Questions and Answers
What unique morphological feature do male nematodes in the order Strongylida possess?
What is a common characteristic of strongyle-type eggs in the Strongylida order?
What is the usual prepatent period for Strongylida nematodes after ingestion of L3 larvae?
How does the periparturient rise phenomenon affect nematode infection in ewes?
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Which of the following nematodes is NOT part of the HOT CO complex?
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What are common clinical signs of Parasitic Gastroenteritis (PGE)?
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What type of life cycle do gastrointestinal nematodes in the Strongylida order exhibit?
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Which of the following best describes the nature of subclinical disease caused by gastrointestinal nematodes?
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What characteristic feature is commonly associated with female Haemonchus spp.?
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Which of the following clinical signs is NOT associated with severe Haemonchus infection?
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What method is primarily used to quantify egg shedding in diagnosing Haemonchus spp. infection?
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What is a significant concern in the management of Haemonchus spp. infections?
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Which life stage of Haemonchus spp. is directly ingested from the environment by the host?
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What immediate effect do Ostertagia spp. have on the abomasum after infection?
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What is the primary clinical manifestation of Type I ostertagiosis?
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Which of the following best describes the life cycle of Ostertagia spp.?
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Which diagnostic tool is most indicative of Ostertagia infection?
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What is a significant consequence of the damage caused by Ostertagia spp. in ruminants?
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What severe condition can Trichostrongylus spp. cause in large numbers within ruminants?
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Which of the following statements about Cooperia spp. is true?
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What type of lesions do Oesophagostomum spp. primarily cause in ruminants?
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What is a unique characteristic of Nematodirus spp. eggs compared to other strongyles?
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Which ruminant species is primarily affected by Oesophagostomum radiatum?
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How do Trichostrongylus spp. and Cooperia spp. contribute to ruminant health issues?
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What is a primary challenge posed by Cooperia spp. in cattle management?
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What happens to Nematodirus spp. eggs under unfavorable environmental conditions?
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What is the primary mode of transmission for Bunostomum spp. to its host?
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Which of the following clinical signs is NOT typically associated with Bunostomum spp. infection?
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What key morphological feature do adult Bunostomum spp. possess that aids in their feeding?
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What is the approximate prepatent period for Bunostomum spp. after larvae infection?
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Which treatment option is specifically labeled for use against Bunostomum spp. in sheep?
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Which pathological effect is primarily caused by the blood-feeding behavior of Bunostomum spp.?
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Which of the following methods is used for the diagnosis of Bunostomum spp. infections?
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What is a potential consequence of heavy Bunostomum spp. infections in young animals?
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What is the primary site of infection for Strongyloides papillosus in ruminants?
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Which stage of Strongyloides papillosus larvae is capable of penetrating the skin of the host?
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What is the primary clinical sign associated with Strongyloides papillosus infections?
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What characteristic of Strongyloides papillosus makes its life cycle unique compared to typical nematodes?
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What is the recommended treatment for infections caused by Strongyloides papillosus?
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What is the role of fecal flotation in the diagnosis of Strongyloides papillosus?
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At what age range do infections of Strongyloides papillosus peak in calves?
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What environmental condition is critical for controlling Strongyloides papillosus infections?
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What is the primary clinical sign that may be observed in young ruminants with heavy infections of Trichuris spp.?
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How is the diagnosis of Trichuris spp. primarily conducted?
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What is the key factor in the life cycle of Trichuris spp. that leads to infection?
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Which treatment option is commonly used against Trichuris spp. infections in ruminants?
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What is the primary morphological feature of adult Trichuris spp. worms?
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What is a significant morphological difference between Thysanosoma spp. and Moniezia spp.?
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What is the public health concern associated with Taenia saginata?
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Where are Thysanosoma spp. mainly located within ruminant hosts?
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Which statement best describes the life cycle of Taenia saginata?
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What are the potential consequences of heavy Thysanosoma spp. infections in ruminants?
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What is the family classification of Moniezia spp.?
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What is a characteristic feature of the eggs of Moniezia spp.?
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Which organism serves as the definitive host for Moniezia spp.?
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How do ruminants typically become infected with Moniezia spp.?
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What is the primary clinical significance of Moniezia spp. in ruminants?
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What is the effective treatment for Moniezia spp. if treatment is necessary?
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Which of the following best describes the life cycle of Moniezia spp.?
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Are there any zoonotic concerns associated with Moniezia spp.?
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What is the common name for Fasciola hepatica?
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In which part of a host is Fasciola hepatica typically found?
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Which of the following is an intermediate host for Fasciola hepatica?
