Questions and Answers
What is the primary method of diagnosing cutaneous habronemiasis?
Which anthelmintic is commonly used to treat equine stomach worms?
What additional treatment may be necessary in severe cases of summer sores?
What is a crucial control measure to reduce exposure to equine stomach worm larvae?
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Which of the following is true regarding zoonotic concerns with equine stomach worms?
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What order do Draschia megastoma, Habronema muscae, and Habronema microstoma belong to?
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Which equine stomach worm is known to cause the most severe clinical lesions?
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What is the main intermediate host in the life cycle of these equine stomach worms?
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What is the prepatent period for the development of adult worms after infection?
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Which clinical sign is most likely associated with heavy infections of equine stomach worms?
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What condition results from L3 larvae being deposited on wounds or moist skin?
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How are equine stomach worms typically diagnosed?
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Where do Draschia megastoma adult worms reside within the horse's body?
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What is the primary age group affected by Parascaris equorum?
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Which of the following clinical signs is NOT associated with heavy infections of Parascaris equorum?
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How does the pathology of Parascaris equorum vary with worm burden?
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What is the recommended treatment approach for foals with heavy infections of Parascaris equorum?
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Which diagnostic method is commonly used to identify Parascaris equorum?
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What environmental control measure is important for managing Parascaris equorum contamination?
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What type of lesions might be observed in the liver due to larval migration of Parascaris equorum?
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Which statement about the zoonotic potential of Parascaris equorum is true?
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What is the primary clinical sign associated with Strongyloides westeri infections in foals?
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Which life cycle characteristic is unique to Strongyloides westeri?
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How does Strongyloides westeri primarily transmit from the mare to the foal?
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What method is most effective in diagnosing Strongyloides westeri?
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What type of medication is commonly used to treat Strongyloides westeri infections?
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Which of the following statements is true regarding the zoonotic potential of Strongyloides westeri?
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What specific feature of Parascaris equorum distinguishes it from Strongyloides westeri?
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What happens to Strongyloides westeri eggs or larvae that are passed in the feces?
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What are Strongylus spp. primarily classified as?
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What is the primary location where Strongylus vulgaris larvae migrate after ingestion?
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Which species of Strongylus has a prepatent period of 6 months?
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What clinical sign is most commonly associated with Strongylus spp. infection in horses?
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Which of the following migrations is generally harmless compared to Strongylus vulgaris?
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How is a Strongylus spp. infection typically diagnosed?
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What is a consequence of S.vulgaris larvae's migration in horses?
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Where do Strongylus equinus larvae migrate to after leaving the peritoneal cavity?
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What is the primary clinical sign of an Oxyuris equi infection in horses?
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How does a horse become infected with Oxyuris equi?
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What is the duration of the prepatent period for Oxyuris equi?
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What treatment is commonly used for controlling Oxyuris equi infection in horses?
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Which method is used to diagnose Oxyuris equi infection?
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What is the potential consequence of hair loss due to excessive rubbing from Oxyuris equi infection?
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What is the shape and structure of Oxyuris equi eggs?
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What hygiene measure is important for controlling Oxyuris equi infection?
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What is a primary consequence of hypobiosis in small strongyle infections?
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Which category of horses is at the highest risk of small strongyle infections?
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What is the prepatent period for small strongyles?
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What method is vital for diagnosing minor strongyle infections?
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Which clinical sign is most likely observed during heavy infections of small strongyles in horses?
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How do small strongyles primarily differ from large strongyles?
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What is a key treatment option for small strongyle infections?
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How can small strongyle infections best be controlled?
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What is the primary consequence of mass emergence of encysted larvae from small strongyles?
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What is the implication of low or negative fecal egg counts in diagnosing larval cyathostominosis?
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What typically occurs to small strongyles after they are ingested by horses?
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What is hypobiosis in the context of small strongyles?
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What is a significant challenge in the treatment of small strongyles?
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Are small strongyle infections considered zoonotic?
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What pathology is associated with the emergence of a large number of encysted small strongyles?
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What happens to small strongyle eggs after they are passed in feces?
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What is the main reason Anoplocephala perfoliata diagnosis is challenging?
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What is included in the treatment plan for Anoplocephala perfoliata?
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How can horses be effectively protected from Anoplocephala perfoliata infections?
