Toxocara canis, T. cati

Toxocara canis, T. cati



NAME: Toxocara canis, Toxocara cati

SYNONYM OR CROSS REFERENCE: Toxocariasis (1-13), visceral larva migrans (1-6, 8-10, 14, 15), ocular larva migrans (1, 3-6, 8), visceral larva migrans visceralis (1, 4), covert toxocariasis (2, 3, 6, 8, 12), neurotoxocarosis (9), dog roundworm (T.canis), cat (or feline) roundworm (T.caiti).

CHARACTERISTICS: T. canis and T.cati are ascarid nematodes (5, 8) in the order Ascaridida, superfamily Ascaridiodea, abd belong to the family Toxocaridae (5). The morphology of the adult worms resembles that of Ascaris lumbricoides, only they are much smaller. Toxocara adult parasites are large, pink, roundworms, measuring 6.5 to 10 cm long for the females and 4 to 6 cm long for the males (3). The male has a curved posterior end which distinguishes it from the straight-tailed female (2, 3, 5). The larvae of T. canis are 290 to 350 μm by 18 to 21 μm. The diameter of the larvae of T. cati is somewhat smaller (3). The brownish eggs of T. canis and T. cati measure approximately 85 by 75 μm and 75 by 65 μm, respectively. The eggs are almost spherical, larger than those of A. lumbricoides and unembryonated when laid. Toxocara is a facultative anaerobe nematode and derives most of its energy from glycogen degradation.


PATHOGENICITY/TOXICITY: The dominant clinical manifestations associated with toxocariasis are classified according to the organs affected. In fact, the majority of infections are asymptomatic (16). There are two main syndromes: visceral larva migrans (VLM), which encompasses diseases associated with the major organs; and ocular larva migrans (OLM), in which the pathological effects are restricted to the eye (2, 4, 5, 8). Two other clinical forms of toxocariasis are now recognised: neurological, in which the target organs are associated with the peripheral or central nervous system (9); and covert, in which the symptoms do not match any of the 3 other forms (2, 3). Typically the manifestation and clinical course are determined by the size of the inoculum, frequency of reinfection, localisation of Toxocara larvae, and the host immunological response (6). In all forms of the disease, fatal cases of toxocariasis are rare (2).

VLM: VLM is primarily diagnosed in children between the ages of 2 and 7 with a history of geophagia and exposure to dogs in the home (8). The acute signs of VLM are associated with hepatic and pulmonary larval infection and often include fever, wheezing or coughing, eosinophilia, and heptomegaly (1-4, 8).

OLM: Typically occurring in children and young adults, the most common symptom is vision loss (2-4, 8), often accompanied by strabismus due to macular damage (3), with onset over a period of days to weeks (8). Closer examination often reveals uveitis endophthalmitits, papillitis, retinal granulomas or inflammatory masses in the peripheral vitreous humour (3-5).

Neurological: The neurological form occurs when Tococara larvae settle in the peripheral or central nervous system (2, 8, 9). There, they can give rise to meningoencephalitis or other neurological manifestations (2, 9), such as eosinophilic meningomyelitis (7), cerebral vasculitis, epilepsy, myelitis, radiculitis, cranial nerve involvement, or skeletal muscle affection (9).

Covert: The symptoms of covert toxocariasis are non-specific, but when grouped together they form a recognisable syndrome (3). These symptoms include recurrent abdominal pain which is often the sole presenting complaint, anorexia, behaviour disturbances, cervical adenitis, wheezing, limb pains, and fever (12, 17, 18).

EPIDEMIOLOGY: Worldwide (1-5, 7, 13, 17), due to human settlement of nearly all landmasses, and prevalence of keeping domesticated animals (5). Seroprevalence is particularly high in developed countries, especially in rural areas (4, 8), and also on some tropical islands (8).

