Diarrhea in Neonatal Ruminants

Several enteropathogens are associated with diarrhea in neonatal ruminants. Their relative prevalence varies geographically; however, the most prevalent infections in most areas are Cryptosporidium parvum, rotavirus, and, to a lesser extent, enterotoxigenic Escherichia coli and coronavirus. Cases of neonatal diarrhea are commonly associated with more than one of these agents, and the cause of most outbreaks is multifactorial.

Determining the particular agents associated with an outbreak of diarrhea can be important, because specific therapy and prophylaxis are available for some. Also, some agents have zoonotic risk.

Diarrhea is also present in neonates with septicemic colibacillosis.

Enteropathogens associated with neonatal diarrhea are commonly found in the feces of healthy calves; whether intestinal infection leads to diarrhea depends on a number of determinants, including differences in virulence of different strains of a pathogen and the presence of more than one pathogen. The resistance of the calf is of major importance and is largely determined by successful transfer of colostral immunoglobulins. Colostrum-deprived calves are highly susceptible to all types of infections, including with enteropathogens, and develop severe and often fatal disease.

The progression of infection, the severity of lesions produced, and the severity of the diarrhea can be modulated by immunoglobulins and other protective compounds received via colostrum. Immunoglobulins act directly on pathogens in the intestinal lumen during the period of colostrum ingestion as well as after, because substantial amounts of circulating immunoglobulins are resecreted into the intestine, especially when the concentration of circulating immunoglobulin is high. The lack of specific antibodies in dams that have not been exposed to specific pathogens, and the use of specific vaccines in these dams, further modulate this influence.

Stress caused by a poor environment, inadequate protection from the weather, or an insufficient or inappropriate diet also increases the risk of diarrhea in neonatal ruminants.

With any of the diarrhea-causing enteropathogens, healthy adult cattle can be carriers and periodically excrete the organism in feces. Excretion can increase around parturition and be more frequent in primiparous cows. This can lead to contaminated calving areas and infection of the udder and perineum of the dam. Other sources of infection include the feces of healthy calves and the feces of diarrheic calves, which contain large numbers of organisms early in the course of infection. A few scouring calves can result in severe contamination of the calf-rearing area.

Transmission of enteropathogens is by fecal-oral contact, fecal aerosol, and, in the case of coronavirus, by respiratory aerosol.

Diarrhea in neonatal ruminants is usually associated with disease of the small intestine and can be caused by hypersecretion or malabsorption. Hypersecretory diarrhea develops when an abnormal amount of fluid is secreted into the gut, exceeding the resorptive capacity of the mucosa. In malabsorptive diarrhea, the capacity of the mucosa to absorb fluid and nutrients is impaired to the extent that it cannot keep up with the normal influx of ingested and secreted fluids. This is usually the result of villous atrophy, in which the loss of mature enterocytes at the tips of the villi results both in a decrease in villous height (with a consequent decrease in the surface area for absorption) and in loss of the brush border digestive enzymes. The extent and distribution of villous atrophy varies with different pathogens and can explain variation in the severity of clinical disease.

Malabsorptive diarrhea can be aggravated by the colonic fermentation of nutrients that normally would have been absorbed in the small intestine. Fermentation products, especially lactic acid, appear to draw water into the colon osmotically, which contributes to the severity of diarrhea.

Inflammation contributes to the pathophysiology of diarrhea in most intestinal infections, and mediators of inflammation can affect ion flux within the intestine. Inflammation also leads to vascular and lymphatic damage and to structural damage of the crypt-villus unit. Inflammation, leading to necrosis of the enterocyte, submucosal inflammatory infiltration, and villous atrophy, is also a major component of the pathophysiology of diarrhea produced by salmonellae, as well as of diarrhea produced by enteropathogenic E coli and by toxigenic C perfringens.

Enterotoxigenic E coli produce the enterotoxin STa, which stimulates marked hypersecretion by activating guanylate cyclase and by inducing a net secretion of sodium and chlorine. The membrane-bound sodium-glucose cotransport system remains functional but cannot compensate for the increased secretory activity. Salmonellae also elaborate enterotoxins. Infections with verotoxin-producing enteropathogenic E coli result in accumulation of fluid within the large intestine and extensive damage to the large intestinal mucosa, with edema, hemorrhage, and erosion and ulceration of the mucosa, which results in blood and mucus in the lumen.