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Which diagnostic method can improve the accuracy of identifying Anoplocephala perfoliata?
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What public health concern is associated with Anoplocephala perfoliata?
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What is the primary intermediate host for Anoplocephala perfoliata?
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Where do Anoplocephala perfoliata tapeworms most commonly attach within the horse's intestines?
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What clinical sign is commonly associated with heavy infections of Anoplocephala perfoliata?
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What period does it typically take for Anoplocephala perfoliata to reach maturity within the horse after infection?
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Which of the following conditions is NOT associated with Anoplocephala perfoliata infections?
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Which group of horses is at heightened risk for clinical disease related to Anoplocephala perfoliata?
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What type of damage does Anoplocephala perfoliata cause to the intestinal mucosa?
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What is the key difference in clinical signs of Dictyocaulus arnfieldi infection between donkeys and horses?
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Which method is effective for diagnosing lungworm infection in horses?
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What is a recommended strategy to control Dictyocaulus arnfieldi infection in equines?
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What is a common misconception about the zoonotic potential of Dictyocaulus arnfieldi?
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Which of the following anthelmintics is effective against Dictyocaulus arnfieldi infection?
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What is the main host species for Dictyocaulus arnfieldi?
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What are the typical clinical signs of Dictyocaulus arnfieldi infection in horses?
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What unique lifecycle characteristic does Dictyocaulus arnfieldi demonstrate?
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What is the prepatent period for Dictyocaulus arnfieldi?
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Which of the following consequences can arise from a heavy infection of Dictyocaulus arnfieldi in horses?
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Why are donkeys considered reservoirs for Dictyocaulus arnfieldi?
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What happens to L1 larvae of Dictyocaulus arnfieldi after being passed in feces?
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What is a common pathology associated with Dictyocaulus arnfieldi infection in horses?
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What is the primary treatment for Onchocerca spp. infections?
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What method can be used to confirm the presence of Onchocerca DNA?
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What is a crucial aspect of controlling Onchocerca spp. infections?
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Which statement regarding the zoonotic potential of Onchocerca spp. is true?
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Why might surgical removal be necessary in Onchocerca spp. treatment?
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What is the primary habitat of adult Onchocerca spp. in horses?
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Which species of vector is primarily associated with the transmission of Onchocerca spp.?
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Which clinical sign is associated with Onchocerca spp. infection in horses?
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What is the typical duration of the prepatent period for Onchocerca spp. after infection?
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What type of life cycle do Onchocerca spp. exhibit?
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Which pathology associated with Onchocerca spp. is primarily due to microfilariae in the skin?
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Which Onchocerca spp. is primarily of relevance to donkeys in Africa?
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Which condition may result from chronic Onchocerca spp. infections in horses?
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What is the primary consequence of larvae being deposited on a horse's skin by flies?
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Which clinical signs are characteristic of cutaneous habronemiasis?
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What role do houseflies and stable flies play in the life cycle of Habronema spp.?
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How does the immune response to larvae in the skin manifest in horses affected by cutaneous habronemiasis?
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What treatment options are available for managing cutaneous habronemiasis?
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Why might cutaneous habronemiasis become a chronic condition if untreated?
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Which environment is most likely to facilitate the transmission of Habronema spp. larvae?
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What is a common method for diagnosing cutaneous habronemiasis?
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What is the primary method for treating Thelazia lacrymalis infections?
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Which of the following is NOT a preventive measure for Thelazia lacrymalis?
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How can Thelazia lacrymalis be diagnosed?
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What zoonotic risk is associated with Thelazia lacrymalis?
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Which treatment is effective in eliminating any remaining larvae or worms after manual removal in Thelazia lacrymalis cases?
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What is the primary natural habitat of Thelazia lacrymalis in horses?
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Which of the following best describes the life cycle of Thelazia lacrymalis?
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What clinical signs are indicative of Thelazia lacrymalis infection in horses?
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How can Thelazia lacrymalis infection primarily be prevented in horses?
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What is the prepatent period for Thelazia lacrymalis in horses?
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What is a potential consequence of prolonged Thelazia lacrymalis infection in horses?
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Which group of horses is most susceptible to Thelazia lacrymalis infection?
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What impact does Thelazia lacrymalis have on the horse's eye?
