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


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Title: Guidelines for Prevention and Treatment of Opportunistic Infections among HIV-Infected Children Fungal Infections

Guidelines for Prevention and Treatment of
Opportunistic Infections among HIV-Infected
Children Fungal Infections
  • Recommendations from Centers for Disease Control
    and Prevention,
  • the National Institutes of Health, the HIV
    Medicine Association of
  • the Infectious Diseases Society of America, the
    Pediatric Infectious
  • Diseases Society, and the American Academy of

About This Presentation
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could become out of date quickly.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
Aspergillosis Epidemiology
  • Aspergillus species are ubiquitous molds found in
    soil, on plants, and in decomposing organic
  • 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 Clinical Manifestations
  • Pulmonary aspergillosis is the most common
  • 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 Diagnosis
  • 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 Diagnosis (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 Prevention
  • 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

Aspergillosis Treatment
  • Voriconazole is recommended for treatment of
    invasive aspergillosis
  • Adult data indicate that voriconazole is superior
    to amphotericin B but data in children are
  • 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 Adverse Effects and Treatment
  • 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

Candida Infections Epidemiology
  • Most common fungal infections in HIV-infected
  • 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

Candida Infections Epidemiology (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 gt90 in
    children with fever and symptoms gt14 days

Candida Infections Clinical 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

Candida Infections Diagnosis
  • 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

Candida Infections Prevention
  • 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

Candida Infections Treatment
  • 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

Candida Infections Treatment (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

Candida Infections Treatment (3)
  • 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)

Candida Infections Treatment (4)
  • 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 lt50 kg
    dosage range 0.8-1.6 mg/kg daily gt50 kg, adult

Candida Infections Treatment (5)
  • 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

Candida Infections Treatment (6)
  • 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)

Candida Infections Treatment (7)
  • 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

Candida Infections Treatment (8)
  • 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

Candida Infections Treatment (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)

Candida Infections Treatment 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

Coccidioidomycosis Epidemiology
  • 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
  • Reports of infection in nonendemic areas usually
    due to reactivation

Coccidioidomycosis Clinical Manifestations
  • Fever and dyspnea most common presentation
  • Chills, weight loss, lymphadenopathy, chest pain,
    diffuse reticulonodular pulmonary infiltrates,
  • Disseminated disease associated with erythema
    multiforme erythema nodosum erythematous
    maculopapular rash arthralgia bone, joint, and
    CNS infection

Coccidioidomycosis Diagnosis
  • 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 gt 116
    correlate with presence and severity of
    extrapulmonary infection

Coccidioidomycosis Prevention
  • 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 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
  • 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 Treatment (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 Monitoring, Adverse Events
and Toxicity
  • Monitoring of complement fixing IgG antibody is
  • 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 Epidemiology
  • 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
  • Usually severely immunosuppressed

Cryptococcosis Clinical 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
  • Translucent, umbilicated, papules, nodules,
    ulcers, infiltrated plaques seen in disseminated
  • Pulmonary cryptococcosis unusual in children

Cryptococcosis Diagnosis
  • 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 Prevention
  • No proven strategies to prevent exposure
  • Believed to be acquired by inhalation of
    aerosolized particles from the environment

Cryptococcosis Treatment
  • Not well studied in children infection is often
    fatal in the absence of treatment
  • CNS 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
  • Fluconazole plus flucytosine is an alternative to
    amphotericin B (limited data in children)

Cryptococcosis Treatment (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

Cryptococcosis Monitoring and 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 Monitoring and Drug Toxicity (2)
  • Flucytosine toxicity
  • Bone marrow anemia, leukopenia, thrombocytopenia
  • Liver, GI, and renal toxicity
  • Fluconazole toxicity
  • Potential interaction with ARV should be
    evaluated before initiating treatment (A III)

Cryptococcosis IRIS and Treatment Failure
  • IRIS related to cryptococcosis can present within
  • 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
  • Consider use of liposomal amphotericin B
  • Experience with posaconazole or voriconazole is

Histoplasmosis Epidemiology
  • Pathogen is Histoplasma capsulatum
  • Incidence of disseminated histoplasmosis in
    HIV-infected children in the United States is
  • 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 Clinical 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
  • Progressive disseminated histoplasmosis (PDH) is
    fatal if untreated

Histoplasmosis Diagnosis
  • 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
  • Skin testing not recommended for diagnosis

Histoplasmosis Diagnosis (2)
  • Culture of Histoplasma from blood or other
  • 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

Histoplasmosis Prevention
  • 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 Treatment
  • Limited data for children recommendations based
    on adult data
  • PDH is fatal without treatment and should be
    treated with either amphotericin B or
  • Fluconazole has been used successfully as an
    alternative for patients with mild disease and
    for those who cannot tolerate itraconazole

Histoplasmosis Treatment (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
  • Liposomal amphotericin B alternative in event of
    amphotericin B intolerance

Histoplasmosis Monitoring 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 jiroveci (carinii) Epidemiology
  • 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 lt1 year pre-ART
  • CD4 T-cell count not a good indicator of risk in
    infants lt1 year old
  • Infection now unusual owing to routine
    prophylaxis with TMP-SMX

Pneumocystis jiroveci (carinii) Clinical
  • 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 jiroveci (carinii) Diagnosis
  • Hypoxia with low arterial oxygen pressure
    (alveolar-arterial oxygen gradient gt30 mmHg)
  • Definitive diagnosis requires demonstrating
  • Induced sputum (difficult lt2 years)
  • Bronchoscopy with bronchoalveolar lavage
  • Fiberoptic bronchoscopy with biopsy generally
    not recommended

Pneumocystis jiroveci (carinii) Diagnosis (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

Pneumocystis jiroveci (carinii) Prevention
  • 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 jiroveci (carinii) Prevention (2)
  • Chemoprophylaxis with TMP-SMX recommended as
    follows, based on CD4 counts and patient age
  • 6 years CD4 count lt200 cells/µL or CD4
    percentage lt15
  • 1 to 5 years CD4 count lt500 cells/µL or CD4
    percentage lt15
  • All HIV-infected infants lt12 months of age
    regardless of CD4 count or percentage

Pneumocystis jiroveci (carinii) Treatment
  • TMP-SMX (A I)
  • gt2 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 jiroveci (carinii) Treatment (2)
  • Adverse reactions
  • Rash
  • Stevens-Johnson syndrome (rare)
  • Neutropenia, thrombocytopenia, megaloblastic or
    aplastic anemia

Pneumocystis jiroveci (carinii) Treatment (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
  • Consider oral atovaquone after 7-10 days (B III)

Pneumocystis jiroveci (carinii) Treatment
  • 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
  • Adverse reactions include rash, nausea, diarrhea,
    increased liver enzymes

Pneumocystis jiroveci (carinii) Treatment
Alternatives (2)
  • Clindamycin/primaquine
  • Used for mild to moderate PCP in adults no data
    in children (C III)
  • Primaquine contraindicated in G6PD deficiency

Pneumocystis jiroveci (carinii) Treatment
Alternatives (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
  • Adverse reactions include rash, nausea, diarrhea,
    pseudomembranous colitis

Pneumocystis jiroveci (carinii) Treatment
Alternatives (4)
  • Dapsone/TMP
  • Use for mild to moderate PCP in adults no data
    in children (C III)
  • Dapsone dosage lt13 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 jiroveci (carinii) Treatment
  • 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 jiroveci (carinii) Treatment
Adjunct (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

Pneumocystis jiroveci (carinii) Monitoring 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

About This Slide Set
  • 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//