Soil-Transmitted Helminthic Zoonoses in Humans and Associated Risk Factors - Soil Contamination - page 44

et al., 2010). These zoonotic infections have significant public health implication in specific
human populations, but are not reviewed in the present work.
2. Toxocara canis and Toxocara cati
The causal agents of human toxocariasis are the ascarid nematodes (roundworms) T. canis
and T. cati , whose definitive hosts are dogs and cats, respectively. Although infection with
these parasites has been described in their usual hosts for more than 200 years, only in the
1950s were they recognized as important human pathogens. When embryonated eggs are
accidentally ingested, larvae hatch in the small intestine, penetrate the intestinal wall and
migrate via the bloodstream to the liver, lungs, muscles, eye and the central nervous system.
Although most infections are asymptomatic, two well-defined syndromes are classically
recognized in human: visceral larva migrans (VLM), a systemic disease caused by larval
migration through major organs, and ocular larva migrans (OLM), a disease limited to the
eye and optic nerve. Less severe syndromes have been described mainly in children (covert
toxocariasis) and in adults (common toxocariasis).
The genus Toxocara belongs to the order Ascaridoidea. The life cycle of T. canis is complex
(Figure 1). Infections are acquired by oral ingestion of infective stages, but also by
transplacental or transmammary routes, and may or may not include migration across the
viscera of the definitive hosts. Female worms produce up to 200,000 eggs a day, which are
shed in dog and cat feces and embryonate in the environment within 2-3 weeks, under ideal
humidity and temperature (25-30C) conditions. Akin to other ascarid eggs, fully
embryonated ova contain third-stage larvae (L3). When dogs ingest embryonated eggs, L3
larvae hatch in the small intestine, penetrate the intestinal wall and are carried by the
bloodstream to several tissues, particularly the liver and the lungs (entero-hepatic-pulmonar
migration). The pulmonary L3 larvae undergo upward tracheal migration and swallowing,
to return to the small intestine, where the final two molts take place. Although larvae will
remain developmentally arrested in most adult dogs, they usually resume development in
pregnant bitches and migrate across the placenta, infecting the foetus. After 4-5 weeks of
infection, eggs shed by female worms are detectable in dogs feces, where the prepatent
period is slightly longer (8 weeks) in T. cati infections of cats. Dogs and other canid species
are also infected by transplacentary and transmammary migration of third-stage larvae.
Although T. canis is often regarded as the main, or sole, cause of human toxocariasis, the
relative contribution of T. cati has possibly been underestimated because these two zoonotic
species could not be reliably differentiated with the identification methods used in most
studies (Fisher, 2003). Serosurvey data from Iceland, however, indicate that T. canis may be
far more important than T. cati as a cause of toxocariasis (Overgaauw, 1997). Dogs have been
banned from Iceland since the 1940s, as a measure to prevent human hydatid disease, but
cats are allowed as pets. Nevertheless, all adult Icelanders exposed to cats (cat breeders and
pet cats owners) tested to date have been seronegative for Toxocara (Woodruff et al., 1982).
The age of definitive hosts, particularly dogs, correlates negatively with the burden of
infection with adult worms. Adult T. canis worms are most commonly observed in puppies
up to three months of age. In dogs up to 5-6 months of age, tracheal migration of larvae
usually results in the development of adult worms. At six months of age, the number of
adult parasites in the intestine decreases drastically, putatively due to acquired immunity
against migrating larvae, while L3 larvae typically undergo somatic migration and
encapsulate in these hosts. In cats, usually more larvae undergo tracheal migration