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First identified in 1929 in a1 human and as intrauterine in origin in 1942 in the United States,2 congenital toxoplasmosis is now considered by neonatologists primarily when they encounter a TORCH (toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus) infection, most often with chorioretinitis, intracerebral calcifications, and hydrocephalus. However, a much broader range of signs and symptoms and additional factors should be considered in the approach to this disease.


The causative agent, Toxoplasma gondii, is a ubiquitous protozoan parasite. It is estimated that more than 30% of the world’s population has been infected, with varying frequencies of infections in different parts of the world and within countries as well. With rare exceptions, first infections of a pregnant woman acquired during gestation cause congenital toxoplasmosis. Primary gestational infections are generally unrecognized and may be asymptomatic or mild and self-limited and therefore go undiagnosed; fetal infections range in severity from asymptomatic at birth to devastating. Congenital toxoplasmosis is both treatable and preventable. Once established, however, infection is lifelong, with risk of recurrence.


Toxoplasma gondii is a 3 × 5 μm parasite in the apicomplexan family. Related apicomplexan parasites that also are pathogenic for humans include Plasmodia, which cause malaria; Cryptosporidia; and Babesia. Toxoplasma gondii exists in 3 primary life-cycle stages as it interfaces with the human host: tachyzoite, bradyzoite, and in the cat intestine, developing stages that mature into sporozoites in oocysts.3, 4, 5, and 6 These life-cycle stages are shown in Figure 57-1.4


A, Schematic diagram of a tachyzoite. B, Transmission and scanning of electron micrographs of a tachyzoite invading a host cell. C, Light micrograph of tachyzoites replicating within a parasitophorous vacuole in the host cell cytoplasm. D, Immunofluorescence assay (IFA) (E Mui) with green fluorescent protein expressing tachyzoites in a parasitophorous vacuole. E, Schematic diagram of a bradyzoite. F, Transmission electron micrographs of a cyst containing bradyzoites. Red arrow in right panel indicates amylopectin granules. G, Light micrograph of a cyst containing bradyzoites. H, Development of oocysts in cat intestine. I, Oocysts in the lumen of a cat intestine. J, Sporulating oocysts that contain sporozoites. (Individual images reproduced with permission from A, McLeod et al133; B, Aikawa et al135; C, E, Long et al132; F, Weiss et al136; G, Remington,137; H, Gardiner et al138; J, Dubey et al.139)

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The rapidly growing tachyzoite form is present in acute postnatal infection (eg, in a pregnant woman), in active congenital infection, and when the infection recrudesces from encysted bradyzoites in recurrent eye disease or with immune suppression.7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18...

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