Visceral Larva Migrans (Toxocariasis)
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DESCRIPTIONNo 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.
Visceral larva migrans (TOXOCARIASIS)
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
 . Thus, visceral larval migrans is principally a disease of children one to five years old, especially
those with a history of geophagus pica  .
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  .
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
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  .
More severe respiratory tract involvement is an uncommon complication of very heavy infection
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  . 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  . The
ocular lesions may resemble retinoblastomas  . (See "Evaluation and management of
strabismus in children").
Other organs systems can also be involved, including the heart and the central nervous system
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  . 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  .
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  .
TREATMENT AND PROGNOSIS Visceral larva migrans is self-limited, subsides slowly, and
requires no therapy in the absence of continuing reinfection  . 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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