Experimental hexachlorophene intoxication in young swine.

Hexachlorophene (HCP) intoxication in swine was studied as a possible model of HCP poisoning in human beings. Swine were topically or orally given HCP each day, and observations were made on central nervous system function, hematologic measurements, serum chemical analyses, necropsy, microscopic examination of tissues, and concentrations of HCP residues in blood and tissue. Intoxication was observed in orally exposed swine, but the syndrome was not consistently produced in topically exposed swine. Signs and microscopic lesions were all related to dysfunction of the central nervous system, e.g., incoordination, paresis, and status spongiosus. Occurrence of signs and lesions, mortality rates, and concentrations of HCP residue were positively correlated with the dosage of HCP given.     

Acute aflatoxicosis in swine: clinical pathology, histopathology, and electron microscopy

Feeder pigs weighing 12 to 15 kg each were given a single oral dose of aflatoxin, 1.2 mg/kg of body weight. Liver-specific serum enzyme activities were compared with gross, microscopic, and ultrastructural hepatic changes in individual pigs euthanatized at 24, 48, and 72 hours after they were given aflatoxin. The greater the morphologic change in liver of the treated pigs, the greater the increase in liver-specific serum enzyme activities. Isocitric dehydrogenase, alkaline phosphatase, sorbitol dehydrogenase, and aspartate aminotransferase activities increased in 6 of 8 treated pigs by 24 hours. Increase in gamma-glutamyl transpeptidase activity was not significant. Microscopic and ultrastructural changes in centrilobular hepatocytes included glycogen deletion, mitochondrial and endoplasmic reticulum swelling, membrane disruption, and nuclear fragmentation at 24 hours. The centrilobular areas had marked extravasation of erythrocytes at 24 hours without basal lamina changes. At 72 hours, the centrilobular hepatocytes had increased lipid vacuoles and acceptable amounts of glycogen. Marked infiltrations of monocytes, plasma cells, and lymphocytes were also present at this time.     

Experimental lead toxicosis in swine

Thirty pigs, weighing 17 to 24 kg, were exposed to lead or sodium acetate orally or intraperitoneally (IP) 6 days each week for 13 weeks. These pigs were extremely tolerant of lead. Only mild clinical signs of lead toxicosis were observed in orally lead-exposed pigs despite blood lead concentrations of up to 290 micrograms/dl. Four IP lead-exposed pigs died, but eight other IP lead-exposed pigs survived the exposure period despite blood lead concentrations up to 14,300 micrograms/dl. Lead exposure caused marked decreases in blood delta-aminolevulinic acid dehydratase activities of all pigs and moderate decreases of blood hemoglobin concentrations, hematocrit percentages, mean corpuscular volumes, mean corpuscular hemoglobin concentrations, and mean corpuscular hemoglobins in IP lead-exposed, but not in orally lead-exposed pigs. Basophilic stippling was observed in erythrocytes of lead-exposed pigs, but not in those of control pigs.     

犬黄曲霉毒素中毒

黄曲霉毒素是由黄曲霉和寄生曲霉产生的有毒代谢产物。当犬采食被黄曲霉和寄生曲霉污染的食物,常可发生中毒。     

Progression of aflatoxicosis in growing barrows

The progression of aflatoxicosis was evaluated in growing crossbred barrows given 0, 1, 2, 3, or 4 mg of aflatoxin (AF)/kg of feed for 28 days (6 to 10 weeks of age). On day 28, pigs were euthanatized and necropsied, and tissues were removed for histologic examination. Body weight gains were decreased in barrows fed 2 mg of AF/kg after 7 days and in barrows fed 1 mg of AF/Kg after 14 days. By 28 days, all barrows fed AF had decreased body weights and weight gains. Compared with decreased in all barrows fed AF. Neither liver weights nor bone ash values were altered, although liver lipid values were increased in barrows fed AF. Serum aspartate transaminase, gamma-glutamyl transferase, and alkaline phosphatase activities were increased in barrows fed AF, whereas creatine kinase activity was decreased. Aflatoxin diets resulted in decreases in serum concentrations of urea nitrogen, phosphorus, cholesterol, albumin, and total protein. Histologic alterations in liver included interlobular fibrosis, periportal lipidosis, bile duct hyperplasia, and periportal lymphocytic infiltration. Lymphocytes in the thymus were depleted, and numbers of granulocytic cells in the bone marrow were reduced. The frequency and severity of lesions increased with increased doses of AF.