Viruses usually produce a malabsorptive diarrhea by destroying the absorptive cells of the mucosa, thus shortening the intestinal villi. The mechanism by which cryptosporidia produce diarrhea is not completely understood; however, it appears to have both malabsorptive and inflammatory components.

Most infectious forms of diarrhea in neonatal ruminants have hypersecretory, inflammatory, and malabsorptive components; however, one usually predominates. These lead to a net loss of water and electrolytes; if severe, the calf develops hypovolemia, acidemia, hypoglycemia, and prerenal azotemia.

Inappropriately formulated milk replacers can produce diarrhea by two mechanisms, both associated with malabsorption. Vegetable (especially soybean) products are commonly used as protein sources in the manufacture of milk replacers. Depending on the degree of refinement, these products can contain carbohydrates that are indigestible in young calves. Such carbohydrates are not absorbed in the small intestine and can contribute to diarrhea via colonic fermentation. In addition, most calves < 3 weeks old appear to have an allergic reaction to soy proteins that results in villous atrophy, leading to diarrhea that is probably malabsorptive.

The clinical presentation of diarrhea in neonatal ruminants can vary greatly, depending on etiology and level of severity. Presentation can range from loose stools in an otherwise healthy animal to recumbency and coma in severely dehydrated and acidotic animals. The major clinical signs include the following:

• diarrhea with loose to watery feces

• varying degrees of dehydration

• dullness and varying degrees of weakness

Age at onset, severity of clinical signs, and course of clinical disease can vary considerably, depending on the causative agents involved.

Diarrhea due to enterotoxigenic E coli occurs in calves < 3–5 days old, rarely later. However, the age of susceptibility can be extended in the presence of other pathogens. Onset is sudden. Profuse amounts of liquid feces are passed, and calves rapidly become depressed and recumbent. Calves can lose > 12% of body weight in fluid within hours, and hypovolemic shock and death can occur in 12–24 hours. Body temperature is sometimes increased but is typically normal or subnormal. If fluid and electrolyte therapy is administered early, response is usually good.

Disease produced by attaching-effacing E coli occurs predominantly in calves from 4 days to 2 months old and can manifest with diarrhea or primarily as dysentery with blood and mucus in the feces. The clinical course is short.

Septicemia, accompanied by high fever and depression progressing to prostration and coma, is the salient clinical sign of salmonellosis in younger calves. Although diarrhea is present, calves die from septicemic shock before showing clinical signs of severe dehydration or hypovolemic shock. The enteric form of salmonellosis is usually not observed in calves < 14 days old. It is characterized by foul-smelling feces that contain blood, fibrin, tissue, and copious amounts of mucus. Affected calves regularly show clinical signs of systemic disease, such as fever, tachycardia, abdominal pain, and tenesmus. Calves with salmonellosis usually deteriorate rapidly and often die, despite vigorous therapy.

Hemorrhagic enterotoxemia due to C perfringens type A, B, or C is characterized by acute onset of depression, weakness, bloody diarrhea, abdominal pain, and death within a few hours. It usually develops in vigorous calves just a few days old that have large appetites and a ready source of milk. Calves affected with C perfringens usually die before treatment can be instituted.

Diarrhea due to rotavirus, coronavirus, and other viruses generally occurs in calves 5–15 days old but can affect calves up to several months old. Affected calves are only moderately depressed and often continue to suck or drink milk. The feces are voluminous, soft to liquid, and often contain large amounts of mucus. Diarrhea commonly persists for 3 to several days; some cases of coronaviral diarrhea become chronic. Cases of viral diarrhea that are uncomplicated by other pathogens commonly respond within a few days to fluid and electrolyte therapy and adequate nutritional support.

