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Hiv  Aids
 

Hiv Aids

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    Hiv  Aids Hiv Aids Presentation Transcript

    • HIV- AIDS By Dr. Osman Sadig
      • Epidemiology
      • - HIV, za cause of AIDS is now za 4 th commonest cause of death world-wide.
      • - In 2000, 34.5 million were infected wz HIV, of whom 24.5 in Sub-Saharan Africa
      • - The human & economic costs are high because of high mortality & fall in life expectancy.
      • - Despite that HIV can be isolated from a wide
      • range of body fluids & tissue, the majority of
      • infections are transmitted via semen, cervical
      • secretions & blood.
      • 1- Sexual transmission ( vaginal & anal):
      • Commonest route & coexistent STDs , sp
      • those causing genital ulceration, enhance
      • transmission. Transmission is more efficient
      • from men to women & to za passive partner
      • in anal intercourse.
      • 2- Mother to Child (vertical): Commonest route in children. Transmission occur during pregnancy,
      • during delivery or after delivery through breast feeding. Most infections occur perinatally. Advanced dis. & high viral load in the mother, prolonged & premature rupture of membranes & chorioamnionitis increase za risk of transmission.
      • Interventions to reduce transmission include use antiretroviral agents, delivery by CS and avoidance of breast feeding.
      • 3- Contaminated blood, blood products & organ
      • donations if not screened.
      • 4- Contaminated needles & instruments . The risk
      • of acquiring HIV following a single needle-stick injury contaminated wz HIV is 0.3%.
      • *** No evidence of HIV transmission by social or household contact or by blood sucking insects.
      • The virus
      • - HIV belongs to retroviral family .
      • - 2 types: HIV-1 & HIV-2 ( West Africa. ? India).
      • HIV-2 is more indolent in nature.
      • - RNA virus & needs a living cell to multiply.
      • -The target cells for HIV are CD4 T-lymphocytes
    •  
      • 1- HIV binds to za host CD4 via za envelope glycoprotein ( gp120 )
      • 2- Reverse transcriptase converts viral RNA to ssDNA and host cell polymerase leads to formation of dsDNA which enters za nucleus of CD4 & inserted into its genome via integrase .
      • 3- With za help of za protease enzyme new viral particles are assembled in za cytoplasm and are budded out of za cell ready to infect other CD4 cells.
      • - Virus production lasts 2 days & is limited by the death of za cell due to direct effect of za virus. The half life of za virus is only 6 hrs, but its
    •  
    •  
      • turnover is very high (10 to za power 9 each day) - Immunosuppression is due to progressive and severe depletion of CD4 T-lymphocytes causing both CM & humoral immune def.
      • - HIV also has a direct effect on za nervous tissue, lymphoid tissue & testes.
      • Diagnosis of HIV infection
      • 1- Detection of virus specific Abs:
      • a/ Abs to gp 120 : - detects Abs against envelop glycoprotein gp 120
      • - Routine test for screening & based on ELIZA .
      • - Window period or serological latency is 3/12
      • - Abs have no protective fn & persist for life.
      • - Abs cross za placenta & not reliable indicator of active infection in za baby & in uninfected babies will be gradually lost over za 1 st 18/12 of life
      • - b/ Abs to p24 ( core protein): detected early
      • in infection & lost as dis progresses.
      • 2- Ag assays by : a/ HIV DNA PCR assay : used in diagn of HIV in babies borne to infected mothers & in the
      • window period
      • b/ HIV RNA PCR assay : superseded za above test.
      • It measures za amount of HIV RNA in za blood
      • ( viral load ). Higher viral load is predictive of
      • faster dis progression. This test is also used to
      • assess za response to anti-viral therapy .
      • The viral load can also be measured by c/branched DNA tehneque .
      • 3- Western blot :
      • - confirmatory test
      • - detects Abs against Ag coded by 3 diff viral
      • genes.
