The congenital infection has attracted attention because of its severe destructive effects on the neonatal brain, as discussed in Chap. 37. Signs of active infection—fever, rash, seizures, hepatosplenomegaly—may be present at birth. More often, chorioretinitis, hydrocephalus or microcephaly, cerebral calcifications, and psychomotor retardation are the major manifestations. These may become evident soon after birth or, more often, the infection is asymptomatic and becomes manifest only several months or years later with choriretinitis. Most infants succumb; others survive with varying degrees of the aforementioned abnormalities.
Serologic surveys indicate that the exposure to toxoplasmosis in adults is widespread (approximately 40 percent of American city dwellers have specific antibodies); cases of clinically evident active infection, however, are rare. It is of interest that in 1975, prior to the AIDS epidemic, the medical literature contained only 45 well-documented cases of acquired adult toxoplasmosis (Townsend et al); moreover, in half of them there was an underlying systemic disease (malignant neoplasms, renal transplants, rheumatologic disease) that had been treated intensively with immunosuppressive agents. Now, innumerable cases of acquired toxoplasmosis are being seen because it is the most common cause of focal cerebral lesions in patients with HIV (see Chap. 33). Frequently, the symptoms and signs of infection with Toxoplasma are assigned to the primary immunosuppressive disease with which toxoplasmosis is associated or to other diseases that cause brain masses.
The prevalent problem, and the one of main interest in this chapter, is of cerebral toxoplasmosis in a patient with HIV (Fig. 31-6). The clinical features are usually a single seizure, focal neurological syndrome, or headache or other symptoms of elevated intracranial pressure. The rim enhancing cerebral lesion or multiple lesions of toxoplasmosis also may be found incidentally on cerebral imaging studies. The lesions may be difficult to differentiate from the less common occurrence of CNS lymphoma that arises in immunosuppressed patients. In general, cerebral toxoplasmosis occurs in patients with HIV and CD4 counts below 100/μl whereas other opportunistic infections and lymphoma may occur with higher counts. In many instances, the cerebral toxoplasmosis syndrome defines the inversion from HIV infection to AIDS.
The clinical picture of systemic toxoplasmosis in patients varies. Most often it is a subclinical process or manifested by a painless lymphadenopathy, a mononucleosis-like syndrome, or acute chorioretinitis. There is a rare fulminant, widely disseminated infection with a rickettsia-like rash, encephalitis, myocarditis, and polymyositis. Sometimes, there are signs of a meningoencephalitis, that is, seizures, mental confusion, meningeal irritation, coma, and a lymphocytic pleocytosis and increased CSF protein. The brain in such cases shows one or more foci of inflammatory necrosis, essentially an abscess, (see Fig. 31-6), with free and encysted T. gondii organisms scattered throughout the white and gray matter. Rarely, large areas of necrosis manifest themselves as one or more mass lesions.
In an immunocompetent patient, a rising or greatly elevated IgG antibody titer or a positive IgM indirect fluorescent antibody or another serologic test are useful. Patients with HIV and those who are otherwise immunocompromised, however, may not display an antibody response or an elevation of titers.