Guidelines For Prevention and Treatment of Opportunistic Infections Among HIV-Infected Children

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 Pediatrics
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become out of date quickly.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
2 July 2009 www.aidsetc.org

Aspergillosis: Epidemiology
 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: Clinical 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: 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 systems

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
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: Adverse Effects
and 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

Candida Infections: Epidemiology
 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

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 >90%
in children with fever and symptoms >14 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
times/day

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

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

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 nephrotoxicity

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 reported
 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,
meningitis
 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 >
1:16 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 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: 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 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: 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 range
 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 countries
 Translucent, umbilicated, papules, nodules, ulcers,
infiltrated plaques seen in disseminated disease
 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 tolerated
 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
long-term

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 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: Epidemiology
 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: 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 transaminases
 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
sensitive
 Skin testing not recommended for diagnosis

Histoplasmosis: Diagnosis (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: 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
itraconazole
 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 itraconazole
 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 <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

Clinical 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

Diagnosis
 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

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 histology

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)

Prevention (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

Treatment
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

Treatment (2)
 Adverse reactions:
 Rash
 Stevens-Johnson syndrome (rare)
 Neutropenia, thrombocytopenia,
megaloblastic or aplastic anemia

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

Treatment 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

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

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

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

Treatment 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

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 11-21

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 treatment

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://www.aidsetc.org

Guidelines For Prevention and Treatment of Opportunistic Infections Among HIV-Infected Children

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Guidelines For Prevention and Treatment of Opportunistic Infections Among HIV-Infected Children

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Guidelines for Prevention and

Treatment of Opportunistic Infections

These slides were developed using the April 2008

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 Fever and dyspnea most common presentation

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 Difficult to avoid exposure in endemic areas

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 Antigen levels should be monitored during

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 Hypoxia with low arterial oxygen pressure

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