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Parasitology > Bovine GI nematodes > Flashcards

Bovine GI nematodes Flashcards

1
Q

Parasitic Gastroenteritis

A
  • Generic term for dz caused by parasitic nematodes in GI
  • Disease of grazing livestock, mainly young stock
  • Adults = generally strong acquired immunity
  • Often caused by mixed species of parasitic nematode
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2
Q

Bovine Abomasal Nematodes

A 
Hemonchus
Ostertagia
Trichostrongylus
**mneumonic = HOT
** ALL three are in trichostrongyloidea family
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3
Q

Bovine Small Intestinal Nematodes

A

**Cooperia
**Nematodirus
**Trichostrongylus
Bunostomum (Strongyolidea- hookworm)
Toxocara (Ascaridoidea)
** = main parasites of concern, all trichostrongyloidea

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4
Q

Bovine Large Intestinal Nematodes

A

Oesophagostomum (strongyloidea - strongyle)

Trichuroidea

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5
Q

Trichostrongyloidea

Common Characteristics

A 
Most important in grazing ruminants
DIRECT life cycle
L3 = infective
Mainly GI (except dictycaulus)
PPP ~ 21days
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6
Q

Bovine Ostertagia species

A

Osteragia ostergai

Ostergia leptospicularis

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7
Q

O. ostergia life cycle - bovine

A

PPP~21d
Eggs hatch in feces –> develop to infective L3 free living in envt (L3 retains L2 cuticle - allows resilience in envt)
L3 = metabolically arrested, only proceed in cycle if taken up by suitable host
L3 ingestion –> penetrate abomasal gland –> L4 (massive change in size) –> either hypobiosis or go to immature adult stage –> larvae erupt at d18 post ingestion into lumen (damage = pathology) –> adults in abomasum –> lay eggs

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8
Q

Ostergiosis Pathogenesis

Heavy infection > 40,000 adults

A

3 possible effects

1) hypoproteinemia
- distention of parasitised gastric gland lumen –> rupture of intracellular jx –> leakage of plasma proteins into lumen –> hypoproteinemia
2) elevated plasma pepsinogen
- distention of parasitised gastric gland lumen –> destruction of parietal cells + replacement w/undifferentiated cells –> decreased HC; secretions –> decrease in abomasal pH (basic)–> fail to activate pepsinogen to pepsin –> leakage of pepisnogen into blood –> elevated plasma pepsinogen
3) bacterial overgrowth
- distention of parasitised gastric gland lumen –> destruction of parietal cells + replacement w/undifferentiated cells –> decreased HC; secretions –> decrease in abomasal pH (basic)–> Bacterial overgrowth

**chief cells not broken down, still make pepsinogen

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9
Q

Osteragiosis nodules: importance

A

Due to heavy parasitization
Distinct nodule w/ puncture wounds where they have larvae have ruptured out
Nodules coalesce and abomasum becomes non-functional (hyperplasia of abomasal mucosa)

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10
Q

Osteragiosis: Two Clinical Forms

A 
Type I:
- First season grazing calves
- July-October
- Due to larvae acquired from pasture 2-3 weeks earlier
Type 2:
- Yearlings (often housed)
- March - May
- Due to maturation of inhibited larvae acquired from pasture during previous autumn (L4 that resume development)
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11
Q

Type I Osteragiosis: Clinical Signs

A
  • Profuse/watery diarrhea
  • Weight loss
  • Dull coats
  • Gather around water sources
  • Occasional submandibular edema (hypoalbuminemia)
  • High morbidity, low mortality (provided animal treated)
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12
Q

Type II Ostertagiosis: Clinical Signs

A
  • Intermittent diarrhea (not always present)
  • Common submandibular edema
  • Weight loss
  • +/- moderate anemia
  • Anorexia and increased thirst
  • Low morbidity, high mortality (b/c of high #s L4s rupturing out at once –> dramatic effect)
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13
Q

Osteragiosis: Diagnosis

A
  • Clinical picture and grazing history
  • Herd dx, not individual
  • Fecal egg counts
  • serum pepsinogen
  • Serum antibody
  • PM
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14
Q

Describe the disadvantages of Fecal Egg Counts in the diagnosis of Osteragiosis.

