Clinical Manual for Management of the HIV-Infected ... - myCME.com

6–106| Clinical Manual for Management of the HIV-Infected Adult/2006
P: Plan
Diagnostic Evaluation
Definitive diagnosis requires identification of T gondii
in tissue biopsy or body fluid samples. Brain biopsy
usually is not performed if toxoplasmosis is strongly
suspected; instead, presumptive diagnosis is made on the
basis of clinical presentation, laboratory and imaging
tests, and response to therapy. Brain biopsy should be
considered in patients who do not respond to therapy or
in whom the diagnosis is unclear.
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Serum Toxoplasma IgG antibody test results are
positive in nearly all patients with toxoplasmic
encephalitis. A negative IgG test result makes
the diagnosis very unlikely but does not rule it
out. (Antibody titer changes are uncommon in
reactivation disease and are not useful in making a
diagnosis.)
CNS imaging with computed tomography (CT)
typically shows multiple contrast-enhancing mass
lesions, but may show a single lesion or no lesions.
Magnetic resonance imaging (MRI) is more
sensitive than CT for CNS toxoplasmosis. Other
imaging studies, such as single photon emission
CT (SPECT), may be useful in distinguishing
toxoplasmic lesions from CNS lymphoma.
Polymerase chain reaction (PCR) tests for T gondii
in the cerebrospinal fluid have poor sensitivity.
Other diagnostic tests should be performed as
indicated to rule out other potential causes of the
patient's symptoms.
Patients with toxoplasmic encephalitis typically
respond quickly to treatment. If clinical
improvement is not seen after 10-14 days of
appropriate treatment, or if clinical worsening is seen
in the first week, consider brain biopsy for alternative
diagnoses.
Treatment
Treatment consists of 2 phases: acute therapy and
chronic maintenance therapy.
Presumptive treatment often is begun on the basis of
clinical presentation, positive Toxoplasma IgG, and
results of brain imaging studies. If patients do not
respond quickly to treatment, other diagnoses should be
considered. The following recommendations are based
on treatment guidelines published by the Centers for
Disease Control and Prevention, National Institutes
of Health, and HIV Medicine Association/Infectious
Diseases Society of America (see References below).
Acute Therapy
Preferred
♦ Pyrimethamine 200 mg orally as a single loading
dose, then 50 mg (60 kg body weight) daily + sulfadiazine 1,000
mg (60 kg body weight) + folinic acid
(leucovorin) 10-20 mg daily.
Dosage adjustments to the lower end of therapeutic
range of pyrimethamine and sulfadiazine may
be considered for patients who have significant
bone marrow suppression despite folinic acid
supplementation. Monitor patients carefully for
cytopenias, especially if they are on other agents that
cause bone marrow suppression, such as zidovudine,
valganciclovir, and ganciclovir.
Note: Patients at risk for G6PD deficiency should
be checked for G6PD deficiency before starting
pyrimethamine.
Alternatives
♦ Pyrimethamine + folinic acid (administered as
described above) + 1 of the following:
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Clindamycin 600 mg orally or intravenously
every 6 hours; recommended for patients with
significant allergic reactions to sulfa medications
Atovaquone 1500 mg orally every 12 hours
Azithromycin 900-1,200 mg orally once daily
Trimethoprim-sulfamethoxazole (TMP-SMX)
5 mg/kg TMP and 25 mg/kg SMX orally or
intravenously every 12 hours. This can be considered
when the availability of other regimens is limited or
when patients need intravenous therapy.