The life cycle of T. canis is complex. Adult T. canis generally inhabit the small intestine of infected dogs. Adult worms do not attach to the mucosa and live on intestinal contents. They shed large numbers of eggs via the faeces into the environment. After predation of Toxocara-infected paratenic hosts (usually rodents) by dogs, larvae are released and develop in most cases, directly to adult worms in the intestinal tract. Larvae can however remain dormant in the animal body for several years. When the bitch becomes pregnant, the larvae activate and migrate across the placenta to the foetus. The larvae migrate also to the intestine of the newborn where they develop to produce eggs at about 2.5 weeks. The lactating bitch becomes reinfected while cleaning the anal region of her pups. Pups/cubs produce the highest number of eggs, although adult dogs also produce eggs but at a lower level. Eggs become infective in the environment within 10 - 21 days after shedding. Faecal egg counts in pups can reach 100,000 eggs/g of faeces. In favourable conditions eggs can survive for 6-12 months; they can develop at 10°C and only heat greater than 30-35°C and desiccation will kill the thick-shelled eggs.
Toxocara eggs are unembryonated and not infectious when passed into the environment. Within a period of between 3-6 weeks and several months, depending on soil type and climatic conditions such as temperature and humidity, eggs will develop to an infectious stage that can survive under optimum conditions for at least a year. When faeces disintegrate, eggs are released into the surrounding soil, becoming a source of infection. The density of eggs in some surveys has been reported as between 0.1 to 23 eggs/g soil (Lloyd, 1993), but many surveys do not differentiate T. canis and T. cati eggs. One survey found egg - positive soil samples in 66% of London parks (Lloyd, 1998).
The shed eggs have a sticky consistency. Because of this flies and other invertebrates (earthworms, cockroaches, beetles and slugs) can be potential carriers to gardens or food. Small rodents are also a source of infection. Some cases of toxocarosis have been described in people who have never owned a dog or had close contact with one.
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The most common route of infection is by ingestion of eggs through contaminated soil. A number of routes are possible: ingestion of contaminated soil containing eggs (pica); poor hygiene; contact with dogs that excrete eggs which may adhere to fingers, toys, food, etc; and by consumption of raw or undercooked meat (although the significance of this route remains undetermined). Direct contact with infected dogs may however be of relatively low potential risk because embryonation of Toxocara ova to the stage of infectivity requires a minimum of 3 weeks. T. canis infections are therefore more likely to be a hazard for people exposed to contaminated environments.
Urban and rural foxes are another source of infection, even in fenced gardens. Infection is very prevalent in foxes: in Bristol 14-73% of foxes older than 2 years were found to be infected (Richards et al. 1993), while >60% rural or mixed urban/rural groups of foxes in Wales and Germany were infected. Surveys have shown a higher prevalence of infection in stray compared to pet dogs. The higher prevalences in stray/wild canid populations are probably dietary; scavenged paratenic hosts being an important food for these animals.
Larvae hatch in the gut and subsequently penetrate the intestinal wall before proceeding on a liver-heart-lung migration (visceral larva migrans). In the human host, larvae at the L2 (second) stage cannot develop into the adult stage but continue to migrate throughout the body. Humans are a dead-end host, able to allow the survival but not the further development of larval parasites. It is the inflammatory response to migrating larvae and their excretory products which is responsible for clinical disease. Clinical manifestations depend on the number of larvae and their anatomic location. Visceral infection may cause several systemic symptoms that last for 6 to 24 months. Ocular infection, which is more likely to occur in older children and adults, may result in permanent loss of visual acuity.
The most at risk group are children, commonly between 2 and 4 years of age, in whom ingestion of contaminated soil is likely to lead to the visceral syndrome. The symptoms are generally hepatosplenomegaly, fever, respiratory signs, pallor, skin lesions and there may be neurological manifestations (e.g. convulsions), with heart problems and occasionally ocular lesions. The ocular syndrome occurs sometimes concurrently with the visceral form. The covert syndrome is being increasingly recognised; symptoms vary, but commonly there is a weakness and lethargy, skin lesions or pruritis, respiratory features, headache, muscular pain and anaemia. The asymptomatic infection is detected by a positive Toxocara antibody result in the absence of other symptoms. Around 2-10% of the population in the Western world are seropositive, with higher rates in children.
