Experimental equine leukoencephalomalacia, toxic hepatosis, and encephalopathy caused by corn naturally contaminated with fumonisins.

A study to evaluate the effects of dietary fumonisin B1 was conducted using 6 ponies (4 test and 2 control). A ration naturally contaminated with fumonisin B1 was fed in 3 phases: 1) 44 ppm fumonisin B1, 2) less than 1 ppm fumonisin B1, and 3) 88 ppm fumonisin B1. All ponies were monitored daily, weighed weekly, and limit fed at a rate of 0.8% body weight plus hay. Feed intake was measured daily, and a serum chemistry panel was completed once or twice weekly. Four to 7 days after initiation of the trial (Phase 1), all 4 test ponies had decreased feed consumption, and selected serum chemistry parameters were markedly elevated. On day 9, 1 pony died acutely with mild encephalopathy and hepatic necrosis. Another pony, euthanized on day 45, also had mild encephalopathy and hepatic necrosis. The remaining 2 test ponies continued the 44 ppm fumonisin B1 diet for 98 days. Phase 2 consisted of a diet with < 1 ppm fumonisin B1 for 120 days. During this phase, the serum chemistry values of the 2 ponies returned to normal. Following Phase 2, the 2 ponies were fed a diet containing 88 ppm fumonisin B1. After 75 days, 1 animal died of equine leukoencephalomalacia with mild hepatic necrosis. On day 78, the remaining pony was euthanized after showing distress; it also had leukoencephalomalacia and hepatic lesions.

Clinical pathologic alterations in horses during a water deprivation test.

A 72-hour water deprivation test was performed in 12 horses to determine clinical pathologic changes. Reference values for electrolyte (X) clearance, expressed as a percentage of creatinine clearance (CLCR; %CLCRX), were also determined. A comparison was made between urine concentration measurement techniques. Results of %CLCRX determination in 12 horses before water deprivation were 0.034 +/- 0.095 %CLCRNa, 42.4 +/- 9.8 %CLCRK, 0.352 +/- 0.190 %CLCRCl, and 0.710 +/- 0.250 %CLCRP. During water deprivation, there was individual variation for electrolyte clearances, but Na excretion increased significantly (P less than 0.01) at 24 and 48 hours. After 48 hours' water deprivation, %CLCRNa decreased significantly, but was still greater than the initial clearance. Plasma protein was a better indicator of water deprivation (dehydration) in the horse than was PCV. Electrolyte concentrations in serum and urine were determined. Little significant (P less than 0.01) change in acid-base values was noticed after 72 hours' water deprivation. Urine osmolality (as determined by osmometry) was compared with sp gr (determined by refractometry) in determining urine concentration. Initially, sp gr correlated well with urine osmolality determinations, but this correlation decreased after 48 hours.

Thymic abnormalities and growth hormone deficiency in dogs.

A high frequency of occurrence of a wasting disease, unthriftiness, and retarded growth was observed in a group of inbred Weimaraner dogs. Affected pups had a small thymus gland, with a marked absence of thymic cortex. A litter of eight pups from a sire and dam that were known to have produced affected offspring was chosen for further study. The pups had normal concentrations of WBC and gamma-globulins and were able to produce antibody in response to Brucella abortus. Two pups in the litter developed a wasting syndrome and responded well to therapy with thymosin fraction 5. One pup that survived the wasting syndrome had a significant (P < 0.05) depression of its lymphocyte blastogenic response to phytohemagglutinin compared with its surviving littermates. Pups from this litter also lacked a normal increase in plasma growth hormone concentration after the injection of clonidine HCl. These pups had concurrent abnormalities of the thymus-dependent immune function and in growth hormone metabolism. The syndrome in these pups has some features in common with the syndrome in the Ames or Snell-Bagg strains of immunodeficient dwarf mice.