Plasma Gastrin Activity and the Diagnosis of Bleeding Abomasal Ulcers in Cattle

Ok, M.; Şen, İsmai̇l; Turgut, K.; Irmak, Kemal

doi:10.1046/j.1439-0442.2001.00389.x

Cited by 26 publications

(16 citation statements)

References 9 publications

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“…In agreement with the findings of a recent report on cows with type-4 abomasal ulcers, 7 which cause diffuse peritonitis, type-3 ulcers occurred predominantly in the first four weeks after calving. 10,17,21,22,27 Of 145 cows with type-2 ulcer, which is associated with severe haemorrhage, 36% were diagnosed in the first four weeks of lactation. 8 A recent review of ulcerogenic factors 19,20 concluded that they consist of various stressors that act on cows in addition to the stress that surrounds parturition causing increased secretion of cortisol, hydrochloric acid and pepsin and decreased secretion of prostaglandin E. 19,20 Owners of cows that had been slaughtered and diagnosed with abomasal ulcers were unable to identify definitive causative factors.…”

Section: Discussionmentioning

confidence: 99%

Clinical and laboratory findings in 60 cows with type-3 abomasal ulcer

Braun¹,

Gerspach²,

Hilbe³

et al. 2019

SAT

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This study involved 60 cows aged 1.9 to 13 years (mean 4.8 ± 2.3 years) with type-3 abomasal ulcer. The most common clinical signs were, in decreasing order of frequency, partial or complete anorexia (98%), obtunded demeanour (95%), decreased skin surface temperature (78%), congested scleral vessels (73%), abdominal guarding (61%), tachypnoea (58%), fever (58%) and tachycardia (55%). One or more concomitant disorders were diagnosed in 86% of the cows. The most common abnormal laboratory findings were hypokalaemia (75%), shortened glutaraldehyde test time (46%) and hyperfibrinogenaemia (43%). The diagnosis of type-3 abomasal ulcer was made in all cows during laparotomy and/or at postmortem examination. Forty-eight (80%) cows were euthanased immediately after the initial examination, during laparotomy or after unsuccessful treatment. Twelve (20%) cows were treated with a solution of sodium chloride and glucose administered via an indwelling jugular catheter, antibiotics, metamizole or flunixin, and discharged from the clinic. Ten cows were still in production two years later.

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Section: Discussionmentioning

confidence: 99%

Clinical and laboratory findings in 60 cows with type-3 abomasal ulcer

Braun¹,

Gerspach²,

Hilbe³

et al. 2019

SAT

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“…In adult cattle and in beef cattle, occurrence of abomasal damage differs between seasons. In adult dairy cattle, this could be related to the seasonality of milk production, because most ulcers develop around parturition, a period marked by stress and a severe change in diet (Smith et al, 1983;Sanford and Josephson, 1988;Ok et al, 2001;Tharwat and Ahmed, 2012). In beef calves, bad weather has often been proposed as a contributing factor (Jensen et al, 1976;Lilley et al, 1985;Mills et al, 1990;Marshall, 2009).…”

Section: Seasonal Effectsmentioning

confidence: 99%

Invited review: Abomasal damage in veal calves

Bus

Stockhofe

Webb

2019

Journal of Dairy Science

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Within all cattle production systems, veal calves are the most severely affected by abomasal damage, with current prevalence at slaughter ranging from 70 to 93% of all animals affected. Although most damage is found in the pyloric region of the abomasum, fundic lesions are also found. Despite past research into the etiology of abomasal damage and the many risk factors that have been proposed, consensus on the causal factors of abomasal damage in veal calves has not yet been reached. The aim of this review was to integrate and analyze available information on the etiology of, and possible risk factors for, abomasal damage in veal calves. We describe various proposed pathways through which risk factors may contribute to damage formation and conclude that the etiology of abomasal damage is most likely multifactorial, with diet being a main contributor. Pyloric lesions, the most common type of damage in veal calves, are likely the result of large and infrequent milk and solid feed meals, whereas fundic lesions may be caused by stress, although the evidence for this is inconclusive. Providing calves with multiple smaller milk and solid feed meals (or ad libitum provision) may decrease abomasal damage. In future research, ulcers, erosions, and scars as well as fundic and pyloric lesions should be recorded separately, because etiologies of these may differ. Further research is required to understand the exact pathway(s) by which milk replacer causes abomasal damage in veal calves; that is, whether low abomasal pH, overloading, or composition are important. Further research is also required to elucidate whether rapid intake of milk replacer and solid feed, which is influenced by restricted amounts fed, inter-calf competition, and calf breed, increases abomasal damage. Research is also needed into the effect of medication and nutrient deficiencies other than iron. The types of experimental designs that can be used for future research could be enhanced if a means to assess abomasal damage antemortem is developed. We conclude that it is unlikely that abomasal or ruminal hairballs, iron deficiency, water provision, and various infections and diseases are significant contributors to abomasal damage in veal calves.

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“…Gastric ulcers regularly occur in calves and adult cattle, with an incidence varying between 2 and 87% (52,96,117,163,206,239). "Candidatus Helicobacter bovis" has been demonstrated in the pyloric part of the abomasums of calves and adult cattle but has not yet been cultivated in vitro (44).…”

Section: Gastric Helicobacters Associated With Ruminantsmentioning

confidence: 99%

Gastric Helicobacters in Domestic Animals and Nonhuman Primates and Their Significance for Human Health

et al. 2009

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SUMMARY Helicobacters other than Helicobacter pylori have been associated with gastritis, gastric ulcers, and gastric mucosa-associated lymphoid tissue lymphoma in humans. These very fastidious microorganisms with a typical large spiral-shaped morphology were provisionally designated “H. heilmannii,” but in fact they comprise at least five different Helicobacter species, all of which are known to colonize the gastric mucosa of animals. H. suis, which has been isolated from the stomachs of pigs, is the most prevalent gastric non-H. pylori Helicobacter species in humans. Other gastric non-H. pylori helicobacters colonizing the human stomach are H. felis, H. salomonis, H. bizzozeronii, and the still-uncultivable “Candidatus Helicobacter heilmannii.” These microorganisms are often detected in the stomachs of dogs and cats. “Candidatus Helicobacter bovis” is highly prevalent in the abomasums of cattle but has only occasionally been detected in the stomachs of humans. There are clear indications that gastric non-H. pylori Helicobacter infections in humans originate from animals, and it is likely that transmission to humans occurs through direct contact. Little is known about the virulence factors of these microorganisms. The recent successes with in vitro isolation of non-H. pylori helicobacters from domestic animals open new perspectives for studying these microorganisms and their interactions with the host.

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Plasma Gastrin Activity and the Diagnosis of Bleeding Abomasal Ulcers in Cattle

Cited by 26 publications

References 9 publications

Clinical and laboratory findings in 60 cows with type-3 abomasal ulcer

Clinical and laboratory findings in 60 cows with type-3 abomasal ulcer

Invited review: Abomasal damage in veal calves

Gastric Helicobacters in Domestic Animals and Nonhuman Primates and Their Significance for Human Health

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