Impaired Intestinal Absorption of Glucose in 4 Foals withLawsonia intracellularisInfection

Abstract

F our weanling foals (age range 4-8 months) were examined because of a history of diarrhea (4/4 foals), lethargy (3/4), decreased appetite (2/4), fever (2/4), weight loss (2/4), and prolonged recumbency (1/4). A presumptive diagnosis of proliferative enteropathy associated with Lawsonia intracellularis was based on clinical signs (4/4 diarrhea, 3/4 poor body condition, 3/4 dehydration, 2/4 generalized weakness, and 1/4 ventral edema), characteristic clinicopathologic abnormalities (4/4 hypoproteinemia [serum total protein o5. , and ultrasonographic appearance of thickened small intestine (3/4). Confirmation of Lawsonia sp. infection was provided by positive fecal PCR (4/4) and high serum titer (2/4; titer 1 : 240) for the causative organism. Foals were treated with antimicrobials (2/4 clarithromycin, 2/4 oxytetracycline, and 1/4 erythromycin), plasma transfusions (4/4), synthetic colloids a (4/4), isotonic fluid therapy b (4/4), parenteral nutrition (2/4), and general supportive care. All foals survived to discharge although 2/4 foals were later reported to be smaller than similar-aged foals. Based on distinctive pathologic findings of small intestinal thickening that occurs with proliferative enteropathy in foals, 1-3 we were interested in the serial evaluation of intestinal absorption of glucose as a surrogate for small intestinal absorptive capacity in these 4 foals using an oral glucose absorption test (OGAT).OGAT was performed in the same manner in all foals by withholding feed for a 10-hour period, followed by administration of 1 g dextrose/kg body weight via nasogastric tube as a 20% solution in water. Blood was collected before and every 30 minutes for 240 minutes after dextrose administration. Blood was placed into heparinzed glass tubes, plasma was separated by centrifugation, and plasma glucose concentrations were determined by an automated chemistry analyzer.c Informed client consent was obtained in all cases. In foal 1, an OGAT was performed on day 1 which revealed complete small intestinal malabsorption of glucose (Fig 1). The foal was hospitalized and on day 8, slight improvement of glucose absorption was observed on repeat OGAT. The foal was discharged at this time but returned for re-examination 15, 29, 36, and 58 days after initial presentation for repeat OGAT and evaluation of serum albumin and total protein concentrations ( Table 1). The OGAT on day 15 demonstrated improvement, yet still abnormal, small intestinal absorption of glucose compared with day 1. The OGAT on day 29 demonstrated a delayed peak glucose concentration suggesting delayed gastric emptying or increased intestinal transit time. Ultrasonographic examination of the abdominal cavity at this time revealed normal small intestinal wall thickness. The OGAT on days 36 and 58 demonstrated partial return of small intestinal absorption with peak plasma glucose concentrations 60-90 minutes after dextrose administration. The serum total protein and albumin concentrations progressively increased over the 58-day period but albumin concent...

Lawsonia intracellularis infection and proliferative enteropathy in foals

“…The exact mechanisms by which hypoalbuminemia develops in affected foals has not been investigated. It appears that a combination of decreased feed intake, coupled with malabsorption and protein-losing enteropathy due to the proliferative nature of the disease may represent likely mechanisms by which low albumin occurs (Wong et al, 2009). Affected foals may also demonstrate non-specific blood abnormalities such as anemia or hemoconcentration, leukocytosis or neutropenia, hyperfibrinogenemia, increased activity of muscle enzymes and electrolyte abnormalities (hypocalcemia, hypochloremia and hyponatremia).…”

Equine proliferative enteropathy – a review of recent developments

“…The exact mechanisms by which hypoalbuminaemia develops in affected foals has not been investigated. It appears that a combination of decreased feed intake, coupled with malabsorption and protein‐losing enteropathy due to the proliferative nature of the disease may represent likely mechanisms by which low albumin occurs . Experimentally infected hamsters had significantly lower intestinal absorption of glucose, potassium and chloride, suggesting that malabsorption is the main mechanism involved in the physiopathology of the diarrhoea in L. intracellularis ‐infected animals .…”

Lawsonia intracellularis proliferative enteropathy in a 3.5‐year‐old miniature horse

“…Although an oral glucose absorption test was not performed on the gelding in this case report, it has been reported in foals with L. intracellularis (Wong et al . ). While receiving enteral nutrition as well as intravenous dextrose solution during hospitalisation, the patient's glucose decreased to as low as 2.3 mmol/l.…”

“…; Frazer ; Wong et al . ). After initial fluid resuscitation, the horse developed a moderate amount of ventral oedema, which has been previously reported secondary to infection with L. intracellularis , as well as other protein losing enteropathies (Lavoie et al .…”