The authors review the clinical, macro- and microscopical features, and pathogenesis of viral haemorrhagic disease (VHD) of rabbits and the European brown hare syndrome (EBHS). The two diseases share similar clinical and pathological manifestations involving an acute syndrome, sometimes accompanied by nervous and respiratory symptoms and epistaxis, and in all cases by severe hepatic damage and multifocal haemorrhages leading to fatal shock. The hepatic lesions (necrosis and inflammation) result from direct cytolytic and indirect microthrombotic effects of the causal agent. Endothelial lesions and a primary or secondary defect of coagulation factors are possible causes of the haemorrhagic syndrome. Typical lesions consist of necrotic hepatitis and congestion, haemorrhaging and oedema of the lungs and trachea. The histological and ultrastructural alterations of the liver are similar to those found in certain cases of acute fatal hepatitis in man. The high correlation between histologically typical hepatic findings and immunohistochemistry and immunoelectron microscopy is of diagnostic value. Both microscopic lesions and pathogenesis favour the unifying definition of "infectious necrotic hepatitis of Leporids" for the two disease entities.

Cloning of cattle, sheep, and mice by somatic cell nuclear transfer (SCNT) can result in apparently healthy offspring, but the probability of a successful and complete pregnancy is less than 5%. Failures of SCNT pregnancy are associated with placental abnormalities, such as placentomegaly, reduced vascularisation, hypoplasia of trophoblastic epithelium, and altered basement membrane. The pathogenesis of these changes is poorly understood, but current evidence implicates aberrant reprogramming of donor nuclei by the recipient oocyte cytoplast, resulting in epigenetic modifications of key regulatory genes essential for normal placental development. The purpose of this review is to provide an overview of the anatomic pathology of abnormal placentae of SCNT clones and to summarize current knowledge concerning underlying pathogenetic mechanisms.

Polychlorinated biphenyls (PCBs) are common environmental contaminants that represent an important risk factor of reproductive disorders in chronically exposed human populations. However, it is not known whether a short accidental exposure of embryos to PCBs before implantation might influence their further development and whether the effect might be reversible. To this aim, in vitro-matured sheep blastocysts were incubated with 2 or 4 µg/ml Aroclor 1254 (A1254), a mixture of 60 PCB congeners for 48h after which blastocyst proliferation and ability for outgrowth in vitro were assessed. Blastocysts exposed to A1254 showed: (i) reduced proliferation and cell number (particularly in the inner cell mass compartment); (ii) accumulation of vacuoles and lipid droplets, diffused mitochondrial damage and up-regulation of autophagy markers (ATG6 and LC3), all signs indicative of deregulated autophagy, and (iii) massive cell death. Although exposed embryos resumed growth following A1254 removal, their subsequent development remained severely perturbed. These findings indicate that short exposure of blastocysts to PCBs leads to its damage characterized by deregulated autophagy and subsequent cell death.