      • 4- Isolation of virus in culture for research.
      • *** NACO guidelines for diagn HIV infection is based on 3 diff ELIZA/rapid tests using 3 diff Ags. AIDS is diagn by using 2 diff ELIZA/rapid
      • tests on diff Ags in za presence of AIDS-related
      • opportunistic infections.
      • Clinical features of HIV infection
      • - It is za result of both direct HIV infection and associated immune dysfn .
      • - AIDS is defined as individuals wz CD4 < 200 with AIDS defining conditions in USA while in Europe it is defined without CD4 level. Both need positive HIV test .
      • - IP is 2-4Ws immediately following infection and is both clinically & serologically silent.
      • 1- Primary HIV infection/ seroconversion
      • 2- Asymptomatic infection/clinical latency
      • 3- Symptomatic infection (ARC)
      • 4- AIDS
    • Acute pry infection CD4>500/microlit . Asymp infection CD4 200->500 Symp infection (ARC) CD4 200-500 AIDS CD4 <200 Acute seroconversion Illness in some pts. PGL in some pts. Oro/vulvovaginal candidiasis, ITP, P. neur Hairy leukopl, constitutional symp (fever, Diah > 1/12, mucocutaneous manifestation Constitutional symp ( Wt loss> 10%, Diah >1/12), neurological dis (dementia, myelopathy, P, neuropath), Kaposi's, NHL and Opportunistic infections .
      • ** Seroconversion illness is a self-limiting non-sp
      • illness occurring 6-8Ws after exposure (sore throat, fever, arthralgia, myalgia, lethargy, LN,
      • mucosal ulcers, +/- MP rash, HA, photophobia,
      • myelopathy, neuropathy & rarely encephalopat)
      • It lasts up to 3Ws & recovery is usually complet .
      • There is cytopenia, CD4 lym depleted, raised liver enzymes, Abs absent early, high viral RNA
      • levels. Pts experiencing seroconversion illness may have a more rapidly progressive course of infection.
      • ** Asymp stage have a median time of 10 years
      • ( period from infections to AIDS). Older age and those experiencing seroconversion have
      • a rapid progression.
      • ** AIDS defining conditions :-
      • 1- Tracheal, bronchial or lung candidiasis
      • 2- Oesophageal candidiasis
      • 3- Invasive cervical Ca.
      • 4- Coccidioidomycosis, disseminated or extrapulmonary
      • 5- Extrapulmonary cryptococcosis, e.g meningitis
      • 6- Cryptosoridiosis, chr intestinal (> 1/12)
      • 7- CMV dis other than liver, spleen or LN.
      • 8- CMV retinitis (wz loss of vision)
      • 9- Encephalopathy, HIV related
      • 10- Herpes simplex, chr ulcers (>1/12), or bronchitis, pneumonitis or oessophagitis.
      • 11- Hitsplasmosis, disseminated or extrapulmon
      • 12- Isosporiasis, chr intestinal (>1/12)
      • 13- Kaposi's sarcoma
      • 14- Lymphoma, NHL or Burkett's
      • 15- Pry lymphoma of za brain
      • 16- Mycobact Tb, any site
      • 17- Mycobact avium complex or kansasi, dissem
      • or extrapulm
      • 18- Pneumocystic carinii pneumonia
      • 19- Recurrent pneumonia
      • 20- Progressive multifocal leucoencephalopathy
      • 21- Salmonella septicemia, recurrent
      • 22- Toxoplasmosis of za brain
      • 23- Wasting syndrome, due to HIV
      • *** Clinical case definition for AIDS :
      • An individual wz +ve test for HIV infection
      • by 2 tests based on 2 diff Ags PLUS any
      • AIDS defining condition
      • *** Common opportunistic infections :
      • - Tb, both M. Tb & atypical mycobact.
      • - candidiasis
      • - Herpes zoster
      • - Diarrhoeal:
      • - protozoal: amoeba, giardia, isospora,
      • cryptosporidium..