A
  • Can’t discriminate b/w different trichostrongyle eggs (except Nematodirus)
  • Not a linear relationship b/w fecal egg count and parasite burden
  • Sometimes dz caused by pre-patent parasites (Type II osteragiosis or Nematodirus battus)
  • LOW FEC from small groups doesn’t rule out PGE dx
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15
Q

Describe the value of serum pepsinogen in regard to Osteragiosis dx.

A
  • Specific for abomasal parasitism
  • Less reliable in older animals with low burdens
  • Useful indicator of burdens at end of grazing season
  • Normal: 1U, parasitized: 3-5U
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16
Q

Value to serum anitbodies in dx of Osteragiosis

A
  • ELISAs
  • Good measure of exposure
  • Not commercially available
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17
Q

Epidemiology of Osteragiosis

A
  • Late winter –> spring: type 2, less prevalent

- Late summer –> early winter, more prevalent

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18
Q

Osteragia Immunity

A
  • Slow to develop
  • Takes at least one grazing season
  • Second season calves and adults generally immune
  • Immune animals still carry burdens (L4 arrested)
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19
Q

Describe overwintering

A
  • L3s in L2 sheath survive over winter protected by sheath
  • In spring = more metabolically active, use more energy stores, must be taken up by host or die
  • Therefore, won’t survive two years in a row
  • By July, pasture is clean
20
Q

Type 1 Osteragiosis epidemiology

A
  • Eggs passed in colder temps take longer to become infective than those in late season (development is temperature dependent)
  • Thus massive numbers of infective L3s mid July –> massive clinical signs

Overwintered L3s survive on pasture from previous grazing season –> calves ingest overwintered L3s and patent infection established in April/May –> 1st generation of adult parasites produces eggs to contaminate pasture in May/July (but insufficient to cause clinical dz) –> Large numbers of L3s appear on pasture July/August and ingested by calves (large numbers of 2nd generation eggs reach L3 at same time) –> 2nd generation of parasites produces clinical signs 2-3 weeks after infection

21
Q

What happens when free-living stages of ostertagia are exposed to low temperatures?

A

Increased probability of inhibition as L4s in abomasal glands

So eaten later in season = more chance of arresting

Type II disease occurs due to reactivation of inhibited larvae in Feb-March

22
Q

Predisposing factors to Type II Osteragia

A

Ingestion of large numbers of L3 in autumn:
Caused by:
1) moving animals to contaminated pasture late in grazing season
2) dry summers delay emergence of larvae from fecal pats (need rain to break open)

23
Q

Ostertagiosis: spring vs autumn calving occurrence

A

Spring: Uncommon
- b/c not weaned until autumn (overwintered larvae are now dead). Little contribution to pasture contamination during early grazing season (adults = low output of eggs)
Autumn: Common
- Weaned in spring - similar to epidemiology of dairy calves in following season

24
Q

Atypical forms of bovine ostertagiosis

A

Early season type 1:
- calves put out early (mar/april) occasionally sufficient overwintered L3 cause dz 4-6 wks after turnout

Ostertagiosis in adults:
- unusual due to acquired immunity, but occasional cases can occur (unexposed stock moved to endemic area), occasionally due to concurrent infection: fasiolosis

25
Q

Treatment of Osteratagiosis

A

Type 1:
Most anthelmenthics, move to clean pasture
Type 2:
Modern benzimidaoles, macrocyclic lactones

26
Q

Ostertagiosis control

A

Grazig management
- avoid grazing heavily contaminated pasture at peak season (dose and move) - need to expose them at some point to get immunity
Monitor
- FEC/growth, so can reduce worming over time
Worm at housing
- stock susceptible to type II dz

27
Q

Trichostrongylus axei

A
  • Abomasum (L3 exsheaths in abomasum)
  • Very small, less than 1cm, thin
  • excretory notch in esophageal region - diagnostic feature
  • infect cattle, sheep, goat, horse
  • cause mucosal erosions
  • Rare in UK, may contribute to PGE as mixed infection
  • Overwinter in sufficient number occasionally to cause clinical problems in spring
28
Q

