Cyathostomins, also termed small strongyles or small red worms, are considered the most prevalent and important equine intestinal parasite. The increasing prevalence of cyathostomins, widespread anthelmintic resistance, and difficulty preventing and treating larval cyathostominosis pose significant challenges for veterinarians.
Cyathostomins comprise over 50 species of small strongyles. Their life cycle is direct and does not involve an intermediate host or extraintestinal migration. The minimum prepatent period is 5 weeks. Adult cyathostomins, located predominantly in the colon and cecum, produce large numbers of eggs, which account for almost all of the strongyle eggs in equine feces. Eggs hatch and develop on pasture, through L1 and L2 stages to the infective L3 stage. L3 acquire a protective sheath which facilitates prolonged survival on pasture, even in freezing conditions, although survival is reduced by hot and dry weather. Ingested L3 penetrate the mucosa and submucosa of the cecum and colon. A small proportion of L3 develop into L4 without interruption, while it is thought that, in some individuals, up to 90% undergo prolonged periods (measured up to 3 years) of inhibited development as encysted early L3. In temperate climates most larvae undergo inhibition in winter, while in tropical climates this may occur in summer. Clinical disease, termed acute larval cyathostominosis, results from en masse ingress or emergence of large numbers (millions) of previously encysted larvae as L4, typically in the fall, winter, or early spring. The host inflammatory response to migrating larvae causes colitis and typhlitis. Water, electrolytes, and proteins leak into the intestinal lumen, and luminal endotoxins are absorbed systemically. Hypoproteinemia may cause peripheral and intestinal edema. Dysmotility and inflammation of the large intestine may cause severe colic. Death may result from hypovolemic and endotoxic shock. Luminal adult cyathostomins (620 mm long) may cause catarrhal colitis, with resultant lethargy, weight loss, and diarrhea, but typically only in young naive horses that have heavy burdens. Cyathostomins may also cause nonspecific colic, nonstrangulated intestinal infarction, granulomatous colitis, cecal tympany, and cecocolic or cecocecal intussusceptions.
All ages can be infested, although young (<5 years old) and geriatric horses are more susceptible. Larval cyathostominosis is more common in young horses.
Other causes of diarrhea including Clostridium difficile, Clostridium perfringens, salmonellosis, and proliferative enteropathy should be considered.
While hypoalbuminemia, hyperglobulinemia, particularly involving the β-globulin fraction, increased acute phase proteins, increased serum alkaline phosphatase, neutrophilia, and microcytic anemia are common, none of these findings is specific for cyathostominosis. Systemic eosinophilia is uncommon.
Histologic examination of rectal mucosal biopsies or biopsies of the large intestine and cecum may identify larvae and/or the associated inflammatory response. Abdominocentesis and fecal culture may aid evaluation of other differential diagnoses.
Abdominal ultrasonography may identify mural edema and thickening of the colon and cecum, liquid colonic and cecal contents, and possibly ascites.
A high suspicion of larval cyathostominosis may be obtained from typical clinical signs, signalment, and history. Confirmation is made by gross observation of large numbers of small red L4 and L5 larvae in feces or on the sleeve used to perform a per rectum examination. To aid detection of larvae, feces can be diluted (1:10 in water) and examined under a microscope × 10. Fecal egg counting is unreliable for diagnosis of larval cyathostominosis; indeed counts are often negative because the infestation may comprise primarily immature larvae.
Large burdens of adult parasites in horses with ill thrift may be evidenced by a high fecal strongyle egg count. Fecal strongyle egg counts are also an essential component of a targeted worming program.
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