Determination of the cause of intestinal disease in cattle is based on clinical, epidemiologic, and laboratory findings. Nonspecific therapy includes oral and parenteral fluid therapy to restore the fluid, electrolyte, and acid-base homeostasis. Specific therapy and prevention are detailed under the individual disease headings. Intestinal diseases of neonates are discussed separately, although some of the causes also affect older animals.
Bovine Viral Diarrhea and Mucosal Disease Complex
Bovine viral diarrhea (BVD) is most common in young cattle (6–24 mo old). The clinical presentation can range from inapparent or subclinical infection to acute and severe enteric disease to the highly fatal mucosal disease complex characterized by profuse enteritis in association with typical mucosal lesions. BVD must be distinguished from other viral diseases that produce diarrhea and mucosal lesions. These include malignant catarrhal fever (see Malignant Catarrhal Fever), which usually is a sporadic disease in more mature cattle, bluetongue (see Bluetongue), and rinderpest (see Rinderpest), which is currently considered to be eradicated worldwide.
Bovine viral diarrhea virus (BVDV), the causal agent of BVD and mucosal disease complex, is classified in the genus Pestivirus in the family Flaviviridae. Although cattle are the primary host for BVDV, several reports suggest most even-toed ungulates are also susceptible. Classically, isolates of BVDV are separated into noncytopathic and cytopathic biotypes based on their ability or lack of ability to cause overt cytopathic change and cell death in cell cultures. Noncytopathic BVDV is the predominant viral biotype in nature, whereas cytopathic BVDV is relatively rare and of little epidemiologic relevance. The cytopathic biotype arises in cattle that are persistently infected with noncytopathic biotype of the same or a genetically similar BVDV strain. The switch in biotype is the result of mutations that often involve recombination of noncytopathic viral RNA with itself, with heterologous viral RNA, or with host cell RNA.
Based on comparisons of nucleotide sequence in the viral RNA, there are at least two viral genotypes (distinct genetic groups) of BVDV that can be further divided into subgenotypes or genogroups. The viral genotypes are termed BVDV type 1 and BVDV type 2, and both cytopathic and noncytopathic BVDV are represented in each viral genotype. In recent years, a new group of atypical pestiviruses, apparently forming a separate species, of which cattle are the most likely host species, have been recognized. Virus of this third Pestivirus genotype are designated as "HoBi"-like pestiviruses. The subgenotypes are clusters of viruses within a viral genotype that are highly similar in nucleotide sequence of the viral RNA. (Subgenotypes are designated by lower case letters; thus, subgenotypes of BVDV genotype 1 are represented as 1a, 1b, 1c, etc.) Currently, at least 12 subgenotypes for BVDV-1 (BVDV-1a to BVDV-1l) and two subgenotypes for BVDV-2 (BVDV-2a and BVDV-2b) are recognized.
BVDV type 1 and type 2 appear to be distributed worldwide; however, the prevalence of each type of virus varies considerably among regions. The distribution of viral subgenotypes is more restricted, with many viral subgenotypes being found only in certain regions of the world and, in some cases, only certain regions of a country. All BVDV, regardless of genotype or subgenotype, are antigenically related. However, serologic assays that use serum obtained from convalescent cattle can distinguish BVDV type 1 from type 2. The extent of antigenic variation among BVDV of different genotypes and subgenotypes remains unknown, but there is concern that the antigenic differences among BVDV may be sufficient to affect protection conferred by vaccination.
Etiology and Epidemiology
Serologic surveys conducted throughout the world suggest that BVDV is endemic in the cattle population of most cattle-producing countries. In some countries, BVD is considered the single most important viral infection of cattle. The prevalence of antiviral antibody in cattle varies greatly among countries and geographic regions because of differing cattle housing practices, population densities, vaccination practices, and implementation of different control or eradication programs. Prevalence of antiviral antibody may be >90% if vaccination is practiced commonly in a geographic region. Although cattle of all ages are susceptible, most cases of overt clinical disease are seen in cattle between 6 mo and 2 yr old.
