Helminths of Ruminants Quiz

Morphological Features of Nematodes (Order Strongylida)

• Presence of a copulatory bursa in male nematodes, aiding in mating.
• Strongyle-type eggs are ellipsoid, thin-shelled, and grayish in color.
• Common parasites (HOT CO complex) include Haemonchus, Ostertagia, Trichostrongylus, Cooperia, Oesophagostomum—eggs are indistinguishable.

Life Cycle of Gastrointestinal Nematodes (Order Strongylida)

• Direct life cycle involving both environmental and host stages.
• Fecal egg shedding begins with eggs developing into L1 larvae, molting to L2, and then becoming infective L3 larvae.
• L3 larvae ingested by the host migrate to specific sites (abomasum, small intestine), developing into L4 and then adults.
• Prepatent period is typically 2-4 weeks.

Periparturient Rise Phenomenon

• Refers to increased nematode egg shedding in pregnant ewes due to reduced immunity.
• Higher prolactin levels lead to the emergence of previously arrested L4 larvae, increasing pasture contamination.

Parasitic Gastroenteritis (PGE)

• Condition caused by multiple gastrointestinal nematodes in ruminants.
• Can present as clinical disease (overt symptoms) or subclinical disease (impact on herd health without clear symptoms).
• Clinical signs: loss of appetite, weight loss, watery diarrhea, dehydration, rough coat, protein loss, pale mucous membranes.

Haemonchus spp.

• Known as "barber pole" worms, large nematodes feeding on blood in the abomasum.
• Females exhibit a distinctive barber pole appearance due to their anatomy.
• Life cycle involves direct ingestion of L3 larvae with potential hypobiosis.
• Clinical signs of infection include severe anemia, pale mucous membranes, submandibular edema (bottle jaw), melena, and emaciation.
• Diagnosis via fecal egg counts and FAMACHA for anemia assessment; management employs strategic deworming and pasture management.

Ostertagia spp.

• "Brown stomach worm," significant in cattle and camelids, causing ostertagiosis.
• Life cycle mirrors that of other Strongylida with L3 larvae in gastric glands.
• Pathophysiology includes gastric gland damage, resulting in protein-losing gastropathy and malabsorption.
• Clinical signs comprise diarrhea, weight loss, and dehydration, diagnosed through fecal egg counts and necropsy findings.

Trichostrongylus spp.

• Small nematodes contributing to PGE but not primary pathogens.
• Lead to severe disease in large populations; associated with dark green diarrhea.
• Direct life cycle with potential for hypobiosis; various species target different parts of the ruminant digestive system.

Cooperia spp.

• Small nematodes prevalent in cow/calf operations, contributing to economic losses through impaired weight gain in calves.
• Direct life cycle with hypobiosis potential; resistance to anthelmintics complicates management.

Oesophagostomum spp.

• Known as nodular worms, found in the large intestine of ruminants.
• Develop nodules in the mucosa, causing inflammation, mucus production, and protein leakage.
• Contribute to PGE, though not primary pathogens.

Nematodirus spp.

• Long, slender nematodes comprising large eggs that require specific environmental conditions for hatching.
• Infective L3 larvae cause malabsorption in the small intestine, leading to PGE.

Bunostomum spp. (Hookworms)

• Nematodes characterized by a large buccal cavity with cutting plates for blood-feeding.
• Direct life cycle involving skin penetration or ingestion of infectious larvae.
• Pathology includes villi loss and significant anemia; clinical signs can be severe, especially in young animals.

Strongyloides papillosus

• Recognized as the threadworm with an alternating life cycle between free-living and parasitic stages.
• Infection leads to diarrhea, dehydration, and potential cardiac arrest in young ruminants.
• Diagnosis involves fecal flotation where characteristic thin-shelled eggs are identified.

Trichuris spp. (Whipworms)

• Found in large intestines with a direct life cycle; can cause mild clinical signs.
• Adult morphology includes a whip-like shape; diagnosis through fecal flotation showing bipolar plugs.

Moniezia spp. (Cestode)

• Common tapeworm in ruminants, typically non-pathogenic but can cause poor growth in young animals.
• Large, segmented body topped with proglottids; direct life cycle involving oribatid mites as intermediate hosts.

Taenia saginata (Beef Tapeworm)

• Cattle intermediate hosts harbor larval cysticerci; humans as definitive hosts.
• Public health concern due to zoonotic potential via undercooked beef; necessitates proper cooking to prevent transmission.