      • - Helmiths: strongyloidosis
      • - Viral: CMV
      • - Toxoplasmosis
      • - Cryptococcal meningitis
      • - CMV retinitis
      • - VL ?
      • Management of HIV positive patient
      • Treatment approach involves :
      • - Inhibiting viral replication & decrease viral load by antiretroviral drugs.
      • - Treatment & prophylaxis of opportunistic infections
      • - Psychological support.
      • 1- Antiretroviral therapy :
      • - Inhibit viral replication & decrease viral load.
      • - Preserve immune fn by increasing CD4 count.
      • - Prevent dis progression
      • - Decrease za incidence of opportunistic infections.
      • - Reduce dis progression
      • - Prolong survival & improve quality of life.
      • - Possibly reduces za risk of transmission
      • ** The goal of antiretroviral therapy is to bring down za viral load to <50 by triple drug therapy over Ws & Ms.
      • Classes of antiretrovirals
      • Antiretrovirals target two key enzymes, protease
      • and reverse transcriptase:
      • 1- Reverse transcriptase inhibitors
      • a/ nucleoside reverse transcriptase
      • inhibitors (NRTs)
      • b/ non-nucleoside reverse transcriptase
      • inhibitors (NNRTs) 2- Protease inhibitors (PIs)
      • NRTIs NNRTIs PIs
      • Zidovudine Nevirapine Indinavir
      • Stavudine Efavirenz Nelfenavir
      • Lamivudine Delavirdine Ritonavir
      • Didanosine Saquinavir
      • Zalcitabine Amprenavir
      • Abacavir Lopinavir
      • When to initiate antiretrovirals?
      • 1- Asym pts = CD4 goes below 350 or HIV RNA
      • above 30-55000 copies/ml
      • 2- All sym pts irrespective of CD4 count or plasma viral load.
      • Combination therapy
      • - 3 drugs should be used in combination to prevent drug resistance ( HAART).
      • - Initiate therapy using: a-2 NRTIs with either one PI or one NNRTIs e.g
      • Zidovudine + Lamivudine + Indinavir
      • Stavudine + Lamivudine + Nevirapine
      • b- 2 PIs + 2 NRTIs, but za following NRTIs
      • combinations should be avoided because of
      • antagonism or overlapping toxicity
      • Zidovudine + Stavudine
      • Zalcitabine + Stavudine or Didanosine
      • How long should za HIV-infected pt
      • continue taking antiretrovirals?
      • - Antiretrovirals should continue indefinitely
      • because they are only suppressive and not
      • curative
      • - The pt should be committed to lifelong therapy.
      • - The virus remain latent in za long lived resting
      • memory CD4 cells & antiretrovirals are not
      • effective against these cells which are not
      • actively multiplying.
      • Follow up of HIV +ve patients using antiretroviral therapy
      • Follow up pts regularly every 3-6/12 by monitoring:
      • - CD4 counts
      • - Viral load using HIV RNA PCR test
      • - Clinically: look for Wt gain & reduction in the No of opportunistic infections.
      • - Adherence (drug combin)
      • - Drug interactions
      • - Drug side effects - Drug access.
      • Patients counselling
      • Before initiating antiretroviral therapy discuss
      • following points wz za pts
      • - Therapy is only suppressive but za pt can lead
      • healthy productive life.
      • - Long life therapy
      • - Drugs free or at low cost
      • - Side effects & drug interactions
      • - The NO of pills taken is large, but can be reduced by combination therapy
      • - Adherence
      • - Avoid blood donation. Protected sex.
