Welcome to I-TECH HIV/AIDS Clinical Seminar Series Opportunistic Infections Dr. Robert Harrington,...

Welcome to I-TECH HIV/AIDS Clinical Seminar Series

Opportunistic Infections

Dr. Robert Harrington, M.D.

December 18, 2008

MMWR 1981

1

10

100

1,000

10,000

100,000

1,000,000

10,000,000

Pla

sma

HIV

RN

A

Plasma RNA Copies

CD4 Cells

4-8 Weeks Up to 12 Years 2-3 Years

CD

4 Cell C

ount

1,000

500

Intermediate Stage AIDS

HIV Infection: Pathogenesis

Typical Course

Viral set point

Anti-HIVT-cell response

Sero-conversionAntibody response

A lot of important stuff happens here

1

10

100

1,000

10,000

100,000

1,000,000

10,000,000

Pla

sma

HIV

RN

A

MAC, CMV, PML, PCNSL, Cryptococcus, MicrosporidiaToxo

PCP

4-8 Weeks Up to 12 Years 2-3 Years

CD4 Cell Count

1,000

500

CD4 Count and Opportunistic Infections

200

100

Bacterial Pneumonia, TB, HSV, Cryptosporidiosis

Thrush, lymphoma, KS

Opportunistic Infections and Geography

Common OIs• PCP• MAC• Candida

Regional Effects• Southwest:

– Coccidiodomycosis

• Midwest:– Histoplasmosis and

Blastomycosis

• South: – Blastomycosis and

Toxoplasmosis

North America

Opportunistic Infections and Geography

The World

TBBacteriaMalariaCryptococcus

CandidaPCPMAC

Holmes, CID, 03Putong, SEA Trop Med, 02Margues, Med Mycol, 2000Amornkul, CID, 03

PCPTBCandidaCryptococcusPenicilliosis

PCPTBCryptococcusIsosporaCryptosporidiosisMicrosporidia

PCP, TBCandida, MACCryptococcusLeishmaniasis

Prophylaxis to Prevent Opportunistic Infections

Considerations for Prophylaxis

• Infection should be common and/or predictable

• Infection should be clinically significant

• Treatment (prophylaxis) should be effective, non-toxic and affordable

Prophylaxis to Prevent Opportunistic Infections in the Developed World

PrimaryPCP CD4 < 200

MTb PPD > 5mm

Toxo IgG+,CD4 < 100

MAC CD4 < 50

VZV Exposure with IgG- or no hstry

S. pneumoniae

HBV

HAV

Influenza

SecondaryPCP

Toxo

MAC

CMV

Cryptococcosis

Histoplasmosis

Coccidioidomycosis

Salmonella species bacteremia

Recurrent HSV

Recurrent Candidiasis

Prophylaxis to Prevent Opportunistic Infections in the Developing World

WHO Guidelines on co-trimoxazole prophylaxis for HIV-related infections among children, adolescents and adults. August, 2006

Primary prophylaxis:

Secondary prophylaxis: for PCP and Cryptococcus

TB prevention

• WHO recommendation: – Treat tuberculin skin test positive HIV-infected

persons without active TB with 6 month regimen isoniazid preventive therapy (IPT)

• Difficulties:

• Lack of tuberculin skin testing– People not screened

– Screen positive do not receive INH

– Screen positive started on INH do not complete regimen

HIV-Associated and Opportunistic Infections

• PCP• MAC• Cryptosporidiosis• Microsporidiosis• Bacterial respiratory

infections• Bacterial enteric infections• Bartonellosis• Coccidiodomycosis• Paracoccidiomycosis• Histoplasmosis• Cryptococcus

• Toxoplasmosis• Candida• TB• Aspergillosis• CMV• HSV• VZV• PML (JCV)• HHV-8• HPV• Penicilliosis• Leshmaniasis

HIV ASSOCIATED MALIGNANCIES

AIDS Defining Malignancies

• Kaposi’s sarcoma

• Primary CNS lymphoma (PCNSL)

• Non-Hodgkin’s lymphoma (NHL)

• Invasive cervical cancer

HIV ASSOCIATED MALIGNANCIES

• Hodgkin’s disease• Anal cancer• Multiple myeloma• Leukemia• Lung cancer

• Head and neck tumors• GI malignancies• Genital cancers• Hypernephroma• Soft tissue tumors

