HIV

Dr Anil Sabharwal MD
• AIDS was first recognized in the United States in the summer
of 1981,
• Unexplained occurrence of Pneumocystis carinii pneumonia
in five previously healthy homosexual men in Los Angeles
• Kaposi's sarcoma (KS) in 26 previously healthy homosexual
men in New York and Los Angeles.
• Within months, the disease became recognized in male and
female injection drug users (IDUs) and soon thereafter in
recipients of blood transfusions and in hemophiliacs.
• It became clear that a microbe transmissible by sexual
(homosexual and heterosexual) contact and blood or blood
products was the most likely etiologic agent of the epidemic
• In 1983, HIV was isolated from a patient with
lymphadenopathy
• 1984 it was demonstrated clearly to be the causative
agent of AIDS.
• In 1985, a sensitive enzyme-linked immunosorbent assay
(ELISA) was developed,
 AIDS
• 1st recognized in US 1981
• In 1983, HIV was isolated from a patient
with lymphadenopathy,
• In 1984 it was demonstrated clearly to be
the causative agent of AIDS.
• In 1985, a sensitive enzyme-linked
immunosorbent assay (ELISA) was
developed
 HIV I & II
• HIV, which belongs to the family of human retroviruses –RNA
virus-HIV-1 (subtypes A,B,C,D,AE )and HIV-2,
HIV2 –differs from HIV 1-
• patient has lower viral load
• Slower CD-4 decline,
• Lower rate of viral transmission
• Slower progress to AIDS
 TRANSMISSION:
• Major route heterosexual(>75%)
• HIV is transmitted by homosexual & heterosexual contact
• Blood and blood products-lab workers;
• Infected mothers to infants either intra partum,
perinatally, or via breast milk.
• There is no evidence that HIV is transmitted by casual
contact or that the virus can be spread by insects, such as
by a mosquito bite.
• World wide there are 40 million persons infected with
HIV
 CD4 & CD8 cells
• After entry HIV is transported to LN via CD4
cells
• CD4 cells (helper inducer) are responsible for cell
mediated immunity
• Any ↓ in CD4 count→ opportunistic infection &
onchogenic virus related tumors
• ↓CD4 cells is correlated with virus load
• CD8 cytotoxic T cells bind & Lyse infected CD4
cells
• B lymphocyte &macrophages are also
infected→↓ humoral immunity
• CD4 count provides important prognostic
information
Clinical features of primary infection
• Many patients with HIV infection remain
asymptomatic with a mean time of 10 years
between exposure development of AIDS
• However hairy lucoplakia & oral thrush should
raise suspicion of HIV
• Fever with rash
• Pharyngitis with cervical lymphadenopathy
• Myalgia/arthalgia
• Headache
• Mucosal ulceration
• Fever, night sweats, weight lost
Pneumocystitis pneumonia is most
common opportunistic infection associated
with AIDS & is difficult to diagnose
because symptoms –fever, cough &
dyspnea are nonspecific
• Diagnosis-chest X-ray-diffuse or perihilar
infiltrates
 CNS
• Toxoplasmosis-most common
• AIDS dementia complex
• Cryptococcus meningitis
• HIV myelopathy
• progressive multifocal leucoencephalopathy
 Others
• Myopathy
• Retinitis
• Oral lesion-candidiasis or hairy leucoplakia
• GIT-candidal esohagitis,hepatic dis
• Endocrinal-hypogonadism
• Skin-Herpes simplex,, herpes zoster,
mmolluscum contagiosum
 HIV related malignancies
• Kaposi sarcoma
• Non-Hodgkin’s lymphoma
• Primary lymphoma of brain
• Non-invasive cervical carcinoma
 Lab investigations
• HIV-ELISA-screening test,15% +ve in 3 weeks, 95%
in 6wks
• Western blot-confirmatory test,
• HIV rapid antibody test-screening test
• CBC-anemia, neutropenia, thrombocytopenia
• Absolute CD4 count risk of opportunistic infection or
malignancy ↑ when CD4<200cells/mcl
• CD4 lymphocyte percentage-risk↑ if %<20 %
• HIV viral load tests-measure amouunt of actively
replicating virus
 Prevention-Primary
• No vaccine
• Education
• Effective precautions regarding sexual practices
• Injection use
• Screening of blood products
• Perinatal HIV prophylaxis practice
• Precautions for lab technicians & blood handlers
 Secondary prevention
• AIDS develops in 10 years in 50 % of sero
positive persons in untreated patients
• ↓in incidence of A IDS reflecting successful
treatment of HIV & successful HIV
prevention is reported in USA & Europe
• Prophylactic regimen can prevent
opportunistic infection & improve survival
HIV risk for health care professional

