Controlling internal parasites in horses

Vet Times The website for the veterinary profession https://www.vettimes.co.uk Controlling internal parasites in horses Author : Kevin Corley Categories : Vets Date : November 29, 2010 Kevin Corley discusses major afflictions affecting equines, including tapeworms and ascarids, and looks at the different treatment regimens available VIRTUALLY all horses, especially those exposed to pasture, continuously experience some level of parasitism 1. Gastrointestinal parasitism is the most common type of infection found in horses and can be subclinical or result in one or several of the following symptoms: weight loss, diarrhoea, colic, ventral abdominal oedema, pyrexia, inappetence or poor body condition 2-6. Migration of these mainly gastrointestinal parasites through other body organs can result in organ damage and associated symptoms 7, 8. Some parasites are not chiefly associated with the gastrointestinal tract, such as lungworm (which can also result in cough and increased respiratory effort) 9 and liver fluke (which can result in weight loss, variable-to-poor appetite and decreased performance) 10. Major horse parasites Cyathostomiasis Cyathostomes ( Figure 1 ), or small strongyles, are the most important intestinal horse parasites, based on prevalence and pathogenic potential. More than 50 species of cyathostomes are known, of which at least 10 are found in horses 11. 1 / 13

The most common clinical sign of cyathostomiasis is weight loss 12. Other clinical signs can include pyrexia, ventral oedema and diarrhoea ( Figure 2 ), which can result in the death of the animal 12-15. Larval cyathostomes have been implicated in cases of caecocaecal and caecocolic intussusception 15. Laboratory signs of infection include hypoalbuminaemia, hyperglobulinaemia and neutrophilia 12. However, none of these laboratory findings are invariably present. Clinical cyathostomosis occurs more commonly in young horses in late winter to early spring. However, lifelong susceptibility to cyathostomes is apparent, and they can cause clinical disease in any age of horse, during any season 12. Cyathostomes are more commonly found on stud farms than in riding schools, and in yearlings rather than in older or younger horses 16. Over the past several years, cyathostomes have become much more clinically important. This is largely because treatment and prevention strategies aimed at large strongyles, while successful, have inadvertently led to the selection of anthelminticresistant cyathostomes 17. The majority of clinical intestinal parasitism cases that reach the author s referral hospital are cyathostomiasis. Tapeworms Anoplocephala perfoliata is the major tapeworm in horses. Anoplocephala magna and Paranoplocephala mamillana are less commonly found. Horses may act as intermediate hosts for other tapeworm species, such as Echinococcus granulosus equinuus 18. Originally thought to be of little pathological significance 18, much current evidence links A perfoliatawith colic, especially ileal impactions 4, 5, spasmodic colic 5, caecal intussusception 19 and colic in general 3. The major pathology associated with A perfoliata is at the ileocaecal junction, where mucosal and submucosal lesions, hypertrophy of the circular muscle layer and damage to the enteric nervous system can be found 20. Large strongyles Strongylus vulgaris is the bestknown of the large strongyles. Horses ingest third-stage larvae (L3) from the environment. The larvae exsheath after passing through the stomach and invade the submucosa of the small 2 / 13

intestine, where they moult to the fourth larval stage (L4) 8. Larvae in the submucosa cause oedema and a marked dilatation of arteries, veins and capillaries, with local haemorrhage. The L4 larvae can be found in the arterioles one week after ingestion of L3 larvae 8. The L4 larvae then migrate to the root of the cranial mesenteric artery, where they moult to L5 larvae. These L5 larvae ultimately return to the caecum by way of the bloodstream and form large nodules in the submucosa, which eventually rupture. The larvae return to the gastrointestinal tract as young adults. After a further six weeks, they become sexually mature and the females begin to shed eggs. It takes approximately six to seven months from the horse s ingestion of L3 larvae to production of eggs by the adult strongyles 1. The main pathology associated with S vulgaris is damage to the arteries and arterioles, particularly to the cranial mesenteric artery 1. The damage has been termed verminous aneurysm, although thinning of the arterial wall is not a feature 8 perhaps verminous arteritis is a more accurate term 1. These lesions can result in colic. The most consistent sign is intermittent colic, with horses often showing sweating and rolling as clear manifestations of abdominal pain 1, 21. Horses are often febrile and depressed, with elevated heart rates and hypermotility of the intestines. Death is a common outcome in many cases 22, and infection with more than 750 infective larvae is invariably fatal 1. Larval migration can also cause ulceration of the colon and caecum, resulting in diarrhoea 23. S edentatus and S equinus are the other two large strongyles in horses 18. They both have a similar life cycle to S vulgaris, but with migration of L3 or L4 stages to the liver rather than the arterioles 18. These strongyles result in clinical signs much less frequently than S vulgaris. In an experimental study, inoculation of pony foals with a large number (15,000) of infective S equinus larvae resulted in diarrhoea 12 weeks after inoculation, and increased blood eosinophil counts and globulin concentrations 24. After experimental infection with S edentatus, no clinical signs attributable to the infestation were observed, but four out of six ponies had increased blood eosinophil counts 25. For both S equinus and S edentatus, the migrating larvae can cause significant tissue damage 25, 26. Large strongyles are now found infrequently in western Europe and the USA 17, 27-29 but remain a significant problem in some other countries. In Poland, S vulgaris was found in 80 per cent of 41 working horses from southern Poland 30. A study in Iran found S edentatus in 22.6 per cent, S equinus in 18.5 per cent and S vulgaris in 6.5 per cent of working horses in the northwest region 31. Ascarids 3 / 13

