Equine Nematodes

Question 1

What is the Superfamly for the equine Nematodes?

Answer 1

Strongylidae

Question 2

What are two major equine nematodes?

Answer 2

1. Cyathostominae (small strongyles)
2. Strongylinae (large stronglyes)

Question 3

What are some key characteristics of cyathostominae regarding their PPP, lifecyle, migration, transmission, and arrested development?

Answer 3

1. direct life cycle
2. non migratory
3. PPP=5-12 weeks
4. propensity for prolonged hypobiosis. (months/ years)

Question 4

Describe the life cycle of Cyathostominae.

Answer 4

1. Eggs in feces
2. L1 moults to L3 (infective stage)
3. L3 ingested and penetrate the mucosa of the Large intestine (Cecum/ Colon).
4. They can either arrest and become hypobiotic or can continue to moult into LL3.
5. If not arresting, will L3 will moult into LL3 and then DL4 still in the mucosa.
6. DL4 will moult to the adult L5 and erupt from the mucosa into the gut lumen.
7. Adult worms are in the L.I and shed eggs into feces.
8. If hypobiosis occurs, this can last for months to years (UNIQUE FEATURE).
9. Will reemerge from its hypobiotic state into from EL3 (encysted) to LL3.
10. LL3 will ensue as normal cycle.

Question 5

What is unique about the Inhibited Development of cyathostominae (hypobiosis)? What effects to anthelmintics have? Any breeds or age more susceptible?

Answer 5

1. Hypobiosis can last for months to years (compared with osteragia which usually just overwinters)
2. The prolonged hypobiosis reflects incomplete immunity of the host.

• incomplete immunity can be found in younger horses (ages 1-3)
• Immunity can be compromised by negative feedback of chemicals from the luminal stages from the L4 and adult larvae

1. Hypobiotic larvae ARE NOT affected by anthelminitcs (In refugia)
2. cause life-threatening illness at any time of year and in any age of horse.

Question 6

When the larvae reemerge from a hypobiotic state what does this indicate of the host?

Answer 6

1. Decreased Immunity of the host and their reemergence may result in disease.

Question 7

What is cyathostominosis? What harm does it cause to the host? When does it occur? How can we diagnose it?

Answer 7

1. When all the arrested larvae erupt synchronously from the mucosa of the L.I tract.
2. Cause protein losing enteropathy due to synchronous eruption.
3. Occurs in late winter/ spring and can sometimes occur post anthelmintic tx.
4. Diagnose fecal larvae and not eggs because hypobiotic larvae do not produce eggs. If given anthelmintic treatment, some adults will die and can be found in the feces.

Question 8

What are some key characteristics of strongylinae regarding their PPP, lifecyle, migration, pathogenicity, transmission, anthelminitc treatment, and arrested development?

Answer 8

1. PPP= 6-10 months
2. direct life cycle
3. migratory life cycle
4. Migration of the larvae is very pathogenic.
5. All levels of larval development are sensitive to anthelmintics.

Question 9

What are the 3 main Large strongyle species?

Answer 9

1. S. Vulgaris
2. S. equinus
3. S. edentatus

Question 10

Describe the pathogencity of strongylinae…

Answer 10

the migratory larvae are very pathogenic and are the main cause of pathogenicity. Adult worms are less pathogenic but are still plug feeders feeding on the mucosa.

Question 11

Describe the Strongylus Vulgaris life cycle…

Answer 11

1. Eggs found in feces.
2. L1–> L3 sheated (infective)
3. L3 ingested and exsheaths in the small intestine, penetrates the intestinal mucosa, and moults to L4 7 days after ingestion.
4. L4’s penetrate the submucosal arteries and migrate along the endothelium to the coelic and colonic arteries around 14 days post infection and eventually make their way to the cranial mesenteric artery by 21 days post infection.
5. After 3-4 months, the L4 larvae have developed into the L5 adult which return to the L.I wall via the lumen of the arteries.
6. Nodules are formed around the L5’s in the walls of the cecum and colon.
7. When the nodules rupture, they release the adult L5’s into the gut lumen where they mature for another 6-8 weeks.

Question 12

What is the epidemiology of Strongylinae? When is their peak infectivity? What kind of environment is lethal to them?

