INTRODUCTION Granulomatous inflammation is a distinctive ...

Toxoplasmosis is caused by an intracellular protozoan. The three forms of the parasite are the
trophozoite, cyst and oocyst. The trophozoites are responsible for the acute infection and the cysts
are present in multiple organs in the latent form (Bia and Barry, 1986). The human beings acquire
the infection by ingestion of the oocyst, the ingestion of poorly cooked infected meat, and by
congenital infection in utero . T. gondii, like other opportunistic pathogens, has a high prevalence
rate in many populated groups and is capable of living in multiple tissues for the entire life of its
host (Bollinger et al., 1995).
After oral ingestion, it is carried as latent infection without causing disease. IgG and IgM are
produced following an infection with T gondii. Cell mediated immunity may be the critical
determinate in controlling toxoplasmosis with assistance of humoral response but it is not fully
protective. Interferon gamma is an absolute requirement for resistance against acquired infection
with T gondii and development of Toxoplasmic encephalitis during the late stage of the infection.?
TE in AIDS patients is most likely from reactivation of latent infection. The most common
affected area is the basal ganglia but other lesions may involve cerebellar and brain stem areas.
Outside the CNS, the lungs, retina, and myocardium may also be affected (Luis, 2006).
Clinical picture
Clinical symptoms depend on the localization of lesions, with acute onset within a few days. The
major signs include focal neurological deficits such as paresis, speech problems or sensory loss
(Porter and Sande 1992). A febrile psychosyndrome with confusion is also frequently an early
sign. It is not unusual to see an epileptic seizure as the initial presentation, in the absence of other
symptoms. Headaches with fever or subfebrile temperatures are always suspicious. Meningitic
signs, however, are less typical. Atypical manifestations in patients with immune reconstitution
under ART have been described (Ghosn et al, 2003).
A fairly rare, but important manifestation is Toxoplasma chorioretinitis. It causes impairment of
vision and is an important differential diagnosis to CMV retinitis and may occur on its own
(Rodgers and Harris, 1996).
The most common clinical presentation of T. gondii infection among patients with AIDS is a focal
encephalitis with headache, confusion, or motor weakness and fever (Luft et al., 1984). Physical
examination might demonstrate focal neurological abnormalities, and in the absence of treatment,
disease progression results in seizures, stupor, and coma. Retinochoroiditis, pneumonia, and
evidence of other multifocal organ system involvement can be seen after dissemination of infection
but are rare manifestations in this patient population (Wong et al., 1984).
Investigations
The serological tests are of limited use in clinical diagnosis owing to the high seronegativity (16%-
22%) in IgG titers in patients confirmed to have CNS toxoplasmosis. These tests prove to be useful
when the non detection of IgG titers along with single lesion in the radiological studies may
indicate the need for a histopathological diagnosis before initiating treatment. A negative
serological test should not be used to exclude the diagnosis of toxoplasmosis in patients with AIDS
(Porter and Sande, 1992).
Detection of T. gondii by polymerase chain reaction (PCR) in cerebrospinal fluid has produced
disappointing results; although specificity is high (96%-100%), sensitivity is low (50%) and the
results usually are negative once specific anti-toxoplasma therapy has been started (Novati et al.,
1994 and Cinque et al., 1997).
CT scan shows multiple, bilateral, hypodense lesions which enhance in the periphery with contrast