In practice, the diagnosis of CNS toxoplasmosis is based on typical clinical and radiological symptoms and signs, and on therapeutic response. Positive serology is present in more than 90%, but the specificity is low: in one large series of European patients, 40% of patients with non-toxoplasmic brain lesions were seropositive as well (Raffi et al. 1997). IgG antibodies are much more common than IgM, pointing to reactivation rather than new infections. In one Danish series of 17 AIDS patients with CNS toxoplasmosis, all were IgG positive but none IgM positive (Smith et al. 1991). Intrathecal antibody production may further support the diagnosis (Potasman et al. 1988), as may PCR on cerebrospinal fluid (Lebech et al. 1992). However, the diagnostic sensitivity of the latter has not been found to be satisfactory (Clinque et al. 1997).
Figure 27.2 CT scan of the brain of an AIDS patient with T. gondii infection: a focal ring enhancing lesion is clearly visible centrally in the left hemisphere, surrounded by oedema, partially compressing and displacing the ventricle system of the brain.
The definitive diagnosis by demonstrating T. gondii in a brain biopsy is rarely practicable: among 17 Danish patients with CNS toxoplasmosis, only three had histologically proven diagnosis, and all three at autopsy (Smith et al. 1991). Pulmonary toxoplasmosis may be confirmed by microscopy of BAL or biopsies (Jacobs et al. 1991); the diagnosis may be supported by extreme elevations of serum LDH (Pugin et al. 1992). Generally, toxoplasmosis of the brain in AIDS patients responds well to treatment with high-dose sulfadiazine plus
pyrimethamine. In case of adverse reactions (seen in 20-40%), clindamycin plus pyrimethamine, or atovaquone may be used (Kovacs 1994). Life-long chemotherapy/ prophylaxis is hardly needed after the introduction of HAART, but resistance to HAART, however, calls for continuousness. Further details on management of toxoplasmosis should be sought in standard textbooks.
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