recommendations from centers for disease control and prevention,

Guidelines for Prevention and Guidelines for Prevention and Treatment of Opportunistic Infections Treatment of Opportunistic Infections among HIV-Infected Childrenamong HIV-Infected Children

Fungal InfectionsFungal InfectionsRecommendations from Centers for Disease Control and Prevention,

the National Institutes of Health, the HIV Medicine Association ofthe Infectious Diseases Society of America, the Pediatric Infectious

Diseases Society, and the American Academy of Pediatrics

July 20092 www.aidsetc.org

These slides were developed using the April 2008 Guidelines. The intended audience is clinicians involved in the care of patients with HIV.

Users are cautioned that, because of the rapidly changing field of HIV care, this information could become out of date quickly. Finally, it is intended that these slides be used as prepared, without changes in either content or attribution. Users are asked to honor this intent. Expert opinion should be sought for complex treatment regimens.

– AETC NRC

About This PresentationAbout This Presentation


Aspergillosis: Aspergillosis: EpidemiologyEpidemiology

Aspergillus species are ubiquitous molds found in soil, on plants, and in decomposing organic materials

The most common species causing aspergillosis are A fumigatus and A flavus

Rare but frequently lethal infection Risk factors include low CD4 count, neutropenia,

corticosteroids, concurrent malignancy with chemotherapy, HIV-related phagocytic impairment, previous respiratory infections, broad-spectrum antibiotic exposure


Aspergillosis: Aspergillosis: Clinical ManifestationsClinical Manifestations

Pulmonary aspergillosis is the most common presentation

Invasive pulmonary aspergillosis associated with fever, cough, dyspnea, pleuritic pain

Additional manifestations include necrotizing tracheobronchitis, pseudomembranous tracheobronchitis, CNS involvement, cutaneous, sinus, middle ear and mastoid infection


Aspergillosis: Aspergillosis: DiagnosisDiagnosis

Usually isolated from the blood but also readily isolated from lung, sinus, brain, and skin biopsy

Definitive diagnosis includes histopathologic demonstration of organisms in biopsy specimens

Presumptive diagnosis of respiratory tract infection can be made if Aspergillus species is recovered from respiratory sample


Aspergillosis: Aspergillosis: Diagnosis Diagnosis (2)(2)

Chest radiograph demonstrates either diffuse interstitial pneumonitis or localized wedge-shaped infiltrates

CT of chest may be used to identify a “halo” sign

Cavitation and air crescent formation in chest CDT more frequent in older children and adults


Aspergillosis: Aspergillosis: PreventionPrevention

Consider excluding plants and flowers from rooms and avoiding food items such as nuts and spices

Erect suitable barriers between patient care and construction sites, clean shower heads routinely as well as hot-water faucets and air-handling systems


Aspergillosis: Aspergillosis: TreatmentTreatment

Voriconazole is recommended for treatment of invasive aspergillosis

Adult data indicate that voriconazole is superior to amphotericin B but data in children are limited

Recommended dosage for children is 6-8 mg/kg IV (or 8 mg/kg orally) Q12H, followed by 7 mg/kg IV or orally twice daily

Treatment is continued for 12 weeks


Aspergillosis: Aspergillosis: Adverse EffectsAdverse Effectsand Treatment Failureand Treatment Failure

Voriconazole side effects include reversible dose-dependent visual disturbances, elevated liver enzymes, and occasional skin rash

Amphotericin toxicity is associated primarily with fever, chills, and nephrotoxicity

Efficacy of antifungal therapy for aspergillosis is poor

Experimental approaches include evaluation of caspofungin


CandidaCandida Infections: Infections: EpidemiologyEpidemiology

Most common fungal infections in HIV-infected children

Thrush and diaper dermatitis occur in 50-85% of HIV-infected children

In pre-ART era, oropharyngeal candidiasis found in 94% of children with Candida esophagitis

Disseminated candidiasis rare in children except those with CMV or HSV coinfection, and those with central venous catheter


CandidaCandida Infections: Infections: Epidemiology Epidemiology (2)(2)

