Progress in the Understanding of Hemorrhagic Bowel Syndrome


Hemorrhagic bowel syndrome (HBS), a deadly digestive tract disease, has been reported with increasing frequency in adult dairy cows. Cattle affected with HBS usually die within 12 to 36 hours after the onset of clinical disease. Cattle present with acute enteritis and concurrent dehydration and shock, with or without signs of abdominal pain. The case fatality rate is 85 to 100%. Pathologic examination of affected animals reveals severe hemorrhagic enteritis with intraluminal hemorrhage or blood clots. Both Clostridium perfringens and Aspergillus fumigatus have been implicated in the development of HBS, though neither has been conclusively demonstrated to be the cause. Suggested risk factors for HBS include a high amount of fermentable carbohydrate in the diet, the level of dry matter (DM) intake, the level of milk production, feeding a total mixed ration, lactation number, herd size, season, and the presence of the causative organism in the feedstuff.

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HBS is a relatively new disorder affecting dairy cattle across North America and throughout the world. HBS is a sporadic, acute intestinal disease of milking cows. The syndrome is characterized by large blood clots in the intestine that result in the obstruction and severe enlargement of the bowel. It was first noted by Bruce Anderson at the University of Idaho in 1991 (Anderson, 1991). At that time, he referred to it as “point source hemorrhage.” It is now referred to by a variety of names including HBS, “jejunal hemorrhagic syndrome” (JHS), “acute hemorrhagic enteritis of the small intestine,” and “dead gut.”

The cause of HBS is not known, but Clostridium perfringens type A and more recently Aspergillus fumigatus have been implicated in the disease syndrome. Clostridium perfringens type A is ubiquitous in the jejunum (small intestine) of all adult cattle and is well known to proliferate rapidly postmortem. A. fumigatus is also ubiquitous in the digestive tract of cattle, making its significance in HBS difficult to ascertain in the absence of visible fungal hyphae in the wall of the affected portion of gut.

HBS was evaluated nationally for the first time during the National Animal Health Monitoring System’s (NAHMS) Dairy 2002 study (USDA: APHIS, 2003). According to the study, herd size, level of production, season, and region were suggested as risk factors for HBS. In other studies, nutritional factors have been suspected to be involved in the development of the disease (Godden et al., 2001; Kirkpatrick et al., 2001).

Review of Hemorrhagic Bowel Syndrome

Clinical syndrome and treatment

HBS is characterized by acute signs of profound depression, decreased milk production, tachycardia (rapid heart rate), ruminal stasis, abdominal distension, and dark clotted blood in the feces (Dennison et al., 2002). At necropsy, segmental lesions localized to the jejunum are observed (Kirkpatrick et al., 2001). These areas consist of frank hemorrhage with immediate clotting, forming a functional occlusion of the lumen of the small intestine. Treating acutely affected cows with antimicrobial agents and supportive therapy (e.g., anti-inflammatories, fluid therapy, and dextrose) has generally been reported to be ineffective (Dennison et al., 2002; Godden et al., 2001; Kirkpatrick et al., 2001). Affected cattle are extremely poor candidates for surgical intervention. Surgical intervention has included intestinal resection and anastomosis or, alternatively, manual massage of the affected area to break down the offending clot (Dennison et al., 2002; Godden et al., 2001; Kirkpatrick et al., 2001). Usually, the prognosis for an affected animal is extremely guarded.


HBS was documented as early as 1966 but with few cases reported in the next 20 years. Over the past five to six years, there has been a significant increase in the number of reported HBS cases. Presentation of HBS has been sporadic, but herd outbreaks involving up to 10% or more of the cows on a given dairy farm have been reported (Kirkpatrick et al., 2001). Morbidity rates of 1 to 2% of the mature cow population would be typical, with mortality approaching 85 to 100% due to the peracute nature and severity of the disease (Kirkpatrick et al., 2001).

Possible risk factors for HBS as suggested by a survey of Minnesota bovine practitioners (Godden et al., 2001), as well as the NAHMS Dairy 2002 study, include:

  1. Parity: more common in second lactation and older cows.
  2. Herd size: more common on large dairy farms (> 100 cows).
  3. Stage of lactation: higher incidence in cows during the first 100 days of lactation.
  4. Feeding system: greater frequency of the disease in herds fed a TMR.
  5. Level of production: the percent of operations with one or more HBS case increased as rolling herd average for milk yield increased.
  6. Region: higher incidence in the western region.
  7. Season: the majority of cases occurred in cooler months (winter and fall).

Some of these factors deserve investigation in future studies, as the association between the disease and some of them may be an artifact. For example, the association between the disease and herd size could be due to the greater likelihood that an animal that dies suddenly will be necropsied on a larger dairy farm, or even just because of larger numbers of animals. The same can be said for other risk factors, such as level of milk production. Higher rolling average for milk yield may be associated with improved management, which may include an increased likelihood that dead cows will be necropsied.

Etiology and pathogenesis

Several investigators have thought that Clostridium perfringens type A may be a cause of HBS (Dennison et al., 2002; Godden et al., 2001; Kirkpatrick et al., 2001; St. Jean and Anderson, 1999). Dennison et al. (2002) conducted a retrospective analysis of all dairy cows examined at the Colorado State University Veterinary Teaching Hospital which were submitted with dysentery, melena (changed blood in the feces), or colic. C. perfringens was isolated from fecal samples in 17 of 20 cows. Genotyping of C. perfringens in 10 cows revealed type A in five cows and type A with the b2 toxin gene in the remaining five cows. Dennison et al. (2002) commented that “it is unclear whether proliferation of C. perfringens is part of the primary disease process in cows with HBS or occurs as a secondary response.” Doubt about this etiological agent has come from the fact that C. perfringens type A is normally found in low numbers in the gastrointestinal (GI) tract of normal, healthy cattle, but its numbers increase rapidly following the death of an animal. Furthermore, immunization against Clostridium spp. does not appear to protect animals from HBS.

