Cominicable Abebaw

Commmunicable Disease
UNIT ONE
INTRODUCTION TO COMMUNICABLE DISEASES AND ITS CONTROL
Introduction to terminologies
Communicable diseases: -These are illnesses due to specific infectious agent or its toxic
products which arise through transmission of that agent or its toxic products.
Communicable disease is also named as Infectious disease or Contagious disease.
Communicable diseases can be conveniently divided based on the mode of transmission
or the causative agent
A. Based on mode of transmission
1. Airborne diseases-Need droplet nuclei or dust for transmission
E.g. Tuberculosis
2. Vehicle borne disease
- Need non-living substance or object for transmission
E.g. Cholera
3. Vector Borne disease
-Need vectors for transmission
E.g. Malaria
4. Other sexually transmitted Diseases, contact diseases, etc
B. Based an the Biologic agent
1. Bacterial diseases e.g. syphilis, gonorrhea, etc
2. Protozoal diseases e.g. Malaria
3. Viral diseases e.g. HIV/AIDS
4. Helminthes diseases e.g. Ascariasis
5. Fungal diseases e.g. candidiasis
Etiology, causative organism or infectious agent: -Agent capable of causing infection
or infectious disease.
Classification of infectious agent by size and sort
1. Metazoa (multicellular organisms e.g. helminthes)
They are made up of many cells. Most of them are visible by naked eye. E.g. Tape worm
2. Protozoa (unicellular organisms e.g. amoeba, Plasmodium)
Single-celled organisms that are smaller and can only be seen by a microscope.
3. Bacteria (e.g. T.pallidum, M.tuberculosis)
They are smaller than protozoa, simple, single celled & seen under a microscope.
4. Rickettsia and Chlamydia are smaller and can only multiply with in cells
5. Viruses: -Smallest of all which cant even be seen with an ordinary microscope
6. Fungus e.g.C.albicans
Reservoir: -Any person, animal, arthropod, plant, soil or substance (or a combination of
these) in which an infectious agent normally lives, multiplies & spreads.
Types of reservoirs
1. Man
There are a number of important pathogens that are especially adapted to man such as
measles, typhoid, M. meningitis, gonorrhea and syphilis. The cycle transmission is from
man to man
2. Animals
Some infective agents have their reservoir in animal.
E.g. Bovine TBc - cow to man
Brucellosis cow, pigs and goats to man
Anthrax
cattle, sheep, goats, horses to man
Rabies
dogs, foxes etc to man
3. Non-living things as a reservoir
E.g.C.botulinum etiology of botulism, C.tetani etiology of tetanus, C.welchi etiology of
gas gangrene; all of them use soil as reservoir.
Carrier: -It is an infected person or animal that does not have apparent clinical disease
but is a potential source of a disease
Types of carriers
A. Healthy or asymptomatic carriers: -These are persons whose infection remains
unapparent through out its course.
B. Incubatory or precocious carriers: -These are individuals or persons who excrete the
pathogens during the incubation period (before the onset of symptoms)
C. Convalescent carriers:-These are those who continue to harbor the infective agent after
recovering from the illness.
D. Chronic carriers: -The carrier state persists for a long period of time.
E.g. Typhoid fever, Hepatitis B virus infection
Portal of exit (mode of escape from the reservoir): -The site through which the agent
escapes
from
the
reservoir.
E.g. GIT = bacillary dysentery, amoebic dysentery, cholera etc.
Respiratory = TBc, common cold etc.
Skin and mucus membrane = syphilis
Portal of entry: -The site in which the infectious agent enters to the susceptible host.
E.g. Mucus membrane = syphilis, HIV
Respiratory tract = TBc, pertusis
GIT = bacillary dysentery, amoebic dysentery, cholera etc
Period of communicability or communicable period:-The period during which an
infectious agent is transmitted from the infected person to the susceptible host.
Susceptible host: -A person or animal not possessing sufficient resistance against a
particular pathogenic agent.
Incubation period: -The time interval between infection of the host and the first
appearance of symptoms and signs of the disease.
Prodromal period: -The time interval between the onset of symptoms of an infectious
disease and the appearance of characteristic manifestations. E.g. In measles from the
onset of fever and coryza to the development of characteristic signs like koplicks spots
and rashes.
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Prepatent period: -The period in people between the time of exposure to a parasite and
the time when the parasite can be detected in blood or in stool.
Endemic: -A disease that is usually present in a population or in an area at a more or less
stable level.
Epidemics: -The occurrence of any disease in a given population in excess of the usual
frequency in that population.
Pandemic: -An epidemic disease which occurs world wide (world wide epidemics).
Sporadic: -A disease that occur in a population, at occasional and irregular intervals.
Infection: -The entry and development or multiplication of an infectious agent in the
body of man or animal.
Infestation: -For persons or animals, the lodgment, development and reproduction of
arthropods on the surface of the body or in the clothing. E.g. Louse infestation.
Chain of disease transmission: -Refers to sequence of factors of a chain that are
essential to the development of the infectious agent and progression of disease.
It has six components
1. The agent
2. Its reservoirs
3. Its portal of exits
4. Its mode of transmission
5. Its portal of entry, and
6. The human host
1. The agent
They range from smaller viruses to complex multicultural organisms( worms)
Infections agents may bring about pathologic effect through different mechanisms
These mechanisms include
1. Direct tissue invasion
2. Production of a toxin
3. Allergic reaction
4. Immune suppression
2. Reservoirs
They include organisms or habitat, in which an infectious agent normally lives,
transforms, develops or multiplies & spreads.
They include human beings, vertebrate animals, invertebrates (arthropods,
molluscs), & environmental sources like plants, soil, water, etc
For some diseases humans are the only reservoirs e.g. STDs, measles, Pertussis
Diseases with environmental reservoirs include cholera (water), Tetanus &
ascariasis (soil).
3. Portal of exit
It is the way through which the infectious agent leaves its reservoir
Possible portal of exit include all body secretions & discharges: mucus, saliva,
tears, breast milk, vaginal & urethral discharges, excretions (feces & urine),
blood, etc
4. Mode of Transmission
It includes the various mechanisms by which agents are conveyed or passed to a
susceptible host
Transmission may be direct or indirect
1. Direct transmission
1.1 Direct contact = refer to the contact of skin, mucosa, or conjunctiva from another
person or vertebrate animal, through
- Touching: Eg Eye- hand eye, Nose-hand-mouth, Mouth- hand- mouth,
Feces-hand- mouth, Skin- skin
- Kissing
- Sexual intercourse e.g. syphilis, HIV AIDS
- Biting e.g. rabies
- Passage through birth canal (e.g. gonococcal ophthalmia neonatarum)
1.2 Direct projection = droplet created by expiration activities such as
coughing, sneezing, spitting, talking, singing, etc.
- Saliva droplets are emitted & can reach another host directly at distances of up
to one meter. E.g. Common cold
1.3 Trans placental transmission
- It is transmission of diseases from mother to her fetus through the placenta.
E.g. TORCHS (Toxoplasmosis, Rubella, Cytomegalovirus infection, Herpes simplex
infection, syphilis, others including HIV/AIDS)
2. Indirect transmission
2.1. Airborne
Two types of particles can result in airborne transmission
a) Dust: - are small infectious particles that arise from, soil, clothes, bedding
contaminated floors and be suspended by air currents.
b) Droplet nuclei: -are small residues resulting from evaporation of fluid
(droplets) from respiratory discharge emitted by an infected host. They usually
remain suspended in the air for long periods of time.
2.2. Vehicle borne
A vehicle is any non- living substance or object by which an infectious agent can
be transported and introduced in to a host.
E.g. food, water, milk, fomites, towels, clothes, etc
2.3. Vector borne A vector is an organism (usually an arthropod such as an insect, tick, or louse),
which transports an infectious agent to a susceptible host or to a suitable vehicle.
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5. Mode of entry: - It is a way in which the infectious agent enters susceptible host.
6. Human host: - Human being that accepts or allow the infection to occur.
Infectivity: -The ability of an agent to invade and multiply in a host.
Pathogenecity: -The ability of an agent to produce clinically apparent disease.
Virulence: -The ability of infectious agent to produce severe disease among infected
persons.
Immunogenicity: -The ability of an agent to produce specific immunity.
Unapparent infection: -The presence of infection in a host with out recognizable clinical
signs and symptoms. It can be identified only by laboratory means (blood).
Asymptomatic, sub clinical and occult infections are synonymous (other names).
Host: -A person or other living animal, that affords substance or lodgment to an
infectious agent under natural conditions.
Nosocomial infection: -An infection occurring in a patient in a hospital or other health
care facility in whom it was not present or including at the time of admission.
Pathogen:- is an infectious agent that can cause clinically apparent infection.
Infectious agent: - is an agent that is capable of causing infection or infectious disease.
Pattern of communicable disease: - different diseases are common in different places
and at different times. Why? To understand this, we need to consider the agent, the host
and the environment. The agents need a suitable environment in which to grow and
multiply and thus be able to spread and infect another host. If they are not successful in
doing this they die out. There is there fore a balance between the agent, the host and the
environment which can be shown as:
HOST
AGENT
ENVIRONMENT
(The host, agent, environment triad)
UNIT TWO
GENERAL METHODS OF PREVENTION AND CONTROL OF
COMMUNICABLE DISEASES
Disease prevention: -Inhibiting the development of a disease before it occurs or if it
occurs interrupting or slowing down the progression of diseases.
Disease control: -Involves all the measures designed to reduce or prevent the incidence,
prevalence and consequence of a disease to a level where it can not be a major public
health problem.
There are three levels of prevention.
1. Primary prevention: The objectives here are to promote health, prevent exposure, and
prevent disease.
A) Health promotion: - any intervention that promotes a healthier and happier life.
This consists of adequately paid jobs; education and vocational training;
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affordable and adequate housing, clothing and food; emotional and social support,
relief of stress, daily physical exercise, balanced diet & etc.
B) Prevention of exposure: - any intervention which prevents the coming in contact
between an infectious agent and a susceptible host. This includes actions such as
provision of safe and adequate water; proper excreta disposal; vector control; safe
environment at home(proper storage of insecticides and medicines), at school and
at work(proper ventilation, monitoring of harmful substances in factories).
C) Prevention of disease: - This occurs during the latency period between exposure
and the biological onset of the disease. An example for this is immunization.
N.B. Immunization against an infectious organism does not prevent it from
invading the immunized host but prevents it from establishing an infection.
Breast feeding is an example of intervention that acts at all three levels of primary
Prevention.
=>Health promotion: by providing optimal nutrition for a young child, either as
the sole diet up to six months of age, or as a supplement in later age.
=>Prevention of exposure: by reducing exposure of the child to contaminated milk.
=>Prevention of disease after exposure: by the provision of ant-infective factors,
including antibodies, WBCs and others.
2. Secondary prevention: This is applied after the biological on set of the disease, but
before permanent damage sets in.
=>The objective here is to stop or slow the progression of disease so as to prevent or
limit permanent damage, through early detection and treatment of diseases.
E.g. Breast cancer (prevention of invasive stage of the disease)
Trachoma (prevention of blindness)
Syphilis (prevention of tertiary or congenital syphilis)
3. Tertiary prevention: After permanent damage sets in, the objective of tertiary
prevention is to limit the impact of that damage. The impact can be physical (physical
disability), psychological, social(social stigma),and financial.
Rehabilitation refers to the retraining of remaining functions for maximum
effectiveness. Rehabilitation should be seen in a very broad sense, not simply limited
to the physical aspect.
Principles of communicable disease control