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What type of reproduction occurs in the freshwater snail host of Fasciola hepatica?
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What pathology is caused by the adult flukes in the bile ducts?
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Which of the following is a clinical sign of fascioliasis in ruminants?
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Which phase of the life cycle involves the release of cercariae from the snail?
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What is the prepatent period for Fasciola hepatica?
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What is a primary clinical sign of chronic disease caused by moderate infections of Fasciola hepatica?
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Which treatment option is effective against different stages of Fasciola hepatica?
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What distinguishes the host response to Fascioloides magna in natural hosts versus aberrant hosts?
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How is Fasciola hepatica primarily diagnosed in animals?
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Which of the following statements is true regarding Zoonotic concerns of Fasciola hepatica?
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What pathologic effect occurs in dead-end hosts infected by Fascioloides magna?
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Which of the following liver trematodes primarily affects the rumen rather than the liver?
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What is the significance of snail management in controlling Fasciola infections?
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Which characteristic distinguishes Fascioloides magna from Fasciola hepatica in natural hosts?
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What is the primary risk involved with Fascioloides magna in domestic livestock?
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What are the primary species of lungworms affecting ruminants?
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What critical role does the L3 larvae play in the life cycle of Dictyocaulus viviparus?
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What is a primary pathological effect caused by Dictyocaulus viviparus infection?
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Which clinical sign is most commonly associated with severe Dictyocaulus viviparus infections in cattle?
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How is Dictyocaulus viviparus primarily diagnosed?
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What is the approximate prepatent period for Dictyocaulus viviparus?
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What environmental factors assist in the development of L3 larvae from L1 larvae?
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What treatment is typically used for managing Dictyocaulus viviparus infections in cattle?
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What is the primary intermediate host for Muellerius capillaris in its life cycle?
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What significant clinical signs are associated with Muellerius capillaris infection in goats?
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How is the diagnosis of Muellerius capillaris typically made?
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Which of the following is a distinguishing characteristic of Muellerius capillaris larvae seen under microscopy?
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What is the prepatent period for Muellerius capillaris?
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What form of treatment is generally not required for Muellerius capillaris infections in sheep?
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What potential economic impact do Muellerius and Dictyocaulus lungworms pose?
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What method can be utilized to control Muellerius capillaris infections?
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What is the common name given to Thelazia spp.?
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Which of the following best describes the definitive hosts of Thelazia spp.?
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What are the intermediate hosts for Thelazia spp.?
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What condition is primarily caused by Thelazia spp. infection?
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In which location do adult Thelazia spp. typically reside in their definitive hosts?
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Which of the following clinical signs is NOT commonly observed in Thelazia infections in ruminants?
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What is a common method for diagnosing Thelazia spp. infection?
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What is the life cycle type exhibited by Thelazia spp.?
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What is the main purpose of effective fly control in preventing Thelazia infection in ruminants?
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Which of the following is NOT associated with Parelaphostrongylus tenuis infection in abnormal hosts?
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What role do land snails and slugs play in the life cycle of Parelaphostrongylus tenuis?
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Which treatment strategy offers the best chance for management of Parelaphostrongylus tenuis in abnormal hosts?
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What is a significant clinical sign of Thelazia infection in ruminants?
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What abnormal host might experience severe neurological disease caused by Parelaphostrongylus tenuis?
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In which environment are human infections of Thelazia spp. most likely to occur?
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Which of the following diagnosis methods is commonly used for identifying Parelaphostrongylus tenuis in white-tailed deer?
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What is the prognosis for animals suffering from Parelaphostrongylus tenuis infection in abnormal hosts?
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What class does Parelaphostrongylus tenuis belong to?
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Which symptom is NOT typically observed in abnormal hosts infected with Parelaphostrongylus tenuis?
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How does Parelaphostrongylus tenuis infect a white-tailed deer?
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What is the best method to prevent Thelazia infection in ruminants during peak fly seasons?
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What symptom is characteristic of Thelazia spp. infections in humans?
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Which of the following statements about zoonotic transmission of Parelaphostrongylus tenuis is true?
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Study Notes
Morphological Features of Strongylida Nematodes
- Males possess a copulatory bursa utilized during mating.
- Shed strongyle-type eggs that are ellipsoid, thin-shelled, and typically grayish.
Strongylida Parasites in Ruminants
- Key genera include Haemochus, Ostertagia, Trichostrongylus, Cooperia, and Oesophagostomum (abbreviated as HOT CO).
- Eggs from these genera are indistinguishable from one another.
Unique Features of Strongylida
- The copulatory bursa is a distinguishing morphological feature in male nematodes of this order.