• Needle stick injury :risk of HIV

transmission is 1:300.Testing done at 6
weeks 3 months & 6 months
• Zidovudine following a needle stick injury
↓ HIV seroconversion by 79 %
Preventing perinatal transmission
• Zidovudine given to mother during
pregnancy, labour & delivery & to their
newborns rate of HIV transmission ↓by
2/3rd
• Breast feeding ↑the rate of transmission by
10-20 %
 Treatment
1. Therapy for opportunistic infection&
malignancy
2. Antiretroviral treatment
3. Hematopoietic stimulating factor
(erythropietin)
4. Prophylaxis of opportunistic infection
 Antiretroviral Drugs
• Zidavudine
• Lamivudine
• Abacavir
• Tenofovir
• Enfuvitide
Cerebral Malaria
 Malaria
• 4 species of Plasmodium – P. vivax, P. Malariae,
P. Ovale & P.falciparum
• Malaria transmitted from person to person by bite
of infected female anopheles mosquitoes
• Resistance of vector to insecticide continue to ↑
• Congenital transmission &through blood
transfusion
• No animal reservoir for human malaria
 Cycle in mosquito
• Mosquito gets infected by ingesting human
blood containing sexual forms of
parasites(micro & macrogametocytes).In
salivary glands the gametocytes develop
into sporozoites.In next bite sporozoites are
injected into human blood
 Cycle in Human
• Sporozoites reach liver through RBC where
merozoites are formed. merozoites again infect
RBC to repeat the cycle of fever
• In vivax & ovale some sporozoites become
inactive (hypnozoite) Reactivation of hypnozoite
can occur after 6-8 months→ relapse
• In falciparum & malarae hepatic phase is not there
so radical treatment is not required.
 Clinical features
• Cold stage-shaking chills-4-6 hours
• Hot stage-fever 410c or higher
• Sweating stage
Fever is either daily or alternate day
Other features-headache, dizziness, GIT
symptoms-nausea ,vomiting ,pain abdomen
Splenomegaly after 4 or more days of fever
 Falciparum Malaria
• P Falciparum is serious infection & may
prove fatal because of heavy parasitemia
(20%)→sequestration of RBC in capillaries
• Complications: 1)hypotension & shock, 2)
cerebral malaria,3)hemolytic anemia.4)
acute tubular necrosis (black water fever)
5)cardic arrhythmia ,6)DIC 7) pulmonary
oedema,
 Lab investigation
• Thick & thin PS-Giemsa stained – samples
to be taken at the time of shivering
• Antibody test + ve after 8-10 days,but can
not differentiate current from past infection
• ↓ hb
 Prevention
• Prevention of mosquito bite
• Empirical treatment
• Treatment-
 Typhoid Fever
• Salmonellae are transmitted to humans orally by contaminated
food or water. The bacteria traverse the gastrointestinal tract,
including the acidic environment of the stomach, to colonize
the small intestines. In the case of enteric fever (a systemic
illness), salmonellae cross the intestinal barrier, where
phagocytosis by macrophages results in their dissemination
throughout the reticuloendothelial system
• In enteric (typhoid) fever, salmonellae (S. typhi or S.
paratyphi) undergo phagocytosis by macrophages after
crossing the epithelial layer of the small intestine. Once
phagocytosed, the bacteria are protected from
polymorphonuclear leukocytes (PMNs), the complement
system, and the acquired immune response (antibodies).
Salmonellae have evolved mechanisms to avoid or delay
killing by macrophages.
 Clinical Features
• Prolonged fever (38.8° to 40.5°C, or 101.8° to 104.9°F).
• Gastrointestinal symptoms - diarrhea or constipation
• Abdominal
• rash ("rose spots"),
• hepatosplenomegaly, epistaxis, and relative bradycardia.
 Complications
Late complications,in the third and fourth weeks of infection, are
most common in untreated adults and include intestinal
perforation and/or gastrointestinal hemorrhage.
Both complications are life-threatening and require immediate
medical and surgical interventions, with broadened antibiotic
coverage for polymicrobial peritonitis
 Rare complications
• pancreatitis, hepatic and splenic abscesses,
endocarditis, pericarditis, orchitis, hepatitis,
meningitis, nephritis, myocarditis, pneumonia,
arthritis, osteomyelitis, and parotitis.
• Despite prompt antibiotic treatment, relapse rates
remain at ~10% in immunocompetent host
 Carrier
• Approximately 1 to 5% of patients with enteric
fever become long-term, asymptomatic, chronic
carriers who shed S. typhi in either urine or stool
for >1 year. The incidence of chronic carriage is
higher among women and among persons with
biliary abnormalities (e.g., gallstones, carcinoma
of the gallbladder) and gastrointestinal
malignancies.
 Diagnosis
• The diagnostic "gold standard" is a culture positive for S. typhi
or S. paratyphi
• Blood cultures is +ve in 90% during the first week of infection
and 50% by the third week
• A diagnosis can also be based on positive cultures of stool,
urine, rose spots, bone marrow, and gastric or intestinal
secretions.
• Bone marrow cultures remain highly (90%) sensitive despite 5
days of antibiotic therapy.
• Widal test for "febrile agglutinins," are available; however,
given high rates of false-positivity and false-negativity, these
tests are not clinically useful
 Treatment
• Ceftriaxone (1 to 2 g intravenously or intramuscularly) for
10 to 14 days is equivalent to oral or intravenous
chloramphenicol in the treatment of susceptible strains.
• Quinolones -Ciprofloxacin (500 mg orally twice a day for
10 days).Ofloxacin (10 to 15 mg/kg in divided doses twice
daily for 2 to 3 days) .
 Prevention
• Improvements in food handling and
water/sewage treatment, enteric fever has
become a rare occurrence in developed
nations
• Vaccine-oral & injectable.