There are three principles:
1. Attacking the source
2. Interrupting the mode of transmission and
3. Protecting the host (decreasing susceptibility)
1. Attacking the source
=> Domestic & Wild animals as reservoirs
i.
Immunization
ii.
Destruction of infected animals e.g. Rabies
=>Humans as reservoirs
i.
Isolation of infected persons & separation of infected persons from others for
the period of communicability.
ii.
Treatment
Of cases (clinical) and carriers
Mass treatment where large proportion are known to have a disease.
iii.
Quarantine the limitation of freedom of movement of apparently healthy
persons or animals who have been exposed to a case or infectious disease.
Cholera, plague, and yellow fever are the 3 internationally quarantinable
diseases by international agreement, b/c these diseases are very infectious.
2. Interrupting transmission
For Transmission by ingestion
i.
Purification of water
ii.
Pasteurization of milk
iii.
Inspection procedures designed to ensure safe food supply
iv.
Improve housing conditions
For Transmission by inhalation
i.
Chemical disinfections of air
ii.
Improving ventilation
Transmission by vector or intermediate hosts
i. Vector control measures
ii.
Environmental manipulation
3. Measures that reduce host susceptibility
i.
Immunization
ii.
Chemoprophylaxis
iii.
Better nutrition
iv.
Personal hygiene: -Protective measures, primarily with in the responsibility of
the individual, that promote health and limit the spread of infectious disease,
chiefly those transmitted by direct contact. It includes := Washing hand in soap and water immediately after evacuating bowel or
bladder and always before handling food or eating.
= Keeping hands and unclean articles, or articles that have been used for toilet
purposes by others, away from the mouth, nose, eyes, genitalia and wounds.
= Avoiding the use of common or unclean eating utensils, drinking cups,
towels, hand kerchiefs, combs, hair brushes and pipes.
= Avoid exposure of other persons to spray from the nose and mouth as in
coughing, sneezing, laughing or talking.
= Washing hands thoroughly after handling a patient or the patients belongings.
= Keeping the body clean by frequent soap and water baths.
N.B:- Effective control of disease is most likely when a combination of methods
attacking the source, interrupting transmission, and protecting the host is used at the same
UNIT THREE
Prevention and control of feco orally transmitted
diseases
Common features
1. The causative organisms are excreted (portal of exit) is the stools of infected
persons (or rarely animals)
2. The portal of entry for these diseases is the mouth
3. Feco-oral transmission occurs mostly through unapparent fecal contamination of
food, water and hands
4. In feco - oral transmission of disease food takes a central position b/c it can be
directly or indirectly contaminated, via polluted water, dirty hands, contaminated
soil or flies
5. The five Fs which play an important role in fecal oral disease transmission are
finger, flies, fomites, food and fluid
Water
Feces
Soil
Food
Mouth
Flies
Finger
N.B There are also diseases that are mainly transmitted through fecally contaminated
water rather than food.
General prevention methods of feco-orally transmitted diseases
1. Early case detection and appropriate Rx of cases
2. Safe human excreta disposal
3. Control of flies
4. Safe water supply
5. Hand washing and sanitary handling of food and utensils
6. Control and check up of food handlers
7. Avoid eating of un cooked foods
Classification of feco-orally transmitted disease
1. As a result of fecally contaminated water
are mainly transmitted through contaminated water rather than food.
1) Typhoid fever
2) Amoebiasis
3) Giardiasis
5) Bacillary dysentery
4) Cholera
6) Infectious hepatitis
2. As a result of fecally contaminated soil
These infections are acquired through exposure to fecally contaminated soil
1) Ascariais
4.Enterobiasis
2) Hook worm 5.Strongloidiasis
3) Trichuriasis
3. As a result of direct contact with feces
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These are diseases transmitted mainly through direct contact with feces of the
infected person.
1) Poliomyelitis
2) Hydatid disease or echinococious
TYPHOID FEVER
Definition: It is a systemic infectious disease characterized by high continuous fever,
malaise and involvement of lymphoid tissues (of intestine).
Etiology: - Salmonella typhi:-Gram negative bacilli
Salmonella enteritidis (rare cause)
EPI: - It occurs world wide, particularly in poor socioeconomic areas
In endemic areas the disease is most commonly in preschool and school aged children (519 years)
Reservoir: - humans
Mode of transmission: - by water and food contaminated by feces and urine of patients
and carriers. Flies may infect foods in which the organisms then multiply to achieve an
infective dose.
Incubation period: - 1 3 weeks
Period of communicability: As long as the bacilli appear in excreta, usually from the
first week through out convalescence.
About 10 % of untreated patients will discharge bacilli for 3 months after onset of
symptoms, and 2% - 5% become chronic carriers.
Susceptibility and resistance: - susceptibility is general and increased in individuals
with gastric achlorhydria or those who are HIV positive.
Relative specific immunity follows recovery from infection; but inadequate to protect
against subsequent ingestion of large no of organisms.
Clinical Manifestations
First Week: - mild illness x-zed by fever rising stepwise (ladder type), for 4- 5 days with
associated chills, myalgia, dry cough, epistaxis, poor appetite, anorexia, lethargy, malaise
and general aches. Dull and continuous frontal headache is prominent. Nose bleeding,
vague abdominal pain and constipation occur in 10%of pts.
Second week: - sustained to (fever), severe illness with weakness, mental dullness or
delirium, abdominal discomfort and distension. Diarrhea is more common than 1st week
and feces may contain blood. Rash on upper abdomen, shoulder, chest and back, slightly
raised rose-red spots fade on pressure, not visible on dark skinned person.
Hepatospleenomegally may occur.
Third week: - patients continue to be febrile and increasingly exhausted. If no
complications occur, pt begins to improve and temperature decrease gradually. In this
week increased toxemia, GI hemorrhage, melena, paralytic ileus, perforation, rigid
abdomen, coma, & death are also may occur.
Clinical Manifestations suggestive of typhoid fever
1. Sustained fever (ladder fashion)
2. Rose spots: - small pallor, blanching, slightly raised macules usually seen on chest
and abdomen in the 1st week in 75% of white people.
3. Relative bradycardia: - slower than would be expected from the level of temperature.
4. Leucopenia: - WBC count is less than 4000/ml of blood
Diagnosis
=>Based on clinical grounds but this confused with wide variety of diseases ( Malaria,
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Typhus fever, Bacillary dysentery, Amoebic liver abscess, Relapsing fever, Non
typhoid salmonellosis etc),
=>Widal & weil flex test
=>Blood culture (first week), feces or urine culture (2nd and 3rd week), bone marrow
culture (most sensitive)
Treatment
CAF or
ciprofloxacin or
ceftriaxone for seriously ill pts
_ Ampicillin or co-trimoxazole for carries (usually for 4 weeks) & mild cases
Prognosis - Untreated 10% die
- Treated 0.1% die
Prevention
1. Treatment of pts and carriers
2. Education on hand washing, particularly food handlers, pts and child care givers.
3. Sanitary disposal of feces and control of flies
4. Provision of safe and adequate water
5. Safe handling of food
6. Exclusion of typhoid carriers and pts from handling of food and patients
7. Immunization for people at special risk e.g. Travelers to endemic areas.
N.B - In paratyphoid fever the disease is almost same to the typhoid fever, except in the
following points:- The cause of Paratyphoid is Salmonella para typhi
- It is less severe
- The course of disease tends to be shorter and milder than typhoid fever
- The onset is often more abrupt with acute enteritis.
- The rash may be more abundant and the intestinal complications less frequent.
Complications of Typhoid fever
GI Hemorrhage, Perforation
Myocarditis
Meningism, Convulsions
Arthritis
Bronchitis
Bronchitis
Leucopenia, thrombocytopenia, DIC
BACILLARY DYSENTERY (SHIGELLOSIS)

Definition: - An acute bacterial disease involving the large and distal small intestine,
caused by the bacteria of the genus shigella.
Etiology: - Four species or serotypes of shigella
1. Group A = shigella dysentriae (most common cause)
2. GP B =
//
flexneri
3. GP C =
//
boydi
4. GP D = //
sonnei
Enteroinvassive E-coli may rarely cause bacillary dysentery
EPI- It occurs world wide, and is endemic in both tropical and temperate climates.
Outbreaks commonly occur under conditions of crowding and where personal hygiene is
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poor, such as in jails, institutions for children, day care centers, mental hospitals and
refugee camps.
Reservoir: - Humans
Mode of transmission:
Mainly by direct or indirect fecal-oral transmission from a patient or carrier
Incubation period: - 12 hrs 4 days (usually 1-3 days)
Period of communicability: -during acute infection and until the infectious agent is no
longer present in feces, usually with in four weeks after illness
Susceptibility and Resistance
Susceptibility is general. The disease is more severe in young children, the elderly and
the malnourished. Breast-feeding is protective for infants and young children.
Clinical manifestation
Fever, rapid pulse, vomiting and abdominal cramp are prominent.
Diarrhea usually appears after 48 hrs with dysentery supervening two days later.
Generalized abdominal tenderness. Tenesmus is present and feces are bloody, mucoid and
of small quantity. Dehydration is common and dangerous- it may cause muscular cramp,
oliguria and shock.
Diagnosis: -Based on clinical grounds
- Stool microscopy (presence of pus cells)
-Stool culture confirms the diagnosis
Treatment: Fluid and electrolyte replacement
Cotrimoxazole or
- Ciprofloxacin or
- Gentamycin or
- Ampicillin
Prevention and control
1. Detection of carriers and Rx of the sick.
2. Hand washing after toilet and before handling or eating food.
3. Proper excreta disposal especially from pts, convalescents and carriers.
4. Adequate and safe water supply
5. Control of flies
6. Cleanliness in food handling and preparation.
AMOEBIC DYSENTERY / AMAEBIASIS)

Definition: - an infection due to a protozoa parasite (E. histolytica) that cause intestinal
or extra intestinal disease
Etiology: - Entameba histolytica
EpI: - It occurs world wide but most common in the tropics and subtropics. Prevalent in
area with poor sanitation, in mental institutions and homosexuals.
Mode of transmission
Fecal-oral transmission by ingestion of food or water contaminated by feces containing
the cyst.
Incubation period: - variable. It ranges from few days to several months or years; but
most commonly 2-4 weeks.
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Period of communicability: During the period of passing cysts of E. histolytica, which

may continue for years.
Susceptibility and resistance
-Susceptibility is general.
Life cycle
Transmissio
n
1. Cysts ingested
in food, water or
from hands
contaminated with
Human host
2 Cysts excyst, forming
trophozoites
3 Multiply & invade the
intestine
4 Trophozoites encyst
5 Infective cysts passes in
feces
* Trophozoites passed in
feces disintegrate
Environment
6 Feces containing
infective cysts
contaminate the
environment
Starts with a prodormal episode of diarrhea, abdominal cramps, nausea, vomiting and
tenesmus.
With dysentery, feces are generally watery, containing mucus and blood
Acute amoebic dysentery poses limited danger
Diagnosis
- Demonstration of entamoeba histolytica cyst or trophozoite in stool microscopy
Rx: Metronidazole or
Tinidazole
1. Adequate Rx of cases
2. Provision of safe drinking water
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3. Proper disposal of human excreta and hand washing following defection

4. Clearing and cooking of local foods (e.g. Raw vegetables) to avoid eating food
contaminated with feces.
GIARDIASIS
Definition: - a protozoan infection principally of the upper small intestine
EPI: - Occurrence world vide distribution. Children are more affected than adults. The
disease is highly prevalent in areas of poor sanitation & overcrowding living situations.
Reservoir: Humans
Mode of transmission:- Feces to mouth transfer of cysts from feces of infected persons
Period of communicability:-entire period of infection, often months.
Asymptomatic carrier rate is high. Infection is frequently self-limited. Persons with AIDS
may have more serious and prolonged infection.
Life cycle: - Similar to E. histolytica.
Clinical Manifestation
- Ranges from asymptomatic infection to severe failure to thrive and mal absorption
- Associated with symptoms of chronic diarrhea, steatorrhea, abdominal cramps,
bloating, frequent loose and pale greasy stools, fatigue and wt loss.
- Young children usually have diarrhea but abdominal distension and bloating are
frequent.
-Adults have abdominal cramps, diarrhea, anorexia, nausea, malaise & bloating
- Many pts complain of sulphur testing (belching)
Diagnosis. Demonstration of G. lamblia cyst or trophozoite in feces.
Treatment. Metronidazole or
Tinidazole.
1. Good personal hygiene and hand washing before food and following toilet use
2. Sanitary disposal of feces
3. Protection of public water supply from contamination of feces
4. Case Rx
5. Safe water supply.
CHOLERA
Definition:-An acute illness caused by an enterotoxin elaborated by vibrio cholera.
Etiology: - Vibrio cholera
EPI: - Has periodic out breaks in different parts of the world and given rise to pandemics.
Endemic predominantly in children.
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Reservoir- Humans
Mode of transmission: - by ingestion of food or water directly or indirectly
contaminated with feces or vomitus of infected person.
Incubation period: - few hours to 5 days. (Usually 2-3 days)
Period of communicability: - for the duration of the stool positive stage, usually only a
few days after recovery. Antibiotics shorten the period of communicability.
Susceptibility and Resistance:
Variable. Gastric achlorhydria increases risk of illness. Breast fed infants are protected.
Abrupt painless watery diarrhea; the diarrhea looks like rice water.
In severe cases, several liters of liquid may be lost in few hours leading to shock &
sudden death.
Severely ill pts are cyanotic, have sunken eyes and cheeks, scaphoid abdomen, poor skin
turgor, and thready or absent pulse.
Loss of fluid continues for 1-7 days
Diagnosis- Based on clinical grounds
- Stool Culture
Treatment (1) prompt replacement of fluids and electrolytes
- Rapid IV infusions of large volumes.
- Isotonic Normal saline solution alternating with isotonic Ringer lactate
(2) Antibiotics like TTC are very effective
1. Safe disposal of human excreta and control of flies
2. Safe public water supply
3. Hand washing and sanitary handling of food
4. Control and mgt of contact cases.
5. Case treatment
GASTROENTERITIS
It is an inflammation of stomach and intestine by bacteria, virus and poisons. Acute
diarrheal disease is a clinical syndrome of this disease. Additionally nausea and /or
vomiting and often fever are also found.
Diarrheal disease affects all the population, but severity varies in different age groups.
Dehydration occurs rapidly in children and is a common cause of death.
Occurrence
=>Low birth weight children and premature children easily get E.coli infections.
=>In the weaning period new type of foods are introduced to children. They are then
exposed to a variety of micro-organisms (pathogenic and non pathogenic).
=>Malnutrition
=>Because of poor economic and educational status of mothers of developing countries
in general bottle fed children develop diarrheal disease. Because they do not have the
facility to clean the bottle properly, and they do not have enough money to buy adequate
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amount of milk and other artificial feeds. The child gets fed with poorly prepared diluted
feeds, and inevitably gets diarrhea.
=>Traveler's diarrhea occurs in people who are exposed to a new environment. It is
thought to be the guts response to new intestinal flora acquired through feco oral contact,
but other factors like changes in food & contamination may also contribute.
N.B. Many organisms can cause diarrhea but it is difficult to prove the particular
organism that is responsible. But Bacteria like E.coli and Rota-viruses are common
causes. There are many strains of E.coli that can cause gastroenteritis.
I/P: l0 hrs to 6 days for most strains.

Mode of transmission: - through contamination of H20, food etc
Clinical Manifestation: Acute onset of watery diarrhea that is usually mild and self
limiting. Malaise, anorexia & abdominal cramps may occur. Some strains can result in
bloody or mucoid diarrhea. Toxins are released from these organisms which increase
intestinal fluid secretion & lead to diarrhea.
Diagnosis - Clinical Features
Stool examination shows fecal leukocytes
Isolation of specific organism in stool specimen (culture)
Treatment: - Rehydration (ORS)
Cotrimoxazole or
- Ciprofloxacin for resistant strains.
ASCARIASIS
Definition: - A helminthic infection of the small intestine generally associated with few
or no symptoms
Etiology Ascaris lumbricoids
EPI: - Common where sanitation is poor. School children (5-10 yrs) are most affected.
Highly prevalent in moist tropical counties
Reservoir: - Humans & ascarid eggs in soil
- Ingestion of infective eggs from soil contaminated with human feces
- Or uncooked food contaminated with soil containing infective eggs; but not directly
from person to person or from fresh feces.
Incubation period- 4-8 weeks
Period of communicability: As long as mature fertilized female worms live in the
intestine. Usual life span of adult worm is12 months
Susceptibility and resistance: susceptibility is general
Life cycle
Transmission
1. Infective eggs ingested in
food or from contaminated
15hands
Human host
2. Larvae hatch in intestine.
3. Migrate through liver and lungs
4. Pass up trachea and are swallowed
5. Worm mature in small
intestine
6. Eggs produced and passed in feces
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Environment (Envt)
6. Eggs become infective
(embryonated) in soil in
30-40 days
7. Infective eggs
contaminate the envt
Most infections go unnoticed until large worms passed in feces and occasionally the
mouth and nose.
- Migrant larvae in lung & trachea may cause itching, wheezing and
dyspnea, fever, productive cough of bloody sputum.
- Abdominal pain may arise from intestinal or duct (billiary, pancreatic)
obstruction.
- Serious complications include bowel obstruction due to knotted or
intertwined worms.
Diagnosis Microscopic identification of eggs in stool sample
- Adult worms pass from anus, mouth or nose.
Treatment- Albendazole
- Mebendazole
- Piperazine
- Levamisole
Prevention and Control
1. Rx of cases
3. Prevent soil contamination in areas where children play
4. promote good personal hygiene (hand washing)
TRICHURIASIS( whip worm)

Definition: - It is a nematode infection of the large intestine (Caecum & upper colon).
Etiology: - Trichuris trichuria (whip worm)
EPI: occurs w/w esp. in warm moist regions. Common in children 3-11 years of age
Reservoir- Humans
Mode of transmission: - indirect, particularly through ingestion of contaminated
vegetables. Not immediately transmissible from person to person.
I/p indefinite
Period of comm.: several years in untreated carriers.
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Susceptibility & Resistance: susceptibility is universal

Life cycle
Transmission
1. Infective eggs ingested in
food or from contaminated
hands.
Envt
5. Eggs become infective
(embryonated) in soil after 3
weeks
6. Infective eggs contaminate the
envt
Human host
2. Larvae hatch. Develop in
small intestine migrate to
Caecum.
Become mature- worms
Clinical 3.
Manifestation:
Most infected people are asymptomatic. Abdominal pain,
4.
Eggs
produced
and
tiredness, nausea and vomiting diarrhea or constipation are complaints by patients. Rectal
passed
in feces.
prolapse may
occur
in heavily infected very young children.
Severity is directly related to the number of infecting worms.
Diagnosis: Stool microscopy (eggs in feces)
Treatment: Albendazole or
Mebendazole
2. Maintaining good personal hygiene (i.e. washing hands and vegetables and other
soil contaminated foods).
3. Cutting nails esp.-in children
4. Rx of cases.
ENTEROBIASIS (OXYURIASIS, PIN WORM INFECTIONS)

