Roundworms (Toxocara canis and Toxascaris leonina) are found in the intestine of dogs and are a major hygienic concern because they are transmissible to people.
The large roundworms (ascaridoid nematodes) of dogs and cats are common, especially in puppies and kittens. Of the 3 species Toxocara canis, Toxascaris leonina, and Toxocara cati, the most important is T canis, not only because its larvae may migrate in people (as do larvae of T cati ), but also because fatal infections may be seen in young pups.
T leonina is seen in adult dogs and in cats. These species also infect wild carnivores, especially those in zoos or other captive settings.
In puppies, the usual mode of infection with T canis is transplacental transfer. If pups <3 mo old ingest embryonated eggs, the hatched larvae penetrate the intestinal mucosa, reach the lungs via the liver and bloodstream, are coughed up, swallowed, and mature to egg-producing adults in the small intestine. However, when embryonated infective eggs of T canis are swallowed by older dogs, the larvae hatch, penetrate the intestinal mucosa, and migrate to the liver, lungs, muscles, connective tissue, kidneys, and many other tissues, where development is arrested. In pregnant bitches, these dormant larvae mobilize and migrate into the developing fetus; they can be found in the intestine of the puppies as early as 1 wk after birth. Some larvae migrate to the mammary gland, so that pups may also be infected via the milk. During this perinatal period, the immunity of the bitch to ascarid infection is partially suppressed, and substantial numbers of eggs may be passed in feces. Development of these patent infections appears to be associated with maturation of arrested larvae in the bitch, which migrate to the intestine via the lungs, and to ingestion and maturation of larvae that are passed in the feces of puppies.
The first indication of infection in young animals is lack of growth and loss of condition. Infected animals have a dull coat and often are “potbellied.” Worms may be vomited and are often voided in the feces. In the early stages, migrating larvae may cause an eosinophilic pneumonia, which can be associated with coughing. Diarrhea with mucus may be evident. In puppies with severe infections, verminous pneumonia, ascites, fatty liver, and mucoid enteritis are common. Cortical kidney granulomas containing larvae are frequent in young dogs.
Disease severity depends not only on the number of larvae ingested but also on the degree of the allergic reaction. Patients with atopy may experience more severe toxocariasis. The pathologic manifestations result from inflammation caused by the immune response directed against the excretory-secretory antigens of larvae. These antigens are released from their outer epicuticle coat, which is readily sloughed off when bound by specific antibodies. These antigens are a mix of glycoproteins, including a potent allergenic component named TBA-1. The inflammatory reaction causes epithelioid cells to surround each larva, and, subsequently, a dense fibrous capsule invests each granuloma.
Although the main clinical manifestations vary depending on the organs infected, the most common characteristic is chronic eosinophilia. Other typical findings follow according to the involved organs. With liver involvement, hepatomegaly, fever, and abdominal pain are common. With lung involvement, pulmonary symptoms (eg, dyspnea, cough, chest tightness), bronchospasm, interstitial pneumonitis, and, possibly, pleural effusion can be present. Ocular toxocariasis can induce decreased visual acuity, uveitis, retinal granuloma, endophthalmitis, and other ocular lesions that often lead to sudden vision loss in the affected eye. If the brain is involved, neurologic manifestations may occur, including seizures.
Infection in dogs and cats is diagnosed by detection of eggs in feces. Distinguishing the spherical, pitted-shelled eggs of Toxocara spp from the oval, smooth-shelled eggs of Toxascaris leonina, is important because of the public health significance of the former.
In dogs, compounds licensed for treatment of roundworm infections include dichlorvos, diethylcarbamazine, fenbendazole, flubendazole, mebendazole, milbemycin, nitroscanate, piperazine, and pyrantel. In Europe, selamectin is approved to treat T canis infections with a single dose, while in Canada approved treatment requires 2 doses 1 mo apart.
The following drug combinations can also be used: praziquantel/pyrantel/febantel, pyrantel/febantel, and pyrantel/oxantel. Preventive programs for heartworm infection using milbemycin oxime, milbemycin/lufenuron, pyrantel/ivermectin, selamectin, or oxibendazole/diethylcarbamazine also control intestinal ascarid infections. However, selamectin is approved for this indication in only some countries.
Environmentally resistant larvated eggs on the ground and somatic larvae in the bitch are the main reservoirs of infection. Perinatal transmission of infection can be greatly reduced by treating bitches with 1) daily doses of fenbendazole (50 mg/kg, PO) from day 40 of gestation to day 14 after whelping, 2) ivermectin (0.3 mg/kg, SC) on days 0, 30, and 60 of gestation, and 10 days after whelping, 3) ivermectin (0.5 mg/kg) on days 38, 41, 44, and 47 of gestation, and 4) ivermectin (1.0 mg/kg) on days 20 and 42 of gestation. Otherwise, to minimize egg output, pups should be treated as early as possible; ideally, treatment should be given 2 wk after birth and repeated at 2- to 3-wk intervals to 3 mo of age. Nursing bitches should be treated at the same times. Because the eggs adhere to many surfaces and become mixed in soil and dust, strict hygiene should be observed by people, particularly children, exposed to potentially contaminated animals or areas.