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Medicine Dr. Ala Lecture 1+2 (Viral Infections)

Definition: Viruses are simple infectious agents consisting of a portion of genetic material, RNA or
DNA, enclosed in a protein coat which is antigenically unique for that species.
They are essentially inert and cannot exist in a free-living state, needing to infect host cells to
survive.
Once it is in the intracellular environment, they utilize host material for protein synthesis and
genetic reproduction.
All viral infections must therefore originate from an infected source by either direct or vector-
mediated spread.
CLASSIFICATION OF HUMAN VIRAL INFECTIONS
Virus involved Clinical syndrom
RNA Viruses
Picornaviruses
Poliovirus
Coxsackie viruses
Echoviruses
Enteroviruses 68-72
Gut/neurological illness
Hepatitis A
Rhinoviruses Upper respiratory tract infection
Rheoviruses
Rheovirus Mild upper respiratory tract infection/gut disease
Rotavirus Gastroenteritis
Togaviruses
Rubella German measles
Yellow fever Yellow/haemorrhagic fever
Dengue
Other arboviruses
Haemorrhagic fevers
Hepatitis C Chronic hepatitis
Calicivirus
Hepatitis E Acute gastroenteritis
Orthomyxoviruses
Influenza A, B
Paramyxoviruses
Measles,Mumps,
Respiratory syncytial virus

Rhabdoviruses Rabies
Retroviruses
HIV-1 and 2 HIV infection syndrome/AIDS
Hepadnavirus, Hepatitis B
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Virus involved Clinical syndrome
DNA Viruses
Adenoviruses
Upper respiratory tract infection/pharyngitis
Acute diarrhoea
Herpes viruses
Herpes simplex types 1 and 2 Acute/recurrent vesicular rash
Varicella zoster Chickenpox/shingles
Cytomegalovirus Acute/recurrent hepatorenal infection
Human herpes virus 6 and 7 Roseola infantum
Epstein-Barr virus
Infectious mononucleosis
Burkitt's lymphoma
Human herpes virus 8
Nasopharyngeal carcinoma
Kaposi's sarcoma
Papovaviruses
Human papillomavirus Common wart
Polyoma
Progressive multifocal
leuco-encephalopathy
Poxviruses
Variola Smallpox
CLASSIFICATION ACCORDING TO THE HOST AND ORGANS INVOLVED:
COMMON VIRAL INFECTIONS AND CHILDHOOD EXANTHEMS.
VIRAL INFECTIONS OF THE SKIN.
SYSTEMIC VIRAL INFECTIONS.
GASTRO-INTESTINAL VIRAL INFECTIONS.
RESPIRATORY VIRAL INFECTIONS.
VIRAL INFECTIONS WITH NEUROLOGICAL INVOLVEMENT.
COMMON VIRAL INFECTONS AND CHILDHOOD EXANTHEMS
MEASELS
RUBELLA (GERMAN MEASELS)
MUMPS
VIRAL INFECTIONS OF THE SKIN
THE HERPES VIRUS GROUP







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Table 13.29 HERPES VIRUS INFECTIONS
Virus Infection
Herpesvirus hominis (herpes simplex, HSV)
Type 1
Herpes labialis ('cold sores')
Keratoconjunctivitis
Finger infections ('whitlows')
Encephalitis
Primary stomatitis
Genital infections
Type 2
Genital infections
Neonatal infection (acquired during
vaginal delivery)
Varicella zoster virus Chickenpox , Shingles (herpes zoster)
Cytomegalovirus (CMV)
Congenital infection
Disease in immunocompromised patients
Pneumonitis
Retinitis
Enteritis
Generalised infection
Epstein-Barr virus (EBV)
Infectious mononucleosis
Burkitt's lymphoma
Nasopharyngeal carcinoma
Oral hairy leucoplakia (AIDS patients)
Human herpes virus 8 Associated with Kaposi's sarcoma
HERPES SIMPLEX VIRUS (HSV)
Types 1 and 2 of this common virus affect humans.
