Paham dan Peduli HIV/AIDS Lecture Series dan Ko-Infeksi...

HIV: Infeksi Oportunistik dan Ko-Infeksi

Lecture SeriesPaham dan Peduli HIV/AIDS

Jumat, 3 Mei 2019Kampus Unika Atmajaya Semanggi

ProfilDr.med. Abraham Simatupang, dr., MKesClinical Clinical PharmacologistPharmacologistFakultas KedokteranUniversitas Kristen Indonesia (UKI)

oDokter – FK UKI (1986)oMKes. – FK UGM (1993)oDoktor Medizine – University of Bonn (1996)

•Direktur – Akademi Fisioterapi (2009-2014)• Direktur Pokja HIV & AIDS (2007-2009)• Kepala Dept. Farmakologi & Terapi (2004-2016)• Direktur Lembaga Penelitian (1998-2004)•Pendiri German-Indonesia Medical Association (DIGM)/Asosiasi Dokter Jerman Indonesia• Pendiri Indostaff (Univ. Staff Development)• Pendiri dan Ketua Rumah Philia (pelayanan Ibu & Anak dengan HIV/AIDS. “Melayani bukan dilayani”

[email protected]

Lab workers Health workers Counselors 3

Learning ObjectivesAt the end of this module, you will be able to:• Describe the difference between HIV infection

and AIDS• Describe the pathogenesis of some opportunistic

infections (OI) e.g. HBV, HCV, Toxoplasmosis, TB, Chronic Diarrhea, CMV, etc

• Describe the prevention and some general approaches to OI


Content Overview• What is HIV?• What is AIDS?• What is the difference between OI and

Infections


What is HIV?

• Human: Infecting human beings

• Immunodeficiency: Decrease or weakness in the body’s ability to fight off infections and illnesses

• Virus: A pathogen having the ability to replicate only inside a living cell


Types of HIV Virus• HIV 1

§ Most common in sub-Saharan Africa and throughout the world

§ Groups M, N, and O§ Pandemic dominated by Group M

§ Group M comprised of subtypes A - J

• HIV 2§ Most often found in West Central Africa, parts

of Europe and India


Structure of HIV

Lab workers Health workers Counselors

Replikasi Virus

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• Enzim Virus: • Reverse Transcriptase: RNA → DNA• Protease: cuts long protein strands into small

functional proteins and enzymes needed to assemble mature virus

• Integrase: integrasi HIV DNA ke dalam DNA sel inang (host)

C:/Users/PORTAL/Videos/HIV Replication 3D Medical Animation - YouTube (360p).mp4


What is AIDS?• Acquired: To come into possession of

something new • Immune Deficiency: Decrease or weakness in

the body’s ability to fight off infections and illnesses

• Syndrome: A group of signs and symptoms that occur together and characterize a particular abnormality

AIDS is the final stage of the disease caused by infection with a type of virus called HIV.


HIV vs. AIDS• HIV is the virus that causes AIDS• Not everyone who is infected with HIV has

AIDS• Everyone with AIDS is infected with HIV• AIDS is result of the progression of HIV

Infection• Anyone infected with HIV, although

healthy, can still transmit the virus to another person


Basic Terms• Antigen: A substance which is

recognized as foreign by the immune system. Antigens can be part of an organism or virus, e.g., envelope, core (p24) and triggers antibody production.

• Antibody: A protein (immunoglobulin) made by the body’s immune system to recognize and attack foreign substances


Testing for Viral Infection and Immune Response • Viral infection

§ Viral Load§ p24 Antigen

• Immune response§ Antibody (IgG, IgM)§ Cellular response (CD4)


Evolution of Antibodies

Window Period


Window Period (Periode jendela)• Time from initial infection with HIV until

antibodies are detected by a single test• Usually 3-8 weeks before antibodies are

detected• May test false-negative for HIV antibodies

during this time period• Can still pass the virus to others during

this period


Disease Progression• Severity of illness is determined by amount

of virus in the body (increasing viral load) and the degree of immune suppression (decreasing CD4+ counts)

• As the CD4 count declines, the immune function decreases.