Life Cycle of Gastrointestinal Nematodes (Strongylida)
- Direct life cycle includes both environmental and host stages.
- Eggs are excreted in feces and develop into first-stage larvae (L1).
- L1 larvae molt to second-stage (L2) and become infective third-stage larvae (L3) in the environment.
- Ingestion of L3 larvae by the host leads to migration to specific sites such as the abomasum and small intestine.
- Development progresses to fourth-stage larvae (L4) and then adulthood.
- Prepatent period from L3 ingestion to egg shedding ranges from 2 to 4 weeks.
Distinction from Nematodirus
- Nematodirus does not belong to the HOT CO complex and has eggs containing more cytoplasm.
- Adult Nematodirus are significantly larger in size compared to other Strongylida.
Periparturient Rise Phenomenon
- Refers to increased nematode egg shedding in pregnant ewes during the periparturient period.
- Associated with a decrease in immunity due to elevated prolactin levels.
- Leads to reactivation of previously arrested L4 larvae, increasing pasture contamination with infective larvae.
- Significant rise in pasture contamination exposes newborn offspring to high levels of infective larvae.
Parasitic Gastroenteritis (PGE)
- PGE results from a complex of gastrointestinal nematodes affecting ruminants.
- Can present as clinical disease with significant symptoms or subclinical disease impacting herd health.
- Clinical signs include:
- Loss of appetite and weight loss
- Watery green diarrhea and dehydration
- Rough hair coat and submandibular edema (due to protein loss)
- Pale mucous membranes indicating possible anemia or protein deficiency.
Morphology of Haemonchus spp.
- Known as the "barber pole" worm; large nematodes located in the abomasum of ruminants.
- Females display a distinct appearance with a white uterus intertwined with a red intestine, signifying their blood-feeding nature.
Life Cycle of Haemonchus spp.
- Direct life cycle; L3 larvae are ingested from the environment.
- Larvae migrate to the abomasum and penetrate the epithelial cells.
- L3 larvae can enter a state of hypobiosis (arrested development) to survive adverse conditions.
Importance of Haemonchus spp.
- Major blood feeders; can induce severe anemia, particularly affecting young ruminants.
- Haemonchus contortus mainly impacts sheep and goats; Haemonchus placei predominantly found in cattle but typically does not cause clinical disease.
Clinical Signs and Pathology
- Infection can manifest as hyperacute, acute, or chronic forms, with severe cases in juvenile animals.
- Clinical indicators include:
- Severe anemia assessed via the FAMACHA system.
- Pale mucous membranes.
- Submandibular edema (bottle jaw).
- Melena (dark feces).
- Wool break, anorexia, and weight loss.
- Death may occur swiftly, often before eggs are detected in feces, due to significant blood loss and anemia linked to the worms' feeding.
Diagnosis and Management of Haemonchus spp.
- Diagnosis typically involves fecal egg counts via the McMaster's technique to gauge egg shedding and pasture contamination levels.
- FAMACHA system used to evaluate anemia severity and inform treatment necessity.
- Management strategies include:
- Strategic deworming and integrated pest management (IPM).
- Implementing pasture rotation and multi-species grazing.
- Selective breeding for resistance against infections.
- Anthelmintic resistance poses significant challenges, necessitating careful management practices.
Importance of Ostertagia spp.
- Ostertagia spp., notably Ostertagia ostertagi, known as the "brown stomach worm," significantly affect cattle and also impact camelid health.
- Causes a disease called ostertagiosis, which impacts ruminant health dramatically.
- Type I ostertagiosis occurs in young cattle grazing for the first time; Type II arises from the synchronous emergence of hypobiotic larvae.
- Worms infest the abomasum, damaging gastric glands and impairing digestion and nutrient absorption.
- Symptoms include diarrhea, weight loss, and can result in death if severe.
Life Cycle and Pathophysiology
- Ostertagia spp. have a direct life cycle; infective L3 larvae are ingested from the environment.
- Larvae penetrate the gastric glands of the abomasum, molting into L4.
- Two outcomes occur after molting: L4 larvae emerge as adults or undergo hypobiosis (arrested development).
- Damage to gastric glands causes increased abomasal pH and decreased pepsin production.
- Increased permeability leads to protein-losing gastropathy, diarrhea, and malabsorption.
- Type I ostertagiosis is connected to recent L3 ingestion; Type II relates to the emergence of arrested larvae after weeks or months.
Related Worms in Small Ruminants
- Teladorsagia sp. is similar but of lesser importance; does not primarily cause disease yet contributes to parasitic gastroenteritis (PGE) in small ruminants.
