timing of maternal infectionThis is an important determinant both for the rate of maternofoetal transmissionand for the congenital damage produced in the baby. Maternofoetal transmissionis rare, about 1% when maternal infection occurs during the first 4 weeks. Itincreases then progressively to reach 90% for infection in the last few weeks of pregnancy.This risk is 14%, 29% and 59% when maternal infection occurs at the endof the first trimester, during the second and during the third trimester, respectively(Desmonts & Couvreur 1974a).

Foetal damage is more often very severe in early pregnancy and almost alwaysabsent when maternal infection occurs in late pregnancy

placentaof infected infants, particularly when the mother has been treated.Spiramycin treatment given to infected mothers significantly reduces infection ofthe placenta (Couvreur et al. 1988) (Table 10.2). If given orally for 1 month or moreas a daily dose of 23 g there is a 50% reduction in the number of congenitallyinfected babies. However, spiramycin does not affect the clinical pattern in infectedfoetuses (Desmonts & Couvreur 1975). The pyrimethaminesulphadiazine combinationgiven to mothers with seroconversion has been said to reduce by 70% the riskof maternofoetal transmission (Krabig 1963).

2.1.2. Symptomatic infectionA minority of healthy persons infected with T. gondiiafter birth develop symptoms, which are usually mild andinclude manifestations such as fever, malaise and lymphadenopathy(Montoya and Liesenfeld, 2004; Remingtonet al., 2006). However, in rare cases, humans who were previouslyhealthy have developed severe and even fatal disease,including pulmonary and multivisceral involvement,possibly from more virulent types of the organism (Carmeet al., 2002; Demar et al., 2007). In addition, up to 2% ofhealthy persons in the USA infected with T. gondii developocular disease (Holland, 2003), usually retinochoroiditis. Ahigher percentage of infected persons have been documentedto develop ocular disease in other parts of theworld, for example, one region of Southern Brazil (17.7%with ocular lesions) (Glasner et al., 1992). Retinochoroiditiscan be due to congenital or post-natally acquired diseaseand can be associated with acute infection orreactivation (Montoya and Remington, 1996; Holland,1999). Current thinking is that the majority of ocular toxoplasmosiscomes from post-natally acquired disease (Holland,1999, 2003). Acute toxoplasmic retinochoroiditisresults in pain, photophobia, tearing and loss of vision.

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