HOST RANGE: Dogs and cats are definitive hosts of T. canis and T. cati respectively (2, 3, 5, 17). Humans and other mammals, such as foxes (2, 13) and wolves (3), are accidental hosts (1, 5)


MODE OF TRANSMISSION: Humans become infected by ingesting either embryonated Toxocara eggs from soil (geophagia, pica) (1, 3, 4, 8, 19), dirty hands, or raw vegetables; or Toxocara larvae from undercooked giblets (mainly liver) (1-3, 8). A new mode of transmission recently proposed is contact with embryonated eggs on a dog’s hair coat (20, 21). Toxocara species cannot complete their life cycle in humans, unlike in their definitive hosts, and instead exist as larvae which migrate throughout the body, invading all organs and damaging tissue (2, 3). The larvae never mature and eventually die in situ, often causing a whole host of inflammatory responses within their host tissues (3).

INCUBATION PERIOD: In children, the incubation period can be weeks or months depending on the intensity of the infection and sensitivity of the patient (1). Ocular manifestations may occur 4 to 10 years after the initial infection. In infections caused by the consumption of infected raw liver, very short incubation periods have been reported.

COMMUNICABIILTY: No evidence for direct human-to-human transmission (1).


RESERVOIR: Dogs (T. canis), and cats (T. cati) (1, 3, 17).

ZOONOSIS: Yes, Toxocara eggs are transmitted to humans by contaminated feces of dogs or cats (2-5, 8).

VECTORS: None; however, earthworms may facilitate the transmission of toxocariasis by altering the distribution of Toxocara eggs in soil (13).


DRUG SUSCEPTIBILITY: Sensitive to anthelminthic drugs such as albendazole, mebendazole (2-4, 7, 8), thiabendazole (1, 4, 8), febendazole (3), and diethylcarbamazine (1, 3, 7).

SUSCEPTIBILITY TO DISINFECTANTS: Due to a resistant outer shell, Toxocara eggs can withstand many disinfectants, including formalin (5, 13, 14), Lysol (13), saturated sodium chloride solution (13), chlorine, phenol, sodium and potassium chloride, quaternary ammonium compounds (19), and various inorganic acids (5, 13, 15). Toxocara (canis) eggs are susceptible to 70% ethanol (15) 2% sodium hypochlorite (15), and various concentration of iodine.

PHYSICAL INACTIVATION: Toxocara eggs are killed by extremes in temperature, desiccation (13-15), and sunlight (15).

SURVIVAL OUTSIDE HOST: Eggs can remain viable for several years in moist, shaded soils when temperatures are cool (2, 5).


SURVEILLANCE: Monitor for symptoms. The most commonly utilised diagnostic test is ELISA (1, 2, 4, 10-12, 17). Toxocariasis can also be detected by Western blot (7, 8), PCR (3), complement-binding reaction (7), indirect haemagglutinin assay (7), indirect immunofluorescence (7), or ophthalmoscopy (for OLM) (4).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Usually only subjects with severe symptoms are treated. Albendazole or mebendazole are the drugs of choice for toxocariasis (1, 3, 5, 7). Symptomatic treatment, including administration of corticosteroids, can be used to help suppress the intense allergic manifestations of the infection (3-5, 7, 8). OLM is treated by surgery (vitrectomy), anthelminthic chemotherapy, and/or corticosteroids (3, 4, 10, 11).


PROPHYLAXIS: No chemoprophylaxis exists; however, effective measures to prevent infection and reinfection exist such as encouraging handwashing in children, discouragement of geophagia, worming of household pets, and the washing of raw vegetables (1, 2, 8, 11). Municipal laws preventing the entry of dogs to parks and playgrounds and the requirement of owners to promptly remove their pet’s faeces from public areas may considerably lower the chances of Toxocara infection (1, 2, 8). Sandpits in public parks can be protected from contamination by covering them with vinyl sheets when not in use (22, 23).



SOURCES/SPECIMENS: Blood and blood products (3, 5), cerebrospinal fluid (7, 9), infected organs (1, 3-5, 8, 17), and dog or cat faeces (1-5, 8).

PRIMARY HAZARDS: Ingestion of eggs, and/or larvae (3, 5, 8, 12, 13).




CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk to splashes (25).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited (25). Additional precautions should be considered with work involving animals or large scale activities.


SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (25).

DISPOSAL: Decontaminate all materials for disposal by steam sterilisation, chemical disinfection, and/or incineration (25).

STORAGE: In sealed containers that are appropriately labelled (25).


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: August 2010.

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©

Public Health Agency of Canada, 2010


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