A substantial percentage of children with fungemia receive oral, systemically absorbable azole antifungals (eg, ketoconazole)

Complications include disseminated infection of bone, liver, and kidney; endophthalmitis

Mortality from disseminated candidiasis >90% in children with fever and symptoms >14 days


CandidaCandida Infections: Infections: Clinical ManifestationsClinical Manifestations

Thrush and erythematous, hyperplastic, and angular cheilitis

Esophageal candidiasis may present with odynophagia, dysphagia, or retrosternal pain

Children may develop nausea, vomiting, or weight loss and dehydration

New onset of fever in individuals with central venous catheters

Systemic fungemia may lead to endophthalmitis


CandidaCandida Infections: Infections: DiagnosisDiagnosis

Culture and KOH preparation with microscopic demonstration of budding yeast cells in wet mounts or biopsy

Blood culture using lysis centrifugation “Cobblestone” appearance on barium swallow Perform endoscopy in refractory cases to look

for CMV, HSV, MAC coinfections Research studies or evaluating detection of

candidate antigens for early diagnosis


CandidaCandida Infections: Infections: PreventionPrevention

Routine primary prophylaxis of candidiasis in HIV-infected children is not indicated

Candida organisms are common commensals on mucosal surfaces in healthy individuals and no measures are available to reduce exposure


CandidaCandida Infections: Infections: TreatmentTreatment

Treat early uncomplicated oropharyngeal candidiasis (OPC) with topical therapy

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


CandidaCandida Infections: Infections: Treatment Treatment (2)(2)

Oral systemic therapy for OPC Fluconazole: 3-6 mg/kg orally once daily for 7-14 days

(A I) Itraconazole: 2.5 mg/kg orally BID for 7-14 days (A I) Ketoconazole: 5-10 mg/kg/day orally divided into 2

doses given for 14 days (D II) Amphotericin oral suspension or IV for OPC refractory

to other treatment



Esophageal disease Treat both diagnosed esophageal disease and

children with OPC and esophageal symptoms (A I) Initiate treatment with:

Fluconazole 6 mg/kg/day orally or IV on day 1 followed by 3-6 mg/kg for 14-21 days (A I)

Itraconazole oral solution 2.5 mg/kg/dose given twice daily or 5 mg/kg once daily for 14-21 days (A I)

Consider low-dose IV amphotericin B minimum of 7 days for refractory disease (B II)



Esophageal disease Other therapies not fully evaluated in children Voriconazole: loading dose of 6 mg/kg IV Q12H on

day 1, followed by 4 mg/kg Q12H thereafter; after stabilization, change to oral dosing

Caspofungin: available only in IV form; <50 kg dosage range 0.8-1.6 mg/kg daily; >50 kg, adult dosing



Invasive disease Remove central venous catheter Amphotericin B (A I)

0.5-1.5 mg/kg once daily IV over course of 1-2 hours, administered in 5% dextrose at final concentration of 0.1 mg/mL

For mild to moderate disease, begin at 0.25-0.5 mg/kg and increase as tolerated to 1.5 mg/kg

Once stabilized, administer 1.5 mg/kg every other day(B III)

Treat for 3 weeks after last positive blood culture of symptoms



Invasive disease: alternative therapy Fluconazole in stable patients with uncomplicated

candidemia without previous azole treatment (identification of Candida species essential; C krusei and C glabrata are resistant) (E III)

Amphotericin lipid formulations (limited pediatric experience) Amphotericin lipid complex (ABLC, Abelcet) Liposomal amphotericin lipid complex

(AmBisome) Amphotericin B cholesteryl sulfate complex

(ABCD)



Treatment under development Caspofungin, micafungin, and anidulafungin

have been studied in battles with HIV infection, neutropenic children at risk of fungal infection in children with documented candidiasis

Data on HIV-infected children are limited



Amphotericin toxicity Nephrotoxicity: azotemia, hypokalemia Nephrotoxicity can be minimized by hydration

with 0.9% saline intravenously 30 minutes before amphotericin B infusion

Infusion-related chills, fever, and vomiting; pretreat with acetaminophen or diphenhydramine

