Toxocariasis

Synonyms: Toxocarosis, Visceral larva migrans, Ocular larva migrans, Covert toxocariasis, Toxocara canis, Toxocara catis

Human toxocariasis is a helminthozoonosis caused by migration of Toxocara larvae through human tissues.

• The usual pathogen is Toxocara canis, which is a gut nematode (roundworm) similar to the human parasite Ascaris lumbricoides.
• Its primary hosts are dogs and cats.
• Humans are an incidental host and do not form part of the worm's life cycle.
• The commonest route of infestation in dogs is transplacental, leading to a high presence of the pathogen amongst young puppies.
• Despite cases of illness due to T. catis (which can be difficult to distinguish from T. canis as they share many common antigens), the importance of this zoonosis has yet to be fully established.¹

• Humans become infected by ingestion of eggs in soil contaminated by dog faeces.
• The appeal to young children of puppies, 'mouthing' of objects, and immature hygiene behaviour put them at particular risk.
• However, direct contact with the animal is not a route of infestation as it takes two weeks for embryonisation of the shed ova.
• Larvae hatch out in small intestine and migrate via liver and lungs to other tissues, though they never mature in humans.
• In most cases the larvae is probably eliminated, but in some a surrounding granuloma may form.
• Rarely, T. catis can mature in humans and be transmitted by vomit or faeces.
• However generally patients with adult T. catis don't have antecedent symptoms, eosinophilia, or antibodies, suggesting that they are acquired by ingestion of adult worms or advanced larval stages from cat vomit or faeces.

• Exposure is undoubtedly common – approximately 2–3% of UK population have antibodies to Toxocara spp.
• Seroprevalence studies in other parts of the world (particularly tropical and relatively undeveloped regions) show that the vast majority of the population have been exposed at some time.²
• Many studies show contamination of children's play areas/sandpits with eggs of T. canis in about 15–25% of those surveyed.^3,4
• An Irish study found a prevalence of ocular toxocariasis of about 6–10/100,000 population, depending on the degree of diagnostic certainty.
• Prevalence rates for visceral larva migrans are difficult to estimate as the disease is largely asymptomatic in many, and presents in a variety of ways.⁵

Risk factors

• Contact with soil contaminated with dog faeces
• Co-habitation with dogs and cats
• Eating without hand washing
• Socioeconomic deprivation
• Rural dwelling
• Travel to areas of high prevalence

• Two main clinical syndromes are recognised, predominantly in children but also affecting some adults: Visceral larva migrans and Ocular larva migrans.
• Covert infestation forms another category, along with some very rare and unusual modes of presentation.
• Manifestations depend upon number of eggs ingested, duration of infestation, anatomical position of larvae and immune reactivity of host.
• Recent studies suggest symptomatic illness may be due to induced autoimmunity associated with the infestation.⁶
• Affected areas include liver, lungs, skin, joints, eyes, heart and brain.

Symptoms

• Visceral: Abdominal pain, decreased appetite, fever, wheezing, cough, urticaria, seizures, joint pain/swelling, fidgeting.
• Ocular: Uniocular decreased visual acuity, strabismus, seeing floaters or 'bubbles', unilateral blindness.
• Occult: Presents similarly to visceral form but less severe/specific symptoms.

Signs

• Visceral: Right upper quadrant tenderness, hepatomegaly, splenomegaly (rarer), wheezing, pleural effusion, monoarthritis, cutaneous vasculitis, urticarial rashes, signs of myocarditis, signs of sub-acute meningitis/encephalitis.
• Ocular: Peripheral retinal lesions, retinal detachment, peripheral retinal exudates, optic neuritis, vitreoretinal bands, uveitis, vitreous abscess.
• Occult: As visceral but fewer/less florid signs.

• Visceral form: Other causes acute hepatitis, adverse drug reactions, pulmonary eosinophilia, other helminthic infestations, allergic bronchopulmonary aspergillosis, angioedema, hypereosinophilic syndrome, eosinophilic pneumonia, SLE.
• The differential diagnoses are legion depending on the mode of presentation.
• Ocular form should be investigated by ophthalmologists to exclude other possible causes.

• Leucocytosis with marked eosinophilia (20-80% of WBC). Eosinophilia is less common in ocular and occult forms.
• Serology may be positive (ELISA); in ocular form test vitreous fluids for antibodies.
• More widespread use of serological tests is detecting more covert cases.
• Ultrasound of liver shows multiple hypoechoic areas.
• Chest x-ray may show nodular infiltrates in pulmonary cases.
• CT/MRI scan of the brain may show meningeal/cerebral involvement.
• Tissue biopsy may be necessary.

Visceral

• Fortunately most patients recover without treatment.
• Anthelmintics, e.g. albendazole, mebendazole, tiabendazole and diethylcarbamazine, are usually used in courses of several days in advanced or highly symptomatic cases or where there is organ damage, under expert guidance.
• Corticosteroids play a role in suppressing intense allergic manifestations of the disease.

Ocular

• Surgical intervention may be required.
• Corticosteroids have an important role in expert hands.

• In ocular form, outcome is variable but uniocular visual loss is not uncommon.
• In visceral form, outcome is usually good, but marked organ damage and even death can occur in extreme cases.

• Removal of pet faeces ("poop scoops", bins, and enforcement fines)
• Personal hygiene
• Regular worming of pets, especially puppies