Visceral Larva Migrans (toxocariasis)

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