Handbook of congenital malformations / edited by Alan Rubin.

Date:
1967
Catalogue details

Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: Handbook of congenital malformations / edited by Alan Rubin. Source: Wellcome Collection.

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    TOXOPLASMOSIS (continued) SO that one or two might fit inside a red blood cell. Although it can be maintained in tissue culture, isolation is usually done by intra¬ peritoneal inoculation of mice. If an exudate is provoked, stained smears are examined for the presence of intracellular parasites. Prenatal infection. Malformations are seen in approximately 20 per cent of cases of congenital toxoplasmosis. These include micro¬ cephaly, microphthalmia, and hydrocephaly. Congenitally infected infants may also have chorioretinitis (65 to 90 per cent), abnormal cerebrospinal fluid (55 to 85 per cent), and anemia (55 to 77 per cent), as well as convulsions, cerebral calcifications, jaundice, fever, splenomegaly, lymphadenopathy, hepatomegaly, vomiting, diarrhea, pneumonitis, and rash. Severe neonatal illness is usually followed by severe neurologic sequelae, including mental retardation and seizures. The chorioretinitis is characteristically bilateral and central. In the active phase the lesions are hemorrhagic with yellowish white or gray foci, show little pigment formation, and are surrounded by coarse and fine vitreous opacifications. The infection involves primarily the vascular or deeper retinal layers with secondary extension to the choroid. Although macular abnormalities are most common, lesions may be found around the optic disc, equatorially or in the periphery. The fundus may show isolated or diffuse chorioretinitis. Anterior uveitis may occur and is characterized by a congested eye, keratic precipitates, anterior chamber flare and floaters and synechiae. Ante¬ rior uveitis not infrequently occurs in association with the posterior uveitis. The inactive phase is characterized by atrophic and deeply pigmented retinal scars. Complicating sequelae include endoph¬ thalmitis, cataract, secondary glaucoma, and retinal detachment. Optic atrophy may follow papillitis or papilledema. Microphthalmia, ocular deviations and impaired visual acuity may also result from congenital infection. Reactivation of the chorioretinitis is common. The majority of postnatal infections are inapparent, although otherwise normal adults may occasionally have an illness of some severity. Acquired infections have been classified according to the predominant clinical manifestation: lymphadenopathic, cerebrospinal, ophthalmic, typhus-like (with rash and intermittent fever), and myocardial. Generalized lymphadenopathy is the most common ab¬ normality and is most marked in the cervical and axillary areas. The infection may be associated with interstitial pneumonia or hepatitis, or it may mimic infectious mononucleosis, with malaise, anorexia, fatigue, fever, splenomegaly, cough, and a transient rash. The diagnosis of congenital toxoplasmosis can be established by the examination of a Wright or Giemsa stained preparation of sedi- mented cells from cerebrospinal fluid or an impression smear from a liver specimen or other tissue. Skin sensitivity is not reliable but, if positive, supports the diagnosis. The best known antibody test is the dye test, although complement-fixation and hemagglutination meth¬ ods are also in use. It is important that the antibody level remain high beyond the time when maternal antibody is no longer detectable in the infant's serum (four to seven months). The demonstration of 360