Rarely: hypotension, arrhythmias, neurotoxicity, hepatic toxicity


CandidaCandida Infections: Infections: TreatmentTreatment (9)(9)

Fluconazole, itraconazole, ketoconazole toxicity

Inhibition of CYP450-dependent hepatic enzymes can result in either decreased levels of azole when administered with other drugs with hepatic metabolism or increased levels of other drugs with hepatic metabolism

Nausea, vomiting, rash, pruritus, Stevens-Johnson syndrome (rare), increased liver enzymes, hepatitis, leukopenia, anemia, hemolytic anemia, alopecia (fluconazole)


CandidaCandida Infections: Infections: TreatmentTreatment Failure Failure

Oral pharyngeal and esophageal candidiasis Initial failure should be treated with oral fluconazole,

itraconazole, oral amphotericin B, or low-dose IV amphotericin B

Invasive disease Amphotericin B lipid formulations can be used for

children who cannot tolerate amphotericin B, have disseminated Candida infection that is resistance to amphotericin B, or are at risk of nephrotoxicity


Coccidioidomycosis: Coccidioidomycosis: EpidemiologyEpidemiology

Increased risk of infection with Coccidioides immitis and Coccidioides posadasii among HIV-infected children in endemic areas (eg, southwestern United States, northern Mexico, Central and South America)

Primary infection of newborn rare In utero and perinatal transmission of

C immitis reported Reports of infection in nonendemic areas

usually due to reactivation


Coccidioidomycosis: Coccidioidomycosis: Clinical Clinical ManifestationsManifestations

Fever and dyspnea most common presentation Chills, weight loss, lymphadenopathy, chest pain,

diffuse reticulonodular pulmonary infiltrates, meningitis

Disseminated disease associated with erythema multiforme; erythema nodosum; erythematous maculopapular rash; arthralgia; bone, joint, and CNS infection


Coccidioidomycosis: Coccidioidomycosis: DiagnosisDiagnosis

Direct examination and culture of respiratory secretions and CSF or biopsy of lesions

Blood cultures positive in 15% of cases Complement fixation assay detects IgG

antibody, positive IgM assays suggest active or recent infection, complement fixation titers > 1:16 correlate with presence and severity of extrapulmonary infection


Coccidioidomycosis: Coccidioidomycosis: PreventionPrevention

Difficult to avoid exposure in endemic areas Exposure can be reduced by avoiding

activities that predispose to inhalation of spores such as disturbing contaminated soil, being outdoors during dust storms


Coccidioidomycosis:Coccidioidomycosis: Treatment Treatment

Limited data in children; recommendations based on adult data

Treat diffuse pulmonary disease or disseminated disease with amphotericin B dosage of 0.5-1.5 mg/kg/day until clinical improvement occurs (A II)

Follow with chronic suppressive fluconazole or itraconazole therapy (A II)

Alterative therapy: fluconazole 5-6 mg/kg BID or itraconazole 4-10 mg/kg BID for 3 days followed by 2-5 mg/kg BID (B III)


Coccidioidomycosis: Coccidioidomycosis: Treatment Treatment (2)(2)

CNS infection, including meningitis High-dose fluconazole 5-6 mg/kg BID If unresponsive to fluconazole, use IV amphotericin

B augmented by intrathecal amphotericin B (C I)


Coccidioidomycosis:Coccidioidomycosis:Monitoring, Adverse Events and ToxicityMonitoring, Adverse Events and Toxicity

Monitoring of complement fixing IgG antibody is useful

Toxicity of antifungal drugs includes fevers, chills, nausea and vomiting, nephrotoxicity

Interaction of all antifungal agents with ARVs should be investigated; fluconazole and itraconazole appear to be safe in combination with ARVs

