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BonnyStatueOfLiberty8607

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Colorado Mountain College

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equine strongyles equine parasites clinical pathology veterinary science

Summary

This document is a lecture on equine parasites, focusing on strongyles. It describes the different types of strongyles, their life cycles, and the damage they cause. The document also covers prevention and treatment strategies.

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CLINICAL PATHOLOGY I – Lecture Equine Parasites: Beginning with Strongyles Common Equine Parasites: Descending Order of Importance Strongyles Ascarid...

CLINICAL PATHOLOGY I – Lecture Equine Parasites: Beginning with Strongyles Common Equine Parasites: Descending Order of Importance Strongyles Ascarid Bots Cestodes Threadworms Protozoa Pinworms Stomach worms Eyeworms Filarial worms The Strongyles o Large and small strongyles o Aka “bloodworms” or “redworms” o Another nematode o Located in large intestine of DH o Ubiquitous o No age-related immunity o Direct life cycle o Infested horses often have both large and small strongyles Species o Large strongyles  Strongylus vulgaris  Strongylus equinus  Strongylus edentatus o Small strongyles: Aka “cyathostomes” or “cyathostomins”  At least 52 species  Most common strongyle observed in horses Large Strongyles 2 to 5 cm long Strongylus vulgaris o Direct life cycle o Fecal-oral transmission o Pre-patent period = 6 months o Adults in cecum and colon (large intestine) o Ingest tissue and blood (aka “bloodworms”) o Ova pass in manure and hatch o Molt to L3 stage in 1 to 2 weeks 12/3/2024 1 o L3 is infectious stage – crawl up blade of grass and ingested by grazing horse o L3 can overwinter on pasture in most U.S. climates -- very resistant to cold and desiccation o Once ingested, L3 penetrates mucosa of small intestine and molts to L4 o L4 migrates upstream to cranial mesenteric artery (primary blood supply for cecum and colon) o L4 spends 3 to 4 months in mesenteric artery maturing to L5 May also enter and damage aorta in heavy infestations o Migration often causes o Aneurysm = Ballooning of arterial wall o Arteritis = Inflammation of artery o Thrombus = Clot attached to interior wall of blood vessel o Embolus = Free floating clot o Infarction = Area of tissue without blood supply o Verminous colic = “Intestinal” colic due to compromised blood supply to GI tract o L5 migrates to cecum and colon via arterial blood supply o L5 encapsulates (wall of large intestine) in bean-sized nodules for final molt o Adult strongyles emerge from nodules to lumen of GI tract, begin reproduction o Prepatent period = 6 months  S. vulgaris ova can be found in feces of foals as young as 12 weeks of age How does this happen?  Fecal samples from infested horses often NOO as larvae are responsible for initial clinical signs o S. vulgaris was #1 cause of colic due to destruction of blood supply to large bowel o Less common in well-managed herds due to effective deworming programs  S. edentatus: Prepatent period = 11 months (Ovum to L3 = 1 to 2 weeks)  S. equinus: Prepatent period = 9 months (Ovum to L3 = 1 to 2 weeks) o Both adults  Twice as large as S. vulgaris  Twice as bloodthirsty as S. vulgaris o Larval stages of both more difficult to remove with anthelmintics o Similar life cycle, except larvae migrate to peritoneum (S. edentatus) and liver (S. equinus and S. edentatus), not cranial mesenteric artery o Larvae generally not as pathogenic as S. vulgaris larvae Damage Caused by Adult Strongyles o Large strongyles are “plug feeders” o Large buccal cavities draw in plug of intestinal mucosa o Mucosa ground up, digested by enzymes o Worm moves to another site to continue feeding o Do not suck blood, but mucosal damage can cause heavy blood loss Clinical Signs of Large Strongyles o Adult strongyles 12/3/2024 2  Anemia  Anorexia  Depression  Weight loss  Dehydration o S. vulgaris larvae  Aneurysm  Arteritis  Thrombus  Embolus  Infarction  Colic o S. edentatus & S. equinus larvae  Peritonitis  Liver damage