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Study Notes
Classification and Prevalence
- Draschia megastoma, Habronema muscae, and Habronema microstoma are classified as nematodes in the order Spirurida.
- These parasites are commonly known as equine stomach worms.
- Habronema muscae is the most prevalent species among the three.
- Draschia megastoma is responsible for the most severe clinical lesions, including large stomach nodules filled with necrotic material.
- Habronema microstoma has not been reported in America.
Life Cycle
- The life cycle is indirect, involving flies as intermediate hosts.
- Adult worms inhabit the horse's stomach and release eggs or L1 larvae, which are ingested by Muscid flies.
- The larvae develop into the infective L3 stage within the fly.
- If L3 larvae are deposited around the horse's mouth, they are ingested and mature into adults in the stomach.
- If the larvae are placed on wounds or moist skin, they result in cutaneous lesions but do not mature into adult worms.
- The prepatent period, from infection to adult worm development, is approximately 2 months.
Clinical Presentation (Ingestion of Larvae)
- Most horses remain asymptomatic upon ingesting infective L3 larvae.
- Heavy infections can lead to gastritis.
- Draschia megastoma causes severe lesions, forming nodules in the stomach that can reach 10 cm in diameter, containing numerous worms and necrotic tissue.
- Nodules may cause mechanical obstruction or rupture, risking fatal peritonitis.
- The parasites are linked to Rhodococcus equi, a pneumonia pathogen in foals.
Clinical Presentation (Deposited on Wounds)
- L3 larvae on wounds or moist skin can lead to cutaneous habronemiasis (summer sores).
- Lesions are characterized by granulomatous, itchy, reddish-brown, and greasy areas with yellow, calcified material resembling rice grains.
- Common sites for skin lesions include legs, face, and near the eyes.
Diagnosis
- Diagnosing equine stomach infections is challenging; eggs are not typically identified in routine fecal flotation.
- Molecular diagnostic methods exist but are seldom employed.
- Adult worms or lesions can be detected via gastroscopy or necropsy.
- Diagnosis of cutaneous habronemiasis is performed by identifying larvae in skin scrapings or biopsies.
Treatment and Control
- Stomach infections are treated with anthelmintics such as moxidectin.
- For summer sores, oral or topical moxidectin may be effective, while severe cases might require surgical removal or cauterization of excessive granulation tissue.
- Control strategies primarily involve managing fly populations around wounds to minimize larval exposure.
Zoonotic Concerns
- There are no significant zoonotic risks associated with Draschia megastoma, Habronema muscae, or Habronema microstoma; these parasites are specific to equines and do not pose a risk to humans.
Strongyloides westeri Classification and Characteristics
- Strongyloides westeri is a nematode belonging to the order Rhabditida, commonly known as the equine threadworm.
- Parasitic females exclusively reside within the host, with eggs or larvae expelled in feces.
Strongyloides westeri Life Cycle
- The life cycle involves direct transmission but is complex, alternating between parasitic and free-living forms.
- Eggs or larvae develop in the environment into free-living adults or infective L3 larvae.
- L3 larvae can penetrate skin or be ingested and then migrate to the small intestine to mature into adult females.
- Transmission can also occur through mare's milk, where larvae reactivated during parturition are passed to foals.
Clinical Presentation in Foals
- Primarily affects foals, causing small intestinal enteritis, diarrhea, and skin irritation from larval penetration.
- Common clinical signs include watery diarrhea, weight loss, dehydration, and behavior termed "frenzied behavior" due to skin irritation.
- Adult horses typically show no clinical symptoms.
Diagnosis of Strongyloides westeri
- Diagnosis involves identifying eggs in feces through flotation methods; eggs are small, oval, and thin-shelled, often containing larvae.
- Skin scraping may help identify larvae in cases of dermal invasion.
Treatment and Control Measures
- Infected foals are treated with anthelmintics such as ivermectin or fenbendazole.
- To prevent transmission, mares should receive ivermectin treatment within 24 hours of foaling.
- Maintaining a clean and dry environment is crucial to reducing the survival of infective larvae.
Zoonotic Concerns
- Strongyloides westeri is not zoonotic, posing no infection risk to humans.
