Intestinal Diseases in Cattle

The etiology of hemorrhagic bowel syndrome is uncertain but may be multifactorial.

Clostridium perfringens type A, a normal inhabitant of the bovine digestive tract (1), has been incriminated as a causative agent, because this organism is isolated from the intestines of cattle with naturally occurring cases of HBS at a higher frequency and in higher numbers than from cattle with other intestinal diseases.

Another proposed potential causative agent of HBS is Aspergillus fumigatus, a common fungus in feed and forages (2).

Despite the suspicion of these two aforementioned pathogens as causes of HBS, a 2023 study on gross pathology, histopathology, culture, and sequencing within HBS lesions did not find evidence to support them as etiological agents in this disease (3).

The primary lesion of HBS is similar to that caused by C perfringens infection in young, rapidly growing animals; it consists of acute, localized, necrotizing, hemorrhagic enteritis of the small intestine that leads to development of an intraluminal blood clot. The clot causes a physical obstruction, resulting in proximal accumulation of intestinal fluid and gas, and development of abdominal distention, dehydration, and varying degrees of anemia.

Hemorrhagic enteritis is progressive. Ischemia and necrosis extend through the intestinal wall, and, if the patient is left untreated, fibrinous peritonitis develops within 24–48 hours, followed by profound toxemia and death.

Hemorrhagic bowel syndrome occurs sporadically, primarily in mature lactating dairy cows in North America and Europe; however, HBS has also been recorded in beef cattle. Most cases occur in mature dairy cattle in the first 3 months of lactation, and the highest incidence rates occur during the cold months of the year.

Possible risk factors for HBS are those associated with management practices aimed at achieving high milk production, such as feeding cattle a diet high in fermentable carbohydrates or feeding a total mixed ration(TMR) diet.

Herd outbreaks of HBS can affect 10% of the herd (4). Mortality in general is high: 80–100% of affected animals die within 48 hours (5, 6).

Cattle affected by hemorrhagic bowel syndrome have a history of the following:

• sudden anorexia and depression

• sudden and pronounced drop in milk production

• abdominal distention and pain, with kicking at the abdomen

• dark, bramble jelly–type feces, scant in amount

• dullness and weakness progressing to recumbency

Clinical findings of HBS include depression, dehydration, increased heart and respiratory rates, and pale mucous membranes. Abdominal distention of the right flank might be mild but progresses rapidly.

Owing to the acute onset of HBS, there can still be good rumen fill; however, the rumen is atonic, and fluid sounds may be elicited by succussion over the right abdomen.

Dark red blood clots with a sticky consistency resembling bramble jelly are present in the feces (see feces image). In cases of complete and prolonged intestinal obstruction, the rectum appears dry and sticky, only containing small amounts of dark feces.

Hemorrhagic bowel syndrome, feces, cow

Image

Feces of a cow with hemorrhagic bowel syndrome. The feces have a sticky consistency and a similar appearance to bramble jelly.

Courtesy of Dr. Walter Grünberg

Distended and firm loops of intestine might be palpable on deep rectal examination. On laparotomy, a segment of the small intestine of variable length is dark red and distended, with a serosal surface covered by tags of fibrin (see small intestine image). The small intestine proximal to the affected segment and the abomasum are distended with gas and fluid.

Hemorrhagic bowel syndrome, bovine small intestine

Image

Bovine small intestine affected by necrohemorrhagic inflammation. Note the serosal layer covered with fibrin. The part proximal to the segment obstructed by a blood clot is distended by fluid accumulation, whereas the distal part of the small intestine appears empty.

Courtesy of Dr. Sameeh M. Abutarbush.

Most cattle with HBS die within 2–4 days after the appearance of clinical signs, despite intensive fluid and electrolyte therapy. Sudden death without prior clinical findings can occur.

The hemogram is variable; serum biochemical analysis reflects obstruction of the upper small intestine and sequestration of abomasal secretions with resultant hypokalemia and hypochloremia. Serum l-lactate concentrations are often markedly elevated (> 5 mmol/L).

• Exploratory laparotomy or necropsy

A tentative diagnosis of hemorrhagic bowel syndrome can be made on the basis of clinical signs of intestinal obstruction and characteristic appearance of the feces. Transabdominal ultrasonography confirms the presence of distended bowel loops, which indicates intestinal obstruction, and possibly also homogenous echogenic content of a bowel segment, which is consistent with a blood clot obstructing the intestinal lumen.

Diagnosis of HBS is confirmed either during exploratory laparotomy or at necropsy and is based on the presence of a characteristic focal necrohemorrhagic enteritis of the distal small intestine. Serum biochemical analysis typically reveals marked hyperlactatemia, hyperglycemia, and hyperchloremia. In some cases, hypocalcemia, presumably resulting from marked inflammation, is observed.

Differential diagnoses for HBS include the following:

• other causes of physical or functional obstruction of the small intestine (eg, intussusception; cecal dilatation and volvulus)

• diffuse peritonitis, from right-sided torsion of the abomasum or torsion at the root of the mesentery

• diseases causing melena (eg, abomasal ulcer)

• Surgery and supportive care

Surgery to localize small intestinal loops affected by hemorrhagic bowel syndrome and manually decrease and dislodge blood clots within the intestinal lumen appears to be the most efficient treatment option in the early stages of HBS. Fluid and electrolyte therapy is also indicated. In advanced stages, resection of the affected segment of the intestine might be required. Prokinetic substances to enhance intestinal passage (eg, neostigmine), administered parenterally in combination with single or repeated large, IV doses of heparin to prevent new clot formation in the intestinal lumen, may be used postoperatively.

The fatality rate among cattle with HBS is high, and the prognosis for individual animals with this disease is grave. No preventive strategies have been identified. A short-term protective effect of a C perfringens type C and D vaccine against HBS in some herds has been reported anecdotally; however, there is no corroborating scientific evidence.

Although the precise etiology of winter dysentery has not been conclusively confirmed, an increasing body of evidence implicates a bovine coronavirus (BCoV) (7), closely related to the virus that causes diarrhea in neonatal calves. Evidence for BCoV as the cause of winter dysentery includes the following:

• Clinical signs and pathological findings are consistent with disease induced by BCoV.

• Seroconversion to BCoV has been demonstrated in affected cattle.

• The virus is frequently isolated from diarrheic feces of cattle that exhibit clinical signs of winter dysentery.

• The disease has been reproduced by briefly exposing BCoV-seronegative lactating cows to a calf experimentally infected with feces from cows with winter dysentery.

However, it has not been possible to consistently reproduce winter dysentery through oral inoculation of adult cattle with BCoV. Concurrent risk factors, such as changes in diet, cold temperatures, closed confinement with high animal density, poor ventilation, and presence of other microorganisms, might be required before BCoV causes clinical disease in adult cattle.

Bovine coronavirus, the suspected causative agent of winter dysentery in cattle, is transmitted via the fecal-oral route through ingestion of feed or water contaminated with feces from clinical cases or clinically healthy carrier animals. Viral particles present in respiratory secretions of affected animals can further enhance transmission. Disease transmission is promoted by close confinement.

Winter dysentery is highly contagious and easily introduced to barns by human visitors with BCoV on their hands, clothing, or boots, as well as by carrier animals and fomites. The disease is common in northern climates, where animals are housed indoors for extended periods during the winter months. It occurs frequently in the northern US, Canada, the UK, Europe, Australia, New Zealand, Israel, and Japan. Coronaviruses survive best at low temperatures and at low UV light intensities, which can lead to a buildup of virus in the environment during the colder months.

Adult lactating cows that have recently calved are most severely affected by winter dysentery; however, the disease can affect younger or older animals and males.

Mortality rates associated with winter dysentery are generally low (1–2%). However, morbidity in affected herds is high: 20–50% of animals in a herd exhibit clinical signs within a few days, and nearly 100% exhibit clinical signs within a week (8). Some degree of immunity to winter dysentery appears to develop, because recurrences, if in the same herd, are noted at 1- to 5-year intervals (8).

Inflammatory mediators that cause hypersecretion in the small intestine and colon are thought to contribute to the voluminous diarrhea observed in cattle with winter dysentery (8). In addition, destruction of epithelial cells in the colonic crypts results in transudation of extracellular fluid and blood, explaining the hemorrhagic nature of the diarrhea in some cases.

Winter dysentery is characterized clinically by an acute onset of fluid diarrhea and a profound decrease in milk production (25–95% production loss). Feces are liquid and homogenous with little odor, dark green to black, and sometimes contain blood (typically in first-lactation heifers) or mucus. A sweet, musty, unpleasant odor can be present in barns with large numbers of affected cattle. Nasolacrimal discharge or cough can accompany or precede the diarrhea.

Other clinical signs of winter dysentery include mild colic, dehydration, depression, a brief period of anorexia, and some decrease in body condition. Occasionally, animals exhibit more severe signs, such as passage of feces with variable amounts of blood, severe dehydration, and weakness. Fatalities are rare.

Diarrhea in individual animals with winter dysentery has a short course, and feces return to normal in 2–3 days in most animals. Disease in the herd typically subsides in 1–2 weeks; however, milk production can take weeks to months to return to normal.

• ELISA

• PCR assay

• Serological testing

A diagnosis of winter dysentery in cattle can be confirmed in one of three ways: by demonstrating coronaviral particles in fecal samples via electron microscopy; by confirming the presence of viral antigen via antigen ELISA; or by confirming the presence of viral DNA via RT-nested PCR assay. Seroconversion to coronavirus in acute and convalescent serum samples, taken 8 weeks apart, also helps confirm the diagnosis.

Differential diagnoses for acute diarrhea in adult cattle include the following:

• bovine viral diarrhea (BVD)

• enteric salmonellosis

• coccidiosis

These diseases can be excluded by absence of mucosal lesions (BVD), negative fecal cultures (Salmonella spp), and negative fecal flotation (coccidiosis), as well as by the characteristic clinical presentation of winter dysentery (rapid onset of diarrheal disease of short duration in a herd with high morbidity but low mortality).

• Supportive care

• Biosecurity

Most cattle affected by winter dysentery recover spontaneously. Fresh water, palatable feed, and free-choice salt should be available at all times. The use of astringents, protectants, and adsorbents is controversial. IV fluid therapy or blood transfusions might be required in severely affected cattle.

There is no vaccine for winter dysentery. Isolation of newly introduced cattle for 2 weeks and isolation of any adult cow with diarrhea is advised to decrease the likelihood of disease introduction into a herd.

In an outbreak of winter dysentery, access to the premises should be restricted, and all humans in contact with affected cattle should ensure that their footwear and clothing are clean before leaving an affected farm.