PID 2 Flashcards

Bovine PGE (35 cards)

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
what does later turnout involve
use of concentrate feeding, economic losses
26
if know when the turnout happens, what can you do?
worm them and move them to clean pasture 'does'n move)
27
dose'n move sequence
let calves in spring and early summer --> move them to clean pasture in mid-summer (any overwintering L3s would have died)
28
(2) problems with dose'n move
not solution for type 2 disease, increased risk of antihelmintic resistance
29
strategic anthelmintic treatment
repeated treatment after mid-July (but temporary control only) OR before mid-July drugs that have residual activity
30
when do you administer drugs with residual activity
one at turnout and one at 8 weeks post turnout
31
why do you delay 2nd treatment by 8 weeks?
because residual activity is 5 weeks and pre-patent period is 3 weeks
32
what period do you cover with 2 treatments
14 weeks
33
what drugs can be administered once?
intra-ruminal boluses have residual activity of 12-14 weeks --> protect calves during whole grazing season
34
examples of drugs
ivomec (withdrawn), paratect (withdrawn), autoworm, panacur bolus BUT expensive
35
when is the treatment required?
when cattle exposed to high quantities of the nematode