Species of veterinary importance include Toxocara canis and Toxocara cati. Both species are zoonotic, and infection can lead to ocular, visceral and cerebral larva migrans in people. Human toxocariasis due to T. canis is widely reported and studied, with fewer reports and investigations for T. cati.

Host range: Definitive hosts for T. canis are dogs and wild canids (coyotes, wolves, foxes). Definitive hosts for T. cati are cats and wild felids. Many animals can act as paratenic hosts (e.g. rodents, pigs, birds, earthworms).

Geographic range: T. canis and T. cati have a worldwide distribution, although prevalence rates vary significantly between regions.

Life cycle: Adult worms live in the small intestine.  In the case of T. canis, there are four routes of infection: (i) Ingestion of eggs containing third-stage (L3) larvae from the environment, (ii) Ingestion of a paratenic host containing somatic L3 larvae, (iii) Transplacental infection of pups by migrating somatic larvae from the pregnant bitch, and (iv) Transmammary infection of neonatal pups by somatic larvae present in the milk of the lactating bitch. In dogs less than 2 months of age, larvae released from ingested eggs or paratenic host tissues undergo a hepatic–tracheal migration ending up as adult worms in the small intestine. In dogs older than 3 months of age, the majority of larvae arrest in somatic tissues. Somatic larvae reactivate during late gestation in pregnant bitches and migrate to the placenta and mammary glands. The prepatent period following T. canis infection is usually 4-5 weeks. However, following transplacental infection, puppies can shed eggs as soon as 2 weeks after birth. In the case of T. cati, the same routes of infection occur as T. canis except that transplacental transmission does not occur. The prepatent period is about 8 weeks, or as soon as 3 weeks after birth for transmammary infections.

Diagnosis: Ascarid-type eggs are detected by microscopy after fecal flotation, or coproantigen can be detected by an ELISA test. The fecal ELISA can detect Toxocara infections prior to patency, detect single-sex infections, and distinguish between active infection and eggs being present in feces due to coprophagy. Young puppies and kittens with heavy infections can present with a combination of poor condition, poor growth, pot-bellied appearance, and sometimes vomiting and diarrhea; very occasionally intestinal impaction can occur. Respiratory signs may also be apparent in puppies or kittens in heavily contaminated environments due to migrating larvae.

Management: Puppies and kittens should be treated with pyrantel pamoate at two, four, six and eight weeks of age and then monthly to six months of age using febantel, fenbendazole, pyrantel pamoate. Nursing bitches and queens should be treated at the same time as puppies and kittens.  To prevent vertical transmission, pregnant bitches can be treated off-label with fenbendazole or high-dose ivermectin. For dogs and cats over 6 months of age, anthelmintic treatment should be based on the results of fecal examinations. Prevention of hunting and scavenging are important to prevent ingestion of larvae from paratenic hosts. 

Host range: Definitive hosts are domestic and wild canids and felids. Paratenic hosts include rodents and birds.

Geographic range: Worldwide distribution, but prevalence generally lower than for Toxocara species.

Life cycle: Adult worms live in the small intestine and eggs are shed in the feces. Dogs and cats are infected by ingestion of larvated eggs from the environment or larvae in paratenic host tissues. Development to the adult stage occurs entirely within the small intestinal tract with no somatic migration. The pre-patent period is ~10 weeks following ingestion of eggs or larvae.

Diagnosis: Detection of smooth-shelled eggs following fecal flotation and microscopy, or detection of coproantigen by fecal ELISA. Clinical impacts are similar to Toxocara, but infection intensities are generally lower and so clinical disease is less common.

Management: Measures recommended to control Toxocara spp. should also control Toxascaris. Since somatic migration does not occur, vertical transmission is not a concern.

Baylisascaris procyonis is the main species of veterinary importance due to its potential for causing particularly severe clinical disease in young children (cerebral and ocular larva migrans).

Host range: The natural host and main reservoir of infection for B. procyonis is the raccoon, but dogs are also a competent definitive host. Over 100 different species of mammals and birds have been described as paratenic hosts, with rodents considered the most important reservoir host among them.

Geographic range: Follows the range of the raccoon host. It is endemic throughout North and Central America and is present in raccoons in BC, AB, SK, MN, ON, QB, NB and NS, with prevalence rates of over 50% in some regions (BC,QB and ON). It has been introduced into Europe and Asia with raccoons.

Life cycle: Adult worms (up to 20 cm in length) reside in the small intestine, and eggs are passed in the feces.  Definitive hosts are infected by ingestion of larvated eggs from the environment or somatic larvae within a paratenic host. Paratenic hosts can be infected by these same routes.

