6.09 – Introduction to Nematodes – The Roundworms Flashcards
Introduction to Nematodes; General Features; morphology and body structure
- elongate tubular bodies
- thick, resistant cuticle
- muscles underlie cuticle
- hydrostatic pressure maintains shape and rigidity
- simple alimentary tract
- separate sexes
Introduction to Nematodes; Anatomy ‐ Male Worms
- single convoluted tube consisting of testes, vas deferens and ejaculatory duct
- sometimes supplemented with cuticular spicules
- some groups have pronounced copulatory bursa
Introduction to Nematodes; Anatomy ‐ Female Worms
- pair of blind‐ended ovaries leading to uteri
- common vagina and vulva
- often store sperm for protracted periods
Introduction to Nematodes; General Life Cycle Strategies
- 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??)
Introduction to Nematodes; General Life Cycle Strategies ‐ Routes of Infection
- 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)
Introduction to Nematodes; General Life Cycle Strategies ‐ Migrations
- 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
Introduction to Ascarids; General Features of the “Roundworms” (ascarids); morphology, site of infection, host specificity, life strategies, egg character
- 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
Typical Life Cycles of the “Roundworms” (ascarids)
- 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
Introduction to Ascarids; Typical Pathogenesis
- 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
Toxocara canis ‐ Roundworms; General Features; site of infectin, morphology of adult and egg, route of infection
- 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
Toxocara canis ‐ Roundworms; Life Cycle, general
- 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…..
Toxocara canis ‐ Roundworms; Life Cycle in Pups
- < 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
Toxocara canis ‐ Roundworms; Transplacental and Transmammary Transmission
- 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)
Toxocara canis ‐ Roundworms; non-vertical routes of transmission
- 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)
Toxocara canis ‐ Roundworms; Pathogenesis/Lesions/Clinical Signs ‐ Intestinal Phase
- 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
Toxocara canis ‐ Roundworms; Pathogenesis/Lesions/Clinical Signs
‐ Migration Phase
- 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)
Toxocara canis ‐ Roundworms; Treatments
- 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
Toxocara cati ‐ Roundworms; General Features; morphology, site of infection, egg morphology
- 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
Toxocara cati ‐ Roundworms; Life Cycle, what type of infection is most important, what type of lifestyle puts older cats at risk
- 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
Toxocara cati ‐ Roundworms; Pathogenicity/Lesions/Clinical Signs
- 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
Toxocara cati ‐ Roundworms; Treatments
- 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]
Toxascaris leonina ‐ Roundworms; General Features; occurence, species affected, morphology of adults and eggs
- 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
Toxascaris leonina ‐ Roundworms; Life Cycle
- 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
Toxascaris leonina ‐ Roundworms; Pathogenicity/Lesions/Clinical Signs
- not as pathogenic as Toxocara spp.
- worm burdens are usually not heavy
Toxascaris leonina ‐ Roundworms; Treatments
- Mostly same treatments as for Toxocara spp. in dogs and cats
- fewer compounds registered for use in cats than in dogs
Parascaris equorum; species affected, adult morphology
Order Ascaridida (Roundworms)
* infects horses, ponies, donkeys
* Adult: Heavy‐bodied, white up to 50 cm long
Parascaris equorum; Egg morphology:
- Sub‐spherical, up to 90 μm
- Thick protein coat on most eggs
Parascaris equorum: Life Cycle;
- Direct life cycle with tracheal migration through liver and lung
Parascaris equorum: PPP
10 - 12 weeks
Parascaris equorum; Pathogenesis and Clinical Signs
- Clinical signs in foals and weanlings
- Unthrifty, loss of appetite, hypoalbuminenia
- Heavy burdens can impact > colic
Parascaris equorum; Diagnosis
- typical eggs in feces of infected young horses
Parascaris equorum; Treatment
- 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
Ascaris suum; adult morphology, host
- infects swine, heavy‐bodied, white up to 40 cm long, males smaller
Ascaris suum; egg morphology
- Sub‐spherical, up to 50 ‐ 80 μm
- Thick protein coat on most eggs
Ascaris suum; Life Cycle:
- Direct life cycle with tracheal migration through liver and lung
Ascaris suum PPP
6 to 8 weeks
Ascaris suum; Pathogenesis and Clinical Signs
- “milk spots” on liver ‐ condemns
- pulmonary hemorrhage/edema
- mild enteritis – growth suffers
Ascaris suum; diagnosis
- typical eggs in feces of infected swine
Ascaris suum; Treatment/Control
- 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
Ascaridia galli; adult morphology
- Heavy‐bodied, white up to 10 cm
Ascaridia galli; egg morphology;
- 70 ‐ 90 μm with smooth shell
Ascaridia galli; life cycle
- 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
Ascaridia galli; Pathogenesis and Clinical Signs
- hemorrhage/diarrhea during larval mucosal migration
- gives decreased production parameters
- low mortality
Ascaridia galli; diagnosis
- typical eggs in feces of infected birds
Would you usually find Ascaridia galli in broiler flocks?
no because PPP in 30 - 50 days
Heterakis gallinarum ‐ “Cecal Worm”; hosts
- chickens, turkeys and many other species
Heterakis gallinarum ‐ “Cecal Worm”; adult morphology
- slender worms (4 to 15 mm) found in ceca
Heterakis gallinarum ‐ “Cecal Worm”; egg morphology
- thick, smooth shell, up to 50 μm long
Heterakis gallinarum ‐ “Cecal Worm”; Life Cycle
- 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
- Eggs in the feces and the embryo in the egg
develops to L3 . - Direct life cycle.
- Oral ingestion of the infective form, the infective egg, with feed or water.
- 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. - Prepatent period = 24 to 30 days.
- Earthworms may be transport or paratenic hosts
Heterakis gallinarum ‐ “Cecal Worm”; significance
- true intermediate host for Histomonas meleagridis
- rare example of an endoparasite acting as a required intermediate host for a second parasitic species
Baylisascaris procyonis; hosts
- Raccoons (DH) and other species (IH’s)
Baylisascaris procyonis; adult morphology
- Large worms up to 20 cm
Baylisascaris procyonis; egg morphology
- thick, smooth shell, up to 50 μm long
