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Questions and Answers
What is a defining feature of male nematodes in the order Strongylida?
Which of the following nematodes is not part of the HOT CO complex?
What is an effect of the periparturient rise phenomenon in ewes?
In the life cycle of Strongylida, what is the prepatent period usually observed?
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Which characteristic is typically associated with strongyle-type eggs?
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What are common clinical signs of Parasitic Gastroenteritis (PGE) in ruminants?
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What ecological consequence is observed due to the periparturient rise in nematode egg shedding?
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How do the eggs of Nematodirus differ from those of Strongylida?
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What is the primary clinical sign associated with severe infection of Haemonchus spp. in young ruminants?
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In the life cycle of Ostertagia spp., what occurs after the larvae penetrate the gastric glands?
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What is a significant economic impact associated with Cooperia spp. in cattle?
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Which of the following is a characteristic feature of Haemonchus spp.?
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What is the term used to describe the arrested development of L3 larvae in Haemonchus spp. to survive unfavorable conditions?
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What distinguishes Type II ostertagiosis from Type I in cattle?
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Which of the following pathogens is most associated with causing clinical disease in cattle among the described nematodes?
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What is a common clinical sign of Ostertagia spp. infection in ruminants?
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How are Nematodirus spp. nematodes primarily characterized in terms of their morphology?
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What management strategy is essential due to the increasing concern with anthelmintic resistance in ruminants?
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Which nematode, while not a primary pathogen, can contribute to parasitic gastroenteritis in small ruminants?
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What is the role of Trichostrongylus spp. in ruminant parasitism?
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Which method is typically used to quantify egg shedding for diagnosing Haemonchus spp. infections?
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What is the primary pathology caused by Oesophagostomum spp. in ruminants?
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Which of the following clinical signs is NOT associated with Bunostomum spp. infection?
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What is the primary method of diagnosis for Strongyloides papillosus?
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Which characteristic feature distinguishes the eggs of Strongyloides papillosus from other nematodes?
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What is the most significant pathway of infection for Bunostomum spp. larvae?
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Which of the following statements regarding the life cycle of Trichuris spp. is true?
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What is one of the main clinical signs of Strongyloides papillosus infection in young ruminants?
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What feature of Bunostomum spp. allows them to feed on blood?
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Which of the following is a common treatment option for Bunostomum spp. infections?
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The pathology associated with Trichuris spp. can lead to which of the following?
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What is the likely result of heavy Bunostomum spp. infection in young animals?
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What class of drugs is primarily used in the treatment of Strongyloides papillosus?
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Which of the following describes the morphology of adult Trichuris spp. worms?
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Why might pasture management be essential in controlling Bunostomum spp. infections?
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What clinical signs may indicate a heavy infection of Trichuris spp. in young animals?
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Which method is primarily used to diagnose Moniezia spp. in ruminants?
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What is the primary mode of transmission for Moniezia spp. in ruminants?
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Which of the following statements about the life cycle of Fasciola hepatica is false?
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What distinguishing feature of Moniezia spp. can be observed in its eggs?
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How do Thysanosoma spp. differ morphologically from Moniezia spp.?
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What is the definitive host for Taenia saginata?
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What is the classification of Fasciola hepatica?
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What is the intermediate host for Fasciola hepatica?
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What effect can heavy infections of Moniezia spp. have on young ruminants?
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Which of the following is NOT a method used for the control of Trichuris spp.?
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Which statement about zoonotic risks of Moniezia spp. is true?
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What treatment is recommended if intervention is needed for Moniezia spp. infections?
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What specific anatomical location does Fasciola hepatica inhabit in its definitive host?
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What severe clinical sign is primarily associated with acute fascioliasis in small ruminants?
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What is a common characteristic of adult Fasciola hepatica in the bile ducts?
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In which way can human infection from Fasciola hepatica occur?
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What is a notable feature of Fascioloides magna's pathology in aberrant hosts?
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What type of management is essential to control Fasciola hepatica infection?
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Which diagnostic method is used to identify Fasciola hepatica eggs?
