Biomedical subjects
Publications and source records attributed to K A Linklater.
Five out of 60 purebred Suffolk lambs died when four to six weeks old with a nephrosis characterised by heavy deposits of crystals resembling calcium oxalate in the tubules. The source of oxalate was not clearly identified but may have resulted from oxalate-forming mould contamination of concentrates fed to both ewes and lambs.
Inocula derived from two sources of typical border disease (BD) and designated BP-77 and H-77 respectively, were prepared and injected into pregnant ewes of four breeds. The BP-77 inoculum produced higher serum neutralising antibody titres to the cytopathic BD virus than to the NADL strain of bovine virus diarrhoea virus. Only typical BD occurred among the progeny of all four breeds. In contrast H-77 produced higher titres to bovine virus diarrhoea than to BD and typical BD occurred only in the progeny of two of the four breeds. Progeny of the other two breeds appeared normal or had a range of malformations of the central nervous system but none of the characteristic clinical or pathological stigmata of BD. The existence of more than one strain of BD virus is confirmed. Virus strain/host genotype interactions may affect the character of disease in the progeny. The possible implications for diagnosis and control are discussed. It is concluded that the generally accepted criteria for diagnosis of BD are no longer adequate and that the disorder should be redesignated.
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An outbreak of acute myopathy occurred in a group of 23 Hereford cross and Aberdeen Angus cross 18-month-old heifers, running outside with a bull in February. One morning two were found recumbent, five were ataxic and one had fallen into a river and drowned. Subsequently two of the ataxic ones became recumbent. Serum creatine phosphokinase values were found to be directly proportional to the severity of the clinical manifestations. Myoglobinuria was not observed. Serum calcium, magnesium and inorganic phosphate levels were all within the normal ranges. Treatment of affected animals with selenium and/or alpha-tocopherol had no clear effect; from biochemical estimations carried out, the selenium and alpha-tocopherol status of both affected and unaffected animals was considered adequate. Five recovered, two spontaneously without treatment, but the two most severely affected did not improve with therapy and had to be slaughtered 13 and 25 days respectively after the onset of symptoms.
A pig which was being immunised with thrombocytes from another pig developed thrombocytopenia and purpura. This appears to be analogous to the post-transfusion purpura syndrome which has been reported in humans and it is suggested that similar systems in pigs could be useful models for experimental studies on the human condition.
Three flocks in which in with one of more sheep had succumbed to polioencephalomalacia (cerebrocortical necrosis) were used for faecal thiaminase studies. Up to one third of the clinically normal animals in these flocks to be excreting thiaminase on any one day and over half the flock could be thiaminase excretors at some time during an outbreak. The possible detrimental effects of sub-clinical thiamine antagonism in sheep are therefore worthy of consideration. Thiaminase excretion by individual animals was variable and sometimes intermittent. It was unaffected by changes in diet, pasture or enviroment. In two of the flocks multiple cases of polioencephalomalacia followed the administration of the anthelmintics, levamisole hydrochloride and thiabendazole. This aspect merits further investigation in view of the widespread use of anthelmintics of this type, especially as the profuse diarrhoea which can be associated with outbreaks of polioencephalomalacia may be wrongly attributed to gastro-intestinal parasitism.
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Two gilts, non-affected members of a litter which had been affected with thrombocytopenic purpura were mated to a boar which was an affected member of the same litter. During pregnancy the gilts were injected with pure thrombocyte suspensions from the boar. Antibodies to the boar's thrombocytes were demonstrated in the sera of both gilts and also in samples of their colostrum at each parturition. The piglets produced from these matings had normal thrombocyte counts at birth but a proportion of them developed thrombocytopenia and purpura similar to that seen in natural cases within a few hours of receiving colostrum. However, despite the fact that this condition was observed in three litters from each of the gilts, a secondary thrombocytopenia at 10 to 14 days of age, characteristic of the naturally occurring condition, was only observed in two piglets in one litter.
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