Hemonchus

A
  • Not important in cattle in UK (more sheep)
  • H. contortus - in sheep
  • L3s dont tolerate cold well (don’t do well in UK)
  • Abomausm
  • Blood feeding- pathology due to adults
  • Barber pole appearance (white ovaries/blood filled intestine)
  • Causes anemia
  • Lancet develops before final molt, feed on mucosal vessels, move freely on mucosal surface
  • Inefficient at feeding - cause more blood loss than they take up, don’t fed in single spot - move around and cause more bleeding
29
Q

Bovine hemonchus immunity

A

2+ years (different than sheep)
Immunity can be broken by drought (poor nutrition/heavy challenge)
Tropics: outbreak during rainy season, end of long dry season

30
Q

Cooperia species in cattle

A

C. oncophora
- temperate (UK), mild pathogen, contribute to PGE
- mild pathogen = larvae dont migrate to tissues
C puntata, C. pectinata = more tropical, more pathogenic b/c infect tissues

31
Q

C. Oncophora

A
  • Temperate regions
  • PGE as mixed infection
  • not very fecund (stable population)
  • Parasitic stages develop on surface of SI mucosa
  • Mild pathogen = inappetance and reduced weight gain
  • Similar epidemiology to Osteragia
32
Q

Anthelmintics concerns with C. oncophora

A
  • Relatively resistant to anthelmintics: dose limiting species
  • needs more to clear parasite
  • most common parasite implicated in anthelmintic resistance
    Indicator species indicating problem with drug resistance
33
Q

What cattle parasite is most commonly implicated in anthelmintic resistance?

A

C. oncophora

34
Q

Trichostrongylus Colubriformis

A
  • Small intestine
  • Adult worm less than 1cm
  • Similar to T. axei
  • Contributes to PGE
  • Pathogenic in large numbers - L3/L4 –> penetrate epithelium causing enteritis
35
Q

Nematodirus helventianus

A
  • Part of mixed infection for PGE
36
Q

Nematodirus battus and spathiger

A
  • In cattle, but more in sheep

- Cattle can act as resevoir

37
Q

Cattle can act as reservoir for sheep for which specie of parasite?

A

N. battus and spathiger

38
Q

Which is the only egg of trichostrongylid species that you can differentiate?

A

Nematodirus (twice the size)

39
Q

Which species of Trichostrongylid eggs look the same?

A

Hemonchus
Ostertagia
Trichostrongylus
Cooperia

40
Q

Bunostomum phlebotomum

A
  • Strongyloidea
  • Cattle hookworm (sucks blood)
  • Small intestine
  • Adult = 1-3 cm with hooked anterior
41
Q

Bunostomum life cycle

A

Typical of hookworm

  • percutaneous - pulmonary migration
  • oral route - no pulmonary migration (ingest larvae and go straight to intestine and develop)

PPP = 6 weeks

  • Need warm and we conditions –> small burdens in UK
42
Q

Bunostomum Pathology

A

Several hundred adult worms needed for clinical signs

  • anemia
  • hypoalbuminemia
  • sometimes diarrhoea
  • pedal dermatitis (penetration of infective larvae)

*remove contamination to avoid recycling of L3s

43
Q

Toxocara vitulorum

A
  • Small intestine
  • Worldwide except UK
  • LARGEST intestinal parasite of cattle
  • Typical ascaridid (thick albuminous pitted shell)
44
Q

T. vituolrum lifecycle + epidemiology

A
  • Similar to T. cati
  • L3 transmammary infection –> arrests (no tissue migration
  • exposed to infection from birth but build up immunity
  • Infection via larvated egg ( no tissue migration in calves, just older animals)
45
Q

Oesophagostomum radiatum

A
  • Large intestinal
  • 2cm stout worms
  • Strongyloidea (but not a hookworm)
  • Not major UK pathogen
  • More in pigs, for nodules on serosal surface of LI associated with larval stages
46
Q

Trichuris globulosa

A
  • Whipworm
  • Large intestine
  • Light infection common
  • Thread head
  • more in pig lectures
47
Q

Bovine PGE most commonly caused by

A

Osteragia osteragi + Cooperia Oncophora

Parasitology (3 decks)

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