Clinical Signs and Diagnosis
- Common clinical signs of Ostertagia infection include:
- Diarrhea
- Weight loss
- Dehydration
- Increased thirst
- Hypoproteinemia
- Submandibular edema
- Severe cases may lead to emaciation and death.
- Diagnosis relies on clinical signs, fecal egg counts, and necropsy findings, which reveal "Moroccan leather" appearance of the abomasal mucosa due to larval nodules.
Trichostrongylus spp. in Ruminant Parasitism
- Small nematodes involved in Parasitic Gastroenteritis (PGE) in ruminants.
- Not primary pathogens but can lead to severe disease in high densities.
- Associated with symptoms like "black scours" or dark green diarrhea.
- Possess a direct life cycle with potential for hypobiosis.
- Trichostrongylus axei affects the abomasum in ruminants and the stomach in horses.
- Trichostrongylus colubriformis primarily targets the small intestine of ruminants.
Economic Importance of Cooperia spp.
- Small nematodes residing in the small intestine of ruminants.
- Contributes to PGE and prevalent in cow/calf operations, leading to economic losses.
- Causes significant weight gain reduction in calves.
- Direct life cycle initiated by ingestion of L3 larvae from the environment, with hypobiosis potential.
- Particularly impacts young animals; resistance to anthelmintics complicates cattle management.
Morphology and Life Cycle of Oesophagostomum spp.
- Known as nodular worms, found in the large intestine of ruminants.
- Direct life cycle where L3 larvae penetrate the mucosa and develop into L4, forming eosinophilic nodules.
- These nodules can cause inflammation and result in hemorrhage, mucus production, and protein leakage.
- Oesophagostomum radiatum affects cattle, while O. columbianum affects sheep and goats.
- Though not primary pathogens, they contribute to PGE and are often noted during necropsies.
Significance of Nematodirus spp. in Ruminant Health
- Long, slender nematodes located in the small intestine of ruminants.
- Unique traits include large eggs that require specific environmental conditions to hatch, leading to seasonal risks.
- Eggs withstand drying and freezing, needing a cold period followed by warmth, particularly common in temperate regions.
- High larval burdens can develop on pastures in spring, posing risks to young animals.
- Infective L3 larvae are ingested, developing in the small intestine mucosa into L4, leading to malabsorption and contributing to PGE.
- Nematodirus helvetianus targets cattle, while N. battus and others affect sheep.
Common Name and Morphological Features
- Bunostomum spp. are commonly known as hookworms.
- These nematodes possess a large buccal cavity equipped with chitinous cutting plates for blood-feeding.
- Adult worms measure approximately 2-3 cm in length.
- They predominantly inhabit the small intestine of ruminants.
- Bunostomum phlebotomy primarily infects cattle, while Bunostomum trigonocephalum targets small ruminants and camelids.
Life Cycle
- Bunostomum spp. have a direct life cycle.
- Infective L3 larvae can be ingested or more commonly penetrate the skin of the host.
- Upon skin penetration, larvae enter the bloodstream, migrate to the lungs, are coughed up, then swallowed to reach the small intestine for maturation.
- If larvae are ingested, they directly enter the small intestine to develop into adults.
- The prepatent period ranges from approximately 2 to 2.5 months.
Associated Pathology
- Significant pathology is attributed to the blood-feeding behavior of Bunostomum spp.
- Consequences include the loss of villi, intestinal inflammation, and hemorrhagic lesions.
- Clinical manifestations include diarrhea, emaciation, anemia, and hypoproteinemia.
- Skin entry by larvae results in irritation, pruritus, and scabs, potentially leading to behaviors like foot stamping and leg licking.
- Severe infections can result in death, particularly in young animals.
Clinical Signs of Infection
- Common signs include diarrhea, weight loss, emaciation, anemia, and hypoproteinemia, which may present as submandibular edema (bottle jaw).
- Skin penetration may cause irritation and pruritus at the entry sites.
- Severe cases may be fatal, posing a higher risk to younger ruminants.
Diagnosis and Treatment
- Diagnosis is conducted through fecal flotation to identify strongyle-type eggs with a rough or thick shell.
- Adult worms can be recognized during necropsy by their characteristic morphology, including chitinous cutting plates and a large buccal cavity.
- Treatment typically involves various anthelmintics, with levamisole specifically labeled for use in sheep.
- Effective management incorporates pasture management and maintaining good hygiene practices.
Classification and Importance
- Strongyloides papillosus, commonly known as the threadworm, is classified under the order Rhabditida.
