Search

In the Dutch national surveillance system, outbreaks of fatal infections by Mannheimia haemolytica (M. haemolytica) in dairy cows and veal calves have become apparent in recent years. These observations prompted an in-depth analysis of available pathology data over the period 2004-2018 to investigate changes in the occurrence and/or expression of M. haemolytica-associated cattle disease. With multilevel logistic regression models, time trends were identified and corrected for farm, season, pathologist and region. Deaths associated with M. haemolytica infection increased over time with dairy cows and veal calves diagnosed with fatal M. haemolytica infections 1.5 and 1.4 times more frequently every following 3-year period between 2004 and 2018, respectively. M. haemolytica-associated disease showed two distinct disease presentations: acute pleuropneumonia in dairy cows and polyserositis in veal calves. The prevalence of both disease presentations with M. haemolytica confirmed increased in each 3-year time period between 2004 and 2018, with an odds ratio (OR) of 1.5 for acute pleuropneumonia in dairy cows and an OR of 1.7 for polyserositis in veal calves. No change was found for M. haemolytica-associated disease in dairy calves. Although M. haemolytica is considered an opportunist bovine pathogen, and the presence of primary pathogens such as BHV-1, BVDV and Mycoplasma species was not completely ruled out in our study, substantial evidence is provided to indicate infections with M. haemolytica were the most likely cause of death. M. haemolytica-associated diseases occurred more often in October-June than July-September, and were detected more often in necropsied animals from the North, South and East Netherlands than the West Netherlands., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

In December 2011, a previously unknown congenital syndrome of arthrogryposis and hydranencephaly in sheep and cattle appeared in the Netherlands as an emerging epizootic due to Schmallenberg virus (SBV). Gross lesions in 102 lambs and 204 calves included porencephaly, hydranencephaly, cerebellar dysplasia and dysplasia of the brainstem and spinal cord, a flattened skull with brachygnathia inferior, arthrogryposis, and vertebral column malformations. Microscopic lesions in the central nervous system showed rarefaction and cavitation in the white matter, as well as degeneration, necrosis, and loss of neurons in the gray matter. Brain and spinal cord lesions were more severe in lambs than in calves. Ovine and bovine cases examined early in the outbreak showed encephalomyelitis. SBV infection was confirmed by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) in brain samples in 46 of 102 lambs (45%) and in 32 of 204 calves (16%). Immunohistochemistry, performed on tissue samples from 18 RT-qPCR-positive lambs, confirmed the presence of bunyaviral antigen in neurons of the brain in 16 cases. SBV antibodies were detected by enzyme-linked immunosorbent assay in fetal blood in 56 of 61 sampled ovine cases (92%). In a virus neutralization test, all tested dams of affected newborns, 46 ewes and 190 cows, were seropositive. Compared with other teratogenic viral infections, the pathogenesis and lesions of SBV in sheep and cattle fetuses are similar to those of other ruminant orthobunyaviruses. However, the loss of spinal ventral motor neurons and their tracts, resulting in micromyelia, distinguishes SBV infection from other viral central nervous system lesions in newborn ruminants., (© The Author(s) 2014.)

An outbreak of hydranencephaly in aborted foetuses and newborn calves occurred following the 2007 epidemic of bluetongue serotype 8 (BTV8\net2006) in the Netherlands. In total 35 aborted foetuses and 20 live-born calves, submitted from September 2007 to May 2008, were examined pathologically. Foetuses with gestational ages between 4 and 9 months (mean 6.8 month) showed varying stages of cerebral malformation. Initial stages were cavitations in the cerebral hemispheres with massive destruction of neuroparenchyma, calcium deposits, and a phagocytic inflammatory response. Later stages showed distinct hydranencephaly, the cerebral hemispheres being almost completely replaced by fluid-filled sacs. In seven cases the cerebellum was affected as well, but brainstem structures were intact. Newborn calves with clinical signs of abnormal behaviour ('dummy calves'), circling, head pressing, incoordination, and blindness were seen from the end of January 2008. The calves were born between 2nd January and 16th March 2008. The calves were euthanized after 1 day up to 14 weeks (mean 4-7 weeks). Brain malformations in these calves were confined to the cerebrum and consisted of varying degrees of hydranencephaly. Spleen tissue was PCR-positive for bluetongue virus (BTV) in 21 of 35 foetuses and in 1 of 20 calves. A higher percentage of PCR-positives was found in foetuses aborted in early gestation than in late gestation, suggesting clearance of BTV during gestation. Fifteen of 33 dams of PCR-negative hydranencephalic foetuses or calves could be traced and all were BTV-seropositive, indicating a previous BTV infection. The timing of hydranencephaly cases in live-born calves during the first months of 2008 was consistent with infection in early gestation during the prior transmission season. Vertical transmission and teratogenic potential have previously been described for modified-live vaccines for bluetongue but are highly unusual for field strains of BTV, which raises the issue whether BTV8\net2006 or its ancestor has been cell- or laboratory-adapted in the past.

Five of eight meat cattle died suddenly without showing prior symptoms of disease. The sudden death occurred in connection with the feeding of mouldy tulip bulbs. A short review is given of the use of flower bulbs as cattle feed, the use of herbicides/fungicides in bulb cultivation, and the relevant legislation. Several toxicological aspects that should be taken into consideration when flower bulbs are used as cattle feed are discussed. Both the Central Veterinary Institute and the State Institute for Public Health and Environmental Hygiene showed, in experiments with mice, the presence of a toxin in extracts of the mouldy tulip bulbs. This toxin is probably produced by moulds present in the tulip bulbs. The death of the animals was probably caused by an as yet unidentified mycotoxin.