Voriconazole should be avoided in patients on PIs or NNRTIs


Cryptococcosis: Cryptococcosis: EpidemiologyEpidemiology

Most infections caused by Cryptococcosis neoformans and Cryptococcosis gattii

Infection occurs primarily in tropical and subtropical areas

Low incidence of infection in children, especially with use of ART

Children usually infected during 6-12 year age range

Usually severely immunosuppressed


Cryptococcosis: Cryptococcosis: Clinical ManifestationsClinical Manifestations

Meningoencephalitis most common manifestation Fever, headache, altered mental status evolving

over days to weeks Acute illness with nuchal rigidity, seizures, focal

neurologic signs observed in developing countries Translucent, umbilicated, papules, nodules, ulcers,

infiltrated plaques seen in disseminated disease Pulmonary cryptococcosis unusual in children


Cryptococcosis: Cryptococcosis: DiagnosisDiagnosis Microscopic examination of CSF on India ink-stained

wet mounts Detection of cryptococcal antigen in CSF, serum,

bronchoalveolar lavage fluid (can be negative in culture-positive meningitis)

Fungal cultures from CSF, sputum, and blood cultures can identify the organism

Antigen levels useful in evaluating response to treatment and relapse

Pulmonary disease diagnosed by bronchoalveolar lavage and direct examination of India ink-stained specimens


Cryptococcosis: Cryptococcosis: PreventionPrevention

No proven strategies to prevent exposure

Believed to be acquired by inhalation of aerosolized particles from the environment


Cryptococcosis: Cryptococcosis: TreatmentTreatment

Not well studied in children; infection is often fatal in the absence of treatmentCNS Disease

Amphotericin B induction (0.7-1.5 mg/kg/day IV) combined with 2 weeks of flucytosine (25 mg/kg/dose given 4 times daily) followed by fluconazole for a minimum of 8 weeks

After symptoms are controlled, treat with fluconazole or itraconazole maintenance

Use amphotericin B alone if flucytosine is not tolerated Fluconazole plus flucytosine is an alternative to

amphotericin B (limited data in children)


Cryptococcosis: Cryptococcosis: Treatment Treatment (2)(2)

Pulmonary and extrapulmonary cryptococcosis No clinical trials on the outcome of non-CNS

cryptococcosis in HIV-infected patients Treat with amphotericin B with or without the

addition of fluconazole (A III) Fluconazole or itraconazole should be continued

long-term


Cryptococcosis:Cryptococcosis: Monitoring Monitoring and Drug Toxicityand Drug Toxicity

Amphotericin toxicity Nephrotoxicity: azotemia, hypokalemia Nephrotoxicity can be minimized by hydration with

0.9% saline intravenously 30 minutes before amphotericin B infusion

Infusion-related chills, fever, and vomiting; pretreat with acetaminophen or diphenhydramine

Rarely: hypotension, arrhythmias, neurotoxicity, hepatic toxicity


Cryptococcosis: Cryptococcosis: Monitoring Monitoring and Drug Toxicity and Drug Toxicity (2)(2)

Flucytosine toxicity Bone marrow: anemia, leukopenia,

thrombocytopenia Liver, GI, and renal toxicityFluconazole toxicity Potential interaction with ARV should be

evaluated before initiating treatment (A III)


Cryptococcosis:Cryptococcosis:IRIS and Treatment FailureIRIS and Treatment Failure

IRIS related to cryptococcosis can present within weeks

Optimal treatment of patients experiencing treatment failure has not been defined

Patients failing initial azole treatment should be switched to amphotericin B in combination with flucytosine

Consider use of liposomal amphotericin B Experience with posaconazole or voriconazole

is limited


Histoplasmosis:Histoplasmosis: EpidemiologyEpidemiology

Pathogen is Histoplasma capsulatum Incidence of disseminated histoplasmosis in

HIV-infected children in the United States is <0.4%

Incidence is higher in countries such as Brazil, Argentina, and Mexico (2.7% to 3.8%)

No evidence of dissemination of maternal infection to the fetus or greater severity of infection during pregnancy


Histoplasmosis:Histoplasmosis: Clinical ManifestationsClinical Manifestations

Prolonged fever is the most common presentation Malaise, weight loss, and nonproductive cough Primary pulmonary focus leads to widespread

dissemination in children Pulmonary manifestations common Physical findings include hepatosplenomegaly,

erythematous nodular coetaneous lesions, CNS involvement with meningitis

Anemia, thrombocytopenia, elevated liver transaminases Progressive disseminated histoplasmosis (PDH) is fatal

if untreated


Histoplasmosis: Histoplasmosis: DiagnosisDiagnosis

Serologic testing using CF and immunodiffusion is insensitive in the presence of HIV infection.

