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Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor
The etiological agent of AIDS is HIV, which belongs to the family of human retroviruses & subfamily of lentiviruses.
Four recognised human retroviruses belongs to two group
Human T lymphotropic viruses (HTLV-1,2)
Human immundeficiency virus (HIV-1,2)
MODES OF TRANSMISSION
Sexual >75% : Homosexual, heterosexual
Parenteral – blood, blood product transfusion
Vertical Transmission : Mother to child
Injection drug use
The transmission risk after exposure is over 90% for blood or blood product, 15 – 40% for vertical route, 0.5 – 1.0% for injection drug use, 0.2 -0.5% for genital mucous membrane.
CLINICAL MANIFESTATION
General | Fever Pharyngitis Lymphadenopathy Headache/retro orbital pain Athralgia/myalgia Lethargy/ malaise Anorexia/weight loss |
Neurologic | Meningitis Encephalitis Peripheral neuropathy Myelopathy |
Dermatologic | Erythematous maculopapular rash Mucocutaneous ulceration |
The asymptomatic stage – Clinical latency
The length of time from initial infection to the development of clinical disease varies greatly, the median time for untreated patients is approx 10yrs.
Individuals remain well during this period with no evidence of disease except for the possible presence of persistent generalised lymphadenopathy. (Defined as enlarged glands at 2 or more extra inguinal sites)
Long term non progressors: They have low levels of HIV RNA , decline in CD4 cells takes over a period of time.
Persons with high levels of RNA progress to symptomatic disease faster than do patients with low levels of HIV RNA.
Some patients remain asymptomatic despite progressive decline CD4 counts , in these patients appearance of an opportunistic disease may be the first manifestation of HIV.
AIDS
A diagnosis of AIDS is made in anyone with HIV infection & a CD4+ T cell count <200/μL & in anyone with HIV infection who develop one of the HIV associated disease considered to be indicative of a severe defect in cell mediated immunity.
AIDS DEFINING DISEASE
Oesophageal candidiasis
Pulmonary/Extrapulmonary TB
Invasive cervical cancer, kaposi's sarcoma
Disseminated mycobacterium avium infection
Pneumocystis jiroveci pneumonia
Cryptosporidial diarrhea
Extrapulmonary histoplasmosis/ coccidodomycosis
Cerebral toxoplasmosis
CNS lymphoma
HIV dementia
Cryptococcal meningitis
CMV retinitis
Progressive multifocal leucoencephalopathy
DIAGNOSIS
The diagnosis of HIV infection depends on demonstration of antibodies to HIV & or the direct detection of HIV or one of its components.
Antibodies to HIV generally appear in the circulation 3-12 weeks following infection.
P24 antigen capture assay:
They detect viral protein p24 in the blood of HIV infected individuals where it exists as free antigen or complexed to anti-p 24 antibodies.
During the first week of infection there is a brisk rise in p24 antigen levels. Once the antibodies develop they decline.
ELISA
Standard screening test for HIV is ELISA (Sensitivity of >99.5%.).
ELISA is an extremely sensitive test, it is not optimal with regard to specificity.
Factors associated with false positive test are antibodies to class II antigens (such as may be seen following pregnancy, blood transfusion or transplantation, auto antibodies, hepatic disease, acute viral infection, recent influenza vaccination).
These people must be subjected to confirmatory test by western blot.
WETERN BLOT
Western blot is based on the fact that multiple HIV antigen of different, well characterized molecular weight elicit the production of specific antibodies,& they can be separated based on molecular weight. The antibodies to each component can be detected as discrete bands on the western blot.
Western blot is considered positive if antibodies exist to two of the three HIV proteins: p24, gp41 & gp 120/160.
Graph showing the relationship between CD4 counts and viral load during the course of disease
Attribute : "Hiv-timecourse" by Jurema Oliveira - Based on Figure 1 in Pantaleo, G et al. (February 1993). "New concepts in the immunopathogenesis of human immunodeficiency virus infection". New England Journal of Medicine 328 (5): 327-335. PMID 8093551.Also available via Figure 4 in The relationship between the human immunodeficiency virus and the acquired immunodeficiency syndrome. US National Institute of Allergy and Infectious Diseases Retrieved on November 3, 2009.Supporting data for this disease course is available in Piutak, M et al. (March 1993). "High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR". Science 259 (510): 1749-54. PMID 8096089.. Licensed under CC BY-SA 3.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Hiv-timecourse.png#mediaviewer/File:Hiv-timecourse.png
CD4+ T CELL COUNTS
They are generally accepted as the best indicator of immediate state of immunologic competence of patient with HIV infection.
