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Parasitology 2 > 6.09 – Introduction to Nematodes – The Roundworms > Flashcards

6.09 – Introduction to Nematodes – The Roundworms Flashcards

1
Q

Introduction to Nematodes; General Features; morphology and body structure

A
  • elongate tubular bodies
  • thick, resistant cuticle
  • muscles underlie cuticle
  • hydrostatic pressure maintains shape and rigidity
  • simple alimentary tract
  • separate sexes
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2
Q

Introduction to Nematodes; Anatomy ‐ Male Worms

A
  • single convoluted tube consisting of testes, vas deferens and ejaculatory duct
  • sometimes supplemented with cuticular spicules
  • some groups have pronounced copulatory bursa
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3
Q

Introduction to Nematodes; Anatomy ‐ Female Worms

A
  • pair of blind‐ended ovaries leading to uteri
  • common vagina and vulva
  • often store sperm for protracted periods
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4
Q

Introduction to Nematodes; General Life Cycle Strategies

A
  • all nematodes (free‐living or parasitic) undergo the same life cycle
  • egg > L1 > L2 > L3 > L4 > L5 > adults
  • like coccidia, the life cycle can be divided among
    different hosts (IH’s, PH’s, DH’s) in different ways
  • most parasites of domestic animals have only a single host (implications??)
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5
Q

Introduction to Nematodes; General Life Cycle Strategies ‐ Routes of Infection

A
  • usually oral ingestion of infective forms (usually fecal‐ oral transmission)
  • may penetrate the skin (e.g. some hookworms)
  • transplacental transmission (e.g. Toxocara)
  • transmammary transmission (e.g. dog hookworms)
  • predator‐prey transmission with IH or PH (e.g. Trichinella)
  • vector‐borne transmission (e.g. heartworm)
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6
Q

Introduction to Nematodes; General Life Cycle Strategies ‐ Migrations

A
  • Tracheal Migration
    ‐ taken by many GI parasites, particularly ascarids ‐ extensive migration leading to alveoli from which larvae move up the airways to the trachea to the gut
  • Somatic Migration (usually associated with tracheal migrations) ‐ stay in bloodstream to be distributed around body
  • Mucosal Migration
    ‐ penetrate gastric pits or mucosa for a period of development prior to returning to lumen as adult
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7
Q

Introduction to Ascarids; General Features of the “Roundworms” (ascarids); morphology, site of infection, host specificity, life strategies, egg character

A
  • generally robust, heavy‐bodied worms
  • infect small intestine of definitive hosts
    (exception: Heterakis gallinarum in cecum)
  • adults highly host specific
  • various (and often complicated) life strategies, most involving a complete tracheal migration
  • ascarid eggs highly resistant to environmental stress
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8
Q

Typical Life Cycles of the “Roundworms” (ascarids)

A
  • direct life cycle
  • prolific (as many as 200,000 eggs/female)
  • eggs mature to contain L3’s in the environment before becoming infective ‐‐ oral infections usually
  • L3’s penetrate small intestine and undergo migration
  • many alternate routes with hypobiosis as well as transmammary and/or transplacental transmission
  • larvae eventually reach the small intestine and rapidly mature to adults and begin to produce eggs
  • PPP variable but usually long if the larvae undergo significant migration(s)
  • paratenic hosts may be involved
  • eggs remain infectious for extended periods
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9
Q

Introduction to Ascarids; Typical Pathogenesis

A
  • poor growth ‐‐ unthriftiness
  • sometimes “potbelly” with or without diarrhea
  • massive numbers can give obstructions
  • minor lesions from migrating stages
  • zoonoses
    ‐ Ocular or Visceral Larval Migrans
    ‐ OLM or VLM
    ‐ associated with tracheal migration
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10
Q

Toxocara canis ‐ Roundworms; General Features; site of infectin, morphology of adult and egg, route of infection

A
  • large roundworm in small intestine of dog
  • large, heavy‐bodied adults up to 18 cm
  • thick shelled, pitted egg (~90μm in diameter) containing a single cell when passed in feces
  • most pups born with this parasite through efficient transplacental route of infection
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11
Q

Toxocara canis ‐ Roundworms; Life Cycle, general

A
  • direct life cycle (no intermediate hosts)
  • larvae develop to L3’s within the pitted egg
  • infective eggs ingested
  • fate of infective larvae in host depends of age and immune status of host…..
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12
Q

Toxocara canis ‐ Roundworms; Life Cycle in Pups

A
  • < 3 months ‐ primarily tracheal migration with a typical PPP of 4 to 5 weeks
  • 3 ‐ 6 months ‐ increasingly somatic migration
  • 6 or older ‐ only somatic migration
  • most pups infected in utero by transplacental migration of larvae from bitch to fetus
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13
Q

