Bursate Nematodes 3

Question 1

What are some other Trichostrongyloidea in cattle? (Less important)

Answer 1

-Cooperia spp. - (C. oncophora, C. curticei, C. pectinata - small intestine)
-Haemonchus placei - abomasum
-Trichostrongylus axei - abomasum

Cooperia and Trichs minor players in bovine PGE
Adults </= 11mm in length
All produce Typical stronglye eggs

Question 2

Bovine PGE summary:

Answer 2

-Ostertagia ostertagi
-Calves, first grazing season
-Pathology of the abomasum

Question 3

Ovine / Caprine PGE (small ruminants)

Answer 3

Multi-factorial (Trichostrongyles)
Lambs, but also older sheep
*peri-parturient rise in egg count
*Abomasum and intestine

Question 4

Teladorsagia (small ruminants)

Answer 4

-Teladorsagia circumcinta (formerly Ostertagia) abomasum
-Similar pathogenesis as bovine ostertagiosis
-Usually present with other pathogens (intestinal)

Question 5

Additional Pathogens in Small Ruminants

Answer 5

-Trichostrongylus colubriformis, T. vitrinus, other Trich spp.
-Cooperia spp. (contributes to bovine PGE also)
-Small intestine
-Loss of villi, malabsorption, stunted growth, diarrhea
-Haemonchus contortus (notorious in small ruminants)

Question 6

Haemonchus contortus

Answer 6

-Abomasal parasite (“barbers pole worm”)
-Voracious blood sucker (female more than males)
-Anemia!!
-Severe problem in warmer climates
-Temperate areas, autumn, spring after hypobiosis
-H. placei in cattle

Question 7

Ovine / Caprine Haemonchosis Clinical Signs

Answer 7

-Anemia
-Compensated, then iron deficiency
-Acute, sub-acute or chronic
-Acute cases more likely in warmer climates
-Temperate areas, cases in spring following hypobiosis
-In summer, following warm weather

Question 8

Haemonchosis - Diagnosis, TX, Control

Answer 8

-Genetic susceptibility, blood type
-Treat acute phase rapidly
-Dose, provide supportive therapy, move off pasture

Question 9

Anemia correspond to __.

Answer 9

Clinical Severity!

Question 10

Seasonality of Trichostrongyle Infections:

Answer 10

Eggs and larvae can overwinter in temperate climates
Build up of infectivity on pastures over the summer
Greatest disease risk is mid-summer -> autumn but there are exceptions!

Question 11

Nematodirus

Answer 11

-N. battus, N. helvetianus, other spp.
*-N. battus is the very pathogenic one
-Variation on typical trichostrongylid life cycle
-Eggs hatch only at L3 (NOT L1)
-Cold conditioning, followed by rise in temperatures stimulates hatching
-Cold resistance
-Anti-freeze in eggs (adaptation to colder climates)

Question 12

Nematodirus stages

Answer 12

N. battus has a little bit more of a “running track” outside than the N. Non battus.

Question 13

Nematodirosis Epidemiology

Answer 13

-Acute disease in lambs in springtime
-Depends on the weather conditions
-Spring comes early, lambs not grazing = no disease
-Spring comes late, lambs develop innate resistance
-10 C critical temp - mean about this stimulates a mass hatch
-sheep acquire strong innate resistance at about 3 months of age
-lamb to lamb transmission (ewes have no role here)
-calves can support parasite and shed eggs, no disease
-climate change = unpredictability

Question 14

Nematodirosis - Path & Clinical Signs

Answer 14

-stunting of intestinal villi
-hypermotility and increased secretions
-type II hypersensitivity response (Th2)
-Blackish D+
-Dehydration, extreme thirst
-Lambs gathered around water trough
-Ewes remain unaffected

Question 15

PGE in small ruminants vs cattle

Answer 15

-Multi factorial (Teladorsagia, Trichostrongylus, others)
-Continued age susceptibility
-Peri-parturient rise in egg production
-High protein decreases clinical signs
-Nematodirus vs Haemonchus

Question 16

Control of PGE in sheep

Answer 16

-Dose ewes, then lambs if necessary
-Forecasts for Nematodiris (tracking based on weather)
-Clean pasture in the spring (Nematodirus can be carried by calves even though they don’t have clinical signs!)
-Good pasture management and minimum dosing
-Targeted selective TX
-Rotate drugs