Type 1 HSV produces mucocutaneous lesions, predominantly of the head and neck
Type 2 disease is a sexually transmitted anogenital infection
The source of infection is a case of primary or active recurrent disease.
Primary infection
Normally occurs as a gingivostomatitis in infancy and may be subclinical or mistaken for 'teething'.
It may present as: - a keratitis (dendritic ulcer), viral paronychia ('whitlow'),
- vulvovaginitis, cervicitis (often unrecognised), balanitis
- or rarely as encephalitis.
Recurrent disease, involving reactivation of HSV from latency in the dorsal root ganglion, produces
the classical 'cold sore' or 'herpes labialis'.
Prodromal hyperaesthesia is followed by rapid vesiculation, pustulation and crusting. Recurrences
can be precipitated by disturbance of local skin integrity by ultraviolet light or systemic upset from
menstruation or fever of any cause.
*** Type 2 (genital) disease is a common cause of recurrent painful genital ulceration

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Complications:
Neonatal HSV disease, contracted from the birth canal, may be disseminated and is potentially
fatal. Active HSV in a pre-term mother is an indication for either elective caesarean section or
antiviral therapy.
*eczema herpeticum, HSV infection in patients with eczema can result in a spreading and
potentially serious infection
Dendritic ulcers may produce corneal scarring and permanently damage eyesight. These require
aggressive antiviral therapy.
Encephalitis, the most serious complication of HSV disease, may occur following either primary or
secondary disease. A haemorrhagic necrotising temporal lobe cerebritis produces temporal lobe
epilepsy and decreasing conscious level/coma. Without treatment, mortality is 80%. Any
suggestion of HSV encephalitis is an indication for immediate empirical systemic antiviral therapy.
DIAGNOSIS
PCR,
Electron microscopy or culture from vesicular fluid.
CSF PCR is very useful in HSV encephalitis.
Serology is of limited value, only confirming primary infection.
Management:
The acyclic antivirals are the treatment of choice for HSV infection.
Therapy must commence in the first 48 hours of clinical disease (primary or recurrent); thereafter
it is unlikely to influence clinical outcome or modify the disease process.
Severe manifestations should be treated regardless of the time of presentation
Primary HSV
- Famciclovir 250 mg 8-hourly
- Valaciclovir 500 mg 12-hourly
- Aciclovir 200 mg 5 times daily
* Severe and preventing oral intake
Aciclovir 5 mg/kg 8-hourly i.v.
*Recurrent HSV-1 or 2
- Aciclovir ointment 3-5 times daily
- Oral aciclovir 200 mg 6-hourly
- Famciclovir 250 mg 12-hourly
- Valaciclovir 500 mg daily
* In immunocompromised
- Aciclovir 400 mg 6-hourly
- Famciclovir 500 mg 12-hourly
- Valaciclovir 1 g 12-hourly
Severe complications
- Aciclovir i.v. 10 mg/kg 8-hourly (up to 20 mg/kg in severe encephalitis)
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CHICKENPOX
Varicella zoster virus (VZV) is dermo- and neurotropic infection. Spread by the aerosol route, it is
highly infectious to susceptible individuals.
Disease in children is usually well tolerated. It is more severe in adults, pregnant women and the
immunocompromised.
Pneumonitis can be fatal and is more likely in smokers, pregnant women & immunocompromised
The incubation period is 14-21 days, after which a vesicular eruption begins, often on mucosal
surfaces first, followed by rapid dissemination in a centripetal distribution (most dense on trunk
and sparse on limbs).
New lesions occur every 2-4 days, each crop associated with fever. The rash progresses from small
pink macules to vesicles and pustules within 24 hours. These then crust. Infectivity lasts until
crusts separate.
Complications
- Due to intense itch secondary bacterial infection from scratching is the most common
complication of primary chickenpox.
- Self-limiting cerebellar ataxia may rarely occur 7-10 days after recovery from the rash.
