Congenital tremor and hypomyelination associated with bovine viral diarrhoea virus in 23 British cattle herds.

This paper presents data from 23 British herds investigated between 1991 and 2007 where neurological disease in calves was caused by bovine viral diarrhoea virus (BVDV) infection. A variety of clinical signs, most commonly tremor or trembling, were apparent in the calves from birth, and most were recumbent or unable to stand unsupported. Severe diffuse neuraxial hypomyelination was present in all of the calves, and immunohistochemistry revealed cerebral neuronal labelling consistent with congenital persistent pestivirus infection in each brain. BVDV was detected in peripheral blood samples from eight of 15 calves tested using an antigen ELISA, and was isolated in culture from samples of viscera, brain or blood collected from 17 of 24 affected calves. TaqMan RT-PCR for pestivirus RNA was positive for BVDV-1 in all six calves tested. Six of the virus isolates on which molecular classification was carried out, obtained from calves in four of the herds, were identified as BVDV-1a, while three isolates from one affected and two unaffected calves on a fifth farm were confirmed as BVDV-1b.

Characterization of canine microsatellites.

Canine DNA was cloned in M13 and screened for the presence of (dC-dA)n.(dG-dT)n repeats. Oligonucleotide primers were synthesised to the microsatellite flanking sequences and used in the polymerase chain reaction to amplify those loci from genomic DNA. The polymorphism of each microsatellite was estimated in a set of unrelated dogs.

Immunological activity of a T-hybrid line. II. Mapping H-2 genes for the SRBC-specific suppressor factor, its acceptor, and suppression of the antibody response.

Studies are reported on the nature and action of a suppressor factor with specificity for sheep red cells produced by a mouse T-hybrid cell line. Absorption of the factor with anti-H-2 reagents indicated that it carries determinants coded between the I-J and D loci. The factor was bound well by spleen cells of certain strains (B10, B10.BR), but not others (B10.S); absorption studies with spleen cells of H-2 recombinant strains suggested that a gene contributing to a cellular acceptor site for the factor also mapped in the region between I-J and D. On the other hand, studies of functional suppression of the anti-SRBC response of different strains in vitro indicated that an H-2 gene in the I-A or I-B subregions controlled suppression. Thus, at least two H-2 genes seem to be involved in the suppressive action of this factor.

Dandy-Walker malformation in two calves.

Two calves with unusual malformations of the skull and brain are described. Both calves showed doming of the posterior skull due to enlargement of the posterior fossa and cyst-like dilatation of the fourth ventricle. The cystic dilatation of the fourth ventricle formed a meningocoele in one calf. Aplasia of the cerebellar vermis was present in both calves. One calf showed agenesis of the corpus callosum. These features are consistent with the Dandy-Walker malformation of man.

A syndrome of anaemia, immunodeficiency and peripheral ganglionopathy in Fell pony foals.

Fell pony foals developed a syndrome of anaemia, immunodeficiency and peripheral ganglionopathy. They became ill in the second or third week, and died in the second or third month of life. Clinical and pathological investigations revealed severe anaemia associated with small numbers of late erythroid precursors in bone marrow, small thymi, an absence of secondary lymphoid follicles, a lack of plasma cells and neuronal chromatolysis involving trigeminal, cranial mesenteric and dorsal root ganglia. Some of the foals had cryptosporidial enteritis and adenoviral bronchopneumonia and pancreatitis. The clinical and pathological findings were compatible with an intrinsic defect.

Determination of the frequency and distribution of vascular and parenchymal amyloid with polyclonal and N-terminal-specific PrP antibodies in scrapie-affected sheep and mice.