Cattle persistently infected with noncytopathic BVDV serve as a natural reservoir for virus. Persistent infection develops when noncytopathic BVDV is transmitted transplacentally during the first 4 mo of fetal development. The calf is born infected with virus, remains infected for life, and usually is immunotolerant to the resident noncytopathic virus. Transplacental infection that occurs later in gestation can result in abortion, congenital malformations, or birth of healthy calves that have antibody against BVDV. The prevalence of persistent infection varies among countries and between regions within a country. The estimated mean animal prevalence of persistent infection with BVDV is ~1%–2% but may approach 4% on dairy farms with endemic BVDV infection. On a given farm, persistently infected cattle are often found in cohorts of animals that are approximately the same age. Persistently infected cattle can shed large amounts of BVDV in their secretions and excretions and readily transmit virus to susceptible herdmates. Clinical disease and reproductive failure often are seen after healthy cattle come in contact with a persistently infected animal. Although persistently infected cattle are important in transmission of BVDV, the virus also may be spread by biting insects, fomites, semen, biologic products, and other animals, including swine, sheep, goats, camelids, and possibly wild ruminants.
Clinical Findings and Lesions
Disease induced by BVDV varies in severity, duration, and organ systems involved. Infection of immunocompetent susceptible animals with either noncytopathic or cytopathic BVDV is termed acute or transient BVD. Inapparent or subclinical infection without any clinical signs that is followed by seroconversion is the most common form of infection in the field. Acute clinical disease may range from mild disease of high morbidity and low mortality to severe enteric disease with considerable mortality. Biphasic fever (~104°F [40°C]), depression, decreased milk production, transient inappetence, rapid respiration, excessive nasal secretion, excessive lacrimation, and diarrhea are typical signs of acute clinical BVD. Clinical signs of disease usually are seen 6–12 days after infection and last 1–3 days. Transient leukopenia may be seen with onset of signs of disease. Recovery is rapid and coincides with production of viral neutralizing antibody. Gross lesions seldom are seen in cases of mild disease. Lymphoid tissue is a primary target for replication of BVDV, which may lead to immunosuppression and enhanced severity of intercurrent infections.
Some isolates of BVDV (BVD type 2) have been associated with severe clinical disease that manifests as high fever (~107°F [41°–42°C]), oral ulcerations, eruptive lesions of the coronary band and interdigital cleft, diarrhea, dehydration, leukopenia, and thrombocytopenia. In thrombocytopenic cattle, petechial hemorrhages may be seen in the conjunctiva, sclera, nictitating membrane of the eyes, and on mucosal surfaces of the mouth and vulva. Prolonged bleeding from injection sites also occurs. Swollen lymph nodes, erosions and ulcerations of the GI tract, petechial and ecchymotic hemorrhages on the serosal surfaces of the viscera, and extensive lymphoid depletion are associated with severe forms of acute BVD. The duration of overt disease may be 3–7 days. High morbidity with a mortality of ≥25% is common. Severity of acute BVD is related to the virulence of the viral strain infecting the animal and does not depend on viral biotype.
In pregnant cattle, BVDV may cross the placental barrier and infect the fetus. The consequences of fetal infection usually are seen several weeks to months after infection of the dam and depend on the stage of fetal development and on the strain of BVDV. Infection of the dam near the time of fertilization may result in reduced conception rates. Infection during the first 4 mo of fetal development may lead to embryonic resorption, abortion, growth retardation, or persistent infection. Congenital malformations of the eye and CNS result from fetal infections that occur between months 4–6 of development. Fetal mummification, premature birth, stillbirth, and birth of weak calves also are seen after fetal infection.
Persistent infection is an important sequela of fetal infection with noncytopathic BVDV. Persistently infected calves may appear healthy and normal in size, or they may show stunted growth and be prone to respiratory or enteric ailments. They often have a short life span, and death before 2 yr of age is common. Persistently infected cows always give birth to persistently infected calves, but most calves sired by a persistently infected bull will not be infected with virus in utero. Lesions attributable to BVDV often are not seen in persistently infected cattle at necropsy. Antibody against BVD seldom is detected in persistently infected cattle in the absence of vaccination or superinfection with an antigenically heterologous BVDV. Persistently infected cattle exposed to BVDV that is antigenically different from their resident noncytopathic virus can produce antiviral antibody. Therefore, screening for persistent infection using serologic tests to identify animals that lack antiviral antibody may not detect some persistently infected cattle.
Mucosal disease is an uncommon but highly fatal form of BVD occurring in persistently infected cattle and can have an acute or chronic presentation. Mucosal disease is induced when persistently infected cattle become superinfected with cytopathic BVDV. The origin of the cytopathic BVDV is usually internal, resulting from a mutation of the resident persistent, noncytopathic BVDV. In those cases, the cytopathic virus is antigenically similar to the resident noncytopathic virus. External origins for cytopathic BVDV include other cattle and modified-live virus vaccines. Cattle that develop mucosal disease due to exposure to a cytopathic virus of external origin often produce antiviral antibody. Prevalence of persistent infection usually is low, and many persistently infected cattle do not develop mucosal disease, regardless of exposure. Acute mucosal disease is characterized by fever, leukopenia, dysenteric diarrhea, inappetence, dehydration, erosive lesions of the nares and mouth, and death within a few days of onset. At necropsy, erosions and ulcerations may be found throughout the GI tract. The mucosa over Peyer's patches may be hemorrhagic and necrotic. Extensive necrosis of lymphoid tissues, especially gut-associated lymphoid tissue, is seen on microscopic examination.