- Maternal infection in early pregnancy carries a 3% risk of neonatal damage, and disease
within 5 days of delivery can lead to severe neonatal varicella.
Diagnosis
Usually this is clinically obvious from the classical appearance of the rash .
Aspiration of vesicular fluid and PCR or tissue culture will confirm the diagnosis.
Electron microscopy cannot distinguish HSV from VZV.
Serological examination for rising titres of antibody is only useful in primary infection.
Chickenpox can recur as a subclinical infection following primary disease.
Management
Aciclovir, valaciclovir and famciclovir, effective if commenced within 48 hours of rash appearance.
They are required in the management of the immunocompromised or any case of pneumonitis .
Note: Aciclovir shortens symptoms in chickenpox by an average of 1 day. In shingles aciclovir
reduces pain by 10 days and the risk of post- herpetic neuralgia by 8%. Aciclovir is therefore cost-
effective in shingles but not chickenpox.
Human VZV immunoglobulin may be used to attenuate infection in highly susceptible contacts of
chickenpox such as:
bone marrow recipients
patients with debilitating disease
HIV-positive contacts without VZV immunity
pregnant women with no known VZV antibody (screen for antibody if in doubt)
Immunosuppressed contacts who have received high-dose corticosteroids in the prev. 3m.
Neonates whose mothers develop chickenpox between 1w before and 4w after delivery.
Neonates in contact with chickenpox/shingles whose mothers have no history of chickenpox
or any demonstrable antibody
Premature infants of less than 30 weeks' gestation, or weighing less than 1 kg at birth who
contact chickenpox or shingles.
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SHINGLES (HERPES ZOSTER)
This is produced by reactivation of latent VZV from the dorsal root ganglion of sensory nerves.
Commonly seen in the elderly,
It may present in younger patients with immune deficiency or after intra-uterine infection.
Although thoracic dermatomes are most commonly involved, the ophthalmic division of the
trigeminal n. is frequently implicated; vesicles may appear on the cornea & lead to ulceration
Geniculate ganglion involvement causes the Ramsay Hunt syndrome of facial palsy, ipsilateral
loss of taste and buccal ulceration, plus a rash in the external auditory canal. This may be
mistaken for Bell's palsy.
Bowel and bladder dysfunction occurs with sacral nerve root involvement.
The virus occasionally causes myelitis or encephalitis.
Clinical features
Burning discomfort in the affected dermatome progresses to frank neuralgia. Discrete vesicles
appear in the dermatome 3-4 days later and often coalesce.
Severe disease, multiple dermatomal involvement or recurrence suggests underlying immune
deficiency.
Complications
The most common and troublesome complication is post-herpetic neuralgia: persistence of pain
for 1-6 months or more following healing of the rash.
Management
Early therapy with aciclovir 800 mg 5 times daily or valaciclovir 1 g 8-hourly, or aciclovir 10 mg/kg
i.v. 8-hourly in severe infection and in the immunocompromised has been shown to reduce both
early- and late-onset pain, especially in patients over 65 .
Post-herpetic neuralgia requires
aggressive analgesia and
the use of transcutaneous nerve stimulation (a 'TENS' machine), along with
neurotransmitter modification with agents such as amitriptyline 25-100 mg daily or
gabapentin (commencing at 300 mg daily and building slowly to 300 mg 12-hourly or more.
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Smallpox (variola)
This severe disease, with a 30% mortality in the unvaccinated patient and no current effective
therapy, was eradicated world-wide in 1980 by a successful international vaccination campaign
coordinated by the WHO.
Interest in the disease has re-emerged due to its potential as a bioterrorist weapon .In view of this
threat some developed countries have reintroduced vaccination for key health-care personnel and
re-evaluated national plans for the containment of disease.
Clinical features
The classical form is characterised by a typical deep-seated centrifugal vesicular/pustular rash,
worst on the face and extremities, with no cropping (i.e. unlike chickenpox);
the rash is accompanied by fever, severe myalgia.

