Parasitic Infections - AETC National Resource Center
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Transcript Parasitic Infections - AETC National Resource Center
Guidelines for Prevention and
Treatment of Opportunistic Infections
among HIV-Infected Children
Parasitic 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become out of date quickly.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
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Cryptosporidiosis/Microsporidiosis:
Epidemiology
Protozoal parasites that cause enteric illness in humans
and animals
Human infection primarily caused by C hominis,
C parvum, C meleagridis
Microsporida include E bieneusi and E intestinalis
Infection results from ingestion of oocysts excreted in
feces of humans or animals
Invade intestinal tract mucosa causing watery,
nonbloody diarrhea, dehydration, malnutrition
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Cryptosporidiosis/Microsporidiosis:
Epidemiology (2)
Person-to-person transmission in child care
centers
Oocysts can contaminate water supplies
Outbreaks associated with contaminated
drinking water and swimming pools
Incidence declined since advent of ART
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Cryptosporidiosis/Microsporidiosis:
Clinical Manifestations
Frequent watery, nonbloody diarrhea
Abdominal cramps, fatigue, vomiting, anorexia, weight
loss, poor weight gain
Fever and vomiting more common in children
Liver involvement causes abdominal pain and elevated
alkaline phosphatase
Less common: myositis, cholangitis, sinusitis, hepatitis,
CNS disease
Different species may cause different clinical
syndromes (eg, Encephalitozoon hellem associated
with keratoconjunctivitis, sinusitis, prostatic abscess)
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Cryptosporidiosis/Microsporidiosis:
Diagnosis
Cryptosporidiosis
Concentrated stool samples demonstrating
oocysts
Evaluate at least 3 separate stool samples
Monoclonal antibody fluorescein stain and EIA
for antigen have enhanced specificity and
sensitivity
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Cryptosporidiosis/Microsporidiosis:
Diagnosis (2)
Microsporidia
Use thin smears of unconcentrated stoolformalin suspension or duodenal aspirates
stained with trichrome or chemofluorescent
agents
Consider endoscopy in all patients with diarrhea
>2 months duration
PCR techniques still in research
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Cryptosporidiosis/Microsporidiosis:
Prevention
Avoid direct contact with fecal material from adults,
diaper-age children, and infected animals
Carefully investigate sources of drinking water and
recreational activities involving water
HIV-infected children should not be allowed to drink
water directly from lakes or rivers
Outbreaks of cryptosporidiosis occasionally have been
linked to municipal water contamination
Some experts recommend that severely
immunocompromised HIV-infected patients should not
share a room with patients who have cryptosporidiosis
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Cryptosporidiosis/Microsporidiosis:
Treatment
Immune restoration following antiretroviral
treatment frequently results in clearing
Supportive care, hydration, electrolyte
replenishment, nutritional supplements
Available treatment inconsistently effective
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Cryptosporidiosis: Treatment
No agents have been consistently effective
Nitazoxanide: effective for Cryptosporidium and
Giardia lamblia (B I for children and C III for HIVinfected children)
Nitazoxanide dosage: 100 mg orally BID for
children 1-3 years; 200 mg BID for children 4-11
years
Limited data: paromomycin, azithromycin
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Microsporidiosis: Treatment
Albendazole: 7.5 mg/kg orally BID; maximum
dosage 400 mg orally BID (A II)
Fumagillin: limited data for adults, no data for
HIV-infected children
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Malaria: Epidemiology
Malaria is caused by the obligate intracellular
protozoa Plasmodium
4 species account for most human infections: P
falciparum (60%), P vivax (25-30%), P ovale and
P malariae
In the United States, 1,200 to 1,400 cases are
reported annually
Most cases of malaria infection in U.S. citizens
are a result of not taking appropriate malaria
chemoprophylaxis
Over 30% of malaria cases in children are
found in newly arrived immigrants
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Malaria: Clinical Manifestations
Clinical studies of malaria present differing conclusions
on whether parasitemia, frequency of malaria,
recurrence, and severity of infection differ in HIV-infected
vs HIV-uninfected children
Fever is the most common symptom of malaria,
accompanied by chills, sweating, headache, myalgias,
malaise, nausea, vomiting, diarrhea, and cough
Chronic symptoms include splenomegaly, fever,
thrombocytopenia, and anemia
Congenital malaria is rare
Malaria may be misdiagnosed as a viral infection or HIV
(HIV also may be misdiagnosed as malaria)
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Malaria: Diagnosis
Thick blood smears are the most sensitive
technique for detecting infection but are not
helpful in determining the infectious species
Giemsa-stained thin blood smear gives the
malaria parasite’s distinctive appearance
Blood smear examination taken at 12-24 hour
intervals may be needed to rule out a diagnosis
A rapid malaria antigen capture assay (Binax
Now) has been approved by the FDA
The test is less sensitive for asymptomatic
individuals
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Malaria: Prevention
HIV-infected children who travel to regions of
endemic malaria should use clothing impregnated
with permethrin
DEET mosquito repellent (30-50% concentration)
is practical and effective
Insecticide-treated bed nets should be provided
Recommendations for chemoprophylaxis are the
same for HIV-infected children and HIVuninfected children
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Malaria: Prevention (2)
Prevention includes mefloquine (Lariam) and
Malarone
Mefloquine chemoprophylaxis is less expensive
and more convenient (once a week) but may be
associated with central nervous system effects
Doxycycline is an alternative chemoprophylaxis
