Toxocariasis is one of the most common
human helminth infections in North America and Europe, with the
highest occurrence among disadvantaged minority populations.1-3 There
are 3 major forms of the disease: visceral larva migrans (VLM),
ocular larva migrans (OLM), and covert toxocariasis.
VLM and OLM are usually caused by helminth larvae of dogs and cats
that ordinarily cannot complete their life cycle in humans (eFig. 331.1).
Migrating larvae of zoonotic ascarids may be associated with significant
pathology by wandering through extraintestinal viscera, causing
tissue necrosis and provoking eosinophilic granulomatous inflammation.
The clinical syndrome of VLM and OLM are most commonly caused by
larvae of the dog ascarid Toxocara canis and, less
frequently, the cat ascarid T cati. Covert toxocariasis
refers to infection with either T canis or T
cati that results in either asymptomatic infection or infection
associated only with asthma and wheezing.2 Seroprevalence
surveys show presence of antibody in up to 50% of African
American and Hispanic children living in poverty in the United States.1-3 Infection
is common in both urban and rural areas, and some studies have linked
environmental exposure to Toxocara larvae as a
contributor to asthma.2,3
Adult Toxocara live in the dog’s small
intestine and are 8 to 12 cm long. The ova are deposited with the
dog’s feces and become infective in approximately 2 weeks.
If swallowed by young dogs, second-stage larvae hatch in the small
intestine, penetrate the intestinal wall, and migrate through canine
tissues where they can undergo arrested development. Some larvae
return to the small intestine, where they mature, mate, and oviposit.
Arrested larval development more often occurs in female dogs than
males, and the dormant larvae in tissues can migrate transplacentally
(or possibly enter the mammary tissues) and thereby serve as a source
of perinatal and postnatal infection in puppies. In the United States,
large numbers of newborn puppies are infected and pose a health
risk to those who handle them.
In humans, most infections have been reported in young children
1 to 4 years of age with a history of pica, especially geophagy.
After a human ingests the embryonated egg, a second-stage larva
emerges in the small intestine, penetrates the intestinal wall,
and initiates somatic migration that may last for many weeks or
The liver and lungs are most often involved with Toxocara, the
former probably because of the mesenteric venous portal drainage.
Tissue granulomas consist of many eosinophils and histiocytes, with
an occasional multinucleated foreign-body giant cell in an area
of necrosis. A portion of a second-stage larva also may be evident.
Granulomas can also be found in lung, kidney, lymph node, eyes,
brain, heart, and skeletal muscle. The syndrome produced by granulomas
from toxocariasis in the eye is termed ocular larva migrans.
In Ireland the incidence of ocular larva migrans has been estimated at
9.7 per 100,000 persons.4
In visceral larva migrans and covert toxocariasis clinical presentations
vary from eosinophilia discovered by chance in an asymptomatic patient
to fever, hepatomegaly, hyperglobulinemia, and marked eosinophilia.
Many infections are subclinical. Some children have pulmonary symptoms
(notably wheezing and rhonchi), signs of myocarditis, cutaneous
nodules, or urticaria. Some children exhibit central nervous system
disease, manifested as either cerebritis or epilepsy, a result of
larvae migrating through the brain.2 The acute
phase may last 2 to 3 weeks, and in some cases the resolution of
eosinophilia and clinical symptoms may take as long as 18 months.
Ocular larva migrans is more common among older children (school-aged
and adolescents). The most dramatic symptoms are due to retinal pathology
and include visual changes, strabismus, and retinal detachment.
Diagnosis usually is made based on a combination of clinical
features and serologic tests. Close association with a dog or cat frequently
is disclosed by history, and a history of pica is commonly elicited
with visceral larva migrans, but not ocular larva migrans. A persistently
elevated eosinophil count, a moderate to high increase in gamma
globulin, and elevated erythrocyte sedimentation rate all support
the diagnosis. If the patient is not blood type AB, one of the antihemagglutinins (anti-A
or anti-B) usually is increased, because Toxocara larvae contain
surface antigens that stimulate isohemagglutinin production. An
enzyme-linked immunoassay for Toxocara antibodies
in serum is available through the Centers for Disease Control and
Prevention (CDC) and through some private laboratories. This assay
detects both IgM and IgG, and the CDC assay is reported to have
a sensitivity of 85% and a specificity of 92%.
Patients with visceral toxocariasis usually have elevated titers
(1:1024), but those with ocular disease alone may have low or absent
antibody titers. Therefore, ocular larva migrans is most frequently
diagnosed on the basis of characteristic lesions seen on fundoscopy.
Larvae may be detected in biopsy specimens, although most patients
do not require surgical procedures for diagnosis. Occasionally,
migrating larvae may also be seen in the retina.
Albendazole is the treatment of choice for visceral larva migrans.5 The
drug should be used with caution because of potential toxicity from
allergic responses to dying parasites. Although mebendazole is commonly
used to treat a number of human helminth infections, the drug is
poorly absorbed from the gastrointestinal tract and therapeutic
levels of the drug are often inadequate to treat the tissue-dwelling
larvae that cause toxocariasis. The benefit of albendazole in the
treatment of covert toxocariasis has not been established. The management
and treatment of ocular larva migrans should be done in consultation
with an ophthalmologist and will often require local use of steroids
or surgical modalities. The benefit of specific anthelminthic therapy
with albendazole for treating ocular larva migrans has not been
established, particularly given the exacerbation of host inflammation
that could result. All dogs and cats should be dewormed periodically.
Puppies and kittens should be dewormed at 2, 4, 6, and 8 weeks of
age, because they usually are heavily infected.