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What significant consequence may arise from chronic fascioliasis infections?
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How do dead-end hosts like cattle respond to Fascioloides magna infections?
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What distinguishes Dicrocoelium dendriticum from Fasciola hepatica?
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Which treatment options are effective against different stages of Fasciola hepatica?
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What is a key outcome of control measures against Fasciola hepatica?
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What effect does feeding by adult Fasciola hepatica have on the host?
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Which feature is true regarding the life cycle of Fascioloides magna?
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How does the presence of Fascioloides magna impact livestock economics?
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What is the primary host for Parelaphostrongylus tenuis?
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Which pathological condition is primarily associated with Thelazia spp.?
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What is a common clinical sign of Parelaphostrongylus tenuis infection in abnormal hosts?
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What is the role of Musca flies in the life cycle of Thelazia spp.?
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Which therapeutic method is typically employed for Thelazia spp. infection treatment?
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What is the primary way to prevent Thelazia infection in ruminants?
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Which of the following symptoms is NOT commonly associated with Thelazia infection in ruminants?
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What technique is most commonly used for diagnosing Parelaphostrongylus tenuis in white-tailed deer?
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What neurological symptoms may result from Parelaphostrongylus tenuis infection in abnormal hosts?
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What is the primary host affected by Dictyocaulus viviparus?
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What contributes to the poor prognosis of Parelaphostrongylus tenuis infections in abnormal hosts?
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Which life cycle type is associated with Muellerius capillaris?
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What is the typical visual expression of Thelazia spp. infection in ruminants?
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What characteristic distinguishes the L1 larvae of Muellerius capillaris from Dictyocaulus species under microscopy?
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Which of the following best describes the epidemiology of Parelaphostrongylus tenuis in abnormal hosts?
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Which clinical sign is commonly observed in severe infections of Dictyocaulus viviparus in cattle?
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What role do fungi like Pilobolus play in the life cycle of Dictyocaulus viviparus?
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Which of the following is a zoonotic concern with Thelazia spp.?
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How is diagnostic confirmation of Dictyocaulus viviparus accomplished?
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What systemic medications may be used for managing Thelazia spp. infections?
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What is a common name associated with the clinical manifestation caused by Dictyocaulus viviparus?
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Which of the following is a characteristic effect of Muellerius capillaris infections in goats?
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What is the typical prepatent period for Dictyocaulus viviparus?
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What factor contributes to the pathogenesis of Dictyocaulus viviparus leading to lung damage?
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Which hosts are definitive for Thelazia spp.?
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What treatment is often not required for Muellerius capillaris infections in sheep?
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What impact do Dictyocaulus and Muellerius lungworms have on livestock?
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What role does the copulatory bursa play in male nematodes of the order Strongylida?
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Which of the following statements accurately describes the lifecycle stages of Strongylida nematodes?
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What is the primary biological reason behind the periparturient rise of nematode egg shedding in pregnant ewes?
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What clinical signs associated with Parasitic Gastroenteritis (PGE) may indicate a significant severity of infection?
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Which nematode is recognized for having a distinct egg morphology that sets it apart from Strongylida?
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What main outcome is associated with the emergence of previously arrested L4 larvae in pregnant ewes due to increased nematode egg shedding?
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Which of the following is NOT a common characteristic observed in Strongylida nematodes?
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In the context of gastrointestinal nematodes, what does 'subclinical disease' refer to?
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What is the primary consequence of blood feeding by Haemonchus spp. in infected young ruminants?
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What pathological condition is primarily caused by the migration of immature Fasciola hepatica flukes through the liver parenchyma?
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What characterizes Type II ostertagiosis in cattle?
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In chronic fascioliasis, which clinical sign is NOT typically observed?
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Which morphological feature is distinctive for diagnosing Oesophagostomum spp. infections?
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What type of cysts do Fascioloides magna form in natural hosts like deer?
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What is a common clinical sign associated with severe infection by Ostertagia spp.?
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In humans, which symptom is associated with fascioliasis caused by Fasciola hepatica?