Clinical signs of chronic mucosal disease may last several weeks to months and are less severe than those of acute mucosal disease. Intermittent diarrhea and gradual wasting are common. Coronitis and eruptive lesions on the skin of the interdigital cleft cause lameness in some cattle. Lesions found at necropsy are less pronounced than, but similar to, those seen in acute mucosal disease. Often, the only gross lesions seen are focal ulcerations in the mucosa of the cecum, proximal colon, or rectum, and the mucosa over Peyer's patches of the small intestine may appear sunken.
BVD is diagnosed tentatively from disease history, clinical signs, and gross and microscopic lesions. Diagnostic laboratory support is required when clinical signs and gross lesions are minimal. Laboratory support also is required in some outbreaks of mucosal disease or clinically severe acute BVD, because either disease may appear similar to rinderpest (see Rinderpest) or malignant catarrhal fever (see Malignant Catarrhal Fever).
Laboratory tests for BVDV include isolation of virus or viral antigen in clinical specimens and tissues, and assays that detect anti-BVDV antibody in serum or milk. Because antibody against BVDV can be highly prevalent in regions with high infection prevalence and/or common use of BVD vaccines, a single serologic test is seldom sufficient for diagnosis of recent infection. A >4-fold increase in antibody titer in paired serum samples obtained ≥2 wk apart is necessary to verify recent infection. Isolation of BVDV from blood, nasal swab specimens, or tissues confirms active infection. Identification of persistent infection requires detection of virus in clinical specimens obtained at least 3 wk apart. Colostral antibody can impair the sensitivity of virus isolation in blood during the first weeks of life. At necropsy, tissues of choice for viral isolation include spleen, lymph node, and ulcerated segments of the GI tract.
Alternatives to viral isolation include antigen-capture ELISA to detect virus in blood, serum, or tissue biopsies; immunohistochemistry to detect viral protein in frozen or fixed tissues; PCR to detect viral RNA in clinical specimens; and PCR or in situ hybridization to detect viral RNA in fresh or fixed tissues. Differentiation of viral genotypes and subgenotypes may be accomplished by PCR assays alone, or by PCR assays followed by analysis of nucleotide sequence, restriction fragment analysis, or palindromic nucleotide substitution analysis. Monoclonal antibody binding assays and viral neutralization assays also differentiate viral genotypes.
Treatment and Control
Treatment of BVD remains limited primarily to supportive therapy. Control is based on sound management practices that include use of biosecurity measures, elimination of persistently infected cattle, and vaccination. Replacement cattle should be tested for persistent infection before entry into the herd. Quarantine or physical separation of replacement cattle from the resident herd for 2–4 wk should be considered, and vaccination of replacement cattle for BVD should be done before commingling with the resident herd. Embryo donors and recipients also should be tested for persistent infection. If vaccination of embryo donors or recipients is warranted, it should be done at least one estrous cycle before embryo transfer is performed. Because BVDV is shed into semen, breeding bulls should be tested for persistent infection before use. Artificial insemination should be done only with semen obtained from bulls free of persistent infection.
Screening cattle herds for persistent infection can be done by PCR assays using skin biopsies, blood, or milk; by classical virus isolation methods using serum or buffy coat cells; by antigen-capture ELISA using serum, buffy coat, milk, or skin biopsies; or by antigen detection using immunochemical methods on tissue or skin biopsies. Several strategies, based on herd size, type of herd being screened, financial limitations of the herd owner, and testing ability of the diagnostic laboratory being used, are available to screen herds for persistent infection. When identified, persistently infected cattle should be removed from the herd as soon as possible, and direct or indirect contact with pregnant cattle should be prevented.
