Measures of Central Tendency: Mean, Median and Mode
nrc_peds_oi_july09_fungal.ppt
1. 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
2. July 2009
2 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become out of date quickly.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 Presentation
3. July 2009
3 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
4. July 2009
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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
5. July 2009
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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
6. July 2009
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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
7. July 2009
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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
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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
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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
10. July 2009
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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
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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
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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
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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
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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
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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
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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
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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)
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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; <50 kg
dosage range 0.8-1.6 mg/kg daily; >50 kg, adult
dosing
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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
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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)
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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
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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
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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)
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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
25. July 2009
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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
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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
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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
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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
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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)
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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)
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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
32. July 2009
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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
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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
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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
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Cryptococcosis: Prevention
No proven strategies to prevent
exposure
Believed to be acquired by
inhalation of aerosolized particles
from the environment
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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)
37. July 2009
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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
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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
39. July 2009
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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)
40. July 2009
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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
41. July 2009
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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
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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
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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
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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
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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
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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
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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
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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
49. July 2009
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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
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Pneumocystis jiroveci (carinii):
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
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Pneumocystis jiroveci (carinii):
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
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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 histology
53. July 2009
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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)
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Pneumocystis jiroveci (carinii):
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
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Pneumocystis jiroveci (carinii):
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
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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 minutes
Consider oral atovaquone after 7-10 days
(B III)
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Pneumocystis jiroveci (carinii):
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
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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
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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 days
Adverse reactions include rash, nausea,
diarrhea, pseudomembranous colitis
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Pneumocystis jiroveci (carinii):
Treatment Alternatives (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
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Pneumocystis jiroveci (carinii):
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
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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 11-21
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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 treatment
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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
About This Slide Set