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Which nematode species is most commonly associated with causing PGE in young ruminants?
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What diagnostic method is generally used to identify Fascioloides magna in aberrant hosts?
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How do Trichostrongylus spp. affect digestion in ruminants?
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Which treatment is specifically noted as effective against all stages of Fasciola hepatica?
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Which of the following factors is a primary challenge in managing Cooperia spp. infections in cattle?
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Which pathology results from the larvae of Ostertagia spp. penetrating gastric glands?
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What is a potential consequence of ignoring snail population control in managing Fasciola hepatica?
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What diagnostic technique is essential for assessing Haemonchus spp. infection severity?
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In aberrant hosts like sheep and goats, the infection with Fascioloides magna can lead to which severe outcome?
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Which of the following is the intermediate host for both Fasciola hepatica and Fascioloides magna?
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What notable appearance does the abomasal mucosa exhibit in severe Ostertagia infection?
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What is a significant characteristic of Nematodirus spp. in terms of their life cycle?
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What management strategy should be implemented due to rising concerns over anthelmintic resistance?
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What is a significant clinical sign associated with heavy infections of Trichuris spp. in young animals?
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Which morphological feature is characteristic of eggs produced by Moniezia spp.?
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What is the primary reason for managing grazing areas in relation to Moniezia spp.?
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What is the main public health concern related to Taenia saginata?
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Which cestode is primarily found in the bile ducts and pancreatic ducts of ruminants?
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In which anatomical location will adult Fasciola hepatica be commonly found within its definitive host?
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What specific stage of Fasciola hepatica is responsible for infecting ruminants?
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What is the definitive host for the cestode Moniezia spp.?
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What is the mode of transmission for Taenia saginata to humans?
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What is a primary treatment option for infection with Moniezia spp. if intervention is deemed necessary?
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Which of the following statements regarding the life cycle of Fasciola hepatica is true?
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What structure is a definitive feature of adult Fasciola hepatica?
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What distinguishes Thysanosoma spp. from Moniezia spp. morphologically?
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What is a common effect of infection with Moniezia spp. in young ruminants?
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Which of the following nematodes predominantly infects small ruminants and camelids?
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What is the typical mode of entry for infective L3 larvae of Bunostomum spp. into the host?
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What is a key clinical sign indicating severe infection of Strongyloides papillosus in young ruminants?
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Which of the following features distinguishes Trichuris spp. from other nematodes?
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In the life cycle of Strongyloides papillosus, what happens to larvated L1 eggs once they are passed in feces?
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What pathology is primarily caused by the blood-feeding behavior of Bunostomum spp.?
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Which of the following morphological features is seen in the adult Strongyloides papillosus?
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What is the prepatent period for Bunostomum spp. after infection?
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What type of eggs are associated with Strongyloides papillosus infections?
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In cases of Bunostomum spp. infection, what secondary symptom can be observed due to skin penetration?
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What is the classification order of Strongyloides papillosus?
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What contributes to the high larval burden of Nematodirus on pasture in spring?
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Which class of drugs is typically not used for treating Trichuris spp. infections?
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Which clinical sign is least associated with severe Trichuris spp. infection in ruminants?
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Study Notes
Morphological Features of Nematodes in Strongylida
- Males possess a copulatory bursa for mating.
- Produce strongyle-type eggs: ellipsoid, thin-shelled, grayish in color.
- Key genera include Haemonchus, Ostertagia, Trichostrongylus, Cooperia, and Oesophagostomum (often referred to as HOT CO).
Life Cycle of Strongylida Nematodes
- Direct life cycle involving eggs and larvae in the environment and definitive hosts (ruminants).
- Eggs shed in feces develop into first-stage larvae (L1), then molt to L2 before becoming infective L3 larvae.
- L3 larvae are ingested by hosts, migrate to specific sites (e.g., abomasum, small intestine), and develop into L4 larvae and adults.
- Prepatent period: 2-4 weeks from L3 ingestion to egg shedding.
Periparturient Rise Phenomenon
- Refers to increased nematode egg shedding in pregnant ewes.