- Primarily affects young ruminants, particularly in the small intestine, causing significant health issues.
- Exhibits a unique life cycle with alternating free-living and parasitic stages, with only parasitic females present in the host.
Life Cycle
- The life cycle can be direct or indirect.
- Parasitic females in the host's small intestine lay eggs containing rhabditiform L1 larvae, expelled in feces.
- In the environment, L1 larvae hatch and can develop into infective L3 larvae or free-living adults reproducing sexually.
- L3 larvae can penetrate the host's skin or be ingested; they migrate to the lungs, are coughed up, then swallowed to mature in the small intestine.
Pathology and Clinical Signs
- Infections mainly affect young ruminants leading to diarrhea, dehydration, anorexia, and emaciation.
- Severe infections can cause ataxia and brain lesions, with cardiac arrest reported in heavily burdened calves and lambs.
- Clinical signs can manifest with as few as 2000-5000 larvae in goats and lambs.
- Peak infection occurs in calves aged 1-3 months and in lambs and kids aged 2-6 weeks.
Diagnosis and Treatment
- Diagnosis is performed through fecal flotation, identifying thin-shelled, larvated L1 eggs.
- Differences in egg morphology: rhabditiform eggs have a dilated esophageal bulb, while filariform eggs have a long esophagus without a bulb.
- Adult worms are small (3-10 mm) and embedded in the intestinal mucosa, making them hard to visualize.
- Treatment options include avermectins (approved for cattle) and thiabendazole.
- Control measures involve maintaining a clean, dry environment to limit the survival of infective L3 larvae.
Significance of Trichuris spp. in Ruminants
- Trichuris spp., or whipworms, primarily inhabit the large intestine of ruminants.
- Infections are mostly subclinical, but can lead to anorexia and severe diarrhea in young animals.
- Heavy infections can cause bloody diarrhea, particularly in vulnerable populations.
Classification of Trichuris spp.
- Classified within the order Enoplida.
- They have a direct life cycle, with no intermediate hosts required for development.
Life Cycle of Trichuris spp.
- Life cycle is direct; eggs containing L1 larvae are passed in feces.
- Eggs develop into infective L1 larvae in the environment.
- Upon ingestion by the host, larvae hatch in the small intestine and migrate to the large intestine.
- Larvae embed in the mucosa of the large intestine and mature into adults.
Morphology of Trichuris spp.
- Adult whipworms measure 3-5 cm in length.
- Characteristic whip-like shape with a narrow anterior end and a thicker posterior end.
Pathology Associated with Trichuris spp.
- Generally causes mild pathology in hosts.
- Heavy infections can result in inflammation and damage to the intestinal mucosa.
- Clinical signs are uncommon but can include anorexia and bloody diarrhea, primarily in young ruminants with heavy burdens.
Diagnosis of Trichuris spp.
- Diagnosis is achieved through fecal flotation to identify characteristic eggs with bipolar plugs.
- Adult worms can be observed during necropsy of infected individuals.
Treatment and Management of Trichuris spp.
- Treatment options include various avermectins effective against whipworm infections.
- Implementing pasture management practices aids in controlling parasite spread and reducing infections.
Cestodes in Ruminants
- Moniezia spp. is the most common cestode found in ruminants.
- Classification: Class Cestoda, Family Anoplocephalidae.
General Morphology of Moniezia spp.
- Large tapeworms, often several meters in length.
- Broad, segmented body known as the strobila, composed of multiple proglottids.
- Each proglottid contains a complete set of reproductive organs.
- Eggs feature a pyriform apparatus, a distinctive pear-shaped structure within them.
Hosts and Life Cycle of Moniezia spp.
- Definitive Hosts: Ruminants such as cattle, sheep, and goats.
- Intermediate Hosts: Free-living oribatid mites, which are small soil-dwelling arthropods.
- Life Cycle: Indirect; adult tapeworms live in the small intestine, releasing gravid proglottids in feces.
- Gravid proglottids shed eggs that are ingested by oribatid mites, developing into cysticercoid larvae.
- Ruminants become infected by ingesting these mites during grazing, where cysticercoid larvae mature into adult tapeworms in the host's small intestine.
Clinical Significance of Moniezia spp.
- Generally non-pathogenic in ruminants; most infections are asymptomatic.
- Heavy infections in young animals may cause poor growth and nutritional competition.
- Detection often occurs incidentally during fecal examinations.
Diagnosis and Treatment of Moniezia spp.
- Diagnosis through fecal flotation to identify characteristic eggs with a pyriform apparatus; proglottids may also be observed.
