Clinical Overview of Toxocariasis

Disease

The manifestations of toxocariasis reflect the number of migrating Toxocara larvae, where the larvae have migrated in the body, and the degree of immune response and inflammation that developed in response to the presence of the larvae. Many infections are asymptomatic.

In heavy infections, large numbers of larvae may migrate through the liver, lungs, or other internal organs, causing inflammation and symptomatic disease (visceral toxocariasis or VT). Rarely, larvae may migrate to the central nervous system (CNS) causing eosinophilic meningoencephalitis or granuloma formation in the CNS.

Signs of VT may include:

• Fever
• Cough
• Wheezing
• Abdominal pain
• Hepatomegaly

Peripheral eosinophilia is often present.

Visceral toxocariasis has been proposed as a cause of asthma; however, there may be multifactorial causes of asthma and further study is needed to establish a causative link between toxocariasis and asthma.

Typically, ocular toxocariasis (OT) is a unilateral disease when a larva penetrates a single eye. Common signs are associated with granulomatous inflammation especially in the retina, uveitis, and/or chorioretinitis. Patients can present with leukocoria and decreased vision in the affected eye which may be confused with retinoblastoma. Diffuse unilateral subacute neuroretinitis or vitreal bands may develop.

Diagnosis

Diagnosis of either visceral toxocariasis or ocular toxocariasis is based on the presence of signs of VT or OT and history of exposure to a potential source of infectious Toxocara eggs or larvae (e.g., in undercooked infected meat or offal). The diagnosis of visceral toxocariasis is based on compatible disease and exposure history with positive results by serological testing.

The currently recommended test is an enzyme-linked immunosorbent assay (ELISA) with larval stage antigens. Usually excretory/secretory antigens are released when infective Toxocara larvae are cultured. The specificity of this assay is good, although cross-reactivity with antibody to the human roundworm, Ascaris lumbricoides, is possible. Assays employing Toxocara excretory/secretory antigens minimize this problem.

Positive serological results should be interpreted with consideration of the patient's clinical status. Detectable antibody may be the result of infection in the past. Also, seropositivity can be present in asymptomatic Toxocara infection. Paired serum samples demonstrating a significant rise in antibody level over time may be useful to confirm active infection.

In ocular toxocariasis, Toxocara antibody levels in serum can be low or absent despite clinical disease. In some cases, Toxocara antibody can be detected in the aqueous or vitreous fluid samples from the affected eye and may be due to local antibody production or leakage of antibody from the circulation. The ocular fluid sample may be tested at a lower dilution than serum to improve ELISA sensitivity.

Signs and symptoms of VT or OT can also be caused by the migrating larvae of other helminths, including Baylisascaris procyonis (both VT and OT), Strongyloides spp. (VT), and Paragonimus spp. (VT).

Careful attention to disease course, exposure history and serological testing can be useful for differential diagnosis. For OT, if a larva is visualized in the eye, measuring size may help differentiate the larger larvae of Baylisascaris from Toxocara or other larvae.

Treatment and recovery

Treat visceral toxocariasis with antiparasitic drugs such as albendazole or mebendazole. Treatment of ocular toxocariasis is more difficult and usually consists of measures to prevent progressive damage to the eye. See Clinical Care and Treatment of Toxocariasis for more information.