Fasciola hepatica (Liver Fluke)

• Classified under Trematoda, affects liver and bile ducts of ruminants, leading to significant pathology.
• Indirect life cycle involving freshwater snail hosts; clinical signs include liver damage and reduced productivity in infected animals.### Fasciola hepatica Overview
• Cercariae released from snails encyst as metacercariae on vegetation.
• Ruminants become infected by ingesting contaminated vegetation.
• Metacercariae excyst in the small intestine, penetrate the intestinal wall, and migrate to the liver; mature into adults in bile ducts.
• Prepatent period lasts about 2-3 months.

Pathology of Fasciola hepatica

• Caused by hepatic and biliary damage.
• Immature flukes cause hepatitis, fibrotic tracts, hemorrhage, and anemia as they migrate through the liver.
• Adult flukes induce biliary duct hyperplasia, fibrosis, calcification, and cholangitis.
• Feeding on blood leads to anemia and hemosiderin build-up, resulting in black excrement.
• Chronic infections pose a risk of significant liver damage and death.

Clinical Signs of Fascioliasis

• Acute disease manifests in small ruminants after consuming many metacercariae; signs include anorexia, anemia, jaundice, ascites, depression, and sudden death.
• Subacute disease results from gradual infection; symptoms involve weight loss, liver failure, and potential death.
• Chronic disease presents as emaciation, anemia, bottle jaw, and subtle production losses from moderate infections.

Diagnosis and Treatment of Fasciola hepatica

• Identified by operculated eggs in fecal sedimentation; eggs are heavy and non-floating.
• Adult flukes or juveniles may be seen at necropsy.
• Treatment options include triclabendazole, albendazole, and clorsulon.
• Control includes managing snail populations and avoiding contaminated pastures.

Zoonotic Concerns of Fasciola hepatica

• Zoonotic potential; can infect humans through contaminated watercress and vegetation.
• Symptoms in humans mirror those in ruminants, such as abdominal pain and jaundice.
• Preventive measures involve proper washing and cooking of vegetables and snail population control.

Fascioloides magna Classification and Hosts

• Classified under class Trematoda, it's also called the deer liver fluke.
• Natural definitive hosts include cervids like white-tailed deer, elk, and moose.

Life Cycle of Fascioloides magna

• Similar to Fasciola hepatica; eggs shed in feces develop in aquatic environments.
• Miracidia infect freshwater snails, developing into cercariae, which encyst on vegetation as metacercariae.
• Definitive hosts ingest metacercariae, leading to liver migration and maturation into cyst-forming adults.

Pathological Effects in Different Hosts

• Natural hosts (deer) exhibit minimal clinical signs, forming thin-walled cysts in the liver.
• Aberrant hosts (sheep and goats) suffer severe liver damage, often leading to death without egg shedding.
• Dead-end hosts (cattle) develop thick-walled non-patent cysts without clinical signs but with potential liver damage.

Clinical Signs in Ruminants

• Aberrant hosts experience sudden death from liver damage or chronic symptoms like weight loss and ascites.
• Dead-end hosts rarely show clinical signs but may reveal liver damage upon necropsy.
• Natural hosts usually present subclinical infections.

Diagnosis and Management of Fascioloides magna

• Identified through fecal sedimentation in natural hosts and post-mortem findings in aberrant hosts.
• Treatment for cervids may include oxyclozanide; control involves preventing grazing in deer-inhabited areas.

Other Liver Trematodes in Ruminants

• Dicrocoelium dendriticum (lancet fluke) and Paramphistomum spp. (rumen flukes) can also infect ruminants.
• Dicrocoelium has a complex life cycle involving snails and ants; less severe liver disease than Fasciola.
• Paramphistomum primarily affects the rumen and is often asymptomatic.

Lungworms in Ruminants

• Key species include Dictyocaulus viviparus (cattle) and Dictyocaulus filaria (small ruminants), both in the order Strongylida.
• Muellerius capillaris affects small ruminants, particularly goats.

Life Cycle and Pathology of Dictyocaulus viviparus

• Direct life cycle; adults reside in lungs, laying eggs that hatch into L1 larvae.
• Larvae develop into infective L3 in the environment; cattle ingest L3, leading to respiratory disease and potential lung damage.