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SYSTEMIC VIRAL INFECTIONS
INFLUENZA
EBV -Infectios mononucleosus
CMV
VIRAL HEMORAGIC FEVER
HIV

INFECTIOUS MONONUCLEOSIS (IM)
Virology and epidemiology
- The disease is caused by the Epstein-Barr virus (EBV), a gamma herpes virus. .
- In developing countries and poorer societies in developed nations subclinical infection in
childhood is virtually universal. In richer communities, particularly among upper
socioeconomic groups, primary infection may be delayed until adolescence or early adult life.
- About 50% of infections result in typical IM. The virus is usually acquired from asymptomatic
excreters.
- Saliva is the main means of spread, either by droplet infection or environmental
contamination in childhood, or by kissing among adolescents and adults. .
- IM is not highly contagious, isolation is unnecessary and documented outbreaks seldom occur.
Clinical features (IM)
lymphadenopathy, especially posterior cervical,
pharyngeal inflammation or exudates,
fever
splenomegaly,
palatal petechiae,
periorbital oedema,
clinical or biochemical evidence of hepatitis,
And a non-specific rash.
20% or more of peripheral lymphocytes must have an atypical morphology
characteristic heterophile antibody. (classical Paul-Bunnell titration or by slide test 'Monospot)).
Specific EBV serology (immunofluoresence)
COMPLICATIONS OF INFECTIOUS MONONUCLEOSIS
Common
Severe pharyngeal oedema
Antibiotic-induced rash
Chronic fatigue syndrome (10%)
Rare
Ruptured spleen
Respiratory obstruction
Arthritis
Agranulocytosis
Agammaglobulinaemia
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Uncommon
Neurological
Cranial nerve palsies
Polyneuritis
Transverse myelitis
Meningoencephalitis
Haematological
Haemolytic anaemia
Thrombocytopenia
Renal
Glomerulonephritis
Interstitial nephritis
Cardiac
Myocarditis
Pericarditis
Pulmonary
Interstitial pneumonitis
Management
Treatment is largely symptomatic:
aspirin gargles to relieve a sore throat.
If a throat culture yields a -haemolytic streptococcus, a course of erythromycin should be
prescribed. Amoxicillin and similar semi-synthetic penicillins should be avoided .
When pharyngeal oedema is severe a short course of corticosteroids, e.g. prednisolone 30 mg
daily for 5 days, may help to relieve the swelling.
contact sports should be avoided until splenomegaly has completely resolved because of the
danger of splenic rupture.
Unfortunately, about 10% of patients with IM suffer a chronic relapsing syndrome.
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ACQUIRED CYTOMEGALOVIRUS INFECTION
Virology and epidemiology
- Cytomegalovirus (CMV) is a beta herpes virus.
- It circulates readily among children, especially in crowded communities.
- Although most primary infections are asymptomatic, many children continue to excrete
virus for months or years.
A second peak in virus acquisition occurs among teenagers and young adults. CMV infection is
persistent, and is characterised by subclinical cycles of active virus replication and by persistent
low-level virus shedding.
Sexual transmission and oral spread are common among adults, but infection may also be
acquired by women caring for children with asymptomatic infections.
The peak incidence occurs between the ages of 25 and 35, rather later than with EBV-related
mononucleosis.
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Clinical features
Most post-childhood CMV infections are subclinical, although some young adults develop a
mononucleosis-like syndrome .
Some patients have a prolonged influenza-like illness lasting 2 weeks or more .
Physical signs such as a palpable liver and spleen resemble those of IM, but in CMV mononucleosis
hepatomegaly is relatively more common, while lymphadenopathy, pharyngitis and tonsillitis are
found less often. Jaundice is uncommon and usually mild.
Complications
- neurological involvement, - autoimmune haemolytic anaemia,
- pericarditis, - pneumonitis . - arthropathy.
Investigations
- Atypical lymphocytosis is not as prominent as in IM
- heterophile antibody tests are negative.