- Caused by relaxation of immunity due to elevated prolactin levels, leading to emergence of previously dormant L4 larvae.
- Contributes to pasture contamination with infective larvae, increasing risk for offspring.
Parasitic Gastroenteritis (PGE)
- Caused by a complex of gastrointestinal nematodes in ruminants.
- Can present as clinical disease (significant symptoms and impacts) or subclinical disease (impacts herd health without overt symptoms).
- Clinical signs include loss of appetite, weight loss, watery diarrhea, dehydration, rough coat, protein loss (submandibular edema), and pale mucous membranes.
Haemonchus spp. Overview
- Known as "barber pole" worms; blood-feeding nematodes that cause severe anemia.
- Females recognizable by a distinctive striped appearance due to their reproductive organs.
- Direct life cycle; larvae undergo hypobiosis to survive unfavorable conditions.
- Severe infections present with anemia, which can be assessed using the FAMACHA system.
Clinical Signs and Pathology of Haemonchus Infection
- Symptoms vary from hyperacute to chronic; young animals are most affected.
- Signs include severe anemia, pale mucous membranes, submandibular edema, dark feces (melena), wool break, anorexia, emaciation, and potential death before eggs are detected in feces.
Ostertagia spp. Significance
- Known as "brown stomach worms"; essential in cattle health.
- Cause ostertagiosis, with clinical Type I occurring in young animals and Type II from emergence of hypobiotic larvae.
- Damage gastric glands, leading to malabsorption, diarrhea, weight loss, and potential death.
Lifecycle and Pathophysiology of Ostertagia
- Direct life cycle with L3 larvae burrowing into gastric glands.
- Larval development causes increased abomasal pH, reduced pepsin production, and protein loss, leading to diarrhea and weight loss.
Other Important Genera
- Teladorsagia spp.: Similar to Ostertagia but less clinically significant in small ruminants.
- Trichostrongylus spp.: Small nematodes causing PGE, leading to dark green diarrhea; also undergo hypobiosis.
- Cooperia spp.: Contribute to PGE with significant prevalence and impact on weight gain in cattle; resistance to anthelmintics is a challenge.
- Oesophagostomum spp.: Nodular worms that form eosinophilic nodules in the large intestine; associated with inflammation and protein loss.
Nematodirus spp. Characteristics
- Unique among strongyles; large eggs that require specific environmental conditions to hatch.
- Infective larvae pose risks to young animals, leading to malabsorption and PGE.
Bunostomum spp. (Hookworms)
- Large buccal cavity with chitinous cutting plates; significant blood-feeding behavior.
- Direct life cycle with skin penetration as the primary infection route, leading to severe anemia and other pathologies.
Strongyloides papillosus Overview
- Threadworm with an alternating free-living and parasitic life cycle; primarily affects young ruminants.
- Clinical signs include diarrhea, emaciation, and possible neurological effects in heavy infections.
Trichuris spp. Classification and Pathology
- Known as whipworms found in the large intestine; generally subclinical but may cause anorexia and diarrhea in severe infestations.
- Characteristic whip-like morphology with a pronounced difference between anterior and posterior ends.
Moniezia spp. Overview
- Common cestode in ruminants, large tapeworms with a segmented body.
- Life cycle involves oribatid mites as intermediate hosts; typically asymptomatic, but can affect growth in heavy infections.
Fasciola hepatica (Liver Fluke)
- Leaf-shaped flukes found in the liver and bile ducts; indirect life cycle involving freshwater snails as intermediate hosts.
- Important health concerns in ruminants due to potential liver damage.
Taenia saginata (Beef Tapeworm)
- Cattle serve as intermediate hosts for cystic larvae; human consumption of undercooked beef leads to infection.
- Public health concern requires proper meat inspection to prevent zoonotic transmission.
Zoonotic Concerns
- Moniezia spp. pose no significant zoonotic risks, being host-specific to ruminants.### Fasciola hepatica Overview
- Cercariae are released from snails, encyst as metacercariae on vegetation, and infect ruminants via contaminated vegetation ingestion.