- Treatment usually unnecessary but effective anthelmintics include praziquantel and albendazole.
- Control measures emphasize reducing exposure to oribatid mites through grazing management.
Zoonotic Concerns
- No significant zoonotic concerns; Moniezia spp. tapeworms are specific to ruminants and do not infect humans.
Other Cestodes in Ruminants
- Thysanosoma spp. (fringed tapeworm) is another cestode found in ruminants.
- Thysanosoma spp. primarily inhabit bile ducts, pancreatic ducts, and the duodenum, unlike Moniezia spp.
- Proglottids of Thysanosoma spp. have a distinctive fringe along the posterior edge, absent in Moniezia spp.
- These cestodes are more common in the western United States and may cause mild bile duct inflammation with heavy infections.
Taenia saginata: Life Cycle and Public Health
- Taenia saginata, known as the beef tapeworm, belongs to the family Taeniidae.
- Cattle serve as intermediate hosts where the larval stage (cysticercus) resides in muscle tissue, leading to "measly beef."
- Humans act as definitive hosts, developing adult tapeworms in the small intestine after consuming undercooked beef containing cysticerci.
- Although Taenia saginata is non-pathogenic in cattle, it poses public health risks due to potential human infection.
- Proper meat inspection and cooking practices are essential to prevent zoonotic transmission.
Fasciola hepatica Overview
- Classified under the class Trematoda, commonly referred to as the liver fluke.
- Found primarily in the bile ducts and liver of hosts.
Morphology
- Adult liver flukes are large and leaf-shaped, measuring 2-4 cm in length.
- They have a broad anterior end with a cone-shaped projection and are dorsoventrally flattened.
Hosts
- Definitive hosts: Ruminants (cattle, sheep, goats), swine, and horses.
- Intermediate host: Freshwater snail from the family Lymnaeidae.
Life Cycle
- Indirect life cycle involving multiple stages:
- Eggs are excreted in feces of definitive hosts, hatch into miracidia in water.
- Miracidia infect freshwater snails, developing into sporocysts, rediae, and cercariae.
- Cercariae exit the snail, encysting as metacercariae on vegetation.
- Ruminants become infected by ingesting contaminated vegetation.
- Metacercariae excyst in the intestine, migrate to the liver, and mature in bile ducts.
- Prepatent period: Approximately 2-3 months.
Pathology
- Causes hepatic and biliary damage; immature flukes induce hepatitis, fibrotic tracts, hemorrhage, and anemia.
- Adult flukes in bile ducts cause hyperplasia, fibrosis, calcification, and cholangitis.
- Chronic infections can lead to significant liver damage, reduced productivity, and potential death.
Clinical Signs of Fascioliasis
- Acute disease: Anorexia, anemia, jaundice, ascites, depression, and sudden death in small ruminants.
- Subacute disease: Decreased weight gain, anemia, liver failure, and potential death.
- Chronic disease: Emaciation, anemia, bottle jaw (submandibular edema), and production losses.
Diagnosis and Treatment
- Diagnosis: Identification of operculated eggs via fecal sedimentation.
- Treatment options: Triclabendazole, albendazole, and clorsulon; effective against various fluke stages.
- Control measures: Management of snail populations and avoiding grazing on contaminated pastures.
Zoonotic Concerns
- Fasciola hepatica can infect humans, typically through ingestion of contaminated aquatic vegetation.
- Human fascioliasis can lead to similar liver and biliary pathology, causing abdominal pain and jaundice.
- Preventive measures include proper washing and cooking of vegetables and snail population control.
Fascioloides magna Overview
- Also classified under the class Trematoda, known as the deer liver fluke.
- Natural definitive hosts include cervids: white-tailed deer, elk, and moose.
Life Cycle
- Similar to Fasciola hepatica: Eggs hatch into miracidia in water, infect snails, develop into cercariae.
- Cercariae encyst as metacercariae on vegetation, ingested by cervids, migrate to liver, and mature into adults.
Pathological Effects in Hosts
- In natural hosts (deer): Forms thin-walled cysts causing minimal disease.
- In aberrant hosts (sheep and goats): Causes severe liver damage and can lead to death.
- In dead-end hosts (cattle): Flukes form thick-walled cysts producing no clinical signs but causing potential liver damage.
Clinical Signs of Fascioloides magna
- In aberrant hosts: Sudden death due to severe liver damage or chronic disease signs like weight loss and ascites.
- In dead-end hosts: Rare clinical signs, with liver damage evident post-mortem.
- In natural hosts: Generally subclinical infections.
