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Bovine parasitic gastro-enteritis - Coggle Diagram
Bovine parasitic gastro-enteritis
characteristic symptoms
diarrhoea
weight loss
poor weight gain
seasonal appearance
hypoalbuminaemia
importance
considerable economic loss
welfare problem
losses
replacement stock
disruption of breeding programme
impaired productivity
treatment/prevention not cheap
important parasite species
abomasum
ostertagia
-
PRIMARY PATHOGEN
small intestine
Cooperia
Nematodirus - clinical, can be transferred from sheep
life cycle of Ostertagia
final host
parasitic stages
L4 - curls up in gastric pits
adult - emerges from gastric pits, lies on submucosa in a film of mucous
pre-patent period
3 weeks - 6+ months
pasture
free-living
eggs, L1-L3
Ostertagia egg
typical strongyle egg
clear shell
epidemiology
balance between
rate of infection
and
host immunity
rate of infection
host appetite
numbers of infective larvae L3 on pasture
dairy herds
most common in calves
high stocking density
grazing permanent pastures
type 1 disease
(dairy)
jan-may
- overwintering L3 on pasture
july-nov
- autoinfection peak
may-aug
- eggs start to appear and start to hatch into L3 (gen 2)
also known as
summer ostertagiosis
type 2 disease
(dairy)
pre-type2 phase
large numbers of larvae arrested in abomasal sbumucosa
larvae picked up by calves grazing late autumn
march-april
- resumed development --> intermittent diarrhoea
epidemiology in beef calves
spring calving
spring mortaility of L3 happens before calves are grazed
beef calves are grazed with their mothers who are
already immune
disease is unlikely
autumn calving
grazed before spring mortality, but mothers eat most of grass
pathogenesis
decrease in appetite, impaired digestion --> poor weight gain
loss of specialised epithelial cells that produce HCl and pepsinogen, distention of gastric gland) --> increase in gastric pH, decrease in pepsinogen conversion
abomasal mucosal nodules - specialised cells repleced by undifferentiated cuboidal cells
blood changes: increase in mucosal permeability (becomes leaky) --> low blood albumin, high pepsinogen
control methods for type 1
use clean pasture (not always avail)
delay turnout to after spring mortality (uneconomic use of pasture)
dose n move
(inceased althelmintic resistance risk?)
move to a new pasture during late summer (when autoimmune peak would occur)
treatment
after mid july
temporary egg control only!
stategic treatment
doramectin injection at 0 and 8 weeks + 5 weeks residual activity
intra-ruminal anthelmintic devices
minimises pasture contamination
expensive
type 2 disease
medium, high challenge in late autumn / cattle of unknown origin --> kill arrested larvae