Bovine GI nematodes Flashcards
Parasitic Gastroenteritis
- 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
Bovine Abomasal Nematodes
Hemonchus Ostertagia Trichostrongylus **mneumonic = HOT ** ALL three are in trichostrongyloidea family
Bovine Small Intestinal Nematodes
**Cooperia
**Nematodirus
**Trichostrongylus
Bunostomum (Strongyolidea- hookworm)
Toxocara (Ascaridoidea)
** = main parasites of concern, all trichostrongyloidea
Bovine Large Intestinal Nematodes
Oesophagostomum (strongyloidea - strongyle)
Trichuroidea
Trichostrongyloidea
Common Characteristics
Most important in grazing ruminants DIRECT life cycle L3 = infective Mainly GI (except dictycaulus) PPP ~ 21days
Bovine Ostertagia species
Osteragia ostergai
Ostergia leptospicularis
O. ostergia life cycle - bovine
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
Ostergiosis Pathogenesis
Heavy infection > 40,000 adults
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
Osteragiosis nodules: importance
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)
Osteragiosis: Two Clinical Forms
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)
Type I Osteragiosis: Clinical Signs
- Profuse/watery diarrhea
- Weight loss
- Dull coats
- Gather around water sources
- Occasional submandibular edema (hypoalbuminemia)
- High morbidity, low mortality (provided animal treated)
Type II Ostertagiosis: Clinical Signs
- 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)
Osteragiosis: Diagnosis
- Clinical picture and grazing history
- Herd dx, not individual
- Fecal egg counts
- serum pepsinogen
- Serum antibody
- PM
Describe the disadvantages of Fecal Egg Counts in the diagnosis of Osteragiosis.
- 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
Describe the value of serum pepsinogen in regard to Osteragiosis dx.
- 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
Value to serum anitbodies in dx of Osteragiosis
- ELISAs
- Good measure of exposure
- Not commercially available
Epidemiology of Osteragiosis
- Late winter –> spring: type 2, less prevalent
- Late summer –> early winter, more prevalent
Osteragia Immunity
- Slow to develop
- Takes at least one grazing season
- Second season calves and adults generally immune
- Immune animals still carry burdens (L4 arrested)
Describe overwintering
- 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
Type 1 Osteragiosis epidemiology
- 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
What happens when free-living stages of ostertagia are exposed to low temperatures?
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
Predisposing factors to Type II Osteragia
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)
Ostertagiosis: spring vs autumn calving occurrence
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
Atypical forms of bovine ostertagiosis
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
