Toxocariasis is an infection caused by the ingestion of larvae of the dog roundworm Toxocara canis or the cat roundworm Toxocara cati. The soil of parks and playgrounds is commonly contaminated with the eggs of T canis, and infection may cause human disease that involves the liver, heart, lung, muscle, eye, and brain.[1, 2]
Three syndromes of Toxocara infection are generally recognized, as follows:
Prevention of toxocariasis is obviously preferable, but eradicating T canis infection is difficult because of the complexity of its life cycle. Good hygiene practices, timely disposal of pet feces, and routine deworming of pets are strategies necessary to reduce ocular toxocariasis in humans.[3]
Diagnosis of toxocariasis is difficult because confirmation of infection requires demonstration of larvae via biopsy. Therefore, clinicians use serologic testing (eg, enzyme-linked immunosorbent assay [ELISA], immunoblot) to infer diagnosis. Fortunately, toxocariasis usually carries a very good prognosis.
Adult worms of the Toxocara species live in the small intestine of dogs and puppies and range from 4-12 cm in length. Almost all puppies are infected at or soon after birth. During the summer, in wet conditions, Toxocara eggs are embryonated in 2-5 weeks and become infective. They survive for years in the environment, and humans typically ingest the eggs via oral contact with contaminated hands. Once introduced into the human intestine, the eggs decorticate, releasing the larvae. The larval form is visible only under a microscope because it is less than 0.5 mm in length and 0.02 mm wide. The larvae penetrate the bowel wall and migrate through vessels to the muscles, liver, and lung and sometimes to the eye and brain.
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.
Because the anti-Toxocara immunoglobulin-positive population is much higher than the prevalence of clinical toxocariasis, most patients are thought to have subclinical infection. In French adults, toxocariasis is termed common toxocariasis and is clinically characterized by the following:
In Irish children with high anti-Toxocara titers, the condition is termed subclinical toxocariasis, and the most frequent clinical findings are as follows:
Toxocariasis should be strongly considered when the patient has eosinophilia, characteristic clinical symptoms, and a positive finding on Toxocara serologic test.
United States
In the United States, about 10,000 cases of Toxocara infection are reported in humans each year. Almost 14% of the US population is infected with Toxocara, a parasite of dogs and cats that can be passed from animals to humans. In Cleveland, Ohio, the prevalence of T canis infection in the cohort ages 2, 3, and 4-10 years was 2%, 12%, and 12%, respectively.[4]
The US Centers for Disease Control and Prevention (CDC) reported on human ocular toxocariasis from 2009 through 2010. They described the results of a Web-based survey distributed to uveitis, retinal, and pediatric ophthalmologic specialists from around the United States. Epidemiologic, demographic, and clinical information was collected on 68 patients. Among the 44 patients, the median patient age was 8.5 years (range, 1-60 y) and 25 patients (57%) lived in the South at the time of diagnosis.[3]
International
Toxocariasis is a worldwide infection. Seroepidemiological surveys show a 2-5% positive rate in healthy adults from urban Western countries and 14.2-37% in rural areas. In tropical countries, surveys show a positive rate of 63.2% in Bali, 86% in Saint Lucia (West Indies), and 92.8% in La Reunion (French Overseas Territories, Indian Ocean).[5, 6] Research also suggests the prevalence of the disease in North America is significant.[7]
Toxocariasis is almost always a benign, asymptomatic, and self-limiting disease, although brain involvement can cause severe morbidity. Brain involvement can evoke meningitis, encephalitis, or epilepsy.
Ocular involvement may cause loss of visual acuity or unilateral blindness.
Pulmonary and hepatic forms can cause protracted symptoms if the patient does not receive treatment.
No ethnic predilection for toxocariasis has been reported. However studies by the US Centers for Disease Control and Prevention (CDC) have found that, among all age groups, toxocariasis is more common in non-Hispanic blacks than in Mexican Americans and non-Hispanic whites.
