TERATOGEN UPDATE

Venezuelan Equine Encephalitis FRANZ WENGER I Head of Department of Pathology, University Hospital and Medical School, Uniuersidad del Zulia, Maracaibo. Venezuela

Epidemics of Equine Encephalitis amongst delivered, with microcephalus, microphthalanimals have been related, through the years, mia, luxation of the hips, severe hypoplasia of to seasons of heavy rain, because of the prolif- the medulla, and only small rests of nervous eration of insect vectors, especially Aedes tissue in the cranial cavity. In the second taeniorynchus, causing the death of horses and case, with maternal encephalitis a t about 20 donkeys. Before 1962, human cases were not weeks of pregnancy, the infant was born on recognized or were only suspected of being term, without active movements, living only encephalitis (Negrette, '60). In 1962, in the by artificial respiration for four hours. There course of a n unusually heavy rainy season, was no cerebellum, the cranial cavity was ocwhich flooded the country, there was an out- cupied by fluid, with only remnants of the break of an epidemic of encephalitis, which basal ganglia and the cerebral cortex. In the affected clearly man as well as animals, and third case, with encephalitis also a t 20 weeks, there were quick passages of the virus from delivery a t 36 weeks of pregnancy, the infant sick animals, mostly equine, through insect lived for two clays, with severe respiratory disvectors to man, from man through insects to tress syndrome, and died with bronchopneuman, and probably even from humans to monia. At autopsy, the findings were similar to the case No. 2, with nervous tissue only humans directly. In 1962, a huge epidemic of encephalitis, slightly better preserved. produced by the Venezuelan type virus of In three cases, with encephalitis a t about equine encephalitis, swept over the North- eight months of pregnancy, and the infants Western part of Venezuela, the Goajira- delivered one month later, there was massive peninsula, whose inhabitants, living in small necrosis softening and hemorrhage of the rural communities, were affected by an acute, cerebrum, and to a lesser degree, of the but usually benign infectious disease. The cor- cerebellum, with signs of resorption of the rect diagnosis was made by culture of the necrotic tissue (phagocytosis and granulation virus and by tests of neutralizing antibodies. tissue). In another case of encephalitis a t From October to December, there were 6,762 eight months of pregnancy, born two weeks officially registered cases, 389 of which were later, there was only massive necrosis and classified as severe, showing significant neu- hemorrhage, without signs of resorption. rological symptoms; 43 patients died (Avilan These latter four cases, in spite of the Rovira, '64). massive, nearly total cortical necrosis, lived From the beginning of the epidemic, fre- from 15 minutes to 7 days clinically with a quent abortions were observed in patients severe respiratory distress syndrome. They who happened to be pregnant from one to died from pulmonary atelectasia or bronchothree months. Later, I had the opportu- pneumonia. nity to examine seven bodies of newborns, All these lesions seem to be the result of a whose mothers had suffered a severe attack of short attack of the virus of Venezuelan encephalitis between the thirteenth and thir- Equine Encephalitis with destruction of the ty-sixth week of pregnancy (Wenger, '67). In fetal cerebral cortex. Time had permitted, in these cases, the fetuses had kept on living and the first three cases, the necrotic tissue to be developing, despite the fact that the virus had removed during several months, with the deproduced a severe damage to the brain. velopment of a condition similar to HydroIn the first case, with severe and proved anencephaly. maternal encephalitis at 13 weeks of pregnancy, there were no fetal movements, and after ' Request8 for reprmts: Dr F. Wenger. ed. El Saman, C. 73A, No 33 weeks of pregnancy, a still-born fetus was 28-45, Maracaibo, Venezuela. TERATOLOGY, 16: 359-362.

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Fig. 1 Still-born fetus, thirty-third week of pregnancy, 20 weeks after attack of maternal encephalitis: microcephalus, microphthalmia. luxation of hip.

Fig. 2 The same case as figure 1: Low power view of eye, which is well developed except for the retina, which consists only of two sheets of pigmented, single-layered epithelium.

VENEZUELAN EQUINE ENCEPHALITIS

Fig. 3 Infant born at term, encephalitis at 20 weeks of pregnancy, with Hydroanencephaly, A small rest of cerebral tissue, which had survived, is seen surrounded by proliferated meningeal tissue.

Fig. 4 Infant born on term, encephalitis one month earlier: there is necrosis of the cerebral cortex, with beginning resorption.

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Fig. 5 Infant born nearly on term; encephalitis two weeks earlier: gross view of cerebrum, showing diffuse softening and hemorrhage.

LITERATURE CITED Negrette, A. 1960 Encefalitis epidemica. Investigaciones Clinicas., 1: 11. Avilan Rovira, J. M. 1964 El Brote de Encephalitis Equina Venezolana a1 Norte del Estado Zulia a fines de

1962. Revista Venezolana de Sanidad y Assistencia Social. Vol. XXIX, 3: 291. Wenger, F. 1967 Necrosis Cerebral Masiva del feto en casos de Encefalitis Equina Venezolana. Investigaciones Clinicas, 21: 13.

The Editors welcome contributions to “Teratogen Update. ” Manuscripts should be sent to Dr. John L. Sever, Teratology Update Editor, Building 36, Room 50-04,National Institutes of Health, Bethesda, Maryland 20014. Articles should concisely summarize the clinical manifestations, etiology, pathogenesis, treatment, and prevention of the phenomena; and be accompanied by high-quality photographs of affected individuals. Color illustrations will be at the authork expense. Please address reprint requests to the author.

Venezuelan equine encephalitis.

TERATOGEN UPDATE Venezuelan Equine Encephalitis FRANZ WENGER I Head of Department of Pathology, University Hospital and Medical School, Uniuersidad d...
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