Definition: A common helminthic infection of Large intestine (Caecum)
Etiology: caused by Enterobius vermicularis
EPI- it occurs world wide affecting all socioeconomic classes. Prevalence is highest in
school-aged (5-10 yrs). Infection usually occurs in more than one family member.
Reservoir- Humans
Mode of transmission: direct transfer of infective eggs by hands from anus to mouth.
=>Or indirectly through clothing, bedding, food or other articles contaminated with eggs
of the parasite.
I/p. 2-6 weeks
Period of communicability: - As long as gravid females are discharging eggs on perianal
skin. Eggs remain infective in an indoor environment for about 2 weeks
Susceptibility and resistance: susceptibility is universal.
Life cycle
1. Ingestion of eggs by man
2. Larvae hatch in duodenum and migrate down to caecum
3. Adult worms mature in caecum
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4. Gravid females migrate through the anus to the perianal skin and deposit eggs
(usually during the night)
5. Eggs become infective in a few hors in perianal area.
Clinical Manifestation: - perianal itching, disturbed sleep, irritability and some times
secondary infection of the scratched skin. The worm may also invade vagina.
Diagnosis: Stool microscopy for eggs or female worms
Treatment: Mebendazole 100mg Po stat or Albendazole-400mg Po stat
1. Educate the public about hygiene (i.e. hand washing, before eating or preparing
food )
2. keeping nails short and discourage nail biting
3. Rx of cases
4. Reduce over crowding in living accommodations
5. Provide adequate toilets
STRONGLOIDIASIS
Definition: An often asymptomatic helminthic infection of the duodenum and upper
jejunum. (Can be through out the small intestine)
Infectious Agent Strongloides stercoralis
EPI- It occurs in tropical and temperate areas more common in warm and wet regions.
Reservoir Humans
Mode of transmission: - infective (filariform) larvae penetrate the skin and enter venous
circulation
I/P: 2-4 weeks
Period of communicability: as long as living worms remain in the intestine; up to 35 yrs
in cases of autoinfection
Susceptibility and resistance: susceptibility is universal. Patients with AIDS or an
immuno - suppressive medications are at risk of dissemination.
Life cycle
1. Infective filariform larvae penetrate skin & enter circulation. E.g. feet.
2. larvae reaches lung, pass up trachea and swallowed
3. Become mature worms in small intestine
4. Eggs laid. Hatch rhabditiform larvae in intestine
5. Rhabditiform larvae
- passed in feces or
- become filariform larvae in intestine, causing autoinfection
6. In soil larvae become free living worms produce more rhabditiform larvae
7. Become infective filariform larvae in the soil
Clinical Manifestation: pneumonia occurs during heavy larval migration. Mild peptic
ulcer like s/s, epigastric discomfort to severe watery diarrhea. Heavy infection may result
in malabsorption syndrome.
Diagnosis- Identification of rhabditiform larvae in stool specimen microscopy.
Treatment- Albendazole 400mg Po per day for 03 days
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- Or thiabendazole 500 mg Po BID for 03 days.

1. Proper disposal of human excreta
2. personal hygiene including use of foot wear
3. Case Rx
HOOK WORM DISEASE(ANCYLOSTOMIASIS AND

NECATORIASIS)
Definition: A common chronic parasitic infection of small intestine with a variety of
symptoms.
Infectious Agent Ancylostoma duodenale and Necator americanus
EPI- Widely endemic in tropical and subtropical countries where sanitary disposal of
human feces is poor. Common in area where soil is wet.
Reservoir-Humans
Mode of transmission: - through skin penetration by the infective larvae (Filariform).
I/P- Few weeks to many months depending on intensity of infection and iron intake of
the host.
Period of communicable: infected people can contaminate the soil for several years in
the absence of Rx.
Susceptibility & Resistance: susceptibility is universal.
Life cycle
1. Infective filariform larvae penetrate the skin & enter circulation.
2. Larvae migrate to lung, pass up trachea and are swallowed
3. Become mature worms in small intestine (attach to wall and suck blood)
4. Eggs produced and passed in feces
5. Eggs develop. Rhabditiform larvae hatch in soil
6. Develop in to infective filariform larvae in about 1 week
7. Filariform larvae contaminate soil
1. Larval migration to the skin
Produces transient (short lasting) localized maculopapular rash associated
with itching called ground itch
2. Larval migration to lungs
Produces cough, wheezing and transient pneumonitis
3. Blood sucking in intestine
Light infection no symptom
Heavy infection result in symptoms of PUD like epigastric pain and
tenderness. Further loss of blood leads to anemia manifested by exertional
dyspnea, weakness and light headedness.
Diagnosis: Demonstration of eggs in stool specimen
Treatment - Mebendazole 200 mg PO BID for 03 days
- Albendazole 400mg PO stat
- Levamisole
Prevention & control
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1. sanitary disposal of feces

2. wearing of shoes
3. Case Rx.
POLIOMYELITIS
Definition: Acute viral infection most often recognized by the acute onset of flaccid
paralysis.
Etiology: Polioviruses (type I. II and III)
EPI: =>Occurs world wide prior to the advent of immunization.
=>It is primarily a disease of infants and young children i.e. 70-80% of cases are
less than three years of age.
=>more than 90% of infections are unapparent and
=> Flaccid paralysis occurs in less than 1 % of infections
Reservoir: Humans, especially children
Mode of transmission: primarily person to person, spread principally through the fecooral route. In rare instances milk, food stuffs and other materials contaminated with feces
have been incriminated as vehicles.
I/P. Commonly 7-14 days
Period of communicability. As long as the virus is excreted (Usually less than 60days)
Susceptibility and resistance: susceptibility is common in children but paralysis rarely
occurs. Infection confers (gives) permanent immunity.
- Usually asymptomatic or non specific fever is manifested in 90% of
cases.
- If it progresses to major illness, severe muscular pain, stiff neck and back
pain with or without flaccid paralysis may occur
- Paralysis is asymptomatic and occurs with in 3 to 4 days of illness
- The legs are more affected than other parts of the body
- Paralysis of respiratory and swallowing muscle is life threatening
Clinical course of the disease
1. Asymptomatic (unapparent infection) 90-95%
-Show no signs and symptoms
2. Abortive infection occurs in 4-8 % of cases
S/S of URTI fever, sore throat, myalgia
- S/S of GI anorexia, nausea, vomiting, loose stool, stomach upset stomach
aches
3. Non-paralytic poliomyelitis
- There is involvement of CNS without signs of paralysis & subsides without
sequel.
- Signs of meningeal irritation, head ache fever nuchal rigidity.
4. Paralytic poliomyelitis
- Flaccid paralysis of a group of muscles associated with fever, myalgia,
neck rigidity,
Diagnosis: Based on clinical and epidemiological grounds
Treatment: symptomatic
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1. Educate public about the advantage of immunization in early child hood
2. Safe disposal of human excreta
Unit 4
AIR-BORNE DISEASES
INTRODUCTION
Air-borne diseases are diseases transmitted through dissemination of microbial

agent by air to a suitable portal of entry, usually the respiratory tract. The organisms
causing the diseases in the air-borne group enter the body via the respiratory tract. When
a patient or carrier of pathogens talks, coughs, laughs, or sneezes, he/she discharges fluid
droplet nuclei. The smallest of these remain up in the air for sometime and may be
inhaled by a new host. Droplets with a size of 1-5 microns are quite easily drawn in to the
lungs and retained there.
Droplets that are bigger in size will not remain air-borne for long but will fall to
the ground. Here however, they dry and mix with dust. When they contain pathogens that
are able to survive drying, these may become air-borne again by wind or something
stirring up the dust, and they can then be inhaled.
Air-borne diseases, obviously, will spread more easily when there is
overcrowding, as in over crowded class rooms, Public transport, canteens, dance halls,
and cinemas. Good ventilation can do much to counteract the effects of overcrowding.
Air borne diseases are mostly acquired through the respiratory tract.
Common cold (Acute Viral Rhinitis or coryza)

Definition An acute catarrhal infection of the nasal mucus membrane.
Infections agent: Rhino viruses (100 serotypes) are the major causes in adults. Para
influenza viruses, respiratory syncytial viruses (RSV), influenza, and adenoviruses are
additional causes of common cold.
EPI: it occurs world wide both in endemic and epidemic forms. Many people averagely
have one to six colds per year. Greater incidence in the highlands. Incidence is high in
children under 5 years and gradually declines with increasing age.
Reservoir: Humans
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Mode of transmission: inhalation of air-borne droplets; and articles freshly soiled

(contaminated) by discharges of nose and throat of an infected person.
I/P: usually 48 hrs, varying with the agent
POC: 24 hrs before on set and for 5 days after onset
S&R: susceptibility is universal. Repeated infections (attacks) are most likely due to
multiplicity of agents.
Clinical features: - Coryza, sneezing, lacrimation, pharyngeal or nasal irritation, chills
and malaise. Dry or painful throat
Diagnosis: Based on clinical grounds
Treatment: No effective Rx but supportive measures like:
1. Bed rest
4. Anti pain
2. Steam inhalation
5. Balanced diet intake
3. High fluid in take
Prevention & control
1 Educate the public about the importance of hand washing, covering the mouth
when coughing and sneezing,
2. Sanitary disposal of nasal and oral discharges.
3. Avoid crowding in living and sleeping quarters esp. in institution.
4. Provide adequate ventilation
Influenza
Definition: An acute viral disease of the respiratory tract (especially trachea).
Infections agent: Three types of influenza virus (A, B & C)
EPI: Occurs in pandemics, epidemics and localized outbreaks
Reservoir: Humans are the primary reservoirs for human infection
Mode of transmission: Air-borne spread *predominates among crowded populations in
closed places such as school buses
I/P: short, usually 1-3 days.
POC: 3-5 days from clinical onset in adults; up to 7 days in young children
P/R: when a new subtype appears, all children and adults are equally susceptible.
Infection produces immunity to the specific infecting agent.
Clinical picture: Fever, headache, myalgia, prostration, sore throat and cough. Cough is
often severe and protracted, but other manifestations are self limited & last long with
recovery in 2-7 days
Diagnosis: based on clinical ground
Treatment: same as common cold, namely
1. Antipain and antipyretic
2. High fluid intake
3. Bed rest
4. Balanced diet
Prevention: 1. Educate the public in basic personal hygiene, esp. the danger of
unprotected coughs and sneezes and hand to mucus membrane transmission
2. Immunization (with available killed virus vaccines for (A & B types) may
provide 70-80 % protection)
3. Amantadine hydrochloride is effective in the chemo prophylaxis of type A virus
but not others. It is used both for Rx (4-5days) and prophylaxis (as long as
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epidemics lasts) 100mg PO BID
Measles (Rubella)
Definition An acute highly communicable viral disease.
Etiology: measles virus
EPI: Prior to wide spread immunization, measles was common in child hood so that
more than 90% of people had been infected up to age 20; few went through life without
any attack. The maximum incidence is b/n 6 months and 5 years.
Reservoir: Humans
Airborne droplets released when an infected person sneezes or coughs
Contact with nose and throat secretions of infected people
Cases can infect others for several days before and after they develop symptoms
Spreads easily in over crowded areas (schools, military barracks, health facilities
etc)
I/P: 7-18 days from exposure to onset of fever
POC: slightly before the s/s appear to four days after the appearance of the rash.
S and R: All those who are non-vaccinated or have not had the disease are susceptible.
Permanent immunity is acquired after natural infection or immunization.
Signs and symptoms
High fever which begins approximately 10 -12 days after exposure and lasts for
several days.
A characteristic slight raised, red blotchy rash appears on the third to seventh day,
beginning inside the cheeks& on the buccal mucosa as small white spot (this is
called kopliks spot), then under the ears, then on the face and neck gradually
spreads to the body and then to the hands & feet and lasting 4-7 days.
Runny nose, conjunctivitis, coryza, cough, red and watery eyes and
Leucopoenia is common
Complications like otitis media, pneumonia, diarrhoea, encephalitis, croup
(laryngotracheo bronchitis) may result from viral replication or bacterial super
infection.
Diagnosis: = Based on clinical and epidemiological grounds
= Fever and rash plus one of these: Cough, coryza or conjunctivitis.
Complications
Unimmunized children, under 5 years and infants are at highest risk of measles
and its complications.
Pneumonia is the most common cause of death as the virus weakens the immune
system
Complications are due to:
1. Bacterial infection
2. Measles virus which damages respiration and intestinal tracts
3. Vitamin A deficiency.
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1. Acute complications:
o Bronchopneumonia:- the most important complication and responsible
for most deaths
o Diarrhoea (dysentery and persistent diarrhoea)
o Laryngo-tracheo bronchitis
o Conjunctivitis and corneal ulceration
o Ottitis media, mastoiditis
o Stomatitis,
o Appendicitis
o Malnutrition
o Acute encephalitis-rare complications
o Febrile convulsions, AGE in children <2yrs
2. Long term complication
o Increase susceptibility to other infection (damages immune system)
o Blindness
o Sub acute sclerosing pan encephalitis
Treatment
No specific Rx
General nutritional support and Rx of Dehydration
Antibiotics are given only to ear and severe respiratory infection
Vitamin A two doses in 24 hours.
Rx of complication
Nursing care
1. Advise pt to have bed rest
2. Relief of fever
3. Provision of non- irritant small frequent diet
4. Shorten the finger nails
Prevention
1. Educate the public about measles immunization
2. Immunization of all children (<5 years of age) who had contact with infected
children
3. Provision of measles vaccine at nine months of age.
4. Initiate measles vaccination at 6 months of age during epidemic and repeat at 9
months of age.
Pertussis (whooping cough)

Definition: An acute disease of the respiratory tract caused by bacteria.
Infections agent: Bordetella pertusis
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EPI: it is an endemic disease common to children esp. young children every where in the
world.
The disease is mostly affects & dangerous in children age less than one year and nonimmunized.
Many children that contract pertussis have coughing spells that lasts for eight weeks
Reservoir- Humans
Mode of transmission: direct contact with discharges from respiratory mucus membrane
of infected persons by air borne route & by handling objects freshly soiled with
nasopharyngeal secretions.
I/p: 1-3 weeks
POC: ranges from 7 days after a person has been exposed to until three weeks after the
start of the coughing: Highly communicable in early stage. Infectiousness decreases after
onset of therapy.
S and R: Susceptibility to non immunized individuals is universal. One attack usually
confers prolonged immunity but may not be life long.
Signs and symptoms
The disease has insidious onset and 3 phases.
1. Catarrhal phase
- Last 1 2 week
- Cough and rhinorhea
2. Paroxysmal phase:
- Explosive, repetitive and prolonged cough
- Child usually vomits at the end of paroxysmal cough
- Expulsion of clear tenacious mucus often followed by vomiting.
- Lasts 2-4 weeks.
-Whoop (inspiratory whoop against closed glottis) between paroxysms.
- Child looks health b/n paroxysms
- Cyanosis and sub conjunctival haemorrhage due to violent cough.
3. Convalescent phase
- The cough may diminish slowly in 1-2 weeks time or may last long time.
- After improvement the disease may recur
Diagnosis: difficult to distinguish it from other URTI
- History and physical examination at phase two ensure the diagnosis
- Marked lymphocytosis.
Treatment: Erythromycin: 30-40mg/kg PO QID for 10days
- Antibiotics for super infection like pneumonia b/c of bacterial invasion due to
damage to cilia.
Nursing care
1. Proper feeding of the child, high fluid intake
2. Encourage breast feeding immediately after an attack of each paroxysm
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3. Proper ventilation-continuous well humidified oxygen administration

