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Flashcards in Parasitology - Bovine PGE Deck (13):
1

Bovine Parasitic Gastro-Enteritis (PGE) is caused by several nematode species that invade different areas of cattle's gastrointestinal tract. 

Which among these are the *most important* for dairy/cattle practice?

Abomasum:

Ostertagia

Trichstrongylus

Haemonchus

Small intestine:

Cooperia

Nematodirus

Trichostrongylus

Bunostomum

Large intestine (colon):

Oesophagostomum

Chabertia

Trichuris

Ostertagia (abomasum)

Cooperia (small intestine)

Nematodirus (small intestine)

Trichuris (colon)

2

What is the PRIMARY PATHOGEN of cattle? What is the species? 

Ostertagia ostertagi 

This is a nematode (round worm) in the Trichostrongyloidea superfamily. This means its eggs are the "strongyle" type.

3

What do the eggs of the Ostertagia ostertagi round worm look like? 

They are typical strongyle eggs, about 80 um long.

4

What is the general appearance of Ostertagia ostertagi in terms of colour & size?

As Trichostrongyloidea, Ostertagia ostertagi look like short lengths of cotton, about 1 cm long.

Colour: Brown, when fresh.

Their heads have no distinct features.

5

What is the life cycle of Ostertagia osteragi, starting with adult in the abomasum of an adult cow?

The life cycle is the same for typical Trichostrongyloidea:

Adult worms mate & produce eggs inside adult cow's abomasum,  → strongyle eggs dropped in cow faeces → eggs hatch → larvae moult L1, L2 → L3 infective → eaten by calf → L4 →  adult worm in calf GIT

Prepatent period (eggs to L3) = 3 weeks

6

The pre-patent period of Ostertagia ostertagi is three weeks, but can go up to 5-6 months. Why? 

The larvae can undergo "arrested development" at the L4 stage in the abomasal wall of the cow, typically in the middle of winter, so that they can be excreted onto fresh pasture in the springtime. 

Up to 500,000 larvae can undergo arrested development. 

7

What is Type I disease of Ostertagiosis in dairy herds?

Type I = normal, no arrested development of L4 larvae within host. This hits CALVES during their first grazing season. 

Calves turned out in March/April/May. Their faeces contains overwintering larvae that reach L3 in three weeks on grass. 

April/May/June - infective larvae in grass, various stages.  Some L3 die off in "spring mortality." Few are eaten by calves. 

October - all reach L3 stage in faeces. Very high L3 count in grass. 

 

8

What is Type II disease of Ostertagiosis in dairy herds?

Type II = this occurs when calves grazing in late autumn eat L3, which reach L4 inside the GIT. In the abomasal wall the L4 undergo arrested development to EL4 over the winter so that they can reach adulthood and start laying eggs in the springtime during turnout.

This typically occurs when cows are brought in to winter housing from about November to late February

In March, EL4 (arrested) wake up, moult into adults and lay eggs that calves put out during first grazing season. 

On grass there will typically be a much heavier load of L3 in the late autumn than in springtime.

9

Which Ostertagiosis has higher mortality - Type I or Type II? 

Type II has higher mortality because the calves end up eating a lot more that have been arrested in development in the springtime. 

 

10

What has greater chance of Ostertagiosis: beef suckler herds born in spring, or beef suckler born in autumn? Why?

Autumn-born beef calves have higher risk -- but it's still low -- of ostertagiosis because they are turned out earlier than spring-born calves and eat grass on which L3 haven't yet died off in Spring Mortality. 

11

How is immunity reached in cows infected with Ostertagia ostertagi?

Does it last a lifetime? 

At what age are they immune?

Immunity is acquired SLOWLY throughout the whole grazing season. 

Immunity WANES during winter housing but is re-established on turn-out.

Adults can be totally immune. 

12

How does Ostertagia ostertagi cause diarrhoea?

The worm parasitises the gastric glands in the abomasum. As a result, specialised glandular cells that make enzymatic secretions, such as parietal cells that make the HCl necessary to turn pepsinogen into pepsin, are replaced by undifferentiated cuboidal cells that DON'T make HCl

Also, tight junctions that block plasma proteins from entering the gastric glands and abomasal lumen disappear.

As a result, there is a high concentration of the zymogens pepsinogen and gastrin in the lumen as well as in the blood. 

Permeability of the lumen is increased, so water follows the plasma proteins into the abomasal mucosa - water diarrhoea, high pH. 

 

13

Knowing the life cycle of Ostertagia ostertagi, how would you treat Type I disease? 

1. Delay turnout until AFTER the spring mortality of L3.

2. Dose repeatedly with anthelminthic (Ivermectin) monthly from mid-July to cover auto-ingestion period.

3. Move to hay & silage feed in mid-July to avoid ingestion of L3 in "auto-infection" period.

Ivermectin has two-week residual, so if you dose before the three-week PPP, you would be covered for five weeks.

Bolus is slow-release but expensive - controls whole period.

Doramectin has five-week residual.

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