- Sep 1, 1997
In the past, the world of equine parasitology was not concerned about small strongyles, also known as cyathostomes. However, veterinarians and horse owners were much more wary of the large strongyles, and in particular Strongylus vulgaris. Indeed, the migrating larvae of S. vulgaris can be very destructive in the arteries of horses and ponies, leading to colic and in severe cases, death.
A number of anthelmintics that are highly effective against the large strongyles, including the migratory larvae, have been available for several years. The modern dewormers, along with well-designed parasite control programs, have resulted in a vastly lowered incidence of large strongyles, according to scientific surveys based on fecal egg counts and necropsy findings. Now, a major focus of research in equine parasitology is on the small strongyles and a disease caused by this group of helminths called larval cyathostomosis, previously referred to as larval cyanthostomiasis.
To better understand this disease and how to control it, it is necessary to describe the life cycle of cyathostomes and the clinical syndrome caused by the larvae of this group of parasites.
Life Cycle Of Small Strongyles
The cyathostomes comprise approximately 40 different species that live in the colon and cecum of horses and ponies. The incidence of small strongyle infection is very high; they are the predominant parasite of grazing horses, and it is not unusual to find thousands of these worms in a horse. The adult parasites lay eggs that are passed in the feces. Once in the environment, the eggs hatch into larvae. This process proceeds quickly when ambient temperatures are warm and adequate moisture is available.
Under favorable conditions, the larvae develop into the third stage (L3)--the stage that is infective to the horse. Third-stage larvae attach to vegetation and are ingested by the grazing horse. The swallowed larvae penetrate the walls of the large intestine and migrate to the mucosa and submucosa of the large colon and cecum. In this location, the larvae become encysted (like a cocoon around a caterpillar).
At this point, two distinctly different alternative pathways can occur: In the first alternative, the L3 will continue to develop into fourth stage (L4) larvae within the cysts, or the L3 can enter a period of arrested development. In the first alternative where development is not inhibited, the larvae spend approximately one to two months in the intestinal wall, then return to the lumen of the large colon and cecum as L4. There they further develop into mature, egg-laying adults to complete the life cycle.
The variable time of residence in the cystic stage might be due to biological differences among the approximately 40 different species of small strongyles.
In the second alternative, where larval development enters an arrested state, it is important to remember that this phenomenon occurs when the larvae are in their early third stage (EL3). The duration of arrested development can persist for prolonged periods--as long as a year or more.
Two different theories have been offered to explain why the development of cyatho-stome EL3 becomes inhibited and at some later date the larvae become active and resume development. One explanation is based on the premise that in some way the larvae are signaled that upcoming climatic conditions will become adverse for survival of the larvae in the environment, which leads to hypobiosis (a form of arrested development). This situation would occur in late fall or early winter in the northern United States. Later in the winter or early spring, the arrested larvae receive a signal that the climate is changing to a stage favorable for their survival, and development is resumed. This scenario is very much like that of Ostertagia ostertagi, the cattle brown stomach worm whose life cycle has been mapped out in detail by scientific research.
Another possible explanation is based on population dynamics of the late stage larvae and adult worms in the intestinal lumen. When there is a large number of worms in the horse--such as at the end of the grazing season in the fall--the arrest signal is received by the encysted larvae. In late winter or early spring, when the adult worm population in the horse has declined, another stimulus results in resumption of development by the encysted larvae. In reality, it might be a combination of both of these situations that causes the arrest of larvae development, then reactivation.
Regardless of the cause, large numbers of arrested cyathostome larvae synchronously resume development, leave the cysts en masse, and return to the intestinal lumen. This migration can involve from thousands up to a million or more larvae, and it causes severe damage to the intestinal mucosa resulting in the clinical symptoms of larval cyathostomosis, which will be described later in this article.
