Bovine PGE

Question 1

Bovine PGE

(parasitic Gastroenteritis)

Answer 1

• Parasitic gastroenteritis (PGE) is a disease complex associated with a number of nematode species (mostly strongyles), either singly or in combination
• Many worm species- few of significance (roundworms)
• Focus:

1. Abomasum: Ostertagia
2. Small Intestine: Cooperia (Numerically imp.,but less patho.), Nematodirus (Clinical signs in 1st year calves)
3. Large Intestine Parasites as well

Question 2

Ostertagia ostertagi

Answer 2

• Primary pathogen, primary cause of gastroenteritis in cattle (temperate regions)
• Adult worms 1cm long, cotton-like, brown (when fresh)
• Found in the Abomasum (fundus)/ abomasa mucosa
• Animal with clinical signs may have 30 thousand
• <1 cm (adult: L5)
• L3 stage (infective) : <1mm
• egg: 80 micrometers (um)

Question 3

Pre-Patent Period

(PPP)

Answer 3

PPP: time it takes for larvae to be ingested and then passed through the faeces

Pre-patent period: time b/w infection

And first appearance of eggs

And larva

Question 4

Ostertagia Life Cycle

Answer 4

1. Calves are infected by ingesting L3 with grass. (over-wintering L3)
2. The swallowed larvae pass through the fore-stomachs

& abomasal gastric glands to the L4 stage

3. Emerge as adult (L5) worms–> abomasal mucosa

after nearly 3 weeks(PPP) (brown, thread-like, ~1cm)

4. Adult female worms –> strongyle eggs–> faeces

Prepatent period: Time between infection & first

appearance of eggs- 3 weeks (5-6 months if arrested)

5. Eggs hatch–> L1–> L2 –>L3 (infective stage)
6. L3 gather in droplets of water on blades of grass

**Has a direct life cycle: involves ONE host –> cattle. The final/definitive host

Question 5

Strongyle Egg

(Ostertagia)

Answer 5

• 80 um long (compare to pollen grain which is smaller)
• Egg stage that is passed through faeces:

Strongyle (rule of thumb for many eggs, remember this size) egg class

• The infective larvae stage (L3) is visible to the naked eye –> Egg stage Molt a few times to become effective infecting larvae
• cna see the larvae on grass blades

Question 6

Epidemiology

Answer 6

Rate of Infection depends on:

• Host appetite: Amount eaten. Calves grazing amount doesn’t vary much over grazing season
• Number of Infective Larvae (L3) on the pasture: Amount of pasture ridden with larvae (density of larvae) - vary enormously!

1. Clinical disease seen in second half of summer
2. Other time is in housed animals in the middle of winter
   * Dairy calves are reared as a single age group
   - 1st season calves graze in separate pasture than other age groups (yearlings as well)
   - Those pastures are reused for the 1st season calves from one year to the next
   - See this infection especially with permanent pasture! (not plowed/re-seeded every year)
   - This pasture is left for one year to the next
   - Large number of calves will be spreading more and more eggs produced by the parasites. More cows the more parasites
   - The worm larvae may be on the pasture left over from last seasons calves (over-wintering larvae)
   * Calves weaned early and put out to graze with other calves of similar age. High disease risk if not controlled and most frequently occurs when calves graze permanent pasture, especially if kept at high stocking rates

Question 7

TImeline of Ostertagia Infection

Answer 7

• Last years calves contam. the first season calve pasture (winter larve will die off in spring if they don’t infect)

Larvae can survive 9-10 months in cold weather:

They survive even longer in cold weather than in warm, but the development takes longer

• Farmer turns out calves and 3 weeks later the eggs appear in feces (modest infection-not disease)
• Outbreaks late winter/ early spring: infective larvae that have survived over winter (over-wintered). Good at surviving cold weather
• Late april/early may: first season calves going out to pastures for the first time, pick up infected larvae
• PPP period: 3 weeks
• 3 weeks after turnout, you will see eggs appear in the calves feces
• will release eggs in faeces everyday for next few weeks
• eggs are not the infective stage so they need to hatch and go to L3 stage and then can infect cows at that stage. Need to go from egg stage to L1 and L2 and L3. Takes longer if colder! Takes less time for egg development as it gets warmer. Can develop into L3 stage quicker if it is warmer. TEMP DEPENDENT!! But all tend to reach L3 stage at about the same time