- LFTs are often abnormal, with an alkaline phosphatase level raised out of proportion to
transaminases.
- Serological diagnosis depends on the detection of CMV-specific IgM antibody.
Management
Only symptomatic treatment.
Amoxicillin and similar antibiotics should not be prescribed because of the risk of a skin reaction.
Since CMV infection in immunocompetent subjects is self-limiting, the use of potentially toxic
antiviral agents is usually inappropriate
In immunosupp. Pt.,
- Ganciclover injection
- valganciclover tab. (valcyte) 450mg ( 2 tab. 12 hourly for 4-6 weeks )
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VIRAL HAEMORRHAGIC FEVERS
The viral haemorrhagic fevers are zoonoses caused by several different viruses .They are endemic
world-wide, examples.:
a. Yellow fever-
Reservoir; Monkeys
Transmission; Mosquitoes
Geography; Tropical Africa, South and Central America-
Mortality rate; 10-60% death
Clinical features; Hepatic failure, Blood oozing
b. * Dengue
Reservoir ; Humans
Transmission; Aedes aegypti-
Geography ; tropical and subtropical coasts
Mortality rate ; Nil-10%
Clinical features - Joint and bone pain, Petechiae

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Pathogenesis
- These viruses cause endothelial dysfunction with the development of leaky capillary syndrome.
- Bleeding is due to this and associated platelet dysfunction.
- Hypovolaemic shock and acute respiratory distress syndrome develop
Clinical features
All viral haemorrhagic fevers have similar non-specific presentations with fever, malaise, body
pains, sore throat and headache.
On examination conjunctivitis, throat congestion, an erythematous or petechial rash,
haemorrhage, lymphadenopathy and bradycardia may be noted.
Investigations
- There is leucopenia,
- thrombocytopenia
- Proteinuria.
- Prolong PT and PTT
Diagnosis
The clue to the viral aetiology will come from the travel and exposure history, so it is important to
be aware of the incubation periods for these illnesses.
The causative virus may be isolated, or antigen detected, in maximum security laboratories from
serum, pharynx, pleural exudate and urine.
Management
It is important to exclude other causes of fever, especially malaria, typhoid and respiratory
tract infections.
Particular care must be taken with body fluids. Patients returning from endemic area with
a fever should be managed in isolation until a diagnosis is made.
General supportive measures, preferably in a special unit, are required.
Ribavirin is given intravenously (100 mg/kg, then 25 mg/kg daily for 3 days and 12.5 mg/kg
daily for 4 days).
Once haemorrhagic fever is confirmed, full pressure isolation is mandatory and good
infection control practices will prevent further transmission.
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GASTROINTESTINAL VIRAL INFECTIONS
ROTAVIRUS
Rotaviruses are the major cause of diarrhoeal illness in young children, accounting for 30-50% of
cases admitted to hospital in developed countries, and 10-20% of deaths due to gastroenteritis in
developing countries.
Infection is endemic in developing countries and there are winter epidemics in developed
countries.
These viruses are easily transmitted and resist alcohol denaturation; person-to-person spread,
especially by health-care workers in hospitals, is well documented.
The virus infects enterocytes, causing decreased surface absorption and loss of enzymes on the
brush border.
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Diagnosis
The incubation period is 48 hours .
Patients present with watery diarrhoea, vomiting, fever and abdominal pain.
Diagnosis is aided by commercially available enzyme immunoassay kits which simply require fresh
or refrigerated stool for effective demonstration of the pathogens.
Treatment
The disease is self-limiting but dehydration needs appropriate management .
Immunity develops to natural infection.
Other GIT viruses
HEPATITUS VIRUSES (A, B, C, D,E, F).
Adenoviruses
Are frequently identified from stool culture and implicated as a cause of diarrhoea.
Two serotypes (40 and 41) appear to be more frequently found in association with diarrhea
rather than the more common upper respiratory types 1-7.