Toxocara canis ‐ Roundworms; Transplacental and Transmammary Transmission

A
  • some (not all) arrested (hypobiotic) larvae are mobilized by pregnancy
  • enter liver and lung of fetus and wait for birth of pup
  • finish (do not undergo complete) tracheal migration
    and form adults ‐‐ PPP shortened to 3 weeks
  • some larvae may enter milk and infect pups by transmammary route (rarely)
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14
Q

Toxocara canis ‐ Roundworms; non-vertical routes of transmission

A
  • bitch may get infected by ingesting larvae in feces of pups
  • ingestion of paratenic hosts containing larvae may give rise to short‐lived patent infections in adult dogs (no migration)
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15
Q

Toxocara canis ‐ Roundworms; Pathogenesis/Lesions/Clinical Signs ‐ Intestinal Phase

A
  • mainly light infections ‐ few clinical signs
  • heavy infections ‐ unthriftiness, stunted growth with dry skin and dull coat (poor‐doing)
  • gait and behaviour may indicate painful abdomen
  • vomition with worms or worms in feces indicate a very heavy infection
  • death may occur prior to patency
  • cachexia associated with huge numbers of worms
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16
Q

Toxocara canis ‐ Roundworms; Pathogenesis/Lesions/Clinical Signs
‐ Migration Phase

A
  • usually non‐pathogenic
  • may cause eosinophilic gastroenteritis or lung problems if numbers of migrating larvae is high
  • dead larvae may leave focal lesions (1 ‐ 2 mm)
  • migrating larvae cause eosinophilia (30 ‐ 50%) in dogs as well as humans (OLM or CLM)
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17
Q

Toxocara canis ‐ Roundworms; Treatments

A
  • numerous treatments available including pyrantel pamoate (Pyr‐a‐Pam®, etc), fenbendazole (Panacur®), nitroscante (Lopatol®), milbemycin (Interceptor®), selamectin (Revolution®), etc., etc.
  • heavy infections should be treated with anthelmintics that do not induce hyperactivity in roundworms or kill worms quickly (possible obstruction problems) – fenbendazole in these cases
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18
Q

Toxocara cati ‐ Roundworms; General Features; morphology, site of infection, egg morphology

A
  • large roundworm of cats, found in small intestine
  • 10 cm worms have cervical alae (cuticular extensions) that give an arrowhead appearance to worm
  • thick shelled, pitted egg (~75 μm in diameter) containing a single cell when passed in feces
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19
Q

Toxocara cati ‐ Roundworms; Life Cycle, what type of infection is most important, what type of lifestyle puts older cats at risk

A
  • direct life cycle
  • infective eggs contain mature L3’s
  • L3’s undergo tracheal migration in kittens and somatic migration in older felines
  • transmammary infection is most important
  • paratenic hosts may give rise to short‐lived infections in older cats with opportunity to hunt
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20
Q

Toxocara cati ‐ Roundworms; Pathogenicity/Lesions/Clinical Signs

A
  • not as pathogenic as Toxocara canis
  • may induce vomiting even with moderate burdens
  • may get unthriftiness and diarrhea with very heavy burdens but this is unusual
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21
Q

Toxocara cati ‐ Roundworms; Treatments

A
  • fewer compounds than with dogs‐can use pyrantel pamoate‐based treatments (Pyr‐a‐Pam®, Pyr‐a‐Pam II®, Pyran®, Drontal® [mixed with praziquantel]) as well as selamectin (Revolution®) or emodepside (Profender®) [mixed with praziquantel]
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22
Q

Toxascaris leonina ‐ Roundworms; General Features; occurence, species affected, morphology of adults and eggs

A
  • not as common as the Toxocara spp.
  • infect both dogs and cats
  • same size (10 cm) as Toxocara cati but without the cervical alae
  • egg shells are smooth on the outside with an undulating membrane on their inner surface
  • the ~85 μm eggs have a single cell (or pair of cells) that do not fill the egg shell
23
Q

Toxascaris leonina ‐ Roundworms; Life Cycle

A
  • direct (and simple) life cycle
  • infective form is the L3 within the egg
  • oral transmission is normal route either from egg or paratenic host(s)
  • eggs release L3’s in intestine and they undergo a mucosal migration (NO tracheal migration)
  • PPP about 2 months
24
Q

Toxascaris leonina ‐ Roundworms; Pathogenicity/Lesions/Clinical Signs

A
  • not as pathogenic as Toxocara spp.
  • worm burdens are usually not heavy
25
Q

Toxascaris leonina ‐ Roundworms; Treatments

A
  • Mostly same treatments as for Toxocara spp. in dogs and cats
  • fewer compounds registered for use in cats than in dogs
26
Q

