Human toxocariasis, or visceral larva migrans, is a zoonotic disease caused by tissue migration of the nematode larva Toxocara canis, a dog ascaris
Human toxocariasis, or visceral larva migrans, is a zoonotic disease caused by tissue migration of the nematode larva Toxocara canis, a dog ascaris. The condition involves the liver and lungs producing eosinophilic inflammation.
Mature dog ascarid worms, T. canis, live in the small intestine of the wild dog, wolf, dingo, and fox. Eggs produced by these worms are unembryonated when passed in feces, and have a subglubose appearance and a pitted shell. They reach the infective stage in three to four weeks, given favorable moisture and temperature conditions.1
Human infection often follows the ingestion of infective- stage eggs in contaminated dog hair, soil, and food. The eggs must contain fully developed larvae for infection to be transmitted. The larvae hatch in the small intestine, penetrate the intestinal wall, flow through the portal vein to reach the liver, migrate within the liver (visceral larva migrans), move to the lungs (hepatopulmonary migration), and distribute throughout the body, including the orbit and central nervous systems, through the general circulation.1-3 Most larvae remain in the tissues and become encapsulated. They do not grow or develop further, but remain viable and infective indefinitely.
This mode of transmission generally occurs in children who are in frequent contact with dogs or who play on ground contaminated with dog feces.1 This is why toxocariasis used to be considered a disease of children. Nowadays, however, the prevalence of toxocariasis in children is very low, owing to improved hygiene. The incidence of ascaris in pet dogs has also been reduced by the widespread use of antihelminthic drugs.
Adult infection typically follows the ingestion of uncooked animal tissues, such as liver, which contain encapsulated infective larvae (Figure 1). The larvae hatch in the small intestine and, as described above, reach the liver and lungs, where they are encapsulated and remain alive for a certain period.1 Visceral larva migrans of T. canis is one of the most important food-borne parasitic diseases in some Asian countries, including South Korea, Japan, and Taiwan, next to trematodiasis such as clonorchiasis and opisthorchiasis. Visceral larva migrans is rarely reported in Western countries.
Animal infection of T. canis takes place in exactly in the same way, that is, by swallowing embryonated eggs or by ingesting animal tissue containing encapsulated larvae. The liver and lungs are the most frequent site of infection in animals, as they are for humans.1,4 Infective larvae become encapsulated without developing into adult worms and may remain viable for up to 3.5 years in chicken liver5 and for the life of the host (up to nine years) in small mammals.1 Encapsulated T. canis larvae in sexually mature female dogs may be transmitted to offspring though the placenta or through milk feeding. Larvae in the liver or lungs of infected offspring or pups migrate through the trachea to the small intestine. Here they grow into adult worms,1 completing the parasite’s life cycle.
The transfer of encapsulated T. canis larvae from the tissues of mammals to another host is a common mode of transmission among carnivorous vertebrates. People who eat raw animal tissue are also at risk of infection via this route. Uncooked liver from cows (Figure 1), pigs, lamb, and chicken, have all been reported as sources of human infection, as has rabbit meat.6-10
The infective larva of T. canis is 0.5 mm in length and 20 µm in diameter.1 It penetrates the portal vein via the intrahepatic portal radicles, and on reaching the parenchyma can cause eosinophilic inflammation, eosinophilic granuloma, or necrotic nodules (Figure 2).
Each lesion is typically oval and measures 1 cm in diameter. It is common to find multiple lesions scattered throughout the liver. They typically consist of central necrosis surrounded by eosinophilic leukocyte infiltration mixed with neutrophils, lymphocytes, and a palisade of epitheloid histiocytes and/or giant cells. Although the larva may be present in the center of a lesion, it will be difficult to identify.
Living larvae move slowly in liver tissue causing visceral larva migrans. The most constant and striking clinical feature is a high, sustained, peripheral eosinophilia.
CT and ultrasound findings reflect the pathology. CT depicts the lesions as multiple small, ovoid, ill-defined nodules with low attenuation.11 The nodules are usually seen best, or seen only, in the portal venous phase (Figure 3). They will be either faint or not seen at all on arterial and equilibrium phase images. These findings seem to be characteristic for eosinophilic infiltration caused by visceral larva migrans of T. canis.
Follow-up CT scans reflect the movement of larvae through the liver tissue, and both the shape and location of the lesions may be different (Figure 4). Eosinophilic abscesses are present in some cases, appearing as persistent, low-attenuating lesions on arterial, portal venous, and equilibrium phase images.
Ultrasound shows multiple small, focal, hypoechoic lesions in the liver parenchyma. The lesions are usually angulated or trapezoid rather than round, and their margins ill-defined. Lesions sometimes mass together to form a large lesion of mixed echogenicity.
Some larvae in liver tissue enter the hepatic vein and move to the lung parenchyma through the pulmonary circulation, resulting in pulmonary eosinophilic inflammation. Characteristic pulmonary lesions measure approximately 1 cm in diameter and are rather round, comprising a central, tiny, dot-like lesion and a surrounding halo of ground-glass opacity (Figure 5). When the infective larvae move in the lung parenchyma, the lesions move to the adjacent lung on serial chest radiographs or CT images.
Larvae that escape the pulmonary circulation may move to any tissue through the general circulation. The most frequent site of infection is the eye, resulting in endophthalmitis, and the central nervous system, which can cause encephalitis or transverse myelitis (Figure 6).12-14