Parascaris equorum eggs containing L2 larvae infect the host after ingestion. After hatching, the larvae migrate to the lungs, up the bronchi and trachea, and are swallowed. They then return to the small intestine 18. The major clinical signs of ascarids in horses are associated with the intestinal phases. They can cause poor growth, anorexia, dull coat and dullness 18, 32. The adults ( Figure 3 ) can cause physical blockage of the small intestine, resulting in colic 33. The migration of larvae through the lungs has also been associated with clinical signs, and can result in coughing 32 and nasal discharge 18. Strongyloides westeri Strongyloides westeri L3 larvae enter the host horse by skin penetration or ingestion, and subsequent migration via the venous system 18. They develop into adult worms in the small intestine. Arrested larvae can remobilise immediately after birth, and migrate from the ventral abdominal wall of the dam to the mammary gland, where they can be excreted in the milk. Therefore, foals can become infected at a very young age 18. In most cases, few or no clinical signs are associated with S westeri infection. In very young animals, diarrhoea, weight loss, anorexia, dullness and reduced growth rate can occur 18. S westeri eggs were found in 1.5 per cent of foal faecal samples in one study in Kentucky, USA 34. Bots The most common bots are Gasterophilus intestinalis ( Figure 4 ), for which the eggs are laid on the hair of the legs and shoulders of the horse, and G nasalis and G haemorrhoidalis, where the eggs are laid around the intermandibular area and around the lips, respectively 18. Once these eggs hatch, larvae either crawl into the mouth or are transferred to the mouth by licking. After penetrating the tongue, they wander in this tissue for several weeks before passing via the oesophagus to the stomach. Larvae stay in this site for 101 to 102 months before being passed out in the faeces 18. Although usually considered benign, reports of perforation of the stomach wall are associated with Gasterophilus infection 35. Furthermore, aberrant migration of the larvae can occur one reported case resulted in colonic perforation and severe septic peritonitis 36. Oxyuris equi 4 / 13

Oxyuris equi (pinworms) are less commonly identified than small strongyles and ascarids 37. The eggs are ingested, and the third-stage larvae develop in the mucosal crypts of the caecum and colon 1. It is possible that they cause local mucosal irritation during this stage, but no clinical syndrome has been ascribed to this. The adult pinworms do not feed on the colonic mucosa, so no gastrointestinal pathology is expected from the adult stages 1. Oxyuris eggs are laid on the perianal skin. These can cause irritation, resulting in horses self-traumatising the tail-head and hindquarters. Lungworm Dictyocaulus arnf ieldi are ingested as L3 larvae. They moult to L4 larvae in the draining lymph nodes of the intestine and migrate to the lungs. Adult worms in the lungs lay eggs that are coughed up or taken to the pharynx by the mucociliary ladder in the trachea. The eggs are swallowed and develop to L1 larvae, which are passed in the faeces 38. Donkeys are a common host, but rarely show clinical signs 38. Most horse cases are in animals that have co-grazed with donkeys. Clinical signs include a harsh, dry paroxysmal cough and increased expiratory effort 9. Liver fluke Clinical signs reported with natural liver fluke infection include loss of performance or condition, and diarrhoea when the diet is changed and urticaria 10. However, other authors have reported minimal clinical signs, and attempts to experimentally infect horses with Fasciola hepatica and F gigantica have proved difficult, suggesting some horses may have infestation resistance 39. Fasciola infections may be very common in some equid populations in developing countries. In a study of donkeys in Ethiopia, an 80 per cent prevalence was found 37. Diagnosis The main infection diagnosis method is either a faecal egg count (FEC) or identification of larvae in the faeces ( Figure 5 ) 18. Although Dictyocaulus arnfieldi is usually identified in faeces 38, it may be possible to identify the organism in mucus recovered from a tracheal wash 9. O equi can be diagnosed by the Sellotape test, where eggs from the perianal region are collected using clear adhesive tape 40. Gasterophilus larvae can often be seen on the non-glandular epithelium on gastroscopy ( Figure 6 ). For cyathostomiasis, weight loss accompanied by neutrophilia, hypergammaglobuli naemia and hypoalbuminaemia would be strongly suspicious of infestation, especially if the horse has not been 5 / 13