4. Reassurance of the mother (care giver)
5. Steam inhalation
Prevention
o Educate the public about the dangers of whooping cough and the advantages of
initiating immunization at 6 weeks of age
o Consider protection of health worker at high risk of exposure by using
erythromycin for 14 days.
o Vaccination (DPT)
Complications
1. Loss of appetite
6. Bronchiectasis
2. Middle ear infection
7. Re activation of latent TB
3. DHN
8. Pneumothorax
4. Bacterial pneumonia
9. Emphysema
5. Convulsions and seizures
10.Encephalopathy
11. Debility and emaciation
Diphtheria
Definition An acute bacterial disease of the mucus membrane of the RT involving
primarily tonsils, pharynx, nose, occasionally other mucus membranes or skin and some
times the conjunctiva or genitalia.
Infections agents: corynebacterium diphtheriae,
EPI: Disease of colder months, involving primarily non-immunized children less than 15
years of age. It is often found among adult population groups whose immunization was
neglected. Unapparent, cutaneous and wound diphtheria cases are much more common in
the tropics.
Reservoir: Humans
Mode of transmission: contact with a pt or carrier i.e. with oral or nasal secretion, or
infected skin; raw milk has served as vehicle.
I/P: usually 2-5 days
POC: variable. Usually 2 weeks or less.
S and R: susceptibility is universal. Prolonged active immunity can be induced by
diphtheria toxoid.
Clinical picture: Characteristic lesion marked by a patch or patches of an adherent
greyish membrane with a surrounding inflammation (pseudo membrane)
-Throat is moderately sore in pharyngotonsillar diphtheria, with cervical lymph nodes
some what enlarged and tender, in severe cases there is marked swelling and oedema
of neck.
- sore throat, cervical adenopathy or swelling, and low grade fever accompanied by
nasal discharge, systemic toxicity, hoarseness, stridor, palatal paralysis with or
without pseudo membrane.
- Patient may recover within 6 10 days
- But late effects of absorption of toxin appearing after 2-6 weeks, including cranial
and peripheral, motor and sensory nerve palsies and myocarditis (which may
occur early) and are often severe.
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Complications
Abnormal heart beats which may lead to heart failure

Inflammation of heart muscles and valves (lead to chronic heart
disease and heart failure)
The most severe complication is respiratory obstruction as a result of
laryngotracheobronchitis (croup) followed by death.
Diagnosis: Bacteriologic exam of discharges from lesions.
Based on clinical and epidemiological grounds.
Treatment
1. Diphteria antitoxin
2. Erythromycin 500mg for 2 weeks but 1 week for cutaneous form or
3. Procaine penicillin IM for 14 days or
Single dose of Bezanthine penicillin IM
Newborn 150,000IU once(stat)
1-12 months 300,000IU once
2-6years 600,000IU once
7-10 years 900,000 IU once
Over 10 years 1,200,000 IU 0nce
Adult1.2 to 2.4 Million IU once
N.B- primary goal of antibiotic therapy for pts or carriers is to eradicate C- diphtheriae
and prevent transmission from the pt to other susceptible contacts.
Prevention
1. Immunization of infants with diphtheria toxoid.( DPT)
2. Concurrent and terminal disinfection of articles in contact with pt and soiled by
discharges of pt
3. Single dose of B. penicillin (IM) or erythromycin 7-10 days course (PO) is
recommended for all persons exposed to diphtheria.
Antitoxic immunity protects against systemic disease but not against local
infection in the nasopharynx.
Definition An acute bacterial disease that causes inflammation of the meninges (esp.
the pia and arachnoid space) the coverings of the brain.
* There may also be varying involvement of the brain parenchyma.
Infectious agent
1. In neonates Gram-ve bacilli-E.coli , Proteus species.
Group B streptococci
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2. Preschool child Haemophilus influenza B

Neisseria meningitides (meningococcus)
Streptococcus pneumonae
3. Older children and Adults N. meningitidis(A, B, C, X, Y, Z, w135)
strep. Pneumonae
=>Meningococcus (N. Meningitidis.) is responsible to Meningococcal meningitis
& type A is know to cause epidemics
EPI - Epidemics occurs irregularly
- Common in children and young adults
- It is a disease of individuals with poor general health and commonly happen in
crowded situations
Reservoir Humans
Mode of transmission Direct contact with respiratory droplets from nose and throat of
infected person
I/p- Varies from 2-10 days, commonly 3-4 days
POC- until the meningococci are no longer present in discharges from nose and mouth.
Meningococci usually disappear from the nasopharynx with in 24 hrs after initiation
of proper Rx.
Susceptibility and Resistance
- Susceptibility is low and decreases with age
- Immunocompromised persons are at high risk
Pathogenesis: Meninges (pia, arachinoid &dura mater) are congested and infiltrated
with inflammatory cells. A thin layer of pus formed and this may later organize to
form adhesions. This may cause obstructions to the free flow of CSF and impedes
absorption of CSF leading to hydrocephalus or they may damage the cranial nerves
at the base of the brain. The CSF pressure rises rapidly, the protein content increases
and the glucose content decreases.
The increased ICP (tension) impedes cerebral blood supply further results in
ischemic damage.
- Sudden onset of fever, intense head ache, nausea and often vomiting. Neck
stiffness, drowsiness, photophobia, seizures are the usual presenting features.
- There may be *purpuric or* petechial rash and circulatory collapse.
- In severe cases the pt may be comatous and later there may be neurological
deficit.
Usual signs of meningeal irritations
- Kernig's sign- pt feels back pain when one of the lower limbs is flexed at the knee
joint and extended forward in an elevated position
Or when the pt is lying with his thigh flexed on the abdomen, he can't completely
extend his leg.
- Brudzinki's sign: when the pt's neck is flexed, the two lower extremities get flexed
at knees and hip joint or raised up:
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Or when passive flexion of the lower extremity of one side is made, a similar
mov't is seen for the opposite extremity.
- Neck rigidity (Nuchal rigidity) on flexion of the neck
* Lateral rotation of the neck doesn't produce pain.
Diagnosis
Based on clinical and epidemiological grounds
Lab investigations
WBC count ( specially neutrophils may be increased)
CSF analysis by lumbar puncture:
o Gram stain of CSF G-ve intra cellular diplococci
o WBC-polymorphs
o Protein level increased possibly by increased capillary
permeability.
o Glucose increased used up by brain, decreased transport via
inflamed membrane.
o Physical appearance turbid
o Pressure on withdrawing the needle
CT-to exclude cerebral abscesses or space occupying lesions.
N.B. Lumbar puncture is mandatory unless there is contraindication.
Treatment
1. Admit the pt and administer high dose of crystalline penicillin IV.
- Crystalline 3 to 4 Million IU IV q 4 hourly and
- CAF l g Iv QID and
- Ampicillin 1 g IV QID
- Monotherapy with ceftriaxone 100mg/kg/day IM BID.
- The usual duration of antibiotic Rx is 14days
2. Fluid replacement
3. Mgt of seizures
- Control by diazepam 10mg IM or IV
4. Cerebral oedema mgt
- by IV manitol 1-2 days followed by oral glycerine (produce osmotic gradient
b/n the plasma and brain, which in turn excrete through the kidneys)
Nursing care
1. Maintain fluid balance (in put and out put)
2. Maintain body temp. to normal
3. Timely administration of antibiotics
4. Monitor vital signs
5. Observe for any neurological disorders
1. reduce direct contact and exposure droplet infection
2. Reduce over crowding in work places, schools, camps etc.
3. Vaccines containing group A,C and Y strains
4. Chemo therapy of case
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5. Chemo prophylaxis e.g. Rifampin 600mg po BID for 2 days or ciprofloxacin

500mg PO
6. Report to the concerned health authority.
Meningococcal infections
- Bacteraemia and meningitis are the most common infection caused by N.
meningitides among an variety of infections
- N- meningitidis is a gram ve diplococcus and has 13 serogroups
- The natural habitat of these bacteria is the nasopharynx and they are continued
entirely to humans
- Sero group A meningococci are the primary cause of epidemics especially in
Africa.
- In the Meningitis belt On sub-Saharan Africa, the incidence of Meningococcal
do rises sharply toward the end of the dry and dusty season and falls with the
onset of rains.
- Outbreaks occur more frequently among the poorest segments of the population,
where overcrowding and poor sanitation are common.
- Invasive meningococcal disease occurs almost exclusively in individuals who
lack protective bacterial antibodies to the infecting strain.
- Infants are protected from meningococcal infection for the first few months of life
by passively transferred maternal antibodies and by a very low rate of
meningococcal acquisition. As maternal antibodies are lost, susceptibility rises,
peaking at 6 to l2 months. It then falls progressively as antibodies are acquired
through colonization with closely related but non pathogenic bacteria such as N.
lactamica, avirulent N. meningitidis. N. lactamica colonizes the nasopharynx .
Complication
- The complication of meningococcal infections include
Recurrent infection and damage to CNS
- Superinfection of the respiratory tract
- Neurological complication may result from direct infection of brain parenchyma
- Cerebritis
- Brain abscess
- Injury to cranial innervations (seizures, focal deficits & paralysis)
- Cerebral edema & raised ICP
- Interruption of CSF pathway (hydrocephalus)
- Effusion in to subdural space
TUBERCULOSIS
A systemic bacterial disease which primarily affects the lung, but other organs may also
be involved depending on the bacteria, dissemination and the host resistance
Infectious agent
- M. tuberculosis- human tubercle bacilli (commonest cause)
- M. bovis-causes cattle and man infection
- M. avium-causes infection in birds and man
EPI- It occurs world wide, however under developed areas are more affected.
- Affects all ages and both sexes, but age groups b/n 15-45 years are mainly
affected.
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- Through aerosolized droplets mainly from persons with active ulcerative lesion of
lung expelled during taking, sneezing, singing or coughing directly.
- Untreated PTB+ cases are the source of infection
- The risk of infection is related to the length of contact an individual shares
volume of air with an infections case i.e. intimate, prolonged or frequent contact
is required.
- Transmission through contaminated fomites (clothes, personal articles) is rare
- Ingestion of unpasteurized milk transmits bovine TB.
* Over crowding and poor housing conditions favour the disease transmission.
Incubation period: depends on the site of involvement
- 4-12 weeks PTBc
- 3-6 mouth meningeal, milliary and pleural disease
- Up to 3 yrs- GI, bone, joint & lymph node disease
- 8 yrs Renal tract disease
Period of communicability:
- As far as the bacilli is present in the sputum. Some untreated or inadequately
treated pts may be sputum positive intermittently for year.
N.B-effective antimicrobial therapy usually eliminates communicability with in 2 weeks.
- Extra pulmonary TB and children with primary TB are generally non-infections
- Every one who is non infected or non-vaccinated can be infected
- Susceptibility to infection is highest among.
o Children under 3 yrs old
o Adolescents
o Young adults
o The very old
o The immunocompromised.
* Children at greater risk of developing TB are
1. Children who are contacts of a newly diagnosed smear positive case
2. Children less than 5 years of age
3. HIV infected children
4. Severely malnourished children.
HIV is an important risk factor for the development of HIV-associated TBc by

facilitating:
1- Reactivation: reactivation of latent TB infection that was acquired prior to
the HIV infection
2- Progression of recent infection= rapid progression of latent TB infection to
TB disease following recent TB infection
3- Reinfection= a re infection with another strain of M. tuberculosis.
Tuberculosis has two major clinical forms
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1. Pulmonary (80%) of the total TB cases.

- Primarily occurs during child hold & secondarily 15-45 yrs or later.
2. Extra pulmonary (20%) affects all parts of the body.
Most common sites are lymph nodes, pleura, GUT, bone and joints, meninges &
peritoneum.
Early signs and symptoms
- Productive cough for more than 3 weeks
- Fever
- Unexplained wt loss
- Night sweats
Late signs and symptoms
- Blood stained sputum
- Difficulty in breathing
- Severe wt loss
- Severely diminished loss of appetite
- Weakness
- Symptoms of other organ involvement
- Enlargement of lymph nodes
EPTB
TB lymphadenitis
- Slowly developing and painless enlargement of lymph nodes followed by
matting and drainage of pus.
Tuberculosis pleurisy
- Pain while breathing in, dull lower chest pain, slight cough, breathlessness on
exertion
TB of bones and joints
- Localized pain and/or swelling, discharging of pus, muscle weakness, paralysis
and stiffness of joint
Intestinal TB
- Los of wt and appetite
- Abdominal pain, diarrhoea and constipation
- Mass in the abdomen
- Fluid in the abdominal cavity (ascites)
Tuberculosis meningitis
- Head ache, fever, vomiting, neck stiffness and mental confusion of insidious
onset.
Diagnosis
1- Clinical Manifestations
2- Sputum smears for AFB the golden standard
However one positive result doesn't justify starting anti TB Rx since errors can
never be excluded.
3- Acid fast stain for AFB can be done for extra Pulmonary TB having discharge
4- Radio logic examination chest x-ray
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- This is unreliable b/c it can be caused by a variety of conditions or previous TB

patients who are healed may have chest x-ray giving the appearance of active TB,
which requires Rx.
5- Histopathological exam: Biopsy for EPTB like TB lymphadenitis
6- Tuberculin skin test (TST or Montoux test) Helpful in non-BCG vaccinated
children under 6 yrs of age
Values of a negative tuberculin test
A tuberculin test is not significant or 'negative' when the diameter of skin indurations is
less than 10mm (or less than 5 mm in an HIV infected child). This is regardless of
whether or not the child has had BCG. A negative tuberculin skin test doesnt exclude
TB. In other words, a negative test is of no help in deciding that some one does not have
TB.
Conditions that may suppress the TSF
- HIV infection
- Malnutrition & Cancer
- Severe bacterial infections, including TB
- Viral infections like measles, chicken pox, glandular fever
- Immunosuppressive drugs like steroids
- Incorrect injection of PPD.
Values of a positive TST
The criterion for a significant or 'positive' tuberculin test depends on whether a child has
previously had BCG vaccination or not. This is because a reaction to tuberculin is usual
after a previous BCG, for several years. This reaction is usually a weaker reaction
(diameter often less than 5mm) than the reaction to natural infection with M. tuberculosis
A tuberculin test is considered significant or 'positive' when the diameter of skin
indurations is 10mm or more. However, if the child is HIV infected, tuberculin test is
considered ''positive'' if the induration is 5mm or more. A positive tuberculin test is only
one piece of evidence in favour of the Dx of TB. The younger the child and the greater
the diameter of indurations, the stronger is the evidence.
7- Sputum culture- complex and sophisticated which takes several weeks
8- ESR
9- Gastric washing for children
10- Trans bronchial biopsy
11- CT scan tuberculoma
12- CSF analysis TB meningitis
13- Pleural fluid analysis and culture-TB pleurisy
14- Pericardial fluid analysis TB pericarditis
Management
Case definitions
1. Relapse (R): A pt who has been declared cured or treatment completed of any
form of TB in the past, but who reports back to the health service and is found to
be AFB smear positive or culture positive.
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2. Rx failure (F): A pt who, while on Rx remained smeary positive or became again

