Haemorrhagic syndrome of cattle associated with the feeding of sweet vernal (Anthoxanthum odoratum) hay containing dicoumarol.

An outbreak of a haemorrhagic diathesis in cattle fed home produced hay is described. A similar syndrome was reproduced experimentally in calves by feeding them the hay. The experimental disease was characterised by increased prothrombin and partial thromboplastin times while the leucocyte and erythrocyte counts remained normal until the terminal haemorrhage. The calves ate well and grew well until the rapid onset of progressive weakness, stiff gait, mucosal pallor, tachycardia, tachypnoea and haematomata ending in sudden death. The absence of blood coagulation was seen at necropsy while petechial, ecchymotic and free haemorrhages were found in most organs. Particularly striking were massive ecchymotic haemorrhages on the peritoneal surface of the rumen, a bloody, gelatinous mass enveloping each kidney and extensive bruising, haemorrhage and haematomata in the subcutis of the limbs. In a second feeding trial the effects of various preparations of vitamin K1 and vitamin K3 were investigated. Oral administration of large quantities of vitamin K1 reduced the elevated prothrombin time; vitamin K3 acted less consistently. Analysis of the hay for trichothecene mycotoxins was negative but floral analysis revealed that sweet vernal grass (Anthoxanthum odoratum) comprised about 80 per cent of the hay. Dicoumarol was detected in the hay and in the serum and ruminal contents of the experimental calves. The diagnosis, treatment, control and importance of this syndrome in the United Kingdom are discussed.

Investigations of a flock heavily infected with maedi-visna virus.

Following the discovery that a flock of sheep in England was infected with the virus of maedi-virus, several seropositive sheep were brought to the Central Veterinary Laboratory and kept isolated and under observation for up to three years before being further examined at necropsy. Meanwhile, sheep in the infected flock which died or were culled were examined after death for evidence of the actual disease. At necropsy pulmonary disease was a common (although not always the sole) finding, the lesions being mostly chronic pasteurellosis and pulmonary adenomatosis. One of the 45 carcases examined showed classical lesions of advanced maedi. In four others, early or incipient lesions of maedi were found in otherwise normal lungs, while in three more, maedi was coincidental with the other pulmonary diseases. No clinical evidence to suggest maedi, other than emaciation, was seen in any of the sheep with lesions of the disease.

Evaluation of autofluorescence as an aid to diagnosis of cerebrocortical necrosis.

A series of brains from sheep, cattle, goats and pigs was examined histopathologically and illuminated by ultraviolet light to test the specificity of autofluorescence in the diagnosis of cerebrocortical necrosis. Fluorescence was seen in only four cases of porcine encephalopathy. In the ruminant brains it occurred in seven out of eight cases of cerebral oedema of lambs; otherwise it was confined to cases of cerebrocortical necrosis, although a few false negative cases were encountered. Ovine cerebral oedema is a disease of unweaned lambs which is unlikely to be confused with cerebrocortical necrosis. Thus bright cerebrocortical autofluorescence in a naturally occurring disease of cattle, sheep and goats is a likely indicator of cerebrocortical necrosis; however, a small proportion of cases will escape detection by this method.

Sudden death and myocardial necrosis in cattle.

Sudden death in cattle, especially calves, is a common problem of farm practice. Some cases are associated with significant cardiac lesions; in others, although necropsy suggests cardiac failure to be the cause of death, histological examination of H & E sections fails to demonstrate conclusively the site and nature of the lesion. We have studied 26 animals which died suddenly and in which the only pathological abnormalities detected were definite or equivocal myocardial necrosis. Three types of necrosis were identified: myodegeneration, contraction band necrosis and coagulation necrosis. Vacuolation of myocytes occurred in control hearts only in the sub-endocardial myocardium, but was found more extensively in diseased hearts. Paraffin sections of myocardium stained by von Kóssa's method or by haematoxylin-basic fuchsin-picric acid improved the detection of myocardial necrosis. Some myocardium was examined by electron microscopy which detected early myocardial necrosis in some equivocal cases and defined the nature of the lesion in more advanced cases. Early changes were an increase in the number of type A mitochondrial inclusions which did not contain significant quantities of calcium but which increased in number after death, albeit to a lesser degree, even in control material. This was followed by deposition of electron-dense granules and spicules (Type B inclusions) and totally electron-opaque mitochondria in association with contraction band necrosis. X-ray microanalysis showed type B inclusions and electron-opaque mitochondria to have peaks for calcium. It is suggested that myocardial cell death in animals having such lesions resulted from mitochondrial calcium overload. The findings are discussed in relation to nutritional myopathies of ruminants and human myocardial disease associated with sudden death, and to experimental myocardial ischaemia.

Diagnostic aspects of cerebrocortical necrosis.

Specimens from cattle and sheep suspected of having cerebrocortical necrosis (CCN) were studied. Rumenal contents were examined for thiaminase-producing bacteria. Thiaminase activity was assessed in rumenal contents. The thiamine concentration of liver, brain and heart was determined and erythrocyte transketolase assessed. Diagnosis in each case, whether positive or negative for CCN, was decided by histopathological examination. There was a substantial agreement between the biochemical findings and the histological diagnosis indicating that a provisional diagnosis may be made on clinical and biochemical data alone. The findings are discussed in relation to other diseases which have the same neuropathological features. Attempts to isolate thiaminase-producing bacteria, which may be implicated in the aetiology of CCN, were inconclusive.

Studies on bovine leukosis as it is seen in England and Wales.

A random series of 14 clinical cases of bovine leukosis as it is seen in England and Wales has been studied clinically, haematologically, serologically (by the indirect fluorescent antibody test and later by agar gel immunodiffusion as well), virologically (for evidence of bovine leukaemia virus--BLV) and using the electron microsocope to count intranuclear pockets in circulating lymphocytes. Additionally calves have been inoculated with whole blood and a tissue lymphocyte suspension from the first six cases and the experimental calves studied periodically by the same methods. Herds of origin of the field cases were examined for clinical evidence of lymphomatosis, for evidence of leukaemia and for serum antibody to BLV. To date no evidence has been found to indicate that the field cases were other than sporadic and non-contagious. Neither BLV nor specific antibody has been demonstrated; no increase in lymphocytic nuclear pockets has been seen; the transmission tests are still apparently negative. It would appear that sporadic bovine leukosis and enzootic bovine leukosis are aetiologically separate entities.