Toxocariasis has no sexual predilection.
CDC studies have shown that transmission of Toxocara larvae is most common in young children and persons younger than 20 years.
Toxocariasis is predominantly a disease of children, typically those aged 2-7 years.
Ocular toxocariasis is most common in older children and young adults.
Toxocariasis is generally a self-limited disease. The prognosis is good when adequately treated, except in some patients with ocular or cerebral involvement.
Properly de-worm kittens and puppies.
Pets should undergo periodic stool examinations by a veterinarian, and they should be treated if examination findings are positive for Toxocara eggs.
Do not bring stray dogs or cats home. If such animals are brought home, they should be examined by a veterinarian for toxocariasis.
Focus on personal hygiene. If dogs or cats have been in the yard, consider it contaminated. Wash hands after lawn work or gardening.
For patient education resources, see the Brain and Nervous System Center, as well as Brain Infection.
Inquire about pets in the home. Ask if children play in a sandbox. Ask about pica and handwashing practices and determine if hygiene practices are poor. Symptoms during the acute phase may include the following:
Tenderness in the right upper quadrant or hepatomegaly may be present in patients with liver involvement.
With pulmonary involvement, wheezing may be heard. Breath sounds may be decreased if a pleural effusion is present.
Patients with ocular involvement may present with the following:
Risk factors of toxocariasis include the following:
Decreased visual acuity may occur if ocular toxocariasis is not identified and treated.
Retinal detachment due to ocular involvement may cause unilateral visual loss.
Seizures may result from cerebral involvement.
The diagnosis of toxocariasis requires a high index of suspicion and depends on serologic testing (eg, ELISA, immunoblot).
Peripheral blood eosinophilia is the most important finding; however, it may be absent in patients with ocular or covert toxocariasis.
Serum total IgE: Patients with toxocariasis often have a marked increase in total IgE levels.
ELISA with Toxocara excretory-secretory antigen (TES-Ag) may show the following:
In a patient with pulmonary involvement, chest radiography may show multiple pulmonary nodules with surrounding ground-glass opacities, or possibly pleural effusion.
Ultrasonography reveals multiple hypoechoic areas in the liver.
Hepatic lesions are of low density.
Pulmonary involvement manifests as multiple pulmonary nodules and surrounding ground-glass opacities or, rarely, pleural effusion.
In the CNS, granulomas appear cortically or subcortically, showing a hyperintense appearance on proton density and T2-weighted images.
 View Image | The image on the left is a posteroanterior chest radiograph in a patient with toxocariasis. The image on the right is a CT scan of the patient with to.... |
An immunoblot is more specific than ELISA when bands from 24-35 kD are considered out of typical 7-band patterns (24, 28, 30, 35, 132, 147, 200 kD).
Funduscopic examination should be performed in patients suspected of having acute toxocariasis.
Biopsy is rarely performed to confirm the presence of Toxocara larvae.
A needle biopsy of the liver is required for histologic diagnosis in cases of liver involvement; however, some results are false-negative because lesions in the liver are very small.
The encapsulated larvae can be found in the liver, lung, brain, and/or enucleated eye. The larvae occur in a matrix of epithelioid cells surrounded by a fibrous capsule with weak inflammatory reactions. In ocular toxocariasis, a mobile larva can be directly observed under the retina.
Chemotherapy is the treatment of choice in most patients with liver, lung, or eye involvement. Occasionally, ocular involvement requires ocular surgery.
Treatment includes mebendazole, thiabendazole, corticosteroids, and specific organ treatment. The prognosis of toxocariasis is generally favorable.
For liver or lung involvement, no surgical care is required.
For ocular involvement with retinal detachment, laser treatment may be considered.
A consultation with an ophthalmologist is indicated in cases of ocular larva migrans.
Consultation with a neurologist is indicated in cases of brain involvement with neurologic symptoms or seizures.
Consultation with an infectious disease specialist may be indicated when questions exist regarding the indications for and selection of treatment for visceral larva migrans.
