Toxoplasmosis pathology and pathogenesis

Toxoplasmosis pathology and pathogenesis

Toxoplasmosis pathology and pathogenesis

Infection is common,20-40% of adults in Britain having antibodies. The mostserious effects are seen after congenital infection or inimmunocompromised patients.Pathology and pathogenesisTrophozoites released at the site of entry multiply andspread via blood and lymphatics to all tissues. They caninvade any cells, and intracellular proliferation leads to celldeath. Development of immunity results in restriction ofproliferation and the organism is eliminated, or formstissue cysts. Cysts 10-200 mm in diameter, containingseveral thousand organisms, may remain in the tissues forlife. Depression of CMI results in reactivation.

Clinical features Congenital infectionCongenital infection usually follows primary asymptomaticinfection of the mother during the third trimester ofpregnancy. The effect on the fetus may be spontaneousabortion, stillbirth, premature birth, or normal birth withsubsequent illness. The latter is most frequent and resultsin disease of the eye, usually bilateral choroidoretinitis, orof the brain, with hydrocephalus, microcephaly, cerebralcalcification or convulsions. Fever, lymphadenopathy,hepatosplenomegaly and rash may also occur.Acquired infectionAsymptomatic infection is common in adults, but theremay be a mild chronic febrile illness with lymphadenopathy.Often a group of enlarged lymph nodes in a single areais the only finding, although more diffuse adenopathy mayoccur with splenomegaly. Sore throat does not occur.Choroidoretinitis is now recognized as a manifestation ofacquired infection.Reactivation in the immunosuppressed patientMost toxoplasmal disease in patients with deficient immunityis caused by reactivation of latent cysts. The mostcommon manifestation, especially in AIDS, is necrotizinglesions in the brain, often presenting as intracerebral masslesions. Primary infections in the immunocompromisedhost cause disseminated infections. This has been recognizedin cardiac transplantation when a seropositive donoris the source of a heart for a seronegative recipient. This isprevented by chemoprophylaxis. Myocarditis and possiblypneumonitis also occur.DiagnosisThis is by serology. The Sabin-Feldman dye test, indirecthaemagglutination or fluorescent antibody test (FAT) areused to measure IgG antibodies, and an ELISA is alsoavailable for measurement of IgM antibodies. Histology ofaffected lymph nodes shows reactive changes which are 3439not specific for toxoplasmosis. The organisms are rarelyseen in tissue sections. Diagnosis of cerebral lesions is byCT or MRI scan.

Management Treatment of acquired infection in normal adults does notaffect outcome and is rarely required. Severe infections aretreated with the synergistic combination of pyrimethamine50 mg daily and sulfadiazine 1.0-1.5g every 6 hours bymouth for 3 weeks, together with folinic acid 15 mg daily,as pyrimethamine is a folic acid antagonist and can causebone marrow suppression. Clindamycin 600 mg every 6hours orally or i.v. can be used as an alternative to sulfadiazinein the event of toxicity. Patients with AIDS mayneed a longer course of treatment and the cerebral lesionsare monitored by CT or MRI. These patients also requiremaintenance therapy with pyrimethamine 75 mg twice perweek and sulfadiazine 1.5g twice daily once a satisfactoryresponse has been achieved. Tissue cysts are not killed bythis treatment, but they may be susceptible to azithromycinor atovaquone.

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