Toxocariasis and Public Health: An Epidemiological Review

An epidemiological review of toxocariasis aimed to underpin its prevalence, proclivity and prognosis was undertaken. Human toxocariasis constitutes one of the most common parasitic infections worldwide, which is more prevalent in developing and tropical countries. Human infection is caused by ingesting the eggs which were shed in the faeces of the defi nite dog or cat host. There is a range of clinical manifestations of toxocariasis in human, but the two classical clinical syndromes often described are visceral and ocular larva migrans. The clinical signs and complications which result from infection with this parasite are mostly dependent on the number and migration locations of Toxocara larvae. Visual identifi cation of larvae in tissues and organs is the gold standard for toxocariasis diagnosis in human, while an enzyme linked immunosorbent assay detecting Imunoglobulin-G antibodies against Toxocara excretory-secretory antigen is the reference test for immunodiagnosis. In human, loss of vision, hypereosinophilia, encephalitis and problems involving the liver, lung and the central nervous system are the most important complications. Poor hygiene, poverty and lack of education can exacerbate the exposure to Toxocara infection. Albendazole is the treatment of choice for toxocariasis. Conclusively, the present review recommends that regular stool examination and frequent chemotherapy of pets can be effective in reducing the egg number deposited in soil; reducing the number of pet animals or limiting contacts of small children with them and good hygiene practices will limit transmission of toxocariasis. Review Article Toxocariasis and Public Health: An Epidemiological Review Anunobi Toochukwu Joy1, Okoye Ikem Chris2 and Nwosu Chigozie Godwin2* 1Science Laboratory Department, Federal Polytechnic, Idah, Kogi State, Nigeria 2Parasitology and Biomedical Diseases Research Unit; Zoology and Environmental Biology Department, University of Nigeria Nsukka, Enugu State, Nigeria Dates: Received: 11 October, 2017; Accepted: 20 November, 2017; Published: 21 November, 2017 *Corresponding author: Nwosu Chigozie Godwin, Parasitology and Biomedical Diseases Research Unit; Zoology and Environmental Biology Department, University of Nigeria Nsukka, Enugu State, Nigeria, E-mail:


Introduction
Toxocariasis is the clinical term applied to infection in the human host with either Toxocara canis (Werner, 1782) or Toxocara cati (Schrank, 1788). Both of these are ascarid nematodes in the order Ascaridida, superfamily Ascaridiodea, and family Toxocaridae. The defi nitive hosts of T. canis and T. cati are the domestic dog and cat respectively. They can be found in different parts of the body, including the liver, heart, lungs, brain, muscle or eye [1]. The clinical signs and complications which result from infection with this parasite are mostly dependent on the number and migration locations of Toxocara larvae [2]. In human, loss of vision, hypereosophilia, encephalitis and problems involving the liver, lung and the central nervous system are most important complications caused by this parasite [2]. Other names applied to toxocariasis include Weingarten's disease, Frimodt-Møller's syndrome, and eosinophilic pseudoleukemia [3], and also nematode ophthalmitis, toxocaral disease, toxocarose, and covert toxocariasis [4]. T. canis and T. cati are distributed worldwide [5], which is more prevalent in tropical, developing countries and poor communities [6]. Human quest for surrounding ourselves with various domestic animals, particularly cats and dogs, has ensured a worldwide distribution for toxocariasis [7,8]. Poor hygiene, poverty and lack of education can exacerbate the exposure to Toxocara spp (Quattrocchi et al., 2012).

