II
index.html
Influenza 211, March 2003

Injection safety 231, revised October 2006 III

Leprosy 101, revised October 2005

http://www.who.int/topics/leprosy/en/
Lymphatic filariasis 102, revised September 2000 IV

index.html

230
Malaria 94, May 2007

Marburg haemorrhagic fever March 2005

http://www.who.int/mediacentre/factsheets/
fs_marburg/en/index.html
Measles 286, revised November 2007

Meningitis 141, revised May 2003

Plague 267, revised February 2005

Poliomyelitis 114, updated January 2008

Rabies 99, revised November 2006

Rift Valley fever 207, revised September 2007

print.html
Salmonella (drug-resistant) 139, revised April 2005

index.html
Schistosomiasis 115, revised July 2007

Tuberculosis 104, revised March 2007

World Health Organization About WHO

http://www.who.int/about/en/
Yellow fever 100, revised December 2001

Water, sanitation and health Introduction to fact sheets on water

http://www.who.int/water_sanitation_health/hygiene/
emergencies/envsanfactsheets/en/print.html

231
ANNEX 5
Flowcharts for the diagnosis of communicable diseases
Suspected
outbreak ACUTE DIARRHOEA AND ACUTE WATERY DIARRHOEA
Definition of Acute onset of diarrhoea and severe illness and absence of

syndrome known predisposing factors
Watery
Viral gastroenteritis
Possible Cholera
diseases/
Enterotoxigenic E. coli
ANNEXES
pathogens
Giardiasis
Cryptosporidium
Specimens required In Cary-Blair I

No transport media required for Faeces transport medium
parasitic and viral examinations)
II
Laboratory
Bacterial:
studies
Faecal leukocytes Viral: Parasitic:
Culture Culture Macroscopic
Antimicrobial Antigen detection and microscopic III
susceptibility Genome detection examination
Serotyping
Toxin identification
IV
Ebola and other haemorrhagic fevers may initially present as bloody diarrhoea. If such an etiology is suspected,
refer to Acute haemorrhagic fever syndrome for appropriate specimen collection guidelines.

232
Suspected
outbreak ACUTE BLOODY DIARRHOEA
Definition of Acute onset of diarrhoea and severe illness and absence of

Shigellosis
Possible
Salmonellosis
diseases/
Campylobacteriosis
pathogens
Amoebic dysentery
Enterohaemorrhagic E. coli
Clostridium difficile
Haemorrhagic fevers
Specimen required and transport Cary-Blair trans-

media port medium;
Faeces
(No transport media required for parasitic and viral for Shigella, refri-
examinations) gerate at 28 C
Laboratory
studies Bacterial:
Viral: Parasitic:
Gram stain
Antigen detection Macroscopic
Faecal leukocytes
Genome detection and microscopic
Culture examination
Culture
Antimicrobial
susceptibility
Serotyping
Ebola and other haemorrhagic fevers may initially present as bloody diarrhoea. If such an etiology is suspected,
refer to Acute haemorrhagic fever syndrome for appropriate specimen collection guidelines.

233
Suspected
outbreak ACUTE HAEMORRHAGIC FEVER SYNDROME
Acute onset of fever of less than 3 weeks duration and any two
of the following:
haemorrhagic or purpuric rash
Definition of epistaxis
syndrome haemoptysis
blood in stool
other haemorrhagic symptom
and absence of known predisposing factors.
Dengue haemorrhagic fever and shock syndrome

Yellow fever
ANNEXES
Other arboviral haemorrhagic fevers (e.g. Rift Valley, CrimeanCongo,
Possible tick-borne flaviviruses)
diseases/ Lassa fever and other arenoviral haemorrhagic fevers
pathogens Ebola or Marburg haemorrhagic fevers
Haemorrhagic fever with renal syndrome (hantaviruses)
Malaria I
Relapsing fever
Blood II
Specimens Blood smear
required Serum
Postmortem tissue specimens (e.g. skin and/or liver biopsy)
III
Viral:
Culture
Laboratory Parasitic:
Antigen detection
studies
Antibody levels
Demonstration of pathogen IV
Genome detection

234
Suspected
outbreak ACUTE JAUNDICE SYNDROME
Definition of Acute onset of jaundice and severe illness and absence of

Possible Leptospirosis and

diseases/ Yellow fever Hepatitis AE other spirochaetal
pathogens diseases
Specimens Postmortem Blood

required Serum
liver biopsy (urine*)
Viral:
Leptospiral:
Culture
Laboratory Culture
Antigen detection
studies Antibody levels
Antibody levels
Serotyping
Genome analysis
* Requires specialized media and handling procedures.