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RESPIRATORY VIRAL INFECTIONS
Adenoviruses,
rhinoviruses
enteroviruses (Coxsackie viruses and echoviruses)
Often produce non-specific symptoms. The individual infections each produce lasting specific
immunity.
** Influenza viruses
Human immunodeficiency virus infection (HIV) and (AIDS)
EPIDEMIOLOGY AND BIOLOGY OF HIV
The acquired immunodeficiency syndrome (AIDS) was first recognized in 1981. It is caused by the
human immunodeficiency virus (HIV-1). HIV-2 causes a similar illness to HIV-1 but is less aggressive
and restricted mainly to western Africa.
Since 1981 AIDS has grown to be the second leading cause of disease burden world-wide and the
leading cause of death in Africa, where it accounts for over 20% of deaths.
* Immune deficiency is a consequence of continuous high-level HIV replication leading to immune-
mediated destruction of the key immune effector cell, the CD4 lymphocyte.
MODES OF TRANSMISSION
HIV is present in blood, semen and other body fluids such as breast milk and saliva.
Exposure to infected fluid leads to a risk of contacting infection, which is dependent on the
integrity of the exposed site, the type and volume of body fluid, and the viral load.
HIV can enter either as free virus or within cells.
The modes of spread are sexual (man to man, heterosexual and oral), parenteral (blood or
blood product recipients, injection drug-users and those experiencing occupational injury)
and vertical.
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VIROLOGY AND IMMUNOLOGY
HIV is a single-stranded RNA retrovirus from the Lentivirus family.
After mucosal exposure, HIV is transported to the lymph nodes via dendritic, CD4 or Langerhans
cells, where infection becomes established.
Free or cell-associated virus is then disseminated widely through the blood with seeding of
'sanctuary' sites (e.g. central nervous system) and latent CD4 cell reservoirs.
With time, there is gradual attrition of the CD4 cell population, resulting in increasing impairment
of cell-mediated immunity and susceptibility to opportunistic infections.

As CD4 cells are pivotal in orchestrating the immune response, any depletion in numbers renders
the body susceptible to opportunistic infections and oncogenic virus-related tumours.
The predominant opportunist infections seen in HIV disease are intracellular parasites (e.g.
Mycobacterium tuberculosis) or pathogens susceptible to cell-mediated rather than antibody-
mediated immune responses.
The reduction in the number of CD4 cells circulating in peripheral blood is tightly correlated with
the amount of plasma viral load.
Both are monitored closely in patients and are used as measures of disease progression.

Virus-specific CD8 cytotoxic T-cell lymphocytes develop rapidly after infection and are the most
important element in recognizing, binding and lysing infected CD4 cells.
They play a crucial role in controlling HIV replication after infection and determine the viral 'set-
point' and subsequent rate of disease progression.
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NATURAL HISTORY AND CLASSIFICATION OF HIV
Primary infection
Asymptomatic infection
HIV SYMPTOMATIC DISEASES
Mildly symptomatic disease
Acquired immunodeficiency syndrome (AIDS)
Primary infection
Fever with rash
Pharyngitis with cervical lymphadenopathy
Myalgia/arthralgia
Headache
Mucosal ulceration
Primary infection is symptomatic in 70-80% of cases and usually occurs 2-6 weeks after exposure.
Rarely, presentation may be neurological (aseptic meningitis, encephalitis, myelitis, polyneuritis).
This coincides with a surge in plasma HIV-RNA levels to > 1 million copies/ml (peak between 4 and
8 weeks), and a fall in the CD4 count to 300-400 cells/mm3, but occasionally to below 200 when
opportunistic infections (e.g. oropharyngeal candidiasis, Pneumocystis carinii (jirovecii)
pneumonia) may rarely occur .
Symptomatic recovery occurs after 1-2 weeks but occasionally may take up to 10 weeks and
parallels the return of the CD4 count and fall in the viral load.
In many patients the illness is mild and only identified by retrospective enquiry at later
presentation.
