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Toxocara canis


Synonym(s): T. canis, dog roundworm




  • Phylum: Nematoda.
  • Class:  Secernentea.
  • Order: Ascaridida.
  • Family: Toxocaridae.
  • Genus: Toxocara.
  • Species: T. Canis.

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Clinical Effects



  • L2 in tissues of any mammal or bird, including dog and man, but also mice, rats, rabbits, domestic farm animals, chickens.
  • Adult worms in small intestine, particularly anterior small intestine, of dogs and foxes.
  • Eggs in environment.


  • See lifecycle diagram Lifecycle Toxocara canis - diagram :
    • Adult male and female.
    • Egg.
    • L2.
    • Paratenic host.
    • Develops to adult.
  • Bitch and her puppies.
  • Adult dogs.
  • Foxes and their cubs.
  • Human infection.


Infection of young puppy

  • Transplacental transfer of L2:
    • Accounts for >95% of L2 transferred.
    • L2 become activated at 40 days of pregnancy → migrate across placenta.
    • L2 in liver and lungs of newborn pup complete migration to intestine → develop to adults that begin to lay eggs in about 2.5 weeks.
  • Transmammary transfer of L2:
    • Accounts for <5% of the transferred L2.
    • L2 transfer via milk to puppies, develop in intestine without migration.
    • This transfer can continue for first 4-5 weeks of lactation.
  • Infection with eggs:
    • L2 in infective eggs ingested by puppies less than 3 months old undergo tracheal migration (via liver, lungs, trachea), to be swallowed and develop into adults with a prepatent period of about 1 month.
  • Infection of lactating bitch
    • Some of immature T. canis puppy acquired from dam are swept out in puppy's feces. These are eaten by lactating bitch while cleaning puppies, and develop to egg-laying adults in bitch's intestine.
    • A few L2 in tissues of bitch may migrate via trachea to intestine to develop to adults.

​​Infection of adult dog

  • Infection with eggs:
    • In some dogs, possibly related to breed, immunosuppression or estrus, L2 from ingested eggs undergo tracheal migration to become adults in intestine.
  • Infection with paratenic hosts:
    • L2 in paratenic hosts, ingested by dogs that hunt, eg rodents, hares, birds or are fed raw meat, develop directly in intestine to adults.
    • This route of infection can account for higher levels of infection withT.canisin stray dogs and foxes. The latter can eat up to 6,000 rodents a year.

Routes of infection for man

  • The surface of T. canis eggs are extremely sticky:
    • Ingestion of infective eggs in or from soil.
    • Ingestion of L2 in meat, eg liver, steak eaten rare or raw.
    • Indirect transfer of eggs from dog feces, perhaps by flies to food or surface of fruit or vegetables contaminated by eggs from feces.

Risk factors for developing VLM or OLM

  • The main source of large numbers of eggs a garden requires to cause VLM is young puppies + dam, (or a vixen and cubs).
  • VLM, induced by large numbers of L2, usually is associated with history of recent (1 year), puppy ownership and geophagia pica by child.
  • OLM, or asymptomatic infection, can be related to lower numbers of L2 which may be acquired from anywhere, including eggs sticking to fingers in soil of parks and gardens contaminated by adult dogs/foxes or through eating rare/raw meat containing L2. Also, through eating foods contaminated by eggs from dog feces, or perhaps contaminated indirectly by eggs carried by flies from feces to food.
  • In households with untreated dogs, eggs may build up in the immediate environment over time.
  • Embryonated eggs have been demonstrated in the coats of dogs. Although eggs have been demonstrated to embryonate in the coat of dogs this does not occur at as great a rate as in soil.

Pathological effects

Intestinal infection with adult parasites

  • Dogs do remain susceptible to direct development of L2 to adult in intestine if these are derived from paratenic hosts or puppies.
  • However, some protective immunity may develop, as lactating bitches infected with large numbers of T. canis do expel these when lactation ceases - this coincident with their cellular immune reactivity returning to normal.
  • In dogs aged from about 3 months, L2 from ingested eggs are increasingly less able to undergo tracheal migration back to the intestine to develop. Whether this is an immunologically- or physiologically-mediated effect is unknown. However, tracheal migration to the intestine does occur in immunosuppressed dogs.

Infection with tissue larvae

  • These can remain alive and migrate in tissues for many years, despite host production of specific antibodies and reactive cells.
  • L2 evade immune response very effectively, through repeated shedding of their surface antigens.

Activation of L2 in pregnancy, lactation and estrus

  • Activation of L2 from about last 20 days in pregnancy through lactation + direct transfer of L2 from ingested eggs to placenta or mammary gland at these times is coincident with a marked depression in lymphocyte responses for last 3-4 weeks of pregnancy and for 4-5 weeks into lactation.

