How to Cite This Chapter: McCullagh D, Alexander P, Paul M, Stefaniak J. Toxocariasis. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed July 15, 2024.
Last Updated: September 28, 2020
Last Reviewed: February 26, 2021
Chapter Information

Definition, Etiology, PathogenesisTop

Toxocariasis is a chronic parasitic zoonosis caused by the larval stage of canine or feline ascarids. The disease involves internal organs and the eye. Humans are accidental intermediate hosts for the parasite. Toxocariasis is epidemiologically one of the most prevalent and ubiquitous human helminth infections across industrialized countries.

1. Etiologic agent: Nematodes of the Toxocara genus, which are accidental human parasites. For years their larvae continue to migrate through tissues and organs (liver, myocardium, lungs, skeletal muscles, eyes, and central nervous system [CNS]) but never reach sexual maturity. The adult form of the nematode develops in a canine (T canis) or feline (T cati) host. Eggs released in the animal feces are deposited in soil, where they continue their biological cycle.

2. Reservoir and transmission: Domestic and wild dogs and cats. Humans become infected as a result of accidental ingestion of infective eggs of Toxocara spp, which are present in soil contaminated with animal feces (eg, sandboxes, parks, recreational areas, private gardens, playgrounds), through unwashed hands, or after consuming raw fruits and vegetables contaminated with soil.

3. Epidemiology: Toxocara spp are prevalent worldwide.

Risk factors for infection: Pica (geophagy), raising dogs or cats, inconsistent deworming of domestic animals (especially young animals, <8 months of age), occupational exposure to animals (veterinarians, farmers) or to soil contaminated with feces (farmers, staff responsible for the maintenance of parks and recreational areas, geologists), consumption of raw fruits and vegetables contaminated with soil. Recreational areas and private gardens in urban areas are associated with a particularly high risk of infection due to the possibility of significant contamination of soil with infective eggs. Several members of the same family may be affected.

4. Incubation and contagious period: From 2 weeks up to a few months or even years. The patient is not contagious.

Clinical Features and Natural HistoryTop

1. Systemic toxocariasis: Symptomatic visceral larva migrans syndrome: fever, hepatomegaly, splenomegaly, eosinophilia, hypergammaglobulinemia, and involvement of the respiratory system; the patient may have only some of the signs and symptoms listed above. Severe symptomatic cases are rare and occur predominantly in children 2 to 5 years of age with geophagy. Larval migration is associated with abdominal pain, loss of appetite, weight loss, cough, attacks of dyspnea, transient cutaneous rashes (urticaria or eczema), lymphadenitis, myalgia, arthralgia, and, less frequently, myocarditis or meningitis.

2. Localized toxocariasis: Ocular toxocariasis (ocular larva migrans syndrome) and CNS toxocariasis (neurotoxocariasis; very rare) result from colonization of the eye or CNS by a small number of larvae or, typically, by a single larva. Ocular toxocariasis is associated with unilateral vision impairment, leukocoria (a white reflection from the retina), strabismus, and occasionally eye pain. Clinical manifestations of CNS toxocariasis are dominated by the signs and symptoms of encephalitis, often with coexisting generalized or partial epileptic seizures.

3. Covert toxocariasis: Various noncharacteristic signs and symptoms, such as acute bronchitis, pneumonia with or without Löffler syndrome, asthma, chronic urticaria, eczema, generalized lymphadenopathy, myositis, or arthritis. It may progress to fully symptomatic visceral larva migrans syndrome or ocular toxocariasis. Covert toxocariasis is most frequently diagnosed on the basis of improvement or resolution of symptoms following antiparasitic treatment.

4. Asymptomatic toxocariasis: Diagnosed most frequently in the patient’s family members on the basis of positive serologic results. Inactive larvae of Toxocara spp remain in tissues for life and may be reactivated and start to migrate at any time.


As the parasite does not develop into an adult stage in a human host, the eggs of Toxocara spp are never detected in human feces. The infection can only be confirmed on the basis of indirect diagnostic tests.

Diagnostic Tests

1. Serology:

1) Specific serum IgG (enzyme-linked immunosorbent assay [ELISA], confirmation by Western blot assay). A positive test result must be interpreted with caution (see point 2) below) and the patient's clinical status needs to be considered.

2) IgG avidity tests allow the differentiation of acute invasion (within <5 months of infection; low avidity) from chronic disease (high avidity).

3) Comparative analysis of the immunologic profile of specific IgG in serum and aqueous humor collected from the anterior eye chamber or intraocular fluid (immunoblotting). In ocular toxocariasis serum antibody levels may be low or absent even in the presence of active disease.

2. Ancillary tests: Complete blood count (CBC) and immunoglobulin levels. In symptomatic patients with visceral larva migrans syndrome the results reveal an increase in the absolute number and percentage of eosinophils, increase in the number of leukocytes in peripheral blood, and serum hypergammaglobulinemia. In patients with eosinophilic encephalitis and meningitis, high eosinophil counts in peripheral blood and cerebrospinal fluid are observed.