smear positive at the end of the five 'months' or later, after commencing Rx.
3. Return after default (D): Apt who had previously been recorded as defaulted
from Rx and returns to the health facility with smear positive sputum
4. New case (N): Apt who has never had Rx for TB or has been on anti TB Rx for
less than four weeks.
5. MDR-TB: A pt who is still smear positive at the completion of re treatment
regimen.
6. Defaulter: A pt who has been on Rx for at least 4 weeks and whose treatment was
interrupted for 8 or more consecutive weeks
7. Rx failure: A pt who remains or becomes again smear positive at the end of 5
months or later during Rx. A pt who was PTB-negative at the beginning and
turned out smear positive at the end of the intensive phase
Drugs used for the chemotherapy of TB:
1. Streptomycin (S)
2. Ethambutol (E)
3. Isoniazid (H)
4. Rifampicin (R)
5. Pyrazinamide (Z)
Phases of chemotherapy Rx of TB has two phases
1. Intensive phase (initial): This phase consists of three or more drugs for the 1st 8
weeks for new cases and 12 weeks for re-treatment cases. It renders the pt non-infectious
by rapidly reducing the load of bacilli in the sputum and minimizing the danger of dev't
of drug resistance.
2. Continuation phase: This phase immediately follows the intensive phase and is
important to ensure that the pt is permanently cured and does not relapse after completion
of Rx. This phase requires at least two drugs to be taken for 4-6 months.
Treatment categories
There are four diff. Rx categories and corresponding Rx regimens.
1. Category I: short course chemotherapy for smear +ve PTB & seriously ill
smear negative PTB and EPTB cases
New smear-positive PTB pts
- New smear-negative PTB pts, who are seriously ill
- Return, after default from SCC, who have smear negative PTB
Seriously ill includes.
- Life threatening disease:
- Acute disseminated miliary TB
- TB meningitis
- TB peritonitis
- Risk of severe disability
- Spinal TB
- TB pericarditis
- Bilateral TB pleural effusion
- Renal TB
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- Extensive x-ray lesions without cavitations in immunocompromised pts e.g. DM, HIV the
Rx: 2(ERHZ) /6 (EH) i.e.
Intensive phase- 2ERHZ The drugs must be collected daily and must be
swallowed under the direct observation of a health worker
Continuation phase 6 EH the drugs must be collected every month and self
administered
2. Category II (Re treatment regimen)
This regimen is to prescribe for pts previously treated for more than one
month with SCC or LCC and who are still smear positive.
- Relapses
- Treatment failures
- Returns after default
- PTB patients who become smear positive after 2 months of Rx
- Re turn after default from re-treatment (only once re- treatment again)
- Relapses after re treatment (only once re treatment again)
Rx: Intensive phase 2 S(ERHZ)
- 1 (ERHZ)
Continuation phase 5 E3 (RH) 3 '3' 3 times a week i.e. in alternate days
N.B- The drugs must be taken under the direct observation of a health worker through
out the duration of re-treatment
3. Category II
short course chemotherapy for smear negative PTB, EPTB and TB in children
who are not seriously ill
o New adult patient with smear negative PTB
o New adult patents with EPTB (milder forms)
TB of the lymph nodes
TB osteomyelitis (Bone TB)
TB arthritis
Adrenal TB
TB with unilateral pleural effusion
Children b/n 7 and 14 yrs old with any type of TB, who are not seriously
ill.
Rx: Intensive phase - 2 (RHZ)
Continuation phase 6 (EH)
-
4. Category IV chronic cases

- Multi drug resistant cases of TB, they are given the least priority
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RxINH prophylaxis for life long or second line anti TB drugs e.g.
Clarithromycin/ azithromycine
Ofloxacine
Protionamide /Ethionamide
Cycloserine
Capreomycin
Para aminosalicylic acid (PAS)
- This category is not being implemented in Ethio.
1. Health education esp. for pts how to dispose sputum and MOT
2. Chemotherapy of cases
3. Chemoprophylaxis for contacts
INH for 06 months blindly or
INH for 03 months then do PPD test
PPD test +ve continue for 03 months
PPD ve stop INH and give BCG for the future
4. Immunization of infants with BCG
5. Educate the public about the modes of disease transmission and methods of
control
- Improved standard of living
- Adequate nutrition
- Healthy housing, ventilation and sunlight exposure (windows open and
transparent)
- Environmental sanitation
- Personal hygiene & Active case finding and Rx.
6. Isolation of PTB +ve case = decreases infectivity
Leprosy (Hansen's disease)

Definition A chronic bacterial disease primarily of the skin, peripheral nerves and in
lepromatous patients, the upper air way and the eyes.
Infections agent: M. leprae, acid fast, rod shaped bacillus
EPI: Although common in rural tropics and subtropics, socio-economic condition may be
more important than climate itself. Endemic in south and southeast Asia, tropical Africa
and Latin America.
Leprosy affects all ages and both sexes. The age group mainly affected is between 15-45
yrs. There are however special groups that are more vulnerable to developing the disease.
Factors related to poverty increase the risk of developing disease.
Under normal circumstance only a very small proportion (less than 5%) of all individuals
who are infected by the leprosy bacilli will develop the disease during their life. In the
majority of people, the immunological defence kills all the bacilli. The disease has a long
incubation period, on average ranging from 3 to5 years, but it may vary from 6 months
to more than 20 yrs. Leprosy can cause severe disability mainly as a result of peripheral
nerve damage.
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Reservoir: untreated multi-bacillary leprosy pts discharging bacilli are the main
reservoir of the disease
Mode of transmission: - Not clearly established.
House hold and prolonged close contact appear to be important. Millions of bacilli are
liberated daily in the nasal discharges of untreated lepromatous pts.
Cutaneous ulcers in lepromatous pts may shed large No of bacilli. Organisms probably
gain access (entrance) through the URTI and possibly through broken skin.
In children less than one year of age, transmission is presumed to be transplacental.
I/P: 8 mouth to 20 yrs
POC: Infectiousness is lost in most instances with in 3 months of continuous and regular
Rx with dapsone or clofazmin and with in 3 days of rifampicin Rx.
Susceptibility and resistance: the presence and format leproly depend on the ability to
develop effective cell mediated immunity.
Clinical Manifestations: vary b/n two polar forms: lepromatous and tuberculoid leprosy.
Lepromatous (multibacillary form)
Nodules, papules, macules and diffused infiltrations are bilaterally symmetrical and
usually numerous and extensive (six or more skin lesions)
Involvement of the nasal mucosa may lead to crusting, obstructed breathing and epistasis.
Ocular involvement leads to iritis and keratitis.
Tuberculoid (paucibacillary form) skin lesions are single or few, are to five leprosy
skin lesions sharply demarcated, anaesthetic or hyperaesthetic and bilaterally
symmetrical, peripheral nerve involvement tends to be sever.
Borderline
Has features of both polar form and is more liable to shift towards the lepromatous
form in untreated patients and toward the tuberculoid form in treated patients
Diagnosis cardinal signs for the diagnosis of leprosy are:1. Hypo-pigmented or reddish skin lesion(s) with definite loss of sensation
2. Definitively enlarged nerves at the sites of predilection and/or damage to the
peripheral nerves, as demonstrated by loss of sensation and weakness of the
muscles of hands, feet or face.
3. The presence of AFB positive skin smears
N.B. The finding of one of these three cardinal signs is diagnostic for leprosy.
The main aim of case-finding is to:
1. Diagnose and treat leprosy cases early, before irreversible damage has occurred.
2. Interrupt transmission of the disease
3. Prevent the occurrence of leprosy related disability
A pt is suspect for leprosy when presenting with
1. Reddish patches on the skin
2. loss of sensation on the skin
3. Numbness and tingling of the hands and/or the feet
4. weakness of eyelids, hands and feet
5. painful and/or tender nerves
6. Burning sensation in the skin
7. Painless swelling in the face and ear lobes
8. Painless wounds or burns on the hands or feet.
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TREATMENT
MDT regimen for MB leprosy
Drugs
0-5yrs
Rifampicin
300mg
Clofazimine
100mg
Clofazimine
50 mg twice
a week
Dapsone
25 mg
6-14yrs
450mg
150mg
50mg every
0ther day
50mg
>15yrs
600mg
300mg
50mg daily
6-14yrs
450mg
50mg
>15yrs
600mg
100mg
100mg
MDT regimen for PB leprosy

Drugs
Rifampicin
Dapsone
0-5yrs
300mg
25mg

1. H/E
2. Case detection and early Rx (particularly infectious mutibacilary)
3. Avoid contact with pt (isolation)
4. Disinfection of articles in contact with nasal discharges of infections pt
UNIT 5
Arthropod-borne
(Intermediate host-borne)or vector borne
diseases
Introduction
Generally speaking a vector is any carrier of disease specially invertebrate hosts (insects
or snails).
Vector borne disease
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1. Mosquito borne diseases

- Malaria
- Filariasis
- Yellow fever
2. Flea-borne Diseases
- Plague
- Endemic typhus (flea-borne typhus)
3. Louse-borne Diseases
- Epidemic typhus
- Relapsing fever
4. Snail-borne Diseases
- Shistosomiasis
- Guinea worm infection (Dracunculiasis)
MALARIA
Definition: Malaria is an acute infection of the blood caused by protozoa of the
genus plasmodium.
Infectious agent
- Plasmodium falciparum/ malignant tertian: invades all ages of RBC, RBC
cycle is 42 hrs
- Plasmodium vivax /benign tertian: invades reticulocytes only. RBC cycle
is 48 hrs
- Plasmodium ovalae /tertian: invades reticulocytes only, RBC cycle is
48hrs
- Plasmodium malarial /quartan malaria: invades reticulocytes only. RBC
cycle is 72 hrs
EPI- Endemic in tropical and subtropical countries of the world. Affects 40% of the word
population
Children less than 5 yrs of age, pregnant women and travellers to endemic areas are risk
groups.
P. falciparum 60% and p. vivax 40% are common in Ethiopia.
Reservoir- humans
- By the bite of an infective female anopheles mosquito which sucks blood
for egg maturation
- Blood transfusion, hypodermic needles, organ transplantation, and mother
to fetus transmission is possible.
- Female Anopheles mosquitos are common vectors in Ethiopia.
Incubation period Varies with species
- P. falciparum-7-14days
- P. vivax -8-14 days
- P. Ovalae-8-14 days
- P. Malariae -7 -30 days
Period of communicability
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Mosquitoes are infective as long as infective gametocytes are present in the blood of
patients. Once infected, mosquito remains infective for life
Susceptibility is universal except in some host resistance factors.
Non specific factors
- Hyperpyrexia-which is said to be schizonticidal
- Sickle cell traits are resistant to p. falciparum
- Because of passive immunity infants are resistant in early life.
- Chills, rigor, fever, head ache, diarrhoea, hallucinations, abdominal pain,
aches, renal or respiratory symptoms & jaundice etc
Diagnosis
- Clinical Manifestations and epidemiological grounds
- Blood film for hemo parasites
- Chest x-ray to rule out pneumonia
Treatment
Management of simple P.falciparum malaria
1. For non pregnant mothers, Adults, and children >5kg
Artemether-Lumefantrine two times daily for 3 days (4 tabs PO BID for 03 days)
2. For pregnant mothers and children <5kg
- Quinine three times daily for 7 days (600mg PO TD for 07dys)
Management of severe (Complicated) P.falciparum malaria
1. Quinine loading dose (20mg/kg) in 500cc D/w to run over 4hrs, 4hrs interval of
rest
2. Quinine maintenance dose (10mg/kg) in 500cc D/W to run over 4hrly until the pt
can take po. At least for the 1st 48 hrs.
3. Give IV glucose 40% (IV push or in the bag) simultaneously with quinine.
4. Nursing Management
5. Discharge the pt with quinine po or Artemether-Lumefantrine for the remaining
period of Rx
6. A loading dose should not be used in pts who has taken any anti malarial in the
preceding 24 hrs or mefloquine with in preceding 7 days.
Management of other forms of malaria
- Chloroquine po daily for 3 days (4,4,2)
Complications
1. Cerebral malaria in a pt with falciparum malaria
2. Anaemia (Hg<5g/dl)
- Due to Acute destruction of RBC & Spontaneous bleeding
3. Renal failure
4. Hypoglycemia (BGL<40g/de)
5. Fluid, electrolyte and acid- base disturbances
6. Pulmonary edema
7. Circulatory collapse, shock
8. Spontaneous bleeding
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9. Hyper pyrexia Hyper parasitemia

- Parasite load or density above 5% or +++++
10. Malarial haemoglobinuria
1. Chemo prophylaxis for travellers to endemic areas
2. Vector control
- Avoiding mosquito breeding sites
- DDT spray or other chemicals
- Personal protection against mosquito bite (use of bed net & mosquito
repellent creams)
3. Chemo therapy of cases
Filariasis
Definition: A disease caused by the reaction of the body to presence of worms in the
lymphatic system
Infectious agent Nematodes
Wucheriria Bancrofti (vectors are culex Anopheles mosquito)
EPI
Widely prevalent in tropical and subtropical areas. It is found in Gambella region
(western Ethiopia)
Reservoir: Humans
Mode of transmission: - by bite of mosquito harbouring infective larvae.
Incubation period: one month.
Period of communicability: microfilariae may persist in human for 5-10 year or longer
after infection. The mosquito becomes infective about 12-14 days after an infective blood
meal.
Susceptibility and resistance: universal. Repeated infections may lead to the severe
manifestations such as elephantiasis.
The presence of worms in the lymph vessels causes allergic reaction.
Three phases may be distinguished.
Acute phase = Lymphadenopathy, Fever, Eosinophilia
Sub acute phase= This occurs after about one year following acute phases.
- lymphangitis, epididymitis. Recurrent attacks will sooner or later lead to
hydrocele.
Lung symptoms may be seen
Chronic phase
- After many years of repeated attacks, lymph glands and lymph vessels
become obstructed; as a result lymphedema is seen in the legs
(elephantiasis) or scrotum. But may also be present in vulva, breasts, or
arms.
Diagnosis
- Clinical and epidemiological grounds
- History of travel to and residence in endemic areas.
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Microfilaria in the peripheral blood film (B/F). That is, microfilarial

appears in the peripheral blood during the night (nocturnal) in most parts
of the world
Treatment
* Diethyl carbamazine (DEC)
- Day 1
50mg
- Day 2
50 mg Po TID
- Day 3
100 mg Po TID
- Day 4-14- 2mg/kg Po TID
OR
* Ivermectin 150-200 mcg/kg/d PO as single dose; repeat q2-3mo.
* Refer the pt for surgical Rx of hydrocele.
1. Reducing the vector population
2. Mass and selective Rx
3. Personal protection against mosquito bite
Epidemic Typhus (Louse -borne typhus)

