Ostertagia is a parasite (nematode ) that is also causes parasitic gastroenteritis in cattle
the disease is called Bovine a ostertagiosis/PGE
PGE-• Disease associated with a number of nematode species (singly or in combination)
→ ROUNDWORMS
• Characterised by:
• diarrhea / weight loss (clinical disease)
• poor weight gain (subclinical disease)
• seasonal appearance
• hypoalbuminemia
PARASITIC GASTRO-ENTERITIS
Economic importance
• Considerable economic importance in grazing livestock
• Potential welfare problem (esp. organicfarms)
• Losses associated with the cost of:
• replacement stock
• disruption of breeding programme
• impaired productivity
• treatment of clinically affected stock
• prophylaxis
what is the primary cause of PGE - ostertagia
BOVINE OSTERTAGIOSIS
caused by: Ostertagia
• PRIMARY pathogen of cattle (temperate regions)
• Adult worms 1cm long, cotton-like, brown (when fresh)
•found in Abomasum of cattle
life-cycle of nematode ostergia . adult is found in abomasum of cow both female and male mate > eggs are released via poo> hatch produce larvae L3 and eaten by another cow > into their abomasum and mucosa and infected . 3 weeks prepatent period > time of infection to eggs in theor poo
1st stage : typical strongyle egg from ostergia and will have an oval shape and thin shell. 3rd stage : go onto L3 larvae stage more visible to naked eye and lives 9-10months in pasture and larvae live sin water droplets and the gets ingested by another cow and take 2-3weeks to develop in adult in gastric gland
larva stage 4 : 1mm long in gastric gland and then adult worm 1cm
risk of disease = rate of infection + host immunity
RATE OF INFECTION depends on:
• Host appetite - cow that eat
• NUMBERS OF INFECTIVE LARVAE (L3) ON PASTURE/grass
times which larvae high in pasture - 1. august to winter and 2. from january until spring
A) risk to grazing animals outside
B) Risk to Housed animals for winter
→ Disease commonest in calves at
• grazing permanent pasture
• kept at high stocking density
whys we see disease at a particular time of year.L3 causes disease.
permanent pasture grazed by cattle last year
LARVEA ON PASTURE FROM LAST YEAR
overwinter L3 good at surviving winter.dont feed, have food reserve
as weather warms up , slowly decline due to lost of food reserves
then cattle turnout - ( cows leave their houses )
pick up/ eat infected larvae
after 3 weeks eggs appear=in their poo
the time for egg to hatch gets shorter as we reach summer
due to higher temperature
all reach L3 same time and then a sudden increase in larvea on pasture = summer ostertagiasis
WINTER OSTERTAGIA - This is the autumn infection peak. From the previous graph.last part of the grazing season here, September, October, November time.what happens if calves are left to graze heavily contaminated pasture.
instead of developing adult worms in 3 weeks they pop into the gastricglands eat and then go to sleep
This is due to coolertemperatures
they come arrested for months at L4 in abomasal mucosa
cattleaccumulates a lot of larvae 500K
no clinical symptoms
Let's see what happens to the parasite if the larvae don't become arrested.
If not arrested, larvae would reach the adult worm stage in L3 w
Eggs would appear on pasture during cold weather
Eggs are lessresilient in cold conditions compared to infective larvae
Many eggs would die off in cold weather
Killing off all the eggs could eliminatelarvae on the pasture
Where larvae become arrested when the L3 are eaten late in the autumn
Around end of January, approximately 20% of arrested worms resume development
Resumed development leads to the adult stage three weeks later, causing clinical signs
Clinical signs appear only when worms reach the adult stage
Following this, another 20% of arrested worms resume development a couple of weeks later
Strategy of staggered development to avoid putting all eggs in the same basket
Aim is to synchronize the waves of infection with periods of favorable weather- for parasite to survive
what triggers Larvae L4 to stop developing and become arrested .
it's prolonged chilling of the same larvae on the grass late in the autumn causes them to become arrested once they're eaten.
Those same larvae on the grass if they're not eaten by calves
will survive through to the following year when they're eaten by next year's calves after turnout.
Tendency to arrested development induced by chilling is turned off by the following spring
Shortchilling induces arrested development, but prolonged chilling turns it off.
Immunity to Ostertagia ostertagi
• SLOW to develop (whole grazing season)
• May FALL over winter
- RE-ESTABLISHED upon turnout (2nd grazing season)
• ADULT cattle solidly IMMUNE (no significant role in disease epidemiology)
CONTROL (TYPE 1 DISEASE) we prevent summer or type one
Use clean pasture
• New leys, pasture not grazed by cattle last year
• BUT not always available
Delay turnout until after spring mortality in L3
• BUT uneconomical use of pasture, supplementary feeding
DOSE ‘N’ MOVE - MID-JULY
Most overwinter larvae die by early summer
Latesummer peak of infection
late summer august type 1 ostertagiasis
Dose and move system involves using a second field for silageproduction in the first half of the year
Cattle are dosed midjuly with a wormer and then moved to fieldB for the rest of the year
This system avoids exposing calves to the significantautumninfectionpeak
BUT will notcontrolearly season disease
• Increased anthelmintic resistance risk?
→ aftermath, that is merely a field that was used that was cut for hay or silage reduction.
IF NO ALTERNATIVE GRAZING AVAILABLE
Strategic anthelmintic treatment
Strategic anthelmintic treatment
Traditional treatments every 3-4 weeks didn't reduce grass larvae.
Doramectin, a modern anthelmintic, used for its lasting effects.
Two doses: one at turnout, another 8 weeks later.
First dose protects for 5 weeks,preventing larvae from establishing and transmission
second dose lasts up to 13weeks.prevents larvae from becoming egg-laying adults at this crucial stage
Prevents contamination of pasture by targeting larvae and overwinter larvae die off.
intraruminalanthelmintic devices like Autoworm minimize pasture contamination.
Administered using a bolus gun, the device sits in the reticular rumen and slowly releases deworming drug.
Provides protection for several months, either intermittently or continuously.
Stops pasture contamination with worm eggs and eliminates autoinfection peak.So that will stop any of the overwinter larvae that are ingested here from growing to adult worms.
→ Therefore no contamination and therefore no auto infection peak.
type two Cattle exposed to MEDIUM / HIGH challenge at pasture in late autumn or cattle of UNKNOWN origin