Answer 12

• enjoy a warm, moist environment (temperate regions)
• Peak pasture infectivity during mid/ late summer.
• Prolonged, dry heat is lethal to the pasture larvae survival.

Question 13

What is meant by the term overdistribution in regards to host susceptibility?

Answer 13

Most adults horses have low levels of infection

80% of parasites are in 20% of hosts (mostly younger horses)

Question 14

Describe Conventional parasite control and whether this is a good strategy to use…

Answer 14

• Frequent invetervals of anthelimintcis given to all the horses of the herd, regardless of age/ infective status.
• Assumes that one size fits all
• Led to anthelmintic resistance in cyathostominae.
• Not a good strategy to use.

Question 15

What are 3 broad spectrum anthelmintics used on Equine Nematodes? Which ones are cyathostominae senstive/ resistant to? Which ones are strongylinae sensitive/ resistant to?

Answer 15

’s 3 and 4 are apart of the same family.

1. Benzimidazoles
2. Pyrantel
3. Ivermectin
4. Moxidectin

• Cyathostominae are resistant to all three anthelmintic drug classes. They have irreversible resistance meaning that if they are exposed and resistant to the anthelmintic, if that same treatment were used 10 years later they would still be resistant.
• Strongylinae are VERY sensitive to anthelmintics.

Question 16

What is meant by the term “ in refugia” ? Give examples

Answer 16

this is the proportion of parasites not exposed to anthelminitc chemical compounds at points when the animals is dosed.

1. Hypobiotic larvae
2. Larve on pasture
3. eggs/ larvae in feces.

Question 17

What is the best practice method of managing Equine parasites?

Answer 17

1. Target selective dosing to control cyathostominae:

• provide monthly FEC to all animals
• provide an anthelmintic dose to the infected animals (>200 epg) based on their body weight.
• Farmers never know the actual body weight of their horses which is a problem when dosing.

1. Monitor anthelmintic resistance.
2. Mixed species co grazing where allow sheep to enter infected pasture and graze therefore ingesting and removing infective larvae (wiil not infect sheep)
3. Caution Harrowing: problem with this method is that this scatters the larvae on the pasture and therefore increases pasture infectivity.
4. Practice pasture hygiene: this removes the feces from pasture before the larvae have time to crawl out and infect pasture. Problem with this method is that you are removing the refugia which could increase the pressure for worms to develop resistance.

Question 18

What anthelmintic is given to treat tapeworms?

Answer 18

praziquantal

Question 19

What anthelmintic is used to treat bots?

Answer 19

Ivermectin.

Question 20

What family does parascars equorum belong to?

Answer 20

ascaridoidea

Question 21

What family does oxyuris equi belong to?

Answer 21

oxyuroidea

Question 22

What family does strongyloides westeri belong to?

Answer 22

rhabditoidea

Question 23

Parascaris equorum is common in what age horses?

Answer 23

Common in foals and yearlings.

infection rates are decreasing from 6 months of age onwards.

Question 24

Describe the life cyle of parascaris equorum and its PPP… What life cycle does this resemble?

Answer 24

1. Egg in feces.
2. L1 (IN THE EGG) moults to L3 **(IN THE EGG) **
3. Once L3 is ingested it unhatches from the egg, travels to the liver via the portal circulation, travels to the lungs, gets coughed up from the bronchi into the trachea.
4. It is swallowed and enter the S.I where the L3 moults to L4.
5. Adults are in the S.I lumen
6. PPP= 10-15 weeks.
7. Resembles life cycle of T. Canis.

Question 25

What is the pathogenesis of Parascaris equorum? What damage is caused?

Answer 25

* The migrating larvae are very pathogen in these parasites. * They will cause liver damage: focal hemorrhaging and fibrosis. * Lung Damage: focal hemorrhage, lymphocyte infiltration, nodules Adult worms in the intestines are not very pathogenic. There are RARELY heavy worm burdens. However if there is a heavy worm burden impaction, protrusion, and peritonitis can occur. This can occur post anthelmintic treatment.

Question 26

What are the clinical signs associated with Parascaris equorum?

Answer 26

1. **Ill thrift** due to the adult worms in the small intestines preventing nutrient absorption. **(COMMON IN FOALS/ YEARLINGS)** 2. This can lead to emaciation if left untreated. 3. Due to the migrating larvae, coughing +/- greyish nasal discharge will also occur, usually concurrent with ill-thrift.

