Dr Nzau Systemic Fungal Infections 3.ppt

detailed presentation of systemic fungal infections. Excludes skin infections. Includes causative organisms, clinical presentation and treatmewnt

1. Systemic Fungal Infections

2. July 20092 www.aidsetc.org
Aspergillosis: Epidemiology
Aspergillusspecies 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

3. July 20093 www.aidsetc.org
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

4. July 20094 www.aidsetc.org
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

5. July 20095 www.aidsetc.org
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

6. July 20096 www.aidsetc.org
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

7. July 20097 www.aidsetc.org
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

8. July 20098 www.aidsetc.org
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

9. July 20099 www.aidsetc.org
CandidaInfections: 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

10. July 200910 www.aidsetc.org
CandidaInfections: 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

11. July 200911 www.aidsetc.org
CandidaInfections: 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

12. July 200912 www.aidsetc.org
CandidaInfections: 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

13. July 200913 www.aidsetc.org
CandidaInfections: Prevention
Routine primary prophylaxis of candidiasis
in HIV-infected children is not indicated
Candidaorganisms are common
commensals on mucosal surfaces in
healthy individuals and no measures are
available to reduce exposure

14. July 200914 www.aidsetc.org
CandidaInfections: 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

15. July 200915 www.aidsetc.org
CandidaInfections: 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

16. July 200916 www.aidsetc.org
CandidaInfections: 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)

17. July 200917 www.aidsetc.org
CandidaInfections: 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

18. July 200918 www.aidsetc.org
CandidaInfections: 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

19. July 200919 www.aidsetc.org
CandidaInfections: Treatment (6)
Invasive disease: alternative therapy
Fluconazole in stable patients with uncomplicated
candidemia without previous azole treatment
(identification of Candidaspecies essential; C
kruseiand C glabrataare 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)

20. July 200920 www.aidsetc.org
CandidaInfections: 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

21. July 200921 www.aidsetc.org
CandidaInfections: 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

22. July 200922 www.aidsetc.org
CandidaInfections: 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)

23. July 200923 www.aidsetc.org
CandidaInfections: TreatmentFailure
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 Candidainfection that is resistance to
amphotericin B, or are at risk of nephrotoxicity

24. July 200924 www.aidsetc.org
Coccidioidomycosis: Epidemiology
Increased risk of infection with Coccidioides
immitisand Coccidioides posadasiiamong
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 immitisreported
Reports of infection in nonendemic areas
usually due to reactivation

25. July 200925 www.aidsetc.org
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

26. July 200926 www.aidsetc.org
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

27. July 200927 www.aidsetc.org
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

28. July 200928 www.aidsetc.org
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)

29. July 200929 www.aidsetc.org
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)

30. July 200930 www.aidsetc.org
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

31. July 200931 www.aidsetc.org
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

32. July 200932 www.aidsetc.org
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

33. July 200933 www.aidsetc.org
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

34. July 200934 www.aidsetc.org
Cryptococcosis: Prevention
No proven strategies to prevent
exposure
Believed to be acquired by
inhalation of aerosolized particles
from the environment

35. July 200935 www.aidsetc.org
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)

36. July 200936 www.aidsetc.org
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

37. July 200937 www.aidsetc.org
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

38. July 200938 www.aidsetc.org
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)

39. July 200939 www.aidsetc.org
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

40. July 200940 www.aidsetc.org
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

41. July 200941 www.aidsetc.org
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

42. July 200942 www.aidsetc.org
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

43. July 200943 www.aidsetc.org
Histoplasmosis: Diagnosis (2)
Culture of Histoplasmafrom blood or other
sources
Detection of H capsulatumpolysaccharide
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

44. July 200944 www.aidsetc.org
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

45. July 200945 www.aidsetc.org
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

46. July 200946 www.aidsetc.org
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

47. July 200947 www.aidsetc.org
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

48. July 200948 www.aidsetc.org
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

49. July 200949 www.aidsetc.org
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

50. July 200950 www.aidsetc.org
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

51. July 200951 www.aidsetc.org
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 PneumocystisMSG gene in
fluids, lavage –sensitive but less specific
than histology

52. July 200952 www.aidsetc.org
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)

53. July 200953 www.aidsetc.org
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/µLor 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

54. July 200954 www.aidsetc.org
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

55. July 200955 www.aidsetc.org
Pneumocystis jiroveci(carinii):
Treatment (2)
Adverse reactions:
Rash
Stevens-Johnson syndrome (rare)
Neutropenia, thrombocytopenia,
megaloblastic or aplastic anemia

56. July 200956 www.aidsetc.org
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)

57. July 200957 www.aidsetc.org
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

58. July 200958 www.aidsetc.org
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

59. July 200959 www.aidsetc.org
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

60. July 200960 www.aidsetc.org
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

61. July 200961 www.aidsetc.org
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

62. July 200962 www.aidsetc.org
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

63. July 200963 www.aidsetc.org
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

64. July 200964 www.aidsetc.org
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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