Visceral larva migrans (TOXOCARIASIS)

Authors

Peter F Weller, MD, FACP

Karin Leder, MBBS, FRACP, PhD, MPH, DTMH Section Editor

Peter F Weller, MD, FACP Deputy Editor

Elinor L Baron, MD, DTMH

Last literature review version 17.1: January 2009 | This topic last updated: October 4, 2007 (More)

INTRODUCTION — Infection with the dog ascarid, Toxocara canis, or less commonly the cat

ascarid, Toxocara catis, produces a syndrome in humans termed visceral larva migrans or

toxocariasis. This disorder may be subclinical; it also may present primarily as an ocular form or a

visceral form. Pulmonary involvement is common in the visceral form. Another form of visceral

larva migrans is caused by humans ingesting eggs of the pig ascarid, Ascaris suum.

EPIDEMIOLOGY — The reservoir for T. canis is latent infection in female dogs. The infection is

reactivated during pregnancy, and is transmitted to puppies through the placenta and in milk.

Most eggs passed into the environment are from puppies and lactating bitches. The eggs are not

infectious when initially shed in the feces of dogs and cats; after about three weeks in the soil,

however, the larvae are able to spread disease.

Human infections are acquired by ingesting Toxocara eggs. People at risk for developing infection

are not those who handle dogs or cats, but those who ingest soil containing the embryonated eggs

[1] . Thus, visceral larval migrans is principally a disease of children one to five years old, especially

those with a history of geophagus pica [2] .

Toxocara canis is common in North America as about 20 percent of adult dogs and 80 percent of

puppies are infected. Areas where dogs defecate, including public playgrounds, frequently harbor

potentially infectious ova [3] .

Ascaris suum may be prevalent on farms where pigs are raised.

CLINICAL MANIFESTATIONS — After ingestion of infectious Toxocara eggs, larvae penetrate the

gastrointestinal mucosa and are carried in the portal circulation to the liver, and then into the

systemic circulation. When larvae encounter vessels too small to allow their passage, they exit into

surrounding tissues.

The manifestations of visceral larva migrans are a consequence of both the damage produced by

migrating larvae, and the evoked eosinophilic granulomatous host response. Mild infections may

be asymptomatic and only suspected by the finding of elevated blood eosinophilia. Heavier

infections may result in malaise, irritability, fever, hepatomegaly, and pruritic cutaneous lesions.

Respiratory symptoms, including dyspnea, wheezing, and a chronic nonproductive cough are

experienced by 20 to 86 percent of children [4,5] . Rales are common on physical examination. The

chest radiograph reveals abnormalities in ≥ 40 percent of patients with symptomatic illness.

Bilateral peribronchial infiltration is most common but prominent infiltrates can also be seen [4-6]

. With both Ascaris suum and Toxocara canis, pulmonary visceral larva migrans appears on CT as

multifocal subpleural nodules with halo or ground-glass opacities and ill-defined margins [7] .

More severe respiratory tract involvement is an uncommon complication of very heavy infection

[8] .

Ocular involvement may occur as the sole manifestation of visceral larva migrans, often presenting

in those without an antecedent history of symptomatic visceral larva migrans [9] . The ocular

lesion is due to larval localization in the eye and the granulomatous response around the larva.

Common symptoms are strabismus and failing vision. The typical lesion is a whitish elevated

granuloma measuring one to two diameters and located in the posterior pole of the retina.

Occasionally, ocular larva migrans (OLM) may present as uveitis or endophthalmitis [10] . The

ocular lesions may resemble retinoblastomas [11] . (See "Evaluation and management of

strabismus in children").

Other organs systems can also be involved, including the heart and the central nervous system

[12] .

Laboratory abnormalities include elevated serum levels of IgG, IgM, and IgE. Marked leukocytosis

with eosinophilia occurs in more than 30 percent of cases, and elevated titers of anti-A or anti-B

isohemagglutinins in about 50 percent of patients. Pulmonary pathology has not been detailed,

but eosinophilic granulomas develop around the larvae in other tissues.

DIAGNOSIS — Definitive diagnosis of visceral larva migrans requires detection of larvae in biopsied

tissue. However, biopsy is rarely indicated. The diagnosis is suspected from the compatible clinical

presentation in a patient with marked leukocytosis, eosinophilia, and hypergammaglobulinemia. It

can then be confirmed by a sensitive and specific enzyme linked immunosorbent assay (ELISA)

antibody assay which can also detect subclinical or mild infections [13,14] .

ELISA antibody assays are not as reliable in the setting of OLM, which is diagnosed on the basis of

clinical criteria during an ophthalmologic examination [15] . Stool examinations are unrewarding,

since the parasite has not reached reproductive maturity at this point.

Pulmonary involvement may result in eosinophilia that is detectable in bronchoalveolar lavage

(BAL) fluid. One case of marked pulmonary infiltration, for example, revealed 64 percent

eosinophils in the BAL analysis [16] .

Ultrasonography and magnetic resonance imaging have been used to detect hepatic and cerebral

lesions [17-19] . With central nervous system involvement, the cerebrospinal fluid may show

eosinophils [20] .

TREATMENT AND PROGNOSIS — Visceral larva migrans is self-limited, subsides slowly, and

requires no therapy in the absence of continuing reinfection [3] . Anthelminthic drugs have been

used, but are of uncertain efficacy, and we do not recommend them for the majority of patients.

Deaths from myocardial or central nervous system involvement are rare. Anecdotal reports

suggest that corticosteroids may be effective in cases of severe respiratory, myocardial, or central

nervous system involvement. Patients with severe disease can be treated with albendazole (400

mg BID for five days) or mebendazole (100 to 200 mg BID for five days); both agents are approved

but considered investigational by the United States Food and Drug Administration (FDA) for the

treatment of this infection.

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