3. Imaging studies:

1) Ultrasonography or computed tomography (CT) of the abdomen reveals hepatomegaly and multiple granulomas forming around the larval stages of the parasite in the liver.

2) CT or magnetic resonance imaging (MRI) of the brain reveals regular, well-demarcated focal lesions in the white matter or within the cerebral cortex, which are often solitary and partially calcified.

3) Chest radiographs may reveal transient pulmonary infiltrates in allergic eosinophilic pneumonia (Löffler syndrome).

4) Ocular ultrasonography in patients with ocular larva migrans syndrome reveals intraorbital or subretinal granulomas. The lesions are usually solitary and unilateral.

4. Other tests: In patients with ocular toxocariasis, ophthalmoscopy may reveal the presence of a grey-white granuloma in the posterior pole or on the periphery of the retina, often with postinflammatory fibrous proliferation and crescent-shaped retinal elevation around the lesion.

Diagnostic Criteria

A positive epidemiologic history (eg, geophagy, close contact with young dogs that have not been dewormed, regular consumption of unwashed homegrown fruits and vegetables, playing in an uncovered sandbox) and fulfillment of ≥1 of the following criteria: presence of specific IgG or IgE in peripheral blood, peripheral blood eosinophilia (>440/microL or >4%), typical clinical manifestations or imaging abnormalities.

Differential Diagnosis

1. Visceral larva migrans syndrome: Infection with Baylisascaris procyonis, tropical pulmonary eosinophilia (Wuchereria bancrofti, Brugia malayi), larval stage of ascariasis, strongyloidiasis, allergic diseases (asthma, urticaria, atopic dermatitis, drug-induced reactions), autoimmune diseases (systemic lupus erythematosus, polyarteritis nodosa, polymyositis and dermatopolymyositis), lymphoproliferative diseases, myeloproliferative diseases, idiopathic eosinophilia.

2. Neurotoxocariasis: Eosinophilic encephalitis due to infection with Gnathostoma spinigerum and Angiostrongylus cantonensis, neurocysticercosis.

3. Ocular larva migrans syndrome: Retinoblastoma and other ocular tumors, ocular toxoplasmosis, ocular tuberculosis, exudative retinitis (Coats disease).


Treatment that includes anthelmintics is advocated for toxocariasis and particularly acute toxocariasis, so as to limit the larvae from reaching the eyes and brain. Specialist consultation is advised. Albendazole and mebendazole are often used. Glucocorticoids (eg, prednisolone) and in some instances ophthalmic surgery are used in more complex infections.

1. Visceral larva migrans syndrome: The first-line drug is oral albendazole 15 mg/kg/d (max 800 mg/d) for 5 to 10 days.Evidence 1Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision. Stürchler D, Schubarth P, Gualzata M, Gottstein B, Oettli A. Thiabendazole vs. albendazole in treatment of toxocariasis: a clinical trial. Ann Trop Med Parasitol. 1989 Oct;83(5):473-8. doi: 10.1080/00034983.1989.11812374. PMID: 2694978. Magnaval JF. Comparative efficacy of diethylcarbamazine and mebendazole for the treatment of human toxocariasis. Parasitology. 1995 Jun;110 (Pt 5):529-33. doi: 10.1017/s0031182000065240. PMID: 7596637.

2. Ocular toxocariasis: Albendazole and glucocorticoids administered systemically or topically as well as surgical treatment (vitrectomy and laser photocoagulation).Evidence 2Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision. Ahn SJ, Woo SJ, Jin Y, et al. Clinical features and course of ocular toxocariasis in adults. PLoS Negl Trop Dis. 2014 Jun 12;8(6):e2938. doi: 10.1371/journal.pntd.0002938. PMID: 24922534; PMCID: PMC4055477.


In the course of albendazole treatment, monitor eosinophilia and blood aminotransferase levels on a regular basis. Treatment should be discontinued if features of liver damage are observed. Fundoscopy should be periodically performed in case of a further decrease of visual acuity.


1. Visceral larva migrans syndrome: Weight loss or failure to thrive, developmental delays, liver failure, pulmonary fibrosis, eosinophilic myocarditis with heart failure.

2. Ocular toxocariasis: Tractional retinal detachment, cataract, phthisis bulbi, strabismus, permanent loss of visual field, vision impairment or loss.

3. Neurotoxocariasis: Behavioral and personality disorders, epilepsy, neurologic deficits.


The prognosis is good in patients with visceral larva migrans syndrome associated with mild signs and symptoms and in patients with covert toxocariasis. Ocular toxocariasis is frequently associated with decreased visual acuity or visual loss. CNS and myocardial disease are rare but can result in death.


Regular deworming of dogs and cats (particularly of young animals), washing of fruits and vegetables prior to consumption, using protective gloves when gardening, removal of dog and cat feces from parks and recreational areas, covering sandboxes to avoid contamination with animal feces.

We use cookies to ensure you get the best browsing experience on our website. Refer to our Cookies Information and Privacy Policy for more details.