Parascaris equorum Classification
- Parascaris equorum is classified as a large roundworm under the order Ascaridida, also called the equine ascarid or large roundworm.
Parascaris equorum Life Cycle
- The life cycle is direct; infective eggs containing L2 larvae are shed in feces and can persist in the environment.
- Upon ingestion, eggs hatch in the small intestine, and larvae migrate through the intestinal wall to the liver and then to the lungs.
- Larvae are coughed up, swallowed, and mature into adults in the small intestine, with a prepatent period of about 10-12 weeks.
Clinical Presentation in Foals
- Primarily affects nursing and weaned foals under one year, with signs including coughing, nasal discharge, weight loss, and reduced growth.
- Heavy infections may cause intestinal impaction and rupture, leading to potential fatality.
- Liver lesions resembling "milk spots" can result from larval migration.
Pathology Based on Worm Burden
- Mild to moderate infections result in mild respiratory signs and growth reduction.
- Heavy infections increase the risk of serious complications, including intestinal blockage, rupture, and respiratory symptoms due to larval migration through the lungs.
Diagnosis of Parascaris equorum
- Diagnosis usually involves identifying characteristic thick-shelled ascarid eggs in feces using flotation methods.
- In severe cases, adult worms may be observed in feces or during necropsy.
Treatment and Control Measures
- Treatment typically includes broad-spectrum anthelmintics such as ivermectin or fenbendazole, with gradual deworming recommended for heavily infected foals to avoid blockage.
- Effective control requires regular manure removal and pasture management since eggs can remain viable in the environment for years.
- Foals are dewormed more frequently than adult horses to prevent heavy infections.
Zoonotic Concerns
- No significant zoonotic risks are associated with Parascaris equorum, as it is specific to horses and does not infect humans.
Classification of Strongylus spp.
- Classified as nematodes under the order Strongylida.
- Commonly known as large strongyles or bloodworms.
- Notable species include Strongylus vulgaris, Strongylus edentatus, and Strongylus equinus.
General Life Cycle of Strongylus spp.
- Life cycle is direct; horses ingest infective L3 larvae while grazing.
- Larvae penetrate gastrointestinal (GI) mucosa, migrating through tissues based on species.
- Larvae return to cecum and colon to mature into adults, ingest blood, and produce eggs shed in feces.
- Prepatent period varies: 6 months for S. vulgaris, 11 months for S. edentatus, 9 months for S. equinus.
Migration of Strongylus vulgaris Larvae
- After ingestion, larvae penetrate the intestinal wall, migrating to the cranial mesenteric artery.
- This migration causes damage to arterial endothelium, leading to arteritis, thrombosis, and possible embolism.
- Larvae then mature and return to the large intestine, completing their life cycle.
Migration of Strongylus edentatus Larvae
- Larvae migrate via portal veins to the liver, residing there for about 2 months.
- They then move through the peritoneal cavity back to the large intestine to mature.
- This migration is relatively harmless compared to S. vulgaris.
Migration of Strongylus equinus Larvae
- Larvae migrate through the peritoneal cavity to the liver and pancreas, staying for several months.
- Eventually, they return to the large intestine to mature.
- This species is less pathogenic compared to S. vulgaris.
Clinical Presentation of Strongylus spp. Infection in Horses
- Common clinical signs include weight loss, lethargy, diarrhea, anemia, and hypoproteinemia.
- Dependent edema may occur due to protein loss.
- S. vulgaris is the most pathogenic, with potential for colic due to mesenteric artery thrombosis, ischemia, and bowel infarction.
Diagnosis of Strongylus spp.
- Diagnosis relies on clinical signs, fecal egg counts, and identification of strongyle-type eggs in feces.
- Eggs cannot be distinguished between large and small strongyles.
- Necropsy may reveal migration damage from S. vulgaris in the cranial mesenteric artery.
Treatment and Control of Strongylus spp.
- Treatment involves broad-spectrum anthelmintics such as ivermectin, moxidectin, or fenbendazole.
- Strategic deworming is necessary due to long prepatent periods targeting larval stages.
- Regular fecal egg counts and pasture management (e.g., manure removal) are crucial for controlling parasite load.
Zoonotic Concerns
- No zoonotic concerns with Strongylus spp.; they are specific to equines and do not pose risks to humans.