Question 27

How do we diagnose Parascaris Equorum?

Answer 27

1. FEC. Females are extremely fecund and will lay thousands of eggs. 2. Eosinophilia during migratory phase of larvae (transient)

Question 28

Describe the 2 kinds of Parascaris equorum eggs. When do the eggs build up on the pasture?

Answer 28

1. Unlarvated, un infective, brown, thick pitted outer shell. 2. Larvated, infective, clear, un pitted outer shell. Eggs are very resistant, sticky, and can survive for long periods in the environment. Eggs build up on the pasture towards the end of the summer.

Question 29

What is the epidemiology of Parascaris equorum?

Answer 29

Adult horses are not a major sourse of contamination however they CAN act as carriers and transmit the infection. Parascaris equorum is mostly transmitted via foal to foal or yearling to yearling. Females are very fecund Eggs are resistant Eggs build up on pasture towards the end of the summer.

Question 30

What is a treatment to control Parascaris Equorum? What are they resistant to? What anthelmintic are they sensitive to?

Answer 30

Control measure aimed at small strongyle control should be used to control parascaris. Resistant: Ivermectin Sensitive: Benzimidazole

Question 31

Which sex is parasitic in Strongyloides westeri? What age group do they predominately infect?

Answer 31

Females are parasitic infects foals \< 6 months old

Question 32

What is the PPP of Strongyloides westeri? What are some unique features about its life cycle?

Answer 32

1. PPP= 8-14 days (short) 2. Free living larvated eggs can cycle in the environment, moult and develop into adults in the environment, and produce new larvated eggs without entering the host. 3. Can enter the host via penetration of the skin or ingestion. 4. If enter the host via penetration of the skin, the L3's can lie dormant in the muscle, and infect the foal via transmammary route (no migration). **This is why this is common for foals to inherit. ** 5. If L3's are swallowed will migrate to the lungs and into the S.I. Once in the S.I. **parthenogenis** occurs (asexual reproduction) therefore the egg doesn't have to be fertilized.

Question 33

What are clinical signs of Strongyloides westeri?

Answer 33

1. Only seen in very young animals and requires a heavy worm burden. 2. Diarrhea 3. Anorexia 4. Dullness 5. Reduced wt. gain.

Question 34

What is the epidemiology of Strongyloides westeri?

Answer 34

L3's are not very resistant in the environment because they are unsheathed. Temperate conditions are optimal for survival. Transmammary route is important...the successive progeny of the same dam ofthen show heavy infections in which case clinical signs will show.

Question 35

What kind of worms are oxyuris equi? Where do they target in the host? What is the infective larval stage?

Answer 35

1. Pinworms 2. L.I 3. L3 IN EGG INFECTIVE

Question 36

Describe the life cycle of oxyuris equi and its PPP...

Answer 36

1. Females lay eggs at anus 2. L1, L2, Infective L3 develop inside the egg. 3. L3 is ingested and hatches. 4. L3 penetrates colonic mucosa and moults to L4. 5. L4 emerges as juvenile adult and enters lumen of the colon. 6. PPP=5 months

Question 37

What are clinical symptoms of oxyuris equi?

Answer 37

Adults in intestine rarely cause clinical signs. Egg laying activity can cause perineal irritation and rubbing. Alopecia/ inflammation of the rump and tail head.

Question 38

How can we diagnose oxyuris equi?

Answer 38

1. clinical signs 2. eggs around perineal region 3. adult worms in feces.

Question 39

What is the epidemiology of oxyuris equi?

Answer 39

1. Infective L3 can develop on the perineal skin. 2. Usually flakes of skin with eggs rub off.

Question 40

How can we control oxyuris equi?

Answer 40

These pinworms are susceptible to most broad spectrum anthelmintics however they may show some resistance to the macrocylic lactones (ivermectin, moxidectin)

Question 41

What is Habronema microstoma a.k.a? What are its hosts? Is it direct or indirect? If indirect what is the IMH? What is its target site? How does it infect? What is its pathogenesis?

Answer 41

1. Summer sores 2. Horses, donkeys 3. Indirect 4. Muscid flies 5. Adults in stomach 6. Flys containing infective L3's are swallowed and the infective L3 emerges and enters stomach to develop. 7. L3 can also be deposited on skin (often around the eyes) and can penetrate but will not further develop.