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Speci c diagnosis depends on the nding of organisms in CSF sediment and occasionally in biopsy specimens of muscle or lymph node A presumptive diagnosis can be made on the basis of a rising antibody titer or a positive IgM indirect uorescent antibody or other serologic test Patients with AIDS and those who are otherwise immunocompromised, however, usually do not display this response (those with lymphoma do have positive serologic tests) Excepting the AIDS cases, a clinical syndrome and radiologic features that are consistent with toxoplasmosis and a greatly elevated IgG titer are thought to be diagnostic In the setting of AIDS, patients with multiple nodular or ring-enhancing brain lesions are treated initially with antibiotics for toxoplasmosis, and further evaluation (mainly for cerebral lymphoma) is undertaken only if there is no response, as discussed in Chap 33 Treatment All patients with a presumptive diagnosis should be treated with oral sulfadiazine (4 g initially, then 2 to 6 g daily) and pyrimethamine (100 to 200 mg initially, then 25 mg daily) Leucovorin, 2 to 10 mg daily, should be given to counteract the antifolate action of pyrimethamine Treatment must be continued for at least 4 weeks In patients with AIDS, treatment is continued until the CD4 count exceeds 200 to 250 for 6 months or more; otherwise treatment must be lifelong in order to prevent relapses Amebic Meningoencephalitis This disease is caused by freeliving agellate amebae, usually of the genus Naegleria and less frequently of the genus Hartmannella (Acanthamoeba and Balamuthia mandrillaris) They are acquired by swimming in ponds or lakes where the water is contaminated One outbreak in Czechoslovakia followed swimming in a chlorinated indoor swimming pool Most of the cases in the United States have occurred in the southeastern states As of 1989, more than 140 cases of primary amebic meningoencephalitis due to Naegleria fowleri and more than 40 cases due to the less virulent Acanthamoeba had been reported (Ma et al) The onset of the illness due to Naegleria is usually abrupt, with severe headache, fever, nausea and vomiting, and stiff neck The course is inexorably progressive with seizures, increasing stupor and coma, and focal neurologic signs and the outcome is practically always fatal, usually within a week of onset The reaction in the CSF is like that in acute bacterial meningitis: increased pressure, a large number of polymorphonuclear leukocytes (not eosinophils, as in the parasitic infestations discussed on page 628), and an increased protein and decreased glucose content The diagnosis depends on eliciting a history of swimming in fresh warm water, particularly of swimming underwater for sustained periods, and on nding viable trophozoites in a wet preparation of unspun spinal uid Gram s stain and ordinary cultures do not reveal the organism Autopsy discloses a purulent meningitis and numerous quasigranulomatous microabscesses in the underlying cortex Subacute and chronic amebic meningoencephalitis is a rare disease in humans Isolated instances, due to Hartmannella species, have been reported in debilitated and immunosuppressed patients (Gonzalez et al) Usually these patients will have amebic abscesses in the liver and sometimes in the lung and brain The organism can be cultured from the CSF during periods of recurrent seizures and confusion A fatal case of ours, in a leukopenic patient who had been receiving granulocyte-stimulating factor, ran a subacute course over 1 month with headache, mild fever, stupor, and unmeasurably low CSF glucose toward the end of life Initially, there were scattered, round, enhancing lesions on the MRI that disappeared with corticosteroids, much like lymphoma; later, there were more irregular.

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Figure 32-7 Toxoplasmosis MRI of the brain in the axial plane showing widespread high-signal lesions with prominent ring enhancement The patient was a 28-year-old man with AIDS Typically, there are fewer lesions than shown here

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con uent white matter lesions A brain biopsy revealed amebae that could have been easily mistaken for macrophages or cellular debris; the organism proved to be Balamuthia (Katz et al) Treatment with the usual antiprotozoal agents is largely ineffective Because of the in vitro sensitivity of Naegleria to amphotericin B, this drug should be used by the same schedule as for cryptococcal meningitis With such a regimen in combination with rifampin, recovery is sometimes possible Malaria A number of other protozoal diseases are of great importance in tropical regions One is cerebral malaria, which complicates about 2 percent of cases of falciparum malaria This is a rapidly fatal disease characterized by headache, seizures, and coma, with diffuse cerebral edema and only very rarely by focal features such as hemiplegia, aphasia, hemianopia, or cerebellar ataxia Cerebral capillaries and venules are packed with parasitized erythrocytes and the brain is dotted with small foci of necrosis surrounded by glia (Durck nodes) These ndings have been the basis of several hypotheses (one of which attributes the cerebral symptoms to mechanical obstruction of the vessels), but none is entirely satisfactory Also, it seems unlikely that a disorder of immune mechanisms is directly involved in the pathogenesis (see reviews by Newton et al and by Turner for a discussion of current hypotheses) Usually the neurologic symptoms appear in the second or third week of the infection, but they may be the initial manifestation Children in hyperendemic regions are the ones most susceptible to cerebral malaria Among adults, only pregnant women and nonimmune individuals who discontinue prophylactic medication are liable to CNS involvement (Toro and Roman) Useful laboratory ndings are anemia and parasitized red blood cells The CSF may be under increased pressure and sometimes contains a few white blood cells, and the glucose content is normal With Plasmodium vivax infections, there may be drowsiness, confusion, and seizures without invasion of the brain by the parasite Treatment Quinine, chloroquine, and related drugs are curative if the cerebral symptoms are not pronounced, but once coma and convulsions supervene, 20 to 30 percent of patients do not survive It has been stated that that the administration of large doses of dexamethasone, given as soon as cerebral symptoms appear, may be lifesaving, but most studies including those of our colleagues have expressed the view that corticosteroids are ineffective Exchange transfusions may confer a small bene t on survival in severe cases Trypanosomiasis This is a common disease in equatorial Africa and in Central and South America The African type ( sleeping sickness ) is caused by Trypanosoma brucei and is transmitted by several species of the tsetse y There has been an alarming increase in this disease in sub-Saharan Africa during the last two decades The infection begins with a chancre at the site of inoculation and localized lymphadenopathy Posterior cervical adenopathy is highly characteristic of CNS infection (Winterbottom sign); another sign of neurologic interest is pronounced pain at sites of minor injury (called Kerandel hyperesthesia) Later, episodes of parasitemia occur, and at some time during this stage of dissemination, usually in the second year of the infection, the trypanosomes give rise to a diffuse meningoencephalitis The latter expresses itself clinically as a chronic progressive neurologic syndrome consisting of a reversal or disruption of circadian sleep rhythm, vacant facial expression, and in some, ptosis and ophthalmoplegia, dysarthria, and then muteness, seizures, progressive apathy, stupor, and coma.

The South American variety of trypanosomiasis (Chagas disease) is caused by Trypanosoma cruzi and is transmitted from infected animals to humans by the bite of reduviid bugs The sequence of local lymphadenopathy, hematogenous dissemination, and chronic meningoencephalitis is like that of African trypanosomiasis Serologic tests are available to con rm the diagnosis Treatment Treatment is with pentavalent arsenicals, mainly melarsoprol, which are more effective in the African than in the South American form of the disease An encephalopathy occurs in one fth of cases during the institution of treatment Unusually high rates of relapse are being reported after treatment A thorough review of the subject of trypanosomiasis is given by Barrett and colleagues They also discuss the important topic of vector control