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.

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.

Twelve male cats were fed 2 diets that differed in the source of P. In diet 1 (1.4% P), 62.7% of P originated from poultry, meat, and fish meal, and the remainder from other organic ingredients of food. In diet 2 (1.6% P), 63.5% of P was derived from neutral monobasic/dibasic salts, and the remainder from other organic ingredients of the food. The P intake was nearly the same with both diets, but there was a significant (P less than 0.05) difference between diets in the percentage of ingested P that was excreted in the urine (14.7 +/- 5.3% for diet 1; 34.9 +/- 8.4% for diet 2), and in 6-day urinary P excretion (774 +/- 290 mg for diet 1; 2,004 +/- 556 mg for diet 2). The P concentrations in urine samples obtained by cystocentesis after cats ate were significantly (P less than 0.05) higher when cats were fed diet 2 than when those same cats were fed diet 1. Plasma P concentrations increased after ingestion of diet 2, but were unchanged after ingestion of diet 1. Seemingly, urinary excretion of P was markedly influenced by dietary composition. Diets with the same P content have potential for different biologic effects because of differences in availability of P.

Terminal renal dysfunction (TRD) was induced in 2 groups of dogs by partial surgical ablation of the kidney. Dogs of a control group and of 1 of the TRD groups were maintained on a diet containing normal phosphorus concentration, whereas dogs of the other TRD group were maintained on a low-phosphorus diet. Mild anemia developed in dogs of both TRD groups and could not be attributed to iron deficiency, increased erthrocyte concentration of 2,3-diphosphoglycerate, or absolute deficiency of erythropoietin (EP). Subsequently, all dogs were acutely depleted of approximately 25% of their blood volume. Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus. The PCV in dogs of the chronic TRD goups had a slight positive correlation with serum EP concentration, and a significant (P lesss than 0.05) negative correlation with plasma PTH and serum phosphorus and creatinine concentrations, using a correlation matrix. There was no longer a significant correlation between plasma PTH concentration and PCV after controlling for serum creatinine concentration by use of a multiple linear regression analysis. A significant (P less than 0.05) negative correlation also was observed between plasma PTH and serum EP concentrations, but not between serum EP and phosphorus or or creatinine concentrations. Significance of the EP and PTH association was reduced when analyzed, using a multiple linear regression analysis that included serum creatinine values. According to these data, PTH does have an independent effect on EP concentration, but the relationship between PTH and EP is not sufficiently strong to account for the genesis of the anemia of chronic TRD.