The introduction of a new batch of feed to 400 pigs aged five to eight weeks resulted in 38 deaths and further morbidity associated with multiple haemorrhages. Signs abated within two days of withdrawal of the feed. Widespread haemorrhages were present in many tissues including the pancreas. Additional pancreatic lesions comprised focal necrosis, atrophy and fibrosis of exocrine tissue. The condition was reproduced experimentally in pigs and vitamin K protected mice against the injurious effects of the feed. The cause was not determined but it is speculated that more than one toxic factor and an imbalance of nutritional factors may have been present in the diet.

Six ten-week old gilts were fed a diet containing 20% soyameal for a period of 14 weeks. Their body weights and vulval measurements were compared with those of six similar gilts fed a soya-free diet. After five weeks, the vulvae of the soya-fed group were slightly larger than those of the controls. The difference was maintained until the end of the experiment and was highly significant over the last five weeks. All 12 gilts were slaughtered after 14 weeks on the test diets and a general post-mortem examination carried out. The reproductive tracts were weighed and samples taken for histological examination; however no significant differences between the two groups were observed.

Four groups of six 12-week-old male Friesian calves were fed diets containing 390 to 540 microgram ochratoxin A per kg, 320 to 500 microgram ochratoxin A plus 12 to 13 microgram aflatoxin B1 per kg, 10 to 13 microgram aflatoxin B1 per kg, or a control diet containing neither toxin. At the end of the 87-day experiment there was no evidence of kidney or liver damage in any group of animals as judged by serial plasma and urine enzyme assays, haematological examinations including the assay of blood coagulation factors, gross appearance at autopsy or histopathological assessment at the light microscopic level. Nor was there any significant alteration in serum IgA, IgM, IgG1 and IgG2 levels or in titres to environmental bacterial and viral antigens. Trace amounts of ochratoxin A were detected in kidneys of five out of the 12 calves exposed to this toxin but all 12 kidneys contained residues of the metabolite ochratoxin alpha (less than 5 to 10 microgram/kg). Traces of aflatoxin B1 and M1 were detected in the liver of one of the 12 calves exposed to aflatoxin B1 but nine kidneys contained the metabolite aflatoxin M1 (less than 0.01 to 0.03 microgram/kg). There was no evidence of interaction between the two toxins.

Three calves were dosed orally with carbon tetrachloride at 0.05, 0.1 or 0.3 ml/kg body-weight. Plasma enzyme activities, clotting times, bilirubin concentrations and bromsulphthalein elimination times increased. These changes are associated with damage to the liver and are discussed in relation to the clinical syndrome. Three groups of seven calves were infected weekly with 10, 50 or 100 Fasciola hepatica metacercariae for 12 consecutive weeks. Maximum glutamate dehydrogenase and gamma glutamyltransferase activities in the plasma were greater with the larger infecting doses but there was no change in plasma clotting times.

Over a period of 13 years 740 samples of various animal feedstuffs were analysed for the presence of aflatoxin B1. Nearly 500 were suspected of causing disease in farm animals but aflatoxin B1 could be detected in only 13.6 per cent of them. Groundnut meal samples nearly always contained the toxin but compounded feeds were contaminated to a varying extent. In particular, none could be detected in 62 poultry feeds. Where mycotoxicosis was suspected in dairy cattle, aflatoxin B1 was present at levels of more than 30 micrograms per kg in about 27 per cent of associated feed samples. In other dairy feeds (178 samples) this level of contamination was present in only about 9 per cent of samples. Concentrations of aflatoxin B1 likely to produce toxic effects (100 micrograms per kg and above) were present in about 4 per cent of suspect dairy concentrates but in 1 per cent or less of others. Contamination of dairy concentrates with aflatoxin B1 is usually at such a level that cows probably excrete the toxic metabolite aflatoxin M1 in milk at very low concentrations of 0.1 micrograms per litre or less.

Fifteen pregnant, bovine virus diarrhoea-mucosal disease (BVD-MD) antibody-free Jersey heifers were infected experimentally with a mixture of 10 cytopathic strains of BVD-MD virus isolated from cattle in Britain. Each cow was inoculated intramuscularly on gestation day 100 with a high or a low dose of virus grown in primary calf testis tissue cultures. None of the cows showed clinical signs of illness following exposure, but all had seroconverted within six weeks. Six fetuses, including one set of twins, died in utero following infection. Of these five were aborted between days 136 and 154; the sixth one was mummified and still retained at day 300. The remaining 10 fetuses survived to term, but all showed evidence of intrauterine growth retardation with or without gross malformation and/or dysmyelination of the central nervous system. Three were clinically affected with congenital nervous disease. Of the 10 liveborn fetuses, two had specific serum antibodies to BVD-MD. Non-cytopathic BVD-MD virus was recovered from all of the remaining eight. When non-immune cows become infected with BVD-MD virus in mid gestation: transplacental infection of the fetus will probably result; apart from the risk of fetal death, with or without abortion, there is a high probability of fetal mal-development which may not always be clinically obvious; the immunological competence of the fetus may be impaired; congenital infection is likely in a substantial proportion of liveborn calves. About one in 16 bovine fetuses in British herds are estimated to be at risk from BVD-MD virus infection.

