Colic and Endotoxic Shock in Horse Secondary to Strongylus Parasitism

History. A 1-year-old Standardbred filly is brought to your clinic by its new owner because the horse has been restless, rolling, kicking at its belly, and pawing the ground. The owner reports that the horse has had a poor appetite for several days and now refuses both hay and grain.

Clinical Examination. The horse is underweight and has a dull hair coat. It is obvious that she is in pain. Physical examination reveals an abnormally high temperature (103.5^o F), rapid labored breathing (40 breaths/min), and an elevated heart rate (80 beats/min). AU limbs feel cool to the touch. The mucous membranes are abnormally dark, and the capillary refill time is prolonged (both these observations indicate sluggish circula­tion). Gastrointestinal auscultation of all four quadrants yields abnormal findings; no abdominal sounds are heard on either the left or the right side, dorsally or ventrally. A rectal exam­ination reveals several distended loops of bowel.

You perform abdominocentesis and withdraw some peri­toneal fluid. Normally, peritoneal fluid is clear and straw colored; the fluid from this horse is darker yellow than normal and has a turbid appearance. Measurements with a refrac­tometer indicate that the peritoneal fluid contains five times more protein than normal. Microscopic examination of the fluid reveals the presence of four times the normal number of WBCs, specifically neutrophils, and the cells contain bacteria.

Outcome. You tell the owner that the filly appears to have a badly damaged bowel and that the prognosis is poor. You inform him that surgical treatment is possible, but expensive postoperative complications are likely because infection appears to have spread into the peritoneum. After considering the options, the owner decides against surgery.

The horse’s condition deteriorates over the next 12 hours. The heart rate increases progressively to IOO beats/min. The mucous membranes show evidence of declining blood flow (darker color and longer capillary refill time). The horse begins to wheeze and becomes lethargic. Bowel sounds continue to be absent. Despite the delivery of IV fluids, there is no output of urine. With the owner’s consent, you euthanize the horse.

Necropsy examination indicates that this horse had thrombi (vascular obstructions) in several major branches of her mesen­teric arteries, probably secondary to a severe infestation of bloodworms (Strongylus vulgaris). Several areas of the intestine were necrotic. Gram-negative bacteria were cultured from both the peritoneal fluid and the blood. The lungs were edematous, and excessive fluid was found in the airways and intrapleural space.

Comment. In horses, S. vulgaris lodges in mesenteric arteries and decreases the blood flow to the intestine. Deworming a severely infested horse can precipitate acute intestinal ischemia, because the worms break away from the walls of major mesen­teric arteries and drift into smaller arteries, which they occlude. Also, the dying worms release substances that trigger the formation of blood clots in the arteries. Digestive processes become disrupted and may cease entirely. Intestinal ischemia and gaseous distention of the bowel cause severe pain. With persistent ischemia, segments of the bowel become perma­nently damaged (infarcted). Ischemic damage to the intestinal epithelium allows intestinal bacteria and bacterial products (endotoxins) to enter the peritoneum and the blood. WBCs move from the bloodstream into the peritoneal fluid, where they combat the bacteria by engulfing them (phagocytosis). However, the infection overwhelms the immune system. Bac­teria and endotoxins (from gram-negative bacteria) cause the body to produce substances that depress the heart and disrupt the capillary endothelium, especially in the lungs. The result­ant combination of heart failure and pulmonary edema leads to respiratory failure and subsequent renal failure. The progres­sion of dysfunction becomes irreversible.