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.

REFERENCES

Glickman, LT, Cypess, RH. Toxocara infection in animal hospital employees. Am J Public Health
1977; 67:1193. Mok, CH. Visceral larva migrans. A discussion based on review of the literature. Clin
Pediatr (Phila) 1968; 7:565. Schantz, PM, Glickman, LT. Toxocaral visceral larval migrans. N Engl J
Med 1978; 298:436. Huntley, CC, Costas, MC, Lyerly, A. Visceral larva migrans syndrome: Clinical
characteristics and immunologic studies in 51 patients. Pediatrics 1965; 36:523. Snyder, C. Visceral
larva migrans — ten years' experience. Pediatrics 1961; 28:85. SHRAND, H. VISCERAL LARVA
MIGRANS. TOXOCARA CANIS INFECTION. Lancet 1964; 18:1357. Sakai, S, Shida, Y, Takahashi, N, et
al. Pulmonary lesions associated with visceral larva migrans due to Ascaris suum or Toxocara canis:
imaging of six cases. AJR Am J Roentgenol 2006; 186:1697. Beshear, JR, Hendley, JO. Severe
pulmonary involvement in visceral larva migrans. Am J Dis Child 1973; 125:599. Good, B, HOlland,
CV, Taylor, MR, et al. Ocular toxocariasis in schoolchildren. Clin Infect Dis 2004; 39:173. Stewart,
JM, Cubillan, LD, Cunningham, ET Jr. Prevalence, clinical features, and causes of vision loss among
patients with ocular toxocariasis. Retina 2005; 25:1005. Chuah, CT, Lim, MC, Seah, LL, et al.
Pseudoretinoblastoma in enucleated eyes of Asian patients. Singapore Med J 2006; 47:617. Marx,
C, Lin, J, Masruha, MR, et al. Toxocariasis of the CNS simulating acute disseminated
encephalomyelitis. Neurology 2007; 69:806. Cypess, RH, Karol, MH, Zidian, JL, et al. Larva-specific
antibodies in patients with visceral larva migrans. J Infect Dis 1977; 135:633. Jones, WE, Schantz,
PM, Foreman, K, et al. Human toxocariasis in a rural community. Am J Dis Child 1980; 134:965.
Despommier. Toxocariasis: Clinical Aspects, Epidemiology, Medical Ecology, and Molecular
Aspects. Clin Microbiol Rev 2003, 16:265. Roig, J, Romeu, J, Riera, C, et al. Acute eosinophilic
pneumonia due to toxocariasis with bronchoalveolar lavage findings. Chest 1992; 102:294.
Ishibashi, H, et al. Hepatic granuloma in toxocaral infection: Role of ultrasonography in
hypereosinophilia. J Clin Ultrasound 1992; 20:204. Jain, R, Sawhney, S, Bhargava, DK. Hepatic
granulomas due to visceral larva migrans in adults: Appearance on US and MRI. Abdom Imaging
1994; 19:253. Zachariah, SB, Zachariah, B, Varghese, R. Neuroimaging studies of cerebral "visceral
larva migrans" syndrome. J Neuroimaging 1994; 4:39. Eberhardt, O, Bialek, R, Nagele, T, Dichgans,
J. Eosinophilic meningomyelitis in toxocariasis: case report and review of the literature. Clin Neurol
Neurosurg 2005; 107:432.

© 2009