Clinical Signs of Dictyocaulus viviparus

• Symptoms include deep cough, tachypnea, and harsh bronchial sounds; severe cases may lead to anorexia and emaciation.

Diagnosis and Treatment of Dictyocaulus viviparus

• Diagnosis by identifying L1 larvae in feces using the Baermann technique; adult worms visible at necropsy.
• Treatment includes anthelmintics and vaccination; prevention via pasture management and strategic deworming.

Life Cycle and Impact of Muellerius capillaris

• Indirect life cycle involving snails as hosts; causes granulomatous nodules in lungs.
• Goats show clinical signs, while sheep infections are often subclinical.

Diagnosis and Management of Muellerius capillaris

• Identified by L1 larvae in feces using the Baermann technique; treatment may be off-label for goats.
• Control focuses on managing snail populations and avoiding contaminated pastures.

Distinguishing Dictyocaulus and Muellerius Morphologically

• Muellerius has a wavy tail with a dorsal spine, while Dictyocaulus has a blunt tail.

Zoonotic Potential of Lungworms

• Does not pose zoonotic risks; specific to ruminants, impacting livestock health.

Thelazia spp. Overview

• Classified under Spirurida, known as eye worms with definitive hosts including ruminants and intermediate hosts being various flies.

Life Cycle of Thelazia spp.

• Indirect life cycle; adult worms in the eye lay L1 in secretions, which are ingested by flies and develop into L3 larvae, infecting new hosts.

Pathology and Clinical Signs of Thelazia Infection

• Causes conjunctivitis, keratitis, and potentially corneal ulcers; symptoms include excessive tearing and squinting.

Diagnosis and Treatment of Thelazia spp.

• Confirmed by observing worms in the eye; treatment involves manual removal and anthelmintics.
• Effective fly control measures are necessary for prevention.

Zoonotic Concerns of Thelazia spp.

• Zoonotic potential; can cause ocular symptoms in humans, especially through contact with infected animals or flies.

Classification and Hosts of Parelaphostrongylus tenuis

• Classified under Strongylida, commonly known as the meningeal worm.
• Natural hosts are white-tailed deer; abnormal hosts include small ruminants and livestock.

Life Cycle of Parelaphostrongylus tenuis

• Indirect; larvae migrate aberrantly in abnormal hosts, causing severe neurological damage.

Pathology and Clinical Signs in Abnormal Hosts

• Severe neurological symptoms include ataxia, paralysis, and other central nervous system deficits; prognosis is generally poor.

Diagnosis and Treatment of Parelaphostrongylus tenuis

• Diagnosis in deer involves L1 identification in feces; abnormal hosts diagnosed via clinical signs and CSF analysis.
• Limited treatment options; prevention includes snail control and avoiding co-grazing with deer.

Zoonotic Concerns of Parelaphostrongylus tenuis

• No zoonotic potential; specific to natural hosts with negative impacts on abnormal hosts.

Morphological Features of Nematodes (Order Strongylida)

• Presence of a copulatory bursa in male nematodes, aiding in mating.
• Strongyle-type eggs are ellipsoid, thin-shelled, and grayish in color.
• Common parasites (HOT CO complex) include Haemonchus, Ostertagia, Trichostrongylus, Cooperia, Oesophagostomum—eggs are indistinguishable.

Life Cycle of Gastrointestinal Nematodes (Order Strongylida)

• Direct life cycle involving both environmental and host stages.
• Fecal egg shedding begins with eggs developing into L1 larvae, molting to L2, and then becoming infective L3 larvae.
• L3 larvae ingested by the host migrate to specific sites (abomasum, small intestine), developing into L4 and then adults.
• Prepatent period is typically 2-4 weeks.

Periparturient Rise Phenomenon

• Refers to increased nematode egg shedding in pregnant ewes due to reduced immunity.
• Higher prolactin levels lead to the emergence of previously arrested L4 larvae, increasing pasture contamination.

Parasitic Gastroenteritis (PGE)

• Condition caused by multiple gastrointestinal nematodes in ruminants.
• Can present as clinical disease (overt symptoms) or subclinical disease (impact on herd health without clear symptoms).
• Clinical signs: loss of appetite, weight loss, watery diarrhea, dehydration, rough coat, protein loss, pale mucous membranes.

Haemonchus spp.

