Parasitology - Equine PGE Flashcards Preview

BVM2 > Parasitology - Equine PGE > Flashcards

Flashcards in Parasitology - Equine PGE Deck (39):
1

What is the most important nematode that causes equine parasitic gastro-enteris (PGE) compex?

Strongylus species - ie., Strongyles also known as RED WORMS

2

What are parasites that invade the horse's large intestine (the large ascending colon)?

Large strongyles aka large redworms:

Strongylus vulgaris

S. edentatus

S. equinus

Triodontophorus spp.


Small strongyles aka small redworms:

Cyathosomins (aka trichonemes) of which there are > 40 species; 
Oxyuris equi aka “pinworms” - invades caecum, large intestine & rectum

3

What is the name of the PGE caused by large red worms / large strongyles?

What parts of the pathogenesis do the different species of Strongylus (large red worms) share?

 Strongylosis

Common Aspects of Pathogenesis:

Horse eats grass infested with L3 stage of Strongylus - can be S. vulgaris, S. edentatus, S. equinus or Triodontophorus

Larvae pass down the intestinal tract & penetrate intestinal mucosa. At this larval stage, S. vulgaris is the most pathogenic, potentially damaging the cranial mesenteric artery & resulting in thrombosis & colitis.

Then, depending on the species, will go through different migrations & pre-patent periods. 

4

What is the condition caused by small red worms / small strongyles in the large intestine?

Cyathosominosis

Type I & more-serious Type II 

5

What is the morphology of the large red worms/large strongyles, 

Strongylus vulgaris

S. edentatus

S. equinus

?

Gross:
- Stout, 1.5-5 cm long
- Large buccal capsule

- Bursa visible to naked
eye in male


Micro (buccal capsule):

- Double row leaf
crowns
(see photo of S. vulgaris)
- Teeth (0,2,3 or more) -
not in S. edentatus

- Dorsal gutter (channel
for enzymatic secretions)

6

All the large red worms (large strongyles) that cause Strongylosis in the large intestine (colon) of the horse share the common initial pathogenic pathway of being ingested at L3 stage by horses eating grass. 

The larvae enter the intestinal tract, penetrating the intestinal mucosa, before they take different paths. 

Describe the path of Strongylus vulgaris.

S. vulgaris, unlike S. edentatus or S. equinus, is potentially highly pathogenic at the larval stage, not just the adult stage. From the ascending colon, the larvae:

→ migrate into anterior (cranial) mesenteric artery over 2 weeks → burrow into intersection of artery & aorta to form verminous endarteritis lesion over 3-4 months → migrate back down via anterior mesenteric artery & moultbore hole into descending colon & exit as adults over 6-8 weeks

As adults, they become plug feeders with their large buccal capsules, penetrating down into the muscularis layer and blood vessels. They leave circular bleeding ulcers that can lead to anaemia if there are many.

PPP = 6-7 months

NB: endarteritis is the inflammation of the intima of one or more arteries

7

All the large red worms (large strongyles) that cause Strongylosis in the large intestine (colon) of the horse share the common initial pathogenic pathway of being ingested at L3 stage by horses eating grass.

The larvae enter the intestinal tract, penetrating the intestinal mucosa, before they take different paths.

Describe the path of Strongylus edentatus.

S. edentatus (without teeth) are relatively non-pathogenic as larvae (unlike S. vulgaris). Their larval migration takes them to roomy tissue like the liver & mesentary that can withstand more damage than the cranial mesentery artery as with S. vulgaris.

After entering the large intestine (ascending colon), S. edentatus larvae:

→ migrate via hepatic portal system to liver → form nodules in liver → moult → exit liver via peritoneum → migrate via periotoneum back to large intestine → exit as adults

PPP = 11-12 months

8

All the large red worms (large strongyles) that cause Strongylosis in the large intestine (colon) of the horse share the common initial pathogenic pathway of being ingested at L3 stage by horses eating grass.

The larvae enter the intestinal tract, penetrating the intestinal mucosa, before they take different paths.

Describe the path of Strongylus equinus.

The larvae of S. equinus is relatively non-pathogenic, unlike S. vulgaris. Like S. edentatus, the larval migration of S. equinus is through roomier tissue such as the liver that is able to withstand damage better than the cranial mesenteric artery as in the case of S. vulgaris. After entering the horse's ascending colon, the larvae:

crosses peritoneal cavity from intestine to liver“wanders around” liver before returning to large intestine via peritoneal cavity again → exits as adult


PPP = 9 months

9

Recap where the larvae of the large redworms go to migrate and moult after they enter the horse's large intestine? 

