Abstract. The present study describes pathologic and virologic findings in 15 sheep and 6 goats that died of natural peste des petits ruminants virus infection in Turkey. Pathologic findings included erosiveulcerative stomatitis, fibrino-necrotic tracheitis, bronchointerstitial pneumonia, multifocal coagulation necroses in the liver, and severe lymphocytolysis in lymphoid tissues. Syncytial cells were conspicuous, especially in the oral mucosa, pulmonary alveoli, liver, and lymphoid tissues. In addition to the typical tissue distribution, eosinophilic intracytoplasmic and/or intranuclear inclusions were observed in epithelial cells lining the renal pelvis and abomasal mucosa. Immunolabeling of the viral antigen was observed in the kidney, brain, rumen, abomasum, heart, and myocytes of the tongue besides its more typical locations. In this study, we report and describe in detail the first peste des petits ruminants endemic in Kirikkale Province, Central Anatolia of Turkey. In conclusion, these previously unreported pathologic findings in natural peste des petits ruminants virus infection establish a basis for resemblance to other morbillivirus infections, such as canine distemper and distemper of sea mammals. Reverse transcriptase-polymerase chain reaction analyses indicated that the 448-bp genome fragment was amplified in 18 cases (18/21, 85.7 %). Phylogenetic analysis showed that viruses belong to lineage 4 in the peste des petits ruminants virus common phylogenetic tree.

Polioencephalomalacia (PEM) in ruminants has been recognized as a consequence of excess sulphur intake. The present study describes clinical, gross and histopathological findings of PEM following an abrupt change of diet in two ranches housing 2750 dairy and 2300 beef cattle. As a result of severe PEM, 256 cattle died or were slaughtered. Clinical findings included circling, hypersensitivity, excessive salivation, hypermetria, incoordination, blindness and death. The first clinical signs occurred in beef calves (6-8 months old) at a holding facility. Clinical signs of the disorder continued intermittently during the 5-month period in both ranches and were more evident in calves and lactating dairy cows. The affected cattle did not respond to thiamine injections. Clinical signs disappeared gradually following removal of barley malt sprouts from the diet. Although macroscopic lesions were not apparent in the brain tissues of some animals, histopathology typical of PEM was found in most cases: spongiosis in the neuropil and neuronal necrosis, haemorrhage, capillary hyperplasia, fibrinoid degeneration in arterioles, multifocal liquefaction necroses in the grey matter and abundance of gitter cells with vacuolar large cytoplasm. Sulphide in rumen fluid of a clinically affected animal was measured as 1.55 mg/dl, which is considerably higher than that collected from two control cows (mean 0.21 mg/dl). The total sulphur content of the diet containing barley malt sprouts was estimated to be 0.45%, which is also higher than the National Research Council (NRC) maximum tolerable levels. In conclusion, PEM can result from excess barley malt sprout intake because of its higher sulphur content. Clinical signs may occur shortly after the intake of barley malt sprout as outbreaks with a higher number of deaths or as an ongoing periodic condition.

Abstract. Concurrent infection with peste des petits ruminants virus (PPRV) and pestivirus was diagnosed in stillborn twin lambs. With the flock history, the findings of epidermal syncytial cells and necrotizing bronchitis/bronchiolitis prompted testing for PPRV infection, and PPRV antigen was detected by immunohistochemistry (IHC) in the skin, lungs, kidneys, rumen, and thymus. Macroscopic anomalies that were typical of border disease included scoliosis, brachygnathism, prognathism, arthrogryposis, hydranencephaly, cerebellar hypoplasia, and hairy fleece; pestiviral antigen was detected by IHC in the brain, liver, lungs, and kidneys. Tissues from both lambs were positive by reverse transcriptase-polymerase chain reaction (RT-PCR) for PPRV and pestivirus. To the authors' knowledge, PPR has not been reported previously as a congenital infection or in combination with pestiviral infection.

No abstract

No abstract