Toxocarosis is not a notifiable disease in England and Wales, so the numbers of cases per year must be estimated from diagnostic laboratory records. The true incidence of cases is unknown due to the asymptomatic form as well as the non-specific signs and symptoms of the disease. The only routine source of national data is based on voluntary reporting of infections to the Health Protection Agency by microbiology laboratories in England and Wales. There is an unascertainable level of under-reporting, especially where diagnoses are based on clinical rather than serological tests. In a survey in one 6-month period in England, 150 of 1182 sera were positive, one third of whom were ocular toxocarosis patients (Gillespie, 1993)
Since 2000, between 1 and 8 newly diagnosed cases have been reported annually, with infections occurring in all age groups.
The detection of antibodies in blood (usually by the ELISA test) is the most commonly used method of diagnosis for visceral disease. In the ocular syndrome, serology is less effective and confirmation is may be done by the examination of vitreous and/or aqueous humour. In all syndromes, parasitological diagnosis is rare, and biopsy often will not detect larvae.
The destruction of eggs is very difficult due to their resistant shell. Control in pet dogs is very effective, although there is no vaccination available. Prevention should be mainly directed towards the destruction of larvae in female dogs. This would eliminate the most important reservoir of parasites and may result in the eradication of the worm. The problem is that unless the animal is heavily infected it does not show any symptoms, but can be excreting eggs. For this reason puppies should be routinely wormed.
Good hand washing is necessary, as well as the control of children at play areas, to prevent their ingestion of soil. The washing of vegetables, wearing gloves when gardening, as well as the fencing of vegetable gardens and suitable disposal of dog faeces are considered very important in the control of this disease.
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The Dogs [Fouling of Land] Act 1996 has been repealed (replaced by the Clean Neighbourhoods and Environment Act 2005), but existing designations remain in force until any Dog Control Order is made on the same land. Controls on dogs include restraint, exclusion from parks and beaches, and requirement for dog owners to collect their dogs' faeces. In many cases the only people who obey the restrictions are responsible pet owners, whose dogs are least likely to be infected; other dogs, stray dogs, cats and foxes remain uncontrolled. Toxocara eggs can survive sewage processing or composting and methods for disposal of canine faeces require further evaluation.
Clean Neighbourhoods and Environment Act 2005, available at: http://www.legislation.gov.uk/ukpga/2005/16/contents
Chapter 1 of the above act refers to dog controls: http://www.legislation.gov.uk/ukpga/2005/16/part/6/chapter/1
Information on responsible dog ownership from Defra: http://archive.defra.gov.uk/environment/quality/local/dogs/owner.htm
Gillespie SH. (1993). The clinical spectrum of human toxocariasis. In: Toxocara and toxocariasis: clinical, epidemiological and molecular perspectives. (Ed. J W Lewis and R M Maizels); pp. 55-61. Institute of Biology and British Society of Parasitology, London.
Lloyd S. (1993). Toxocara canis: the dog. In: Toxocara and toxocariasis; clinical, epidemiological and molecular perspectives. (Ed. J W Lewis and R M Maizels); pp. 11-24. Institute of Biology and British Society of Parasitology, London.
Lloyd S. (1998). Toxocarosis. In: Zoonoses. Biology, Clinical Practice and Public Health Control. (Ed: S R Palmer, Lord Soulsby, and D I H Simpson); pp. 841-854. Oxford University Press, Oxford.
Richards D T, Harris S, and Lewis J W (1993); Epidemiology of Toxocara canis in red foxes ( Vulpes vulpes) from urban areas of Bristol. Parasitology, 107, 167-73.
Overgaauw P A M and van Knapen F. (2000). Dogs and Nematode Zoonoses. In: Dogs, Zoonoses and Public Health (Ed: C N L Macpherson, F X Meslin and A L Wanderler) pp. 213-256. CABI Publishing, Wallingford.
Last reviewed: 25 May 2011