Mid to late July: Auto infection peak, number of infective larvae that appear on the pasture as a result of the overwinter peak

Calves will succumb to disease (summer or type I ostertagiosis) if autoinfection peak passes a certain threshold

• See outbreak of ostertagiosis in LATE SUMMER
• Auto infection: same calves will go down with clinical disease. They get it from pasture they infected

Question 8

Type I Disease (Summer)

Answer 8

• Modest numbers of L3 survive over winter, drop during mid-summer
• Dairy calves are turned out in April when there is still L3 which has

over-wintered present on the pasture

• Calves consume the L3, although relatively low numbers at first so

appear healthy & 3 weeks later the now mature Ostertagi–> eggs

and contaminate the pasture (~May)

• The eggs aren’t infective yet they must mature to L3 first the lag time for this is temperature dependent: ↑ temp –> ↓Lag Time
• Type 1 disease- Affects calves between mid-July and October due to L3 ingested 3-4 weeks earlier
• Clinical signs: diarrhoea, weight loss, reduced appetite- ↑ morbidity / ↓ mortality

Question 9

Why do we see an outbreak in housed animals over winter??

Answer 9

• Calves grazing contaminated pasture in late autumn
• The larvae ingested will actually go into arrested development (sleep).
• Stop developing after about 4 days (at EL4 phase) and sit in abomasal mucosa
• These calves are not showing clinical signs even though they ingested thousands of larvae –> Type II Phase
• Eggs arent good at developing in winter!! (PPP 3 weeks if they continue to develop rather than arrest)
• Wont develop, no infective larvae and they would die out. Larvae can survive winter weather, but the eggs will die out and not develop! HENCE: they go through arrested dev.

Question 10

What triggers the arrested development stage?

Answer 10

What triggers arrested dev??

• larvae become arrested due to temperature of prolonged chill. TEMP BASED signal
• become arrested about for days in of being ingested (be arrested for about 2 or 3 months and then resume becoming adult worms)
• 20% will become adult worms and then another 20% will come out of arrested phase

-why not all resume development at once? –> don’t put all eggs into one basket. Eggs are passed in waves to try and hit the right type of weather so you can ensure some amount of survival on the farm. DO not want to die out.

Question 11

Pre-Type II Phase

Answer 11

Pre-Type 2 Phase

• Calves at end of first grazing season (from October) continue to ingest more L3, but won’t develop to L5 in 3 weeks, they’ll become arrested
• –> Accumulation of large population (>100,000) of Ostertagia EL4 (arrested stage) (PPP is now several months)
• Not a disease yet as there are no clinical signs
• Larvae will have been conditioned by the time they are eaten and be arrested in development about 4 days into being ingested

-go to sleep effectively for about 2-3 months

Question 12

Larval Stages Ostertagia

Answer 12

• Eggs hatch to produce L1
• L1 to L2 on pasture
• L3 - infectious (at auto infection peak are 2 or 3 months old at least)

-Same larvae that would cause type I disease in august would cause type II later in winter if they encounter temps that make them arrest dev.

• L3 will molt into early 4th larval stage in gastric gland (and stay that way over winter if arrested)–> around Feb. (if arrested) will molt to L5
• L4 -L5 causes diarrhea/egg release
• L5 emerges from gastric gland and causes disease

Question 13

Type II Disease

Answer 13

Type 2 Disease

• Affects yearlings housed after first grazing season (February - May)
• The EL4 are preprogrammed to resume development after long periods of cold.
• Eggs are released in waves to increase the chance of optimal conditions for some of them ↓ morbidity / ↑ mortality (exposed to large amounts)
• Clinical signs: diarrhoea, weight loss, reduced appetite, submandibular oedema

Question 14

Epidemiology- Beef Sucklers

Answer 14

• Calves suckle and graze with their dams
• Calves are susceptible, but cows are immune
• Overt disease is much less common than in dairy herds

Question 15

Beef: Spring-Calving Herds

Answer 15

Spring-calving herds (BEEF SUCKLERS)

• Spring mortality of L3 occurs before calves eat significant amounts of grass, so there won’t be much infective larvae on grass when they start eating so only ↓ level infections will occur
• Immune cows take in lots of L3, but pass very few worm eggs leading to development of very few L3
• Net result: Disease in spring= very unlikely
• Disease risk is low in SPRING born beef calves

Question 16

Autumn- calving Herds (BEEF)

Answer 16

Autumn-calving herds (BEEF SUCKLERS)