Definition: An acute rickettsial disease often with sudden onset.
Infectious agent :- Rickettsia Prowazeki
Epidemiology
Occurrence- In colder areas where people may live under unhygienic conditions and are
louse-infected. Occurs sporadically or in major epidemics, for example during wars or
famine, when personal hygiene deteriorates and body lice flourish.
Reservoir- Humans. Infected lice die and dont serve as a reservoir.
Mode of transmission- The body louse and head louse are infected by feeding on the
blood of a patient with acute typhus fever. Infected lice excrete rickettsiae in their feces
and usually defecate at the time of feeding. People are infected by rubbing feces or
crushed lice into the bite or into superficial abrasions (scratch inoculation).
Incubation period- From 1 to 2 weeks, commonly 12 days
Period of communicability- Patients are infective for lice during febrile illness and
possibly for 2-3 days after the temperature returns to normal. Infected lice pass rickettsiae
in their feces within 2-6 days after the blood meal; it is infective earlier if crushed. The
louse die within 2 weeks after infection.
Rickettsiae may remain viable in the dead louse for weeks.
Susceptibility and resistance- Susceptibility is general. One attack usually confers longlasting immunity.
Early symptoms of fever, headache, mayalgia, macular eruption appear on the body.
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Patient may have pneumonia, renal or CNS involvement, gastrointestinal disease, skin
rash singly or in
combination.
Disease usually terminates by rapid lysis after 2 weeks of fever.
Diagnosis
Based on clinical and epidemiologic grounds
Serologic test (weil-felix agglutination test)
Treatment
Treatment consists of either tetracycline (25 mg/ kg/d in four divided doses) or
chloramphenicol (50100 mg/kg/d in four divided doses) for 410 days.
1. Delousing of clothes by insecticides or dipping into boiling water
2. Public education on personal hygiene
3. Treatment of cases
4. Chemoprophylaxis for contacts.
Endemic typhus (Flea-borne typhus) (Murine Typhus fever)

Definition: A rickettsial disease whose course resembles that of louse borne typhus, but
is milder.
Infections agent - Rickettsia typhi ( Rickettsia mooseri)
EPI occurs world wide, found in areas where people and rats occupy the same
buildings.
Reservoir: Rats & mice. Infection is maintained in nature by a rat flea-rat cycle.
* Infected fleas defecate rickettsia while sucking blood, contaminating the bite site and
other fresh skin wounds.
* Rarely inhalation of dried infective flea feces.
Incubation period = commonly 12 days
Not directly transmitted from person to person. Once infected, fleas remain so for life (up
to 1 year)
Susceptibility is general. One attack confers immunity
- Prodromal symptoms of head ache, myalgia, arthralgia nausea, and
malaise for 1 to 3 days. Then abrupt onset of chills and fever. Nearly all
patients experience nausea and vomiting early in the illness.
- The duration of untreated illness averages 12 days.
- Rash is present in only 13% of patients
- Pulmonary involvement: non productive cough and pneumonia.
Dx
- Epidemiological ground
- Weil felix agglutination test (serology)
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Rx - .Doxycycline (single dose) OR

- Chloramphenicol or TTC 500mg Po QID for 7days
1. Destroy rats from burrows and harbourages
2. Use insecticides to abolish flea from living quarters
3. Treatment of patients.
Relapsing fever
Definition: An acute infectious bacterial disease characterized by alternating febrile
periods (recurrent pyrexia attacks)
Infections agent
Borrelia recurrentis causes of louse borne relapsing fever
Borrelia duttoni cause of tick borne relapsing fever
EPI Occurs in Asia, eastern Africa (Ethiopia and Sudan) the high lands areas of central
Africa and South America.
Reservoir: Humans for Borrelia recurrentis;
Wild rodents and soft ticks for tick borne relapsing fever.
By crushing an infected louse so that it contaminates the bite wound or an abrasion
Incubation period usually 8 days
Period of communicability: Louse becomes infective 4-5 days after ingestion of blood
from an infected person and remains so for life (20-40days)
Susceptibility is general.
Clinical manifestations
- Sudden onset of illness with chills, fever and prostration, head ache,
myalgia and arthralgia.
- There may be nausea and vomiting, jaundice and liver swelling.
After 4-5 days the temperature comes down, the patient stays free for 8-12 days and then
a relapse follows with the same signs but less intense. In untreated cases there may be up
to 10 relapses.
Diagnosis
- clinical and epidemiological grounds
- Blood film(B/F)
Treatment
1. Admit the pt
2. Open vein (start IV line with Normal saline) before administering penicillin
3. Administer 400,000 IU procaine penicillin IM stat
4. TTC 500 mg po QID during discharge for 3 days
5. Chloramphenicol in infants and children can be used in place of TTC
6. Nursing care (monitor vital signs & any Reaction, shaving hair)
1. Control of vectors (louse)
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2.
3.
4.
5.
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Personal hygiene
H/E about hygiene and modes of disease transmission
Delousing of pt's clothes and his/her family
Chemotherapy of cases and chemoprophylaxis (TTC) for contacts when risk of
acquiring the infection is high
UNIT 6
Prevention and control of zoonotic diseases
Introduction
Infectious diseases transmitted between vertebrate animals and men are called zoonosis.
For most of these diseases, man is a dead end of the transmission cycle. This means under
normal conditions, man will not infect other human beings
1. When animals used as a food
- Teaniasis
- Brucellosis
- Trichinellosis or trichinosis
- Toxoplasmosis
2. Animal Bite diseases
- Rabies
3. Direct contact diseases
- Anthrax
4. Animal reservoir diseases
- Leishmaniasis
- African trypanosomiasis
Teaniasis
Definition: -Teaniasis is an intestinal infection with the adult stage of large tapeworms.
Cysticercosis is a tissue infection with the larval stage
Infection agent Taenia saginata (beef take worm)
Taenia solium (pork tape worm)
EPI Frequent where beef or pork is eaten raw or insufficiently cooked and where
sanitary conditions permit pigs and cattle to have access to human faeces.
Reservoir
Humans are definitive hosts of both species of Taenia; cattle are the intermediate hosts
for Taenia saginata and pigs for Taenia solium.
Eggs of Taenia saginata passed in the stool of an infected person are infectious
only to cattle. They develop into "cysticercus bovis"(larva) in the flesh of the cattle.
In human, infection follows after ingestion of raw or under corked beef containing
cysticerci. The adult worm develops in the intestine.
Or in case of Taenia solium the larvae penetrate the intestinal wall and are carried
to the various tissues where they develop to produce the human disease of cysticercosis
and even neurocysticercosis.
I/P: - 8-14 weeks
Period of communicability: - T. saginata is not directly transmitted from person to
person but T. solium may be. Eggs may remain viable in the environment for months.
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Susceptibility and resistance: - susceptibility is general.

Clinical Manifestation (for both species)
Symptoms of cysticercosis may appear after some days and stay for 10 years after
infection
Passage of proglottidis (segmented adult worms) in the faeces and perianal discomfort.
Minimal or mild abdominal pain or discomfort, nausea, change in appetite, weakness and
wt loss Epigastria discomfort, nausea a sensation of hunger, wt loss, nervousness, and
anorexia.
Diagnosis - Identification of proglottidis (segments)
- Eggs in faeces or anal swab
- Palpable subcutaneous cysticercus in microscopic exam of an excised tissue
Treatment - Single dose of praziquantel is highly effective
- Niclosamide or
- Dechlorophil or
- Mebendazole or
- Albendazole
T. Solium
Rx is the same as to T saginata but praziquantel can evoke an inflammatory response in
the CNS if cysticercosis is present in CNS.
Cysticercus Mgt - Combination of praziquantel and Albendazole
- Surgery and supportive medical MGT
- High dose of glucocorticoid can be used to decrease inflammation.
1. prevent faecal contamination of soil, water, human & animal food
2. Cook beef and pork thoroughly
3. Use latrines
4. Identification and immediate RX of Cases
5. Freezing of pork/ beef below -5oc for more than 4 days kills the cysticerci
effectively or cooking to a To of 56oc for 5 minutes destroys cysticerci
6. Deny swine access to latrines and human faeces
Brucellosis
Definition: Brucellosis is a systemic bacterial disease with acute or insidious onset
transmitted to humans from infected animals
Infection agent
- Brucella melitensis (most common world wide) acquired primarily from
goats, sheep and camels
- B. Abortus from cattle
- B. Suis from pigs
- B. Canis from dogs
EPI Occurs world wide. Predominantly an occupational disease of those working with
infected animals or their tissues especially farm workers, veterinarians and abattoir
workers, which is more frequent among males.
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Reservoir- cattle, swine, goats and sheep, pet dogs

Mode of transmission: by contact with tissues, blood, urine, vaginal discharges, aborted
foetuses and especially placentas (through breaks in the skin). Most commonly through
ingestion of raw milk and dairy products from infected animals (raw meat or bone
marrow). Airborne infection occurs rarely
Incubation period: - usually 1-3 weeks
Period of communicability: - no evidence of communicability from person to person.
Susceptibility and resistance - General
- Abrupt onset of Fever, chills, diaphoresis, head ache, myalgia, fatigue,
anorexia, joint and low back pain, wt loss, constipation, sore throat, and
dry cough
- Often no abnormalities and pt looks well.
- Some patients are acutely ill, with pallor, lymphadenopathy,
hepatosplenomegally, arthritis, spinal tenderness, epididymo orchitis, skin
rash, meningitis, cardiac murmurs or pneumonia.
Diagnosis
- Epidemiological & clinical features
- Serology-raised levels of B. agglutinin
- Blood or bone marrow culture
Treatment- Doxycycline + Streptomycin for 2 weeks followed by Doxycycline +
Rifampcin for 4-8 weeks is the most effective regimen.
- In pregnancy and in children less than 7 years bacterium and rifampcin for
8-12 weeks
1. Educate people not to drink untreated milk or eat products made from untreated
milk.
2. Educate farmers and slaughter house workers and those in meat processing plants
and butcher shops as to the nature of the disease and the risk in the handling of
carcasses and products of potentially infected animals
3. Educate hunters to use barrier precaution (gloves and clothing)
4. Pasteurize milk; cook meat and bone well
5. Proper disposal of placenta, discharges or foetus from an aborted animal.
Disinfect contaminated areas.
Toxoplasmosis
Definition: Toxoplasmosis is a systemic protozoal disease that can be either acute or
chronic type with intracellular parasite
Infectious agent: -Toxoplasma Gondi(protozoa)
EPI - It occurs world wide in mammals and birds. Infection in man is common
Reservoir
The definitive hosts are cats and other felines. They acquire the infection mainly from
eating infected rodents or birds. The intermediate hosts include sheep, goats, rodents,
cattle, chicken, birds & man
1. Ingestion of raw or undercooked infected meat containing Toxoplasma cysts
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2. Ingestion of food, drink or from hands contaminated with faeces of an infected cat
3. Tran placental
4. Blood transfusion & Organ transplantation
The parasites form tissue cysts, most commonly in skeletal muscle, myocardium,
and brain; these cysts may remain throughout the life of the host.
I/P: - from 10-23 days.
Not directly transmitted from person to person, except in utero.
Cysts in the flesh of an infected animal are infective if eaten uncooked
Susceptibility to infection is general. Most infections are asymptomatic. Pt taking
immune suppressive therapy or pts with AIDS are at risk of developing the disease.
Symptoms are generally mild, except in immuno suppression or some rare cases.
The acute form of this disease is characterized by fatigue, lymphadenitis, chills, fever,
head ache and myalgia. In addition to chronic disease, the pt may develop maculopapular
rash, encephalomyelitis and hepatitis; retinochorditis with subsequent blindness has been
known to occur on rare occasions
Diagnosis - Clinical sign and symptom
- Serological test & Cell culture
Treatment
1. No treatment for a healthy immunocompetent host; except in sever disease.
2. The preferred Rx for those with severe symptomatic disease is pyrimethamine
combined with sulfadiazine or fansider and folinic acid for four weeks.
3. For pregnant women, spirmycin is commonly used to prevent placental infectionTreatment for infants
1. Pyrimethamine
2. Sulfadiazine
3. Folinic acid
1. Avoid eating under cooked or raw meat and
2. Avoid cyst-contaminated materials
3. Meat should be heated or frozen well
4. Hands should be washed thoroughly after work in the garden and all fruits and
vegetables should be washed
5. Discourage cats from hunting
6. Dispose cats faeces daily
7. Pts with HIV/ AIDS who have severe symptomatic toxoplasmosis should receive
prophylactic Rx (pyrimethamine, sulfadiazine, folinic acid) throughout their life
span.
Rabies
Definition: It is acute viral encephalomyelitis (attacking brain and meninges).It is
almost 100% fatal if untreated.
Infections agent-Rabies virus
EPI-occur world wide. It is primarily a disease of animals (zoonotic).
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Reservoir: - Dog, wild carnivores and bats

Mode of transmission: - Transmitted with saliva of rabid animal introduced by a bite
or scratch.
I/P- Usually 3-8 weeks
POC- 3-7 days before the disease and throughout the course of the disease.
Susceptibility & resistance: - General
Clinical Management
1. Prodromal phase:-A sense of apprehension, head ache, fever and nausea,
abnormal sensation at the site of inoculation (bite)(paraesthesia, tingling
sensations at the bite site)
2. Excitatory phase or aerophobia: slightest sound or wind excite the victim,
irritability, restlessness, nervousness, tendency to bite, are some of the symptoms
3. Paralytic phase: - spasm of swallowing muscles leads to drooling of saliva and
fear of water (hydrophobia). Delirium and convulsions. Death is often due to
respiratory muscle paralysis.
Diagnosis- history of bite by known rabid animal.
- The rabid animal usually dies in 10 days.
Treatment
1) Wound care
- Wash the wound with soap and water thoroughly to decrease the viral load
- If there is bleeding cover the wound
- Never suture the wound.
2) Start anti rabies vaccine immediately if it is proved to be rabid animal bite.
1. Immunize all dogs and cats
2. Detain & clinically observe for 10 days any healthy appearing dog or cat known
to have bitten a person
3. Post exposure prophylaxis
4. Keep dogs and cats at home
5. Destroy stray animals where rabies is endemic
Definition: An acute bacterial disease usually affecting the skin & rarely the
oropharynx, lowers respiratory tract, mediastinum or intestinal tract.
Infections agent Bacillus anthracis, spore forming bacteria
EPI-occurs world wide. It is Primarily a disease of herbivores. Humans and
carnivores are incidental hosts. Primarily an occupational disease who process &
hides, hair (esp. from goats), bone and bone products and wool: and of veterinarians
and agriculture and wild life workers who handle infected animals.
Reservoir: - Animals, normally herbivore. The spores of B. anthracis, are very
resistant to adverse environmental conditions and disinfections.
1. Cutaneous anthrax: contact with tissues of infected animals (cattle, sheep, goats,
horses, pigs and others). Contamination with hair, wool, hides, or products made
from them such as drums or brushes or contact with soil associated with infected
animals.
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2. Inhalation anthrax: - Inhalation of spores in risky industrial processes such as

tanning of hides, or wool or bone processing, where aerosols of B. anthracis
spores may be produced.
3. Intestinal and oropharyngeal anthrax: ingestion of contaminated meat; but not
milk.
- Vultures have been reported to spread the organism from one area to another
IP: - Most cases within 48 hours
POC: - Transmission from person to person is very rare. Articles and soil contaminated
with spores may remain infective for decade.
Susceptibility & resistance - Uncertain
Clinical Manifestation Is different according to the site of infection
1. Cutaneous anthrax
- Approximately 95% of human cases of anthrax are cutaneous
- Small red macules & papule appear
- An ulcer with blackened necrotic eschar surrounded by oedema.
-The lesion may be pruritic but painless
- regional lymphadenitis is common.
- Spontaneous healing occurs in 80-90% of untreated cases but edema may
persist for weeks
- In 10-20% of cases, infection progresses, bacteria develops and is often
associated with high fever sever shock and rapid death.
2. Inhalation anthrax
- Increasing fever, dyspnoea, stridor, hypoxia, and hypotension usually
leading to death with in 24 hrs
3. Gastrointestinal Anthrax
- Fever, nausea and vomiting, abdominal pain, bloody diarrhoea, and
sometimes rapidly developing ascites.
- Diarrhoea is occasional and massive in volume
- Usually death will occur within 48 hours.
4. Oropharyngeal anthrax
- Fever, sore throat, dysphagia, painful regional lymphadenopathy,
Inflammation of the tonsil, toxaemia, respiratory distress may be evident
Diagnosis
- Clinical data
- Gram stain of wound discharge
- Culture from the wound discharge or blood
Treatment
For cutaneous anthrax
1. Penicillin-G IV until edema subsides and with subsequent oral penicillin to
complete the course (adults).
=>For penicillin-sensitive adults Ciprofloxacin, erythromycin, TTC, CAF can be
substituted.
2. Clean and cover the cutaneous lesions
For inhalation anthrax, GI and Anthrax meningitis
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- High dose of IV penicillin is recommended