Increased Rates of Other Cancers in HIV

EFFECTS OF HAART ON OPPORTUNISTIC INFECTIONS

• Declining incidence

• Reduced need for prophylaxis (primary and secondary)

• Spontaneous improvements and cure

• Immune reconstitution effects

EFFECT OF HAART ON INCIDENCE OF OPPORTUNISTIC INFECTIONS

J.E. Kaplan et al. CID 2000;30:S5-S14 (Kovacks, NEJM, 2000)

Effect of HAART on Opportunistic Infections: Reduced Need for Prophylaxis

Primary Prophylaxis

PCP When CD4 > 200 for 3 months

MAC When CD4 > 100 for 3 months

Toxo When CD4 > 200 for 3 months

Effect of HAART on Opportunistic Infections: Reduced Need for Prophylaxis

Secondary Prophylaxis or Maintenance TherapyPCP When CD4 > 200 for 3 monthsCMV When CD4 > 100-150 for 6 monthsMAC When CD4 > 100 for 6 months, no

symptoms of MAC and after 12 months of MAC Rx

Toxo When CD4 > 200 for 6 months and completed initial Toxo Rx

Cryptococcus When CD4 > 100-200 for 6 months and completed initial Crypto Rx

Opportunistic Infections Treatable with HAART alone

• Progressive Multifocal Leukoencephalopathy (PML)• Cryptosporidiosis• Microsporidiosis• Kaposi’s sarcoma• Mycobacterium avium complex (sometimes)

Case 1

• A 40 yo male with severe bipolar disease presents with cough, weight loss, dyspnea and low grade fever.

• His PMH is notable for recurrent bacterial pneumonia, methamphetamine and alcohol abuse. He has refused all medications.

• On exam he is thin and in mild respiratory distress. T 38C, BP 100/70, HR 100, RR 18, O2 saturation 89% at rest. Lung exam reveals fine rales at lung bases.

Case 1

CXR of Case 1

(www.learningradiology.com)

http://www.learning/

Case 1

• What diagnostic studies do you want?

(www.tulane.edu)

Case 1

• Treatment: – TMP-SMX, pentamidine– Timethoprim-dapsone, clindamycin and primaquine,

atovoqone– Trimetrexate and leucovorin– Severe disease (paO2 < 70 or Aa gradient > 35): add

steroids

How would you treat this patient?

Case 1

• Over the next 10 days the patient slowly improves.

• His CD4 T-cell count returns at 60 cells/uL.

• Should he receive HAART and, if so, when should he start?

Timing of HAART

#142: Immediate Vs Delayed ART in Setting of Acute OI, Zolopa, Powderly, et.al. (ACTG 5164)

• Randomized study of ARV given within 14 days of Rx for OI Vs delayed (at least 4 wks)

• Patients with TB excluded• Primary endpoint: 48 week combination of 3 categorical

variables – 1. Death or alive with new AIDS diagnosis – 2. Alive with HIV RNA > 50 and no new AIDS diagnosis– 3. Alive with HIV RNA < 50 and no new AIDS diagnosis

Timing of HAART

#142: Immediate Vs Delayed ART in Setting of Acute OI, Zolopa, Powderly, et.al. (ACTG 5164)

• Patients (N=282)– Median age 38– Median CD4 = 29 and log10 HIV RNA level = 5.07– OIs

• PCP 63%• Cryptococcal meningitis 13%• Pneumonia 10%

– Median time to starting ART 12 Vs 45 days

05

101520253035404550

Death or NewOI

VL > 50 VL < 50

Immediate

Delayed

Timing of HAART

• No significant difference between immediate Vs delayed for the composite endpoint

• Immediate arm had fewer deaths/new AIDS diagnosis

• Immediate arm had longer time to death/new AIDS diagnosis (HR 0.53)

P=0.035

ACTG 5164: Results

Case 2

• RT is an asymptomatic 47 yo Asian male with newly diagnosed HIV who presents for care.

• His PMH is notable for multiple STDs and “hepatitis”• PE is notable only for thrush, mild cervical adenopathy

and seborrheic dermatitis.• CD4 is 380, HIVRNA is 80K, ALT is 240, HepAAB+,

HepCAB and RNA negative, HepBsAG+, cAB+, eAG+ and HBV DNA 40 million

Case 2

• How common is chronic Hepatitis B infection and why do you suppose he has it?

• What about co-infection with HIV?

