University of Illinois Extension

Illini DairyNet Papers

Atresia coli in Calves: Cause and Surgical Management
Peter D. Constable and Dawn E. Morin
11/15/2000

TAKE HOME MESSAGES

  • Calves born with atresia coli have a section of their large bowel missing and will die within 2 weeks of birth unless surgical correction is performed.
  • Holstein-Friesian calves are at much greater risk for atresia coli than all other breeds.
  • During pregnancy examination, early (day 42 of gestation) palpation per rectum of the amniotic vesicle can damage the fetal intestinal blood supply and increase the risk of atresia coli.
  • Surgical correction of atresia coli has a poor overall success rate, with a short term survival rate of <50% and a long term survival rate of <35%.

INTRODUCTION

Atresia coli is a developmental abnormality in cattle that is lethal without surgical correction. The inheritance of atresia coli remains controversial and not completely understood. Because surgical correction of atresia coli in calves is being attempted with increasing frequency, producing affected cattle that can reproduce if they survive to adulthood, an important issue to be resolved is whether atresia coli is a heritable condition in cattle. The primary purpose of this study was therefore to evaluate breed as a risk factor for atresia coli, specifically to confirm suggestions that Holstein-Friesian cattle are predisposed to developing atresia coli. The secondary objective was to develop a cohesive hypothesis for the development of atresia coli that accounts for the apparent breed predisposition and association with palpation per rectum for pregnancy diagnosis. The final objective was to provide recommendations for the best method to surgically correct calves with atresia coli.

MATERIALS AND METHODS

Articles on atresia coli published since 1973 were examined and information regarding breed and surgical management of affected calves recorded. In addition, information concerning selected epidemiologic factors of calves with atresia coli was obtained by a computer-assisted search of hospital records performed by the Veterinary Medical Data Program. The computer search identified all calves diagnosed with atresia coli that were admitted to 18 North American veterinary schools over a 29 year period and all similarly aged, unaffected calves admitted over the same period. A hospital-based case-control study was then conducted to evaluate breed as a risk factor for atresia coli.

RESULTS AND DISCUSSION

Thirty-seven articles describing atresia coli in cattle were obtained. Of these articles, 22 studies provided sufficient information regarding breed of affected calves. Atresia coli has been reported in 10 breeds, with the marked preponderance of cases occurring in Holstein-Friesian calves. Cases have been reported in 497 dairy calves: 485 Holstein-Friesian, 8 Holstein-Friesian x Jersey crossbred, 2 Ayrshire, 1 Guernsey and 1 Brown Swiss. Cases have also been reported in 17 beef or crossbred calves: 6 Angus, 4 Simmental, 2 Shorthorn, 2 crossbred, 1 Maine-Anjou, 1 Hereford, and 1 Polled Hereford. Cases have been reported in 12 countries, including Australia, Belgium, Canada, France, Germany, Great Britain, Italy, Ireland, Japan, the Netherlands, Switzerland, and the United States.

The Veterinary Medical Data Program search produced 10.3 cases of atresia coli per 1,000 admissions. The risk of being born with atresia coli was 4.6 times greater for Holstein-Friesian calves than for all other dairy cattle breeds combined (P <0.0001), and 7.1 times greater for all other dairy and beef cattle breeds combined (P <0.0001), whereas there was no difference in the risk of atresia coli between other dairy cattle breeds (not Holstein-Friesian) and beef cattle breeds. Comparing individual cattle breeds, Holstein-Friesian calves were at significantly greater risk of developing atresia coli than all other breeds except Brown Swiss, Ayrshire, Guernsey, Limousin, Chianina, and Maine-Anjou. These 6 breeds all had fewer than 400 animals examined over the study period, decreasing the statistical power of the comparison.

Our findings indicate that atresia coli can occur spontaneously but rarely in cattle that are not Holstein-Friesians. It is likely that atresia coli occurs in all cattle breeds secondary to vascular insufficiency of the developing spiral colon, and that in familial lines of Holstein-Friesian cattle the developing spiral colon grows at a faster rate and to a longer length than in other cattle breeds, predisposing the Holstein-Friesian fetus to atresia coli. Rapid embryonic and early fetal growth places an added stress on the colonic vasculature of the Holstein-Friesian calf as the vasculature migrates with the developing ascending and spiral colon, predisposing the developing colon to ischemia and subsequent atresia.

