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Ocular Toxocariasis


Key Concepts

  • Toxocariasis is a zoonotic infection caused by the roundworms Toxocara canis and Toxocara cati.

  • Although ocular toxocariasis is relatively uncommon, it mostly affects young children and frequently causes permanent vision loss, including blindness.

  • The diagnosis is predominantly based on clinical findings and exposure to puppies or kittens.

  • Enzyme-linked immunosorbent assay (ELISA) is the most reliable and readily available test for the evaluation of antibodies directed against this organism and may be helpful in the diagnosis of the disease.

  • Most Toxocara infections are self-limiting and resolve without therapy.

  • Corticosteroids may be useful to control inflammation in infected tissues, including the eye, lungs, heart, and central nervous system (CNS).

  • Although the use of available anthelmintic drugs, including albendazole and mebendazole, have not been conclusively shown to alter the course of the disease, the combination of anthelmintics and corticosteroids appears useful in some cases of ocular toxocariasis.

  • Surgery may be useful in treating ophthalmic complications of infection, including retinal detachment.

  • Prevention is the best approach. Routine deworming of pets and avoidance of contaminated areas are warranted.

Ocular toxocariasis is a zoonotic infection that is caused by the roundworms Toxocara canis and Toxocara cati. Humans become infected with Toxocara by ingesting embryonated eggs that can be shed in the feces of infected dogs and cats. The roundworms can cause damage as they migrate through the tissues in the body, and the resultant disease has been termed larva migrans syndrome. Other parasitic worms that can cause larva migrans syndrome include Ascaris suum. T. canis, T. cati, and A. suum. These are all large intestinal roundworms that belong to the family Ascarididae. In addition to causing similar clinical diseases in humans, they share biological features that cause similar risk factors for infection.

Life Cycle

T. canis is an ascarid that can only complete its life cycle in the dog. Fig. 17.1 shows the life cycle of Toxocara species. Toxocara can follow a direct (single host) or indirect (multiple host) life cycle. An adult dog can acquire the infection by ingesting eggs with stage I encapsulated larvae that are found in the soil; by ingesting second-stage larvae from infected meat from animals, such as mice or rabbits; or by ingesting advanced-stage larvae from the feces of prenatally infected pups. In some parts of the United States, toxocariasis is found in 100% of puppies less than 6 months of age. Eggs in the intestine will ultimately hatch, and the larvae will migrate out of the intestine to all parts of the body. Most of the eggs will encyst as stage II larvae and not develop further. However, pregnancy can reactivate some of these dormant larvae, allowing them to re-enter the bloodstream and pass through the placenta to infest the growing pups. At birth, the larvae will migrate to the lungs and reach stage III. These can be coughed up and then swallowed, whereupon these larvae develop into stage IV eggs that then develop into the adult worm. These adult worms lay massive numbers of eggs that pass out of the host in feces.

Fig. 17.1, Life cycle of Toxocara. Toxocara spp. can have a direct (one host) or indirect (multiple host) life cycle. Unembryonated eggs are shed in the feces of the definitive host (canids: T. canis; felids: T. cati ). Eggs embryonate over a period of 1 to 4 weeks in the environment and become infective, containing third-stage (L3) larvae. After ingestion by a definitive host, the infective eggs hatch, and larvae penetrate the gut wall. In younger dogs (T. canis) and in cats (T. cati), the larvae migrate through the lungs, bronchial tree, and esophagus, where they are coughed up and swallowed into the gastrointestinal tract; adult worms develop and oviposit in the small intestine. In older dogs, patent (egg-producing) infections can also occur, but larvae more commonly become arrested in tissues. Arrested larvae are reactivated in female dogs during late gestation and may infect pups by the transplacental (major) and transmammary (minor) routes; in the small intestine of the pup, adult worms become established. In cats, T. cati larvae can be transmitted via the transmammary route to kittens if the dam is infected during gestation, but somatic larval arrest and reactivation do not appear to be important as in T. canis. Toxocara spp. can also be transmitted indirectly through ingestion of paratenic hosts. Eggs ingested by suitable paratenic hosts hatch, and larvae penetrate the gut wall and migrate into various tissues, where they encyst. The life cycle is completed when definitive hosts consume the larvae within the paratenic host tissue, and the larvae develop into adult worms in the small intestine. Humans are accidental hosts and become infected by ingesting infective eggs or undercooked meat/viscera of infected paratenic hosts. After ingestion, the eggs hatch, and larvae penetrate the intestinal wall and are carried by the circulation to a variety of tissues (liver, heart, lungs, brain, muscle, eyes). Although the larvae do not undergo any further development in these sites, they can cause local reactions and mechanical damage that causes clinical toxocariasis.

Humans can then be infected when they ingest soil, food, or other materials contaminated by the eggs. Once in the human intestine, the stage II larva will enter the bloodstream, migrating throughout the body until the vascular lumen becomes small enough to block its progress. At this point, the larva bores into the tissue and encysts. In addition to the eye, Toxocara cysts are frequently found in the brain, liver, and lungs. Because the larvae cannot migrate out of the tissue, the life cycle ends at the stage II larval state, and Toxocara eggs are not found in the feces of infected persons.

The encysted larvae may stay dormant without causing any clinically overt symptoms, even when present in large numbers. However, two clinical syndromes have been well described: visceral larva migrans and ocular toxocariasis.

T. cati has a life cycle similar to that of T. canis (see Fig. 17.1 ). Humans usually become infected either by contact with eggs in contaminated litter boxes or by petting the infected animals and then touching the mouth because the eggs can adhere to the animal’s fur. Clinical signs of T. cati in the cat include vomiting, decreased appetite, and stunted growth; however, mild infections with small numbers of worms may have no obvious signs or symptoms. Ocular disease caused by T. cati is similar to that caused by T. canis.