Outcome of Hepatitis B by Age of Acquisition

Symptomatic Infection

Chronic Infection

Age at Infection

Ch

ron

ic I

nfe

ctio

n (

%)

Sym

pto

mat

ic I

nfe

ctio

n (

%)

Birth 1-6 months 7-12 months 1-4 years Older Childrenand Adults

0

20

40

60

80

100100

80

60

40

20

0

IgM anti-HBc

Total anti-HBc

HBsAg

Acute(6 months)

HBeAg

Chronic(Years)

anti-HBe

0 4 8 12 16 20 24 28 32 36 52 Years

Natural History: Acute HBV Infection with Progression to Chronic Infection

Weeks after Exposure

Titer

Natural History: Chronic HBV Definitions: NIH Workshop

(Hoofnagle, Hepatology 2007;45:1056-1075)

Immune Tolerant

ImmuneActive(Clearance)

Inactive ChronicCarrier

PerinatalTransmission

60-80%

20-40%

Horizontal Transmission

Natural History: Chronic HBV Definitions: NIH Workshop

• HBsAg-positive for at least 6 months• Phases of Chronic hepatitis B

– Immune Tolerant Phase: HBeAg+, normal ALT, HBV DNA > 200,000 IU/ml (>1 million copies)

– Immune Active or Clearance Phase: elevated ALT, HBV DNA > 2,000 IU/ml, HBeAg or anti-HBe

– Inactive Hepatitis B carrier: anti-HBe, ALT WNL, HBV DNA < 2,000 IU/ml

• Reactivation of hepatitis• Clearance of HBsAg

(Hoofnagle, Hepatology 2007;45:1056-1075)

Hepatitis B: Epidemiology

2 billion people have evidence of HBV infection 1/3 of world’s populations

350 million people chronically infected 15% to 25% will develop HBV-related chronic liver

disease (cirrhosis, hepatocellular carcinoma) and die without intervention

Up to 1 million deaths worldwide each year from HBV-related chronic liver disease

HBsAg Prevalence

8% - High 2-7% - Intermediate <2% - Low


• Among all the chronic hepatitis B carriers worldwide, 75% are Asians

• While the overall incidence of chronic hepatitis B in the US population is less than 1 in 200, the incidence among Asian Americans is 1 in 10 (Source: Asian Liver Center of Stanford University)

• 9-16% of HIV infected patients in the US are co-infected with HBV


Case 2

….back to the case• He is not inclined to start HAART but wants to

discuss it with you.

• Should you be worried about his HBV infection and why?

• Does it influence your decision to recommend HAART?

Natural History: Long-Term Outcome of Chronic HBV

• Hepatocellular carcinoma (HCC)– 25%-40% of males– 10-15% females

• Cirrhosis– 10% to 20% of males and females

Beasley. Cancer 1988;61:1942-66McMahon. Ann Intern Med 2001;135:759-768

Elevated HBV DNA as Risk for HCC: R.E.V.E.A.L.-HBV Study*

• 23,820 residents 7 townships in Taiwan– 4,155 HBsAg-positive– 3,653 tested for HBV DNA at entry– Median age 46 years; follow-up 11.4 years– Findings: Risk factors for HCC at study entry using

Regression analysis• HBV DNA > 104 copies/ml• Liver cirrhosis• Age

Chen JAMA 2006;295:65-73*Funded by Bristol Myers Squib

Chen, C.-J. et al. JAMA 2006;295:65-73. APPLIES TO ADULTS > 40WITH GENOTYPES B&C

Chen, C.-J. et al. JAMA 2006;295:65-73.

Cumulative Incidence of Hepatocellular Carcinoma by Serum HBV DNA Level at Study Entry

Natural History: Chronic HBV: Factors Associated with Progression

• HBV– HBV DNA level– Genotype– Pre-core mutant– Core Promoter mutations

• Other viruses: HIV, DELTA, HCV• Demographic: Age, male sex • Environmental and Social

