Acquired Immune Deficiency Syndrome (AIDS)

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Acquired Immune Deficiency Syndrome (AIDS)

Caused by the human immunodefficiency virus (HIV). AIDS is the clinical syndrome caused by infection with HIV and the resultant immunodeficiency  predisposes to infections and cancers. First described in 1981.

HIV virus:
two types – HIV-1 & HIV-2
HIV-1 is primary cause

Diagnosis of AIDS:
• defined as the development of one or more AIDS indicating conditions when positive for HIV and a CD4 lymphocyte count <200 x 106/l AIDS indicating conditions – pneumocystis pneumonia, non-Hodgkin’s lymphoma, primary CNS lymphoma. progressive multifocal leukoencephalopathy, Kaposi’s sarcoma, oesophageal candidiasis, cancer of the cervix, mycobacterium avium intracellulare, CNS toxoplasmosis, tuberculosis, Wasting syndrome, CMV retinitis; dementia, cryptococcal meningitisHIV is transmitted by: • sexual contact (vaginal or anal) with infected individuals – 75% of cases worldwide; in developing countries; in developing countries, this is most heterosexual • exposure to infected blood or blood products (screening of blood in most countries have reduced this mode of transmissions to minimal levels) • IV drug use with contaminated needle • improper infection control procedures by health professional (eg needle stick injury) • infected mother to neonate It is not transmitted by salvia, tears, body contact, sweat, objects touched by HIV positive persons.Time between HIV infection to developing AIDS can be as high as 10 years  public health problem to control spread of disease.Epidemiology: • about 16000 new case per daily world wide (1600 children)Relative risks of transmission: Blood transfusion – 1:1 Seropositive mother to neonate – 1:4 Seropositive male to female during intercourse – 1:3 to 1:2500 Health care worker with needle stick injury exposed to HIV infected blood – 1:300 Casual contact with HIV infected person – no reported cases Cutaneous exposure to blood infected with HIV – no reported caseTransmission to health care workers: • very rare • greatest risk if from needle stick injury with HIV contaminated blood • risk of transmission following needle stick injury is 1 in 300Pathogenesis: HIV binds to CD4 receptors on helper T-cells (CD4 cells), monocytes and neural cells Seroconversion  dissemination of virus to lymphoid organs Helper T- cells die  release of new virions  infect other cells  more virions produced (turnover of CD4 cells on a daily basis is in the billions) When body can no longer replace CD4 cells  immunodefficiencyClinical features: Following initial HIV infection (primary infection)  latent period of a few weeks  intense viraemia, followed by seroconversion (antibodies detectable)  fall in viraemia symptoms – 50-90% have acute brief illness of fever, malaise, headache, joint symptoms, muscle aches, rash, tender lymphadenopathy (seroconversion illness)  then asymptomatic phase. Progression from this stage is very variable.General features of HIV disease: Fatigue; fever; malaise; weight loss; diarrhoea; lymphadenopathy; oral candida, splenomegalyDiagnosis – must have high index of suspicion; most develop antibodies within 3 months of exposure; PCR can detect virus prior to seroconversionEarly diagnosis important so access can be gained to treatment while immune system still has some good capacity and to prevent further transmissionDisseminated Disease in AID’s: • infections (cytomegaloviirus (CMV) infection; bacterial septicaemia (eg penumococcal); M. tuberculosis infection; toxoplasmosis; cryptococcosis; histoplasmosis) • neoplasms (Kaposi’s sarcoma; non-Hodgkin’s lymphoma)Organ specific complications: Skin: • Involvement of skin is very common. • Usually – seborrhoeic dermatitis; folliculitis; impetigo; cellulitis; secondary syphilis; herpes simplex; herpes zoster; molluscum contagiosum; fungal infections; Kaposi’s sarcoma; drug eruptionsOral: • Mouth lesions are very common  need for good oral care. • Usually – candidiasis; angular stomatitis; peridontal disease; gingivitis; hairy leucoplakia; ulcers; warts; Kaposi’s sarcoma.Gastrointestinal: Weight loss is common and is a contributor to death in many AID’s patients. Pathogens  diarrhoea;Respiratory: • Infections common. Most serious is Pneumocyctis carinii – commonly the AID’s confirming diagnosis and is most common life threatening infection.Neurological: • Can have – encephalitis, meningitis, myelopathy, peripheral neuropathyHaematological: • In early stages  idiopathic thrombocytopenia purpuraMusculoskeletal: • See Rheumatology ChapterNeedle stick injury/occupational exposure: • seroconversion rate is very low (<0.5% if ‘donor’ is HIV positive) • after injury  wash area, encourage bleeding • report incidence • store blood from both parties and ascertain HIV status • counselling as to risk • Test at 3, 6 and 8 months • if high risk  zidovudineManagement: No cure is yet available.3 types of antiretroviral: • Protease inhibitors (eg indinavir, nelfinavir, ritonavir) • Nucleoside reverse transcriptase inhibitors (eg zidovudine, didanosine, zalcitabine) • Nonnucleoside reverse transcriptase inhibitors (eg nevirapine, delavirdine)Drugs are usually used in combination to inhibit HIV replication.

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