It is important to note that the occurrence of this parasitic disease is reported to transpire from approximately November to May in the northern temperate zones of Europe and the United States, compatible with the scenario discussed above. Another important consideration is that at any given point during this late fall to early spring period, there very likely will be a mixed population of cyathostomes in the horse, consisting of arrested early L3, developing L3, and L4 in the intestinal wall as well as larval and adult worms in the lumen of the intestine. Using a dewormer that has a high degree of activity against all the stages of cyathostomes is critical to the success of controlling larval cyathostomosis.
Signs Of Larval Cyathostomosis
The true evidence of larval cyathostomosis is unknown, but increasingly the disease is being reported from Europe and the United States. Several reports indicate that the disease occurs in grazing horses even though regular deworming programs have been employed. Routine deworming with available products at standard doses has only minimal effect on the encysted larvae. Also, larvae that are picked up between dewormings enter the intestinal mucosa and accumulate there.
Diagnosis of larval cyathostomosis is very difficult because there are no specific diagnostic tests, although certain serum analyses can provide clues. In published reports of the disease, the diagnosis has been made at necropsy or on the basis of finding cyathostome larvae in the feces. Strongyle eggs are not found in the feces because the horses often have been dewormed, leading to removal of the adult worms. The disease, however, is caused by immature parasites that are not laying eggs.
Because small stron-gyle infections are so common in horses and ponies, the potential for larval cyathostomosis to occur can be assumed to be quite high.
As a result of the damage caused by the larvae synchronously emerging from the mucosal cysts, the affected horse or pony will experience a sudden onset of diarrhea, which may become chronic; weight loss is rapid and dramatic, even though feed and water intake typically remain normal. The animal becomes weakened, but usually not depressed. A low-grade colic can occur that tends to be intermittent. Death can occur in more severe cases. Edema of the limbs and ventral abdomen might develop associated with lowered serum protein levels.
With milder cases, the clinical manifestation can be an unexplained weight loss during the winter, with or without ventral edema. In very mild cases, the only symptom observed in competitive horses might be a less-than-expected performance level; otherwise, the animal appears normal.
Control Of Larval Cyathostomosis
Because of the sudden onset of clinical symptoms and the potential for a fatal outcome, considering the disease occurs quite predictably in the late fall to early spring months (at least in the northern temperate zone, this timing might need some adjustment in the southern zone), and because treatment of the acute disease is frequently unsatisfactory, it seems reasonable to prevent larval cyathostomosis rather than attempting to treat the disease after the onset of symptoms.
As mentioned above, it is important to select anthemintics that have a high degree of efficacy against the arrested (EL3) and developing (LL3/L4) larvae in the intestinal wall in order to control larval cyath-ostomosis successfully.
Based on available scientific reports, it appears that the avermectins and fenbendazole (Panacur/SafeGuard) have activity against strongyle larvae. Of the avermectins, ivermectin (Eqvalan) is labeled for control of tissue (migratory) stages of Strongylus vulgaris and S. edentatus, as well as fourth-stage cyathostome larvae, but not the tissue stages.
Moxidectin (Quest), which has been available in some other parts of the world with label claims to control late (developing) encysted stages of small stron-gyle larvae, now is available in the United States. Fenbendazole is labeled in the United States for removal of fourth-stage larvae of S. vulgaris at the laricidal dose of 10mg/kg body weight daily for five days. In Europe, the United Kingdom, and Ireland, fenbendazole is labeled for removal of fourth-stage S. vulgaris larvae as well as early-inhibited and later-encysted mucosal cyathostome larvae ata daily dose of 7.5mg/kg body weightfor five days.
Tables 1 through 3 list the summary results of controlled efficacy studies. In these studies, the test drugs were compared to untreated controls and
larvae/worm counts were made at necropsy. The following abbreviations are used in these Tables: EL3=early third-stage cyathostome larvae (the stage that is known to become arrested); LL3/L4=late third-stage and fourth-stage larvae that are developing.