Classification
- Oxyuris equi is a nematode classified under the order Oxyurida.
- Commonly known as the equine pinworm.
Life Cycle
- Life cycle is direct, with no intermediate hosts.
- Horses ingest eggs containing infective L3 larvae.
- Larvae emerge in the small intestine and migrate to the cecum and colon to mature into adults.
- Adult females migrate to the perianal region to deposit eggs on the skin around the anus.
- Eggs become infective in 3-5 days.
- Prepatent period lasts about 5 months.
Clinical Presentation
- Primary symptom is intense itching around the tail and perianal region due to egg deposition.
- Excessive tail rubbing leads to hair loss, broken tails, and potential secondary bacterial infections.
- Itching may cause horses to rub against objects, damaging skin and coat.
- Possible intestinal ulcers from larval feeding on the intestinal mucosa.
Diagnosis
- Diagnosed using the "scotch tape test," which collects eggs for microscopic examination.
- Eggs are elongated, oval with a flattened side, and possess a distinct operculum (cap).
- Adult worms can be seen around the anus or in feces.
Treatment and Control
- Treated with anthelmintics such as ivermectin, pyrantel pamoate, or fenbendazole.
- Hygiene measures are vital due to the stickiness of eggs; cleaning the perianal area is crucial.
- Disinfection of the environment, including bedding and grooming equipment, helps reduce contamination.
Zoonotic Concerns
- No zoonotic risks associated with Oxyuris equi.
- Pinworm infections are specific to horses and do not affect humans.
Classification of Small Strongyles
- Small strongyles, or cyathostomins, belong to the superfamily Strongyloidea and order Strongylida.
- Over 40 species of small strongyles infect horses.
Life Cycle and Migration Differences
- Cyathostomins do not migrate outside the gastrointestinal tract, contrasting with large strongyles.
- After ingestion, L3 larvae enter the cecum and colon mucosa, where they encyst.
- Encysted larvae may undergo hypobiosis before maturing and feeding on the mucosal surface.
Life Cycle of Small Strongyles
- Direct life cycle where horses ingest infective L3 larvae from contaminated pastures.
- Larvae encyst in the cecum and colon mucosa and may remain dormant until conditions are favorable.
- After weeks to months, larvae emerge, mature into adults, and begin feeding.
- Adult worms mate and shed eggs in feces, which hatch into L1 larvae and develop to L3 larvae in the environment.
- Prepatent period is 6-12 weeks based on environmental factors.
Clinical Presentation of Infection
- Light infections may show no clinical signs.
- Heavy infections can cause unthriftiness, lethargy, diarrhea, anemia, and hypoproteinemia.
- Sudden mass emergence of larvae may lead to colitis and severe diarrhea, termed larval cyathostominosis, prevalent in late winter or early spring.
Pathology Associated with Small Strongyles
- Massive emergence of encysted larvae damages the mucosal lining, causing inflammation, edema, and fibrosis.
- This disrupts nutrient absorption, leading to weight loss and colitis.
- Adult worms contribute less to pathology than encysted larvae.
Impact of Hypobiosis
- Hypobiosis allows larvae to survive adverse conditions and synchronize their emergence.
- This can overwhelm the host's immune response, causing clinical disease.
- Horses may show no symptoms during hypobiosis; signs appear when larvae emerge.
Susceptible Horses
- All age groups can be infected, but younger horses and those in poorly managed pastures are at higher risk.
- Heavily stocked pastures increase exposure to high egg shedding.
Diagnosis of Small Strongyle Infections
- Diagnosis primarily involves fecal egg counts (FEC) to detect strongyle-type eggs.
- Eggs cannot differentiate between small and large strongyles.
- Low or negative FEC may occur in larval cyathostominosis due to the presence of immature larvae.
- Necropsy can reveal encysted larvae in the intestinal mucosa.
Treatment Options
- Treatment includes anthelmintics like ivermectin, moxidectin, or fenbendazole, with moxidectin effective against encysted larvae.
- Resistance, particularly to fenbendazole and pyrantel, has been reported, highlighting the need for resistance management.
- Targeted deworming based on FEC is recommended to minimize resistance.
Prevention and Control
- Good pasture management includes rotating pastures, avoiding overstocking, and manure removal.