• Known as "barber pole" worms, large nematodes feeding on blood in the abomasum.
• Females exhibit a distinctive barber pole appearance due to their anatomy.
• Life cycle involves direct ingestion of L3 larvae with potential hypobiosis.
• Clinical signs of infection include severe anemia, pale mucous membranes, submandibular edema (bottle jaw), melena, and emaciation.
• Diagnosis via fecal egg counts and FAMACHA for anemia assessment; management employs strategic deworming and pasture management.

Ostertagia spp.

• "Brown stomach worm," significant in cattle and camelids, causing ostertagiosis.
• Life cycle mirrors that of other Strongylida with L3 larvae in gastric glands.
• Pathophysiology includes gastric gland damage, resulting in protein-losing gastropathy and malabsorption.
• Clinical signs comprise diarrhea, weight loss, and dehydration, diagnosed through fecal egg counts and necropsy findings.

Trichostrongylus spp.

• Small nematodes contributing to PGE but not primary pathogens.
• Lead to severe disease in large populations; associated with dark green diarrhea.
• Direct life cycle with potential for hypobiosis; various species target different parts of the ruminant digestive system.

Cooperia spp.

• Small nematodes prevalent in cow/calf operations, contributing to economic losses through impaired weight gain in calves.
• Direct life cycle with hypobiosis potential; resistance to anthelmintics complicates management.

Oesophagostomum spp.

• Known as nodular worms, found in the large intestine of ruminants.
• Develop nodules in the mucosa, causing inflammation, mucus production, and protein leakage.
• Contribute to PGE, though not primary pathogens.

Nematodirus spp.

• Long, slender nematodes comprising large eggs that require specific environmental conditions for hatching.
• Infective L3 larvae cause malabsorption in the small intestine, leading to PGE.

Bunostomum spp. (Hookworms)

• Nematodes characterized by a large buccal cavity with cutting plates for blood-feeding.
• Direct life cycle involving skin penetration or ingestion of infectious larvae.
• Pathology includes villi loss and significant anemia; clinical signs can be severe, especially in young animals.

Strongyloides papillosus

• Recognized as the threadworm with an alternating life cycle between free-living and parasitic stages.
• Infection leads to diarrhea, dehydration, and potential cardiac arrest in young ruminants.
• Diagnosis involves fecal flotation where characteristic thin-shelled eggs are identified.

Trichuris spp. (Whipworms)

• Found in large intestines with a direct life cycle; can cause mild clinical signs.
• Adult morphology includes a whip-like shape; diagnosis through fecal flotation showing bipolar plugs.

Moniezia spp. (Cestode)

• Common tapeworm in ruminants, typically non-pathogenic but can cause poor growth in young animals.
• Large, segmented body topped with proglottids; direct life cycle involving oribatid mites as intermediate hosts.

Taenia saginata (Beef Tapeworm)

• Cattle intermediate hosts harbor larval cysticerci; humans as definitive hosts.
• Public health concern due to zoonotic potential via undercooked beef; necessitates proper cooking to prevent transmission.

Fasciola hepatica (Liver Fluke)

• Classified under Trematoda, affects liver and bile ducts of ruminants, leading to significant pathology.
• Indirect life cycle involving freshwater snail hosts; clinical signs include liver damage and reduced productivity in infected animals.### Fasciola hepatica Overview
• Cercariae released from snails encyst as metacercariae on vegetation.
• Ruminants become infected by ingesting contaminated vegetation.
• Metacercariae excyst in the small intestine, penetrate the intestinal wall, and migrate to the liver; mature into adults in bile ducts.
• Prepatent period lasts about 2-3 months.

Pathology of Fasciola hepatica

• Caused by hepatic and biliary damage.
• Immature flukes cause hepatitis, fibrotic tracts, hemorrhage, and anemia as they migrate through the liver.
• Adult flukes induce biliary duct hyperplasia, fibrosis, calcification, and cholangitis.
• Feeding on blood leads to anemia and hemosiderin build-up, resulting in black excrement.
• Chronic infections pose a risk of significant liver damage and death.

Clinical Signs of Fascioliasis

• Acute disease manifests in small ruminants after consuming many metacercariae; signs include anorexia, anemia, jaundice, ascites, depression, and sudden death.
• Subacute disease results from gradual infection; symptoms involve weight loss, liver failure, and potential death.
• Chronic disease presents as emaciation, anemia, bottle jaw, and subtle production losses from moderate infections.

