The toxic effects of citrinin in turkeys and ducklings was studied in four trials. Citrinin dissolved in dimethyl sulfoxide-70% ethanol solution (3: 1, volume/volume) was administered by gavage to male turkey poults and male white Pekin ducklings. When seven-day-old ducklings were given doses of citrinin between 30 to 110 mg/kg body weight, most of the treated ducklings which died (49/80) did so within four to 12 hours. Blood samples were collected sequentially at 3, 6, 12, and 24 hours after administration from seven-day-old ducklings given the single lethal dose (LD 50 ). The alterations included hyperkalemia (P ≤ 0.01) and metabolic acidosis characterized by reduced blood pH (P ≤ 0.01) and base excess (P ≤ 0.01). Fourteen-day-old turkeys and ducklings given 56 or 57 mg/kg, respectively, were killed at 1,3, 6, 12, 24, 48, and 72 hours after treatment. The principal alteration in both species was nephrosis that was more severe in turkeys than in ducklings. Tubular necrosis was the dominant lesion at three to 72 hours in turkeys and at six to 24 hours in ducklings. Hepatic and lymphoid lesions occurred in both turkeys and ducklings treated with citrinin.
Citrinin was mixed in the diet (100, 250, 500 parts/10(6)) and fed to 1-day-old male White Pekin ducklings (Trial I), or it was dissolved in dimethyl-sulphoxide-70% ethanol (3:1, v/v) and administered by crop gavage to 14-day-old male White Pekin ducklings (Trial II) or 7-day-old male turkey poults (Trial III). Ducklings given 250 or 500 parts/10(6) citrinin diet for 15 days had clinical signs of citrinin toxicity. Body weight gain was significantly decreased by the 500 parts/10(6) diet (P < 0.05). Ducklings fed 250 and 500 parts/10(6) developed nephropathy that was more severe in the 500 parts/10(6) group. The nephropathy was characterised by degeneration, necrosis, mineralisation and regeneration of tubular epithelial cells of both the cortical and medullary regions. Interstitial fibrosis was found in the medullary regions of the 500 parts/10(6) group only and focally was accompanied by interstitial nephritis. Seven daily doses of citrinin equal to a half or three-quarters of the single-dose LD(50) produced no additive toxic effects in either ducklings or turkeys, but body weight gain was significantly decreased in duckling given three-quarters of the single-dose LD(50).
6-Aminonicotinamide (6-AN), a niacin antagonist, was administered sc to pregnant female (1.0, 3.0, or 6.0 mg 6-AN/kg body weight) and neonatal male (1.5, 3.0, 6.0 or 12.0 mg 6-AN/kg body weight) Sprague-Dawley rats on the 15th, 17th and 19th days of gestation or the 5th, 7th and 9th days of life, respectively, to determine the effects of the antimetabolite on testicular morphology and development. In prenatal males, microscopic alterations were present in testes of fetuses from females treated with 6.0 mg 6-AN/kg and consisted of necrosis and loss of gonocytes, and vacuolation of interstitial cells. Histologic changes in testes of neonatal rats treated with 3.0, 6.0 or 12.0 mg 6-AN/kg were qualitatively similar with necrosis and loss of spermatogonia and supporting cells, and increased cross-sectional areas of affected tubules. Quantitation of the number of nuclei/cm2 of seminiferous tubule indicated 6-AN caused a significant reduction in the numbers of supporting cells and spermatogonia/tubular cross-section.
Persistent hematuria in a neutered male Collie failed to resolve after treatment for adult Dirofilaria immitis. Excretory urography revealed normal opacification and an hourglass-shaped right kidney, with distortion of the renal pelvis and diverticula. After ureteronephrectomy, recovery was uncomplicated, and hematuria ceased 2 weeks after surgery. The middle of the excised kidney had been replaced with blood-filled spaces that were consistent with histopathologic diagnosis of hemangioma.
Mycotoxicosis Caused by Either T-2 Toxin or Diacetoxyscirpenol in the Diet of Broiler Chickens. Hoerr, F.J., Carlton, W.W., Yagen, B. and Joffe, A.Z. (1982). Fundam. Appl. Toxicol. 2:121-124. Seven-day-old male broiler chickens were fed either T-2 toxin or diacetoxyscirpenol at 4 and 16 ppm for 21 days and had reductions of feed consumption and of weight gain. Focal, yellow, oral plaques developed by day 2 and were located around salivary duct openings on the palate, tongue, and buccal floor. The plaques progressed to raised, yellowish-gray crusts which covered ulcers. Microscopically, the ulcers had a base of granulation tissue and inflammatory cells, and the crusts comprised exudate, bacterial colonies and feed components. T-2 toxin and diacetoxyscirpenol produced similar effects at these concentrations. Comparable lesions also occurred in chickens fed T-2 toxin at 50, 100, or 300 ppm for 7 days. Six of 10 chickens died in the 300-ppm group which received an average daily exposure of about 10 mg T-2 toxin/kg body weight. In dead chickens, the lymphoid and hematopoietic tissues and alimentary mucosa were necrotic. Necrosis was seen less frequently in the liver, kidney and the feather. Survivors of the 7-day studies had atrophied lymphoid organs and were anemic.
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