Post on 22-May-2017
HIV/ AIDS and Related Diseases
Dr. Musofa Rusli, Sp.PD Div. of Tropical – Infectious Disease, Dept. of Internal Medicine
Faculty of Medicine Universitas Airlangga
Master Class Lecture
Lecture Contents Background – Epidemiology – Transmission – Natural history
Clinical features of HIV – Diseases that define HIV infection – Clinical stadium
Opportunistic infections – Viral infections – Fungal infections – Parasitic infections – Bacterial infections
Immune Reconstitution Inflammatory Syndrome Other diseases related to HIV infection – Malignancy – Common co-infections
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HIV/ AIDS Global Epidemy (Approximate numbers in 2012)
34.000.000 in the world
180.000 in Indonesia
3.500 in Jawa Timur
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Discovery of HIV/ AIDS
Kluster kasus Kaposi’s sarcoma dan PCP pada orang gay di AS (1981)
Nama awal:
– Limfadenopati
– KS dengan infeksi oportunistik
– GRID (gay-related immune deficiency)
– 4H (Haitians, homosexual, hemophiliacs and heroin users) disease
US CDC: AIDS (1982)
Clinical Manifestation of AIDS prior to ARV Era
Co-discoverer of HIV Luc Montagnier*
Institute of Pasteur France Robert Gallo
National Cancer Institute USA
“LAV” “HTLV-III”
Francoise Barre-Sinoussi* Institute of Pasteur France
*Awarded Nobel Prize 2008
1985: AIDS is caused by HIV 1988: World AIDS Day (December 1)
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HIV Replication Cycle
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HIV Initial Infection and Dissemination
Induction of HIV-specific immune responses, beginning with CD8 + T cells and following
with antibodies that provide incomplete control of viremia
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HIV Initial Infection and Dissemination
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The stages and natural history of HIV infection
HIV-1 infection is divided into stages – primary infection with seroconversion – clinical latency – early symptomatic disease – AIDS.
The mode of acquisition: heterosexual transmission, MSM Risk factors for transmission include high plasma HIV viral load and presence of ulcerative genital sexually transmitted diseases. During the period of asymptomatic infection, patients generally have no findings on physical examination except for lymphadenopathy. Despite the lack of symptoms, high rates of HIV replication and CD4 T cell destruction may be occurring.
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HIV Natural History
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Conditions that define an AIDS diagnosis P. carinii pneumonia — 42.6 percent
Esophageal candidiasis - 15.0 percent
Wasting — 10.7 percent
Kaposi's sarcoma — 10.7 percent
Disseminated M. avium infection — 4.8 percent
Tuberculosis — 4.5 percent
Cytomegalovirus disease — 3.7 percent
HIV-associated dementia — 3.6 percent
Recurrent bacterial pneumonia — 3.0 percent
Toxoplasmosis — 2.6 percent
Immunoblastic lymphoma - 1.9 percent
Chronic cryptosporidiosis - 1.5 percent
Burkitt lymphoma - 1.5 percent
Disseminated histoplasmosis - 1.0 percent
Invasive cervical cancer - 0.9 percent
Chronic Herpes simplex — 0.5 percent 11/7/2013
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Lymphadenopathy
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ACUTE EXANTHEM OF HIV INFECTION
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Opportunistic Infections
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Pneumocystis jirovecii Pneumonia
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CYTOMEGALOVIRUS INFECTIONS
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HERPES SIMPLEX VIRUS INFECTIONS
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Human papillomavirus
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VARICELLA-ZOSTER VIRUS INFECTIONS
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PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY
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CANDIDIASIS
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CRYPTOCOCCOSIS
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ASPERGILLOSIS
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Nontuberculous Mycobacterial Infections
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TOXOPLASMOSIS
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Tuberculosis in HIV
HIV infection is a potent risk factor for the development of active tuberculosis (TB).
This may result from: – high risk of reactivation of latent Mycobacterium
tuberculosis infection;
– increased risk of exposure to TB;
– greater risk of infection with M. tuberculosis following exposure to an infectious source;
– progression of M. tuberculosis infection to primary active TB.
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SKIN INFECTIONS
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Eosinophilic folliculitis
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Kaposi’s Sarcoma
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Non-Hodgkin’s Lymphoma
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The Burden of HIV,HBV and HCV Worldwide
Estimated number in million.
350
175
40
12 4
1
0,5
HBV HCV
HIV
Worldwide prevalence of hepatitis and HIV
Infection Worldwide U.S.
HIV 31 million 860,000
Hepatitis B (chronic) 300 million 1 million
Hepatitis C (chronic) 170 million 4 million
Epidemiology
About 400,000 HIV/HCV + in U.S.
● overall 30-50% of HIV+ are co-infected
Prevalence of HCV in HIV+ individuals:
● approx. 90% in IVDU
● 60-85% in hemophiliacs
● 4-8% in HIV+ MSM
HIV/HCV Coinfection
Almost all HIV positive IDU are HCV coinfected
HIV/HCV100% (n=117) Iran
HIV/HCV 98% (n=131)Vietnam
HIV/HCV 99.3% (n=138) China
HIV/HCV 99% (n=131) Chiang Mai
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Certain principles underlie the decision to use prophylaxis
the incidence and prevalence of specific infections in HIV-infected individuals the potential severity of disease in terms of morbidity and mortality the level of immunosuppression at which each disease is likely to occur the feasibility and efficacy of preventive measures, and in particular their impact on quality of life and survival the potential for emergence of organisms resistant to the agents used for prophylaxis the risk of toxicities and drug interactions with antiretrovirals and other drugs used by HIV-infected patients the issue of compliance the cost-effectiveness of prophylaxis.
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DURATION OF PROPHYLAXIS AGAINST OPPORTUNISTIC INFECTIONS
Susceptibility to opportunistic infections can be accurately assessed by the CD4 + T-cell count stop primary or secondary prophylaxis in patients whose immunity has improved as a consequence of HAART and whose T cells have risen above the threshold of increased susceptibity
This is particularly true for patients with complete viral suppression, as ongoing improvements in immune function can be expected
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IMMUNE RECONSTITUTION SYNDROMES
HIV-infected patients who initiate potent antiretroviral therapy with low CD4 T-cell counts, especially less than 100 cells/µL, are at risk for developing immune reconstitution inflammatory syndrome (IRIS) Opportunistic organisms, sometimes at high titer, may be present in HIV-infected hosts who are unable to mount immune responses to clear these pathogens. As immune responses are reconstituted on antiretroviral therapy, however, these microbes can stimulate profound immune reactions The presenting signs of IRIS are usually pathogen specific and relate to the tissues, organs, or compartments that are involved Distinguishing IRIS from clinical worsening of the underlying opportunistic infection can be challenging; cultures and biopsies sometimes help to clarify the picture. Treatment of IRIS may involve anti-inflammatory agents such as nonsteroidal anti-inflammatory drugs or corticosteroids.
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Nucleoside reverse transcriptase inhibitor-associated skin effects
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Terima Kasih
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