Positive in most patients but not useful for diagnosis of acute infection

For diagnosis of CNS disease, a combination of CSF antibody, antigen, and culture is most sensitive

Skin testing not recommended for diagnosis


Histoplasmosis: Histoplasmosis: Diagnosis Diagnosis (2)(2)

Culture of Histoplasma from blood or other sources

Detection of H capsulatum polysaccharide antigen in urine, blood, CSF, or bronchoalveolar lavage using EIA

EIA sensitivity greater in disseminated disease or acute pulmonary disease; greater in urine than in serum

Antigen levels decline with treatment and correlate with both response to treatment and relapse


Histoplasmosis: Histoplasmosis: PreventionPrevention

Most infections occur without a recognized history of exposure

Sites and conditions commonly implicated include outbreaks of soil contamination with bird or bat droppings, older urban and rural structures, and decaying vegetation


Histoplasmosis: Histoplasmosis: TreatmentTreatment

Limited data for children; recommendations based on adult data

PDH is fatal without treatment and should be treated with either amphotericin B or itraconazole

Fluconazole has been used successfully as an alternative for patients with mild disease and for those who cannot tolerate itraconazole


Histoplasmosis: Histoplasmosis: Treatment Treatment (2)(2)

Amphotericin B for patients with severe disseminated disease requiring hospitalization and for those who are immunocompromised

Amphotericin B induction dosage: 1 mg/kg for 4-6 weeks followed by itraconazole chronic suppressive therapy for 12 months (A I)

After successful treatment of acute disease, use chronic lifelong suppressive therapy with itraconazole

Liposomal amphotericin B alternative in event of amphotericin B intolerance


Histoplasmosis:Histoplasmosis:Monitoring and Adverse EffectsMonitoring and Adverse Effects

Antigen levels should be monitored during treatment and for 1 year thereafter

Adverse effects of amphotericin B include nephrotoxicity, infusion related fever, chills, nausea, and vomiting

Azole drugs inhibit CYP450-dependent hepatic enzymes, warranting careful review of drug interactions when using ARVs


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): EpidemiologyEpidemiology

Organisms are found worldwide in the lungs of humans and lower animals

Antibody in 80% of normal children by 4 years Most common AIDS indicator disease in children Incidence highest in first year of life, peaking at 3-6

months Accounted for 57% of AIDS-defining illnesses in

infants age <1 year pre-ART CD4 T-cell count not a good indicator of risk in

infants <1 year old Infection now unusual owing to routine prophylaxis

with TMP-SMX


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):):Clinical ManifestationsClinical Manifestations

Fever, tachypnea, cough, dyspnea, poor feeding, weight loss

Abrupt or insidious onset Bibasilar rales with evidence of hypoxia and

respiratory distress Extrapulmonary locations: spleen, liver, colon,

pancreas, ear, eye, GI tract, bone marrow, heart, kidney, lymph nodes, CNS


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): DiagnosisDiagnosis

Hypoxia with low arterial oxygen pressure (alveolar-arterial oxygen gradient >30 mmHg)

Definitive diagnosis requires demonstrating organism

Induced sputum (difficult <2 years) Bronchoscopy with bronchoalveolar lavage Fiberoptic bronchoscopy with biopsy –

generally not recommended


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Diagnosis Diagnosis (2)(2)

Open lung biopsy most sensitive Requires thoracotomy, chest tube drainage Organisms seen on biopsy with:

Gomori methenamine silver stain Toluidine blue stain Giemsa or Wright stain Monoclonal antibody

DNA PCR for Pneumocystis MSG gene in fluids, lavage – sensitive but less specific than histology


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): PreventionPrevention

Need for isolation of hospitalized patients has not been demonstrated, but when prophylaxis cannot be given, may need to isolate patient or susceptible contacts

Infants born to HIV-infected mothers should be considered for prophylaxis at 4-6 weeks of age and continued until 1 year of age (A II)


