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Toxocara canis, T. cati (Pathogen – Tissue Nematode)
Cause of Visceral Larva Migrans (VLM) and Ocular larva Migrans (OLM)

Organism:
The VLM syndrome was described by Beaver and colleagues in New Orleans in 1952. This syndrome is caused by the migration of larvae of Toxocara canis, T. cati, and some other animal helminths. Within 10 years of the initial report, more than 2,000 cases had been reported from 48 countries and from every region of the United States. The disease, frequently seen in young children, usually does not cause severe problems, although it persists for months to more than a year. One serious possible complication is invasion of the eye (OLM), often resulting in a granulomatous reaction in the retina. Larva migrans caused by Toxocara spp. are widely recognized as zoonotic infections throughout the world and may be much more common than previously thought.    
Puppies are often infected by vertical transfer of larvae from their dams transplacentally or lactogenically, and egg shedding by puppies can begin as early as 2 weeks of age.  In cats, lactogenic but not transplacental transmission occurs.  Young kittens and puppies tend to recover from the infections between 3 and 6 months of age.  Infections in older animals are acquired by the ingestion of infective eggs from the soil or ingestion of larvae in infected rodents, birds, or other paratenic hosts.  Eggs are shed in the feces and take about 2 to 3 weeks to mature and become infective.    

Toxocara adult worms Egg containing larva Granuloma

Life Cycle:
Humans acquire the infection by ingesting infective eggs of the dog (primarily) or cat ascarid T. canis or T. cati. After the eggs are accidentally ingested by a human, the larvae hatch in the small intestine, penetrating the intestinal mucosa, and migrating to the liver. Migratory routes include the lungs and/or other parts of the body, or the larvae may remain in the liver. During this migration, the larvae do not mature, even if they make their way back into the intestine.

Acquired:
Infection in humans is acquired through ingestion of eggs in contaminated soil.

Epidemiology:
Given that (i) Toxocara worms are commonly found in dogs and cats, (ii) puppies and kittens are infected early in life, and (iii) pets and children are often found in the same household, it is not surprising that a combination of small children playing in contaminated soil and pets passing large numbers of infective eggs leads to VLM and/or OLM. However, it is important to remember that this disease can also occur in adults. The eggs will become infective in about 3 weeks and will remain viable in the soil for months. Examination of soil from parks and playgrounds in various areas of the world has demonstrated infective Toxocara eggs that contribute to the high infection rate seen in dogs.

Clinical Features:
Clinical symptoms depend on the number of migrating larvae and the tissue or tissues involved.  Infections may range from asymptomatic to severe disease. Larvae often remain in the liver and/or lungs, where they become encapsulated in dense fibrous tissue. Other larvae may continue to migrate throughout the body, causing inflammation and granuloma formation. The most outstanding feature of the disease is a high peripheral eosinophilia, which may reach 90%. The overall severity of the clinical picture depends on the initial dose of infective eggs. As few as 200 T. canis larvae in small children may produce a peripheral eosinophilia of 20 to 40% for more than a year, with no other detectable symptoms. Patients with 50% eosinophilia usually have symptoms, which might include fever, hepatomegaly, hyperglobulinemia, pulmonary infiltrates, cough, neurologic disturbances, and endophthalmitis. Although a rare complication of toxocariasis, CNS involvement can cause seizures, neuropsychiatric symptoms, or encephalopathy (8, 88). 

Clinical Specimen:
Serum:  Acute and convalescent titers demonstrate several-fold increases in both serum and CSF antibody levels.

Laboratory Diagnosis:
Serology:  Serologic tests are recommended. Serum samples can be sent to the appropriate state Department of Public Health (check the applicable state submission requirements). These specimens are often sent to the Centers for Disease Control and Prevention. History information is required, and each sample must be specified as "serum," or "eye fluid," so that a correct interpretation of the results can be made.
Tissue: Tissue specimens containing larvae can be referred to a reference center (university or Armed Forces Institute of Pathology, Washington, D.C.).

Organism Description:
Egg: B. procyonis eggs are somewhat oval, dark brown, and measure from 63 to 88 µm by 50 to 70 µm.  The eggs contain a single-celled embryo and a thick shell with a finely granular surface; they are not infective immediately after being passed, but can survive in moist soil for years.  Toxocara eggs tend to be somewhat larger and have a coarsely pitted thick shell.
Larvae:  Cross‑sections of larvae tend to measure 60 to 70 μm, and the larvae have prominent, single lateral alae and paired, conical excretory columns (smaller than central intestine). 

Laboratory Report:
Serology results indicated (with interpretation)

Treatment:
Diethylcarbamizine, thiabendazole, ivermectin, and albendazole are effective in some cases but not in others. Corticosteroids may also be given to patients with VLM or OLM. Destruction of the larva by photocoagulation is recommended when the larva is visible in the eye. (Specific drug and dosage information is provided in chapter 25.) Even when the eye is involved, the prognosis is usually favorable, particularly when a prompt diagnosis is made and treatment is effective.  Albendazole is the treatment of choice.  Although mebendazole is poorly absorbed outside the gastrointestinal tract, it has been used with some success.
Garcia, L.S. 2007.  Diagnostic Medical Parasitology, 5th ed., ASM Press, Washington, D.C.

Control:
One preventive measure includes worming dogs and cats periodically with mebendazole to keep them free of worms. Another recommendation is preventing children from eating dirt, particularly soil that could be contaminated by neighborhood or family pets. Proper curbing of dogs in the street during defecation has also been recommended.  Another approach involves protection of sandpits in public parks from Toxocara egg contamination. The recommendation is to cover the sandpits with clear vinyl sheets at night and on rainy days.
 In summary, the following preventive measures should be emphasized:  regular deworming of dogs and cats, beginning at 2 weeks of age; removing cat and dog feces in places adjacent to homes and children’s playgrounds; keeping children’s sand boxes covered when not being used; regular hand washing after handling soil and before eating; and teaching children not to put dirty objects into their mouths.