– Alcohol– NAFLD– Aflatoxin

Natural History: Chronic HBV/HIV Co-infection

• Co-infected patients have– Higher HBV DNA levels– Lower rates of spontaneous HBeAg clearance– More severe liver disease and higher liver-related

mortality– May experience severe hepatitis flares due to immune

reconstitution after HAART– May have “occult” HBV infection with high HBV

DNA levels but with negative HBsAg. • Any HIV+ patient who tests + for either HBsAg or HBcAB

should be tested for HBV DNA

Long-Term Goals of Antiviral Therapy

• Decrease risk of development of cirrhosis• If cirrhosis is present, decrease risk of

decompensation• If decompensated cirrhosis present, treat to

revert patient to compensated cirrhosis• Decrease risk of development of

hepatocellular carcinoma

HBsAg +

HBeAg

Positive

ALT < 1 X ULN ALT 1-2 X ULN ALT >2 X ULN

Q 6 mo ALTQ 12 mo HBeAg

Q 3 mo ALTQ 6 mo HBeAgLiver bx if persistent or age > 40, Rx as needed

Q 1-3 mo ALT, HBeAgIf persistent, Liver bx & Rx;Immediate Rx if jaundice or decompensated

* HCC surveillance if indicated

AASLD Practice Guidelines, 2007*

Lok & McMahon. Hepatology 2007;45:507-539. Available at aasld.org

HBsAg +

Negative

ALT > 2X ULNDNA > 20,000 IU/mL

ALT 1-2X ULNDNA 2,000-20,000 IU/ml

ALT < 1X ULNDNA < 2,000 IU/mL

Liver bx & Rx Q 3 mo ALT & DNAIf results persist, liver bx, treat as needed

Q 3 mo ALT X 3, Then Q 6-12 mo If ALT still WNL

* HCC surveillance if indicated

AASLD Practice Guidelines, 2007*

HBeAg

Lok & McMahon. Hepatology 2007;45:507-539. Available at aasld.org

Treatment of HBV/HIV Co-infection

• All HBV/HIV patients should be offered HAART• If treating HBV only can use IFN or adefovir• When treating both HIV and HBV - Rx with TDF and FTC

is preferred• Patients already on HAART with agents not active against

HBV can be treated with the addition of IFN, adefovir or entecavir

• Patients with lamivudine resistant HBV can be treated with the addition of TDF

• When altering HAART, consider the need to continue HBV therapy unless the patient has cleared HBeAg

Case 3

• A 38 yo South African male presents with a 10 kg weight loss, 10 weeks of cough and intermittent fever. He has no past medical history.

• On exam he is thin, T 38.8 C, BP 100/70, HR 104, RR 20. He has prominent cervical adenopathy, oral thrush and course breath sounds over his R upper and mid lung zones.

Case 3

• HIV test is + and Sputum smear stains 3+ for AFB

What diagnostic testing do you want?

Case 3

• He is admitted to a hospital ward with similar patients and started on “RIPE” therapy.

• After a week his constitutional symptoms improve. His CD4 T-cell count measures 15 cells/uL.

• Should he be offered HAART? – If so, when should HAART be started?

– Are there TB and HIV drug interactions of concern?

WHO/DHHS: Treatment

Start TB therapyHAART as soon as TB Rx tolerated (b/n 2-8 wks)Some experts would wait until 8 weeks (avoid IRIS)

Start TB therapyHAART after intensive phase of TB Rx(HAART earlier if severely immunocompromised)

Start TB therapyMonitor CD4 count and start HAART when indicated

TB therapy Improving, no OIs HAART when TB Rxcomplete

CD4 not available

CD4 100-200

CD4 200-350

CD4 > 350

HIV-TB

Extrapulmonary TBPulmonary TB

Start TB therapy, start HAART in 2 weeksCD4 < 100

Treatment and Outcome

Thailand• Retrospective study of

1103 HIV+ patients with TB

• 411 received HAART• Risk factors for death

– No HAART– Delay of HAART > 6

months– MDR TB– Gastrointestinal TB

Survival

(Manosuthi, J Acquir Immune Defic Syndr 2006;43:42-46)

Timing of HAART and TB

CROI 2007: Abst # 81: Early Mortality Among Patients with HIV and TB in Africa, Lawn, et, al.

• Observational study of mortality before and during first 16 weeks of ART in patients with (n=213) and without (n=675) TB

• MV analysis: mortality associated only with CD4 < 100 and WHO stage 4

• Among 73 patients who had TB diagnosed prior to HAART there were 14 deaths– 10 occurred among patients waiting for HAART– 4 occurred after HAART - 2 due to IRS

COD in Patients with TB

CROI 2007: Abst # 82: Cause of Death in HIV + Patients with TB in Soweto, South Africa,