However, the CD4 count rarely recovers to its previous value.
Diagnosis is made by
1- detecting HIV-RNA in the serum or
2- immunoblot assay (which shows antibodies developing to early proteins).
The appearance of specific anti-HIV antibodies in serum (seroconversion) takes place later at 3-12
weeks (median 8 weeks), although very rarely seroconversion may take place after 3 months.
Factors likely to indicate a faster progression of HIV are
1- the presence and duration of symptoms,
2- evidence of candidiasis, and
3- Neurological involvement.
4- The level of the viral load post-seroconversion strongly correlates with subsequent
progression of disease.
The differential diagnosis of primary HIV includes
acute Epstein-Barr virus (EBV),
cytomegalovirus (CMV),
streptococcal pharyngitis,
toxoplasmosis
Secondary syphilis.
Asymptomatic infection
Category A disease in the Centers for Disease Control (CDC) classification
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Follows and lasts for a variable period, during which the infected individual remains well with no
evidence of disease except for the possible presence of persistent generalised lymphadenopathy
(PGL, defined as enlarged glands at 2 extra-inguinal sites).
At this stage the bulk of virus replication takes place within lymphoid tissue (e.g. follicular
dendritic cells).
There is sustained viraemia with a decline in CD4 count dependent on the height of the viral load
but usually between 50 and 150 cells/cc/year
HIV SYMPTOMATIC DISEASES
Oral hairy leucoplakia
Recurrent oropharyngeal candidiasis
Recurrent vaginal candidiasis
Severe pelvic inflammatory disease
Bacillary angiomatosis
Cervical dysplasia
Idiopathic thrombocytopenic purpura
Weight loss*
Chronic diarrhoea*
Herpes zoster
Peripheral neuropathy
Low-grade fever/night sweats*
Mildly symptomatic disease
Centers for Disease Control (CDC)
Classification category B disease.
indicating some impairment of the
cellular immune system.
These diseases correspond to AIDS-
related complex (ARC) conditions but by
definition are not AIDS-defining.
The median interval from infection to the development of symptoms is around 7-10 years,
although subgroups of patients exhibit 'fast' or 'slow' rates of progression.
Acquired immunodeficiency syndrome (AIDS)
AIDS (CDC Classification category C disease)
is defined by the development of specified opportunistic infections, tumours etc.
There is correlation between CD4 count and HIV-related diseases (type of the disease). ( box 14.7)
AIDS-DEFINING DISEASE (box14.6 )
- Oesophageal candidiasis - Cryptococcal meningitis
- Chronic cryptosporidial diarrhoea - CMV retinitis or colitis
- Chronic mucocutaneous herpes simplex - Disseminated Mycobacterium avium intracellulare
- Pulmonary or extrapulmonary TB - Pneumocystis carinii (jirovecii) pneumonia
- Cerebral toxoplasmosis - Progressive multifocal leucoencephalopathy
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- Extrapulmonary coccidioidomycosis - Recurrent non-typhi Salmonella septicaemia
- Invasive cervical cancer - Extrapulmonary histoplasmosis
- Kaposi's sarcoma - Non-Hodgkin lymphoma
- Primary cerebral lymphoma - HIV-associated wasting
- HIV-associated dementia
DIFFERENTIAL DIAGNOSIS OF HIV-RELATED SKIN DISEASE
A. Early HIV
Infection: Herpes simplex, Varicella zoster, Human papillomavirus (HPV), Impetigo,
Dermatophytosis, Scabies, Syphilis, HIV seroconversion
Other: Xeroderma, Pruritus, Seborrhoeic dermatitis, Drug reaction (co-trimoxazole/nevirapine),
Itchy folliculitis, Psoriasis, Acne
B. Late HIV
Common
Kaposi's sarcoma
Molluscum contagiosum
Chronic mucocutaneous herpes simplex
Rare
Bacillary angiomatosis
CMV
Non-Hodgkin lymphoma
Cryptococcus
Histoplasmosis
Mycobacterial (tuberculosis/atypical)
Figure 14.5 Presentation and differential diagnosis of HIV-related gastrointestinal disorder

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Figure 14.9 Presentation and differential diagnosis of HIV-related neurological disorders

MANAGEMENT OF HIV
Management of HIV involves both treatment of the virus and prevention of opportunistic
infections. The aims of HIV treatment are to:
1- reduce the viral load to an undetectable level (< 50 copies/ml) for as long as possible
2- improve the CD4 count (above 200 cells/mm3 ,when the significant HIV-related events
rarely occur)
3- increase the quantity and improve the quality of life without unacceptable drug-related
side-effects or lifestyle alteration
4- reduce transmission (mother-to-child and person-to-person).
