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Contributed by Stefan Isenmann, MD, Christian Aepinus, MD, Martin Skalej, MD, Antje Bornemann, MD, Ernst H. Grote, MDFINAL DIAGNOSIS: CEREBRAL TOXOPLASMOSIS
DISCUSSION:
In light of the parasitic nature of the lesion, HIV serology was initiated. Two independent sera were positive for anti-HIV-antibodies, and Western blot analysis confirmed the presence of specific bands. Further blood tests showed a low CD4+/CD8+ ratio, and quantitative PCR from the blood revealed a high virus load. Taken together, these findings not only established advanced HIV infection, but also founded the diagnosis of AIDS, with the cerebral lesion constituting the AIDS-defining disease (1). Only after being confronted with these results, the patient gave notice of being homosexual.
Following diagnosis, the patient was treated with pyrimethamine, sulfalene, and folate. During the entire postoperative course, there were no signs of aphasia present. A control CT scan seven weeks after surgery and five weeks following the initiation of the antiparasitic drug regimen showed an almost complete remission of the temporal lesion (Fig. 1c). At this time, antiretroviral triple therapy was started. Six months after the initial admission, the patient was free of symptoms, and the EEG focus was no more detectable. He intended to go back to work.
Toxoplasmic encephalitis is the most frequent cause of acute neurological deterioration in AIDS patients. It occurs due to reactivation following a previous inapparent infection in immune-compromised individuals (8). Although toxoplasma lesions can present as ring enhancing lesions in CT and MRI, singular manifestations are less common (3,8), especially in severely immunosuppressed patients who often present with encephalitic symptoms (8,9). In patients with an established diagnosis of AIDS, CNS symptoms, and brain masses, toxoplasmosis and primary CNS lymphoma are the most likely causes (3). It is now established that in this constellation, anti-Toxoplasma drug therapy is started, and biopsy only carried out if the patient deteriorates (7). However, gliomas have also been reported in AIDS patients (2), and in our patient, imaging was suggestive of glioma, while there was no evidence for HIV infection at the time of admission.
Our report stresses the importance of considering undiagnosed HIV infection in patients of risk groups presenting with a cerebral mass lesion. Moreover, this case underlines the value of molecular pathological tools as a supplement to conventional histological and immuno-cytochemical examinations on biopsy specimens (4,5,6). Using modern triple antiretroviral regimens, the prognosis of this condition has improved considerably over the past years.
REFERENCES:
Contributed by Stefan Isenmann, MD, Christian Aepinus, MD, Martin Skalej, MD, Antje Bornemann, MD, Ernst H. Grote, MD
International Society of Neuropathology