3-months old female calf

SIGNALMENT: (age, breed, sex, species, and scientific name) 
3-months old female calf (Bos Taurus), breed unspecified 

TREATMENT PROTOCOL: (including test  compound)
During a 7-week period, 5 calves from a 170-head beef herd developed clinical signs of weakness, ataxia, depression, dehydration, diarrhea, and loss of appetite. Four of the affected animals died. Following the death of the fourth calf, a dumpsite was discovered in the pasture where the cattle grazed. Within the debris was an open metal container containing white powder, which is identified by the owner as an old potato dust. The white powder was found to contain 70% arsenic trioxide.

Unavailable (done by the referring veterinarian).

LABORATORY RESULTS: (clinical pathology, microbiology, etc…)
Hematological examination revealed leukopenia, neutropenia, and hemoconcentration. A bovine serum chemistry profile revealed abnormal elevation in urea, creatinine, creatine kinase, glutamic dehydrogenase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and the total and conjugated bilirubin. These results suggested hepatopathy and severe renal dysfunction.

Liver arsenic content was 353 ppm (reference level is 0.004-0.4 ppm) and rumen content arsenic level was 1200 ppm

1. Small intestine: enteritis, necrotizing and hemorrhagic, acute severe, multifocal, with mild necrotizing vasculitis.
2. Liver: acute multifocal necrosis, severe.
3. Kidney (images are not submitted): Acute moderate tubulonephrosis.
4. Abomasum (images are not submitted): Mild acute necrotizing abomasitis.

The outstanding lesion of acute inorganic arsenic poisoning is severe gastritis or gastroenteritis, often hemorrhagic. The lesions produced by acute poisoning can largely be explained on the basis of vascular injury and the direct   necrotizing effect on mucosal surfaces.  However, the hepatotoxic effect of arsenic is mostly attributed to its interference with the sulfhydryl groups of the hepatocellular enzymes. Arsenic may cross the blood brain barrier and causes diffuse cerebral edema and petechiation. No significant lesions are present in the brain of this calf.

Inorganic arsenic poisoning is no longer common due to the decreased use of herbicides and insecticides containing arsenic. However, many sources are still available and animals may be poisoned through ingestion or percutaneous absorption.    Arsenic does not stay in the tissues very long. It is partially methylated in the liver and kidney and is rapidly excreted in urine, feces, bile, milk, saliva, and sweat.

Organic arsenicals, p-aminophenylarsonic acid (arsanilic acid) and 3-nitro-4-hydroxyphenylarsonic acid (3-Nitro), are commonly used as feed additives for swine, to promote growth and control enteric disease. Two syndromes related to accidental poisoning by these compounds have been described. Unlike inorganic arsenicals, lesions are mostly confined to the central nervous system.

1. Storts RW and Montogomery DL, The nervous sytem. In: Thomson’s Special Veterinary Pathology, 3rd 2001, edited by McGavin MD et al., Mosby Inc, St.louis, Missouri, PP.415.

2. Jones TC, et al., Veterinary Pathology, 6th 1997, Williams & Wilkins, Baltimore, Maryland, pp.699-700.



Figs 1 & 2: Small intestine: Acute necrohemorrhagic enteritis with moderate submucosal edema. H&E. (objective =16).


Fig 2: Small intestine. Acute necrohemorrhagic enteritis with moderate submucosal edema. H&E. (objective =16).


Fig.3: Small intestine: severe non-selective necrosis of the mucosal layer with marked cryptal necrosis (arrows) and moderate submucosal edema.H&E. (objective =25).


Figs 4 & 5. Liver: Acute multifocal hepatic necrosis, particularly in the periportal zone. H&E. (objectives are 16 and 25 respectively).


Fig 5.


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