Diagnosis and Treatment of Fasciola hepatica

• Identified by operculated eggs in fecal sedimentation; eggs are heavy and non-floating.
• Adult flukes or juveniles may be seen at necropsy.
• Treatment options include triclabendazole, albendazole, and clorsulon.
• Control includes managing snail populations and avoiding contaminated pastures.

Zoonotic Concerns of Fasciola hepatica

• Zoonotic potential; can infect humans through contaminated watercress and vegetation.
• Symptoms in humans mirror those in ruminants, such as abdominal pain and jaundice.
• Preventive measures involve proper washing and cooking of vegetables and snail population control.

Fascioloides magna Classification and Hosts

• Classified under class Trematoda, it's also called the deer liver fluke.
• Natural definitive hosts include cervids like white-tailed deer, elk, and moose.

Life Cycle of Fascioloides magna

• Similar to Fasciola hepatica; eggs shed in feces develop in aquatic environments.
• Miracidia infect freshwater snails, developing into cercariae, which encyst on vegetation as metacercariae.
• Definitive hosts ingest metacercariae, leading to liver migration and maturation into cyst-forming adults.

Pathological Effects in Different Hosts

• Natural hosts (deer) exhibit minimal clinical signs, forming thin-walled cysts in the liver.
• Aberrant hosts (sheep and goats) suffer severe liver damage, often leading to death without egg shedding.
• Dead-end hosts (cattle) develop thick-walled non-patent cysts without clinical signs but with potential liver damage.

Clinical Signs in Ruminants

• Aberrant hosts experience sudden death from liver damage or chronic symptoms like weight loss and ascites.
• Dead-end hosts rarely show clinical signs but may reveal liver damage upon necropsy.
• Natural hosts usually present subclinical infections.

Diagnosis and Management of Fascioloides magna

• Identified through fecal sedimentation in natural hosts and post-mortem findings in aberrant hosts.
• Treatment for cervids may include oxyclozanide; control involves preventing grazing in deer-inhabited areas.

Other Liver Trematodes in Ruminants

• Dicrocoelium dendriticum (lancet fluke) and Paramphistomum spp. (rumen flukes) can also infect ruminants.
• Dicrocoelium has a complex life cycle involving snails and ants; less severe liver disease than Fasciola.
• Paramphistomum primarily affects the rumen and is often asymptomatic.

Lungworms in Ruminants

• Key species include Dictyocaulus viviparus (cattle) and Dictyocaulus filaria (small ruminants), both in the order Strongylida.
• Muellerius capillaris affects small ruminants, particularly goats.

Life Cycle and Pathology of Dictyocaulus viviparus

• Direct life cycle; adults reside in lungs, laying eggs that hatch into L1 larvae.
• Larvae develop into infective L3 in the environment; cattle ingest L3, leading to respiratory disease and potential lung damage.

Clinical Signs of Dictyocaulus viviparus

• Symptoms include deep cough, tachypnea, and harsh bronchial sounds; severe cases may lead to anorexia and emaciation.

Diagnosis and Treatment of Dictyocaulus viviparus

• Diagnosis by identifying L1 larvae in feces using the Baermann technique; adult worms visible at necropsy.
• Treatment includes anthelmintics and vaccination; prevention via pasture management and strategic deworming.

Life Cycle and Impact of Muellerius capillaris

• Indirect life cycle involving snails as hosts; causes granulomatous nodules in lungs.
• Goats show clinical signs, while sheep infections are often subclinical.

Diagnosis and Management of Muellerius capillaris

• Identified by L1 larvae in feces using the Baermann technique; treatment may be off-label for goats.
• Control focuses on managing snail populations and avoiding contaminated pastures.

Distinguishing Dictyocaulus and Muellerius Morphologically

• Muellerius has a wavy tail with a dorsal spine, while Dictyocaulus has a blunt tail.

Zoonotic Potential of Lungworms

• Does not pose zoonotic risks; specific to ruminants, impacting livestock health.

Thelazia spp. Overview

• Classified under Spirurida, known as eye worms with definitive hosts including ruminants and intermediate hosts being various flies.

Life Cycle of Thelazia spp.

• Indirect life cycle; adult worms in the eye lay L1 in secretions, which are ingested by flies and develop into L3 larvae, infecting new hosts.