The eggs of Toxocara species are widespread in parks, playgrounds, yards, and in homes and apartments where the occupants have dogs or cats. Elimination of eggs from the environment is not possible; therefore, prevention depends on proper hygiene, including handwashing after contact with pets.
Dogs and cats can be de-wormed. However, this does not eliminate eggs from the larger environment.
Public policies that have attempted to eradicate Toxocara infection in dogs and cats have had limited success.
Puppies and kittens acquire Toxocara infection transplacentally and should be de-wormed at 2, 4, 6, and 8 weeks.
Sandboxes should be covered when not in use.
Dog and cat feces should be disposed of properly.
After playing in public parks and in sandboxes, children should wash their hands before eating.
For more information, visit CDC’s Guidelines for Veterinarians.[8]
Perform a follow-up examination of the lesion and a serum titer for TES-Ag using IgG, IgE with ELISA, or immunoblotting.
For significant lung involvement, obtain follow-up chest radiography to confirm the resolution of any acute infiltrate.
Serum transaminases and alkaline phosphatase can be used to monitor the degree of liver involvement.
For ocular involvement, monthly or bimonthly funduscopic examinations are recommended, according to the patient's state of remission.
In a patient with acute symptoms of toxocariasis (ie, dyspnea, chest tightness) due to lung involvement, hospitalization may be necessary.
In a patient with liver or ocular involvement, hospitalization may be needed for diagnostic and/or therapeutic procedures such as biopsy or laser surgery.
Continue anthelmintic therapy for 1 month after completing a course of steroids. If symptoms persist after a full course of anthelmintic therapy, extend steroid administration and taper according to lung symptoms.
In general, blood eosinophilia combined with a positive serologic test result indicates active toxocariasis and requires treatment. Deciding whether to treat covert or subclinical toxocariasis that does not show eosinophilia is controversial. Consider treatment in patients with a total serum IgE level over 500 IU/mL. Mebendazole or diethylcarbamazine kills the nematode larvae. Prednisone can be used as an adjunct to antihelminthic therapy in patients with wheezing or other signs of tissue inflammation.
Clinical Context: DOC. Adverse effects are negligible, except headaches during early therapy. These symptoms are from metabolites secreted from nematodes that are killed by the drug. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestines where helminths dwell.
Clinical Context: Second DOC if mebendazole is difficult to obtain. Decreases ATP production in the worm, causing energy depletion, immobilization, and, finally, death.
Clinical Context: Synthetic organic compound highly specific for several common parasites. Does not contain any toxic metallic elements. Not recommended as the DOC because of more severe adverse effects. Recommended if therapy with mebendazole fails or mebendazole is not available.
Funduscopic examination of the right eye of a patient with ocular toxocariasis showing rhegmatogenous retinal detachment.
The image on the left is a posteroanterior chest radiograph in a patient with toxocariasis. The image on the right is a CT scan of the patient with toxocariasis showing multiple pulmonary nodules with surrounding ground-glass opacities at first visit.
The image on the left is a posteroanterior chest radiograph in a patient with toxocariasis. The image on the right is a CT scan of the patient with toxocariasis showing multiple pulmonary nodules with surrounding ground-glass opacities at first visit.
Funduscopic examination of the right eye of a patient with ocular toxocariasis showing rhegmatogenous retinal detachment.
Immunogold finding of Toxocara canis larva reacted with a seropositive human serum. Arrows indicate each particle. (A) High-density immunogold particles are distributed in the large columnlike secretory cell (LCSC), excretory duct (ED), and cuticle(C); (B) high-density immunogold particles are shown in the secretory cell (SC), excretory duct (ED), and cuticle; (C) immunogold particles are distributed in the excretory duct (ED); (D) high-density particles are displayed in the microvilli of the intestine (MI); (E) immunogold particles are shown in the excretory duct; and (F) high-density immunogold particles are distributed in the cuticle(C).
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