Strongylus vulgaris

S. edentatus

S. equinus

Strongylus vulgaris - cranial mesenteric artery to junction of artery & aorta, then back to colon via mesenteric artery

S. edentatus - hepatic portal system to liver then back to colon via peritoneum

S. equinus - peritoneal cavity to liver then back to colon via pernitoneal cavity

10

All the large red worms (large strongyles) that cause Strongylosis in the large intestine (colon) of the horse share the common initial pathogenic pathway of being ingested at L3 stage by horses eating grass.

The larvae enter the intestinal tract, penetrating the intestinal mucosa, before they take different paths.

Describe the path of Triodontophorus.

Unlike the other large red worms, Strongylus vulgaris, S. edentatus & S. equinus, Triodontophorus is non-migratory. Instead, it just stays in the large intestine and moults there into an adult, where it feeds in "herds".

After entering the large intestine of the horse, the larvae:

→ moves around wall of large intestine → moults to L4 → exits as adults

As adults, it causes superficial damage with its small buccal cavity, but feeds in herds, leaving large large, superficial ulcers several cm across that leave scars after they heal.


PPP = 2-3 months

11

Aside from large redworms (large strongyles), what other nematode types cause PGE in the horse's large intestine? 

Small redworms (Cyathosomins, aka Trichonemes)

Pinworms (Oxyuris equi)

12

What is the morphology of the small red worms, also known as Cyathostomins or Trichonemes? How do they differ in appearance from the large strongyles?

They look a lot like the large strongyles/red worms, but they are smaller, less than 1.5 cm (large redworms are 1.5-5 cm long).

They have small, shallow buccal capsules with double row of leaf crown and possibly teeth.

See photo.

13

What happens to the small redworms, Cyathostomins, after they enter the large intestine of the horse as L3 with grass?

Cyathstomins are confined to the gut wall, but can take two life-cycle routes:

1. L3 can become arrested in gut wall for several months → moults to L4 → emerges as adult in gut lumen

OR


2. L3 moults to L4 → emerges as adult in gut lumen

PPP = 8-12 weeks

14

Why would a small redworm, Cyathostomins aka Trichoneme, become arrested at L3 for several months or years in the large intestine of the horse rather than moult from L3 to L4 to adult in its normal 8-12-week PPP?

Similar to ostertagia in calves, the larvae become arrested in the gut wall (potentially for years) if they were ingested in late summer or early autumn. They become hypobiotic throughout the winter and emerge in late winter or early spring, and this is quite harsh for the horse.

15

What is different about the hypobiotic larval stage of Cyathostomins compared with Ostertagia?

Cyathostomins, aka small red worms, become arrested as L3 and they can stay hypobiotic for years.

Ostertagia become arrested at L4 and typically are hypobiotic until the next grazing season.

16

What is the name of the condition caused by Cyathostomins aka Trichonemes aka small red worms, and what are the different types?

Cyathostominosis.

Type I Cyathostominosis:
- Initial infection (L3) → local inflammation
- larval emergence in summer/autumn
+ plug-feeding adults = wormy horse

Larval / Type 2 Cyathostominosis:
- larval emergence (late winter/early spring) → severe diarrhoea → severe weight loss

NB this is like ostertagia in calves sheep, which can accumulate L3 that become hypobiotic & then attack harshly as adults

17

When do small redworms become plug feeders?

Small redworms, Cyathostomins, are plug feeders as larvae & adults.

The large redworms Strongylus vulgaris and Triodontophorus are only a plug feeders as adults.

18

What are the clinical signs of Cyathostominosis Type I, aka "wormy horse"? How many adult and larval worms are present?

Unthriftiness, poor coat, anaemia, diarrhoea

 10s or 100s of thousands of adults and millions of mucosal larvae present.

19

What are the clinical signs of Cyathostominosis Type II, aka "wormy horse"? How many adult and larval worms are present?

Massive inflammatory infiltration, serious diease characterised by severe diarrhoea &/or weight loss

20

In what age of horse does Strongylosis typically occur? In what type of environment?

Young horses on permanent pasture

Adult horses especially if there is overcrowding or poor hygiene

 

21

What are the sources of Strongylosis infection?