agent
Emerging evidence suggests that TMP-SMX
may protect against new or recurrent cases of
malaria
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Malaria: Treatment
HIV infection status should not determine the
choice of treatment (A II)
Chloroquine-sensitive P falciparum should be
treated with chloroquine
In the United States, resistant P falciparum
treatment choices include atovaquoneproguanil, quinine with clindamycin, or
doxycycline or mefloquine
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Malaria: Treatment (2)
Severe P falciparum should be treated with IV
quinidine gluconate (or IV quinine when
available)
Ritonavir inhibits quinidine metabolism and is
contraindicated
Artemisinin, artesunate and other derivatives
combined with additional antimalarial drugs
have not been approved in the United States
but may be available through the CDC
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Malaria: Treatment (3)
P vivax, P ovale, P malariae
The drug of choice for non-P falciparum is
chloroquine
The drug is well tolerated and side effects
are usually limited to itching
Resistance to chloroquine may exist,
warranting treatment with quinine plus
clindamycin or doxycycline, atovaquoneproguanil, or mefloquine
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Malaria: Adverse Events
Severe malaria commonly induces
hypoglycemia in children, especially when
treated with IV quinine/quinidine
Cardiac monitoring and intensive care
monitoring are recommended when using
quinine/quinidine
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Toxoplasmosis: Epidemiology
Primarily perinatal transmission from primary
infection of mothers during pregnancy
Older children acquire toxoplasmosis from poorly
cooked food and from ingestion of sporulated
oocysts in soil, water, or food
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Toxoplasmosis: Epidemiology (2)
Risk of transmission in HIV-uninfected
mothers with primary infection during
pregnancy = 29% (lower if maternal
infection in 1st trimester)
Perinatal toxoplasmosis infection may
occur in HIV-positive women with chronic
infection
<1% of AIDS-defining illnesses in
children
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Toxoplasmosis: Clinical Manifestations
Non-immunocompromised infants are usually
asymptomatic at birth but majority develop late
manifestations: retinitis, neurologic impairment
Newborn symptoms can include:
Rash, lymphadenopathy, jaundice, hematologic
abnormalities, seizures, microcephaly, chorioretinitis,
hydrocephalus
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Toxoplasmosis: Clinical Manifestations (2)
Toxoplasmosis acquired after birth is initially
asymptomatic, followed by infectious
mononucleosis-like syndrome
Chronic toxoplasmosis can reactivate in HIVinfected children
Isolated ocular toxoplasmosis is rare is usually
associate with CNS disease
Less frequently observed presentations
include pneumonitis, hepatitis, myocarditis
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Toxoplasmosis: Diagnosis
Test all HIV-infected pregnant women for
toxoplasmosis
If positive, evaluate infant for congenital
toxoplasmosis
Use antibody assay to detect IgM-, IgA-, or
IgE-specific antibody in first 6 months or
persistence of IgG antibody after 12 months
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Toxoplasmosis: Diagnosis (2)
Additional methods include isolation of
toxoplasmosis from body fluids or blood
Negative antibody does not exclude
toxoplasmosis – may require CT, MRI, or
brain biopsy in case of encephalitis
In the United States, routine screening for
Toxoplasma is not recommended in HIVinfected children when the mother does not
have Toxoplasma infection
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Toxoplasmosis: Prevention
Council all HIV-infected children and their caregivers
regarding sources of Toxoplasma gondii infection
Advise not to eat raw or undercooked meat
Hands should be washed after contact with raw meat or
when gardening or in contact with soil
Vegetables should be washed well and never eaten raw
Stray cats should not be handled or adopted
Toxoplasma-seropositive adolescents and adult
patients with CD4 counts of <100 cells/µL and
Toxoplasma-seropositive children with CD4 percentage
<15% should be administered prophylaxis with TMPSMX
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Toxoplasmosis: Treatment
If HIV-infected mother has symptomatic toxoplasmosis
during pregnancy, infant should be treated (B III)
Preferred treatment – congenital toxoplasmosis:
Pyrimethamine loading dose of 2 mg/kg orally once
daily for 2 days; then 1 mg/kg orally once daily for
2-6 months; then 1 mg/kg orally 3 times/week with
sulfadiazine 50 gm/kg/dose BID and with leucovorin
(folinic acid) 10 mg orally with each dose of
sulfadiazine (A II)
Optimal duration of treatment: 12 months
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Toxoplasmosis: Treatment (2)
Treatment of HIV-infected children with acquired
CNS, ocular, or systemic toxoplasmosis
Pyrimethamine: 2 mg/kg/day (maximum 50 mg/kg) orally
for 3 days; then 1 mg/kg/day orally and leucovorin 10-25
mg/day plus sulfadiazine 25-50 mg/kg/dose orally, given
4 times daily
Continue acute therapy for 6 weeks
Lifelong therapy should be provided
Alternative to pyrimethamine and leucovorin in sulfasensitive individuals is clindamycin
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Toxoplasmosis: Alternative Treatment
Azithromycin: 900-1,200 mg/kg/day with
pyrimethamine and leucovorin (B II), but not
evaluated in children
Clindamycin with pyrimethamine leucovorin
Adults – atovaquone: 1,500 mg orally BID
plus pyrimethamine and leucovorin (C III), but
not evaluated in children
Limited use of corticosteroids as adjuvant
therapy with CNS disease
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Toxoplasmosis: Adverse Events
Pyrimethamine: rash, Stevens-Johnson
syndrome, nausea, reversible bone marrow
toxicity
Sulfadiazine: rash, fever, leukopenia, hepatitis,
nausea, vomiting, diarrhea, crystalluria
IRIS rare in patients with HIV in toxoplasmosis
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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
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