Toxoplasma gondii Clinical presentation

Toxoplasmosis is - next to PCP - the most important opportunistic tissue protozoan infection in patients with AIDS. Soon after the recognition of the AIDS syndrome, outbreaks of central nervous system (CNS) toxoplasmosis in Western Europe and North America were observed (Luft et al. 1983). The CNS remains the most common localization in AIDS patients, underlining the seriousness of this condition. It is found in 5-10% of North European AIDS patients (Smith et al. 1991), but rarely if the HIV positive patient takes regular chemoprophylaxis with co-trimoxazole (sulfamethoxazole-trimethoprim) (Gallant et al. 1994) or sulphone-pyrimethamine. The CD4+ count at the time of diagnosis is generally lower than for PCP, 100 or below versus 200-300mio./l, respectively (Masur et al. 1989). The clinical presentation may be acute with high fever, confusion, gross neurological deficits, seizures, and even life-threatening brain oedema, closely resembling CNS lymphoma - another common event in severely immunocompromised HIV positive patients. Or it may be insidious with tiredness, discrete mental changes, and low-grade fever, mimicking AIDS dementia.

On computed tomography (CT) scan or magnetic resonance imaging (MRI) scan of the brain, toxoplasmosis most often presents as a focal or multifocal hypodense or ring enhancing lesions (Figure 27.2). Unfortunately, CNS lymphoma may present similarly. If a brain biopsy is not wanted or possible, it is justified to treat the patient empirically with high-dose sulfadiazine plus pyrimethamine. A therapeutic response should be observed clinically within days and on CT scans after 2 weeks. Raffi et al. (1997) showed that 40% of AIDS patients suspected of CNS toxoplasmosis and given specific therapy, were actually not having toxoplasmosis. Thus, more sensitive and specific diagnostic tools are warranted. Even with adequate therapy and life-long maintenance therapy, the prognosis is relatively poor, and relapses not uncommon. New, potent anti-HIV drug combinations (HAART), reduces the need for life-long suppressive therapy of toxoplasmosis (Kirk et al. 1999), but one recent study showed that the incidence of cerebral toxoplasmosis as an AIDS-defining illness remained stable after introduction of HAART (Ives et al. 2001).

Other organs may be affected by toxoplasmosis, with or without simultaneous CNS involvement. Chorioretinitis may be caused by T. gondii in AIDS patients, but is much more often caused by cytomegalovirus (Mathiesen and Lundgren 1997). Detection of intra-ocular antibody production and PCR analysis may be helpful (Verbraak et al. 1996). Pulmonary toxoplasmosis has been reported with increasing frequency (Pomeroy and Filice 1992), mimicking PCP. Next to the brain and the lungs, the myocardium is the site most commonly

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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.

involved in disseminated toxoplasmosis (Jacobs et al. 1991). Necrotizing pancreatitis and multiorgan failure associated with toxoplasmosis has also been described in AIDS (Ahuja et al. 1993).

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