- Regular FEC monitoring helps identify high egg shedders and guides deworming strategies.
- AAEP recommends deworming based on FEC results and routine treatments for encysted larvae (powerpac with double dose of fenbendazole for 5 days).
Zoonotic Concerns
- There are no zoonotic risks associated with cyathostomins; they are equine-specific and do not affect humans.
Classification
- Anoplocephala perfoliata is a cestode (tapeworm) under the order Cyclophyllidea and family Anoplocephalidae.
- It is the most common tapeworm species found in horses.
Life Cycle
- The life cycle is indirect, involving an intermediate host, the oribatid mite.
- Mites ingest tapeworm eggs shed in horse feces, leading to the development of infective cysticercoid larvae.
- Horses become infected by ingesting mites while grazing, releasing larvae in their intestines.
- The larvae attach to the intestinal mucosa, usually at the ileocecal junction, and mature into adults.
- The prepatent period for infection is approximately 6-10 weeks.
Typical Location in Horses
- Tapeworms typically attach at the ileocecal junction, ileum, and cecum.
- In heavy infections, tapeworms can cluster in these areas, leading to serious clinical issues.
Clinical Presentation
- Many horses remain asymptomatic despite infection.
- Heavy infections can lead to colic, weight loss, diarrhea, and poor body condition.
- Associated complications include ileocecal impaction, spasmodic colic, intussusception, and cecal rupture, all of which can be life-threatening.
- Inflammation from the tapeworm attachment contributes to these symptoms.
Pathology
- Anoplocephala perfoliata causes localized inflammation and damage to the intestinal mucosa at the ileocecal junction.
- This inflammation can impair intestinal motility and increase the risk of ileal impaction and cecal intussusception.
- Severe cases may lead to rupture of the cecum or other intestinal sections.
- The inflammation and physical blockage from large worm populations are primary pathology contributors.
Risk Factors for Clinical Disease
- Horses of all ages can be infected; however, younger horses and those with poor pasture management are more vulnerable.
- Pastures with high populations of oribatid mites, particularly in dense vegetation and humid conditions, increase the risk of infection.
Diagnosis
- Diagnosing tapeworm infections is challenging due to inconsistency in egg shedding.
- Fecal flotation can detect eggs, but sensitivity is low.
- Modified flotation techniques or ELISA-based tests for antibodies or antigens increase diagnostic accuracy.
- Post-mortem diagnosis can occur by finding adult tapeworms attached to the ileocecal junction.
Treatment and Control
- Treatment involves anthelmintics like praziquantel or a double dose of pyrantel pamoate.
- Horses should be dewormed at least once a year, typically in fall or winter when mite activity lessens.
- Preventive measures include managing pasture conditions and reducing overgrazing to limit exposure to oribatid mites.
Public Health or Zoonotic Concerns
- Anoplocephala perfoliata poses no zoonotic concerns, as it is specific to equines and does not affect humans.
Classification
- Dictyocaulus arnfieldi is a nematode in the order Strongylida.
- It is the primary lungworm affecting equines.
Hosts Affected
- Natural hosts are donkeys, which often remain asymptomatic.
- Horses can become infected when sharing pastures with donkeys and exhibit clinical symptoms.
Life Cycle
- The life cycle is direct and begins in the bronchi and bronchioles of the host.
- Adult worms lay embryonated eggs that are coughed up, swallowed, and excreted in feces as eggs or L1 larvae.
- L1 larvae develop into infective L3 larvae in the environment.
- Infection occurs when horses or donkeys ingest L3 larvae while grazing.
- L3 larvae penetrate the gastrointestinal mucosa and migrate to the lungs through lymphatics and blood vessels.
- In the lungs, larvae mature into adults, causing respiratory disease, with a prepatent period of approximately 4 weeks.
Clinical Presentation
- Horses exhibit coughing, nasal discharge, dyspnea, and exercise intolerance due to lungworm infection.
- Wheezing or abnormal lung sounds may be present; severity depends on the number of adult worms.
- Donkeys typically do not show clinical signs despite being carriers.
Pathology
- Adult lungworms in the bronchi and bronchioles cause irritation and inflammation.
- This leads to bronchitis, excess mucus production, airway obstruction, and reduced lung function.
- Secondary bacterial infections may complicate respiratory symptoms in severe cases.