Cryptosporidiosis occurs in calves 5–35 days old but most often affects calves in the second week of life. It is characterized by persistent diarrhea that does not respond to therapy. Diarrhea caused solely by Cryptosporidium spp is often mild and self-limiting; however, severity can be related to the general strength of the calf and the intensity of challenge with the organism. Combination infections with cryptosporidia, rotavirus, and other enteropathogens are common and result in persistent diarrhea often characterized by emaciation and death. Death from hypoglycemia also occurs as a sequela of cryptosporidiosis in calves 3–4 weeks old that have recovered from diarrhea but are still emaciated. Death often occurs during a bout of cold weather and is more likely to occur on farms with a policy of decreasing the amount of milk fed to calves during periods of diarrhea.

Dietary diarrhea occurs in calves < 3 weeks old and is characterized by voluminous feces of pasty to gelatinous consistency. Initially, calves are bright and alert and have good appetites. Eventually, they become weak and emaciated if the diet is not corrected. Infectious forms of diarrhea are often complicated by poor-quality diets or insufficient nutritional intake.

• Calfside test kits for pathogen identification

• Necropsy

A definitive etiological diagnosis for diarrhea in neonatal ruminants cannot be made based solely on clinical findings. However, history, age, and clinical presentation can permit a presumptive etiological diagnosis. Fecal samples can then be tested with calfside test kits using immune chromatography to identify antigens of common neonatal diarrhea pathogens, or samples can be submitted to a diagnostic laboratory for isolation and characterization of enteropathogens. For a diagnosis at herd level, samples should be obtained from several untreated calves in the early stages of diarrhea. Interpretation of fecal microbiological test results can be difficult because of mixed infections and because enteropathogens are commonly present in the feces of healthy calves.

Necropsy allows for examination of intestinal mucosa for evidence of diagnostic lesions and for the presence of enteropathogens, such as cryptosporidia, at the site of intestinal lesions. Necropsy might be the only way to diagnose some forms of disease, such as that associated with attaching-effacing strains of E coli. The diagnostic value of postmortem examination diminishes quickly with time after death; important lesions can disappear within minutes as a result of autolysis.

Blood biochemical, blood gas, and hematologic analyses are of limited value in making an etiological diagnosis; however, they can help determine the severity of metabolic disturbances such as dehydration, acid-base imbalances, electrolyte imbalances, and glycemia. Complete laboratory evaluation can, however, be expensive, and dehydration and acidemia severity can be determined with reasonable precision by physical examination.

• Supportive care

Many factors involved in disease resistance are nonspecific; thus, important preventive measures can be taken, and therapy can be started, before an etiological diagnosis is established. Treatment for diarrhea in neonatal ruminants includes the following:

• fluid therapy to facilitate water and electrolyte replacement and correction of acid-base disturbances

• alteration of the diet

• anti-inflammatory therapy

In severely affected patients, the need for antimicrobial therapy often must be assessed before a definitive etiological diagnosis is available.

Fluid and electrolyte therapy is essential and should be started as soon as possible, regardless of whether clinical signs of dehydration are present, as these might not develop until the calf has lost ≥ 6% of its body weight in fluid. Calves still able to stand and willing and able to suck can often be treated with oral electrolyte solutions alone. Fluids for oral rehydration should promote the cotransport of sodium with glucose and amino acids and should contain sodium, glucose, glycine or alanine, potassium, and an alkalinizing agent (bicarbonate, citrate, or acetate). Oral electrolyte solutions should be offered, alternating with whole milk or milk replacer. Numerous commercial preparations are available for this purpose. Solutions containing carbohydrates, as most oral electrolyte solutions do, should not be administered by stomach tube. Repeatedly tube-feeding calves with these solutions can result in rumen acidosis and ruminal drinking.

Feeding milk can increase fecal volume; however, it provides energy to the calf and can promote gut healing. Calves have large energy requirements and little reserve. Electrolyte solutions do not meet calf energy requirements, and milk should not be withheld.

Recumbent calves, calves showing evidence of ≥ 8% dehydration of body weight, and calves unwilling or unable to voluntarily ingest fluids orally require IV fluid therapy. In these cases, dehydration is usually associated with acidemia and in some cases also with hypoglycemia. Fluid and base deficits can be corrected by first rapidly infusing a hypertonic solution of sodium bicarbonate (either 500 mL of a 4.2% solution or 250 mL of an 8.4% solution), followed by a physiologically balanced electrolyte solution administered at an infusion rate of approximately 40 mL/kg/hour until the volume deficit is corrected (4). Even with severe dehydration of 10–15% of body weight, correction of the volume and base deficit can safely be achieved within 2–3 hours using this protocol.

