Bacterial Diarrhea in Foals

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.