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Parasitology > Equine Nematodes > Flashcards

Equine Nematodes Flashcards

1
Q

What is the Superfamly for the equine Nematodes?

A

Strongylidae

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2
Q

What are two major equine nematodes?

A
  1. Cyathostominae (small strongyles)
  2. Strongylinae (large stronglyes)
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3
Q

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

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

Describe the life cycle of Cyathostominae.

A
  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.
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5
Q

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

A
  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.
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6
Q

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

A
  1. Decreased Immunity of the host and their reemergence may result in disease.
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7
Q

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

A
  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.
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8
Q

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

A
  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.
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9
Q

What are the 3 main Large strongyle species?

A
  1. S. Vulgaris
  2. S. equinus
  3. S. edentatus
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10
Q

Describe the pathogencity of strongylinae…

A

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.

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11
Q

Describe the Strongylus Vulgaris life cycle…

A
  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.
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12
Q

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

A
  • enjoy a warm, moist environment (temperate regions)
  • Peak pasture infectivity during mid/ late summer.
  • Prolonged, dry heat is lethal to the pasture larvae survival.
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13
Q

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

A

Most adults horses have low levels of infection

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

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14
Q

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

A
  • 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.
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15
Q

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

A

’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.
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16
Q

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

A

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.
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17
Q

What is the best practice method of managing Equine parasites?

A
  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.
18
Q

What anthelmintic is given to treat tapeworms?

A

praziquantal

19
Q

What anthelmintic is used to treat bots?

A

Ivermectin.

20
Q

What family does parascars equorum belong to?

A

ascaridoidea

21
Q

What family does oxyuris equi belong to?

A

oxyuroidea

22
Q

What family does strongyloides westeri belong to?

A

rhabditoidea

23
Q

Parascaris equorum is common in what age horses?

A

Common in foals and yearlings.

infection rates are decreasing from 6 months of age onwards.

24
Q

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

A
  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.
25
Q

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

A
  • 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.

26
Q

What are the clinical signs associated with Parascaris equorum?

A
  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.
27
Q

How do we diagnose Parascaris Equorum?

A
  1. FEC. Females are extremely fecund and will lay thousands of eggs.
  2. Eosinophilia during migratory phase of larvae (transient)
28
Q

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

A
  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.

29
Q

What is the epidemiology of Parascaris equorum?

A

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.

30
Q

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

A

Control measure aimed at small strongyle control should be used to control parascaris.

Resistant: Ivermectin

Sensitive: Benzimidazole

31
Q

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

A

Females are parasitic

infects foals < 6 months old

32
Q

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

A
  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.
33
Q

What are clinical signs of Strongyloides westeri?

A
  1. Only seen in very young animals and requires a heavy worm burden.
  2. Diarrhea
  3. Anorexia
  4. Dullness
  5. Reduced wt. gain.
34
Q

What is the epidemiology of Strongyloides westeri?

A

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.

35
Q

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

A
  1. Pinworms
  2. L.I
  3. L3 IN EGG INFECTIVE
36
Q

Describe the life cycle of oxyuris equi and its PPP…

A
  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
37
Q

What are clinical symptoms of oxyuris equi?

A

Adults in intestine rarely cause clinical signs.

Egg laying activity can cause perineal irritation and rubbing.

Alopecia/ inflammation of the rump and tail head.

38
Q

How can we diagnose oxyuris equi?

A
  1. clinical signs
  2. eggs around perineal region
  3. adult worms in feces.
39
Q

What is the epidemiology of oxyuris equi?

A
  1. Infective L3 can develop on the perineal skin.
  2. Usually flakes of skin with eggs rub off.
40
Q

How can we control oxyuris equi?

A

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

41
Q

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?

A
  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.

Parasitology (10 decks)

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