Pathology and Clinical Signs of Thelazia Infection

• Causes conjunctivitis, keratitis, and potentially corneal ulcers; symptoms include excessive tearing and squinting.

Diagnosis and Treatment of Thelazia spp.

• Confirmed by observing worms in the eye; treatment involves manual removal and anthelmintics.
• Effective fly control measures are necessary for prevention.

Zoonotic Concerns of Thelazia spp.

• Zoonotic potential; can cause ocular symptoms in humans, especially through contact with infected animals or flies.

Classification and Hosts of Parelaphostrongylus tenuis

• Classified under Strongylida, commonly known as the meningeal worm.
• Natural hosts are white-tailed deer; abnormal hosts include small ruminants and livestock.

Life Cycle of Parelaphostrongylus tenuis

• Indirect; larvae migrate aberrantly in abnormal hosts, causing severe neurological damage.

Pathology and Clinical Signs in Abnormal Hosts

• Severe neurological symptoms include ataxia, paralysis, and other central nervous system deficits; prognosis is generally poor.

Diagnosis and Treatment of Parelaphostrongylus tenuis

• Diagnosis in deer involves L1 identification in feces; abnormal hosts diagnosed via clinical signs and CSF analysis.
• Limited treatment options; prevention includes snail control and avoiding co-grazing with deer.

Zoonotic Concerns of Parelaphostrongylus tenuis

• No zoonotic potential; specific to natural hosts with negative impacts on abnormal hosts.

Morphological Features of Nematodes (Order Strongylida)

• Presence of a copulatory bursa in male nematodes, aiding in mating.
• Strongyle-type eggs are ellipsoid, thin-shelled, and grayish in color.
• Common parasites (HOT CO complex) include Haemonchus, Ostertagia, Trichostrongylus, Cooperia, Oesophagostomum—eggs are indistinguishable.

Life Cycle of Gastrointestinal Nematodes (Order Strongylida)

• Direct life cycle involving both environmental and host stages.
• Fecal egg shedding begins with eggs developing into L1 larvae, molting to L2, and then becoming infective L3 larvae.
• L3 larvae ingested by the host migrate to specific sites (abomasum, small intestine), developing into L4 and then adults.
• Prepatent period is typically 2-4 weeks.

Periparturient Rise Phenomenon

• Refers to increased nematode egg shedding in pregnant ewes due to reduced immunity.
• Higher prolactin levels lead to the emergence of previously arrested L4 larvae, increasing pasture contamination.

Parasitic Gastroenteritis (PGE)

• Condition caused by multiple gastrointestinal nematodes in ruminants.
• Can present as clinical disease (overt symptoms) or subclinical disease (impact on herd health without clear symptoms).
• Clinical signs: loss of appetite, weight loss, watery diarrhea, dehydration, rough coat, protein loss, pale mucous membranes.

Haemonchus spp.

• Known as "barber pole" worms, large nematodes feeding on blood in the abomasum.
• Females exhibit a distinctive barber pole appearance due to their anatomy.
• Life cycle involves direct ingestion of L3 larvae with potential hypobiosis.
• Clinical signs of infection include severe anemia, pale mucous membranes, submandibular edema (bottle jaw), melena, and emaciation.
• Diagnosis via fecal egg counts and FAMACHA for anemia assessment; management employs strategic deworming and pasture management.

Ostertagia spp.

• "Brown stomach worm," significant in cattle and camelids, causing ostertagiosis.
• Life cycle mirrors that of other Strongylida with L3 larvae in gastric glands.
• Pathophysiology includes gastric gland damage, resulting in protein-losing gastropathy and malabsorption.
• Clinical signs comprise diarrhea, weight loss, and dehydration, diagnosed through fecal egg counts and necropsy findings.

Trichostrongylus spp.

• Small nematodes contributing to PGE but not primary pathogens.
• Lead to severe disease in large populations; associated with dark green diarrhea.
• Direct life cycle with potential for hypobiosis; various species target different parts of the ruminant digestive system.

Cooperia spp.

• Small nematodes prevalent in cow/calf operations, contributing to economic losses through impaired weight gain in calves.
• Direct life cycle with hypobiosis potential; resistance to anthelmintics complicates management.

Oesophagostomum spp.

• Known as nodular worms, found in the large intestine of ruminants.
• Develop nodules in the mucosa, causing inflammation, mucus production, and protein leakage.
• Contribute to PGE, though not primary pathogens.

