Parasitology - 10.8.10 - Horse Strongyles - 2Nd Year - Fall

Front 1

Which are a bigger problem, small strongyles or large strongyles?

Back 1

Large strongyles

Front 2

What are the three species of strongylus of importance to horses?

Back 2

Strongylus vulgaris, S. edentatus and
S. equinus

Front 3

What is the strongyle life cycle? Do they travel extraintestinally? Where do you find L4?

Back 3

There is extraintestinal migration.
L4 live in the mesenteric arteries for 5-11 months before they become adults. They actually wander through the walls of the vasculature.

Front 4

Describe the migration of the s. vulgaris larvae? Include timing.

Back 4

After ingestion, S. vulgaris L3s exsheath in the small intestine, penetrate the intestinal mucosa and moult to L4s by 7 days after infection(B).  These L4s penetrate submucosal arteries and migrate along the endothelium to the cecal and colic arteries (by 14 days post infection) and then to the root of the cranial mesenteric artery and its main branches (C) which they reach by day 21 after infection.   After a period of development of 3-4 months, the larvae have molted to immature adults (L5s) but retain the fourth-stage cuticle as an external sheath. They return to the intestinal wall via the lumen of arteries.  Nodules are formed around the L5s mainly in the wall of the cecum and colon (D) Subsequent rupture of these nodules releases the young adult parasites into the lumen of the intestine where they mature in another 4 to 8 weeks.

Front 5

What life stage causes the most problems in s. vulgaris?

What are the symptoms of both larval and adult stages?

Back 5

most damage due to larvae in
blood vessels

L4 in mesenteric arteries: Aneurysms, verminous arteritis
Disruption of intestinal blood flow

Adults: heavy infections cause diarrhea, blood loss

Front 6

What is the harmful stage of s. edentatus?

Back 6

Immature adults causing nodules in the large intestine causing problems.

Front 7

What is there to know about S. edentatus?

Back 7

Ingested L3s ….. gut wall to liver
Wander around the visceral cavity for several months
Migrate back to cecum and colon
Form nodules
Maturation: large intestine
Prepatent period: about 11 months
Pathology: hepatitis, peritonitis

Front 8

In what stage do s. edentatus get ingested, then what path do they take?

How long is the prepatency period?

What pathology to they cause?

Back 8

Ingested L3s ….. gut wall to liver
Wander around the visceral cavity for several months
Migrate back to cecum and colon
Form nodules
Maturation: large intestine
Prepatent period: about 11 months
Pathology: hepatitis, peritonitis

Front 9

What is the migration route to s. equinus?

What is their pathology?

Back 9

Similar migration route (gut to liver to gut) as S. edentatus

Hemorrhagic nodulescaused by migrating larvae

Front 10

What are the "small strongyles"

Back 10

Cyathostomes

Genera include:
Cyathostomum
Cylicostephanus
Cylicocyclus
Cylicodontophorus
Poteriostomum
Gyalocephalus

But we will refer to them as cyathostomes

Front 11

Compare and contrast small vs large strongyles.

Length, buccal cavity

Back 11

Somewhat relative terms
e.g. the ‘large’ strongyles (Strongylus vulgaris, S. edentatus, S. equinus) range in length from 1.5- 4cm
e.g. the ‘small’ strongyles (cyathostomes) range from 1-2 cm in length
In ‘large’ the buccal capsule is well developed
In ‘small’ it is less developed with adults not attached to the mucosa

Front 12

Why are cyathostomes some of the most important internal parasites of horses?

Back 12

Now ivermectin and benzimidazoles have reduced the impact of Strongylus vulgaris.
Often cause sub-clinical impairment of intestinal function
→ poor performance and weight loss.
Overt disease with diarrhoea, severe weight loss and edema.

Front 13

What is cyathostome morphology of adult worms?

Do the adults attach to the mucosa and feed on blood?

Do they have a leaf crown?

Back 13

White to dark red worms
1-2 cm in length
Buccal capsule less-developed than in large strongyles
Leaf crown present
Adults not attached to mucosa
Adults do not feed on blood

Front 14

What is the life cycle of the small strongyle?

Back 14

See picture

Front 15

What worm is this intestinal lining indicative of?

Back 15

Gross examination of the mucosal lining of a horse suffering from acute larval cyathostomosis.

Demonstrates the swollen and edematous mucosal surface disrupted by the synchronous emergence of encysted larvae.

Colon section - mucosal folds are swollen (edema). reddish-brown foci represent embedded nematode (Cyathostome) larvae.