When the severity of acidemia is determined by blood gas analysis, the amount of sodium bicarbonate required to correct the base deficit can be calculated from the base excess and the patient's body weight, using the following equation (5):

1. Amount of Bicarbonate (mmol) = Base Excess (mmol/kg) x Body Weight (kg) x 0.6

To determine the volume of sodium bicarbonate solution required, note that the amount of bicarbonate in millimoles corresponds to the volume of 8.4% sodium bicarbonate in milliliters or twice that volume of 4.2% sodium bicarbonate.

To address hypoglycemia (a frequent concomitant finding in diarrheic calves), adding 25–50 g of dextrose to the fluid volume to be administered in the first 2–3 hours is beneficial (6).

Once the appropriate volume of fluids to correct dehydration and acidemia has been administered, the patient must be reassessed to determine whether IV fluid therapy should be continued. With adequate hydration and suckle reflex, the patient can usually be switched to oral rehydration therapy.Oral electrolyte solutions should be used concurrently with and after IV fluid therapy to compensate for ongoing fluid and electrolyte losses. Studies have reported improved and faster recovery when colostrum is added to the milk fed to diarrheic calves for 2–4 days (7).

Diarrhea per se is not an indication for antimicrobial therapy; however, parenteral antimicrobial therapy should be considered whenever calves are systemically ill and show clinical signs suggestive of septicemia. Field studies revealed that at least 30% of diarrheic calves with systemic disease are bacteremic—a clear indication for parenteral antimicrobial therapy (8, 9). Because the large majority of cases of bacteremia and septicemia in neonatal calves are associated with E coli, the chosen antimicrobial should be effective against gram-negative bacteria.

In several studies, severely affected diarrheic calves treated with NSAIDs and fluid therapy showed fewer clinical signs of pain, made a faster recovery, and had better weight gains in the convalescent period than those not treated with NSAIDs and fluid therapy (10). These effects, reported for several NSAIDs, have been attributed to their analgesic, anti-inflammatory, antipyretic, and antisecretory properties.

Diarrheic calves should always have access to plain water offered from a bowel or bucket so that water is ingested from a surface rather than from a nipple. This is advisable because hypernatremia and salt intoxication, resulting from either repeated infusion of hypertonic solutions or incorrectly reconstituted oral rehydration solutions, are common complications observed in the field. These can easily be prevented if the patient can ingest plain water ad libitum.

The use of drugs that decrease intestinal motility, such as hyoscine-N-butylbromide or atropine, is sometimes advocated, because they decrease fecal output. Although decreasing fecal production might be interpreted as a positive treatment outcome, it can also represent sequestration of gut fluid containing bacteria, toxins, and undigested nutrients in the intestinal tract. The literature does not provide any strong supportive evidence for or against the use of antimotility drugs in diarrheic calves.

Intestinal gels and adsorbents, such as kaolin and pectin, are in general use. However, their only established effect is to increase fecal consistency; they do not decrease the loss of water and ions.

Because of the complex nature of diarrhea in neonatal ruminants, it is unrealistic to expect total prevention—economical control is the major objective. The incidence of clinical disease and the case fatality rate depend on the balance between the levels of exposure to infectious agents and the resistance in the calf. Differences in herd size; availability of facilities, land, and labor; and general management objectives make it impossible to recommend specific management procedures applicable to all situations. However, several broad principles apply in all herds:

• Practice good general hygiene, in particular in maternity and calf-rearing areas.

• Decrease exposure of neonates to pathogens by separating maternity pens, calf-rearing areas, and hospital pens on the premises.

• Practice good colostrum management.

• Avoid mingling older calves with neonates.

• Assure access to plain, clean water for calves from the first day of life.