Aetiologic Agents
Zoonotic Toxocara species include Toxocara canis, T. cati, and possibly T. vitulorum and T. pteropodis. These nematode parasites all belong to the family Toxocaridae. T. canis is generally thought to be more important than T. cati in human disease. T. cati has been implicated particularly in ocular toxocariasis [9,10]. T. vitulorum infection is thought to be a low level zoonosis mainly affecting children in the tropics. T. pteropodis, a nematode of fruit bats, was implicated in an outbreak of hepatitis associated with feces-contaminated fruit in Palm Island, Australia [11]. This association has been questioned by some authors.
Two new species have recently been identifi ed: T. malayasiensis [12], in the domestic cat and T. lyncus in caracals [13]. The zoonotic potential of these two organisms is unresolved [11,14,15]. Toxocara canis (Werner, 1782) and Toxcara cati (Schrank, 1788) are common intestinal roundworms of canids and felids, respectively that are often implicated in human toxocariasis. however identifi ed what Werner had described as a member of the genus Toxocara and established by Stiles in 1905. Fülleborn speculated that T canis larvae might cause granulomatous nodules in humans. In 1947, Perlingiero and Gyorgy described the fi rst case of what was probably toxocariasis. Their patient was a 2-year-old boy from Florida who had classical symptoms and esoinophilic necrotizing granulomas [3]. In 1950, Campbell-Wilder was the fi rst to describe toxocariasis in humans; she published a paper describing ocular granulomas in patients with endophthalmitis, Coat's disease, or pseudoglioma. Two years later, Beaver et al published the presence of Toxocara larvae in granulomas removed from patients with symptoms similar to those in Wilder's patients [16,7,9].
Habi tat: The eggs of T. canis are ex creted in the feces of an in fected canid host. The em bry onated eggs can live in the feces for up to three weeks. The feces are often de posited in soil or sandy areas. A host must in gest the eggs for the life cycle to con tinue. If in gested, the new habi tat be comes the in ter nal organs of the host. The gut is the fi rst area T. canis lar vae re side.
If the host has not been pre vi ously in fected, hatched ju ve niles go throught the cir cu la tion to the lungs, then back to the gut. If in a canid host, they take up res i dence in the in tes tine and develop into adults. If hosts have been pre vi ously "im mu nized" jun ve niles go to the body tis sues and be come dor mant as if they were in a paratenic host. Often the in fec tious lar vae stay in the mam mary glands until a preg nancy where they are passed on to a nurs ing pup. If in a human or other non-canid host the lar vae will won der through out the or gans. These wan dering lar vae are called vis ceral larva mi grans. They may travel to the eyes, lungs, brain, heart, mus cles, liver, and other or gans.
Here they do not de velop fur ther but can cause se vere local reac tions [17,18].
Morphology of Toxocara species: T. canis and T.cati are ascarid nematodes [19,7], in the order Ascaridida, superfamily Ascaridiodea, and belong to the family Toxocaridae [7]. Toxo cara canis is smaller than most of the other species in the fam ily As cari di dae. It has a com plete gut in the form of a simple tube. It is a "round worm" im ply ing the shape of the outer layer to be round (if seen in a cross sec tion). De pend ing on the host the worm gets into, T. canis will have dif fer ent num ber of lar val stages. Most worms have three lar val stages be fore be com ing in fec tive. The larvae of T. canis are 290 to 350 μm by 18 to 21 μm. The diameter of the larvae of T. cati is somewhat smaller. The morphology of the adult worms resembles that of Ascaris lumbricoides, but they are much smaller. Tox o cara canis is dioe cious hav ing mor phol ogy dis tinctly dif fer ent for the male and fe male. Toxocara adult parasites are large, pink, roundworms, measuring 6.5 to 10 cm long for the females and 4 to 6 cm long for the males [20]. The male's pos te rior end is curved ven trally and the tail is bluntly pointed which distinguishes it from straight-tailed female [7]. The male has a sin gle tubu lar testis. He also has sim ple spicules, which allows for di rect sperm trans fer. The fe male worms are gen er ally around 6.5 cm but can be as long as 15 cm long. In the fe male the vulva is about one-third the body length from the an te rior end. The ovaries are very large and ex ten sive. The uteri con tain up to 27 mil lion eggs at a time.
Both males and fe males have three promi nent lips. Each lip has a dentiger ous ridge. The lateral hy po der mal cords are vis i ble with the naked eye. No gubernaculums is pre sent. In both sexes there are promi nent cer vi cal alae [21]. The eggs are brown ish and al most spher i cal. The brownish eggs of T. canis and T. cati measure approximately 85 by 75 μm and 75 by 65 μm, respectively. The eggs are almost spherical, larger than those of A. lumbricoides and unembryonated when laid. The eggs are em bry onated when laid and have sur fi cial pits. These eggs are very re sis tant to var i ous weather and chem i cal con ditions [22,23] (Figures 1,2).
Com mu ni ca tion and per cep tion: Ne ma todes within the Secer nen tea have phas mids, which are uni cel lu lar glands. Phasmids likely func tion as chemore cep tors. Fe males may pro duce pheromones to at tract males. Ne ma todes in gen eral have papillae, setae and am phids as the main sense or gans. Setae de tect mo tion (mechanore cep tors), while am phids de tect chem i cals (chemore cep tors) [24,23].   body fl u ids. Ex tra cel lu lar di ges tion be gins within the lumen and is fi n ished in tra cel lu larly (Barnes, 1987 [33]. Post mortem examination of rats (Rattus norvegicus) which had been experimentally infected with T. canis revealed L3s in muscle, eye, liver, kidney, brain and lung [34]. The same situation may apply to T. cati.

