Lecture 11- Gastrointestinal Nematode Parasites of Domestic Production Animals (Cattle)

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73 Terms

1
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What type of nematodes are Trichostrongylid parasites?

Small gut-dwelling nematodes

2
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Do Trichostrongylid parasites undergo extensive tissue migration?

No, they do not undergo extensive tissue migration.

3
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What type of life cycle do Trichostrongylid parasites have?

A simple, direct life cycle.

4
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What is "Arrested Development" (Hypobiosis) in Trichostrongylid parasites?

A survival adaptation where recently ingested larvae stop developing and remain in a juvenile state for months.

5
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Why is "Arrested Development" important for Trichostrongylid parasites?

It allows the parasite to survive during hostile environmental conditions and ensures pasture contamination each season.

6
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Why are Trichostrongylid parasites a primary target of producer-initiated parasite control programs?

They significantly impact livestock health and production.

7
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Where do recently ingested larvae go during hypobiosis?

They enter the gut tissue and stop developing.

8
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How long can arrested larvae remain in a juvenile state?

Several months.

9
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When do arrested larvae resume development?

When environmental conditions are favorable for parasite reproduction.

10
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What are the benefits of arrested development for parasite populations?

It allows survival during adverse environmental conditions and ensures pasture contamination in future grazing seasons.

11
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Where do adult Ostertagia spp. worms reside?

In the abomasum of cattle.

12
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How can you describe the size and morphology of Ostertagia spp.?

Small, sexually dimorphic worms:

Males: 6-7 mm, with a copulatory bursa.

Females: 8-9 mm.

Spicule morphology is diagnostic.

13
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What type of life cycle does Ostertagia spp. have?

A direct life cycle with arrested development in gastric pits.

14
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What is the significance of arrested development in Ostertagia spp.?

It has both pathologic and epidemiologic significance in cattle.

15
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Why is Ostertagia spp. considered highly pathogenic?

It causes Type I and Type II disease, leading to tissue damage in the abomasum.

16
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What is the most economically significant parasitism of cattle?

Ostertagia spp. infestation.

17
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What is the primary clinical consequence of Haemonchus contortus infection in small ruminants?

Fatal anemia

18
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Where do adult Trichostrongylid worms live?

In the gut of the host.

19
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How do Trichostrongylid worms reproduce?

they lay eggs that are passed in feces

20
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What happens to Trichostrongylid eggs after they are passed in feces?

They develop into larvae and hatch

21
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How do Trichostrongylid larvae become infective?

Free-living larvae develop into infective stages on pasture.

22
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What environmental factor influences Trichostrongylid larval development?

Climatic conditions.

23
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How do animals become infected with Trichostrongylid parasites?

By grazing on contaminated pasture.

24
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What is the approximate pre-patent period for Trichostrongylid infections?

About 21 days from infection.

25
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What are the key components of periodic herd health assessments for diagnosing Trichostrongylid nematodes?

Identifying high FEC shedders, evaluating treatment efficacy, and occasionally testing sick animals.

26
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Why are Trichostrongylid nematode eggs not useful for species identification?

The eggs (70‐90 x 40‐45 µm) are morphologically indistinguishable across species.

27
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How is the risk of parasite disease attributed to Trichostrongylid nematodes?

Based on host species and the predominant parasite affecting that host.

28
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What are the main diagnostic methods for Trichostrongylid nematodes?

Fecal Flotation (semi-quantitative)

McMasters Quantitative Test (Fecal Egg Count)

29
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What is the significance of Trichostrongylus sp. in cattle?

It is a common but less pathogenic parasite, with disease occurring in cases of high worm burden (10,000 to 100,000 worms).

30
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Which animals are most at risk for disease from Trichostrongylus sp.?

Young and nutritionally stressed animals.

31
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What type of cattle is Cooperia sp. most associated with?

Calves, where it causes subclinical production losses in Average Daily Gain (ADG).

32
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What is the economic impact of deworming against Cooperia sp.?

Dewormed cattle show an approximate $75 increase in sale price per head.

33
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When does Nematodirus spp. infection typically occur?

Seasonal (spring) hatching concentrates infective worms, with disease most common in late spring calves.

34
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Based on NAHMS statistical sampling, which Trichostrongylid parasite is most prevalent in U.S. cattle?

Cooperia spp. was found in 91% of all cattle by PCR.

35
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What percentage of U.S. cattle were found to be infected with Ostertagia spp. by PCR?

80% of cattle

36
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What is the emerging concern with Cooperia spp.?

Drug resistance to macrocyclic lactones (ML), which are dose-limiting species for these drugs.

37
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What factor may have contributed to decreased efficacy of macrocyclic lactones against Cooperia?

The use of pour-on ML treatments for fly and lice control may have led to reduced anthelmintic efficacy.

38
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How is Ostertagia spp. still effectively controlled?

Through Smart Deworming strategies.

39
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What conditions favor Type 1 Ostertagiosis?

Many worms acquired over a short period, typically in young cattle (first grazing season) under favorable environmental conditions.

40
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Where do Type 1 larvae mature, and what causes damage?

Larvae mature in gastric glands, with damage occurring as they leave the glands to become adults and reproduce.

41
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Why is Type 1 Ostertagiosis progressive?