A number of studies have observed that pregnancy diagnosis in the first 42 days (6 weeks) of gestation by per rectal amniotic vesicle palpation markedly increases the risk of atresia coli in the fetus. Strangulation or damage to the blood vessels supplying the developing embryonic or fetal colon may be followed by colonic ischemia, leading to missing (atretic) segments. The period of spiral colon development in the calf (days 22 to 112 of gestation) encompass the period that pregnancy diagnosis by palpation is most commonly undertaken in dairy cattle. The primitive embryonic gut is first visible at day 22, and the colon appears as a single tube with its associated mesentery by day 37, and extends from the embryo mid-section into the umbilical cord. By day 45, the first evidence of looping of the proximal colon is observed, and the cecum and a portion of the ascending colon remains in the umbilical cord until day 56. Extensive spiraling of the colon and associated blood supply begins at day 56 of gestation, and is complete by day 112. Pregnancy diagnosis by per rectal amniotic vesicle palpation can increase intravesicular pressure vesicle and predispose fetal cells to injury. Cells most at risk for pressure-induced injury are probably those in the embryonic or fetal abdomen and those in the umbilical cord (such as the small and large intestine), as these cells have minimal supporting structures to protect against a palpation-induced increase in intravesicular pressure. We suspect that the association between amniotic vesicle palpation during pregnancy diagnosis and atresia coli results from palpation-induced damage to the developing colonic vasculature when the colon is located in the umbilical cord or coelomic cavity.

Based on the above, the disproportionate number of cases in Holstein-Friesian calves may reflect the widespread practice of early pregnancy diagnosis in dairy cattle and associated palpation-induced damage to the developing embryonic or fetal intestinal vasculature. However, the significantly greater risk of atresia coli in Holstein-Friesian cattle compared with that of all other dairy cattle breeds cannot be satisfactorily explained by breed differences in palpation rates or gestational age when pregnancy diagnosis is performed, as there is no data to support the hypothesis that pregnancy diagnosis by per rectal palpation per rectum occurs earlier in gestation in Holstein-Friesian cattle than in other dairy breeds.

We speculate that Holstein-Friesian cattle have a longer intestine than other cattle breeds as a result of selection for the ingestion of concentrates and milk production. This hypothesis is consistent with findings that intestinal length is positively correlated with milk production and that Holstein-Friesian cattle have the highest average annual milk production and longer small and large intestines than other cattle breeds. We suspect that familial lines of Holstein-Friesian cattle have a proportionately longer large intestine, resulting in an increased risk of vascular compromise during embryonic and fetal development of the colon.

Of the 9 articles that described the surgical management in sufficient detail, it appeared that approximately 40% of calves that had a colocolic anastomosis or cecostomy performed left the veterinary hospital alive. Long term follow-up information was scant. In general, it appeared that no more than 16% of calves undergoing colocolic anastomosis and 0% of calves undergoing cecostomy or colostomy survived until 2 years of age. Although some of the animals discharged from hospital were slaughtered for meat as veal calves or yearlings, there still appeared to be a higher than expected mortality rate in surgically corrected animals. Moreover, some of the surviving animals were reported to have slower growth rates and more watery feces than their herd mates.

In summary, Holstein-Friesian cattle appear genetically predisposed to atresia coli and early (before day 42 of gestation) or vigorous palpation per rectum of the amniotic vesicle can increase the probability of developing atresia coli during embryonic and fetal life. We therefore recommend that surgical correction of atresia coli should not be routinely undertaken in Holstein-Friesian calves destined for use as breeding animals without strongly emphasizing the potential for propagation of a genetic defect. Sires and dams of affected Holstein-Friesian calves should be suspected to be carriers for an allele representing a proportionately longer colon and/or rapid growth of the colon during the embryonic and early fetal period. This is thought to predispose the calf to development of atresia coli, but may also be associated with increased milk production because of increased intestinal length. Routine culling of the sire and dam of an affected calf is not recommended, as atresia coli can also occur spontaneously, as evidenced by the comparatively rarer occurrence of atresia coli in other cattle breeds.

SELECTED REFERENCES

Constable PD, Rings DM, Hull BL, Hoffsis GF, Robertson JT. Atresia coli in calves: 26 cases (1977-1987). J Am Vet Med Assoc 1989;195:118-123.

Syed M, Shanks RD. Atresia coli inherited in Holstein cattle. J Dairy Sci 1992;75:1105-1111.

Syed M, Shanks RD. Incidence of atresia coli and relationships among the affected calves in one herd of Holstein cattle. J Dairy Sci 1992;75:1357-1364.

Syed M, Shanks RD. What causes atresia coli in Holstein calves? Cornell Vet 1993;83:261-263.

Constable PD, Shanks RD, Huhn J, Morin DE. Assessment of breed as a risk factor for atresia coli in cattle. Theriogenology, 1997;48:775-790.

Constable PD, Rings DM: Atresia coli. In, Howard JL, Smith R, eds. Current Veterinary Therapy - Food Animal Practice. 4th edition, 1998:542-543.

Constable PD, Huhn JC, Morin DE, Nelson DR. Atresia coli in calves: etiopathogenesis and surgical management. Bovine Practitioner 1999;33:70-73.