Reservoir Status of Donkeys
- Donkeys are asymptomatic carriers, shedding infective larvae without showing disease signs.
- Co-grazing with donkeys increases the risk of lungworm infection in horses.
- The asymptomatic nature of the infection in donkeys complicates detection and management.
Infection Variability
- Donkeys, as the natural hosts, often show no clinical signs even with heavy infections.
- Horses are more likely to develop significant respiratory symptoms when infected.
Diagnosis
- Diagnosis in horses is achieved by identifying L1 larvae in fresh feces using the Baermann technique.
- Adult worms or larvae may be found in bronchoalveolar lavage (BAL) or tracheal wash fluid.
- Diagnosis may also rely on clinical signs, history of co-grazing, and auscultation findings.
Treatment and Control
- Treat infections with anthelmintics like ivermectin or moxidectin, effective against adults and migrating larvae.
- Control strategies include separating grazing areas for horses and donkeys or regularly deworming donkeys.
- Monitoring donkey fecal output can help assess infection risks in shared pastures.
Zoonotic Concerns
- Dictyocaulus arnfieldi poses no zoonotic risk; it specifically affects equines and is not a threat to humans.
Classification and Host
- Onchocerca spp. are nematodes classified under the order Spirurida.
- These are filarial worms that primarily impact the skin and connective tissues of horses.
Affected Species and Vectors
- Horses are the primary species affected by Onchocerca spp.
- Transmission vectors include biting flies, especially:
- Culicoides species (biting midges)
- Simulium species (black flies)
Relevant Onchocerca Species in Equines
- Key Onchocerca species affecting horses include:
- Onchocerca cervicalis
- Onchocerca reticulata
- Onchocerca railliti, primarily affecting donkeys in Africa
Life Cycle
- The life cycle is indirect, involving several stages:
- Adult worms inhabit connective tissues, notably the nuchal ligament.
- Microfilariae produced by adults migrate to the skin and are ingested by biting flies.
- Within the fly, microfilariae develop into infective L3 larvae.
- The larvae are transmitted to a new host upon the fly's next bite.
- Larvae mature into adult worms within the host's subcutaneous tissues.
- The prepatent period lasts approximately 4-6 months.
Clinical Signs
- Most Onchocerca spp. infections are asymptomatic, particularly in adult worms.
- Microfilariae presence can cause:
- Dermatitis
- Fistulous withers
- Poll evil
- Uveitis
- Common symptoms include itching (pruritus), hair loss, crusting, and depigmentation.
- O. cervicalis can cause localized swelling or nodules in the nuchal ligament.
- O. reticulata may lead to increased reactions in distal limb connective tissue.
- Eye inflammation can result in conjunctivitis or uveitis.
Pathology
- Pathology is primarily caused by microfilariae in the skin, leading to:
- Localized inflammation and dermatitis
- Possible ocular lesions
- Chronic infections can form nodules or fibrous masses in affected tissues
- Chronic eye involvement may result in recurrent uveitis or other ocular issues
Diagnosis
- Diagnosis relies on clinical signs, such as itching and nodules, with a history of fly exposure.
- Skin biopsies can identify microfilariae, while serological tests or PCR detect Onchocerca DNA.
Treatment and Control
- Treatment options include:
- Ivermectin or moxidectin effective against microfilariae but limited on adult worms.
- Surgical removal may be necessary for adult worm-induced nodules.
- Control measures aim at reducing fly exposure through:
- Insect repellents and fly masks
- Environmental management, like reducing standing water, to limit fly breeding.
Zoonotic Concerns
- No zoonotic risks are associated with Onchocerca spp.; these parasites are specific to horses and do not affect humans.
Classification of Habronema spp.
- Habronema spp. are nematodes in the order Spirurida.
- Primarily inhabit the stomach of horses.
- Larvae can lead to cutaneous lesions, known as summer sores.
Life Cycle Related to Cutaneous Form
- Life cycle of Habronema spp. is indirect.
- Adult worms release eggs or larvae in the horse's stomach, passed through feces.
- Flies (houseflies and stable flies) ingest larvae while feeding on feces.
- Larvae develop into infective L3 larvae inside the flies.
- Flies deposit L3 larvae on moist areas of the horse’s skin, particularly wounds and around the eyes.