Persons with CD4+ T cell counts <200/μL are at high risk of developing P. jiroveci.
Persons with CD4+ Tcells count <50/μL are at high risk for CMV, Mycobacterium avium complex, T. gondii.
CD4+ T cell counts should be measured at the time of diagnosis & then every 3-6 months.
If CD4+ T cell count is <200/μL prophylaxis for P. jiroveci should be started.
If CD4+ Tcell count is <50//μL primary prophylaxis for MAC is indicated.
A CD4+ T cell percent of 15 is comparable to CD4+ T cell count of 200//μL
In persons with hypersplenism or splenectomy & in patients on bone marrow suppressing drugs, THE CD4+ T cell percentage may be a more reliable indication of immune function.
Viral Load
It is used a prognostic marker & for starting the HAART.
Optimal viral suppression is defined as a viral load persistently below the level of detection < 20 -75 copies/ml.
Plasma viral load is measured before initiation of therapy and preferably within 2-4 weeks after treatment initiation or modification.
In patients with stable ART viral load is checked every 3-4 months.
INITIAL EVALUATION OF THE PATIENT WITH HIV INFECTION
History & physical examination
Routine chemistry & hematology
AST, ALT , direct & indirect bilirubin
Lipid profile & fasting glucose
CD4+T COUNTS
Two plasma HIV RNA level
HIV resistance checking
HLA-B5701 screening
VDRL test
Anti toxoplasma antibody titer
PPD skin test
Mini mental status examination
Serologies for hepatitis A,B &C
Immunisation with pneumococcal polysaccharide, influenza as indicated
Immunization with hepatitis A &B if negative
Counseling regarding natural history & transmission
Help contacting others who might be infected.
ANTIRETROVIRAL THERAPY
INDICATIONS
All patients with AIDS defining illness
All patients with CD4 <200 cells/mm3.
CD4 200 to 350 cells/mm3 should be offered HAART
HIV RNA >10000 copies/ml
Pregnancy
HAART REGIMEN
NNRTI BASED REGIMEN (1NNRTI + 2 NRTI)
Efavirenz 600mg HS + Tenofovir 300mg + Emtricitabin 200mg (Single Tab HS)
Efavirenz 600mg HS (after 2 hrs of food) + Lamivudine 150mg BD + Zidovudine 300mg BD. (T. Lazid E, T. Duovir E) or Stavudine/didanosine
Nevirapine 200mg OD for 1st 14 days, then 200mg BD + Lamivudine+ Zidovudine 300mg BD or stavudine/didanosine
PI BASED REGIMEN
Single PI or Ritonavir boosted PI regime + 2NRTI is used
NRTI | NNRTI | PI |
Zidovudine 300mg BD Lamivudine 150mg BD Tenofovir 300mg OD Emtricitabine 200mg OD Abacavir 300mg OD Zalcitabine 0.75mg TID Stavudine 40mg BD(>60kg) Didanosine 400mg OD (>60kg ) | Nevirapine 200mg OD for 1st 14 days then 200mg BD Efavirenz 600 HS Delaviridine 400mg TID | Atazanavir Indinavir Lopinavir Nelpinavir Ritonavir Saquinavir Darunavir |
Trade Name | Composition |
Vonaday /Trioday
| Efavirenz 600mg + Lamivudine 300mg + Tenofovir 300mg one/day |
Vonavir/ Viraday | Efavirenz 600mg + Emtricitabine 200mg + Tenofovir 300mg one/day
|
Lazid E, Duovir E | Efavirenz 600 mg + Lamivudine 150 mg + Zidovudine 300mg |
Lazid N | Lamivudine 150mg + Nevirapine 200mg + Zidovudine 300mg |
Lazid | Lamivudine 150mg + Zidovudine 300mg |
Updated on 1/1/2015
Reference
Harrison 18th edition
Davidson
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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor