Intestinal Diseases in Cattle

The etiology of HBS is uncertain but believed to be multifactorial. Clostridium perfringens type A, a normal inhabitant of the bovine digestive tract, has been incriminated as a causative agent, because this organism is isolated from the intestines of naturally occurring cases at a higher frequency and in higher numbers than from cattle with other intestinal diseases.

Another proposed potential causative agent is Aspergillus fumigatus, a common fungus in feed and forages. The primary lesion is similar to that caused by C perfringens in young, rapidly growing animals and consists of an acute, localized, necrotizing, hemorrhagic enteritis of the small intestine that leads to development of an intraluminal blood clot. The clot causes a physical obstruction, with proximal accumulation of intestinal fluid and gas and development of abdominal distension, dehydration, and varying degrees of anemia. The hemorrhagic enteritis is progressive. Ischemia and necrosis extends through the intestinal wall, and, if untreated, there is a fibrinous peritonitis 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, but it has also been recorded in beef cattle. Most cases occur in mature dairy cattle in the first 3 months of lactation, with highest incidence rates during the cold months of the year. Possible risk factors for disease are those associated with management practices aimed at achieving high milk production, such as high fermentable carbohydrate content of the diet and feeding a total mixed ration. The animal-level disease incidence rate is estimated to be 1%–2%, but outbreaks in a herd can be associated with morbidity rates of ≥10%. Mortality in general is high, with 80%–100% of affected animals dying within 48 hours.

Cattle affected by hemorrhagic bowel syndrome have a history of:

• 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 include depression, dehydration, increased heart and respiratory rates, and pale mucous membranes. Abdominal distension of the right flank may be mild but progresses rapidly. Due to the acute onset, there can still be good rumen fill, but the rumen is atonic, and fluid sounds may be elicited by succussion over the right abdomen. Dark red blood clots with a sticky bramble jelly-type consistency are present in the feces. In cases of complete and prolonged intestinal obstruction, the rectum appears dry and sticky, only containing small amounts of dark feces. Distended and firm loops of intestine may 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. The small intestine proximal to the affected segment and the abomasum are distended with gas and fluid. Ultrasonography may aid in diagnosis.

Feces of cow with hemorrhagic bowel syndrome

Image

Courtesy of Dr. Walter Grünberg

Most affected cattle die within 2–4 days despite intensive fluid and electrolyte therapy. Sudden death without prior clinical findings may occur. The hemogram is variable; serum biochemistry 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, with values >5 mmol/L.

Lesions

Hemorrhagic bowel syndrome

Image

Courtesy of Dr. Sameeh M. Abutarbush.

Necrohemorrhagic enteritis can occur anywhere in the small intestine and is characterized by severe but localized intraluminal hemorrhage. The affected segment of intestine is dark red and dilated, with tags of fibrin on the serosal surface. The lumen contains a firm blood clot adherent to the mucosa, and at advanced stages the affected segment of intestine becomes necrotic and feels friable on palpation.

• Characteristic lesions in the small intestine determined during exploratory laparotomy or at necropsy

A first, tentative diagnosis of hemorrhagic bowel syndrome can be made based on signs of intestinal obstruction in combination with the characteristic appearance of the feces. Diagnosis is confirmed either during an exploratory laparotomy or at necropsy and is based on the presence of a characteristic focal necrohemorrhagic enteritis of the distal small intestine.

Differential diagnoses include:

• 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 reduce and dislodge blood clots within the intestinal lumen appears to be the most efficient treatment option in the early stages. Fluid and electrolyte therapy is also indicated. In advanced stages, resection of the affected segment of the intestine may be required. Prokinetic substances to enhance intestinal passage administered parenterally combined 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 is high, and the prognosis is grave. No preventive strategies have been identified. A short-term protective effect of a C perfringens type C and D vaccine against hemorrhagic bowel syndrome in some herds has been reported anecdotally, but there is currently 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), closely related to the virus that causes diarrhea in neonatal calves. Evidence for BCoV as the cause of winter dysentery includes the following:

1. Clinical signs and pathologic findings are consistent with disease induced by BCoV

2. Seroconversion to BCoV has been demonstrated in affected cattle

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

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

Notwithstanding, 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, may be required before BCoV causes clinical disease in adult cattle.

BCoV 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 may further enhance transmission. Transmission of disease is promoted by close confinement. Winter dysentery is highly contagious and easily introduced to barns by visitors, carrier animals, and fomites. Winter dysentery is common in northern climates where animals are housed indoors for extended periods during the winter months. It is seen frequently in the northern USA, Canada, the UK, Europe, Australia, New Zealand, Israel, and Japan. Coronaviruses survive best at low temperatures and at low ultraviolet 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, but the disease can affect younger or older animals and males.

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

Inflammatory mediators that cause hypersecretion in the small intestine and colon are thought to contribute to the voluminous diarrhea seen in cattle with winter dysentery. 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 may contain blood (typically in first-lactation heifers) or mucus. A sweet, musty, unpleasant odor is reported in barns with large numbers of affected cattle. Nasolacrimal discharge or cough may accompany or precede the diarrhea. Other signs 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 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, but milk production may take weeks to months to return to normal.

• PCR and serology

A diagnosis of winter dysentery can be confirmed by demonstrating coronaviral particles in fecal samples via electron microscopy or by confirming the presence of viral antigen or viral DNA via antigen ELISA or reverse transcription/nested PCR, respectively. 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 bovine viral diarrhea (BVD), enteric salmonellosis, and 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).

• Symptomatic and supportive care

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 may 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, access to the premises should be restricted, and all persons in contact with affected cattle should ensure that their footwear and clothing are clean before leaving an affected farm.