- Metacercariae excyst in the small intestine, penetrate the intestinal wall, migrate to the liver, and mature into adults in bile ducts.
- The prepatent period lasts approximately 2-3 months.
Pathology of Fasciola hepatica
- Causes both hepatic and biliary damage:
- Immature flukes induce hepatitis, fibrotic tracts, hemorrhage, and anemia while migrating through the liver.
- Adult flukes in bile ducts lead to biliary duct hyperplasia, fibrosis, and calcification, resulting in cholangitis.
- Feeding can cause anemia, contributing to hemosiderin deposition in excrement.
- Chronic infections result in substantial liver damage, reduced productivity, and can lead to death.
Clinical Signs of Fascioliasis
- Acute disease in small ruminants:
- Symptoms include anorexia, anemia, jaundice, ascites, depression, and sudden death.
- Subacute disease follows lower infection levels, presenting as decreased weight gain, anemia, liver failure, and potential death.
- Chronic disease from moderate infections leads to emaciation, anemia, bottle jaw, and production losses.
Diagnosis and Treatment of Fasciola hepatica
- Diagnosis: Identification of operculated eggs in fecal sedimentation; adults may be seen during necropsy.
- Treatments include:
- Triclabendazole, albendazole, and clorsulon target various fluke life stages.
- Control measures focus on snail management and avoiding grazing on contaminated pastures.
Zoonotic Concerns with Fasciola hepatica
- Fasciola hepatica is zoonotic; humans can be infected by contaminated watercress or aquatic vegetation.
- Symptoms in humans mirror those in ruminants: abdominal pain, jaundice, and systemic symptoms.
- Preventive measures include proper washing of vegetables and snail population control.
Fascioloides magna Overview
- Also known as the deer liver fluke, classified under the class Trematoda.
- Natural definitive hosts include cervids such as white-tailed deer, elk, and moose.
Life Cycle of Fascioloides magna
- Similar to Fasciola hepatica:
- Eggs released in feces hatch into miracidia in aquatic environments.
- Miracidia infect freshwater snails, develop into cercariae, which encyst as metacercariae on vegetation.
- The juvenile flukes migrate to the liver and mature into adults.
Pathological Effects of Fascioloides magna
- In natural hosts (deer), thin-walled cysts form in the liver with minimal clinical signs.
- In aberrant hosts (sheep and goats), severe lesions arise, causing traumatic hepatitis, hemorrhage, and necrosis, often leading to death.
- Dead-end hosts (cattle) develop thick-walled cysts without egg shedding; clinical signs are rarely observed.
Clinical Signs of Fascioloides magna Infection
- Aberrant hosts show sudden death due to severe liver damage or chronic signs like weight loss and ascites.
- Dead-end hosts typically show no clinical signs, though liver damage may be evident post-mortem.
Diagnosis and Management of Fascioloides magna
- Diagnosis in deer is through fecal sedimentation to identify operculated eggs.
- In aberrant hosts, flukes may be found post-mortem, with no eggs present in feces.
- Management focuses on deer and snail population control.
Other Liver Trematodes in Ruminants
- Dicrocoelium dendriticum (lancet fluke) and Paramphistomum spp. (rumen flukes) can infect ruminants.
- Dicrocoelium uses land snails and ants as intermediate hosts, generally causing milder liver disease than Fasciola.
- Paramphistomum primarily resides in the rumen and is usually incidental with minimal clinical impact.
Key Lungworm Species in Ruminants
- Dictyocaulus viviparus (cattle), Dictyocaulus filaria (small ruminants), and Muellerius capillaris (small ruminants, especially goats) are significant lungworm species.
Life Cycle of Dictyocaulus viviparus
- Direct life cycle; adult worms reside in the lungs of cattle.
- Eggs are coughed up and hatch into L1 larvae, which develop into infective L3 larvae in the environment.
- Cattle are infected through ingestion of L3 larvae.
Pathology of Dictyocaulus viviparus
- Causes parasitic bronchitis ("husk"), leading to airway obstruction, difficulty breathing, and secondary bacterial infections.