Diagnosis and Management
- Diagnosis in natural hosts involves fecal sedimentation to identify operculated eggs.
- Aberrant hosts diagnosed post-mortem; no eggs in feces.
- Treatment for cervids may include anthelmintics like oxyclozanide; control through prevention of grazing near deer populations.
Zoonotic Concerns
- No significant zoonotic risk with Fascioloides magna; does not infect humans.
- Economic and animal health concerns arise from its presence in wildlife and spillover into domestic livestock.
Other Liver Trematodes
- Dicrocoelium dendriticum (lancet fluke): Uses land snail and ants as intermediate hosts; less severe liver disease than Fasciola.
- Paramphistomum spp. (rumen flukes): Found in the rumen, generally considered incidental and typically not causing clinical disease.
Key Species of Lungworms in Ruminants
- Key lungworm species include Dictyocaulus viviparus and Dictyocaulus filaria (order Strongylida, superfamily Trichostrongyloidea) and Muellerius capillaris (order Strongylida, superfamily Metastrongyloidea).
- Dictyocaulus viviparus primarily affects cattle, while Dictyocaulus filaria is found in small ruminants.
- Muellerius capillaris is more prevalent in small ruminants, especially goats.
Life Cycle of Dictyocaulus viviparus
- Life cycle is direct; adult worms inhabit the trachea, bronchi, and bronchioles of cattle.
- Adult worms lay embryonated eggs that are coughed up, swallowed, and excreted as L1 larvae in feces.
- L1 larvae develop into infective L3 larvae in the environment, aided by fungi like Pilobolus.
- Cattle ingest L3 larvae, which penetrate the intestinal wall and migrate through lymphatics and bloodstream to lungs.
- Adults mature in the lungs with a prepatent period of approximately 1 month.
Pathology Associated with Dictyocaulus viviparus
- Causes parasitic bronchitis, also known as "husk" or "hoose."
- Inflammatory exudates obstruct small airways, causing breathing difficulties, fibrotic alveoli, and potential atelectasis.
- Severe infections lead to significant lung damage and can result in secondary bacterial infections.
Clinical Signs of Dictyocaulus viviparus Infection
- Respiratory symptoms: deep, moist cough, tachypnea (rapid breathing), and harsh bronchial sounds.
- Severe cases may cause anorexia, emaciation, and fever due to secondary infections.
- Untreated severe infections can be fatal.
Diagnosis and Treatment of Dictyocaulus viviparus
- Diagnosis achieved by identifying L1 larvae in fresh feces using the Baermann technique.
- Adult worms can be observed during necropsy.
- Treatment involves anthelmintics approved for cattle, with vaccination available for clinical disease prevention.
- Control measures focus on pasture management and strategic deworming.
Life Cycle of Muellerius capillaris
- Life cycle is indirect; adult worms reside in the lung parenchyma of small ruminants.
- They lay eggs that hatch into L1 larvae in the lungs, which are then coughed up, swallowed, and excreted.
- L1 larvae are ingested by land snails, their intermediate host, becoming L3 larvae.
- Small ruminants become infected by consuming snails with L3 larvae, which migrate to lungs, forming granulomatous nodules.
- Prepatent period lasts about 1.5 months.
Pathology Associated with Muellerius capillaris
- Causes granulomatous nodules in lungs containing various parasite stages.
- Infections in sheep are often subclinical, whereas goats may show symptoms like coughing, dyspnea, and weight loss.
- Goats are more predisposed to developing clinical disease compared to sheep.
Diagnosis and Treatment of Muellerius capillaris
- Diagnosis involves identifying L1 larvae in fresh feces using the Baermann technique.
- L1 can also be detected in histopathology but not grossly visible during necropsy.
- Distinctive characteristics include wavy tail with dorsal spine (Muellerius) versus blunt tail (Dictyocaulus).
- Treatment typically not needed in sheep; goats may require off-label anthelmintics if symptoms arise.
- Control measures should focus on managing snail populations and minimizing exposure to contaminated areas.
Morphological Differences Between Dictyocaulus and Muellerius
- Muellerius capillaris: L1 larvae are not grossly visible, exhibit a wavy tail with a dorsal spine.
- Dictyocaulus viviparus: L1 larvae are grossly visible with a blunt tail.
Zoonotic Concerns
- No significant zoonotic risks are associated with either Dictyocaulus or Muellerius lungworms.
- These parasites are specific to ruminants and do not present risk to humans, although they have economic impacts on livestock health and productivity.
Thelazia spp. (Eye Worms)
- Classified under the order Spirurida.
- Commonly known as eye worms.