Martinson, et.al.Results of complete autopsies, N=47

Immediate Cause of Death

Pulmonary TB 19

Bacterial pneumonia 4

Disseminated TB 4*

CMV pneumonia 7

PCP 3* Contributed to another 28

Immune Reconstitution Syndrome

• TB-associated IRS in South Africa– 160 patients receiving Rx for

TB at the time HAART initiated

– Median CD4 68 – IRS in 12% overall, 32% in

those who started HAART within 2 months of TB Rx

– MV analysis: IRS risks• Low CD4• Early HAART – OR for

starting HAART < 30 days = 69.5

– 2 IRS deaths (both had disseminated TB

TB-IRS and CD4 and HAART

(Lawn, AIDS 2007;21:335-41)

TB/HIV Co-infection: Principles of Treatment

• Treatment generally the same as in HIV- patients (4 drugs for 2 months and 2 drugs for 4 months)

• Sub-optimal response (culture + after 2 months) – give 9 months, skeletal TB – 6 to 9 months, CNS TB – 9 to 12 months

• If using regimens without INH or a rifamycin - duration should be 12 to 15 months

Principles of Treatment:Importance of Rifamycin

• Treatment with NON rifamycin-containing regimens is associated with:

• Higher relapse rates

• Higher mortality

Wallis, et al. (1996) Tuber Lung Dis 77:516-23Hawken, et al. (1993) Lancet 342:332-38Perriens, et al. (1991) AM Rev Resp Dis 144:750-55Korwnromp, et al. (2003) CID 37:101-12

Principles of Treatment

• Be wary of drug interactions between the rifamycins and HIV medications

• Do not use TB treatment regimens that are dosed weekly (e.g. INH-rifapentine) or even twice weekly in patients with CD4 counts < 100

• Consider measuring drugs levels if there is concern for malabsorption or increased elimination of TB therapies


Drug Interactions: The P450 system

• Isoform CYP 3A is affected and/or involved in the metabolism of rifamycins, NNRTI and PIs

• Rifamycins: Induce CYP 3A– Rifampin > rifapentine > rifabutin

– Rifampin is not metabolized by CYP 3A (level not affected by other drugs that influence CYP 3A)

– Rifabutin is metabolized by CYP 3A (level is affected by other drugs that also affect CYP 3A)


Drug Interactions: The P450 system

• NNRTIs (efavirenz and nevirapine)– Induce CYP 3A

• Protease Inhibitors (many)– Inhibit CYP 3A


• If using rifampin - avoid PI-based HAART - use NNRTIs instead

• If using rifabutin - can use PIs or NNRTI - but will have to dose adjust the rifabutin in most cases


Drug Interactions: Rifamycins and PIs

PI Rifabutin RifampinATZ 400/d 150 QOD No

AMP 1200 BID 150 QD (300 3x/wk) No

IDV 1000 q8hr 150 QD (300 3x/wk) No

LPV/r 3 caps BID 150 QD (150 3x/wk) 600 QD +R*

NLF 1250 BID 150 QD (300 3x/wk) No

(*Extra RTV 300 BID)


Drug Interactions: Rifamycins and PIs

PI Rifabutin RifampinSQV/RTV 400/400 BID 150 QOD (150 3x/wk) NoIDV/RTV 800/200 BID 150 QOD (150 3x/wk) NoATZ/RTV 300/100 QD 150 QOD (150 3x/wk) No dataAPV/RTV 600/100 BID 150 QOD (150 3x/wk) No dataTPV/RTV 500/200 BID 150 QOD (150 3x/wk) No dataDRV/RTV 600/100 BID 150 QOD (150 3x/wk) No data


Drug Interactions: Rifamycins and NNRTIs

NNRTI Rifabutin Rifampin

EFV 600 QD 450 QD (600 3x/wk) 600 QD

NVP 200 BID 300 QD 600 QD

DLV No No

Web site for more complete table showing dosages:www.cdc.gov/nchstp/tb/TB_HIV_Drugs/TOC.htm

Case 3

…back to the case• 10 days into his TB therapy he is started on

HAART.• 3 weeks later his fever and cough return

Case 3

What are you worried about and what are you going to do?

XDR TB

# 143: Exogenous Re-infection with MDR and XDR TB Among TB/HIV Infected Patients in Rural South Africa,

Andrews, et.al.

• Case control study of patient with pulmonary TB at Church of Scotland Hospital, South Africa from 2005-06

• N=170; 43 had baseline and follow-up cultures; 23 developed MDR or XDR TB

XDR TB# 143: Exogenous Re-infection with MDR and XDR TB Among

TB/HIV Infected Patients in Rural South Africa, Andrews, et.al.