      • 2- Treatment of common opportunistic infections
      • 1- Tb = Anti-Tb drugs + ciprof in resist. cases
      • 2- MAC = Azith + ETB +/- RIF
      • 3-Oropharyngeal candidiasis= topical anti-fungal
      • 4- Oesophageal or tracheal candidiasis= system
      • ketoconazole or fluconazole
      • 5- Herpes simplex/Zoster= Acyclovir
      • 6- CMV retinitis= Ganciclovir
      • 7- Pneumocystic carinii= Co- trimoxazole
      • 8- Toxoplasmosis= pyrimeth & sulfadiazine
      • 9- Cryptococcal meningitis= Amph-B + flucytosin
      • OR Fluconazole + flucytosine & maintain on fluconazole
      • 10- NHL= Chemotherapy
      • 11- Kaposi's sarcoma= Chemotherapy depending on za extent of za dis.
      • 12- Diarrhoea due to:
      • - Salmonella/ shigella= Ciprof, Co- trimoxazole
      • - Campylobacter= erythro/ Azith
      • - Clostridium difficile= metronidazole
      • - Amoeba & giardia= Metronidazole
      • - Isospora= Co- trimoxazole
      • - Stronyloides= Mebendazole
      • - CMV= Ganciclovir
      • - HSV= Acyclovir
      • - VL= SSG.
      • Pediatric HIV infection
      • - ELIZA testing is reliable only after za age of 18/12 since maternal Abs cross za placenta.
      • - HIV DNA PCR is recommended for diagn in children < 18/12 .
      • - Antiretroviral therapy is recommended in all children wz clinical symptoms or evidence of immune suppression regardless of age or viral
      • load
      • - In asym children <1 year start TR soon after diagn regardless of clinical or immune status or viral load.
      • - In asym children aged 1 year or above, start TR immediately or defer if immune status is normal wz regular follow up.
      • - triple therapy is recommended.
      • Maternal transmission of HIV
      • (Vertical transmission)
      • - It is za pry means for infants infection
      • - The risk is 7-40%. 50-70% of transmission occur in late pregnancy or during labour and delivery.
      • - Transmission occurs in utero, during labour and delivery or via breast feeding.
      • - Increased risk of maternal HIV transmission is associated with:
      • - high maternal viral load - low CD4 count
      • - advanced clinical dis - pry infection
      • - chorioamnionitis - mode of delivery - - >4 hr ruptured membr. - breast feeding
      • - Decrease risk of transmission by :
      • - Prophylactic antiretroviral therapy for mother and child to prevent maternal HIV transmission
      • - Use of formula feeding reduces risk of transmis
      • via breast milk as delivery by CS.
      • ** Zidovudine & nevirapine are effective
      • Post-exposure prophylaxis for healthcare personal (PEP)
      • - Contact wz blood or bloody fluids or other potentially infectious fluids (CSF, synovial, pleural, pericardial and amniotic fluid) from HIV +ve pts is hazardous
      • - The risk of infection after percutaneous exposure is 0.3% & depends on za size & type of needle, depth & severity of exposure, volume of blood involved & viral load of pt. The risk after mucus membr exposure is 0.09%
      • - Semen, vaginal secretions & fluids wz visible blood potentially transmit HIV.
      • - PEP aborts infection by inhibiting HIV replication
      • 1- Consider expanded regimen for severe percutaneous exposure. Consider basic regimen if source HIV status unknown
      • 2- For large volume splash over mucosa or non intact skin or less severe percutaneous exposure recommend expanded or basic regimen if source is HIV +ve. Basic regimen if source HIV status unknown.
      • 3- For small volume splash over mucosa & non intact skin consider basic regimen if source is HIV +ve. Basic regimen if source HIV status unknown.
      • 4- For exposure to intact skin PFP is not needed.
      • *** Basic regimen (28 days):
      • Zidov 300 mg tid + lamiv 150 mg bid OR
      • Stavu 750 mg bid + Lamiv 150 mg bid
      • *** Expanded regimen (28 days):
      • As above + indinavir 800 mg tid OR
      • Efavirenz od at bedtime OR
      • Nelfinavir 750 mg tid.