Adult T. canis in the intestine

  • Light to moderate infections → malabsorption, villous atrophy + increased thickness of intestinal muscle layers, the degree of change correlates directly with level of infection.
  • Heavy infections (>100 worms) → villous flattening, marked hypertrophy of muscle layers of anterior small intestine, marked distension of anterior small intestine, pot belly and possibly intestinal obstruction.
  • Burdens of 300-400 worms may kill a Beagle-sized puppy.
  • OLM has been described occasionally in dogs.

Other Host Effects

  • The inter-relationship between hormonal effects, directly or indirectly via immune system, in relation to larval migration and development, is unknown.

Immunopathological response to migrating larvae in man

  • L2 in the tissues (liver, muscles, eye, etc), induce an eosinophilic, granulomatous response.


Control via animal

  • Anthelmintic treatment should be vigorous as T. canis is preventable cause of disease in children.

Treatment of lactating bitch and pups

  • Two programmes available:
    Either Treat bitch daily from day 40 post mating until 2 days post parturition with fenbendazole 25 mg/kg to kill L2 as they activate to move to fetuses. This may not be 100% effective, particularly if bitch is heavily infected or she and her pups are acquiring infection from heavily infected environment, so subsequent treatment of bitch and pups in lactation may be considered.
    Or Treat pups at 2 weeks old, every 2 weeks until 2 weeks post weaning and then monthly until 6 months old. The lactating bitch should also be treated at 2 weeks post parturition and at weaning. Further treatments for the bitch when treating the puppies may also be considered to reduce shedding from auto infection. This will markedly reduce egg counts.
    Do not use piperazine as it only kills adult form ofT. canis, which are immediately replaced with newly maturing worms

Treatment of dogs from 12 weeks to adulthood

  • Even though parasites are normally harmless in adult dogs, dogs should be treated for T. canis every 1-3 months because:
    • The prepatent period for T. canis from eggs or paratenic hosts is 1 month.
    • NO information available on reinfection following treatment.
    • Difficult to identify infected dogs.
    • Just a very few eggs from infected dog can cause OLM.
    • Every 3 months may be more practicable in view of necessity for owner compliance and has been demonstrated to reduce egg shedding.

Control via chemotherapies

Control via environment

  • Eggs are extremely resistant, survive several years. Will even survive >1 year when feces composted.
  • Dessication in dry heat over many days lethal to eggs.
  • Sodium hypochlorite (concentrated), when in contact with eggs for some 10 mins or more, strips off outer surface → eggs less sticky → wash away in drains. More prolonged contact with sodium hypochlorite dissolves shell to kill egg.
  • Measures to reduce dog fouling.
  • Keeping dogs out of public children's playgrounds/sport pitches.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Keegan J D & Holland C V (2012) A comparison of Toxocara canis embryonation under controlled conditions in soil and hair. J Helminthol 87 (1), 78-84 PubMed.
  • Wright I & Wolfe A (2007) Prevalence of zoonotic nematode species in dogs in Lancashire. Vet Rec 161 (23), 790 PubMed.
  • Laus J L, Canola J C, Mamede F V et al (2003) Orbital cellulitis associated with Toxocara canis in a dog. Vet Ophthalmol (4), 333-336 PubMed.
  • Wolfe A & Wright I (2003) Human toxocariasis and direct contact with dogs. Vet Rec 152 (14), 419-422 PubMed.
  • Wolfe A, Hogan S, Maguire D et al (2001) Red foxes (Vulpes vulpes) in Ireland as hosts for parasites of potential zzonotic and veterinary significance. Vet Rec 149 (25), 759-763 PubMed.
  • Blagburn B L, Lindsay D S, Vaughan J L et al (1996) Prevalence of canine parasites based on fecal flotation. Comp Cont Ed Pract Vet 18 (5), 483-509 VetMedResource.
  • Fisher M A, Jacobs D E, Hutchinson M J et al (1994) Studies on the control of Toxocara canis in breeding kennels. Vet Parasitol 55 (1-2), 87-92 PubMed.
  • Richards D T, Harris S & Lewis J W (1993) Epidemiology of Toxocara canis in red foxes (Vulpes vulpes) from urban areas of Bristol. Parasitol 107 (Pt 2), 167-173 PubMed.
  • Lloyd S (1985) Toxocara canis: infection, treatment and control. Vet Annual 25, 368-375 VetMedResource.
  • Sprent J F A & Barrett M G (1964) Large roundworms of dogs and cats: differentiation of Toxocara canis and Toxascaris leonina. Aus Vet J 40, 166-171 VetMedResource.
  • Nichols R L (1956) The etiology of visceral larva migrans. I. Diagnostic morphology of infective second-stage Toxocara larvae. J Parasitol 42 (4 Section 1), 349-362 PubMed.

Other sources of information

  • Lewis J W & Maizels R M (eds) (1993) Toxocara and toxocariasis. Clinical, epidemiological and molecular perspectives. Institute of Biology. pp 169.

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