170 patients with TB

43 had both initial and follow up cultures done

23 developed MDR or XDR TB

17 had paired spoligotypes performed

17/17 pairs were NOT matched

XDR TB# 143: Exogenous Re-infection with MDR and XDR TB Among

TB/HIV Infected Patients in Rural South Africa, Andrews, et.al.

23 developed MDR or XDR TB

17 had paired spoligotypes performed

17/17 pairs were NOT matched

All 17 patients had been hospitalized15/17 who were HIV tested were +


(Raviglione, NEJM 2007;356:656-59)

MDR and XDR TB

http://content.nejm.org/content/vol356/issue7/images/large/02f1.jpeg


• XDR TB– Report of 53 cases in rural

South Africa– 55% had never been treated

for TB– 67% had recently been

hospitalized– 44 (100%)/44 tested for

HIV were + (median CD4 63)

– 52 (98%)/53 died, median survival of 16 days

• 49 cases in USA: HIV+: 74% (1993-99) Vs 10% (2000-06)

Survival

(Gandhi, Lancet, 2006; 368: 1575-80)(MMWR, 2007; 56(11): 250-53)

XDR TB

# 112: Confronting the Catastrophe of M/XDR TB, Gerald Friedland

• Infection with resistant organisms acquired in healthcare settings is central to recent MDR/XDR outbreaks

• Need– Better diagnosis and infection control procedures– De-centralization of care– Better integration of HIV and TB care

–Better diagnosis and infection control procedures–De-centralization of care–Better integration of HIV and TB care

Case 4

• A 46 yo Ethiopian male with untreated HIV and a CD4 T-cell count of 110 presents with mild dysphagia, weight loss, abdominal fullness and fatigue.

• On exam he appears chronically ill. T 38 C, BP 110/60, HR 98, RR12. He has thrush, a palpable liver and spleen tip and several nodular skin lesions.

• His Hct is 24, WBC 1800, plts 90. AST 110, ALT 123, AP 200, bili 2.3.

Case 4

Skin lesions for Case 4

(www.dermatology.cdlib.org)

Case 4

• What is your differential diagnosis for this patient?

• What diagnostic tests will you perform?

Case 4

• Blood smear or buffy coat or BM of Leishmania amastigotes

Leishmaniasis and HIV

• An intracellular protozoa• Transmitted to humans by phlebotomine sand flies• Most cases reported in southern Europe (Spain,

Italy, France), Ethiopia, central and south America


(www.who.int)

Reported cases of Leishmania and HIV Co-infection - 1998


Clinically• Cutaneous, mucosal or visceral disease• HIV patients:

– Disseminated visceral disease – Cytopenias– Atypical locations: GI, lung, pleura and peritoneal

spaces, unusual cutaneous lesions


Treatment: HAART +• AmB 0.5 to 1.0mg/kg/d (to total dose of 1.5-2.0

gms)• Liposomal AmB 2-4mg/kg/d (to total dose of 20

to 60 mg/kg)• Pentavalent antimony 20 mg/kg/d for 3-4 weeks

• Secondary prophylaxis q 3 to 4 weeks• Consider discontinuing if CD4 > 350

Opportunistic Infections - not discussed

• MAC• Cryptosporidiosis• Microsporidiosis• Bacterial respiratory

infections• Bacterial enteric

infections• Bartonellosis• Coccidiodomycosis• Paracoccidiomycosis• Histoplasmosis• Cryptococcus

• Toxoplasmosis

• Candida

• Aspergillosis

• CMV

• HSV

• VZV

• PML (JCV)

• HHV-8

• HPV

• Penicilliosis

• Malaria

Summary

• Opportunistic infections are predictable based on a patients immune status and environment

• Disseminated and atypical presentations are the rule with extreme immune suppression

• Prophylaxis against certain OIs is indicated if the OI is common and the prophylaxis is affordable, effective and well tolerated

• HAART alone is treatment enough for certain OIs and can eliminate the need for prophylaxis

• The timing of HAART relative to OI therapy is controversial but should probably be early…..however, watch out for IRIS!

Thank you!

Next session: January 8th, 2009Listserv: [email protected]

Email: [email protected]

Welcome to I-TECH HIV/AIDS Clinical Seminar Series

Next session: January 8th, 2009Lisa FrenkelPediatric HIV

Welcome to I-TECH HIV/AIDS Clinical Seminar Series Opportunistic Infections Dr. Robert Harrington,...

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