wormed with an avermectin-containing wormer. An ELISA has been developed for detection of Anoplocephala perfoliata infection in horses 41, 42. However, the optimum cut-off point for diagnosis of infection and the utility of this test, compared to an FEC in the individual animal 43, is a controversial issue. Cy-GALA-1 is a protein that appears to be specific to encysted cyathostomes. An ELISA test detecting antibodies to this protein might, in the future, allow serological detection of encysted cyathostomes in affected horses 44. Prevention Good pasture management and targeted treatment of affected individuals are prevention mainstays. One study has highlighted a number of risk factors for infestation with strongyles and Parascaris equorum 16. For strongyles, stud farms had a higher incidence of infection than riding schools, and yearlings were found to be at higher risk of shedding eggs than either foals or older horses. Clipping rough areas in the pasture decreased the infection odds by a factor of two. For P equorum, deep litter stabling increased the odds of infection by a factor of three, and spreading horse manure as a fertiliser on the fields increased the odds of infection by 44. Treatment Anthelmintics Benzimidazoles The benzimadoles are a large group of anthelmintics, of which a number have been used in horses. These include fenbendazole (5mg/kg for general worming, 10mg/kg for treating Parascaris equorum), albendazole (25mg/kg to 50mg/kg), cambendazole (20mg/kg), oxfendazole (10mg/kg), oxibendazole (10mg/ kg to 15mg/kg), mebendazole (8.8mg/kg for general worming, 15mg/kg to 20mg/kg for treatment of Dictyocaulus arnfieldi) and thiabendazole (44mg/kg to 88mg/kg) 45, 46. Fenbendazole appears to be the most commonly used of these in the UK and Ireland. It is effective against ascarids (94 per cent egg count reduction in one study) 47, but cyathostome resistance to fenbendazole has been reported in some areas. For example, fenbendazole did not result in any reduction in faecal strongyle egg shedding in a study of foals in Kentucky, USA. In the same study, ivermectin resulted in a 100 per cent reduction in strongyle eggs 47. 6 / 13

Fenbendazole (84 per cent reduction) and oxibendazole (94 per cent reduction) were effective against P equorum in a study where the ascarids appeared completely resistant to ivermectin 47. Triclabendazole (12mg/kg) has been reported to be effective for treatment of Fasciola hepatica 48. Avermectins Avermectins are macrocyclic lactones and include ivermectin, moxidectin and doramectin. These anthelmintics are broad-spectrum and are effective against large strongyles, small strongyles and pinworms 49-52. They have variable activity against Gasterophilus intestinalis larvae. Ivermectin is reasonably effective, but moxidectin is much less effective 53, 54. Their effectiveness against ascarids is variable, and has been excellent in some studies but minimal in others 47, 52, 55. Ivermectin still appears to be highly effective against cyathostomes 47, 49, 56, with reductions in FEC of 99.5 to 100 per cent. Ivermectin toxicosis characterised by depression, forelimb and hindlimb ataxia, drooping of the superior and inferior lips, and muscle fasciculations has been reported in adult horses administered an appropriate dose orally. This rare condition might be a result of an interaction with a plant increasing the permeability of the blood-brain barrier, such as silverleaf nightshade 57. Moxidectin is highly effective for at least 12 weeks after treatment, and in some horses it may still be effective after 16 weeks 51. Moxidectin is fairly effective against encysted cyathostomes, in contrast to ivermectin, which is fairly ineffective against this stage 53, 54. A moxidectin overdose is relatively easy to achieve in foals, and may result in coma 58. Affected foals can be supported through the toxicosis, but this may involve mechanical ventilation, as breathing may be severely inhibited. Moxidectin is labelled not for use in foals less than four months old and in pregnant animals. Doramectin was found to reduce the FEC by 90 per cent two weeks after intramuscular injection at 0.2mg/ kg. The egg reappearance period was 10 weeks 59. Pyrantel In two studies, pyrantel was found to be at least 95 per cent effective against Anoplocephala perfoliata 60, 61. It also has good efficacy against Oxyuris equi 50. Pyrantel also has activity against cyathostomes and large strongyles. However, marked resistance of cyathostomes to pyrantel has been reported in some geographical areas, and has been linked to frequent use of this product 62, 63. Praziquantel Praziquantel is highly effective against A perfoliata. In one study, it was 100 per cent effective in horses in Canada, Germany and New Zealand, and 90 per cent effective in horses in France 64. 7 / 13