- Definitive hosts primarily include ruminants like cattle, sheep, and goats.
- Intermediate hosts are mainly flies from the genus Musca, such as houseflies and face flies.
Life Cycle of Thelazia spp.
- Indirect life cycle involving adult worms in the conjunctival sac and lacrimal ducts of definitive hosts.
- Adult worms lay first-stage larvae (L1) in the eye's secretions.
- Flies ingest L1 larvae while feeding on eye secretions, developing them into infective third-stage larvae (L3) over 2-4 weeks.
- L3 larvae migrate to the mouthparts of the fly and are deposited back into the conjunctival sac of a new host during feeding.
- Once in the eye, larvae mature into adult worms.
Pathology Associated with Thelazia spp.
- Causes irritation and inflammation of the eye, leading to conjunctivitis and keratitis.
- Severe cases may result in corneal ulcers and excessive tearing (epiphora).
- Chronic infections can lead to long-term eye damage and impaired vision.
Clinical Signs of Thelazia Infection in Ruminants
- Signs include excessive tearing, conjunctivitis, squinting, photophobia, and visible worms in the eye.
- Corneal ulcers may occur, causing cloudiness and decreased vision.
- Infected animals often show discomfort, characterized by frequent blinking or rubbing of their eyes.
Diagnosis and Treatment of Thelazia spp.
- Diagnosis typically involves direct observation of adult worms in the conjunctival sac.
- Slit-lamp examination can provide detailed visualization.
- Treatment includes manual removal of worms under local anesthesia and the use of anthelmintics like ivermectin or doramectin.
- Fly control measures are essential for preventing reinfection.
Preventive Measures for Thelazia Infection
- Effective fly control to reduce Musca populations is crucial.
- Use of insecticides, fly repellents, and practices to manage fly breeding sites.
- Physical barriers like fly masks during peak fly seasons can help prevent infection.
Zoonotic Concerns of Thelazia spp.
- Thelazia spp. are zoonotic and can infect humans, causing ocular symptoms similar to those in animals.
- Human infections generally result from contact with infected animals or the same fly species.
- Good hygiene and fly control measures are important to minimize zoonotic transmission.
Parelaphostrongylus tenuis (Meningeal Worm)
- Classified under the order Strongylida and superfamily Metastrongyloidea.
- Commonly known as the meningeal or brain worm.
- Natural definitive host is the white-tailed deer, where it typically causes little to no clinical disease.
- Abnormal hosts include small ruminants (sheep, goats), camelids (alpacas, llamas), and other wildlife, leading to severe neurological disease.
Life Cycle of Parelaphostrongylus tenuis
- Indirect life cycle with adult nematodes in the subdural space of white-tailed deer.
- Eggs are carried to the lungs via the venous system, hatching into L1 larvae.
- Larvae are coughed up, swallowed, and passed in feces, then ingested by land snails or slugs.
- Infective L3 larvae develop in the intermediate hosts and are transmitted to ruminants through ingestion.
- L3 larvae migrate to the spinal cord and brain in deer; in abnormal hosts, they cause neurological damage through aberrant migration.
Pathology of Parelaphostrongylus tenuis in Abnormal Hosts
- Causes severe neurological damage due to migration within the CNS.
- Leads to encephalitis, neural tissue damage, and symptoms like ataxia, paraplegia, and tetraplegia.
- Damage is often irreversible, resulting in poor prognosis.
Clinical Signs of Parelaphostrongylus tenuis Infection
- Symptoms in abnormal hosts include progressive neurological dysfunction: ataxia, paraplegia, tetraplegia, head tilt, circling, and potential blindness.
- Signs typically worsen over time, potentially leading to recumbency and death.
Diagnosis of Parelaphostrongylus tenuis
- In deer, L1 larvae can be identified in fresh feces using the Baermann technique and PCR.
- In abnormal hosts, diagnosis relies on clinical signs, history of exposure, CSF analysis, and necropsy findings.
- Larvae or adults are rarely found ante-mortem in abnormal hosts.
Treatment and Prevention of Parelaphostrongylus tenuis
- Treatment options for abnormal hosts are limited with a generally poor prognosis.
- May involve anthelmintics like ivermectin or fenbendazole combined with anti-inflammatory medications for CNS inflammation.
- Preventative measures include controlling snail and slug populations and avoiding co-grazing with white-tailed deer.
Zoonotic Concerns of Parelaphostrongylus tenuis
- Parelaphostrongylus tenuis does not pose zoonotic risks as it does not infect humans.
- Primarily affects its natural hosts, exhibiting significant health impacts primarily in abnormal hosts like livestock.
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