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The species discussed herein are all nematodes that invade tissues, either in their adult or larval stages. A common feature among many of these species is low host specificity, which facilitates zoonotic transmission. Associated disease varies widely by the tissue impacted, and some manifestations such as invasion of the central nervous system (CNS) may prove fatal. Diagnosis is difficult for several discussed agents due to a lack of infectious stages shed in feces or blood and relies on serology, imaging, or biopsy. Thus, the true incidence and impact of tissue nematode infections could be underestimated Table 127-1.


The larvae of the common ascarid roundworms of dogs and cats, Toxocara canis and Toxocara cati, respectively, may infect humans. The adult worms live in the small intestines of their animal hosts, and eggs are shed in the feces. The eggs develop in the environment over 2–4 weeks, and both definitive and paratenic hosts (including many species of birds and mammals) may acquire infection following the ingestion of these infectious eggs. Definitive hosts may also become infected by consuming encysted larvae from tissues of an infected paratenic host. Larval migration follows a hepatotracheal route to the gastrointestinal tract in the definitive host, while somatic migration via circulation to visceral organs occurs in the paratenic host (including humans) and to some extent in the definitive host.1 Transmission to humans primarily occurs through the fecal-oral route, from eggs in the environment or adhering to animal hair, but Toxocara spp. may also be a foodborne agent if undercooked meat from paratenic host tissue containing larvae is eaten. Foodborne cases have been reported after eating raw bovine and poultry livers; the liver is a common site for accumulation of larvae in paratenic hosts.2,3 Larvae of T. cati in meat have been shown to be tolerant of refrigeration and short-term freezing (up to 2 weeks).4

The most significant clinical manifestation of human toxocariasis is visceral larva migrans (VLM) caused by mechanical damage and inflammation incurred during the migration of Toxocara larvae through visceral organs, particularly the liver and lungs. Migrating larvae are attacked by the host immune system and eventually become trapped in granulomas (Fig. 127-1A). Clinical symptoms and signs are fairly nonspecific. Hepatomegaly and pneumonitis may occur alone or together, and are usually accompanied by peripheral hypereosinophilia and sometimes hyperglobulinemia. Fever, malaise, and anorexia may occur. Severe cases may involve myocarditis, nephritis, and neurological manifestations if the respective organs are sufficiently impacted. Causal links between mild or subclinical cases and pulmonary insufficiency, cognitive deficits, and unexplained urticaria have been proposed.5–7 Toxocara spp. larvae sometimes enter the eyes; this is referred to as ocular larva migrans (OLM). OLM is often associated with diffuse unilateral subacute neuroretinitis (DUSN), endopthalmitis, retinitis, and granuloma formation, which can result in retinal detachment and permanent vision defects.1

Figure 127-1

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