Transmission: Eating uncooked meat or contact with faeces of an infected dog or cat. (definitive hosts) There are two forms of toxoplasmosis:
CONGENITAL - when a previously unaffected woman contracts infection during pregnancy (subclinical infection); transplacental spread results in fetal infection.
Premature delivery occurs in 25%.
- aqueduct stenosis,
- microcephaly. Non-neurological features:
- skin rash, jaundice, hepatosplenomegaly, choroidoretinitis.
Skull X-ray shows:
- curvilinear calcification (basal ganglion and periventricular regions).
Varying degrees of organ involvement may occur. The only manifestation may be choroidoretinitis in an otherwise healthy child.
ACQUIRED - symptomatic infection is uncommon and may be associated with underlying systemic disease or immunosuppression, (e.g. AIDS)
Fever and fatigue with muscle weakness and lymphadenopathy result. Abnormal lymphocytes in peripheral blood leads to confusion with infectious mononucleosis. The neurological features are those of a meningoencephalitis with focal signs and depressed conscious level. Choroidoretinitis occasionally occurs.
I----Areas of atrophic
I----Areas of atrophic choroid, exposing the white sclera.
Retinal pigment epithelium becomes hyperplastic -Diagnosis: densely pigmented areas result.
Organisms are seldom identified.
IgG antibodies indicate previous exposure, positive IgM and high or rising IgG confirm active infection. Serological tests are negative in AIDS.
In acquired infection CT shows characteristic ring shaped contrast enhancement (page 125). MRI is even more sensitive. Brain biopsy is necessary for exclusion of CNS lymphoma and for definitive diagnosis. N.B. Rubella, cytomegalovirus and herpes simplex can also spread transplacental^ and cause jaundice and hepatosplenomegaly. Cytomegalovirus may also produce choroidoretinitis and intracranial calcification. Treatment
Sulphadiazine and pyrimethamine (Dapaprim) with folinic acid for 3 weeks or longer in immunocompromised patients. Give steroids when choroidoretinitis is present.
Plasmodium falciparum, the agent of malignant tertiary malaria, is responsible for cerebral malaria. Infected red blood cells adhere to vascular endothelium and block the microcirculation. Endothelial damage produces cerebral oedema. Confusion, focal signs, convulsions and coma occur. Diagnosis depends on demonstrating parasites in peripheral blood. Parenteral anti malaria treatment (chloroquine), exchange transfusion and supportive therapy may be life saving. Overall mortality is 10%. Complete recovery without sequelae is expected in survivors.
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