More recently, a group at Oregon State University has reported that infection of dairy cattle by a common mold (Aspergillus fumigatus) likely is a cause of the disease (Forsberg, 2003). The hemorrhagic condition seen in HBS cows is similar to enteric hemorrhagic diseases caused by A. fumigatus in immuno-suppressed humans. The A. fumigatus is one of the few mold species which has the ability to digest its way through the GI tract or pulmonary epithelium and to enter the blood. Once in the blood, A. fumigatus continues to secrete toxins which suppress blood clotting. As a result, uncontrolled bleeding is typical of spreading aspergillosis and in humans can result in bleeding into the jejunum. Forsberg (2003) proposed that A. fumigatus may infect cows that are stressed and/or immuno-suppressed that are fed feedstuffs containing the common mold A. fumigatus.

The investigations involved samples collected from eight HBS cows and 17 healthy cows from Idaho, Iowa, Oregon, and Washington.

Samples included feed, blood, gut contents, and tissues (gut wall, mesenteric lymph node, and liver) from HBS cows, while only blood samples were taken from the negative control cows. All cows with HBS were infected with A. fumigatus in blood and tissues. Fourteen negative control cows have tested negative for A. fumigatus, while the remaining cows contained very low levels of the organism. C. perfringens was not detected in all HBS cows. Moreover, A. fumigatus was detected in three of three feed samples. However, limitations of this analysis exist, such as the small data set and lack of GI tissues from negative control cows. In addition, A. fumigatus is ubiquitous in the GI tract of cattle. Finally, the investigators evaluated antifungal compounds for their potential to inhibit the growth of A. fumigatus in culture and in the field. The investigators formulated a combination of GRAS (generally recognized as safe) ingredients based on their abilities to inhibit fungal growth in the laboratory and then tested them in the field. The field trial involved 1,700 cows that had experienced incidence of HBS. The study revealed that the experimental product appeared to successfully prevent the occurrence of HBS (Forsberg, 2003). However, neither the data nor the identity of the ingredients have yet been published

HBS and Nutrition

High fermentable carbohydrate

Consumption of large amounts of fermentable carbohydrate could be considered as a potential risk factor. Kirkpatrick et al. (2001) reported an association of increased death rates with increased management-level milk. Maximal milk production is a product of carbohydrate consumption and dry matter intake, both of which could be considered as possible risk factors for HBS.

Feeding TMR

Feeding TMR has been suggested as a risk factor for HBS. The Minnesota survey (Godden et al., 2001) found that 83% of affected herds were fed a TMR. The identification of TMR feeding as a risk factor is supported by the fact that only 38% of the herds in Minnesota at the time of the survey were fed a TMR.

Presence of the organism in the feedstuff

The presence of both C. perfringens and A. fumigatus has been reported in the feedstuffs of affected herds. Kirkpatrick et al. (2001) isolated C. perfringens type A from alfalfa haylage that had been fed to the cows. No outbreaks occurred during times when alfalfa haylage was not in the ration. Likewise, Forsberg (2003) detected A. fumigatus in all three of the feed samples that were tested. Additionally, when an antifungal product was used in the field study, the incidence of the disease was reduced (Forsberg, 2003). Therefore, the presence of the causative organism in the feedstuff may be a risk factor for the development of HBS. However, the wide range of investigational items would suggest that the presentation of HBS may not be solely dependent on presence of a causative organism but on the combination of a range of conditions.


HBS is a highly fatal intestinal disease. Animals with HBS have a poor prognosis, regardless of treatment. HBS is more prevalent in large herds, herds with high production, and herds in the western region. However, HBS has been a significant problem in herds of all sizes, production levels, and regions of the country. The cause of the disease is not known yet, but C. perfringens and A. fumigatus have been suggested as causative agents. However, the ubiquitous nature of both of these organisms makes its significance in HBS difficult to ascertain. Some nutritional factors are also suspected to be risk factors for the disease. However, more studies and research need to be done to illuminate the disease process.

Author Information

Myassar O. Alekish
Department of Veterinary Clinical Sciences
Purdue University


Anderson, B.C. 1991. “Point source” hemorrhage in cows. Vet. Rec. 128:619-620.

Dennison, A., D. VanMetre, R. Callan, P. Dinsmore, G. Mason, and R. Ellis. 2002. Hemorrhagic bowel syndrome in dairy cattle: 22 cases (1997-2000). J. Am. Vet. Med. Assoc. 331:686-689.

Forsberg, N. 2003. New findings on jejunal hemorrhagic syndrome. Hoard’s Dairyman 148(8):311, April issue.

Godden, S., R. Frank, and T. Ames. 2001. Survey of Minnesota dairy veterinarians on the occurrence of and potential risk factors for jejunal hemorrhage syndrome in adult dairy cows. The Bovine Practitioner 35:97-103.

Kirkpatrick, M.A., L.L. Timms, K.W. Kersting, and J.M. Kinyon. 2001. Case report: jejunal hemorrhage syndrome of dairy cattle. The Bovine Practitioner 35:104-116.