WHO HIV/AIDS Classification SystemStage I

Asymptomatic

Stage IIMinor

Symptoms

Stage IIIModerate

Symptoms

Stage IV

AIDS


Perjalanan penyakit HIV dan komplikasinya


Gejela-gejala utama AIDS

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Mulut: KandidaEnsefalitis, Meningitis, Toksoplasmosis

Paru2: TB, Pneumosistis pneumonia

Kulit: Tumor Sarkoma Kaposi

Pencernaan: Esofagitis, Diare kronis, Tumor

Berat Badan turun drastis,Fatigue


Toxoplasmosis• Penyebab: Toxoplasma gondii (protozoa)• Paling sering toxoplasma encephalitis• Biasanya CD4 < 200 sel/mm3 (risiko

meningkat bila CD4 < 50 sel/mm3• Profilaksis: TMP-SMX (double strength:

160 mg TMP-800 mg SMX) 2 x/hari selama 14 hari

• Infeksi akut: Pirimetamine-Sulfadiazine


Kandidiasis• Infeksi jamur tersering pada

ODHA• Bisa bertambah berat sampai

ke daerah kerongkongan (esofagus) → kesulitan makan dan minum§ Cotrimoxazole: 10 mg troches 4-5

times/day for 2 weeks (B II)§ Nystatin suspension: 4-6 mL

(400,000-600,000 units/mL) 4 times/day

§ Amphotericin B suspension: (100 mg/mL) 1 mL 4 times/day


Pneumonia - Pneumocystis jiroveci (carinii)• Organisme di

dapatkan di seluruh dunia

• Antibodi pada 80% anak normal umur 4 tahun

• Bisa dicegah dengan profilaksis TMP-SMX


.


INTERACTION OF TB & HIV• HIV -↑number of TB cases and alters the

clinical course of TB disease.• As HIV infection progresses → CD4+ T-

lymphocytes decline in number and function.

• Thus, the immune system becomes less able to prevent the growth and local spread of M. tuberculosis

• The most common types of TB in HIV are disseminated and extra pulmonary TB


Skrining TB aktifAlat skrining: TB ücough of any durationü fever of any durationüexcessive night sweatsü loss of weight >3kg/1moüTempat: klinik,VCT,PMTCT, Puskesmas,

dll/.ü Cough registers


Kolaborasi TB-HIV• Semua pasien HIV → skrining TB• Anamnesis: Batuk lama, keringat malam, BB

Turun• Positif? → Rontgen Toraks, Sputum BTA• Rawat ruang isolasi TB• Semua pasien TB → skrining HIV• Positif?• Terapi ARV tanpa tunggu hasil CD4• Terapi TB dimulai dulu 2 minggu→ + ARV


ISONIAZID PREVENTIVE THERAPY(IPT)ü Tab 300mg OD INH selama 6 bulan.ü Diulang setiap 2 tahunü Eligibility: - Tidak ada hepatitis- Tidak mendapatkan terapi TB dalam 2 tahun terakhir- Tingkat kepatuhan tinggi/adherence- Tidak ada penyalahgunaan alkohol- Tidak ada obat kontraindikasi dengan INH- Tidak ada tanda neuritis perifer


Major Hepatitis VirusesVirus Means of transmission

Hepatitis A Fecal-oral: Contaminated food or water

Hepatitis B Sexual, mother-to-child, blood exposure (transfusion, IDU, tattoo)

Hepatitis C Blood exposure (transfusion, IDU, tattoo); sexual, mother-to-child less common


HBsAg Prevalence³8% - High

2-7% - Intermediate <2% - Low

Geographic Distribution of Chronic HBV Infection

CDC


• Sexual

• Parenteral

• Perinatal

HBV Modes of Transmission

CDC


Hepatitis B• Acute and chronic forms

§ 2-10% develop chronic disease over 5 years of age

• Asymptomatic or symptomatic§ Clinical illness <5 yrs of age: <10%

(jaundice) >5 yrs of age: 30%-50%• Incubation: 45 – 180 days

§ Average 60-90 days• Most common cause of cirrhosis and

hepatocellular carcinoma worldwideCDC


United United States States 3-4 M3-4 M

AmericasAmericas12-15 M12-15 M

Africa Africa 30-40 30-40

MM

Southeast AsiaSoutheast Asia30-35 M30-35 M

AustraliaAustralia0.2 M0.2 M

World Health Organization. Weekly epidemiological record. World Health Organization. Weekly epidemiological record. 1999;74:421-428.1999;74:421-428.