- Larvae invade skin instead of maturing in the stomach, causing summer sores through granulomatous reaction.
Clinical Signs of Cutaneous Habronemiasis (Summer Sores)
- Characterized by granulomatous, ulcerative skin lesions that do not heal.
- Commonly located on the face, eyes, legs, and near wounds.
- Lesions are reddish-brown, greasy, and may contain calcified debris resembling rice grains.
- Affected horses may experience itching and irritation, leading to scratching or rubbing.
Pathology Associated with Cutaneous Habronemiasis
- Inflammatory reaction from larvae presence in the skin triggers immune response.
- Granuloma formation can become chronic if untreated.
- Secondary bacterial infections may arise, complicating the condition and hindering healing.
Diagnosis of Cutaneous Habronemiasis
- Diagnosis based on non-healing, granulomatous skin lesions, particularly in fly-bite areas.
- Identification of larvae may occur in skin scrapings or biopsies from lesions.
- History of fly exposure during warmer months supports diagnosis.
Treatment and Control of Cutaneous Habronemiasis
- Systemic anthelmintics like ivermectin or moxidectin are used to eliminate larvae.
- Topical treatments such as corticosteroids and antibiotic ointments help reduce inflammation and secondary infections.
- Severe cases may necessitate surgical removal of affected tissue.
- Effective fly control strategies include repellents, fly masks, and environmental management to lower fly populations.
Zoonotic Concerns with Habronema spp.
- No zoonotic risks; Habronema spp. parasites are specific to equines and do not infect humans.
- Fly control is crucial to minimize the spread of these parasites and other equine diseases.
Classification
- Thelazia lacrymalis is a nematode classified under the order Spirurida.
- Commonly referred to as the equine eyeworm.
Natural Habitat
- Resides in the conjunctival sac and tear ducts of horses.
- Feeds on the tear film, leading to irritation of the eye.
Life Cycle
- The life cycle is indirect, involving adult worms in the conjunctival sac.
- Adult worms mate and produce eggs, which are consumed by flies, particularly Musca species (e.g., face flies).
- Inside the fly, larvae develop into infective L3 larvae.
- L3 larvae are deposited back onto the horse's eyes, maturing into adult worms.
- Prepatent period lasts about 3-6 weeks:
- 2-4 weeks for egg to L3 in the fly,
- 10-11 weeks for L3 to become adults in the horse.
Clinical Signs
- Symptoms can range from mild to severe ocular irritation.
- Common signs include excessive tearing (epiphora), conjunctivitis, eyelid swelling, squinting (blepharospasm), photophobia, and eye rubbing.
- Severe cases may lead to corneal ulcers and secondary bacterial infections.
- Adult worms may be visible in the eye or conjunctival sac.
Pathology
- Primarily causes irritation and inflammation of the conjunctiva and tear ducts.
- Inflammation results in excess tear production, redness, and swelling.
- Prolonged infections can cause corneal damage, vision impairment, and increase the risk of secondary infections.
- The movement of worms results in physical irritation and discomfort.
Risk Factors
- Horses in areas with high fly populations, especially where Musca species thrive, are at greater risk.
- Wet, warm environments contribute to large fly populations.
- Poor fly control around stables or grazing areas elevates infection risk.
Diagnosis
- Diagnosis often involves direct observation of adult worms in the conjunctival sac or tear ducts.
- Worms are thin, white, and visible to the naked eye or under magnification.
- Excessive tearing and conjunctivitis may prompt further examination.
- Microscopic examination can reveal larvae or adult worms in eye secretions.
Treatment and Control
- Treatment usually involves manual removal of worms using fine forceps, often under sedation or local anesthesia.
- Topical and systemic anthelmintics, such as ivermectin, are effective in eliminating remaining worms or larvae.
- Preventive measures include fly control strategies like fly masks, repellents, and managing fly populations.
- Reducing horse exposure to flies during peak seasons minimizes infection risk.
Zoonotic Concerns
- Thelazia lacrymalis is not known to be zoonotic, though some Thelazia species can infect humans.
- Zoonotic infections in humans are more closely associated with Thelazia callipaeda.
- Good hygiene and effective fly control are essential to reduce the risk of zoonotic infections from other species.
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