Front 16

What is the immune effect of treating a horse for small strongyles?

Back 16

Larvae emerge following removal of adults by treatment – loss of premunition

Front 17

What seasons are the high risk periods of infection for cyathostomes?

Back 17

Spring and fall

monitoring pasture infectivity has shown high levels of infective larvae present on turnout paddocks, even in January after snow.

“winter worming” must be considered as well as during summer grazing.

In autumn, their development is prolonged as hypobiotic larvae within the gut wall.

in the late winter or spring, these larvae resume their development.

Front 18

Finish this statement from slide 31 of 10.8 lecture

Redworm larvae can develop into adults within a period of 5 weeks
Versus _____ for large strongyles

Back 18

Is this talking about prepatency?

Front 19

Why are fecal egg counts not useful in the diagnosis of small strongyles?

What are useful?

Back 19

FEC not useful……WHY??
Clinical signs, response to appropriate treatment, and larvae and immature adults in feces.
Necropsy

Front 20

What drugs are successful against cyathostome? What are their problems?

Back 20

Fenbendazole (Panacur) – 5 day, double dose - effective against L3s, but resistance problems - ideal when the horses aren't showing resistance.

Moxidectin (Quest) – one dose, but not as effective against L3. Possible toxicity problems

Ivermectin – not as effective as moxidectin agains L3 and does not hit larvae - not the drug of choice when you start having clinical problems with small strongyles.

Pyrantel – resistance problems


Take home - use Panacur, but don't be shocked if the worms are resistant

Front 21

Treatment Strategies: Horse Paddock vs Sheep Pasture
Where is the refugia?

Back 21

Refugia is the proportion of the population that is not selected by drug treatment, it dilutes the resistant genes in a population. By treating the top 30% of the herd only, you enable 95% of the surviving worms to by refugia.

So horses are still being treated all at once. The refugia is on the ground, not in the horse. (and this is bad...ask him to be sure you know why).

And the sheep are treated as above, so the refugia is in the sheep.

Front 22

What are the species that trichostrongyles mainly harass? What about true strongyles?

Back 22

Cattle and sheep

Horses

Front 23

Are oesophagostomum spp. host specific?

Back 23

Yes.

The same species that infects cattle will not infect sheep and same for pigs. We don't need to know the species, just that they are different.

Front 24

What is the buccal cavity of oesophagostomum spp like? Where do they infect? How long are they?

Do they have leaf crowns?

Back 24

posterior small intestine and large intestine
cattle, sheep, and pigs
adults 1-2.5 cm long, white in color
buccal capsule cylindrical, narrow
internal and external leaf crowns present
pharynx strongyliform
cervical papillae prominent

Front 25

Why would being a naive host be advantageous to oesophagostomum infections?

Back 25

In lambs or sheep with no resistance all worms take straightforward path to colon
If host has been sensitised, larvae may induce reaction of localised inflammation around each worm.
larvae may remain in nodules with caseous or calcified contents for up to three months.
Nodules may have small opening but many larvae never escape so there are few adults in colon.

So the egg burdens won't reflect the clinically the infection, but the tissue damage will be immense.

Adult worms do not suck blood (not as pathogenic as larvae) but cause thickening of bowel wall, congestion and mucus production - profound effect on appetite and wool growth.

Chronic infection - extreme emaciation, atrophy of muscles, and complete prostration followed by death.

Front 26

What are the harmful stages of oesophagostomum?

What is the outcome of chronic infection?

Back 26

Adult worms do not suck blood (not as pathogenic as larvae) but cause thickening of bowel wall, congestion and mucus production - profound effect on appetite and wool growth.

Chronic infection - extreme emaciation, atrophy of muscles, and complete prostration followed by death.

Front 27

What is the pre-patency period of oesophagostomum?

What is the difference in reinfection?

What environment are oesophagostomum more prevalent?

Back 27

Pre-patent period – 4-6 weeks in most (3 weeks in pigs)

In older animals (i.e. immune primed) or on reinfection, hypobiotic larvae may arrest for months → either die or develop when immune relaxation occurs (periparturient) → postparturient rise in epg feces.

Generally Oesophagostomum spp more prevalent in warm, humid areas – larvae in soil subject to desiccation.

Front 28

Which worm is the barber-pole worm? What species is that in?

Back 28

Haemonchus

sheep and cattle

Front 29

What organ does ostertagia infect? What is this worm's "nick name"?

Back 29

abomasum, brown stomach worm

Front 30

What is nematodirus is notable for?

Back 30

Its large strongyle-type egg