Like ostertagia, L3 on pasture, spring rise, overwintered L3

22

In what age of horse does cyathostominosis typically occur? 

Young horses less than 5 years old. 

23

The pinworm - aka Oxyuris equi - also attacks the large intestine in the horse, causing PGE. What is the morphology of the pinworm?

Females large: <10 cm long, white, with thin, pointed “pin-like” tails (see photo)

Males small: <1 cm long, difficult to see

24

Where are the preferred targets of the pinworm in the horse GIT?

Caecum

Large intestine (colon)

Rectum

 

 

25

What is the life cycle of the pinworm, Oxyuris equi, after its L3 is ingested by a horse?

L3 invades colonic mucosa → moults inside egghatches as L4 → L4 feed on colonic mucosa → develop to adulthood → adults migrate to rectum females lay eggs on perianal hair → operculate eggs, 80-90 μm flattened on one side, fall to ground


PPP = 5 months

26

What is the pathogenic stage of the pinworm, Oxyuris equi -- larval or adult?

Larval:

L4 feed on colonic mucosa by nipping off epithelium, causing erosion; NOT true plug- feeders

Adults are non-pathogenic as they feed on gut contents.

However, egg-laying causes pruritus ani aka “seat itch”: broken hair & bare patches at rump & tail head

27

What is the largest type of nematode found in the horse to cause PGE? 

How big does it grow to and what are its other distinguishing morphological features?

Parascaris equorum, an ascarid

- Really huge: up to 50 cm (18 inches) long
- Three large lips around mouth (seen in all ascarid worms)

28

What is the target organ of the Parascaris equorum larvae?

Small intestine via liver, heart & lungs

(hepato-tracheal migration)

29

Which age of horse is most susceptible to Parascaris equorum infestation? How is it transmitted? 

Mostly young foals < 4-6 months old

(like Nematodirus in sheep)

Transmission is from one year’s foals to next; usually first month of life; adult horses might be carriers as they carry only a few worms (like Nematodirus in sheep)

30

What is the life cycle of the Parascaris equorum L2 embryonated egg after it is ingested and enters the foal's intestines?

hepato- tracheal migration: intestine to hepatic portal system to liver → right side of heart → punches through lungs → up to trachea where it is coughed up and swallowed into small intestine → adult lays unembryonated egg with thick, sticky shell → in a couple of weeks it becomes L2 with larva inside


PPP = 10-12 weeks

31

What is so different about the infectious stage of the Parascaris equorum worm?

It is ingested during its embryonated egg stage (L2). It reaches L4 inside the egg. 

32

What is special about the Parascaris equorum egg?

In the unembryonated stage in faeces, it is very strong with a thick, pitted shell that is sticky and can last for up to a year. Its stickiness means it can facilitate passive spread on fomites.

33

The Parascaris equorum worm is very pathogenic. Describe the fecundity of the female as well as the damage caused by the larvae and the adults.

High fecundity of female - lay millions of eggs per day in infected foal.

LARVAE: leave eosiniphilic tracts & haemhorrages in lungs → nasal discharge


ADULTS: cause unthriftiness, weight loss, intestinal impaction & performation (rare)

34

What is the first parasite to which foals are exposed and causes PGE?

Strongyloides westeri

This is a Rhabditoid - NOT A STRONGYLE

35

What is the morphology of Strongyloides westeri?

- Very small, < 6 mm long
- similar to small trichostrongyles like Ostertagia
- long oesophagus (1/3 of body length)
- only female is parasitic

36

What organ(s) does the Strongyloides westeri worm target in the foal?

The small intestine via the liver, right side of heart & lungs (hepato-tracheal migration). 

37

Why is the Strongyloides westeri considered facultatively parasitic?

What is its life cycle?

It can choose parasitic OR non- parasitic life cycle, depending on previous generation’s cycle:


Foal ingests L3 in mare’s milk and/or L3 with grass and/or skin penetration → hepato- tracheal migration → female lays larvated ie., embryonated eggs (50-60 μm), which are passed in faeces
PPP= 1 week

38

Why is Strongyloides westeri considered the first parasite to which foals are exposed? 

Because the L3 can be transmitted in mare's milk. 

39

What is the immunity of mares?

Adults are normally immune, may act as carriers

Decks in BVM2 Class (88):