Small Strongyles (Aka “cyathostomes”, “cyathostomins”) < 1.5 cm long (“Cyathostomiasis”) Small Strongyles o Many species (at least 52) o Direct life cycle o Fecal-oral transmission o Prepatent period = Short as 40 days; may be months (or years) long due to hypobiosis o Adults in cecum and colon o Ovum passes in feces, molts to L3 in < 1 week, ingested by horse o L3 undergoes mucosal migration in wall of cecum and colon -- L3 encysts in gut wall, molts to L4 → hypobiosis o Very resistant to anthelmintics while encysted, are susceptible to large doses of fenbendazole or moxidectin o Fecal samples often NOO as encysted larvae cause clinical signs, not adults Hypobiosis o Hypobiosis = Low environmental temps stimulate L3/L4 to remain dormant for months o L4 emerge en masse in spring  Months of larval waste released into intestine = GI inflammation  Large numbers of L5 mature to adults simultaneously Clinical Signs of “Cyathostomiasis” and “Larval Cyathostomiasis” o Adult cyathostomes cause 12/3/2024 3  Clinical signs similar adult large strongyles; signs milder due to smaller size and feeding method o Cyathostome larvae cause  Diarrhea  Weight loss  Copious production of mucus in large intestine Diagnosis: Both Large and Small Strongyles o Typical “strongyle-type” egg on fecal flotation o Cyathostome L4 and L5 recovered from feces via Baermann apparatus o Unable to differentiate various species of strongyle ova Prevention of Strongyles o Perform fecals on new horses and deworm prior to introduction to herd o Pasture management  Drag or harrow weekly when weather is hot and dry  Perform during summer months and...  Leave vacant for two weeks (southern U.S.) or 4 weeks (northern U.S.)  Graze horses on pasture that has been  Vacant for two months during warm season  Grazed by other livestock species  Reduce density of horses  Remove feces every few days  Do not spread manure Traditional Deworming of Horses – No Longer Recommended o Treat all horses at frequent intervals (4 to 6 x per year), use different classes of anthelmintics at each deworming o Treatment regimen extremely successful in reducing morbidity and mortality of S. vulgaris, however... o Resulted in resistance to anthelmintics  Benzimidazoles (“BZD”): Fenbendazole, oxibendazole  Macrocyclic lactones: Ivermectin, moxidectin  Tetrahydropyrimidines: Pyrantel (tartrate and pamoate) o New classes of anthelmintics could decrease resistance, but... o No new anthelmintics introduced since 1980s, unlikely new deworming agents approved in near future o Must avoid increased drug resistance Evidence-based Deworming of Horses o Three-pronged approach  Treat horses responsible for significant environmental contamination  Restrict anthelmintic treatment to transmission seasons 12/3/2024 4  Preserve parasite refugia  “Wild-type” parasites that haven’t been exposed to anthelmintics and lack anthelmintic-resistant genes  Parasite refugia  Parasites outside host; i.e., on pasture  Parasites encysted in host  Parasites in untreated horses o 1) Use  Correct drug  For correct parasite life stage  At appropriate time of year o 2) Determine which horses require frequent treatment based on FEC o 3) Evaluate overall success by regularly monitoring FEC of all horses on property  FEC = “Fecal egg count”  Quantitative fecal analysis  Measured amount of feces examined, all eggs counted  Results = Number of eggs per gram; i.e., “EPG”  Deworm only when FEC reaches significant level; e.g., > 100 EPG Anthelmintic Classes o Macrocyclic lactones (aka “macrolides”)  Avermectins  Ivermectin  Selamectin  Milbemycins  Moxidectin  Milbemycin oxime o Benzimidazoles (aka “BZDs”)  Fenbendazole  Oxibendazole o Tetrahydropyrimidine  Pyrantel pamoate  Pyrantel tartrate Anthelmintics for Strongyles o Large strongyles  Ivermectin  Moxidectin: Kills encysted larvae  Fenbendazole: Kills encysted larvae  Oxibendazole  Pyrantel (pamoate and tartrate) 12/3/2024 5 o Cyathostomes o Ivermectin o Moxidectin: Kills encysted larvae o Fenbendazole: Kills encysted larvae o Oxibendazole o Pyrantel (pamoate and tartrate) 12/3/2024 6

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