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2012; Vol.1,No.1 APRIL - JUNE
ISSN 2319 – 4154

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TOXOPLASMOSIS REVISITED

Sheela Mathew, MD
Infectious Diseases Department, Government Medical College Hospital Trivandrum – 695011, India
Email: dr.sneha.n@gmail.com

  • Infection inimmunocompromised patients

    Most cases oftoxoplasmosis in immunocompromised patients are a consequence oflatent infection and reactivation. In patients with AIDS, T gondiitissue cysts can reactivate with CD4 counts less than 200 cells/μL. When CD4 counts are less than 100 cells/μ L, clinical diseaseis more likely. Patients with CD4 counts less than 100 cell/μ Land T gondii IgG positivity have a 30% risk of eventually developingreactivation disease, if adequate prophylaxis is not given or immunefunction is not restored. Although toxoplasmosis in immunocompromisedpatients may manifest as chorioretinitis, reactivation disease inthese individuals is typically in the central nervous system withbrain involvement being common.

    Toxoplasmicencephalitis and brainabscess presents most commonly as headache, focal neurologicdeficits and seizures. Lumbar puncture studies performed when thereis no evidence of raised ICT reveals a picture mimicking tuberculousmeningitis. With significant disease, patients may also have thesigns and symptoms of elevated intracranial pressure. Cerebraltoxoplasmosis is generally identified on CECT scan as multiplering-enhancing lesions; solitary lesions may also be seen. Absence oflesions in CT or MRI scans does not rule out the diagnosis of centralnervous system toxoplasmosis. When plain CT scan of a patient revealsan infarct like picture, contrast study must be done, as many casesare misdiagnosed as vascular events. In a patient who isimmunosuppressed and has focal neurologic deficits, if CT scan isnormal, MRI scan is advisable.7

    Aside from centralnervous system toxoplasmosis, toxoplasmic pneumonitis, myocarditis,as well as disseminated toxoplasmosis are also commonly identified inimmunocompromised patients. Toxoplasmic pneumonitis typicallypresents with symptoms, which are typical for an infectious pulmonaryprocess. Symptoms include fever, dyspnea, and cough. Chestradiography is often nonspecific, but findings may be similar to thatofPneumocystisjiroveci pneumonia. Diagnosis is establishedvia broncho-alveolar lavage (BAL). Most patients with extra-centralnervous system manifestations of toxoplasmosis will also be noted tohave central nervous system lesions when appropriate radiographicstudies have been performed.

    toxoplasmosis

    Figure 2. ContrastEnhanced Computed Tomographic scan(CECT) of brain. Multiple ring enhancing lesions can be seen.

  • Toxoplasmicencephalitis and brain abscess can result in permanent neurologicsequelae depending on the location of the lesion and the extent oflocal damage and inflammation.8

    Diagnosis

    Diagnosis isconfirmed by isolation of toxoplasma from blood or body fluids,demonstration of parasite in tissues, detection of specific nucleicacid sequence with DNA probes, or detection of toxoplasma specificimmunoglobulin. Polymerase chain reaction (PCR) amplification is usedto detect the DNA in body fluids and tissues. Amniotic fluid, braintissue, BAL fluid, cerebrospinal fluid, vitreous and aqueous fluid,urine and peripheral blood can be used for PCR. IgM levels areestimated to demonstrate acute infection. IgG levels are assayed fordiagnosing past infection. Many tests for avidity of Toxoplasma IgGantibodies have been introduced to differentiate between recentlyacquired and distant infection.9

    Treatment

    Immuno-competent,non-pregnant patients do not require treatment. If there is eye involvement or central nervous system involvement,treatment should be started. Treatment includes six-week regimenofpyrimethamine(100 mg loading dose per orally followed by 25-50 mg/d) plussulfadiazine (2-4 g/d divided four times a day) or pyrimethamine (100mg loading dose per orally followed by 25-50 mg/d) plus clindamycin(300 mgper orally four times a day) and folinic acid (leucovorin)(10-25 mg/d) to prevent hematologic toxicity of pyrimethamine.Trimethoprim (10 mg/kg daily) and sulfamethoxasole (50 mg/kg/daily)can also be used. In patients with history of allergy to the formerdrugs azithromycin 500 mg daily or atovaquone 750 mg twice a day canbe considered. Atovaquone is a promising alternative for thetreatment of ocular toxoplasmosis in immune competent patients.Atovaquone tablets (750 mg four times a day) for 3 months along withprednisolone (40 mg) tablets on tapering dose added on day 3 onwardsis as effective as conventional therapy. Consider administration ofsteroids in patients with radiologic midline shift, clinicaldeterioration after 48 hours, or elevated intracranial pressure.