1. Decontaminate wool and goats hair and improvement of working condition for
handlers of animal products
2. Vaccination of humans & herbivores
3. Carcasses of animals should be buried intact or burned
4. Butchering of infected animals should be avoided
5. Dust control and proper ventilation in hazardous industries
6. Treat all animals exposed to anthrax with TTC or penicillin
Tetanus
Definition: - Tetanus is an acute disease caused by a toxin produce by tetanus bacilli and
is characterized by painful contraction of voluntary muscles
It is also called lock jaw.
Infectious agent
Clostridium Tetani. It is Gram negative rods, Spore forming & anaerobe organism.
Epidemiology
- Move common in rural than town
- It is almost 100 % fatal if untreated
- Normally tetanus bacilli live in the bowel of man & animal
* The source of infection is soil, street dust & Faeces containing spores
Tetanus is more likely to develop is patents with deep penetrating necrotic wound
Wounds which favor tetanus are
Umbilical stump in new born (necrosis)
Crush wound (Necrosis ,poor blood supply)
Stab wound (deep)
Wound with foreign bodies (always infected)
Human & animal bite
Burns (Necrosis , poor blood supply )
Surgical wound (from dressing instrument)
Chronic ear discharge
Endogenous infection (during bowl surgery)
Tetanus bacilli harmful only when they are lodged in the tissue b/c from
there the toxin can be transported to CNS.
Incubation period
- The usual I/P 5-21 days
- But it can range from 3 days 3 months
Susceptibility (high risk group)
- New born
- Children
- Farmers
- Any one with dirty wound
- Soldiers
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Clinical Picture
Increased tone of the jaw muscle - causing trismus & risus sardomicus (devils
grin)
Later the spasm become generalized involving all muscles and painful
Sever spasm results in pain, disturbance of swallowing & respiration.
Spasm of the neck muscle resemble neck stiffness of meningitis
Negative neurological signs (no drowsiness, no change in consciousness)
Low grade fever
Arrhythmias, Asphyxia , Cyanosis, pain at wound site ,Risus sardomicus (fixed
smile )Hydrophobia/ photophobia, Stiffness of jaw, Sudden bradycardia,
Irritability, Tachycardia ,Muscle rigidity & sudden cardiac arrest can occur
= Death occurs due to asphyxia due to Spasm of glottis, thoracic muscle & diaphragm
= In the new born first sign of tetanus is
- Inability to suck, spasm, Apnea & cyanosis
- Extended spine with clenched fists & mouth and flexed toes.
Dx - History of the pt.
- Culture from the wound
Complications
-
Respiratory arrest
Cardiac failure
Pulmonary embolism
Secondary bacterial infection
Dehydration
Air way obstruction

Anoxia
Urinary retention
constipation
pneumonia
Management
Patient must be referred to hospital quickly
Spasm: (caused by toxin of bacilli)
- Diazepam (valium) in high dose
- Start with 10-40mg IV + chlorpromazine 20-50mg IM alternately 6 hourly
- When spasm continue more diazepam should be given (max dose 500 mg / day
- Reduce the dose if the pt. is over sedated.
- Or phenobarbitone(100mg 4 hourly) + chlorpromazine (20-50mg IM 6 hourly)
Secondary infection
To combat secondary infection & tetanus bacilli
- Doxycycline
- Crystalline penicillin (1Mil. IU)
- Clindamycin
- PPF(1.2 Mil IU) daily for 5 days
ATS (anti tetanus serum) ( also known as TAT)
- 10,000 units IM /IV for both adult& children
- Do skin test first. Have adrenaline at hand.
Surgical RX
- Look for wound & clean with savalon
- Tracheostomy ( sever case)
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Intensive care unit(ICU)

- Give care in dark & isolated room
- Mouth- mouth respiration if Pt. develops breathing arrest (tetanus do not pass
through mouth to mouth contact)
- Semi-prone position (never on his back)
- Change position every 2 hrs
- Rise to foot of bed to stimulate lug drainage to prevent pneumonia.
Tetanus Toxoid (TT)
- Patients with Tetanus do not develop immunity so they must be immunized with
TT after recovery to prevent re occurrence.
Prevention & Control

Active Immunization (DPT) ( For Infants )
Active immunization with TT ( specially for pregnant women )
Passive protection ATS is only for 10 days so it should not be given with out
active immunization
UNIT 7
Food Borne Diseases (Food Poisoning, Food borne
Intoxications, Food-borne infection)
Introduction
Food-born diseases, including food borne intoxications and food-borne infections, are
terms applied to illnesses acquired by consumption of contaminated food.
Staphylococcal food poisoning(Intoxication)

It is intoxication (not infection) of abrupt and some times violent onset.
Infections agent (toxic agent)
Enterotoxins of staphylococcus aureus.
Staphylococci multiply in food and produce the toxins
Reservoir: Humans & occasionally cows with infected udders .
MOT- By ingestion of a food product containing staphylococcal enterotoxin.
Food handlers infected with S. aureus ( from purulent discharges of an infected finger or
eye, abscesses, nasopharyngeal secretions) will contaminate the food. When these foods
remain at room temperature for several hours before being eaten, toxin producing
staphylococci multiply and elaborate the heat stable toxin.
I/p: 30 minutes to 8hrs, usually 2-4 hrs
POC- not applicable
S/R Most people are susceptible
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- Sudden onset of vomiting and watery diarrhoea

- Fever and abdominal cramp
- If the illness is severe it may require hospitalization
Diagnosis
- short interval between eating and the onset of symptoms
- Culture & detection of enterotoxin from food
Rx. Fluid and electrolyte replacement.
1. Strict food hygiene, hand washing, cleaning of finger nails, cover wounds on the
skin.
2. Reduce food handling time to an absolute minimum, with no more then 4hrs at
ambient temperature. Keep perishable food hot (>600C or cold (below 100C).
3. Exclude people with boils, abscesses and purulent lesion from food handling.
Botulism( Intoxication )
A paralytic disease that begins with cranial nerve and progresses to the extremities.
I/A - Toxin produced by clostridium botulinum (Neurotoxin)
EPI - World wide occurrence. Home canned foods, particularly vegetables, fruits and
less commonly with meat and fish. Outbreaks have occurred from contamination through
cans damaged after processing.
Reservoir - The bacteria is found in the soil and in the intestine of animals
MOT- Food infection in which the toxin is found.
I/P: usually 12-36 hours, some times several days, after eating contaminated food
POC: not communicable
S and R Susceptibility is general
- Illness varies from a mild condition to very severe disease that can result in death
within 24 hours.
- Symmetric descending paralysis is characteristic and can lead to respiratory
failure and death.
- Cranial nerve damage produce diplopia (double vision) dysphasia (difficult in
swallowing) & general body weakness
- Nausea, vomiting, abdominal pain occur following paralysis.
- Dizziness, blurred vision, dry mouth, and occasionally sore throat.
- No fever
- Paralytic ileus, severe constipation and urinary retention are common.
Dx - Afebrile, mentally well patients who have symmetric descending paralysis
- Demonstration of organisms or its toxin in vomitus, gastric fluid or stool
Treatment 1 .Hospitalize the pt and monitor closely
2. Intubation and mechanical ventilation may be needed
3. Antitoxin administration after hypersensitivity test to horse serum
4. Emesis and lavage if short time after ingestion of food to decrease the toxin
Prevention and control.
1. Effective control of processing of canned and preserved food
2. Education about home canning and other food preservation techniques regarding
the proper time, pressure and temperature required to destroy spores.
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3. Adequate refrigeration & boiling canned foods9 Specially vegetables) for at least
10 minutes to destroy botulinal toxin.
4. Canned foods in bulging containers should not be used eaten or tasted.
Salmonellosis (Infection)
A bacterial disease commonly manifested by an acute enterocolitis.
I/A- Salmonella typhimurium and salmonella enteritidis
EPI: It occurs world wide
Reservoir - Animals including poultry, swine, cattle, rodents, pets and humans
MOT- ingestion of food ( specially raw fruits & vegetables raw and under cooked eggs
and egg products, raw milk and its products, poultry) contaminated by faeces of an
infected animal
I/P: from 6-72 hours, usually about 12-36 hours
POC- usually several days to several weeks
S/ R Susceptibility is general and increased by achlorhydria, antacid therapy, GI surgery
, immuno suppression and malnutrition.
S/S. - Self limited fever and diarrhoea (Bloody or dysenteric when colon is involved),
nausea, vomiting, abdominal cramp & leukocytosis
DX Blood culture initially & Stool culture later
Rx Symptomatic ( Mainly fluid replacement & Analgesics)
- If there is an underlying immunosuppressive disease (condition like AIDS,
lymphoma, immunosuppressive treatment) treat the underlying cause
1. Quality testing of the known and commonly contaminated foods
2. Avoid consuming raw or partially cooked ages
3. Wear gowns and gloves when handling stool and urine and hand washing after
patient contact.
VI. Prevention & Control of STI

Syndromic approach to the management of STI
The control of STI, is based on three principles
1. Education on the mode and means of reducing the transmission of STI
2. Provision of effective Management for symptomatic pts with STIs
3. Detection of infection in asymptomatic individuals by screening patients
attending routine services like family planning or antenatal clinics.
Advantages of syndromic case management over etiologic
1. Solves the problem of scarce human resources and lab facilities where these are
significant limitations for mgt based on the identification of the etiologic agent of
a specific STI.
2. Saves the time spent to isolate the specific pathogen and the inaccessibility of
such facilities
3. Saves financial expenditure to get lab services
N.B. The syndromic case met requires identification of distinct syndromes that are known
to be associated with STI rather than identifying specific diseases
* One of the means of controlling AIDS is effective control of STI. Because:
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1. Both infections, share similar epidemiologic determinants

2. STIs increase the susceptibility to infections as well as the spread of HIV.
The public health importance of STIs
The occurrence of STI in an individual is an indicator of unprotected sexual activity that
increases the chance of acquiring another STI including HIV. There fore the
epidemiological determinants of STI and HIV infection are similar b/c both infections
result from risky sexual behaviour. STI promote the spread of HIV in the community; for
instance men with gonococcal urethritis have eight times higher concentration of the
virus in their semen than men without it. This increases the probability of infection in
their partners. Similarly, women with vaginosis have large number of CD4 cells in the
vagina resulting in high chance of acquiring HIV infection. STIs are also important
causes of cervical and penile cancer. Infertility and other obstetric complications like
ectopic pregnancy occur following inadequately treated STIs.
Impact of HIV on conventions STI,
The interaction of HIV and conventional STIs is bi-directional. This is because HIV
affects the Mgt of STI and conventional STIs predispose for HIV infection.
The clinical features of various types of STIs are affected by co-infection with HIV.
Syphilis can have atypical presentation with a tendency to rapidly progress to
neurosyphilis. Atypical lesions of chancroid are common and tend to be less purulent
often with indurations mimicking primary syphilis. The lesions could as well be extensive
and multiple which could be associated with fever and chills. Recurrent or persistent
genital ulcers caused by herpes simplex virus are common among pts with HIV and they
are often multiple and extensive. The Rx of conventional STIs is also affected by
infection with HIV. The risk of Rx failure following single injection of benzathine
penicillin is increased among pts with primary syphilis. Topical antifungal drugs are less
effective and hence oral drugs like ketoconazole are frequently indicated.
Examination of a pt with STI
- Like any other disease, the diagnosis of STIs relies on paper history taking and
physical exam. This entails privacy and confidentiality in order to promote health
seeking behaviour and avoid stigmatization.
- The demographic characteristics of the pt that include age, sex, and marital status
are important components of the history.
- The occupation of the pt is also important because long truck drivers and solders are
at increased risk for STIs. Multiple sexual partnership and history of STIs in the pt
or his/her partner are also important risk factors for STIs.
* Urethral discharge or burning on micturation in men
- Onset, unprotected casual sex, the amount of discharge should be inquired.
* Vaginal discharge in women
- Vaginal discharge is abnormal when the women notice change in colour, amount
and odour. History of STI in her partner, multiple sexual partners and change in
Partner is important risk factor to consider in the history.
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* Genital ulcer in men and women.