Table 1 shows a summary of six published studies where ivermectin was evaluated for efficacy against the mucosal and lumenal stages of cyathostomes. All but one of these studies, Love (1995), utilized natural infections of small strongyles. The results show that the labeled dose (0.2 mg/kg) and five times the labeled dose had limited efficacy (0-10% reduction) of the EL3 in the mucosa. The EL3 and LL3/L4 were not differentiated in the two studies that used the higher doses of ivermectin, Klei (1993) and Lyons (1994), but the reported reductions of 35% and 42%, respectively, indicate only limited efficacy. The one study reported by Love (1995) showed a reduction of LL3/L4 by 77%, which were thought to be in the EL3 stage (but not inhibited) at the time of the treatment.
The difference in the results of this study compared to the other five studies is likely to have been due to the use of artificial rather than natural infections and/or the ponies used in the Love study were younger than those used by the other investigators and the younger ponies had no previous exposure to cyathostome infections.
While removal of larvae and adult cyathostomes in the intestinal lumen was mainly highly efficacious, the limited activity demonstrated against the mucosal larvae would not make ivermectin the drug of choice to prevent larval cyathostomosis in equines.
Table 2 summarizes the results of five studies with moxidectin used at doses ranging from 0.2 to 0.5 mg/kg body weight. In three of these studies, the mucosal larvae were differentiated and showed that variable efficacy against the EL3 (0-81%) and LL3/L4 (0-92%) was obtained. Interestingly, the results against the mucosal larvae were not related to dosage level.
Results reported by DiPietro (1992) and Bello (1994) did not differentiate the EL3 from the LL3/L4 stages; therefore, efficacy against the EL3 cannot be deduced. The results of DiPietro (1992) were somewhat different depending on the method used to recover and identify larvae. Reduction of the lumenal larvae and adult cyathostomes was in the high 90% to 100% range, but the variability against the mucosal stages would not make moxidectin the ideal drug to use for prevention of larval cyathostomosis in equines.
Results of six studies with larvicidal doses of fenbendazole are summarized in Table 3. In his first study, Duncan (1977) used single, elevated doses of fenbendazole against developing mucosal stages of cyathostomes and found increasing efficacy with higher doses. Subsequent work showed the larvicidal activity of fenbendazole was enhanced when lower doses were administered daily over a five-day period.
The remainder of the studies in Table 1 employed the five-day regime with either the European daily dose of 7.5mg/kg or the United States daily dose of 10 mg/kg. In Duncan's second study (1980), as well as the studies by Abbott (1993) and Lyons (1994), there was no differentiation made between EL3 and LL3/L4 stages.
The horses used in the Abbott (1993) study originated in a herd where benzimidazole-resistant small strongyles had been confirmed. There might be a biological difference in the larvae and adult resistant cyathostomes as demonstrated by the reduction of larvae by 91% and the adults by 80%.
Of the five studies that utilized the multiple-day dosage of fenbendazole, only one reported efficacy against mucosal larvae of less than 90%; Lyons (1994) reported a reduction of 80%, but the investigator stated, "that all larvae found were considered alive so as not to overestimate the efficacy, obviously some of these larvae were dead or dying."
In the study reported by Abbott (1996), 92% of the EL3 and 96-99+% of the developing larvae were removed with fenbendazole. The 1997 study results are pooled from three locations (DiPietro, Illinois; Klei, Louisiana; Reinemyer, Tennessee) all using the same protocol. Excellent efficacy of 98% reduction of EL3 and 92-96% reduction LL3/L4 was achieved, depending on the method of recovery. The mean numbers of EL3 found in the untreated control animals in this trial were 5535.5 compared to 1821.7 of LL3/L4. This emphasizes the importance of selecting a product that has uniformly high efficacy against all the mucosal stages of cyathostomes. Based on the results of the studies summarized in Tables 1 to 3, the larvicidal dose of fenbendazole would be preferred treatment to prevent larval cyathostomosis.
About the Author
John Paul, DVM, MS, is a career-long parasite researcher and American Association of Equine Practioners member of 28 years.
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