Toxoplasmosis

Toxoplasmosis is a common cause of focal neurological abnormalities in advanced HIV infection, particularly in those with a CD4 cell count less than 200 per microlitre.59,60 It almost always results from reactivation of latent cysts of Toxoplasma gondii. These rapidly divide, resulting in tissue destruction and progressively enlarging necrotic lesions, mainly in the brain (particularly the basal ganglia), but also in the eye and lung.

The onset of symptoms is usually subacute with the most common abnormalities being a hemiparesis or speech problem. Brain stem involvement may result in cranial nerve abnormalities. Occasionally the onset is more abrupt with seizures or cerebral haemorrhage. Confirming a diagnosis of toxoplasmosis can be difficult. Serology is unhelpful as disease is secondary to reactivation of latent infection and thus detectable IgG to T. gondii does not differentiate latent from active infection. If CSF can be safely obtained, PCR for T. gondii may be diagnostic.61 CT or MRI scanning typically demonstrates solitary or multiple, ring-enhancing cerebral lesions, most commonly in the basal ganglia or cerebral hemispheres (Figure 9.1). Whilst ring-enhancing lesions are not diagnostic of cerebral toxoplasmosis, in a patient with AIDS the positive predictive value of detectable toxoplasma IgG and multiple ring-enhancing lesions on CT or MRI is nearly 80%.60 Thus a presumptive diagnosis may be made if there is a favourable response to treatment. Serial scanning can

Figure 9.1 CT scan of a patient with AIDS showing multiple ring-enhancing lesions of cerebral toxoplasmosis

be used to monitor lesions. Ninety per cent of patients will have demonstrable clinical and radiological improvement after two to three weeks of appropriate treatment. If improvement does not occur, if there is clinical deterioration, or if diagnostic doubt remains, a cerebral biopsy should take place.

Treatment for cerebral toxoplasmosis is usually with pyrimethamine and sulfadiazine, plus folinic acid to reduce bone marrow suppression.59 This will result in a clinical response in 68-95% of patients, but 40% will suffer side effects. Pyrimethamine and clindamycin is one of a number of alternative regimens.62 Steroids are used frequently but there has been no definite benefit described and their use can make the interpretation of the results of empirical therapy difficult. After completion of initial therapy patients should take lifelong suppressive therapy unless immune reconstitution occurs after use of HAART.57

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