The onset, history of recurrence, presence of pain, location and whether the ulcer
is single or multiple should be described in the history.
* Lower abdominal pain in women.
The onset, quality of pain radiation, severity presence of vaginal discharge, last
menstrual period, and systemic symptoms like fever, nausea and vomiting are
essential components of the history.
* Scrotal swelling
The health worker should ask the onset, presence of pain, history of trauma and
for concomitant urethral discharge
* Inguinal bubo.
Presence of pain, ulceration, discharges and the locations of the swelling are
essential components of the history
Common syndromes in STIs

1. Urethral Discharge and/or burning on urination in men
Burning on micturation and urethral discharge are common symptoms of
urethritis
Aetiology
N. gonorrhea
C. Trachomatis
Commonest causes of urethral discharge & dysuria
M. Genitalium
T. Vaginalis
Rare causes of urethritis
U Uraelyticum
Urethritis caused by N-gonorrhoea has usually an acute onset with profuse and
purulent discharge while that of C. trachomitis will be of subacute onset with scanty
mucopurulent discharge. However, mixed infections by both organisms can occur in
20% of pts.
Examination
Look for evidence of spontaneous discharge
-Note the colour, quality, and quantity of the discharge
-The evidence of mild discharge may be crusting at the meatus and meatal redness
should also be sought
-Milk the urethra to bring the discharge forward, if no discharge is found on meatus.
Complications
- Disseminated gonoccocal infection (N.g)
- Prostatitis (N.g)
- Conjunctivitis (both)
- Urethral stricture (both)
- Enhanced transmission of HIV (both)
Mgt
2. Genital Ulcer
-
Primary syphilis, genital herpes, chancroid, LGV, and granuloma inguinale are
common ulcerative lesions of the genitalia in men and women.
Aetiology
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Common causes of genital ulcer are

1. Treponema palidum syphilis
2. Herpes simplex virus herpes genitalia (genital herpes)
3. Haemophilus ducreyi-chancroid
4. Chylamidia trachomatis serovars L1, L2 and L3 LGV
5. Chlymmatobacterium granulomatis GI
Clinical Features
Syphilis (Hard chancre)
- A disease characterized by a primary lesion, a later secondary eruption on the skin
and mucus membranes, then a long period of latency, and finally late lesion, of skin,
bones, viscera, CNS and CVS
Etioiopy Treponema pallidum, a spirochete
Three stages are described in the clinical presentation of syphilis. Genital ulcer occurs in
the primary stage of the disease. It starts as a small papular lesion that rapidly ulcerates to
produce a non tender, indurated lesion with a clean base and a raised edge known as
hard chancre.
The clinical presentation is divided in to three stages
1. Primary syphilis
Consists of hard chancre, the primary lesion of syphilis, together with regional
lymphadenitis. The hard chancre is a single, painless ulcer on the genitalia or
elsewhere (lips, tongue, breasts) and heals spontaneously in a few weeks with out
Rx. The lymph glands are bilaterally enlarged and not painful. There will not be
suppuration.
2. Secondary syphilis
After 4-6 weeks of the primary infection, a generalized secondary eruption
appears, often accompanied by mild constitutional symptoms. These early rashes
tend to be symmetrical, quickly passing and dont itch. These early skin lesions
are highly infective and many spirochetes are demonstrated in them.
3. Tertiary syphilis
This stage is characterized by destructive, non-infectious lesions of the skin,
bones, viscera, and mucosal surfaces. Other disabling manifestations occur in the
CVS (aortic incompetence, aneurysms) or CNS (dementia paralytica, tabes
dorsalis)
Herpes genitalia (Genital herpes)
Latency and frequent recurrence characterise herpes genitalias producing a life long
infection after the primary infection. The lesions are painful initially presenting
erythematous macules, which then progress to vesicles, pustules, ulcers and finally
crusts. Prolonged and severe disease with extensive tissue involvement and higher
rate of dissemination occur in patients with HIV infection.
First episode primary genital herpes is x-zed by fever, head ache, malaise and
myalgias.
Pain, itching, dysuria, vaginal and urethral discharge, and tender inguinal lymph
adenopathy are the predominant local symptoms.
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Chancroid /soft chancre/

- It is a bacterial infection characterized by single or multiple painful necrotizing
ulcers at the site of infection. The lesions are painful progressing from a small
papule to pustule and then ulcer with soft margins described as soft chancre.
Inguinal adenopathy that becomes necrotic and fluctuant (buboes) follow the
ulcer. It is endemic and the commonest cause of genital ulcer in many developing
countries. Most frequently diagnosed in men, especially those who frequently
prostitutes.
LGV
The diseaese starts as a small painless papule that develops to an ulcer. After a week
or so painful regional lymphadenopathy develops with symptoms of fever, chills,
head ache, malaise, anorexia and wt loss.
Elephantiasis of genitalia, scrotum and vulva occur in either sex.
Granuloma Inguinale
It is a chronically progressive ulcerative disease with out systemic symptoms. The pt
usually presents with a non-supportive genital lesion, which develop from a small
firm papule to a painless ulcer with a beefy red appearance and non purulent base.
Complications
1. Syphilis Secondary syphilis
- Latent syphilis
- Aortitis with valvulitis
- Aortic aneurysm
- Gumma
- Neurosyphilis
2. Genital herpes Recurrence
- Aseptic meningitis and encephalitis
3. Chancroid Penile auto amputation
4. LGV Genital edema
- Salphingitis
- Infertility
- PID
5. GI Genital pseudo elephantiasis
- Adhesion
- Urethral, vaginal or rectal stenosis.
Recommended Rx for genital ulcer
B. Penicillin 2.4 miu lm stat
or ( in penicillin allergy)
Doxycycline 100mg BID for 15 days Plus
Erythromycin 500 mg po QID for 7 days.
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3. Vaginal Discharge
Causes of vaginal discharge
1. Neisseria gonorrhoea
2. Chylamydia trachomatis
3. Trichomonas vaginalis
4. Gardnerella vaginalis
5. Candida albicans
The first three are sexually acquired and the last two are endogenous infections. The first
two cause cervicitis while the last three cause vaginitis.
The presence of vaginal discharge may represent either cervical or vaginal pathology.
There fore, the initial evaluation of a pt that has vaginal discharge includes risk
assessment and clinical examination with a speculum to determine the site of infection
Vaginitis
Bacterial vaginosis, vaginal thrush or trichomoniasis are the usual causes of vaginitis.
Bacterial vaginosis and trichomoniasis are more frequent among sexually active women
while vaginal thrush occurs when there is impairment of local or systemic defence
mechanisms. Risk assessment is usually negative and cervix looks healthy and discharge
is not coming from the cervical opening in isolated vaginitis
Cervicitis
The presence of purulent or mucopurulent exudation from the cervical os frequently
indicates gonococcal or chlamydial, infection. The risk factors include age less than 25
yrs, single status, multiple sexual partners, a change of sexual partner recently and history
of STI previously either in the pt or in the partner. On speculum examination the presence
of redness, contact bleeding, spotting and endocervical discharge suggests the diagnosis
of cervicitis
Complications
1. PID
2. PROM
3. PTL (preterm labour
Recommended treatment for V. discharge
Risk assessment positive
Ciprofloxacin 500 mg po stat
Or
Spectinomycin 2g Im stat
Plus
Doxycycline 100mg po BID for 7 days
Plus
Metronidazole 500 mg po BID for 10 days
Risk assessment negative
Metronidazole 500 mg PO BID for 7 days
Plus
Clotrimazole vaginal tab 200mg at bed time for 3 days
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4. Lower abdominal pain due to PID

PID refers to an acute clinical syndrome that results from ascending infection from the
cervix and or vagina. The upper structures of the female genital organs are affected. The
term PID includes endometritis, parametritis, salphingitis, oophoritis, pelvic peritonitis,
tuboovarian abscess and inflammation around the liver, spleen, or appendix.
The common pathogens associated with PID, which are transmitted through sexual route,
include N. gonorrhoea, C. trachomatis, M. Homonis and bacteroides. Other organism like
streptococcus species E.coli and H. influenza may some times cause PID but their
transmission is not via the sexual route.
PID and STI share many of the same risk factors and in most instances PID is caused by
STIs.
Clinical Features
- The occurrence of vaginal discharge may be an antecedent event and supports the
diagnosis of PID.
- Bilateral lower abdominal pain or pelvic pain is the most common clinical
complaints but ranges from abrupt and fulminant presentation to a sub acute form
with mild symptoms often described as dull pain.
- Lower abdominal and adenexal tenderness together with cervical excitation
tenderness are indicative of PID.
- Other causes of lower abdominal pain like appendicitis ectopic pregnancy, and
cholecystitis should be ruled out by proper examination.
Recommended Rx for PID
0utpatient
Ciprofloxacin 500 mg PO stat
Or
Spectinomicin 2g Im stat
Plus
Doxycycline 100mg PO BID for 14 days
Plus
Metronidazole 500mg PO BID for 14 days
- Remove IUD and do counselling for contraception
- Admit if there is no improvement with in 72 hrs
Inpatient
Ciprofloxacin 500mg PO BID
Or
Spectinomicin 2g IM BID
Plus
Doxycycline 100mg PO BID for 14 days
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Plus
Metronidazole 500mg PO BID for 14 days
Inpatient regimen is given for at least 48 hrs after the pt clinically
improves
After discharge from hospital the pt hast to continue with the oral Rx.
5. Scrotal swelling
The cause of scrotal swelling can vary depending on the age of the pt. Among pts who are
younger than 35 years, the swelling is likely to be caused by N. gonorrhoea and c.
trachomatis. However scrotal swelling among patients older than 35 yrs is commonly
caused by gram-negative organisms and rarely TBc. Other infectious causes of scrotal
swelling could be brucellosis, mumps, onchocerciasis or infection with w. bancrofti.
It is important to exclude other causes of scrotal swelling like testicular torsion, trauma
and incarcerated inguinal hernia as they may require urgent referral for proper surgical
evaluation and Rx.
Complications
- Epididymitis
- Infertility
- Impotence
- Prostatitis
Recommended Rx of scrotal swelling
The Rx of scrotal swelling suspected to be of STI origin is similar to that of a urethral
discharge.
Ciprofloxacin 500mg PO stat
Or
Spectinomycin 2gm IM stat
Plus
Doxycycline 100mg PO BID for 7days
Or
TTC 500mg PO BID for 7 days
6. Inguinal bubo
It is swelling of inguinal lymph nodes as a result of STI, it should be remembered that
infections on the lower extremities or in the perineum could produce swelling of the
inguinal lymph nodes
The common sexually transmitted pathogens that cause inguinal swelling include T.
pallidum, C. trachomatis, (serovars L1, L2, L3), H. ducreyi and C. granulomatis. However,
unlike other causes of inguinal bubo, syphilis doesnt cause necrosis and abscess
collection in the lymph nodes. In conditions where the clinical examination doesnt reveal
fluctuant bubo, syphilis should be considered and be treated accordingly. Surgical
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incisions are contraindicated and the pus should only be aspirated using a hypodermic
needle.
Recommended Treatment
B. Penicillin 2.4 MIU IM stat
Plus
Erythromycin 500mg PO QID for 15 days
Or
Co-trimoxazole double strength tablet PO BID for 15 days.
7. Neonatal infections due to STIs

1. Congenital syphilis
Infection of the fetus by T. pallidum usually occurs starting from the second
trimester of pregnancy. The infection may result in still birth or produce multiple
systemic complications, which affect the infant after birth. Early manifestations of
congenital syphilis occur in the first two years of life and may include fever, nasal
discharge, hepatosplenomegally or failure to thrive. The late onset manifestations
of congenital syphilis include keratitis, deafness, Hutchinson's teeth or bone
damage.
Treat any infant whose mother had untreated or inadequately treated syphilis at
delivery regardless of signs and symptoms in the infant
Treatment crystalline penicillin 50,000 iu/kg IV daily for 10 days
Or
PP.50, 000 iu/kg lm daily for 10 days
2. Neonatal conjunctivitis
It is acquired during birth as a result of genital infection of the mother by N.
gonorrhoea and C. trachomitis. The clinical features include periorbital swelling,
redness of the eyes with sticky eye lids and purulent discharge from the eyes.
Treatment Spectinomycin 50 mg /kg IM stat
Plus
Erythromycin 50 mg/kg PO in 4 divided doses for 10 days.
3. Neonatal herpes
Neonatal herpes occurs after birth of a neonate from a mother with active herpes
genitalis. In fact vaginal delivery is CI if the mother is found to have active
genital herpes in order to avoid neonatal infection. The neonate may develop
aseptic meningitis or encephalitis and it is frequently fatal.
Treatment Acyclovir 5-10 mg/kg IV daily for 10 days
1. Treatment of cases
2. Treatment of contacts and source of infection
3. Health education on safe sex (sex education for high risk groups)
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4. Controlling STIs among commercial sex workers

Monthly check up and Rx of cases
Provision of condom
5. Screening of clients (e.g. VDRL in pregnant to prevent congenital syphilis)
6. Screening of blood before transfusion (syphilis)
7. Thorough washing of genitalia with soap and water promptly after intercourse is
very effective (chancroid)
8. Consistent use of condoms (herpes genitalia)
9. Application of 1% TTC in both eyes of new borne as soon as delivered
(Gonorrhoea)
Reference:
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65
1) Jan Eshuis and peter Manschot, communicable diseases , a manual for rural
health workers African medical and research foundation, Nairobi 1978
2) Abram S. Benson, 14th edition, control of communicable disease in man
interdisciplinary books pamphlets and periodicals, Washington 1985.
3) National guide line on HIV /AIDS . MOH Addis Ababa , 1998
4) National guide line on selected epidemic diseases in Ethiopia , MOH, Addis
Ababa .
5) National guide line on MTCT, MOH Addis Aabab
6) National Management guide line on Malaria for health workers in Ethiopia,
MOH, Addis Ababa
7) National Guide line on prevention and control of malaria in Ethiopia MOH,
Addis Ababa
8) Mansons tropical diseases, 4th edition UK
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66

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Cominicable Abebaw

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Commmunicable Disease

Principles of communicable disease control

BACILLARY DYSENTERY (SHIGELLOSIS)

AMOEBIC DYSENTERY / AMAEBIASIS)

Period of communicability: During the period of passing cysts of E. histolytica, which

3. Proper disposal of human excreta and hand washing following defection

I/P: l0 hrs to 6 days for most strains.

TRICHURIASIS( whip worm)

Susceptibility & Resistance: susceptibility is universal

ENTEROBIASIS (OXYURIASIS, PIN WORM INFECTIONS)

- Or thiabendazole 500 mg Po BID for 03 days.

HOOK WORM DISEASE(ANCYLOSTOMIASIS AND

1. sanitary disposal of feces

Prevention and control

Air-borne diseases are diseases transmitted through dissemination of microbial

Common cold (Acute Viral Rhinitis or coryza)

Mode of transmission: inhalation of air-borne droplets; and articles freshly soiled

epidemics lasts) 100mg PO BID

Pertussis (whooping cough)

3. Proper ventilation-continuous well humidified oxygen administration

Abnormal heart beats which may lead to heart failure

2. Preschool child Haemophilus influenza B

5. Chemo prophylaxis e.g. Rifampin 600mg po BID for 2 days or ciprofloxacin

HIV is an important risk factor for the development of HIV-associated TBc by

1. Pulmonary (80%) of the total TB cases.

- This is unreliable b/c it can be caused by a variety of conditions or previous TB

2. Rx failure (F): A pt who, while on Rx remained smeary positive or became again

4. Category IV chronic cases

Leprosy (Hansen's disease)

MDT regimen for PB leprosy

Prevention and control

1. Mosquito borne diseases

9. Hyper pyrexia Hyper parasitemia

Microfilaria in the peripheral blood film (B/F). That is, microfilarial

Epidemic Typhus (Louse -borne typhus)

Endemic typhus (Flea-borne typhus) (Murine Typhus fever)

Rx - .Doxycycline (single dose) OR

Susceptibility and resistance: - susceptibility is general.

Reservoir- cattle, swine, goats and sheep, pet dogs

Reservoir: - Dog, wild carnivores and bats

2. Inhalation anthrax: - Inhalation of spores in risky industrial processes such as

- High dose of IV penicillin is recommended

Air way obstruction

Intensive care unit(ICU)

Prevention & Control

Staphylococcal food poisoning(Intoxication)

- Sudden onset of vomiting and watery diarrhoea

VI. Prevention & Control of STI

1. Both infections, share similar epidemiologic determinants

* Genital ulcer in men and women.

Common syndromes in STIs

Common causes of genital ulcer are

Chancroid /soft chancre/

4. Lower abdominal pain due to PID

7. Neonatal infections due to STIs

4. Controlling STIs among commercial sex workers

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