235
Suspected
ACUTE NEUROLOGICAL SYNDROME
outbreak
Acute neurological dysfunction with one or more of the following:

deterioration of mental function
acute paralysis
Definition of convulsions
syndrome signs of meningeal irritation
involuntary movements
other neurological symptoms
and severe illness and absence of predisposing factors.
Possible Poliomyelitis or Viral, bacterial, fungal

diseases/ GuillainBarr or parasitic menin- Rabies
pathogens syndrome goencephalitis
ANNEXES
CSF Serum
Blood Postmortem speci-
Specimens Blood smears mens (e.g. corneal
Faeces
required Serum impressions, brain
Throat swab tissue, skin biopsy
Lymph from neck) I
Laboratory studies
II
Bacterial
(including
leptospiral): Parasitological
(HAT) Viral:
Gram stain and other
Viral: microscopic techniques Lymph node aspirate Culture III
Culture Blood concentration Antigen detection
Culture
methods Antibody levels
Antimicrobial
susceptibility CSF concentration Genome analysis
methods
Antigen detection IV
Serotyping

236
Suspected
ACUTE RESPIRATORY SYNDROME
outbreak
Definition of Acute onset of cough or respiratory distress and severe illness and
syndrome absence of known predisposing factors
Possible
diseases/
pathogens
Bacterial pneumo-
Influenza nia, including:
Pertussis Pneumococcal
Diphtheria Hantavirus Legionellosis
pulmonary Respiratory Haemophilus
Streptococcal influenzae
syndrome syncytial virus
pharyngitis Mycoplasma
(RSV) Respiratory
Scarlet fever anthrax
Pneumonic plague
Specimens
required
Blood culture
Serum
Nasopharyngeal
Throat swab Serum Sputum
swab
Urine (for
Legionella)
Bacterial or viral:
Culture
Antimicrobial susceptibility (for bacteria)
Laboratory Antigen detection
studies Antibody levels
Genome analysis
Serotyping
Adapted from: Guidelines for the collection of clinical specimens during field investigation of outbreaks. Geneva,
WHO, 2000 (WHO/CDS/CSR/EDC/2000.4).

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COMMUNICABLE DISEASE

Central African Republic and Chad

Disease Control in Humanitarian Emergencies (DCE)

The information provided aims to assist with the public

Diseases have been included if they fulfil one or more of the

World Health Organization

Central African Republic and Chad

World Health Organization 2009

All rights reserved.

Printed by the WHO Document Production Services, Geneva, Switzerland

Communicable disease epidemiological profile

Communicable disease epidemiological profile

Leishmaniasis (cutaneous and mucosal) ............................................................................................. 90

Pertussis (whooping cough) ........................................................................................................................... 139

Communicable disease epidemiological profile

This document was edited by the unit on Disease Control in Humanitarian

Communicable disease epidemiological profile

Michael Nathan, Benjamin Nkowane, Asiya Odugleh-Kolev, William Perea, Cathy

Communicable disease epidemiological profile

Communicable disease epidemiological profile

Political boundaries of the Central African Republic, Chad and Sudan

Communicable disease epidemiological profile

Communicable disease epidemiological profile

compromised. This is reflected as a lack of epidemiological information for some

Priority high-burden communicable diseases in CAR

For the vaccine-preventable, high-burden communicable diseases, routine immuni-

Communicable disease epidemiological profile

Summary of recent communicable disease

Central African Republic: communicable disease outbreaks, as reported

Month/year Diseasea Cases Deaths Case-fatality ratio (%)

April 2008 Yellow fever 2 1 50

April 2008 Polio (imported WPV1) 1 0 0

SUMMARY OF RECENT COMMUNICABLE DISEASE OUTBREAKS

November 2007 Meningococcal disease 45 5 11.1

November 2006 Yellow fever 1 0 0

JanuaryJune 2005 Measles 195 18 9.2

December 2003 Measles 225 36 16.0

MarchApril 2004 Meningococcal disease 43 7 16.2

JanuaryJune 2004 Measles 1040 80 13.0

JuneOctober 2003 Shigellosis 379 23 6.1

JanuaryMay 2003 Measles 443 86 19.4

2002 Yellow fever 1 0 0

JanuaryApril 2002 Measles 287 19 6.6

FebruaryJune 2001 Meningococcal disease 1816 343 18.8

Communicable disease epidemiological profile

Chad: communicable disease outbreaks, as reported to WHO from

Month/year Diseasea Cases Deaths Case-fatality ratio (%)

MarchApril 2007 Meningococcal disease 350 17 5.1

MarchMay 2007 Meningococcal disease 31 3 9.7

FebruaryJune 2007 Measles 147 1 0.7

JuneDecember 2006 Cholera 1633 68 4.1

MarchApril 2006 Meningococcal disease 200 16 8

JanuaryMarch 2005 Menigococcal disease 387 53 13.7

January 2005 Meningococcal disease 8 0 0

JanuaryMay 2005 Measles 20278 516 2.5

September 2004 Hepatitis E 1442 46 3.2

JuneSeptember 2004 Cholera 3910 164 4.2

April 2004 Meningococcal disease 19 4 21

2003present Poliomyelitis (WPV1 and 86 0 0

JulyAugust 2001 Cholera 3557 113 3.2

December 2000 Menigococcal disease 3579 401 11.2

Communicable disease epidemiological profile

Country-specific disease information and