Clinical Signs of Dictyocaulus viviparus
- Symptoms include a deep, moist cough, tachypnea, and potential anorexia and fever in severe cases.
Diagnosis and Treatment of Dictyocaulus viviparus
- Diagnosed via Baermann technique to identify L1 larvae in fresh feces; adult worms visible during necropsy.
- Treatment includes various anthelmintics and vaccination, alongside good pasture management.
Life Cycle and Significance of Muellerius capillaris
- Indirect life cycle involving land snails as intermediate hosts.
- Causes pulmonary granulomatous nodules; subclinical in sheep but symptomatic in heavily infected goats.
Diagnosis and Treatment of Muellerius capillaris
- Diagnosed using the Baermann technique for L1 larvae; histopathological examination may reveal infection.
- Treatment is rarely necessary in sheep; goats may receive anthelmintics if symptomatic.
Morphological Differences of Lungworms
- Muellerius L1 larvae exhibit a wavy tail with a dorsal spine; Dictyocaulus L1 larvae have a blunt tail and are grossly visible.
Zoonotic Concerns of Lungworms
- Dictyocaulus and Muellerius lungworms pose no significant zoonotic risks to humans but can impact livestock health.
Thelazia spp. Overview
- Classified under Spirurida; commonly known as eye worms.
- Definitive hosts include a range of mammals, primarily ruminants, with flies as intermediate hosts.
Life Cycle of Thelazia spp.
- Indirect life cycle; adult worms reside in the eye, laying L1 larvae in secretions ingested by flies.
- Flies develop L1 into infective L3 larvae to infect new hosts during feeding.
Pathology of Thelazia spp.
- Causes ocular irritation and inflammation, leading to conjunctivitis and keratitis, with potential for corneal ulcers and impaired vision.
Clinical Signs of Thelazia Infection
- Signs include excessive tearing, conjunctivitis, visible worms in the eye, and potential corneal issues.
Diagnosis and Treatment of Thelazia spp.
- Diagnosed by direct observation of worms; treatment involves manual removal, anthelmintics, and fly control measures.
Preventive Measures for Thelazia Infection
- Effective fly control, use of insecticides, and protective measures during peak fly seasons reduce infection risk.
Zoonotic Concerns of Thelazia spp.
- Thelazia spp. are zoonotic and can infect humans, causing conjunctivitis and similar symptoms through exposure to infected flies or animals.
Parelaphostrongylus tenuis Overview
- Classified under Strongylida; known as the meningeal worm or brain worm.
- White-tailed deer are natural hosts, while abnormal hosts include sheep, goats, and various livestock.
Life Cycle of Parelaphostrongylus tenuis
- Indirect cycle; adult worms reside in deer, laying eggs that hatch into larvae and are ingested by snails or slugs.
- Grazing animals then ingest infected snails, leading to potential neurological damage.
Pathology Associated with Parelaphostrongylus tenuis
- In abnormal hosts, larvae migration causes severe neurological damage, resulting in irreversible symptoms like ataxia and paralysis.
Clinical Signs of Parelaphostrongylus tenuis Infection
- Signs in abnormal hosts include progressive neurological symptoms, leading to significant mobility issues and potentially death.
Diagnosis of Parelaphostrongylus tenuis
- Diagnosis in deer involves L1 larvae identification; in abnormal hosts, it relies on clinical signs, CSF analysis, and necropsy.
Treatment and Prevention of Parelaphostrongylus tenuis
- Limited treatment options; anthelmintics can reduce inflammation but offer poor prognosis.
- Prevention focuses on snail control and avoiding co-grazing with deer to reduce transmission risks.
Zoonotic Concerns of Parelaphostrongylus tenuis
- No zoonotic risk to humans; significant impacts mainly observed in livestock and other non-deer species.
Morphological Features of Nematodes in Strongylida
- Males possess a copulatory bursa for mating.
- Produce strongyle-type eggs: ellipsoid, thin-shelled, grayish in color.
