The effect of low levels of dietary cobalt on the chemiluminescence response of polymorphonuclear leukocytes of goats.

Twenty ten-week-old newly weaned male Batinah goats were randomly assigned to a control (n=10) and a treated (n=10) group and were fed a diet containing 0.1mg/kg DM cobalt (Co). Goats in the treated group received bi-monthly subcutaneous injections of 2000 microg of hydroxycobalamin. The phagocytic function of the polymorphonuclear leukocytes (PMN) were tested using a luminol-dependent chemiluminescence assay with opsonized zymosan as the phagocytic target. One month after the onset of the experiment PMN from the control group exhibited a significantly (p<0.05) lower CL response, which continued for the second month. The results of the present study demonstrated that low levels of dietary cobalt leads to an early impairment of phagocytic function. This may at least in part, be an explanation as to why at the field level in Oman young goats fed diets containing low levels of Co appear to be more susceptible to infections.

Comparative chemiluminescence of neonatal and adult ovine polymorphonuclear leukocytes.

Polymorphonuclear leukocytes (PMN) serve on the first line of the immunological defense of ruminants. However, despite the high morbidity and mortality of neonatal lambs to a wide range of infections there have been no definitive studies undertaken to ascertain whether there might be functional differences in PMN from neonatal lambs when compared to those from adult sheep. To determine whether there were differences in the oxidative respiratory burst of PMN, luminol-dependent chemiluminescence (CL) measurements were made of PMN from lambs at 1 week, 1, 2 and 3 months of age and at the same time from their respective dams. PMN isolated from lambs exhibited significantly lower levels of CL until 2 months of age. At 3 months of age the PMN produced levels of CL equal to that of their dams. As CL mirrors the ability of PMN to efficiently phagocytize and kill pathogens the present findings would suggest that PMN of neonatal lambs during the first 2 months are likely less capable of defending them from pathogenic organisms.

Effects of low concentrations of dietary cobalt on liveweight gains, haematology, serum vitamin B(12) and biochemistry of Omani goats.

Seventy-three, 10-week-old, newly weaned Omani goats of three different breeds, namely Dhofari (D), Batinah (B) and Jebel Akhdar (JA) were randomly divided into a control (n=38) and a treated group (n=35) for an experimental period of 10 months. Goats in both groups were fed 150 g/day per head of a pelleted concentrate, based on body weight and their requirements and Rhodes grass hay ad libitum, containing 0.12 and 0.10 mg/kg DM cobalt, respectively. Goats in the treated group also received bi-monthly subcutaneous injections of 2000 microg hydroxycobalamin. In contrast to the treated goats, the control animals of all breeds experienced a severe decrease in their serum vitamin B(12) levels, developed pale mucous membranes, appeared scruffy and two breeds (D and B) had significantly lower weight gains from month 5. Untreated kids of all breeds had significant decreases in their red blood cell counts and erythrocyte indices after approximately four months. Controls developed low total serum protein levels whilst activities of alkaline phosphatase and aspartate aminotransferase significantly increased. Although it is widely assumed that goats are more resistant to cobalt deficiency than sheep this is apparently not true for Omani goats. Based on experimental data from previously reported studies and those from the present study it can be concluded that the reduction in weight gains in D and B goats is related to their lower digestibility coefficients for dry matter, crude protein and energy while the increase in alkaline phosphatase and aspartate aminotransferase are associated with developing hepatic lipidosis.

Caprine hepatic lipidosis induced through the intake of low levels of dietary cobalt.

Forty-one, 10-week-old newly weaned goats were randomly allocated into two groups, namely control (n=22) and treated (n=19). Kids in both groups were fed Rhodegrass hay ad libitum that contained < 0.1 mg/kg DM cobalt and 150 g/day of a commercially prepared ruminant concentrate that contained approximately 0.12 mg/kg DM cobalt. This diet provided the minimum daily requirement of cobalt as specified for sheep. The treated goats were supplemented with bi-monthly subcutaneous injections of 2000 microg of hydroxycobalamin. All goats were weighed and blood samples collected monthly for haematological, clinical biochemical and serum vitamin B12 analysis. After a 10-month experimental period the goats were slaughtered. The control animals exhibited significantly (P<0.05) lower weight gains, and had dry scruffy hair coats. In addition, there was a decline in erythrocyte counts, mean haemoglobin, packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration. Controls also exhibited significantly (P<0.05) lower levels of total serum proteins and elevated levels of serum alkaline phosphatase compared to treated goats. Fourteen (63.6%) of the control goats developed pathology consistent with reported field cases of hepatic lipidosis associated with low liver levels of cobalt. Only one (5.3%) of the treated goats developed hepatic lipidosis. Contrary to previous reports that suggested that goats are less sensitive to low levels of dietary cobalt than sheep, it is apparent that this is not the case with Omani goats. This is the first report of the induction of hepatic lipidosis in goats due to feeding low levels of cobalt in their diet.