Visceral Larva Migrans (Toxocariasis)

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No me explico hasta ahora porque en las evaluaciones prequirurgicas se sigue pidiendo examenes parasitologicos en heces cuando un hemograma nos alerta sobre una hipereosinofilia. Sabemos desde la poca de estudiantes que una hipereosinofilia (numero total igual o mayor de 1,500) nos orienta hacia el diagnostico de fasciolasis, hidatidosis o toxocariasis. Provenientes de Lima un gran porcentaje de nuestros pacientes, deberamos entonces orientar el diagnostico sobre esta ltima patologa. En nuestro hospital solicitamos Ig G antitoxocara. Les dejo con una revisin U-P-T-O-D-A-T-E 2009 y a reorientar diagnosticos.

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  • 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

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    2009