• Calves graze before spring mortality of L3 occurs and will contaminate pasture
• But relatively few calves on pasture (as most of the grass is needed by the cows)
• Net result: relatively few eggs dropped onto pasture, disease possible but lower risk than dairy

Question 17

Immunity

(Epidemiology-Ostertagia)

Answer 17

• Ostertagia only increases in numbers of infective larvae on the grass late in the grazing season - takes almost a whole grazing season for calves to develop any reasonable immunity
• Acquired immunity is slow to develop (takes whole grazing season)-For first season calves to develop any reasonable immunity
• Immunity may wane during winter housing (deprived of antigenic stimulation) –> rapidly re-established upon turnout
• Adult cattle solidly immune (no significant role in epidemiology of disease)-Have developed Immunity (after 2 or 3 grazing seasons)
• This is all more relative to first season calves affecting following years of calves

Question 18

Diagnosis of Ostertagiosis

Answer 18

• Seasonal incidence, previous grazing history, clinical signs
• Faecal examination (worm egg count: Type 1 disease: >1,000 e.p.g.; Type 2 disease: variable, often zero)
• Blood pepsinogen or gastrin (elevated; s_pecific indicators of abomasal damage_ in groups of animals)
• Post mortem (fundic nodules, ↑ gastric pH, putrid smell, >40,000 adult worms in lumen on mucosal surface, larvae in mucosa

Question 19

Control of Ostertagiosis

(Type I Disease)

Answer 19

• Use clean pasture (e.g. newly seeded, pasture not grazed by cattle/ grazed by other livestock such as sheep the previous year but not always available)
• Delay turnout until after spring mortality of L3 (But uneconomical use of pasture & supplementary feeding may be required –> ↑ costs.
• Also if it’s a cool spring, larvae may survive longer than normal.
• Dose and move to aftermath

​-aftermath: field where cuts of grass were used for hay or some other purpose. Grass that is left after a cut has been taken for sialage or something.

-goal is to take cows of the infected field and move them before the auto-infection peak in mid July (take them off mid to early July)

​- leave calves on contaminated pasture until mid-July & then dose with wormer and move to clean pasture for the rest of the grazing period (BUT will not control early season disease caused by farmers spreading contaminated slurry on the pasture & may ↑ anthelmintic drug resistance)- can increase the risk whent they are first turned out by using slurry as a cheap fertilizer and the larvae survive well in this

• Field A is the filed the calves are turned out on initially (when the calves are first turned out in Spring, there arent many larvae on the field to infect them) - Late summer is where you see auto-peak and type I disease
• then deworm them and move them to a different pasture (B) before the auto-infection peak hits (filed A will still be dangerous)

Question 20

Control of Type I Ostertagiosis

(No alternative Grazing Available)

Answer 20

• Repeated anthelmintic treatment (deworm)
• Either monthly from mid-July (calves already met auto-infection peak) (calves temporarily better, but constantly being reinfected. BUT temporary control of egg output only, cattle reinfected)- not ideal strategy
• Stop calves from contaminating: Or before mid-July on 2 or 3 occasions, e.g. doramectin 0 and 8 week treatment post turnout (relies on residual activity of 5 weeks + 3 week worm PPP)(Gap allows calves to develop some immunity). GIve this drug at turnout and then 8 weeks later. dormacting has a 5 week residual activity, will kill any incoming larvae for the next 5 weeks
• after turnout dormaectin wears off is where the infective larvae will first start to become established (will mature and lay eggs 3 weeks later)

-between week 5 and 8 is the 3 week PPP

-cows will be protected until week 13 (another 8 weeks): SAFE–> 13 weeks after turnout, beyond point where over-wintered larvae have died off

• Intra-ruminal anthelmintic devices (intraruminal bulous) :
• give around turnout to prevent over-wintered larvae from establishing
• no contamination, no autoinfection peak
• Sit in reticular rumen & –> anthelmintic drug continuously/ in pulses- ↓ pasture contamination & size of autoinfection peak BUT expensive

Question 21

Type II Disease Control

(Winter Form)

Answer 21

Type 2 disease

• Cattle that are exposed to ↓ challenge at pasture in late autumn (if farmer tried to control already for type I) are unlikely to require treatment at housing
• Only if Cattle exposed to medium/high challenge in late autumn (late season) or animals of unknown origin are likely to require treatment at housing (using an anthelmintic active against arrested larvae)