PID 2 Flashcards

Bovine PGE

1
Q

pge acronym

A

parasite gastroenteritis, more than one parasite causing this diesease

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2
Q

what kind of parasite is it associated with

A

nematodes, either alone or incombination

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3
Q

signs

A

diarrhoea, weight loss (in clinical disease), LOP (loss of production), hypoalbuminea

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4
Q

economic importance

A

grazing livestock, esp organic farm

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5
Q

association of economic losses

A

replacement of stock, breeding programme, impaired productivity, treatment and prophylaxis

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6
Q

nematodes in abomasum

A

ostertagia, trichostrongylus, haemonchus

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7
Q

nematodes in small intestine

A

cooperia, nematodirus, trichostrongylus

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8
Q

ostertagia

A

primary pathogen of cattle, adults 1cm long, cotton-like, brown (‘brown stomach worm’), found in glandular =/fundus abomasum

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9
Q

lifecycle ostertagia

A

direct lifecycle:

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10
Q

prepatent period (IMP)

A

3 weeks, time between infection and egg shedding (parasite visible) BUT, can be as long as 6 months

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11
Q

why can it be as long as 6 months?

A

because larvae L3 can survive overwinter via overwintering (because L3 retain sheath the protects them against harsh conditions) + arrested development (hypobiosis) –> L3 undergo arrested development in the host

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12
Q

what do L3 do

A

climb up the grass, survive in droplets, penetrate gastric glands in the fundus of abomasum

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13
Q

what do they do in the host

A

emerge from the fundus –> causes trauma

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14
Q

what is epidemiology (risk of disease) dependent on?

A

rate of infection (larvae cow ingests) vs host immunity

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15
Q

so what determines rate of infection

A

appetite of cow, density of larvae

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16
Q

what population most common?

A

calves, high stocking density

17
Q

how does pasture larval count evolve through the year? (IMP)

A

from january to june –> over-wintering L3, if not ingested die + turnout of cows around spring (btw March and May) –> cows start ingesting L3s –> 3 weeks later start shedding eggs –> end of summer: accumulation of L3s on pasture ==> auto-infection peak because larvae developed from eggs that the cows themselves have shed earlier in the season

18
Q

when does type 1 disease develop?

A

when nb of L3 exceed level

19
Q

when does type 1 disease develop (IMP)

A

at the end of the grazing season

20
Q

what happens after summer?

A

arrested L4s in abomasal mucosa –> L4s resume development and emerge in waves

21
Q

in beef herds, what is the difference that counts for epidemiology?

A

mums and calves put together, mums immune to the disease –> very unlikely in spring calving

22
Q

what happens in autumn calving in beef herds? (VERY IMPORTANT)

A

calves inside until spring when put on pasture –> put on larvae but because raised with mums –> mums ingest must larvae –> auto-infection peak not as high to cause disease

23
Q

immunity of ostertagia ostertagi

A

slow to develop (whole grazing season), may fall overwinter, re-established upon turnout (2nd grazing season), adults are solidly immune –> nb of eggs they shed is smaller

24
Q

how do we avoid clinical disease?

A

use clean pasture, not always available OR later turnout of calves because most wintering L3s would have died

25
Q

what does later turnout involve

A

use of concentrate feeding, economic losses

26
Q

if know when the turnout happens, what can you do?

A

worm them and move them to clean pasture ‘does’n move)

27
Q

dose’n move sequence

A

let calves in spring and early summer –> move them to clean pasture in mid-summer (any overwintering L3s would have died)

28
Q

(2) problems with dose’n move

A

not solution for type 2 disease, increased risk of antihelmintic resistance

29
Q

strategic anthelmintic treatment

A

repeated treatment after mid-July (but temporary control only) OR before mid-July drugs that have residual activity

30
Q

when do you administer drugs with residual activity

A

one at turnout and one at 8 weeks post turnout

31
Q

why do you delay 2nd treatment by 8 weeks?

A

because residual activity is 5 weeks and pre-patent period is 3 weeks

32
Q

what period do you cover with 2 treatments

A

14 weeks

33
Q

what drugs can be administered once?

A

intra-ruminal boluses have residual activity of 12-14 weeks –> protect calves during whole grazing season

34
Q

examples of drugs

A

ivomec (withdrawn), paratect (withdrawn), autoworm, panacur bolus BUT expensive

35
Q

when is the treatment required?

A

when cattle exposed to high quantities of the nematode