- Key genera include Haemonchus, Ostertagia, Trichostrongylus, Cooperia, and Oesophagostomum (often referred to as HOT CO).
Life Cycle of Strongylida Nematodes
- Direct life cycle involving eggs and larvae in the environment and definitive hosts (ruminants).
- Eggs shed in feces develop into first-stage larvae (L1), then molt to L2 before becoming infective L3 larvae.
- L3 larvae are ingested by hosts, migrate to specific sites (e.g., abomasum, small intestine), and develop into L4 larvae and adults.
- Prepatent period: 2-4 weeks from L3 ingestion to egg shedding.
Periparturient Rise Phenomenon
- Refers to increased nematode egg shedding in pregnant ewes.
- Caused by relaxation of immunity due to elevated prolactin levels, leading to emergence of previously dormant L4 larvae.
- Contributes to pasture contamination with infective larvae, increasing risk for offspring.
Parasitic Gastroenteritis (PGE)
- Caused by a complex of gastrointestinal nematodes in ruminants.
- Can present as clinical disease (significant symptoms and impacts) or subclinical disease (impacts herd health without overt symptoms).
- Clinical signs include loss of appetite, weight loss, watery diarrhea, dehydration, rough coat, protein loss (submandibular edema), and pale mucous membranes.
Haemonchus spp. Overview
- Known as "barber pole" worms; blood-feeding nematodes that cause severe anemia.
- Females recognizable by a distinctive striped appearance due to their reproductive organs.
- Direct life cycle; larvae undergo hypobiosis to survive unfavorable conditions.
- Severe infections present with anemia, which can be assessed using the FAMACHA system.
Clinical Signs and Pathology of Haemonchus Infection
- Symptoms vary from hyperacute to chronic; young animals are most affected.
- Signs include severe anemia, pale mucous membranes, submandibular edema, dark feces (melena), wool break, anorexia, emaciation, and potential death before eggs are detected in feces.
Ostertagia spp. Significance
- Known as "brown stomach worms"; essential in cattle health.
- Cause ostertagiosis, with clinical Type I occurring in young animals and Type II from emergence of hypobiotic larvae.
- Damage gastric glands, leading to malabsorption, diarrhea, weight loss, and potential death.
Lifecycle and Pathophysiology of Ostertagia
- Direct life cycle with L3 larvae burrowing into gastric glands.
- Larval development causes increased abomasal pH, reduced pepsin production, and protein loss, leading to diarrhea and weight loss.
Other Important Genera
- Teladorsagia spp.: Similar to Ostertagia but less clinically significant in small ruminants.
- Trichostrongylus spp.: Small nematodes causing PGE, leading to dark green diarrhea; also undergo hypobiosis.
- Cooperia spp.: Contribute to PGE with significant prevalence and impact on weight gain in cattle; resistance to anthelmintics is a challenge.
- Oesophagostomum spp.: Nodular worms that form eosinophilic nodules in the large intestine; associated with inflammation and protein loss.
Nematodirus spp. Characteristics
- Unique among strongyles; large eggs that require specific environmental conditions to hatch.
- Infective larvae pose risks to young animals, leading to malabsorption and PGE.
Bunostomum spp. (Hookworms)
- Large buccal cavity with chitinous cutting plates; significant blood-feeding behavior.
- Direct life cycle with skin penetration as the primary infection route, leading to severe anemia and other pathologies.
Strongyloides papillosus Overview
- Threadworm with an alternating free-living and parasitic life cycle; primarily affects young ruminants.
- Clinical signs include diarrhea, emaciation, and possible neurological effects in heavy infections.
Trichuris spp. Classification and Pathology
- Known as whipworms found in the large intestine; generally subclinical but may cause anorexia and diarrhea in severe infestations.
- Characteristic whip-like morphology with a pronounced difference between anterior and posterior ends.
Moniezia spp. Overview
- Common cestode in ruminants, large tapeworms with a segmented body.
- Life cycle involves oribatid mites as intermediate hosts; typically asymptomatic, but can affect growth in heavy infections.
