Cattle Case: Jejunal Hemorrhage Syndrome

Crystal Riczu, ,  March 2013



Last year, a 3 year old Angus bull (Bull 1) was presented with anorexia, weight loss, and dark tarry feces. A comprehensive diagnostic work came back inconclusive. The bull was treated with gastroprotectants, seemed to improve over the next month, but then was found dead with no significant post mortem (autopsy) findings.

Two weeks ago, Bull 2 (a 2 year old Angus bull) also presented with anorexia, weight loss, and dark hemorrhagic diarrhea at the same time that Bull 3 (a 2 year old Angus bull) who had been losing weight over the winter, seemed to “not be doing right”. Over the next week the diarrhea resolved for Bull 2, and the health of both bulls seemed to be improving. This morning, Bull 3 was found down and reluctant to get up, and by the afternoon was found dead in the pasture.

A post mortem was performed on Bull 3 with the only lesion being a 3 foot long firm blood clot inside the middle of the jejunum (the middle portion of the small intestine) followed by dark bloody fluid with smaller free blood clots inside the rest of the jejunum. The ileum (last portion of the small intestine) contained green-yellow watery fecal material.

Three samples of the intestine were collected containing either the blood clot, bloody fluid, or feces, and sent to the lab (with various other tissue and organ samples of this bull) for further diagnostic work-up.

A dark red, firm blood clot, approximately 3 feet in length, found in the jejunum of an animal suspected to be affected with Jejunal Hemorrhage Syndrome.

Based on the history and post mortem findings, this bull was tentatively diagnosed with jejunal hemorrhage syndrome (JHS).

On histopathology (examination of the tissues under a microscope), no changes were found in the anatomy of the intestines to explain the hemorrhage or associate the hemorrhage with jejunal hemorrhage syndrome. At this point the tentative diagnosis of jejunal hemorrhage syndrome could not be confirmed or definitively ruled out.The samples were also submitted for culture to determine if the cause was a bacterial organism.


Two bacterial organisms were isolated in the samples: Clostridium perfringens and Escherichia coli.  Although both of these bacteria are normal inhabitants of the bovine gastrointestinal tract, certain types  of these bacteria have specific genes capable of producing toxins which have been associated as the cause of jejunal hemorrhagic syndrome:  Shiga-toxin producing E-coli (STEC) and Clostridium perfringens Type A.  As such, the two bacteria were further tested to determine their exact genotype using multiplex polymerase chain reaction (PCR). The PCR test showed the the E. coli in the sample were non-enteropathogenic, meaning that they are not the type to produce Shiga toxin. However, the C. perfringens isolated in the sample was positive for Alpha toxin, meaning that it is a C. perfringens Type A, a bacterium associated with causing JHS .  This result, in combination with our history, post-mortem findings and bacterial culture was enough to reach a final diagnosis.

What is Jejunal Hemorrhagic Syndrome (JHS)?

Jejunal hemorrhage syndrome (JHS), also known as hemorrhagic bowel syndrome (HBS), was first reported in 1991 as an emerging, economically important, acute sporadic small intestinal disease of adult cattle. This disease occurs more common in mature dairy cattle (in the first 3 months of lactation) than beef cattle.

Post-mortem findings of a enlarged, congested jejunum with associated inflamed lymph nodes.

How is it caused?

Although the exact cause remains unknown, two theories are found in the literature. Most commonly reported is the increased consumption of high energy diets in high producing cattle provides a perfect environment for Clostridium perfringens Type A and β2 toxin producing strains to produce enterotoxins in the intestine leading to the disease. More recently it has been suggested that mycotoxins in the feed cause severe congestion and damage to the barrier function in the intestine, as well as diarrhea and abdominal pain. This sets up an ideal environment for pathogens such as Shiga-toxin producing Escherichia Coli (STEC) to colonize, grow, and produce toxins which contributes to developing severe hemorrhage in the intestine.Both causes lead to a similar primary lesion of an acute, localized necrotic and hemorrhagic small intestinal enteritis (inflammation of the small intestine) resulting in development of a blood clot that physically obstructs the small intestine.

What clinical signs to look for:

Affected animals may be found dead, but typically demonstrate a sudden onset of depression, lethargy, reduced milk production, anorexia, weight loss, right abdominal distension and discomfort, and scant dark black tarry (bloody) feces. As the condition progresses we see sternal recumbency, shock (pale or congested mucous membranes) and death.


Jejunal hemorrhage syndrome must be differentiated from other causes of intestinal obstruction, dysentery, and melena from abomasal ulcers. Transrectal exam would find intestinal distension and scant to absent feces containing digested and/or clotted blood. Blood work would suggest a moderate inflammatory process with biochemistry values consistent with a proximal intestinal obstruction (hypochloremic, hypokalemic metabolic alkalosis). Transabdominal ultrasound may show signs of an intestinal obstruction (slow or non-moving distended loops of intestine that may or may not contain blood clots).  On post mortem they would find segmental necrohemorrhagic enteritis (bloody necrotic inflammation) of the small intestine (primarily jejunum) with hematoma (localized collection of blood) and ulceration of the intestinal wall and associated blood clot inside the intestine.  On histopathology we would expect to find segmental submucosa hemorrhage, edema, and mucosal necrosis.


Despite intensive medical and surgical treatment, there is a 77-100% mortality rate with most cases dying within 2-4 days.

Aggressive early medical treatment includes cathartics (to accelerate defecation), anti-inflammatories and intensive fluid and electrolyte therapy, which improves medium and long term survival by reducing recurrence rate of the disease. Use of antibiotic treatment is controversial as antibiotics containing trimethoprim (Trivetrin) can increase the amount of shiga-toxin producing E-coli, and contribute to the development or worsening clinical symptoms of JHS. A novel prebiotic has been suggested to bind mycotoxins and prevent STEC colonization of the intestines thus preventing the mycotoxin: STEC interaction improving recovery of symptomatic beef calves

Surgical treatment consists of an exploratory laparotomy to determine the severity of the lesion, then the clot it removed either by manual massage (manually dissolve the clot and allow it to pass), enterotomy (cut a window in the intestines and remove the clot) or enterectomy (remove the affected piece of intestine with the clot and re-attach the healthy intestines). Of those surviving surgery, there has been a 39% recurrence rate reported.


As an emerging disease, very few prevention strategies are known. Feeding practices to ensure adequate fiber length and quantity in diet, as well as ensuring good quality, non-moldy feed. Currently there is no vaccine against C. perfringens type A as the commercially available 7-way clostridial vaccine does not appear to protect against the development of HBS.



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