Pediatric Toxocariasis

Updated: Mar 10, 2015
  • Author: Germaine L Defendi, MD, MS, FAAP; Chief Editor: Russell W Steele, MD  more...
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Overview

Background

Toxocariasis is caused by Toxocara canis (T. canis) and, less frequently, Toxocara catis (T. catis), which are intestinal nematodes (roundworms) found in dogs and cats, respectively. In humans, toxocariasis is considered an aberrant infection because humans are incidental hosts, as the parasites cannot successfully reach full maturity in the human body. Instead, the invasive larvae migrate for months through different organs until they are overcome by the human inflammatory reaction and die. The larvae can survive in tissues for at least 9 years and, possibly, for the entire life of the host.

Three clinical forms of toxocariasis are traditionally described; these are visceral larva migrans (VLM), ocular larva migrans (OLM), and covert toxocariasis (common toxocariasis). [1] A constellation of differing disease manifestations have been attributed to each of these clinical forms. [2]

Diagnosis is based on clinical and serologic findings. In addition to enzyme-linked immunosorbent assay (ELISA), polymerase chain reaction (PCR) is being researched as a possible diagnostic tool. Stool examination for Toxocara larvae is not a helpful diagnostic test for toxocariasis. Whether or not the infection should be treated and, if so, when and how it should be treated is controversial. The anthelmintic agents, mebendazole, thiabendazole, albendazole, and diethylcarbamazine, are medication options used in treatment. Corticosteroids also have a significant role in therapy. See the images below.

Diagram of the Toxocara canis life cycle image. Co Diagram of the Toxocara canis life cycle image. Courtesy of the Centers for Disease Control and Prevention.

Toxocara canis eggs are passed in dog feces, espe Toxocara canis eggs are passed in dog feces, especially puppies' feces. Humans do not produce or excrete eggs; therefore, the presence of these eggs is not a diagnostic finding in human toxocariasis. The egg to the left is fertilized but not yet embryonated, whereas the egg to the right contains a well-developed larva. The latter egg is infectious if it is ingested by a human (frequently, a child). Courtesy of the Centers for Disease Control and Prevention.
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Pathophysiology

Most frequently, human toxocariasis is caused by T. canis, a nematode roundworm of the family Ascaridae. Adult T. canis female worms are usually found in young puppies and lactating female dogs. The adult T. canis female worms can excrete as many as 200,000 eggs per day. These eggs require about 2 to 5 weeks of optimal environmental conditions (temperatures of 10-35°C, high soil humidity) to develop from a noninfective unembryonated form to an infective embryonated egg. Embryonated eggs are resistant to freezing, moisture, and extreme pH levels.

When a dog ingests infective eggs, the eggs hatch into larvae in the proximal small intestine. The larvae then penetrate the intestinal wall, and gain access to the blood and lymphatic circulation. The larvae invade the dog’s liver, lungs, and other tissues. In most dogs, the larval maturation process is arrested in most tissues. However in the pregnant female, T. canis continues developing and migrates across the placenta, infecting canine fetuses. After the birth of the puppies, the larvae continue to mature migrating from the lungs to the gastrointestinal tract via the trachea. The larvae reach maturity in the puppies' intestinal tracts. Post-partum, the lactating female dog is re-infected while caring for her young. Therefore, the primary sources of T. canis eggs are puppies less than 3 months old and lactating female dogs.

Humans are paratenic hosts for T. canis. Paratenic hosts are transport hosts in which the larvae never mature into adult worms. The infection is acquired through ingestion of soil containing infective T. canis eggs. Theseeggs are found in areas where dogs defecate, such as playgrounds, outdoor public areas and dog parks. As much as 20-30% of soil samples from public parks and children's sandboxes are contaminated with Toxocara eggs. Infections acquired through ingestion of raw snails and raw lamb have also been reported.

The cat roundworm, T. catis, has a similar life cycle to T. canis. A noted difference is that vertical transmission is due to lactation more than transplacental transmission. Humans are paratenic hosts; however, there have been some cases reported of mature worm T. catis intestinal infections in children. Overall, T. catis causes fewer cases of human infection than T. canis, probably due to the defecation patterns of cats, which make environmental infestation less frequent. As such, this article focuses on T. canis infections.