Thirty pregnant, BVD antibody-free Dorset Horn ewes were divided into three equal groups and infected experimentally with a mixture of 10 strains of BVD virus isolated from cattle in Britain. Ewes of groups I and II were inoculated intramuscularly at day 25 to 40 of gestation with a high and low dose of virus respectively. Ewes of group III received inoculum partially inactivated by heat. Ten additional pregnant ewes served as uninoculated controls. None of the inoculated ewes showed any evidence of malaise, but all had seroconverted within 42 days.

Six dairy cows consuming a diet contaminated with approximately 10 μg aflatoxin B1/kg excreted aflatoxin M1 in the milk, the concentration varying between 0·01 and 0·33 μg/litre with a mean value of 0·.19 μg/litre. Approximately 2·2% of ingested aflatoxin B1 appeared in the milk daily as the metabolite aflatoxin M1. This was a more consistent index of aflatoxin ‘carry over’ than the ratio of toxin concentrations in feed and milk.

Penitrem A or an unknown tremorgenic toxin, "X," was produced by 10 of 60 fungal isolates obtained from a pasture involved in an outbreak in cattle and sheep resembling migram and ryegrass staggers. Tremorgenic properties of extracts containing penitrem A or toxin X were confirmed by bioassay.

Pregnant Dorset horn gimmers inoculated with a non-cytopathic strain of the border disease virus produced "hairy shaker" lambs that were individually affected to a varying degree. Surviving lambs were observed for a period of up to 20 weeks when neurological signs were seen to gradually disappear. During this time live virus was isolated from a wide variety of sites in nearly all of the infected lambs. The infected animals grew at a significantly slower rate compared with the controls, particularly during the first 15 weeks. Several morphological defects are described the most consistent being the decreased weight of the central nervous system. By 20 weeks body-weights were about 20 per cent lower and carcase quality scores were reduced. An assessment is made of the economic losses attributable to BD taking into consideration carcase quality at 20 weeks and the perinatal losses.

Piglets and calves were dosed orally with pure diacetoxyscirpenol (DAS) and T-2 toxin, crude extracts of Fusarium tricinctum containing T-2 toxin, and whole cultures of F tricinctum containing T-2 toxin at a constant daily rate of 0.1 mg toxin per kg body-weight (piglets) or 0.2 mg toxin per kg body-weight (calves). The treatment continued for periods of seven to 78 days but it failed to induce clinical haemorrhagic syndromes. Increasing the dose of F tricinctum culture five-fold for eight days following 78 days at the lower dose was equally ineffective. The lack of an effect by daily intakes of toxin that could have been ingested with naturally contaminated feedstuffs suggests that DAS, T-2 toxin and other metabolites of F tricinctum probably have little or no part to play in the aetiology of feed associated haemorrhagic disease.

Abstract— In a neurochemical study of experimental Border Disease in lambs it was found that the fresh weights of four parts of the CNS (cerebrum, cerebellum, brain stem and spinal cord) from clinically affected lambs were significantly smaller than those of controls at birth but by 20 weeks of age the cerebrum, cerebellum and brain stem had reached near normal weights. The spinal cord was still considerably smaller, however. Clinical symptoms of the disease (muscular spasms and‘hairy’birthcoat) had disappeared during this period, accompanied by a regression in the neurochemical abnormalities seen at birth. Thus the deficiency of myelin lipids was partially made up by the rapid deposition of cerebrosides and by 20 weeks differences in the fatty acid composition of this lipid fraction were no longer apparent. Myelin degeneration as indicated by the presence of elevated levels of esterified cholesterol was apparently absent at 20 weeks of age and this was parallelled by a fall in the level of‘anti‐myelin’antibodies in the sera of affected lambs. The altered distribution of copper in spinal cord myelin seen at birth had also become nearly normal at the end of the period.

Concentrate rations containing 385–1925 μg zearalenone/kg or 317–1125 μg ochratoxin A/kg were prepared from naturally contaminated cerals and were each fed to two adult cows, the zearalenone ration for 7 wk and the ochratoxin ration for 11 wk before slaughter. Aflatoxin B1 was fortuitously present in both rations at a concentration of 20 μg/kg. Residues of zearalenone, ochratoxin α and aflatoxin B1 were not detected in muscle, liver, kidney, serum, milk or urine, but ochratoxin A was detected in the kidneys of one cow at a concentration of about 5 μg/kg and aflatoxin M1 was detected in the kidneys, milk and urine of all animals at concentrations varying from trace amounts to 0·6 μg/kg.

The reliability of erythrocyte glutathione peroxidase activity as an indicator of selenium status in livestock is discussed. Based on this measurement, a survey is described of the biological selenium status of sheep on each of 329 farms in Britain. Results showed that 47 per cent of these farms were probably unable to provide grazing livestock with sufficient selenium to maintain blood levels greater than 0.075 microgram per ml. Increased selenium deficiency from the increasing use of home grown feeds as a major constituent of livestock rations may be causally related to the increase of white muscle disease and other selenium responsive diseases in Britain.

Two liver-specific enzymes in the plasma of young cattle were used to study their resistance to reinfection with Fasciola hepatica. Although plasma glutamate dehydrogenase and gamma-glutamyltransferase activities rose sharply after infection with 1000 metacercariae of F. hepatica, reinfection 35 or 54 weeks later produced no such effect. The ventral lobe of the liver almost completely disappeared 35 weeks after infection, with a thickening of the remaining liver. Ten weeks after a second infection fibrin tags were observed on the surface of the liver, but there was less traumatic damage in the subcapsular tissue than in singly infected calves. No effect of infection on weight gain was observed.