Pathology in Practice

Cynthia M. Bell Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706.

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 MS, DVM
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Howard Steinberg Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706.

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 VMD, PhD, DACVP

History

A Holstein heifer calf was born during an uneventful parturition in the evening and received 4 quarts of maternal colostrum within 2 hours after birth. The following morning, the calf was bloated and repeated attempts by both the owners and the referring veterinarian to reduce the abdominal distension by orogastric intubation were unsuccessful. The referring veterinarian was able to extract a small amount of feces from the rectum. On the farm, the calf received treatment with flunixin meglumine, penicillin, and electrolytes.

Clinical and Gross Findings

The 24-hour-old calf was evaluated at the University of Wisconsin-Madison Veterinary Medical Teaching Hospital because of irreducible bloat and suspected atresia coli. At the evaluation, the calf had a severely distended abdomen and was tachycardic (220 beats/min), tachypneic (88 breaths/min), and afebrile (38.5°C [101.3°F]). Rectal examination revealed a small amount of mucus but no feces. Again, orogastric intubation was unsuccessful in reducing the abdominal distension.

Hematologic analysis revealed moderate neutrophilia with left shift and toxic change. Electrolyte abnormalities detected via serum biochemical analysis included hypercalcemia, hyperphosphatemia, and hypermagnesemia. Creatinine concentration and activities of creatine kinase, alkaline phosphatase, and γ-glutamyl transferase were high. The calf was mildly hypoalbuminemic and mildly hypoglobulinemic.

The calf received boluses of dextrose, hypertonic saline (7% NaCl) solution, and polyionic crystalloid solution IV. Another dose of flunixin meglumine was administered. Abdominal radiography revealed a severely gas-distended abomasum, gas within the small intestine, and no evidence of intestinal atresia. With perioperative antimicrobial treatment, an exploratory, right paralumbar celiotomy was performed to evaluate possible pyloric outflow obstruction. According to the surgeon, the abomasum was dilated and filled with gas and fluid and the walls were markedly edematous (particularly the pyloric region) and multifocally hemorrhagic and emphysematous and were considered devitalized. Owing to the poor prognosis, the calf was euthanized and tissue samples from the abomasum were obtained immediately for histologic evaluation and bacterial culture.

At gross postmortem examination, the carcass was not autolyzed, the abomasotomy site was observed to be sutured closed, and the abomasum contained red-tinged, curdled milk. The abomasal mucosa was diffusely gelatinous in texture (edema) and red to dark red (congestion and hemorrhage), and many of the mucosal folds were brown (possibly necrotic) at the distal ridge (Figure 1). There was crepitus on palpation of the abomasal wall (emphysema). Few segments of the jejunal and cecal wall were dark red, and there was a cast of clotted blood within the lumen of the jejunum (presumed surgical hemorrhage). Several joints had red-tinged, low-viscosity synovial fluid and congested synovial membranes. Intestinal atresia was not present. The umbilicus was dry and contracted and lacked redness or swelling.

Figure 1—
Figure 1—

Photograph of the forestomachs, abomasum, and proximal portion of the duodenum (white asterisk) of a Holstein heifer calf that was evaluated because of irreducible bloat and suspected atresia coli. The abomasal mucosa is thick, gelatinous (edema), and red to dark red to brown (hemorrhage, congestion, and necrosis). The rumen (black asterisk), reticulum, and omasum have mild to moderate hyperemia.

Citation: Journal of the American Veterinary Medical Association 240, 6; 10.2460/javma.240.6.681

Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn page

Histopathologic and Microbiological Findings

Specimens of the abomasum (collected immediately following euthanasia), omasum, a mesenteric lymph node, lungs, and synovial fluid underwent histologic evaluation. The submucosa of the abomasum was expanded to > 4 times the thickness expected in a healthy calf by emphysema that created pockets of clear space separated by thin bands of collagenous stroma (Figure 2). All layers of the abomasal wall were edematous and hemorrhagic and contained many neutrophils. Blood vessels in the abomasal wall were dilated and congested, and a solid layer of neutrophils often pavemented the intimal surface of vessels. The lamina propria was severely congested, and there was necrosis of the mucosal surface epithelium (Figure 3). In some areas, there was full-thickness mucosal necrosis with ulceration and the necrotic mucosal epithelium was lined by many bacilli (approx 10 × 2 μm). These organisms reacted positively with a tissue Gram (modified Brown-Brenn) stain. A small number of gram-negative bacteria were evident.

Figure 2—
Figure 2—

Photomicrograph of a section through the abomasal wall of the calf in Figure 1. All layers of the abomasum are edematous, resulting in the pallor and loose arrangement of the connective tissue stroma (single asterisk). The submucosa (bracket) of the abomasum is also severely expanded by emphysema that creates large pockets of clear space (double asterisk) separated by thin bands of stroma (arrows). The mucosa is severely congested. H&E stain; bar = 500 μm.

