Toxocara canis Intestinal Roundworm of Dogs		Contents		Rev 10/25/2025
		Classification		Biology and Ecology
		Morphology and Anatomy		Life Cycle
Return to Toxocara menu				Ecosystem Functions and Services
		Distribution		Management
Return to Ascarididae Menu		Feeding		References
		Go to Nemaplex Main Menu		Go to Dictionary of Terminology

Classification:

Class:    Chromadorea

Subclass: Chromadoria

Order:   Rhabditida 

Suborder: Spirurina

Superfamily: Ascaridoidea

Family:  Ascarididae

 

        Toxocara canis (Werner, 1782) Stiles, 1905

Morphology and Anatomy:

• Adults are white to cream colored and stout bodied with a pear-shaped cervical ala

Males:

• Length 4-10 cm, width 2-2.5 mm
• Spicules slightly unequal, curved, winged 750-1300 um long
• Small finger-like process on the tail.

Females:

• Length 5-18 cm (usually about 6.6) , width 2.5-3 mm
• Dark brownish, subspherical with a thick, finely-pitted cuticle. Eggs are 85-90 x 75 um and contain a single cell when laid

Ref: Cruthers et al., 2020

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Distribution:

Worldwide

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Economic Importance:

May cause death in canines and larval visceral migrans in humans.

Toxocara canis is parasitic in the small intestine of dogs worldwide and can cause visceral larva migrans in humans

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Hosts:

Common among wild and domestic animals.

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Feeding:

Intestinal mucosa

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Life Cycle:

Complex life cycle with four modes of transmission in dogs:

1.

• Eggs passed in the feces of infected dogs (700 eggs/g feces/day) develop to the infective L2 in 4 weeks under optimal conditions and can survive for years in soil.
• L2 hatch are ingested by young dogs, penetrate the small intestine and travel to the liver and lungs by way of the bloodstream.
• The L2 molts to the L3 which returns to the small intestine via tracheal migration, soughing and swallowing, and molts to the adult stages.

2.

•  In dogs older than 3 months, hepatic-tracheal migration decreases and ceases in dogs 6 months of age. Instead, the L2 undergo a somatic migration to many tissue within the dog becoming larvae with arrested development. Prenatal infection occurs in the pregnant bitch with the arrested-development larvae becoming mobilized about 3 weeks prior to parturition.
• The L2 migrate to the lungs of the fetus and molt to the L3 just before birth.
• The L3 travels to the small intestine of the newborn pup via tracheal migration and the final molts take place to complete the life cycle.

3.

•  Suckling pups can be infected by ingestion of larvae in the milk during the first 3 weeks of lactation..

4.

•  Paratenic host (earthworms, rodents, birds, sheep, pigs, monkeys, and humans), in which the L2 become arrested, also serve as a transmission route for infection of dogs.

 The prepatent period is 4-5 weeks by direct infection following ingestion of eggs or larvae or a paratenic host, or 3 weeks by prenatal infection.

Children ingesting T. canis eggs when eating contaminated soil become infected. The infection causes sustained eosinophilia called visceral larva migrans and granulomatous retinitis

Ref:  Cruthers et al., 2020

For Ecophysiological Parameters for this species, click	If species level data are not available, click for genus level parameters

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Damage:

Visceral larval migrans in paratenic human hosts, usually children.

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Management:

Sanitation

Anthelminthics

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References:

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