Nematodirus spp.

• Long, slender nematodes comprising large eggs that require specific environmental conditions for hatching.
• Infective L3 larvae cause malabsorption in the small intestine, leading to PGE.

Bunostomum spp. (Hookworms)

• Nematodes characterized by a large buccal cavity with cutting plates for blood-feeding.
• Direct life cycle involving skin penetration or ingestion of infectious larvae.
• Pathology includes villi loss and significant anemia; clinical signs can be severe, especially in young animals.

Strongyloides papillosus

• Recognized as the threadworm with an alternating life cycle between free-living and parasitic stages.
• Infection leads to diarrhea, dehydration, and potential cardiac arrest in young ruminants.
• Diagnosis involves fecal flotation where characteristic thin-shelled eggs are identified.

Trichuris spp. (Whipworms)

• Found in large intestines with a direct life cycle; can cause mild clinical signs.
• Adult morphology includes a whip-like shape; diagnosis through fecal flotation showing bipolar plugs.

Moniezia spp. (Cestode)

• Common tapeworm in ruminants, typically non-pathogenic but can cause poor growth in young animals.
• Large, segmented body topped with proglottids; direct life cycle involving oribatid mites as intermediate hosts.

Taenia saginata (Beef Tapeworm)

• Cattle intermediate hosts harbor larval cysticerci; humans as definitive hosts.
• Public health concern due to zoonotic potential via undercooked beef; necessitates proper cooking to prevent transmission.

Fasciola hepatica (Liver Fluke)

• Classified under Trematoda, affects liver and bile ducts of ruminants, leading to significant pathology.
• Indirect life cycle involving freshwater snail hosts; clinical signs include liver damage and reduced productivity in infected animals.### Fasciola hepatica Overview
• Cercariae released from snails encyst as metacercariae on vegetation.
• Ruminants become infected by ingesting contaminated vegetation.
• Metacercariae excyst in the small intestine, penetrate the intestinal wall, and migrate to the liver; mature into adults in bile ducts.
• Prepatent period lasts about 2-3 months.

Pathology of Fasciola hepatica

• Caused by hepatic and biliary damage.
• Immature flukes cause hepatitis, fibrotic tracts, hemorrhage, and anemia as they migrate through the liver.
• Adult flukes induce biliary duct hyperplasia, fibrosis, calcification, and cholangitis.
• Feeding on blood leads to anemia and hemosiderin build-up, resulting in black excrement.
• Chronic infections pose a risk of significant liver damage and death.

Clinical Signs of Fascioliasis

• Acute disease manifests in small ruminants after consuming many metacercariae; signs include anorexia, anemia, jaundice, ascites, depression, and sudden death.
• Subacute disease results from gradual infection; symptoms involve weight loss, liver failure, and potential death.
• Chronic disease presents as emaciation, anemia, bottle jaw, and subtle production losses from moderate infections.

Diagnosis and Treatment of Fasciola hepatica

• Identified by operculated eggs in fecal sedimentation; eggs are heavy and non-floating.
• Adult flukes or juveniles may be seen at necropsy.
• Treatment options include triclabendazole, albendazole, and clorsulon.
• Control includes managing snail populations and avoiding contaminated pastures.

Zoonotic Concerns of Fasciola hepatica

• Zoonotic potential; can infect humans through contaminated watercress and vegetation.
• Symptoms in humans mirror those in ruminants, such as abdominal pain and jaundice.
• Preventive measures involve proper washing and cooking of vegetables and snail population control.

Fascioloides magna Classification and Hosts

• Classified under class Trematoda, it's also called the deer liver fluke.
• Natural definitive hosts include cervids like white-tailed deer, elk, and moose.

Life Cycle of Fascioloides magna

• Similar to Fasciola hepatica; eggs shed in feces develop in aquatic environments.
• Miracidia infect freshwater snails, developing into cercariae, which encyst on vegetation as metacercariae.
• Definitive hosts ingest metacercariae, leading to liver migration and maturation into cyst-forming adults.

Pathological Effects in Different Hosts

• Natural hosts (deer) exhibit minimal clinical signs, forming thin-walled cysts in the liver.
• Aberrant hosts (sheep and goats) suffer severe liver damage, often leading to death without egg shedding.
• Dead-end hosts (cattle) develop thick-walled non-patent cysts without clinical signs but with potential liver damage.