The process is continuous and cumulative.

42
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When does Type 2 disease occur?

Months after initial infection, when accumulated parasites suddenly emerge from dormancy.

43
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Which animals are most affected by Type 2 Ostertagiosis?

Older cattle (second grazing season), especially under stress (nutritional stress, post-calving, etc.).

44
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Why might fecal exams be negative in Type 2 Ostertagiosis?

Disease is caused by larvae emerging from tissues, not by active egg-laying adults.

45
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How does Type 2 Ostertagiosis compare to Type 1 in severity and response to treatment?

More severe, often with higher mortality and poor response to deworming.

46
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When do young cattle acquire substantial worm burdens in the Southern U.S.?

While grazing October-March under medium temperature/moisture conditions.

47
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What happens to infective larvae between April and September? (type 1 ostertagiosis)

they begin arrested development in tissues due to high temperatures and drier conditions.

48
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What are the key clinical signs of Type 1 Ostertagiosis?

Profuse watery diarrhea, often bright green from lush pasture grazing.

Bottle jaw due to tissue leakage and impaired digestion.

Loss of appetite, failure to gain weight, loss of body condition.

49
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What is the response to treatment for Type 1 Ostertagiosis?

Positive response to timely treatment.

50
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When do infective larvae enter dormancy in the gastric glands?

During late spring months.

51
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When do larvae emerge en masse, causing damage?

During late summer to fall months.

52
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What is the pattern of disease progression in Type 2 Ostertagiosis?

May be catastrophic or protracted.

53
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What are the key clinical signs of Type 2 Ostertagiosis?

Brown watery diarrhea

Loss of appetite & body condition

Rumen pH approaches neutral

Negative fecal exams

54
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Which animals are most severely affected by Type 2 Ostertagiosis?

Older cattle (second grazing season).

55
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How effective is deworming in Type 2 Ostertagiosis?

Poor response to treatment.

56
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How is Type 2 Ostertagiosis diagnosed?

Based on clinical signs and seasonal disease onset from emerging larvae.

57
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Why is it not feasible to eliminate parasites from cattle herds?

Parasites are endemic in grazing systems, and complete eradication is impractical; the goal is to reduce pasture contamination and hazardous re-infection.

58
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What is the primary goal of parasite control in cattle herds?

reduce pasture contamination and hazardous reinfection while mapping disease risk

59
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What factors increase the risk of Type 1 Ostertagiosis in a herd?

Young cattle (1st grazing season)

Lack of prior exposure → inadequate immunity

High fecal egg counts (FECs) due to accumulating worm burdens

Favorable environmental conditions for larval development & transmission

60
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What factors increase the risk of Type 2 Ostertagiosis in a herd?

Older heifers (2nd grazing season)

Mass emergence of arrested larvae

Negative fecal exams (due to larvae still in tissue phase)

61
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Why is treating older adult cattle with subclinical infections not practical or cost-effective?

They typically have effective immunity

Low worm burdens

Low FECs

Over-treatment may promote drug resistance

62
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Why should stockers & new additions be dewormed upon arrival?

To prevent importation of resistant parasites and reduce hazardous pasture contamination.

63
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What are key principles of Smart Deworming?

Treat animals based on seasonal parasite biology & host risk

Use the fewest annual treatments possible

Consider the persistent activity of dewormers

64
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How does persistent activity of dewormers affect parasite control?

Longer ERP (Egg Reappearance Period) allows for safer grazing intervals

Reduces reinfection rates

Helps mitigate resistance development

65
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What is the Egg Reappearance Period (ERP) and how does it affect parasite management?

Time before new egg shedding resumes post-treatment

Affects timing of next deworming

ERP depends on drug class & persistent activity

66
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Which drug classes only remove adult worms and provide an ERP of ~21 days?

Benzimidazoles

Imidazothiazoles

Tetrahydropyrimidines (These are ideal for parasites like Cooperia, where drug resistance is an issue.)

67
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How do Macrocyclic Lactones (MLs) differ from other dewormers?

Kill adult worms

Effective against inhibited larvae

Provide 14-21 days of protection from reinfection

ERP of 35-42 days (14 days persistent activity + 21-day prepatent period = 35-day ERP)

68
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What is the goal of Strategic Deworming?

Removal of parasites by targeting seasonal biology and exploiting parasite life cycle vulnerabilities.

69
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What are the key elements of Strategic Deworming?

Targeting inhibited larvae

Differential selectivity against larval stages

Removing adult parasites to reduce overall worm burden

70
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How does Selective Deworming differ from Strategic Deworming?

Instead of treating all animals, it removes parasites from selected hosts, allowing some parasites to survive and reproduce without drug selection pressure.

71
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What is the importance of refugia in parasite control?

Refugia = parasite populations not exposed to dewormers

Helps maintain genetic diversity of parasites

Reduces resistance development

72
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How are hosts selected for Selective Deworming?

Young animals vs. older animals

High FEC shedders

Clinically ill vs. asymptomatic animals

73
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How do Strategic and Selective Deworming complement each other?

Young animals are treated to prevent disease & reduce pasture contamination.

High FEC shedders are treated to reduce pasture contamination.

Inhibited larvae are targeted with effective drugs to reduce seasonal outbreaks.