Small Strongyles

What you need to know

Probably now the most commonest parasite. Part of the lifecycle involves the larvae becoming ‘encysted’ (forming a protective membrane around themselves) in the gut wall. They may remain in this state for months or even years before suddenly all emerging together and causing severe illness with diarrhoea, weight loss or colic. If this ‘larval cyathostominosis’ is not prevented, the success rate for treatment is only about 50%. Unfortunately, the encysted larvae are well protected and very few drugs are able to remove this most important stage of the worm.

Effective wormer chemicals. Ivermectin, but not for encysted. Encysted worms Moxidectin and Fenbendazole.

More information

Many species in several genera of "small strongyles" are found in the cecum and colon. Most of them are appreciably smaller than the "large strongyles," but some (eg, Triodontophorus spp , which are sometimes classified as no migratory large strongyles) may be almost as large as Strongylus vulgaris . One species, T tenuicollis , produces rather severe ulcers in the wall of the colon. Small strongyles belong to the subfamily Cyathostominae of the family Strongylidae. Over 40 species of small strongyles have been described from domestic equids and ~10 species are known to be most prevalent. There is apparently no extra intestinal migration of the larvae in the host; larvae develop in the wall of the large intestine, where they may undergo hypobiosis and remain dormant over prolonged periods. Adult cyathostomes within the lumen of the large intestine are of minor clinical importance. It is common to recover thousands of adult cyathostomes from horses that have received limited anthelmintic treatment. Generally, 10% of adult cyathostomes reside in the cecum, and the rest are distributed in the dorsal and ventral colon; specific species of adult cyathostomes have site preferences within the dorsal or ventral colon. At necropsy, some adult cyathostomes are found at the ingesta-mucosal interface; the intestinal tract of the worm may contain plant material or ciliates. Many of the small strongyles feed superficially on the intestinal mucosa, while others may be attached to the mucosa by their buccal capsule. These worms emerge from the gut wall, suck a plug of mucosa into their buccal capsule, break up the mucosal plug, may eventually rupture capillaries, and ingest small quantities of blood. Generally, erosions of the mucosa by single adult cyathostomes is slight and hard to visualize; however, in heavy infections, disruption may be extensive enough to disturb digestive and absorptive function, resulting in a catarrhal enteritis of the large intestine. In temperate areas, an acute syndrome of diarrhoea and death in young ponies and horses in late winter and spring has been reported. This is associated with the mass emergence of larvae from the intestinal wall and may have some similarity to Type II ostertagiasis ( Haemonchus, Ostertagia, and Trichostrongylus spp) in young cattle. Somatic larvae of cyathostomes have been associated with a diarrhoeal syndrome in Europe. The syndrome occurs less commonly in the USA; verminous diarrhoea in horses has been reported in New York and Tennessee. Response to treatment is variable, and the condition is best prevented by a good parasite control program. For treatment and control, see large strongyles, Large Strongyles .

Horses with larval cyathostomiasis generally have a neutrophilia and
hypoalbuminemia. Hyperglobulinemia, particularly involving the _-globulin fraction described as characteristic in some reports, has been a less consistent finding. Eosinophilia is not a consistent finding. Often, free strongyle eggs are not seen on faecal examination. However, gross observation of fourth- or fifth-stage larvae, which are often bright red in colour, in the faeces is helpful in making a diagnosis. Biopsy of large intestine via laparotomy may assist in diagnosis; rectal biopsy is less reliable. Gross pathologic findings include typhilitis or colitis with mucosal hyperaemia, haemorrhage, congestion, ulceration, or necrosis; in protracted cases, there may be only mucosal thickening. Cyathostome larvae can be seen as small gray dots (1-2 mm) in the mucosa, giving it a gritty sensation on palpation. Transillumination of the mucosa from the serosal surface may aid in visualizing the larvae present in the mucosa.

Adult cyathostomes are easily removed from the gut lumen by anthelmintic treatment. Infection may be prevented by daily administration of pyrantel tartrate. A population of small strongyles has been described as cross-resistant to the benzimidazoles. Resistance is heritable and most likely not reversible. Treatments effective against benzimidazole-resistant populations include ivermectin, pyrantel salts, or mixtures of benzimidazole and piperazine. Drug efficacy and the presence of anthlemintic resistance may be determined by comparing the worm egg count at the time of treatment and 10-14 days later; an effective drug should reduce the egg count to 0 or to very low levels.

Somatic small strongyle larvae are much more difficult to effectively remove with anthelmintics. Horses with larval cyathostomiasis may not respond to treatment if submucosal inflammation is too severe. Treatment with large doses of fenbendazole (10 mg/kg for 5 consecutive days) has been reported as effective. Ivermectin has been used with mixed results; lack of efficacy has been reported at label dosages as well as at higher dosages. Corticosteroid therapy, in addition to anthelmintics, has also benefited some horses with somatic small strongyle disease.