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Prevention Prevention (2)(2)

Chemoprophylaxis with TMP-SMX recommended as follows, based on CD4 counts and patient age:

6 years: CD4 count <200 cells/µL or CD4 percentage <15%

1 to 5 years: CD4 count <500 cells/µL or CD4 percentage <15%

All HIV-infected infants <12 months of age regardless of CD4 count or percentage


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): TreatmentTreatment

TMP-SMX (A I) >2 months 15-20 mg/kg/day of TMP

component IV in 3-4 divided doses Infuse over course of 1 hour Administer for 21 days Can be given orally in children with mild to

moderate disease Lifelong prophylaxis indicated


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii): ): Treatment Treatment (2)(2)

Adverse reactions: Rash Stevens-Johnson syndrome (rare) Neutropenia, thrombocytopenia,

megaloblastic or aplastic anemia


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii): ): Treatment Treatment (3)(3)

Pentamidine isethionate Recommended for patients with intolerance

to TMP-SMX or clinical failure with TMP-SMX (A I); do not combine use

4 mg/kg/day IV once daily over period of 60-90 minutes

Consider oral atovaquone after 7-10 days(B III)


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Treatment AlternativesTreatment Alternatives

Atovaquone (B I) Limited data in children 30-40 mg/kg/day divided into 2 doses, given

with fatty foods Infants 3-24 months may require 45

mg/kg/day divided into 2 doses, given with fatty foods (A II)

Adverse reactions include rash, nausea, diarrhea, increased liver enzymes


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Treatment Alternatives Treatment Alternatives (2)(2)

Clindamycin/primaquine Used for mild to moderate PCP in adults;

no data in children (C III) Primaquine contraindicated in G6PD

deficiency


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii): ): Treatment Alternatives Treatment Alternatives (3)(3)

Clindamycin/primaquine Pediatric clindamycin dosing based on other

uses: 20-40 mg/kg/day IV divided into 3 or 4 doses, administered for 21 days

Primaquine dosing based on malaria: 0.3 mg/kg daily of the base, administered orally for 21 days

Adverse reactions include rash, nausea, diarrhea, pseudomembranous colitis


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Treatment Alternatives Treatment Alternatives (4)(4)

Dapsone/TMP Use for mild to moderate PCP in adults; no

data in children (C III) Dapsone dosage <13 years 2 mg/kg/day

orally once daily (A II) for 21 days TMP 15/mg/kg/day orally divided into 3 daily

doses for 21 days Adverse reactions include rash, anemia,

thrombocytopenia, increased liver enzymes


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Treatment AdjunctTreatment Adjunct

Corticosteroids Consider use in moderate to severe

PCP Use within 72 hours of diagnosis Results in reduced respiratory failure,

decreased ventilation requirements, and decreased mortality


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii): ): Treatment Adjunct Treatment Adjunct (2)(2)

Corticosteroids Dosing recommendations vary

Prednisone: 40 mg BID for 1-5 days; 40 mg once daily days 6-10; 20 mg once daily days 11-21

Alternative: prednisone 1 mg/kg BID days 1-5; 0.5 mg/kg BID days 6-10; 0.5 mg/kg once daily days 11-21


Pneumocystis jiroveciPneumocystis jiroveci ( (cariniicarinii):): Monitoring and Adverse EventsMonitoring and Adverse Events

Short courses of corticosteroids have been used in some cases of PCP of moderate to severe intensity starting within 72 hours of diagnosis (A I)

As with other coinfection, IRIS may occur following initiation of ART but has been described infrequently in PCP

Most common adverse reaction to TMP-SMX includes rash and rarely erythema multiforme or Stevens-Johnson syndrome

Pentamidine is associated with renal toxicity, usually occurring 2 weeks after initiation of treatment


This presentation was prepared by Arthur Ammann, MD, Clinical Professor of Pediatrics University of California and President of Global Strategies for HIV Prevention for the AETC National Resource Center, in July 2009

See the AETC NRC website for the most current version of this presentation:

http://www.aidsetc.org

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