Diagnosis: Detection of ascarid-type eggs by microscopy following fecal flotation, or detection of coproantigen by fecal ELISA. Eggs are similar to those of Toxocara but are slightly smaller, more finely pitted, and darker in colour.  Infections with adult worms in definitive hosts are asymptomatic. Migration of L3 in paratenic hosts, including humans, can cause a range of signs varying from mild behavioural changes to severe disability, coma, and death.

Management: Routine fecal examination and treatment of dogs as applied for Toxocara. Preventing dogs from hunting, scavenging, and encountering raccoon latrines will greatly reduce risk of exposure. Prevention of human disease is focused on public education of the dangers of contact with raccoons or their feces, particularly for young children who are prone to geophagia.

Species of veterinary importance include Ancylostoma caninum, Ancylostoma braziliense, and Ancylostoma tubaeforme. A. braziliense and, to a lesser degree, A. caninum are zoonotic parasites causing cutaneous larval migrans in people. A. caninum is also rarely reported to cause eosinophilic enteritis in people.

Host range: Definitive hosts of A. caninum are dogs and wild canids. Definitive hosts of A. tubaeforme are cats and wild felids. Both canids and felids serve as definitive hosts of A. braziliense.

Geographic range: Mainly occur in warmer tropical and subtropical climates, although A. caninum and A. tubaeforme are endemic in parts of North America including Canada – particularly in the eastern provinces, albeit at a low prevalence. Animals at highest risk in Canada are imported dogs or cats or those returning from travel to warmer regions. In North America, A. braziliense occurs in the southeastern and southcentral US coastal states.

Life cycle: Ancylostoma adults are 1-2 cm in length and attach to the small intestinal mucosa, feeding off blood. Eggs are shed in the feces and develop in the environment, with a first-stage larva hatching out and moulting two times.  Infective L3 enter the host by ingestion or by skin penetration. In the latter case, larvae migrate via the bloodstream to the lungs and then to the small intestine via the respiratory tract. The prepatent period is 14-21 days. In the case of A. caninum, a proportion of L3 pass from the lungs to skeletal muscle and can remain dormant for many years, reactivating in pregnant bitches to infect puppies through the transmammary route.

Diagnosis: Detection of strongyle-type eggs on fecal flotation or coproantigen by ELISA. Eggs are very similar to Uncinaria but smaller in size. A. caninum can cause anaemia and bloody diarrhea which is generally seen in animals less than 1 year of age or in young puppies following transmammary transmission; infection can be fatal in severe cases. Lower worm burdens can cause chronic malaise and poor condition. Other Ancylostoma species are considered to be milder pathogens. Migrating larvae can cause skin lesions, particularly pedal dermatitis.

Management: Measures recommended to screen and control Toxocara species should also control Ancylostoma infection. Deworming of dogs and cats following importation or travel to an endemic region is recommended.

Host range: Domestic and wild canids and felids.

Geographic range: U. stenocephala is often called the “northern hookworm” as it is endemic in temperate and cooler regions. It is present in all Canadian provinces, albeit at a low prevalence.

Life cycle: Adults (up to 1 cm in length) attach to the small intestinal mucosa and feed on blood. Eggs are shed in the feces and develop in the environment, with a first-stage larva hatching out and moulting two times. The definitive host is generally infected via ingestion of L3. Skin penetration by infective L3 can cause dermatitis but doesn’t generally result in a patent infection.

Diagnosis: Detection of strongyle-type eggs on fecal flotation or coproantigen by ELISA. Eggs are similar to Ancylostoma but larger in size. Adult worms are of low pathogenicity but migrating larvae can cause pedal dermatitis and, more rarely, a more generalised dermatitis.

Management: Measures recommended to screen and control Toxocara species should also control Uncinaria infection.

Host range: Domestic and wild canids; coyotes are considered to be an important reservoir. 

Geographic range: Worldwide.

Life cycle: Adult worms (up to 8 cm in length) reside in the cecum and colon with their anterior end embedded in the mucosa. Eggs are shed in the feces and develop to first-stage larvae within the egg.

After ingestion by the dog, larvae hatch out and develop in the distal small intestinal and large intestinal mucosal glands. The prepatent period is around 3 months.

Diagnosis: Detection of characteristic eggs in fecal flotation (small “lemon-shaped” eggs with bipolar mucus plugs); the long prepatent period and low egg output of adult worms can lead to false negatives. A fecal ELISA test for coproantigen can detect infection prior to patency.  Heavily infected dogs have been reported to have colitis leading to mucus and blood in stools. Reduced growth has been reported in puppies.

Management: Measures recommended to screen and control Toxocara species should also control Trichuris infection.