DRUGS
A. ANTIRETROVIRAL DRUGS
Nucleoside reverse transcriptase inhibitors (NRTIs)
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Protease inhibitors (PIs)
Others
The drugs that are currently used, their side-effects and a glossary of terms and abbreviations are
given in Boxes 14.22, 14.23 and 14.24. in Davidsons
B. Nucleoside reverse transcriptase inhibitors (NRTIs)
- Zalcitabine (ddC) - Didanosine (ddI) - Lamivudine (3TC)
- Zidovudine (ZDV) - Stavudine (d4T) - Abacavir - Emitricitabine (FTC)
C. Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
- Nevirapine - Efavirenz - Delavirdine1
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D. Protease inhibitors (PIs):
- Indinavir2 - Ritonavir - Nelfinavir
- Lopinavir3 - Atazanavir2 - Fosamprenavir2
- Saquinavir2 - Amprenavir1,2 - Tipranavir1,2
E. Others: - Tenofovir - Enfuvirtide (T-20)
Notes about HIV drugs
The inclusion of two NRTIs, or one NRTI and tenofovir, remains the cornerstone of HAART. (highly
active anti-retroviral therapy)=combination treatment
Resistance to all NRTIs will occur unless they are part of a maximally suppressive HAART regimen .
* More recently, two PIs (atazanavir and osamprenavir) have become available; they allow for
once-daily administration with fewer tablets. The subsequent fall in morbidity and mortality can
be directly linked to the introduction of these drugs and their use in HAART. When they are given
with two NRTIs the combination controls viral replication in plasma and tissues, and allows
reconstitution of the immune system.
Short- and long-term side-effects are not infrequent. Fat redistribution occurred in 20-30% of
patients treated with HAART including a PI after 2 years. The syndrome is characterised by
peripheral fat-wasting (cheeks, temples, limbs and buttocks), localised collections (buffalo hump,
peripheral lipomatosis, and breast enlargement in women) and central adiposity.
Enfuvirtide (T-20) is a new class of antiretroviral drug which prevents viral entry into cells and
preventing fusion. It is highly active but has to be injected subcutaneously 12-hourly and therefore
is reserved for patients with more advanced disease and fewer options.
FACTORS TO CONSIDER WHEN CHOOSING HAART
Ease of compliance
Fit of the drug regimen around the patient's lifestyle
Wishes of the patient
Stage of disease
Coexisting/past medical history
Possibility of additive side-effects (e.g. ddI and neuropathy)
Potential for drug interactions with non-HIV medications
Antagonistic NRTI combinations (ZDV/d4T and ddC/3TC)
CNS penetration
Possibility of acquisition of resistant virus
POST-EXPOSURE PROPHYLAXIS
Combination therapy is now recommended for occupational post-exposure prophylaxis (PEP)
where the risk is deemed to be significant, although there is no evidence for this practice. The first
dose should be given as soon as possible. However, protection is not absolute and health-care
workers have been reported to seroconvert despite taking a full course of three drugs started
within hours of exposure.
Recommended PEP is ZDV, 3TC and indinavir or nelfinavir for 28 days.
Vaccine development is slow.
* Some pics. Expl. medical terms are omitted from the handout; you can check out for your interest