Inactivated and modified-live virus vaccines are available. They contain a variety of strains of BVDV representing both viral biotypes and viral genotypes 1 and 2. Antigenic diversity among BVDV may affect the efficacy of a given vaccine if the vaccine virus or viruses differ significantly from the challenge virus. Proper and safe immunization of cattle with either inactivated or modified-live virus vaccines requires adherence to the manufacturer's instructions. Because BVDV is fetotropic and immunosuppressive, use of modified-live virus vaccines is not recommended in cattle that are pregnant or showing signs of disease. Inactivated viral vaccines may be used in pregnant cattle. Protection conferred by inactivated vaccines may be of short duration, and frequent vaccination may be necessary to prevent disease or reproductive failure. Colostral antibody confers partial to complete protection against disease in most calves for 3–6 mo after birth. Vaccination of neonatal cattle that have acquired colostral antibody may not stimulate a protective immune response, and revaccination at 5–9 mo of age may be necessary. A booster dose of vaccine is often administered before first breeding, and additional booster doses of vaccine may be administered in subsequent years before breeding.
Jejunal Hemorrhage Syndrome
(Hemorrhagic bowel syndrome of cattle)
Jejunal hemorrhage syndrome is a sporadic disease of uncertain etiology that is observed with increasing frequency in cattle. It is manifest by sudden onset of abdominal pain, progressing to sternal recumbency, shock, and death.
Etiology and Pathogenesis
The etiology of jejunal hemorrhage syndrome is uncertain but is believed to be multifactorial. Clostridium perfringens type A, a normal inhabitant of the bovine digestive tract, has been incriminated as an important 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 hypochloremia, hypokalemia, dehydration, and varying degrees of anemia. The hemorrhagic enteritis is progressive. Ischemia and necrosis extends through the intestinal wall, and within 24–48 hr, there is a fibrinous peritonitis, continued electrolyte imbalance, profound toxemia, and death.
Jejunal hemorrhage 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 mo 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 hr.
Cattle affected by jejunal hemorrhage syndrome have a history of sudden anorexia and depression, a pronounced reduction in milk production, abdominal distension and pain with kicking at the abdomen, and weakness progressing to recumbency. Clinical findings include depression, dehydration, increased heart and respiratory rates, and pale mucous membranes. The abdomen may be moderately distended on the right side, the rumen is atonic, and fluid sounds may be elicited by succussion over the right abdomen. Dark red blood clots may be found in the feces and rectum. Distended and firm loops of intestine may be palpable on deep rectal examination. On laparotomy, a segment of the small intestine 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.
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.
Necrohemorrhagic jejunitis with intraluminal hemorrhage is severe. 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 the affected segment of intestine is necrotic.
Diagnosis of jejunal hemorrhage syndrome can be made 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 such as intussusception (see Acute Intestinal Obstructions in Large Animals), cecal dilatation and volvulus, and diffuse peritonitis (see Peritonitis), from right-sided torsion of the abomasum (see Diseases of the Abomasum) and torsion at the root of the mesentery, and from diseases with melena such as abomasal ulcer (see Abomasal Ulcers).
Treatment and Control
Fluid and electrolyte therapy and laparotomy with massage of affected bowel loops to break down obstructing blood clots and, in advanced stages, resection of the affected segment of the intestine are treatment options for jejunal hemorrhage syndrome. Even with such treatment, the fatality rate is very 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.
Winter dysentery is an acute, highly contagious GI disorder that affects housed adult dairy cattle, primarily during winter. Clinical features include explosive diarrhea (sometimes accompanied by dysentery), a profound drop in milk production, variable anorexia and depression, and mild respiratory signs such as coughing. The disease has a high morbidity but low mortality, and spontaneous recovery within a few days is typical.
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, and 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.
Transmission, Epidemiology, and Pathogenesis
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-yr 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 wk, but milk production may take weeks to months to return to normal.
The small intestine may be dilated and flaccid. Lesions are primarily seen in the large intestine and consist of cecal and colonic mucosal hyperemia, linear streaks or pinpoint-sized hemorrhages mostly along the colonic mucosal ridges, and blood in the lumen of the large intestine. Histologic findings may include widespread degeneration and necrosis of colonic glandular epithelium.
A diagnosis of winter dysentery can be confirmed by demonstrating coronaviral particles in fecal samples via ELISA or electron microscopy. Seroconversion to coronavirus in acute and convalescent serum samples, taken 8 wk 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).
Treatment and Control
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 wk 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.
Other Intestinal Diseases of Cattle
Infection with Salmonella spp (see Salmonellosis) can produce diarrhea in animals of all ages, especially those that are stressed, closely stocked, or exposed to a heavily contaminated feed or water supply. In older animals, the disease is manifest by dysentery and toxemia, and mortality can be significant.