Fasciola hepatica (Liver Fluke)
- Leaf-shaped flukes found in the liver and bile ducts; indirect life cycle involving freshwater snails as intermediate hosts.
- Important health concerns in ruminants due to potential liver damage.
Taenia saginata (Beef Tapeworm)
- Cattle serve as intermediate hosts for cystic larvae; human consumption of undercooked beef leads to infection.
- Public health concern requires proper meat inspection to prevent zoonotic transmission.
Zoonotic Concerns
- Moniezia spp. pose no significant zoonotic risks, being host-specific to ruminants.### Fasciola hepatica Life Cycle
- Cercariae released from snails encyst as metacercariae on vegetation.
- Ruminants ingest contaminated vegetation, leading to infection.
- Metacercariae excyst in the small intestine, penetrate the intestinal wall, and migrate to the liver.
- Maturation into adults occurs in the bile ducts, with a prepatent period of 2-3 months.
Pathology of Fasciola hepatica
- Causes hepatic and biliary damage through immature flukes migrating in the liver.
- Associated with hepatitis, fibrotic tracts, hemorrhage, and anemia.
- Adult flukes in bile ducts lead to biliary duct hyperplasia, fibrosis, calcification, and cholangitis.
- Feeding by flukes may result in anemia and contributes to hemosiderin and black excrement.
- Chronic infections can cause severe liver damage, reduced productivity, and possibly death.
Clinical Signs of Fascioliasis
- Acute disease in small ruminants leads to anorexia, anemia, jaundice, ascites, depression, and sudden death.
- Subacute disease presents with decreased weight gain, ongoing anemia, liver failure, and potential death.
- Chronic disease features include emaciation, anemia, bottle jaw (submandibular edema), and minor production losses.
Diagnosis and Treatment of Fasciola hepatica
- Diagnosis involves identifying operculated eggs in fecal sedimentation; eggs are heavy and sink.
- Adult flukes may be observed at necropsy.
- Treatment options: triclabendazole, albendazole, and clorsulon effective against various fluke stages.
- Control measures focus on managing snail populations and avoiding grazing on contaminated pastures.
Zoonotic Concerns
- Fasciola hepatica is zoonotic, infecting humans primarily through contaminated watercress or vegetation.
- Human infections can result in liver and biliary pathology, with symptoms such as abdominal pain and jaundice.
- Preventative measures include thorough washing and cooking of vegetables and controlling snail populations.
Fascioloides magna Classification and Hosts
- Fascioloides magna, or deer liver fluke, belongs to the class Trematoda.
- Natural hosts include cervids like white-tailed deer, elk, and moose.
Life Cycle of Fascioloides magna
- Eggs are shed in feces of definitive hosts and develop in aquatic environments into miracidia.
- Miracidia infect freshwater snails, the intermediate host, developing into cercariae.
- Cercariae encyst as metacercariae on vegetation, leading to ingestion by definitive hosts.
- Juvenile flukes migrate to the liver of cervids, maturing into adults and forming cysts communicating with bile ducts, facilitating egg shedding.
Pathological Effects of Fascioloides magna
- In natural hosts (deer), flukes create thin-walled cysts in the liver, usually causing minimal disease.
- Aberrant hosts (sheep and goats) exhibit severe issues due to continuous migration, resulting in hepatitis, hemorrhage, necrosis, and potential mortality with no egg shedding.
- In dead-end hosts (cattle), thick-walled non-patent cysts form in the liver, typically without clinical signs, although liver damage may occur.
Clinical Signs of Fascioloides magna Infection
- In aberrant hosts like sheep and goats, signs can include sudden death from extensive liver damage or chronic symptoms like weight loss and ascites.
- Dead-end hosts rarely show clinical signs but may exhibit liver damage upon necropsy.
- In natural hosts such as deer, infections are generally subclinical.
Diagnosis and Management of Fascioloides magna
- In natural hosts, diagnosis involves fecal sedimentation to identify operculated eggs.
- In aberrant hosts, presence of flukes may be confirmed post-mortem.
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