PubMed · 4942200
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D W Fewkes, K J Parker, A J Vlitos. 1971. Sucrose.. https://pubmed.ncbi.nlm.nih.gov/4942200/
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Secondary Cu deficiency, Cr deficiency and molybdenosis were suggested causes of the 'mysterious' disease afflicting moose (Alces alces L.) in a region in south-west Sweden affected by acid rain. A model experiment with goats was performed to study the clinical chemical parameters, determine the tissue contents of trace and minor elements, to perform pathological and histopathological investigations and to compare the findings with those in moose disease. Twenty 3-month-old male goats were assigned to four dietary treatments (five animals each) in an experiment lasting for 20 months. The four groups in the study were: control group, Cu-deficient group (group 1), Cr-deficient group (group 2), and Cu- and Cr-deficient group (group 3). The animals were fed a basic semi-synthetic diet. At the end of the study the three surviving animals of group 3 were supplemented with additional tetrathiomolybdate (TTM) during the last 2 months. Feed consumption and weight development of the animals were monitored and are presented. The feed consumption of the two Cu-deficient groups of goats (group 1 and group 3) supported the previously described observations in copper deficiency in ruminants, e.g. decreased appetite and feed intake. A previously unreported effect of Cr deficiency in ruminants is now described in goats. Chromium deficiency at adequate Cu supplementation (group 2), caused increased lipid synthesis and a weight gain of 32 kg compared with that of the control group (20 kg). A possible explanation for this unexpected weight increase in only Cr deficiency is discussed. It is concluded that the feeding experiment does not support the hypothesis concerning the relation of Cr deficiency to the moose disease.
The purpose of this study was to determine whether methods used to control swine dysentery (SD), caused by the intestinal spirochaete Brachyspira (Serpulina) hyodysenteriae, would also be effective in controlling porcine intestinal spirochaetosis (PIS) caused by the related spirochaete Brachyspira (Serpulina) pilosicoli. Weaner pigs in Groups I (n=8) and II (n=6) received a standard weaner pig diet based on wheat and lupins, whilst Group III (n=6) received an experimental diet based on cooked white rice and animal protein. Pigs in Group II were vaccinated intramuscularly twice at a 3-week-interval with a formalinised bacterin made from B. pilosicoli porcine strain 95/1000 resuspended in Freund's incomplete adjuvant. Eleven days later pigs in all groups were infected orally with 10(10) cells of strain 95/1000 on three successive days. One control pig in Group I developed acute diarrhoea, and at post-mortem had a severe erosive colitis with end-on attachment of spirochaetes to the colonic epithelium. All other pigs developed transient mild diarrhoea and had moderate patchy colitis at post-mortem 3 weeks later. B. pilosicoli was isolated from the faeces of all pigs, except for one fed rice, and was isolated from the mesenteric nodes of three pigs from Group I and from one vaccinated pig in Group II. Consumption of the rice-based diet, but not vaccination, delayed and significantly (p<0.001) reduced the onset of faecal excretion of B. pilosicoli after experimental challenge. Vaccination induced a primary and secondary serological response to B. pilosicoli, as measured using sonicated whole cells of strain 95/1000 as an ELISA plate coating antigen. Antibody titres in the vaccinated pigs then declined, despite intestinal colonisation by B. pilosicoli. Both groups of unvaccinated animals also failed to develop a post-infection increase in circulating antibody titres.
Twin 17-day-old crossbred male lambs were examined to determine the cause of weakness and failure to thrive. Hypercalcemia attributable to hypervitaminosis D was diagnosed. The milk replacer or an accidental overdose of an injectable vitamin D product was suspected to be the source, although a definite cause was not confirmed. Lambs responded favorably to palliative treatment (administration of saline [0.9% NaCl] solution to induce calcium diuresis) and changing the diet to another milk replacer.