Proper colostrum management deserves particular attention because the prevalence of failure of passive transfer in calves is still disturbingly high. A substantial portion of both naturally sucking dairy calves and calves handfed colostrum do not acquire adequate amounts of immunoglobulin because of delayed sucking or feeding, ingestion of an inadequate volume of colostrum, or ingestion of inferior-quality colostrum. When time constraints on labor preclude an ensured intake of colostrum by nipple-bottle feeding, administration of 4 L of colostrum by esophageal feeder within the first 2 hours of life can be the best colostrum feeding policy (11). (Also see Management of Reproduction: Cattle.)

Vaccination of dams late in pregnancy to boost the immunoglobulin content against rotavirus, coronavirus, enterotoxigenic E coli, or Cryptosporidium parvumin colostrum can be useful in herds in which these pathogens are known to contribute to the neonatal diarrhea problem. The pregnant dam is vaccinated 6 and 3 weeks before parturition to stimulate antibody production against specific pathogens of the neonatal diarrhea complex; these antibodies are then passed on to the newborn calf through the colostrum (provided the calf ingests it). A single booster is given in subsequent years.

A vaccine against cryptosporidiosis for cows in late pregnancyhas become available in some countries (12). Colostrum from vaccinated dams enhances protection of calves against diarrhea caused by C parvum infection. For best results, excellent colostrum management at calving and feeding the calf milk from vaccinated dams for the first 4–5 days of life is advised in conjunction with this vaccine.

Vaccination of pregnant cows with rotavirus and coronavirus vaccines increases the amount of specific antibody in colostrum and milk; however, the concentration of antibodies in milk might be insufficient to provide local antibody in the intestinal lumen during the period of peak prevalence of infection, which, in calves, is 5–15 days after birth. Controlled trials of commercial vaccines have shown variable results (13). The addition of small amounts of immune colostrum to milk fed during the period of susceptibility can provide some protection against disease.

Monoclonal F5 (K99) E coli antibody is commercially available for oral administration to calves immediately after birth. This treatment should be considered in herds where enterotoxigenic E coli was previously isolated. It should be administered in combination with good-quality colostrum, because this passive immunization only improves resistance to one specific pathogen.

The common practice of not offering water to calves < 2 weeks old, in combination with feeding only a limited volume of milk, hampers the ability of calves with early stage diarrhea and mild dehydration to prevent further dehydration. Free access to clean water offered from a bucket or bowl improves the resilience of calves against overt dehydration from diarrhea. Calves are able to correct dehydration of up to 4% just by increasing the volume of water consumed in early stages of diarrhea (14).

Several of the agents that produce diarrhea in neonatal calves can also produce diarrheal disease in humans. Cryptosporidium parvum and Salmonella spp can produce serious disease, particularly in immunocompromised individuals. These organisms are commonly present as subclinical infections in the gut of calves and lambs, which emphasizes the importance of personal hygiene when handling calves. Immunocompromised humans should avoid contact with young ruminants and possibly all farm animals. (Learn more about cryptosporidiosis and salmonellosis in humans.)

Cattle, including calves, are one of the reservoirs for the verotoxic E coli serotype O157:H7 associated with human hemorrhagic colitis and the hemolytic uremic syndrome. Infection in humans is usually acquired by consumption of contaminated food; however, the infective dose is low, and the possibility of infection by direct contact exists. (Learn more about E coli O157:H7 gastroenteritis in humans.) Other verotoxic E coli serotypes associated with human disease can be isolated from the feces of healthy cattle.

Human disease from infection with enteric livestock pathogens has occurred after seemingly trivial contact associated with visits to livestock fairs, petting zoos, and farm educational tours. Hand cleansing and disinfection should be a component of these visits.

• Carter HSM, Renaud DL, Steele MA, Fischer-Tlustos AJ, Costa JHC. A narrative review on the unexplored potential of colostrum as a preventative treatment and therapy for diarrhea in neonatal dairy calves. Animals (Basel). 2021;11(8):2221.

• Holschbach CL, Peek SF. Salmonella in dairy cattle. Vet Clin North Am Food Anim Pract. 2018;34(1):133-154.

• Wyatt CR, Riggs MW, Fayer R. Cryptosporidiosis in neonatal calves. Vet Clin North Am Food Anim Pract. 2010;26(1):89-103.

• Learn more about cryptosporidiosis, salmonellosis, andE coli O157:H7 gastroenteritis in humans in the MSD Manual for medical professionals.

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