Clinical Signs in Ruminants

• Aberrant hosts experience sudden death from liver damage or chronic symptoms like weight loss and ascites.
• Dead-end hosts rarely show clinical signs but may reveal liver damage upon necropsy.
• Natural hosts usually present subclinical infections.

Diagnosis and Management of Fascioloides magna

• Identified through fecal sedimentation in natural hosts and post-mortem findings in aberrant hosts.
• Treatment for cervids may include oxyclozanide; control involves preventing grazing in deer-inhabited areas.

Other Liver Trematodes in Ruminants

• Dicrocoelium dendriticum (lancet fluke) and Paramphistomum spp. (rumen flukes) can also infect ruminants.
• Dicrocoelium has a complex life cycle involving snails and ants; less severe liver disease than Fasciola.
• Paramphistomum primarily affects the rumen and is often asymptomatic.

Lungworms in Ruminants

• Key species include Dictyocaulus viviparus (cattle) and Dictyocaulus filaria (small ruminants), both in the order Strongylida.
• Muellerius capillaris affects small ruminants, particularly goats.

Life Cycle and Pathology of Dictyocaulus viviparus

• Direct life cycle; adults reside in lungs, laying eggs that hatch into L1 larvae.
• Larvae develop into infective L3 in the environment; cattle ingest L3, leading to respiratory disease and potential lung damage.

Clinical Signs of Dictyocaulus viviparus

• Symptoms include deep cough, tachypnea, and harsh bronchial sounds; severe cases may lead to anorexia and emaciation.

Diagnosis and Treatment of Dictyocaulus viviparus

• Diagnosis by identifying L1 larvae in feces using the Baermann technique; adult worms visible at necropsy.
• Treatment includes anthelmintics and vaccination; prevention via pasture management and strategic deworming.

Life Cycle and Impact of Muellerius capillaris

• Indirect life cycle involving snails as hosts; causes granulomatous nodules in lungs.
• Goats show clinical signs, while sheep infections are often subclinical.

Diagnosis and Management of Muellerius capillaris

• Identified by L1 larvae in feces using the Baermann technique; treatment may be off-label for goats.
• Control focuses on managing snail populations and avoiding contaminated pastures.

Distinguishing Dictyocaulus and Muellerius Morphologically

• Muellerius has a wavy tail with a dorsal spine, while Dictyocaulus has a blunt tail.

Zoonotic Potential of Lungworms

• Does not pose zoonotic risks; specific to ruminants, impacting livestock health.

Thelazia spp. Overview

• Classified under Spirurida, known as eye worms with definitive hosts including ruminants and intermediate hosts being various flies.

Life Cycle of Thelazia spp.

• Indirect life cycle; adult worms in the eye lay L1 in secretions, which are ingested by flies and develop into L3 larvae, infecting new hosts.

Pathology and Clinical Signs of Thelazia Infection

• Causes conjunctivitis, keratitis, and potentially corneal ulcers; symptoms include excessive tearing and squinting.

Diagnosis and Treatment of Thelazia spp.

• Confirmed by observing worms in the eye; treatment involves manual removal and anthelmintics.
• Effective fly control measures are necessary for prevention.

Zoonotic Concerns of Thelazia spp.

• Zoonotic potential; can cause ocular symptoms in humans, especially through contact with infected animals or flies.

Classification and Hosts of Parelaphostrongylus tenuis

• Classified under Strongylida, commonly known as the meningeal worm.
• Natural hosts are white-tailed deer; abnormal hosts include small ruminants and livestock.

Life Cycle of Parelaphostrongylus tenuis

• Indirect; larvae migrate aberrantly in abnormal hosts, causing severe neurological damage.

Pathology and Clinical Signs in Abnormal Hosts

• Severe neurological symptoms include ataxia, paralysis, and other central nervous system deficits; prognosis is generally poor.

Diagnosis and Treatment of Parelaphostrongylus tenuis

• Diagnosis in deer involves L1 identification in feces; abnormal hosts diagnosed via clinical signs and CSF analysis.
• Limited treatment options; prevention includes snail control and avoiding co-grazing with deer.

Zoonotic Concerns of Parelaphostrongylus tenuis

• No zoonotic potential; specific to natural hosts with negative impacts on abnormal hosts.