Laboratory Findings Associated with Abomasal Ulcers/Tympany in Range Calves

Mills, Ken; Johnson, Jerre L.; Jensen, R; Woodard, L.F.; Doster, Alan R.

doi:10.1177/104063879000200310

Cited by 35 publications

(27 citation statements)

References 9 publications

(13 reference statements)

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“…58 Copper deficiency has been associated with abomasitis and abomasal ulcers in beef calves. [61][62][63] However, Roeder and colleagues 51 showed that abomasitis can occur spontaneously and be induced experimentally in the absence of copper deficiency. Thus, although copper deficiency may act as a contributory factor for abomasitis and enteric disease of calves, it does not seem to be a requisite factor for either condition.…”

Section: Clostridial Abomasitismentioning

confidence: 99%

Clostridial Abomasitis and Enteritis in Ruminants

Simpson

Callan

Metre

2018

Veterinary Clinics of North America: Food Animal Practice

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Clostridial abomasitis and enteritis are important alimentary diseases observed in all domestic ruminant species. These diseases most commonly result from overgrowth of Clostridium perfringens types A, B, C, D, and E with the associated release of bacterial exotoxins that result in necrosis of the abomasal or intestinal mucosa. Clostridium difficile may also be associated with enteritis in calves but is much less common than disease caused by C perfringens. This article reviews the causes, pathophysiology, clinical signs, diagnosis, treatment, and prevention of clostridial gastrointestinal diseases in ruminants. Particular emphasis is given to describing the various forms of disease and treatment of individual cases.

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Section: Clostridial Abomasitismentioning

confidence: 99%

Clostridial Abomasitis and Enteritis in Ruminants

Simpson

Callan

Metre

2018

Veterinary Clinics of North America: Food Animal Practice

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“…Clostridial infections of the gastrointestinal tract of calves remain a common problem [1][2][3][4][5], in spite of the widespread availability of effective immunoprophylactic products [6]. Neonatal infection by Clostridium perfringens type C (Table 1) is widely recognized [7], and, like other infections by toxin types of C. perfringens, type C may colonize rapidly in the absence of established normal flora [6].…”

Section: Introductionmentioning

confidence: 99%

Clostridial abomasitis in calves: Case report and review of the literature

Songer

Miskimins

2005

Anaerobe

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Infections by Clostridium perfringens type A are perhaps the most common causes of clostridial hemorrhagic enteritis in neonatal ruminants. Affected calves exhibit tympany, hemorrhagic abomasitis, and abomasal ulceration. Gram-positive bacilli are often found on affected mucosa and in submucosa. Aspects of etiology beyond the infecting organism are little understood, but probably include dietary issues, perhaps relating to overfeeding, feeding of barely thawed or contaminated colostrum, or conditions which effect decreased gut motility. Fatal hemorrhagic enteritis in a cloned gaur calf is illustrative of the syndrome. The calf developed pasty yellow and bloody diarrhea, and the abdomen became distended and painful. In spite of intensive therapy, the calf died approximately 48 h after birth. At necropsy, the distended abomasum contained clotted milk and bloody fluid, and the abomasal and omasal walls were thickened and hemorrhagic. The proximal duodenum was hemorrhagic and emphysematous, and microscopic examination revealed Gram-positive rods in association with acute, necrotizing, hemorrhagic mucosal inflammation. Isolates of C. perfringens from this calf were PCR positive for cpb2, the gene encoding beta2 toxin. This finding is of unknown significance; only 14.3% (8/56) of isolates from other calves with the syndrome have been cpb2 positive, and only 50% of cpb2 positive bovine isolates express CPB2. The most prominent needs to further our understanding of this problem are consistent experimental reproduction of the disease, elucidation of virulence attributes, and development and application of prevention and control strategies.

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“…6,9,14,25 Copper deficiency has become associated with a variety of disease problems. 9,11,12,14,15 Data regarding the association of subclinical copper deficiency and disease are equivical, as effects of subclinical copper deficiency on the immune system have not been clearly documented in vivo. 1,22,23,25 In vitro studies demonstate inconsistent effects on humoral immune response, acute phase protein response, and stimulus-dependent changes in lymphocyte blastogensis.…”

mentioning

confidence: 99%

“…1,13,16,25 Epidemiologic studies have associated subclinical copper deficiencies in calves with abomasal ulcers and calf diarrhea. 9,11,12,14,15 Based on these studies, producers sometimes begin supplementation programs without first assessing herd copper status. This approach can lead to unnecessary expense with no appreciable decrease in disease prevalence and, occasionally, poisoning.…”

mentioning

confidence: 99%