Brains from 17 histopathologically confirmed cases of scrapie, five of which had congophilic vascular amyloid, were stained immunohistochemically for prion protein (PrP) using a polyclonal antibody. Two clinically suspect but pathologically unconfirmed cases of natural sheep scrapie and the brains of four mice infected with the 111A murine scrapie strain were also examined. Selected sections containing amyloid were stained with each of two peptide antibodies which recognise the N-terminal amino acid residues which are lost following protease digestion of the disease-specific isoform of PrP. The mice infected with the 111A murine scrapie strain had large numbers of hypermature plaques. All the amyloid plaques from both natural sheep scrapie brains and experimental murine brains were heavily immunostained by the polyclonal and both peptide antibodies. In addition, disease-specific accumulations of PrP were detected in endothelial cells or in the intima of blood vessels of the cerebral cortex of sheep scrapie brains. The affected blood vessels were located in areas which otherwise lacked typical scrapie pathology. Vascular accumulations of PrP were also found in leptomeningeal and choroid plexus blood vessels. Vascular amyloid was found mainly in the neocortex. Vascular amyloid and disease-specific parenchymal accumulations of PrP were found in two sheep which showed clinical signs of scrapie but lacked its typical vacuolar pathology. These results show that the mature amyloid of scrapie is composed of, or contains a substantial proportion of, whole length PrP protein. Thus truncation of PrP is not essential for the aggregation of PrP into amyloid. The vascular amyloid of natural sheep scrapie originates from the accumulation and release of PrP from endothelial cells presumably following systemic scrapie infection. The topography of vascular amyloid distribution in Great Britain differs from that reported in the Netherlands. As amyloid deposition in mice is largely controlled by the strain of the infecting agent it is possible that the strain of the agent may influence vascular amyloid deposition.

Acute nephropathy in young lambs.

Acute renal failure was diagnosed by clinical, necropsy and histological criteria in 39 flocks (20 low ground, 13 hill and six marginal upland) in areas served by six veterinary investigation centres. Forty-eight lambs of 12 different breeds or crosses were investigated. The mean age of affected lambs was 38 days (range seven to 84 days); 21 lambs (44 per cent) were aged seven to 28 days, while only eight (17 per cent) were older than two months. Mortality in clinically affected lambs was almost 100 per cent, with no response to various treatments. Histological examination showed that 40 lambs (83 per cent) had nephrosis, while the rest had toxic tubular necrosis, interstitial nephritis or tubular damage associated with oxalate crystal deposits. Only about half of the lambs had any evidence of enteric infections or enteropathy. Acutely ill lambs had azotaemia, haemoconcentration and proteinuria; some lambs had glycosuria or haematuria. Samples of plasma from 22 lambs with nephrosis were compared with similar samples from 82 incontact but asymptomatic lambs. The clinically affected group had significantly elevated plasma urea, creatinine, total protein, globulin, phosphorus and chloride concentrations and significantly reduced plasma calcium concentrations compared with healthy lambs. Affected lambs had a significant reduction also in the calcium:phosphorus ratio. No significant differences between groups was found in plasma concentrations of albumin, glucose, lactate, glycerol, creatine kinase, alkaline phosphatase, sodium, potassium or magnesium.

Lack of evidence for an association between MHC diversity and the development of bovine neonatal pancytopenia in Holstein dairy cattle.

Bovine neonatal pancytopenia (BNP), a disease of neonatal calves, has been described in a number of European countries since 2006. The disease results in high mortality of calves aged 1-4 weeks and is characterised by severe bone marrow pathology resulting in profound thrombocytopenia and consequent haemorrhagic diathesis. A number of hypotheses including a novel virus infection, plant toxins, a vaccine associated isoimmune disease, or a genetic defect have been suggested to explain the aetiology of this disease. However, as the number of cases in affected herds remains small, it is hypothesised that the genetic background of the calf may influence disease susceptibility. To test this we focused on the class II region of the major histocompatibility complex (MHC) which is often associated with variations in immune response and susceptibility to antibody mediated autoimmune disease. Forty-three cases of BNP and sixty-eight controls were genotyped at the polymorphic class II MHC-DRB3 locus. Twenty DRB3 alleles were identified with seven appearing at frequencies ≥ 0.05. A comparison of the allelic frequencies between diseased and control groups showed that there was no evidence for any significant differences, suggesting that the MHC does not appear to be a predisposing risk factor in the development of BNP in Holstein dairy cattle.