Rotavirus and coronavirus occasionally cause outbreaks of diarrhea in suckling calves up to 2–3 mo old. The feces are voluminous and may contain mucus. Toxemia is not evident and mortality is negligible, but growth is decreased. (Also see Diarrhea in Neonatal Ruminants.)
Necrotic enteritis of unknown etiology is seen in beef cattle 5–12 wk old, commonly affecting several calves within the herd. There is sudden onset of fever, depression, and profuse diarrhea. The feces are initially dark green, contain blood, and frequently stain the perineum. Circular erosions may be present in the oral mucosa. A proportion of calves recover after a clinical course of 3–5 days. The clinical course is longer in fatal cases; animals have scant mucohemorrhagic feces that are passed with tenesmus and develop a severe nonregenerative leukopenia. A secondary fibrinous bronchopneumonia may develop. Mortality is high despite intensive antibiotic treatment. At necropsy, there is ulcerative necrosis of the terminal small intestine and the large intestine.
Coccidiosis (see Coccidiosis) usually is seen in calves >2 mo old but <1 yr old, especially in situations of heavy stocking density and overgrazing. It is characterized by dysentery and tenesmus and may be accompanied by nervous signs. Intestinal helminthiasis, particularly ostertagiasis (see Gastrointestinal Parasites of Cattle), is seen in cattle of the same age group. Type I ostertagiasis is seen in cattle on pasture, but Type II ostertagiasis may be seen in housed animals.
Explosive outbreaks of diarrhea in mature cattle are associated most commonly with winter dysentery (see Winter Dysentery) but also with salmonellosis when there is heavy contamination of feed or water.
Chronic diarrhea and wasting often in combination with good appetite, occurring as a sporadic disease in adult cattle is typical for paratuberculosis (see Paratuberculosis). Chronic diarrhea and wasting also occurring in younger animals may be caused by chronic salmonellosis and chronic BVD infection. Other possible causes of chronic diarrhea include congestive heart failure, uremia, and chronic peritonitis. Persistent diarrhea with unthriftiness, and occasionally wasting in yearling and mature cattle, can be associated with a secondary copper deficiency due to excess molybdenum in the pastures. Diarrhea may also accompany selenium-responsive ill-thrift syndromes in growing cattle.
Individual cases or outbreaks of diarrhea may be associated with dietary indiscretions. Diarrhea may follow cases of simple indigestion and is common in grain overload (see Grain Overload in Ruminants). It also follows ingestion of toxic amounts of chemicals (eg, arsenic, copper, zinc, and molybdenum) or certain poisonous plants and mycotoxicoses; dipyridyl and organophosphate poisoning can also cause diarrhea.
Cattle may also harbor organisms such as Escherichia coli O157:H7, Yersinia enterocolitica, and Campylobacter jejuni in the intestine; although these are rarely associated with clinical disease in cows, fecal contamination of milk may lead to outbreaks of gastroenteritis in people who consume unpasteurized milk or cheese products. Retail meat products can also be infected if there has been fecal contamination of the carcass at slaughter.
Intestinal adenocarcinoma, commonly seen in association with bovine enzootic hematuria, is believed to result from the interaction of a carcinogen (ptaquiloside) in bracken fern (Pteridium spp, see Bracken Fern Poisoning) and papilloma virus.
Intestinal obstructions are seen sporadically (see Acute Intestinal Obstructions in Large Animals). Cecal dilatation and volvulus are seen predominantly in adult cattle in the postparturient period. Intussusception occurring at the distal jejunum or proximal ileum is the most common cause of complete obstruction in both adult cattle and calves. Ileocecocolic, cecocolic, and colonic intussusceptions are seen less frequently in calves and not at all in adult cattle because of the greater strength of the ileocecal ligament and the presence of mesenteric fat, which stabilize this region of the bowel in older cattle. Intestinal volvulus and volvulus around the mesenteric root are seen sporadically at all ages. Rarely, intestinal obstruction is caused by incarceration and entrapment of the small intestine by persistent urachal or umbilical remnants, by obstruction of the small intestine or descending colon by phytobezoars and enteroliths, or by compression from fat necrosis or lipoma. Intestinal obstruction can also be caused by congenital disease (see Congenital and Inherited Anomalies of the Small and Large Intestine), most commonly by atresia coli (which is seen both sporadically and in clusters on a farm and may be caused by rectal palpation of the amniotic vesicle at 35 and 41 days of pregnancy) but also by atresia ani (which may be accompanied by urogenital defects and defects of the tail).
Last full review/revision August 2014 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM