To evaluate the effect of exogenous testosterone on the development of T-2 toxin-induced necrosis of adrenal glands, mice were allotted to 3 treatment groups. Each treatment group contained castrated male, and castrated and sexually intact female mice. Each mouse in group 1 was given 0.16 mg testosterone propionate at 48-hour intervals for a total of 12 infections, group-2 mice were given similar injections of only the vehicle, and group-3 mice were given no treatment. Twenty-four hours after the last injection, the mice in all 3 groups were exposed for 10 minutes to an aerosol of T-2 toxin. All mice alive at 24 hours after exposure were euthanatized and the adrenal glands and thymuses were examined histologically. Necrosis of the adrenal cortex was not found in any of the mice given preexposure treatment with exogenous testosterone, whereas all mice given vehicle only or no treatment had T-2 toxin-induced necrosis of the inner portion of the adrenal cortex. Lymphocytolysis in the cortex of the thymus confirmed that each mouse of all 3 treatment groups had experienced systemic mycotoxicosis. The uniform severity of the lesion in all mice suggests that the thymus was not protected by exogenous testosterone administration or by the castration status of the mice. We propose that T-2 toxin-induced adrenal necrosis in mice is prevented by the presence of testosterone.

Administration of vitamin K1, SC, to anticoagulant-poisonsed (diphenadione) dogs provided diagnostic information within 4 hours, when vitamin K1 and its epoxide were measured in canine sera. Twelve dogs (2 groups of 6) were given 2.5 mg of diphenadione/kg of body weight for 3 days. Dogs were treated with vitamin K1, 2.5 (n = 6) or 5 mg/kg/day (n = 6) SC for 21 days, and their responses were compared. Four nonexposed control dogs were given 5 mg of vitamin K1/kg/day. Serum concentration of vitamin K epoxide was significantly (P less than 0.02) higher in diphenadione-exposed dogs than in control dogs 1 to 4 hours after the initial vitamin K1 treatment on day 4. Vitamin K epoxide/vitamin K1 ratios were similarly higher and became more distinct. Cessation of vitamin K1 therapy on day 24 resulted in prolongation of one-stage prothrombin times in diphenadione-exposed dogs, becoming clearly evident on day 27. Serum vitamin K1 concentrations were not detectable on day 27 in diphenadione-exposed dogs, whereas serum vitamin K1 concentrations were readily detectable in control dogs. One stage prothrombin time changes, during days 24 to 32, indicated 5 mg of vitamin K1/kg provided better protection than did 2.5 mg of vitamin K1/kg. Coagulopathy in the dogs was resolved by day 32.

In 2 studies, the effects of dietary aflatoxin (AF) and deoxynivalenol (DON) were evaluated in growing crossbred barrows. The first study consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 2.5 mg of DON/kg of feed, 0.75 mg of AF/kg of feed, and 2.5 mg of DON + 0.75 mg of AF/kg of feed. Pigs were fed their respective diets for 21 days. Treatment with DON caused decreases in weight gains, but no other treatment-related differences could be attributed to diets. In a second study, the experimental design consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 3 mg of DON/kg of feed, 3 mg of AF/kg of feed, and 3 mg of DON + 3 mg of AF/kg of feed fed ad libitum for 28 days. The pigs were observed twice daily for clinical signs, hematologic and serum biochemical measurements were made weekly, and body weights and feed consumption were determined weekly. Body weight gains were significantly depressed by the AF and the AF + DON treatments for days 7, 14, 21, and 28. Body weights and body weight gains were only slightly reduced in the DON treatment. Changes in serum enzymatic activities of alkaline phosphatase, aspartate transaminase, creatine kinase, and gamma-glutamyl transferase were noticed in pigs given treatments with AF alone and those given AF + DON. Total iron binding capacity and serum total protein, albumin, cholesterol, BUN, and glucose concentrations were decreased, whereas prothrombin and activated thromboplastin times were increased by AF and AF + DON treatments. Lesions in the AF-treated groups were compatible with a diagnosis of aflatoxicosis. The control and DON-treated pigs had no abnormalities. These data provide a description of the effects of dietary AF and DON, singly and in combination, in growing barrows.

Ruminal microorganisms in cattle at a Florida agriculture research station did not have the ability to detoxify leucaena by degradation of 3-hydroxy-4(lH)-pyridone (3,4,-DHP), but a DHP isomer (2,3-DHP) was degraded in some cattle. Cattle with microorganisms that degraded 2,3-DHP were mostly Senepol cattle imported from St. Croix, US Virgin Islands, where leucaena is an indigenous species. Hereford cattle at the research station in Florida generally did not degrade 3,4-DHP or 2,3-DHP. An experiment was conducted in which a pure culture of 3,4-DHP-degrading bacteria was inoculated into Hereford cattle (with ruminal fistula) grazing leucaena. The bacteria successfully colonized the rumen of recipient cattle and persisted through the following winter when there was no leucaena in the diet.

Sixteen primiparous sows were bred and fed either a control ration (n = 8) or a diet containing purified zearalenone (n = 8; 1 mg/kg of body weight) from days 7 to 10 after breeding. On day 7 after breeding, the jugular vein of each sow was cannulated and blood was collected at 20-minute intervals for 4 hours before feeding and 4 hour after feeding. On day 10 after breeding, blood samples were collected from 4 control sows and 4 zearalenonefed sows at 20-minute intervals for 4 hours before collection of blastocysts. A similar blood sampling schedule was followed for the remaining 4 control and 4 zearalenone sows on day 14 after breeding. On day 10 after breeding, spherical blastocysts were recovered from all control sows and from 3 of 4 zearalenone-treated sows. Average diameter of blastocysts from zearalenone-treated sows were similar to that of control sows. On day 14 after breeding, blastocysts were recovered from all control sows and 3 of 4 zearalenone-treated sows. Blastocysts from the control sows were filamentous, whereas blastocysts from zearalenone-treated sows were fragmented and contained foci of necrosis. Incidence of luteinizing hormone (LH) secretory spikes per sow was less (P less than 0.01) in zearalenone-treated sows (0.25 +/- 0.25/4 h) than control sows (1.75 +/- 0.25/4 h) on day 10 after breeding. Incidence of follicle-stimulating hormone (FSH) secretory spikes was simillar (P = 0.45) among treatments on days 7, 10, and 14 after breeding. Mean serum concentrations of LH were less on day 10 (P = 0.07) and day 14 (P less than 0.01) in zearalenone-treated sows than in control sows (3.3 +/- 0.2 ng/ml vs 6.2 +/- 1.3). These data indicate that administration of zearalenone on days 7 to 10 after breeding altered secretory patterns of serum LH during days 10 and 14 after breeding, which may have contributed to the death of blastocysts by day 14 after breeding.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCA/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF. Aflatoxin alone induced decreased serum concentrations of urea nitrogen, albumin, total protein, calcium, phosphorus, cholesterol, and glucose, as well as serum total iron-binding capacity, whereas HSCAS or HSCAS plus AF did not induce such effects. Liver weight was increased in barrows of the AF-alone treatment group, compared with control barrows. Hepatic lesions in barrows of the AF-alone treatment group were charaterized as peripheral lobular lipidosis accompanied by periportal and interlobular fibrosis and bile duct hyperplasia. Hepatic lesions were not observed in barrows of the 0.5% HSCAS plus AF or 2.0% HSCAS plus AF treatment groups. These findings suggested that HSCAS can modulate the toxicity of AF in growing barrows (perhaps via sequestration and reduced bioavailability in vivo) and may offer a novel approach to the preventive management of aflatoxicosis in animals.

Changes in renal function, determined by pharmacokinetics of phenolsulfonphthalein (PSP), and renal morphologic features were examined in adult pony mares given 20 mg of gentamicin sulfate/kg of body weight, IV, q 8 h (group A) n = 7 or isotonic saline solution, IV, q 8 h, n = 5 (group B) for 14 days. Susceptibility of ponies to gentamicin-induced nephrotoxicosis was varied. Two group-A ponies developed acute renal failure and were euthanatized before treatment day 14, whereas 5 group-A ponies did not develop physical or behavioral abnormalities after 14 days of gentamicin administration. All group-A ponies but none of group-B ponies developed ultrastructural abnormalities of the proximal tubular epithelium, consistent with gentamicin-induced nephrotoxicosis. Significant (P less than 0.05) differences were not detected in pharmacokinetic values of either group. Clearance of PSP was reduced in 4 group-A ponies that developed the most severe gentamicin-induced nephrotoxicosis. Changes in clearance of PSP were significantly (P less than 0.05) correlated with changes in the serum creatinine concentration.

The effects of dietary aflatoxin and ochratoxin, fed singly and in combination, were evaluated in growing crossbred pigs. Five barrows (7 weeks old at beginning of study) per group were fed either control feed, 2.0 mg of aflatoxin (AF)/kg of feed, 2.0 mg of ochratoxin (OA)/kg of feed, or 2.0 mg of AF and 2.0 mg of OA/kg of feed for 28 days. Production performance, serum biochemical, hematologic, and pathologic evaluations were made. Body weights were reduced by the combination treatment, whereas body weight gain was decreased by all toxin treatments. The effect of AF and OA in combination on body weight gain was additive. Liver weights were increased by the combination treatment, whereas kidney weights were increased only in the OA group. Aflatoxin caused decreases in serum calcium, sodium, phosphorus, urea nitrogen, cholesterol, and glucose concentrations, whereas OA alone caused decreases in serum phosphorus, cholesterol, and hematologic values. The AF-OA treatment induced decreases in mean corpuscular volume, packed cell volume, and in serum concentrations of phosphorus, cholesterol, and urea nitrogen. The AF-OA treatment increased serum alkaline phosphatase activities and triglycerides. It was concluded that AF and OA, singly or in combination, can affect clinical preformance, serum biochemical and hematologic values, and organ weights of barrows. Although values of some measurements were affected more by the combination than by either toxin alone and suggested synergism or antagonism, the toxic interactions could best be described as additive.

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary juction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of the liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.

In addition to the 3-striped blister beetles (Epicauta temexa and E occidentalis), other sources of equine cantharidin toxicosis were identified at the Texas Veterinary Medical Diagnostic Laboratory and included E albida and E attrivittata and the previously incriminated E pardalis and E pennsylvanica. Improved methods for diagnosing cantharidin or blister beetle toxicosis involve partial purification of urine and gastric content extracts, using silica cartridges, followed by analysis, using capillary gas chromatography/mass spectrometry. During a 26-month period, 53 episodes of cantharidin toxicosis in horses were confirmed at our diagnostic laboratory. Concentrations of cantharidin in urine and gastric contents ranged from 0.0003 to 3.50 microgram/g. Peak incidences were observed in late summer and early fall.