Toxocariasis

Ocular toxocariasis (OT) is a zoonotic infection caused by Toxocara canis and Toxocara cati. Dogs and cats, the definitive hosts of the roundworm, pass unembryonated eggs via their feces into the environment (often into the soil). According to the CDC, 30% of dogs younger than 6 months may deposit Toxocara eggs in their feces, and 25% of cats are infected with Toxocara cati. After 2–4 weeks, those eggs embryonate and become infectious. Transmission to humans occurs through ingestion of soil or contaminated food, or the fecal–oral route. Exposure to playgrounds, sandboxes, kittens, and puppies, as well as the pica eating disorder, are risk factors. Rarely, humans may acquire the infection from undercooked meat. NHANES data from 2011–2014 suggested an overall seroprevalence in the United States of 5.1%. In children, an increased rate of antibody positivity correlated to lack of health insurance. The prevalence was recently estimated to be 1% of a large uveitic population treated at tertiary care centers in northern California.

The organisms grow in the small intestine, enter the portal circulation, and disseminate hematogenously. In humans, the Toxocara larvae may migrate to different parts of the body, including the liver, heart, lungs, brains, muscles, or eyes. The larvae do not undergo further development in the human but rather cause a local inflammatory reaction. Because ova are not shed in the gastrointestinal tract, stool analysis for larvae is not useful.

Visceral toxocariasis (VT) may include fever, coughing, enlarged liver, pneumonia, and meningoencephalitis. It more often affects children younger than age 3, and those patients may show peripheral eosinophilia. Ocular toxocariasis is found in older children, typically without significant eosinophilia. These infections rarely present simultaneously.

Ophthalmic presentations include a chronic endophthalmitis (25%), a posterior pole granuloma (25%; Fig 11-34), or a peripheral granuloma, sometimes with fibrous bands in the vitreous that may extend posteriorly (50%; Fig 11-35). Any of these presentations may produce leukocoria. Uncommon variants include unilateral pars planitis with diffuse peripheral inflammatory exudates, granulomas involving the optic nerve, and a diffuse unilateral subacute neuroretinitis. Table 11-2 lists the characteristics of each presentation.

Ocular toxocariasis is principally a clinical diagnosis. Serologic testing may suggest prior exposure. However, patients with OT may have negative serum serology. Antibody testing of ocular fluids may be positive despite negative serum. Polymerase chain reaction testing is not readily available. Larvae have been recovered from vitrectomy specimens (Fig 11-36). In cases of media opacity, B-scan ultrasonography and/or computed tomography may show vitreous membranes and/or tractional detachment and confirm the absence of calcium, a potential finding in retinoblastoma.

Figure 11-34 Fundus photograph showing Toxocara posterior pole granuloma causing macular pucker.

(Courtesy of H. Michael Lambert, MD, and the Retina Image Bank, American Society of Retina Specialists.)

Figure 11-35 Toxocara peripheral granuloma.

(Courtesy of Thomas M. Aaberg, MD, and Thomas M. Aaberg Jr, MD, and the Retina Image Bank, American Society of Retina Specialists.)

Table 11-2 Patterns of Manifestation of Ocular Toxocariasis

The differential diagnosis includes retinoblastoma, infectious endophthalmitis, Coats disease, familial exudative vitreoretinopathy, persistent fetal vasculature, toxoplasmosis, undifferentiated intermediate uveitis/pars/planitis, retinopathy of prematurity, combined hamartoma of the retina and RPE, and diffuse unilateral subacute neuroretinitis (DUSN). The migrating larvae of other helminths such as Baylisascaris procyonis may simulate OT. In contrast to OT, children with retinoblastoma are typically younger, lack significant inflammation, and show lesion growth.

Patients with VT are usually treated with oral albendazole. For OT, the use of antihelminthic therapy is not established but may be considered if the larvae appear active. Typically, local and systemic corticosteroids are used to reduce inflammation and minimize structural complications, which may later be amenable to vitreoretinal surgical techniques.

• Centers for Disease Control and Prevention. Ocular toxocariasis—United States, 2009–2010. MMWR. 2011;60(22):734–736.

• Farmer A, Beltran T, Choi YS. Prevalence of Toxocara species infection in the U.S.: Results from the National Health and Nutrition Examination Survey, 2011–2014. PLoS Negl Trop Dis. 2017;11(7):e0005818.

Figure 11-36 Toxocariasis. Histopathology of an eosinophilic vitreous abscess. The organism is in the center of the abscess.

• Schneier AJ, Durand ML. Ocular toxocariasis: advances in diagnosis and treatment. Int Ophthalmol Clin. 2011;51(4):135–144.

• Stewart JM, Cubillan LD, Cunningham ET Jr. Prevalence, clinical features, and causes of vision loss among patients with ocular toxocariasis. Retina. 2005;25(8):1005–1013.

• Woodhall D, Starr MC, Montgomery SP, et al. Ocular toxocariasis: epidemiologic, anatomic, and therapeutic variations based on a survey of ophthalmic subspecialists. Ophthalmology. 2012;119(6):1211–1217.

Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.