Western Western Europe Europe

5 M5 M

170-200 Million (M) Carriers Worldwide170-200 Million (M) Carriers WorldwideHepatitis C: A Global Health Problem

Eastern Eastern Europe Europe 10 M10 M

Far East Far East AsiaAsia60 M60 M


Acute Hepatitis CAcute Hepatitis C

Chronic Hepatitis Chronic Hepatitis 75%-85 %75%-85 %

Cirrhosis 20 %Cirrhosis 20 %

10-20 years

Hoofnagle JH Hepatology. 1997;26 (suppl 1): 15S-20SDi Bisceglie, Hepatology, 2000

Natural History of Hepatitis CMost patients with chronic HCV infection are asymptomatic


Hepatitis C: Pathophysiology• Hepatitis C virus (HCV) replicates in liver cells

(hepatocytes)• Immune system responds with inflammation• Inflammation leads to fibrosis and eventually, in

some cases, cirrhosis (scarring)


Complications of Cirrhosis

• Dangerous impairment of liver function§ Inability to clear toxins from the circulation => jaundice;

hepatic encephalopathy§ Inability to synthesize key proteins (albumin, clotting

factors)• Cancer (hepatocellular carcinoma)• Blockage of portal vein blood flow through the

liver, leading to ascites§ Bacterial peritonitis (infection of the ascites)§ Esophageal varices

http://ahcuk.50megs.com/images/cirrhosis.jpg


Edema


Ascites


Massive ascites due to hepatocellular carcinoma, with collateral venous dilation


Other Extrahepatic Manifestations of Hepatitis C• Hematologic:

§ Cryoglobulinemia§ lymphoma

• Rheumatologic: rheumatoid arthritis• Renal: Glomerulonephritis• Dermatologic:

§ Porphyria cutanea tarda§ Cutaneous necrotizing vasculitis§ Lichen planus

• CNS: depression• Systemic: fatigue

Management of Hepatitis C. NIH Consensus Statement, 2002.


Hepatitis CHIV/HCV COINFECTION• 10%-30% w/ HIV also have HCV• Rate of HCV depends on risk factor

§ Hemophiliacs – >90%§ IDUs – 70%-90%§ MSM – 5%-10%


HCV/HIV Coinfection• HIV accelerates Hep C liver disease (may

cut time to cirrhosis in half!)

• Hep C may impair immune reconstitution after HAART

• HCC may occur at an earlier age with coinfection


Hepatitis CHIV/HCV COINFECTION• HCV liver disease is more severe in HIV+• HCV liver disease is now more important

§ HIV deaths are decreasing§ Deaths related to liver disease are increasing

• Effect of HCV infection on HIV/AIDS progression is not known


Hepatitis CHIV/HCV COINFECTION• HIV treatments can cause liver

problems/liver enzyme elevations§ In some studies these liver problems are

increased in those w/HCV• Some report worsening of HCV liver

disease after HIV treatment is started


HIV/HCV Treatment• Predictors of success in achieving a

sustained viral response:

• CD4 count greater than 500• HIV RNA levels below 10,000 copies• No alcohol consumption


Drug interactions in Co-infection

• ddI and d4T plus interferon/ribavirin appear to cause mitochondrial toxicity

• result: lactic acidosis, peripheral neuropathy

• Avoid starting these drugs if plan to treat HCV later


Prevention & Treatment Strategies


Ringkasan• HIV yang tidak segera diberi ARV → AIDS• AIDS pintu masuk untuk terjadinya Infeksi

Oportunistik (IO) • Infeksi Oportunistik diterapi sesuai jenis

penyakitnya• Ko-infeksi, infeksi bersamaan dengan HIV• Ko-infeksi tersering HBV, HCV• Terapi ko-infeksi tidak mudah terkait interaksi

obat, efek samping obat dan biaya


Impact of a healing community…

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