Ochratoxicosis in Beagle Dogs

Szczech, George M.; Carlton, William W.; Hinsman, E. J.

doi:10.1177/030098587401100501

Cited by 27 publications

(20 citation statements)

References 31 publications

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“…Selective destruction by the toxin of only the epithelium of the proximal convoluted tubule is unusual, and the existence of only proximal tubule damage would not explain the hyposthenuria since the distal convoluted tubule and loop of Henle play major roles in concentrating the glomerular filtrate. Tubular dilatation was described in ochratoxicosis of rats [26,27] and was seen by us in ochratoxicosis of swine [31] but did not occur in the test dogs.…”

Section: Discussionmentioning

confidence: 73%

Ochratoxicosis in Beagle Dogs. II. Pathology

1973

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(With 1 color plate)Absruact. The gross lesions in 23 young male Beagle dogs given daily oral doses of 0.2-3.0 nig/kg body weight ochratoxin A consisted of moderate to severe niucohemorrhagic enteritis of the cecum, colon, and rectum; tonsillitis; and enlargement of lymph nodes, which were edematous, hyperemic, and focally necrotic. Histopathologic alterations in the kidneys consisted of necrosis and desquamation of epithelial cells mainly in, but not limited to, proximal convoluted tubules. Many proximal and distal convoluted tubules contained eosinophilic, granular casts. Necrosis of lymphoid tissues was a prominent feature of the niycotoxicosis and focally occurred in, but was not limited to, germinal centers in the spleen, tonsils, thymus, and lymph nodes and the lymphoid nodules of the jejunum, ileum, cecum, colon, rectum and nictitating membrane. Necrosis did not occur in bone marrow. Hepatic alterations consisted of slight to moderate centrilobular necrosis and fatty change and occurred mainly in dogs receiving 0.2-0.3 mg/kg body weight ochratoxin A daily for 11-14 days.In a companion paper [30], we described the clinical and clinicopathologic features of ochratoxicosis in Beagle dogs. Ochratoxins, the principal one of which is ochratoxin A, are fungal metabolites first isolated from Aspergillus ochraceus [33] and later identified as metabolites of Penicillium viridicatum [34] and other members of the A . ochraceus group [13, 191. The pathologic changes produced by ochratoxin A have been studied in the duckling [26,32], rat [23, 25, 27, 28, 321, chick [3, 10, 241 and trout 191. In the species studied, ochratoxicosis is characterized by renal and hepatic damage and alterations in the intestinal and lymphoid tissues. The severity of the lesions varies somewhat with species and dose of ochratoxin.The present report describes the gross and microscopic pathologic alterations produced in dogs by either an ochratoxin-A-containing rice culture of A . ochraceus or commercial ochratoxin A.

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Section: Discussionmentioning

confidence: 73%

Ochratoxicosis in Beagle Dogs. II. Pathology

1973

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“…Ochratoxin A, at the doses given also caused moderate to severe necrotizing lesions of the gastrointestinal niucosa, but they were not limited to the cecum, colon, and rectum as in dogs given ochratoxin A [37]. Necrosis of lymphoid tissues was slight and hepatic changes were limited t o fatty change mainly at the periphery of lobules.…”

Section: Discussionmentioning

confidence: 82%

Ochratoxin A Toxicosis in Swine

et al. 1973

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Abstract. Ochratoxicosis was induced in young female swine by a diet contaminated with a rice culture of Aspergillus ostiantrs that contained ochratoxin A and by daily oral doses of 2.0 or I .O mg/kg body weight pure ochratoxin A. Mycotoxicosis was characterized early by depression and reduction in feed intake and loss of body weight, followed by diarrhea, polyuria, polydipsia and dehydration. The pigs given pure ochratoxin A were dead or moribund in 5 to 6 days. Packed cell volume, hemoglobin, total plasma protein, and blood urea nitrogen were increased. Progressive leukocytosis, neutrophilia and moderate left shift in the differential count occurred. Concentrations of lactic dehydrogenase, isocitric dehydrogenase and glutamic-oxalacetic transaminase in the serum and urine were increased by the fourth to sixth day, but only the increase in urinary concentrations was significant. Gross findings included dehydration, enteritis, pale tan discoloration of the liver, and edema and hyperemia of the mesenteric and other lymph nodes. Microscopic lesions were most frequent and severe in the kidney and gastrointestinal tract. Necrosis of renal tubular epithelium was most frequent in the convoluted tubules. Many renal tubules were dilated. The intestinal lesions were focal and necrotizing and occurred in most anatomic regions. Fatty change was demonstrated in most of the livers. In lymphoid tissues the changes were edema, hyperemia and focal necrosis of lymphocytes within germinal centers and around follicles.

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“…Ochratoxin A and citrinin, which are both produced by various Aspergillus and Penicillium species found on grapes and raisins, 48 have been shown experimentally to damage the proximal tubular epithelium in dogs. 49,50 Naturally occurring renal damage from ochratoxin A or citrinin generally is a result of chronic exposure and has a progressive clinical course. 51 Neither mycotoxin has been demonstrated to cause acute disease in dogs through environmental exposure.…”

Section: Discussionmentioning

confidence: 99%

Acute Renal Failure in Dogs After the Ingestion of Grapes or Raisins: A Retrospective Evaluation of 43 Dogs (1992-2002)

Eubig

Brady

Gwaltney‐Brant

et al. 2005

Journal of Veterinary Internal Medicine

101

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A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium x phosphorus product (Ca x P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca x P, and peak Ca x P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.

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Ochratoxicosis in Beagle Dogs

Cited by 27 publications

References 31 publications

Ochratoxicosis in Beagle Dogs. II. Pathology

Ochratoxicosis in Beagle Dogs. II. Pathology

Ochratoxin A Toxicosis in Swine

Acute Renal Failure in Dogs After the Ingestion of Grapes or Raisins: A Retrospective Evaluation of 43 Dogs (1992-2002)

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