Citation: Journal of the American Veterinary Medical Association 240, 6; 10.2460/javma.240.6.681

Figure 3—
Figure 3—

Photomicrograph of a section of the mucosa of the abomasum of the calf in Figure 1. The abomasal mucosa is hemorrhagic and edematous with necrosis of the surface epithelium (arrows) and emphysema of the submucosa (asterisk). H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 240, 6; 10.2460/javma.240.6.681

Segments of the forestomachs had multifocal mucosal hemorrhage and edema, which were most severe and transmural in the omasum. There was diffuse mesenteric edema and sinus histiocytosis with neutrophilia of the mesenteric lymph node. The calf also had severe pulmonary interstitial and alveolar edema with multifocal suppurative bronchointerstitial pneumonia. There was moderate fibrinosuppurative synovitis in the joints that were examined.

Anaerobic and aerobic bacterial cultures of samples of the abomasal mucosa yielded moderate growth of Clostridium perfringens and moderate growth of Escherichia coli, respectively. The C perfringens was not genotyped.

Morphologic Diagnosis

Severe, acute, multifocal, necrohemorrhagic abomasitis with marked submucosal and mucosal emphysema and transmural edema with myriad surface gram-positive bacilli.

Comments

Overall interpretation of the pathological findings in the case described in this report was primary abomasitis with evidence of systemic inflammation in the lungs and joints. Although the particular isolate of C perfringens from this calf was not genotyped, the pattern of disease attributable to the various subtypes was indicative of type A. In 1988, Roeder et al1 experimentally induced abdominal tympany, abomasitis, and abomasal ulceration in calves inoculated with C perfringens type A. There have been a few case reports2,3 of clostridial abomasitis in neonatal calves since that time. As in the calf of the present report, affected calves generally have emphysematous and hemorrhagic abomasitis and tympany. Risk factors that have been implicated include overfeeding, feeding cold colostrum, and inadequate hygiene of colostrum feeding, particularly fecal contamination.3

Clostridium septicum, the etiologic agent of abomasitis (braxy) in calves and lambs, is associated with colonization of the abomasum and subsequent bacteremia.2 Clostridium perfringens type C is a fairly common cause of hemorrhagic necrotic enteritis and enterotoxemia in calves that are < 10 days old but is generally not associated with abomastitis.2 Necrotizing enteritis and enterotoxemia in fowl, neonatal pigs, and lambs is associated with C perfringens type A.

Although not detected in the calf of this report, bacteria of the genus Sarcinia have been identified in the abomasal mucosa of calves with similar lesions, including calves in which C perfringens type A was also found.2,3 A recent report4 cites Sarcinia spp as the primary cause of bloat in lambs and calves with abomasal edema, emphysema, and hemorrhage; however, it is not clear that C perfringens was ruled out in those cases. Also, similar lesions in a calf attributed to infection with Salmonella enterica serotype Typhimurium phagetype DT104 have been described.5

For the calf of this report, it was not clear from the history whether the fed colostrum was warm or cold or how the colostrum was administered. The hygiene, method of feeding, and temperature of colostrum may be important factors in the development of abomasal bloat in neonatal calves. Nasogastric intubation commonly fails to relieve the bloat because gas is trapped within the abomasum. Revision of hygiene, colostrum feeding, antimicrobial programs,3 or vaccination protocols1 has been shown to decrease the incidence of bloat and abomasitis in some populations of calves.

References

  • 1.

    Roeder BL, Chengappa MM, Nagaraja TG, et al. Experimental induction of abdominal tymphany, abomasitis, and abomasal ulceration by intraruminal inoculation of Clostridium perfringens type A in neonatal calves. Am J Vet Res 1988; 49:201207.

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  • 2.

    Songer JG, Miskimins DW. Clostridial abomasitis in calves: case report and review of the literature. Anaerobe 2005; 11:290294.

  • 3.

    Van Kruiningen HJ, Nyaoke CA, Sidor IF, et al. Clostridial abomasal disease in Connecticut dairy calves. Can Vet J 2009; 50:857860.

  • 4.

    Edwards GT, Woodger NGA, Barlow AM, et al. Sarcina-like bacteria associated with bloat in young lambs and calves. Vet Rec 2008; 163:391393.

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  • 5.

    Carlson SA, Stoffregen WC, Bolin SR. Abomasitis associated with multiple antibiotic resistant Salmonella entericia serotype Typhimurium phagetype DT104. Vet Microbiol 2002; 85:233240.

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