Epidemiology

Toxocara infection is one of the most common zoonotic infections worldwide, but because most infections are asymptomatic, it remains relatively unknown to the public and is often overlooked by clinicians. The first nematode infection of the eye was reported by Calhoun, in 1937, who observed a larva in the anterior chamber of an 8-year-old boy; and that the larva was ultimately was resorbed. The description of the organism led to its being considered an ascarid. In 1950, Wilder described endophthalmitis caused by nematodes, and Nichols subsequently identified T. canis as the etiologic factor.

Toxocara spp. can be found across the globe. Seropositivity varies widely by study and geographic area. In one study, seropositivity to Toxocara in adults on the island of Réunion was reported to be 92.8%. Human disease caused by Toxocara has been reported in countries worldwide, with most cases occurring in France, Austria, India, Japan, Korea, China, the United States, and Brazil. In this review, the authors stated that 823 cases of ocular toxocariasis had been reported. Over a 20-year period, at the Francis I. Proctor Foundation at the University of California, San Francisco, of the 22,185 cases encountered, 22 were diagnosed with ocular toxocariasis ( Table 17.1 ). In a study of school children, the prevalence of consultant-diagnosed ocular toxocariasis was 6.6 cases per 100,000 persons. It should be mentioned here that another member of the Ascarididae family, T. cati, also needs to be considered in the differential diagnosis.

TABLE 17.1
Demographics and Other Information on Toxocara Patients Seen at the Proctor Foundation, University of California, San Francisco
From Stewart JM, Cubillan LD, Cunningham ET, Jr. Prevalence, clinical features, and causes of vision loss among patients with ocular toxocariasis. Retina . 2005;25:1005–1013, with permission.
Variable Finding
Sex (%)
Male 10 (45.5)
Female 12 (54.5)
Ethnicity (%)
Non-Hispanic, white 15 (68.1)
Hispanic 3 (13.6)
Asian 4 (18.1)
Residence (%)
United States 20 (90.9)
California 18 (81.8)
International 2 (9.1)
Ophthalmologist Referral (%) 22 (100)
Puppy/kitten Exposure (%) 18 (81.8)
Mean/median age at presentation in years (range)
All patients 16.5/14 (1–37)
Male 15.3/11.5 (3–34)
Female 17.4/17.5 (1–37)
Mean/median time from onset to presentation in months (range)
All patients 18.8/5.5 (< 1–212)
Male 7.9/6.3 (< 1–22)
Female 28/5.5 (< 1–212)

T. canis and T. cati are very common parasites of most domestic and peridomestic dogs and cats, with even higher rates of infection found in puppies and kittens. The incidence of infected puppies has been estimated to vary: 33% in London; 98% in Columbus, Ohio; and 100% in Brisbane, Australia. In one case-control study comparing patients with visceral larvae migrans (VLM) with age- and sex-matched control subjects, 23 of the 24 patients had dogs in their homes some time before their illness, and there was a significant association between puppies in the household within 1 year of symptoms and VLM. Having a litter of puppies in the home was identified as a significant risk factor for toxocariasis. In a study by Good et al., dog ownership in the past 2 years, convulsion, and geophagia were identified as risk factors for toxocariasis ( Table 17.2 ).

TABLE 17.2
Risk Factors for Toxocariasis in a European Population
From Good B, Holland CV, Taylor MR, et al. Ocular toxocariasis in schoolchildren. Clin Infect Dis . 2004;39(2):173–178, with permission.
Factor Patients, n/N (%) a Controls n/N (%) a OR (95% CI) P
Dog ownership ever 10/11 (90.9) 24/44 (54.5) 7.6 (0.97–394.4) 0.0552
Cat ownership ever 4/9 (44.4) 22/44 (50) 0.55 (0.05–4.2) 0.8214
Bird ownership ever 3/9 (33.3) 8/44 (18.2) 2.2 (0.31–12.7) 0.5248
Dog ownership in the past 2 years 9/11 (81.8) 18/44 (40.9) 5.5 (1.04–56.1) 0.0422
Cat ownership in the past 2 years 4/8 (50) 20/44 (45.5) 0.82 (0.08–6.7) 1
Bird ownership in the past 2 years 3/8 (37.5) 4/44 (9.1) 4.1 (0.54–28.1) 0.1884
Wheezing in the past 12 months 4/11 (36.4) 8/44 (18.2) 2.5 (0.43–13.3) 0.3687
Asthma 3/11 (27.3) 3/44 (6.8) 8.9 (0.62–498.4) 0.1312
Eczema 1/11 (9.1) 4/44 (9.1) 1 (0.02–14.1) 1
Hay fever 3/11 (27.3) 7/44 (15.9) 2.3 (0.25–20.0) 0.6149
Convulsion 4/10 (40) 1/44 (2.3) 16 (1.58–788) 0.0134
Geophagia 5/9 (55.6) 4.44 (9.1) 8.2 (1.4–62.2) 0.0183
Additional matching factors were age, sex, and urban/rural residence (patients, n = 11; controls n = 44).

a Number positive for the factor/replying to the question.

Parks, playgrounds, and yards frequented by dogs and cats are common sources for Toxocara infection. In addition, increasing populations of semiwild cats and dogs are contributing to high levels of Toxocara eggs in the environment. Preventing dog and cat feces being deposited in play areas appears to be the best way to control infection. Routine deworming of pets and nonferal cats and dogs are also important health measures to limit human exposure.

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