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In view of the scarce references concerning the histological data in congenital parvovirus human B19 infection, we intend to provide a description of the pathological features observed in six autopsies. The virus was detected by DNA hybridization (ISH-DBH), PCR and electronmicroscopy (EM) in paraffin-embedded feto-placentary tissues. These cases constitute a subset from 86 Non Immunologic Hydrops Fetalis (NIHF) cases, in which a systemic complex of inflammatory/degenerative lesions of unknown etiology was visualized by optical microscopy. In one case a syphilitic process was detected, typefying a double infection. All fetuses showed a similar pathology--hydrops, hepato-splenomegaly, lung hypoplasia and erythroblastemia, the specific histological feature being the presence of intranuclear inclusions in the erythroid progenitors, in the erythropoietic visceral tissue and in blood marrow. Complex cardiopathy allied to abnormal lung lobulation and polisplenia were observed once; in 2 cases endocardial fibroelastosis was diagnosed. The pulmonary lesions were represented by dysmaturity allied to interstitial mononuclear infiltration. The hepatic consisted of cholestasis, portal fibrosis, canalicular proliferation, hemossiderosis, focal necroses and giant cell transformation. The central nervous system lesions were predominantly anoxic although the autolysis impaired a correct diagnosis.

from 1974, 1980, 1982, 1987 and 1988, four of which occurred during the second half of the year, confirming the seasonality of the disease.

Extensive calcification of the heart, involving predominantly the right ventricle and interventricular septum, was observed in a 3-h-old baby. The aetiology of the condition was attributed to infection by Toxoplasma gondii, based on the presence of several visceral lesions allied to the identification of the microorganism. The case is reported in view of the rarity of the type of the heart lesion. It is considered that calcification of the myocardium is secondary to vascular, inflammatory or toxic condition. The factors implicated in the pathogenesis of this unusual myocardial lesion are discussed.

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Development and differentiation of bile ducts have been studied for the understanding of pathogenesis of biliary atresia and other diseases of the intrahepatic biliary tree. The aim of this study is to correlate the type of biliary structure with the size of the portal tract and the gestational age. Twenty-four human livers were studied. Fetuses were assigned to four gestational age groups: group I, up to 20 postfecundation weeks (PFW); group II, from 21-26 PFW; group III, from 27-32 PFW; and group IV, from 33-38 PFW. In each specimen, 30 portal tracts were classified as small, medium, or large according to the diameter of the portal vein. In order to identify the bile duct cells, the sections were immunolabeled with anti-cytokeratin antibody, and the biliary structure was classified as absent (bile ducts (BD) 0), presence of bile duct cells without lumen (BD 1), or presence of bile duct with lumen (BD 2). In the small portal tracts, either there were no biliary structures or just a few. There was a substantial increase in the number of medium portal tracts that included a bile duct as a function of gestational age. The majority of large portal tracts exhibited a bile duct. In human fetus up to 20 PFW, it is possible to find 70% of portal tracts without bile ducts, and at 38 PFW it is expected that more than 50% of the portal tract has a BD 0. We suggest the use of the diameter of the portal vein and the gestational age for the quantification of biliary structures and the evaluation of maturity of intrahepatic biliary tree. Anat.

We present an unusual case of extralobar pulmonary sequestration associated with hyaline membrane disease (HMD) that caused the death of a premature baby in the first day of life. The sequestered parenchyma was nourished by an aberrant aortic vessel. Notable was the presence of typical HMD in all the lung parenchyma perfused by the pulmonary artery; the sequestered lung tissue presented a dysplastic structure compatible with CCAM. A few similar cases have been found in the literature. In all of the reported cases there are morphologic aspects characteristic of HMD in the portions normally receiving blood from the pulmonary artery. These findings suggest the importance of the blood pulmonary circulation in the pathogenesis of HMD, whose exact causes are not fully known.