Tissue damage in Toxocariasis is due to the host inflammatory reaction more than the infection itself. The larvae produce glycosylated proteins, usually referred to as Toxocara excretory-secretory (TES) antigens. These antigens induce a Th2-type CD4+ T-cell immune response characterized by production of interleukin 4 (IL-4) that promotes the switching of B-cell isotypes to the production of immunoglobulin E (IgE) and interleukin 5 (IL-5). These, in turn, promote eosinophil differentiation and vascular adhesion.

Although Toxocara organisms are the most common causes of visceral larva migrans (VLM) syndrome, case reports have cited other zoonotic nematodes that cause VLM, including Ascaris suum, [3] Baylisascaris procyonis (raccoon ascarid), and Lagochilascaris minor (opossum ascarid).

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Epidemiology

Frequency

T. canis infections occur in canine animals throughout the world, as confirmed by seroepidemiologic studies. The prevalence of seropositivity varies not only from country to country but also in different regions within a country. [4] The real prevalence of toxocariasis is difficult to estimate because serologic diagnostic tests are performed only when the diagnosis is suspected, and most human Toxocara infections are asymptomatic.

United States

Toxocariasis is a public health problem. The prevalence of infection in different communities is directly proportional to the infection rates among canines and the free access of dogs to public places. Obviously, the higher the rate of infected dogs and the easier their access to public places, the more easily humans are exposed to infective eggs. Because eggs need weeks in the soil to become infective, direct contact with young puppies is not a risk factor for acquiring disease. Young children are at higher risk because of their play habits and their tendency to have oral behaviors such as putting their fingers in their mouths. Children with geophagic pica (the compulsion to consume earth, soil, or clay), children who have contact with puppy litters, and children who are mentally challenged with abnormal oral behaviors are particularly at risk. In tropical climates, clay soil types, warm temperature and humidity favor the embryonization and viability of Toxocara eggs.

In the United States, the seroprevalence of children, as measured with enzyme-linked immunosorbent assay (ELISA) that employs TES antigens, varies from 4-8%. Seroprevalence is higher in Puerto Rico and the southeastern states and then in the western, mid-western and mid-Atlantic states. Black and Latino peoples have rates of 16-30%. Prevalence is also higher in underserved urban areas of the United States. [5] Immigrants from Latin America are also at risk for VLM. [6]

International

The prevalence of human toxocariasis in tropical regions of the world is higher than in the United States. [7, 8, 9, 10, 11, 12] The highest seroprevalence ever recorded was in a village of Santa Lucia, West Indies. Here, the prevalence was 86% in children aged 6 months to 6 years. This community had an extraordinarily high rate of T. canis infection explained by peridomestic areas contaminated with canine waste and geophagic pica behavior among children. Serologic surveys in different countries reveal seropositivity rates of 19% in the Netherlands, 2.5% in Germany, 39% in Brazil, 5.8-36% in the Czech Republic, 0-37% in Spain, 5.2% in Cuba, [13, 14] 10.9 % in Jordan, 47.5% in Colombia, 81% in Nepal, and 13% in the Slovak Republic. [15]

A study conducted in a tropical region of Venezuela illustrates the greater risk for disadvantaged sectors of society in acquiring this infection. [16] In this study, only 1.8% of middle-class urban subjects had positive findings, compared with 20% of urban-slum dwellers, 25% of rural farmers, and 35% of Amazon Indians. In Bolivia, toxocariasis was thought to be a significant cause of epilepsy, particularly partial epilepsy.

In an epidemiological, cross-sectional study in 252 schoolchildren (ages 1-12 years old) in Brazil, seroprevalence of IgG anti-Toxocara antibodies was found to be 15.5%. An ELISA test based on TES antigens was used to determine outcomes. Geophagic pica was associated with increased prevalence. Thorough hand-washing before meals was associated with decreased seroprevalence. [17]

Mortality/Morbidity

Although sudden death due to T. canis infestation has been reported, mortality is unusual. The major morbid condition is decreased visual acuity caused by ocular larva migrans (OLM). Evidence suggests that toxocariasis may be a causative factor for allergic asthma.

Sex

Boys usually have higher seroprevalence than girls. This is probably related to differences in play behavior.

Age

Individuals of all ages are at risk. VLM associated with severe symptoms occurs mainly in young children, age 18 months to 3 years old. Children within this age group who engage in geophagic pica have greater risk in an environment contaminated with Toxocara eggs. The infective worm burden along with the host response, determines the level of infestation and disease severity. [18] Overall, VLM is diagnosed primarily in children, age 1-7 years. OLM occurs more often in older children, adolescents and young adults.

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