PROFESSIONAL VERSION

Clostridial Abomasitis in Calves, Lambs, and Goat Kids

Full Review: Sept 2026 ByErin L. Goodrich, DVM, DACVPM, Cornell University, College of Veterinary Medicine | Peer reviewed byAngel Abuelo, DVM, PhD, DABVP, DECBHM, FHEA, MRCVS, Michigan State University, College of Veterinary Medicine
Last updated: Sept 2026
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Multiple clostridial species are implicated in clostridial abomasitis, a disease that occurs in young calves, lambs, and kids.

Abomasitis Associated With Clostridium septicum in Lambs and Calves

Clostridium septicum is well described as a causative agent associated with wound infections known as gas gangrene (1). It also can cause abomasal infection and toxemia. In lambs and sometimes calves, this condition is known as braxy.

Braxy tends to affect animals in colder climates after trauma to the abomasal mucosa (see ), which can occur when animals are ingesting stemmy forages contaminated with C septicum spores from the soil.

Clinical signs: The onset of abomasitis associated with C septicum is acute and results in anorexia, with signs of abdominal discomfort and bloat, and sometimes fever, followed by death within 12–36 hours. The abomasal wall is congested and edematous with mucosal necrosis, and the contents might be hemorrhagic.

Diagnosis: Diagnosis of abomasitis associated with C septicum is based on the presence of compatible clinical signs and lesions, along with detection of C septicum on culture, by PCR assay, via immunohistochemistry, or via fluorescent antibody testing. Because C septicum can be a postmortem contaminant, it is necessary to take intestinal samples for culture immediately after death and to interpret results in older samples with caution.

Pearls & Pitfalls

  • Because Clostridium septicum can be a postmortem contaminant, it is necessary to take intestinal samples for culture immediately after death from C septicum–associated abomasitis and to interpret results in older samples with caution.

Prevention and treatment: Commercially available bacterin toxoids containing C septicum can be effective at preventing associated abomasitis. These toxoids can be administered to pregnant dams 3–4 weeks before parturition. Animals vaccinated for the first time should receive two doses 4 weeks apart, followed by annual boosters. Treatment with antimicrobials is generally not effective, because of the rapid progression of disease.

Abomasitis Associated With Other Clostridial Species in Calves, Lambs, and Goat Kids

Abomasitis can also occur in calves, lambs, and goat kids in association with one or more other clostridial species,including Sarcina spp (which belong to the genus Clostridium phylogenetically); however, the disease is not well understood.

Specific clostridial species that appear to be associated with clostridial abomasitis, either alone or in combination, include Clostridium perfringens type A, Paraclostridium sordellii, and Sarcina spp. Acute onset of disease is most common and can include signs of severe abomasal bloat, sometimes also with deep or even perforating abomasal ulceration.

The pathogenesis of clostridial abomasitis likely involves the fermentation of milk carbohydrates in the abomasum, with mucosal damage resulting from both the products of that fermentation and the toxins produced by the clostridial species involved.

Calves with clostridial abomasitis tend to range in age from 2 days up to 3 weeks, and changes in diet such as the introduction of course roughage can predispose them to this condition. Overfeeding milk or offering larger volumes at infrequent intervals, along with feeding cold or contaminated colostrum or milk replacer, can contribute to this disease.

Calves with clostridial abomasitis tend to show signs of abdominal discomfort, bloat, and diarrhea, which can quickly progress to death. They can also have peritonitis secondary to perforating ulcers.

Lambs with clostridial abomasitis are typically approximately 2–5 weeks old but can be up to 10 weeks old. Offering large, infrequent, or free-choice consumption of warm milk appears to be a risk factor because of the propensity for lambs to overeat. Feeding cooler milk (20°C [68°F]) is a recommended prevention strategy. Affected lambs show signs of abdominal pain, bloat, and anorexia, or they might be found dead. They do not generally present with diarrhea.

Goat kids fed milk replacer or solid supplements can experience bloat, sometimes with hemorrhage and ulcers. Clostridial abomasitis in goats appears to be caused by exposure to contaminated feeding equipment, along with, like lambs, being fed infrequent high-volume meals of warm milk replacer (2). The most common clinical sign in goats is sudden death; sometimes, however, bloat, diarrhea, or recumbency is observed. Diarrhea is not common.

Lesions of clostridial abomasitis in all species typically include dilation of the abomasum and congestion, hemorrhage, edema, mucosal necrosis, and ulceration of the abomasal wall. The contents can appear red-brown, and emphysema might be present in the abomasal folds. Rarely, lambs and goat kids might also have mesenteric volvulus and abomasal perforation. Young lambs with disease associated with Sarcina spp might show only abomasal ulcers.

Diagnosis of clostridial abomasitis in calves, lambs, and kids relies on identification of the clinical signs and compatible lesions, along with isolation of one of the associated organisms on anaerobic culture, followed by identification using biochemical methods, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), or PCR assay.

A C perfringens type A toxoid for the control of abomasitis is available in the US, for use in pregnant cows or calves at least 4 weeks old. Multivalent clostridial vaccines available for the vaccination of pregnant ewes contain Paraclostridium sordellii; however, their efficacy against abomasitis is unknown. No vaccines are available for the prevention of Sarcina-associated disease.

Other strategies to prevent clostridial abomasitis include decreasing the amount of milk replacer fed at each meal by increasing the meal frequency; minimizing the contamination of colostrum, milk replacer, and milk-feeding equipment; and improving the hygiene of the environment where neonates are housed.

Key Points

  • Clostridial abomasitis involves fermentation of milk carbohydrates in the abomasum, in conjunction with the effects of clostridial toxins, resulting in abomasal damage.

  • Risk factors include large and infrequent milk feedings, overfeeding, contaminated or cold milk or colostrum, and poor feeding hygiene.

  • In addition to vaccination for specific clostridia, prevention strategies include optimal neonatal feeding practices and hygiene.

For More Information

  • Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.

References

  1. Junior CAO, Silva ROS, Lobato FCF, Navarro MA, Uzal FA. Gas gangrene in mammals: a review. J Vet Diagn Invest. 2020;32(2):175-183. doi:10.1177/1040638720905830

  2. Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.

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