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Bacterial Diarrhea in Foals


Allison J. Stewart

, BVSC (Hons), MS, DACVIM-LA, DACVECC, MANZCVS, PhD, The University of Queensland

Last full review/revision Sep 2013 | Content last modified Sep 2022

Bacterial enterocolitis in neonatal foals can be a component of neonatal septicemia, and diarrhea can be seen with bacteremia of any cause. Organisms commonly involved in neonatal bacteremia and subsequent diarrhea in neonatal foals include Salmonella spp, Escherichia coli, and Actinobacillus spp. Although E coli is the most important mediator of systemic sepsis in newborn foals, it is not as common as a primary cause of diarrhea in foals as it is in calves and piglets.

Intensive antimicrobial treatment, correction of fluid loss and electrolyte abnormalities, and nursing care are needed. Foals should be evaluated to determine whether adequate passive transfer of colostral antibodies has occurred; if not, a plasma transfusion is indicated. (Also see Sepsis in Foals Sepsis in Foals Sepsis is a clinical syndrome defined by the development of a systemic inflammatory response syndrome (SIRS) in response to proven or suspected infection. The condition implies an extensive... read more .) Markedly hypoproteinemic foals will benefit from plasma transfusion and/or the administration of a plasma substitute such as hetastarch to improve oncotic pressure. IV fluid treatment without correction of the severe hypoproteinemia may induce pulmonary or peripheral edema.

An acute, fulminant, hemorrhagic diarrhea syndrome with high mortality in young foals <10 days old and commonly <3 days old has been associated with Clostridium perfringens type C infection ( see Clostridia-associated Enterocolitis in Horses Clostridia-associated Enterocolitis in Horses Clostridium difficile and C perfringens are common causes of enterocolitis in horses and foals. Antimicrobial administration has been associated with C difficile diarrhea... read more ). Enterocolitis has also been associated with C perfringens type A with or without β2 toxin gene. The significance of this association is less clear than with type C, because type A has been identified in the feces in >90% of healthy neonatal foals in a farm-based study. It is possible that the number of bacteria and the phase of growth predispose to disease from type A. Infections may be sporadic or seen as outbreaks in multiple foals on a farm. Severe lethargy and rapid deterioration of cardiovascular status is followed by death in 24–48 hr in many cases. Intraluminal hemorrhage and extensive mucosal necrosis of the small intestine and, in some cases, the colon are found on necropsy.

Other bacteria that have been associated with diarrhea in foals are Bacteroides fragilis, C difficile ( see Clostridia-associated Enterocolitis in Horses Clostridia-associated Enterocolitis in Horses Clostridium difficile and C perfringens are common causes of enterocolitis in horses and foals. Antimicrobial administration has been associated with C difficile diarrhea... read more ), Aeromonas hydrophila, and Rhodococcus equi. Although R equi primarily causes respiratory disease ( see Rhodococcus equi Pneumonia in Foals Rhodococcus equi Pneumonia in Foals Rhodococcus equi is the most serious cause of pneumonia in foals 1–4 mo old. It is not the most common cause of pneumonia in this age group; however, it has significant economic consequences... read more ), both acute and chronic enteritis can cause diarrhea in foals 1–4 mo old. The diagnosis is more straightforward if pneumonia is also present. When cultured from tracheal wash fluid, R equi is considered a pathogen; however, a positive fecal culture is not as helpful because R equi can be found in the feces of healthy foals. Clarithromycin combined with rifampin is the treatment of choice for R equi infection in foals. Other macrolides such as azithromycin or erythromycin can be used, but erythromycin can predispose to diarrhea and hyperthermia.

Equine Proliferative Enteropathy

Enteric infection with Lawsonia intracellularis causes proliferative enteropathy, resulting in outbreaks of diarrhea, rapid weight loss, colic, lethargy, subcutaneous edema, and protein-losing enteropathy in weanling foals. Lawsonia has a worldwide distribution and can affect many other species, including pigs, rodents, and ratites; it can survive in the environment for 2 wk, and a fecal-oral route of infection is speculated. L intracellularis enters the enterocytes, avoiding lysosomal destruction. Infected cells continue to divide, resulting in hyperplastic crypts of immature epithelial cells that have a poorly developed brush border, leading to decreased enzymatic activity and absorptive function. Decreased disaccharide activity results in maldigestion with subsequent overload of carbohydrates to the large colon and osmotic diarrhea. Hypoproteinemia results from a combination of malabsorption of amino acids and increased small-intestinal permeability and leads to low plasma oncotic pressure and subsequent ventral edema. Maldigestion and absorption of nutrients and protein-losing enteropathy result in weight loss and failure to thrive.

Affected foals range from 3–12 mo old, but those 4–6 mo old are most commonly infected. Stress may be a predisposing factor. Because of their debilitated state, infected foals are predisposed to secondary GI, skin, and respiratory infections. Morbidity and mortality rates are low if animals are treated appropriately, although sudden death has been reported. Marked hypoproteinemia (<4 mg/dL) with hypoalbuminemia (<1.5 g/dL) are the most common laboratory findings. The WBC count and fibrinogen concentrations tend to be normal to moderately increased. Anemia, hyponatremia, hypochloremia, and hypocalcemia may be seen. CK concentration is often mildly increased.

Diagnosis can be confirmed at necropsy with characteristic intracellular bacteria observed in silver-stained tissues. L intracellularis can be confirmed using PCR analysis and immunohistochemistry on tissues collected at necropsy. Because Lawsonia is an intracellular organism, it does not grow on standard microbiologic culture media, and permissive cell lines are required for isolation. PCR can be used to detect L intracellularis DNA in feces, but false-negative results can occur. Serology to detect antibodies to L intracellularis is more sensitive than fecal PCR, but discrimination between infected foals and exposed foals can be difficult. Indirect fluorescent antibody test and immunoperoxidase monolayer antibody tests are currently the best serologic tests available. An ELISA is also available. Both fecal PCR and serologic testing are recommended. If either test is positive in the presence of hypoproteinemia, then treatment is warranted. Foals can remain seropositive for 6 mo after clinical signs resolve. Frequently, transabdominal ultrasonography reveals a markedly thickened small-intestine wall.

Differential diagnoses for proliferative enteropathy include salmonellosis, clostridiosis, Neorickettsia risticii, R equi, parasitic infections, and any cause of infiltrative/inflammatory bowel disease. Response to treatment is considered confirmation of the diagnosis. Lack of response to therapy after 7–10 days should prompt reassessment of the diagnosis.

Lawsonia is an intracellular pathogen, so antimicrobials must be lipophilic or amphoteric to concentrate within the host cytoplasm. Treatment with oxytetracycline (6.6 mg/kg, IV, bid for 3–7 days) followed by doxycycline (10 mg/kg, bid for 14 days) has been successful. Mild cases respond to oral doxycycline alone. Alternatives include erythromycin (alone or in combination with rifampin) for 3–4 wk or chloramphenicol. Plasma transfusions are required only in the most severely affected foals. Glucocorticoids are not recommended. Response to therapy is indicated by improvement in attitude, appetite, and weight gain. Resolution of hypoproteinemia may take 4–5 wk and small-intestinal thickening 4–8 wk. With treatment, ~90% of foals usually survive.

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