Background
Toxocariasis is caused by Toxocara canis and, less frequently, Toxocara 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, and the parasites cannot completely mature 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 life of the host.
Three clinical forms of toxocariasis are traditionally described; these include visceral larva migrans (VLM), ocular larva migrans (OLM), and covert toxocariasis. Numerous disease manifestations have also been attributed to these parasites.
Diagnosis is based on serologic findings. Polymerase chain reaction (PCR) has been introduced as a diagnostic tool. Examination of stools has no role in the evaluation of toxocariasis. Whether or not the infection should be treated and, if so, when and how it should be treated is controversial. Mebendazole, thiabendazole, albendazole, and diethylcarbamazine, among others, are agents used in the treatment. Corticosteroids also have a significant role in therapy. See the images below.
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, 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. Pathophysiology
Most frequently, human toxocariasis is caused by T canis, a canine roundworm. 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 need several weeks of optimal environmental conditions (10-35°C, high soil humidity) to develop from noninfective unembryonated forms to infective embryonated eggs. The embryonated eggs are resistant to freezing, moisture, and extreme pH levels.
When a dog ingests the infective eggs, the larvae hatch in the small intestine, penetrate the intestinal wall, and gain access to the blood and lymphatic circulation. The larvae invade the liver, lungs, and other tissues. In most dogs, the larval maturation process is arrested in most tissues, but in a pregnant female, T canis resumes development and migrates across the placenta, infecting the fetus. After the birth of the puppies, the larvae continue their maturation process, migrating from the lungs to the GI tract via the trachea; they achieve their mature forms in the puppies' intestinal tracts. Female dogs then become reinfected while caring for their puppies. The main sources of eggs, therefore, are puppies younger than 3 months and lactating female dogs.
Humans are paratenic hosts for T canis. Paratenic hosts are transport hosts in which the larvae never develop into adult worms. The infection is acquired by ingesting T canis embryonated eggs. Sources of these eggs include areas where dogs defecate, such as parks. As much as 20-30% of soil samples from public parks and children's sandboxes are contaminated with Toxocara eggs. Infections acquired by ingestion of raw snails and raw lamb have also been reported.
The cat roundworm, T catis, has a life cycle similar to that of T canis except that vertical transmission is due to lactation more than transplacental transmission. One report documents 4 cases of adult T catis intestinal infection in children. However, in most cases, humans are paratenic hosts. T catis causes fewer cases of human infection than T canis, probably because of the defecation patterns of cats, which make environmental infestation less frequent.
Tissue damage is due to the host inflammatory reaction more than the infection itself. The larvae produce glycosylated proteins, usually referred to as Toxocara excretory secretory antigens. These antigens induce a Th2-type CD4+ cellular immune response characterized by the production of interleukin 4 that promotes the switching of B-cell isotypes to the production of immunoglobulin E (IgE) and interleukin 5. These, in turn, promote eosinophil differentiation and vascular adhesion.
Although Toxocara organisms are the most common causes of VLM, case reports have noted other zoonotic nematodes that cause VLM, including Ascaris suum,[1] Baylisascaris procyonis (raccoon ascarid), and Lagochilascaris minor (opossum ascarid).
Epidemiology
Frequency
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 tendency to place their fingers in their mouths. Children with pica (geophagia) and children who have contact with puppy litters are particularly at risk, as are children with mental retardation. In tropical climates, the high temperature and humidity favor the embryonization of eggs.
The prevalence of seropositivity varies not only from country to country but also in different regions within a country. The real prevalence of toxocariasis is difficult to estimate because tests are performed only when the diagnosis is suspected, and most infections are asymptomatic. The seroprevalence of children, as measured with enzyme-linked immunosorbent assay (ELISA), varies from 4-8%. Seroprevalence is higher in the southeastern United States and Puerto Rico. Minorities, such as black and Hispanic groups, have rates as high as 16-30%. Immigrants from Latin America are also at risk for VLM.[2]
International
The prevalence of human toxocariasis in tropical regions is higher than that in the United States.[3, 4, 5, 6, 7, 8] The highest seroprevalence ever recorded was in a village of Santa Lucia, West Indies, where the prevalence was 86% in children aged 6 months to 6 years. This community had an extraordinarily high rate of canine T canis infection combined with peridomestic areas contaminated with canine waste and pica habits among the 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, 10.9 % in Jordan, 47.5% in Colombia, 81% in Nepal, and 13% in the Slovak Republic.[9]
An interesting study in Venezuela stresses the higher risk of the disadvantaged sectors of society for acquiring the infection.[10] 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 one of the causes of the higher prevalence of epilepsy, particularly partial epilepsy.
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 OLM. Evidence suggests that toxocariasis may be one of the causative factors of allergic asthma.
Race
No racial predilection has been noted.
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. Although the seroprevalence increases with age, VLM with more severe symptoms occurs mainly in young children. VLM is diagnosed mainly in children aged 1-7 years. OLM is more common in older children and young adults.
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