Combination products of praziquantel and an avermectin are highly effective against strongyles 65, 66. Carbamate compounds Netobimin (10mg/kg) is metabolised to albendazole, which is the active metbolite. It was found to reduce the strongyle FEC by 100 per cent for four weeks after administration in naturally infected horses 67. Netobimin should not be given to pregnant animals. Treatment regimes Traditional treatment has consisted of regular dosing (every six to eight weeks) of all horses on a farm, irrespective of their parasite burden. Considerable concern has been expressed that this approach has led to drug resistance in cyathostomes 17 and ascarids 47. Although cyathostome resistance to ivermectin has not yet been reported, egg reappearance in five weeks has been reported on two German farms (decreased from nine weeks in earlier studies), which may be the first signs of ivermectin resistance development 68. However, it has been argued that this early egg reappearance represents incomplete elimination of L4-stage larvae and that ivermectin is still highly effective against adult larvae 69. The efficacy of ivermectin against L4 cyathostomes has always been variable, and substantially less than that of moxidectin 54. The blanket whole-farm approach to worming does not take into account that some animals, such as young horses, are more susceptible to infestation, and that others may have little parasite burden 16, 70. This has led to more strategic worming plans being developed. These may include treating animals joining the herd, anti-larvicidal treatment during winter (moxidectin for nonpregnant animals more than four months old, or a high-dose, five-day course of fenbendazole for young and pregnant animals), and then monitoring of the FEC and further treatment only of horses shedding a high number of eggs (such as more than 300 eggs per gram) 70. The advantage of such programmes is that horses that only shed low numbers of eggs are only treated once a year, reducing the chance of resistance developing. The disadvantage is that any cut-offs for FEC have been chosen arbitrarily, and we do not yet have good evidence this technique adequately protects individual horses or that it prevents resistance development 70. Another commonly used technique to prevent resistance development, namely rotation of different classes of anthelmintic, has not been proven to be effective 71. Traditional treatment on thoroughbred yards has included delivery of the wormer by nasogastric tube. Using this presents no advantage over paste formulations 72 and it may limit the products that 8 / 13

can be used. However, one management practice that should be strongly encouraged is the removal of faeces from the pasture after worming or stabling of horses for 24 hours. High levels of pasture contamination with small strongyles have been found after treatment with ivermectin, despite effective killing 27. Conclusion Parasitism is a major cause of morbidity in horses. However, current treatment strategies have led to widespread resistance of some parasites to commonly used anthelmintics. Treatment strategies are evolving to try to prevent the development of further resistance. However, evidence still needs to be gathered on the efficacy of these strategies, so that optimum treatment can be delivered both to individual farms and individual animals. To download published Veterinary Times articles, log on to www.vetsonline.com References 1. Reinemeyer C R and Nielsen M K (2009). Parasitism and colic, Vet Clin North Am Equine Pract 25(2): 233-245. 2. Lyons E T, Drudge J H and Tolliver S C (2000). Larval cyathostomiasis, Vet Clin North Am Equine Pract 16(3): 501-513. 3. Boswinkel M and Sloet van Oldruitenborgh-Oosterbaan M M (2007). Correlation between colic and antibody levels against Anoplocephala perfoliata in horses in The Netherlands, Tijdschr Diergeneeskd 132(13): 508-512. 4. Little D and Blikslager A T (2002). Factors associated with development of ileal impaction in horses with surgical colic: 78 cases (1986-2000), Equine Vet J 34(5): 464-468. 5. Proudman C J, French N P and Trees A J (1998). Tapeworm infection is a significant risk factor for spasmodic colic and ileal impaction colic in the horse, Equine Vet J 30(3): 194-199. 6. Thamsborg S M, Leifsson P S, Grondahl C et al (1998). Impact of mixed strongyle infections in foals after one month on pasture, Equine Vet J 30(3): 240-245. 7. Little P B, Lwin U S and Fretz P (1974). Verminous encephalitis of horses: experimental induction with Strongylus vulgaris larvae, Am J Vet Res 35(12): 1,501-1,510. 8. Duncan J L (1973). The life cycle, pathogenisis and epidemiology of S vulgaris in the horse, Equine Vet J 5(1): 20-25. 9. George L W, Tanner M L, Roberson E L and Burke T M (1981). Chronic respiratory disease in a horse infected with Dictyocaulus arnfieldi, J Am Vet Med Assoc 179(8): 820-822. 10. Owen J M (1977). Liver fluke infection in horses and ponies, Equine Vet J 9(1): 29-31. 11. Matthews J B, Hodgkinson J E, Dowdall S M and Proudman C J (2004). Recent developments in research into the Cyathostominae and Anoplocephala perfoliata, Vet Res 9 / 13

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