Parascaris equorum; species affected, adult morphology

A

Order Ascaridida (Roundworms)
* infects horses, ponies, donkeys
* Adult: Heavy‐bodied, white up to 50 cm long

27
Q

Parascaris equorum; Egg morphology:

A
  • Sub‐spherical, up to 90 μm
  • Thick protein coat on most eggs
28
Q

Parascaris equorum: Life Cycle;

A
  • Direct life cycle with tracheal migration through liver and lung
29
Q

Parascaris equorum: PPP

A

10 - 12 weeks

30
Q

Parascaris equorum; Pathogenesis and Clinical Signs

A
  • Clinical signs in foals and weanlings
  • Unthrifty, loss of appetite, hypoalbuminenia
  • Heavy burdens can impact > colic
31
Q

Parascaris equorum; Diagnosis

A
  • typical eggs in feces of infected young horses
32
Q

Parascaris equorum; Treatment

A
  • Many registered compounds–must avoid using compounds that cause rapid worm death or spastic paralysis of the worms if heavy infection – risk of impaction – fenbendazole in these cases
33
Q

Ascaris suum; adult morphology, host

A
  • infects swine, heavy‐bodied, white up to 40 cm long, males smaller
34
Q

Ascaris suum; egg morphology

A
  • Sub‐spherical, up to 50 ‐ 80 μm
  • Thick protein coat on most eggs
35
Q

Ascaris suum; Life Cycle:

A
  • Direct life cycle with tracheal migration through liver and lung
36
Q

Ascaris suum PPP

A

6 to 8 weeks

37
Q

Ascaris suum; Pathogenesis and Clinical Signs

A
  • “milk spots” on liver ‐ condemns
  • pulmonary hemorrhage/edema
  • mild enteritis – growth suffers
38
Q

Ascaris suum; diagnosis

A
  • typical eggs in feces of infected swine
39
Q

Ascaris suum; Treatment/Control

A
  • all‐in/all‐out farrowing facilities with good hygiene
  • deworming of sows prior to farrowing
  • in‐feed anthelmintics (e.g. levamisole) to decrease burden in young
40
Q

Ascaridia galli; adult morphology

A
  • Heavy‐bodied, white up to 10 cm
41
Q

Ascaridia galli; egg morphology;

A
  • 70 ‐ 90 μm with smooth shell
42
Q

Ascaridia galli; life cycle

A
  • L3 in larvated eggs are infective
    ‐ egg hatches → L3 enters mucosal → L3 → L4 → re‐enters lumen of small intestine → adults
    PPP: 30 to 50 days
43
Q

Ascaridia galli; Pathogenesis and Clinical Signs

A
  • hemorrhage/diarrhea during larval mucosal migration
  • gives decreased production parameters
  • low mortality
44
Q

Ascaridia galli; diagnosis

A
  • typical eggs in feces of infected birds
45
Q

Would you usually find Ascaridia galli in broiler flocks?

A

no because PPP in 30 - 50 days

46
Q

Heterakis gallinarum ‐ “Cecal Worm”; hosts

A
  • chickens, turkeys and many other species
47
Q

Heterakis gallinarum ‐ “Cecal Worm”; adult morphology

A
  • slender worms (4 to 15 mm) found in ceca
48
Q

Heterakis gallinarum ‐ “Cecal Worm”; egg morphology

A
  • thick, smooth shell, up to 50 μm long
49
Q

Heterakis gallinarum ‐ “Cecal Worm”; Life Cycle

A
  • eggs embryonate after passing to give infective larvae
  • infective eggs or infected paratenic hosts
  • larvae migrate to ceca and enter mucosa
  • larvae move to lumen again > 3 molts > adults

PPP
* 24‐30days

  1. Eggs in the feces and the embryo in the egg
    develops to L3 .
  2. Direct life cycle.
  3. Oral ingestion of the infective form, the infective egg, with feed or water.
  4. Eggs hatch in the gastrointestinal tract of the host. Larva migrates in mucosa of cecum
    and re-enters the lumen in two to five days. Here it molts two times to give rise to adult males
    and females.
  5. Prepatent period = 24 to 30 days.
  6. Earthworms may be transport or paratenic hosts
50
Q

Heterakis gallinarum ‐ “Cecal Worm”; significance

A
  • true intermediate host for Histomonas meleagridis
  • rare example of an endoparasite acting as a required intermediate host for a second parasitic species
51
Q

Baylisascaris procyonis; hosts

A
  • Raccoons (DH) and other species (IH’s)
52
Q

Baylisascaris procyonis; adult morphology

A
  • Large worms up to 20 cm
53
Q

Baylisascaris procyonis; egg morphology

A
  • thick, smooth shell, up to 50 μm long

Parasitology 2 (6 decks)

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