Toxocara transmission in defi nitive host:
There are four ways of in fec tion or trans mis sion from one host to the next. Tox o cara canis can be trans mit ted to nurs ing pups by trans mam mary trans mis sion from lar vae that were in their mother's milk. This is the least com mon form of trans mis sion.
The in gested milk con tain ing the in fected stage three lar vae  [35,15], and up to eight weeks in T. canis. Under optimum conditions, eggs will embryonate and become infective within 6 weeks, but this can be delayed for several months' lower temperatures [36]. sheathed L3, in fec tious stage. When ingested by a canine host, T. canis larvae hatch in the small intestine, burrow through the intestinal mucosa, enter the bloodstream and travel via the liver to the lungs [35]. From here, the larvae either migrate up the trachea where they are swallowed and returned to the small intestine to develop into adult worms or undergo somatic migration and enter a wide range of tissues including the liver, lungs, heart, brain and muscle [15]. The larvae can become mobilised from the tissues and migrate across the placenta infecting puppies in utero, leading to tracheal migration in the pup and eggs being shed in the faeces 2-3 weeks after birth, or they can migrate to the mammary glands and infect puppies during lactation. There is no transplacental transmission with T. cati [15] (Figures 3-5).

Distribution of Toxocara
Ge o graphic range and distribution of Toxocara: Tox co cara has a world wide dis tri b u tion [15]. It is preva lent in all lo cations that have do mes tic dogs, pup pies, and other canids. Toxo cara is also found in places that have other var i ous mam mals such as mice, pigs, birds, and foxes, but these hosts are only paratenic hosts. Hosts are ter res trial mam mals and there fore T. canis is mainly found in ter res trial ter rain [17]. The eggs of these species occur in 2-88% of soil samples collected in various countries and regions. T. vitulorum is found mainly in the tropics; cases have been reported from 50° north of the equator to 40° south. T. vitulorum is present in the U.S. but the prevalence of infection is low. The high ambient temperatures and humidity of the tropics favor the transmission of Toxocara species. In Iceland, where dogs have been banned since the 1940s, visceral larva migrans is very rare and 0 of 300 human adults had antibodies to Toxocara spp.
Soil contamination of Toxocara spp, eggs survival and dispersal: In Nigeria, reports on soil contamination by Toxocara eggs have been reported in Nsukka, Enugu state [37]; Calabar [38]; Kaduna [39] and other places. It is estimated that the contamination of soil with Toxocara eggs may be more than the 90% of the investigated areas worldwide Joanna, 2015 [40]. This is explained by the fact that mature eggs of ascarids can survive in contaminated soil even in harsh conditions (e.g. they may resist to chemicals, broad temperature ranges and several degrees of moisture), thus are available for ingestion at any time by susceptible hosts [7]. Also, viability and infectivity of environmental larvated eggs persist for years, thus explaining the high number of chances that dogs have of becoming infected and the diffi culties in controlling these intestinal parasitoses [41]. Moreover, larvated eggs of T. canis are an effi cient environmental source of infection for various animals, which act as paratenic hosts. These animals greatly contribute to maintaining the biological cycle of toxocariasis everywhere.
In fact, dogs can become infected by Toxocara by ingesting tissues of invertebrates (e.g. earthworms), ruminants (e.g. sheep), rodents, birds (e.g. chicken) [42]. The role of wildlife is another exogenous factor contributing to the environmental contamination. In fact, movements of wildlife to sub-urban and urban environments due to destruction or reduction of their habitat is another source of soil contamination by T. canis.
The key example is represented by synantropic fox populations, which reinforce environmental contamination and risk of infection for humans and stray and domestic dogs [43]. Thus, a combination of these factors is the basis for an extremely high environmental contamination and a life-long risk of infection for dogs living in contaminated areas [44]. Once expelled, T. canis eggs require 2-6 weeks at temperatures of 10-30 C before the eggs are fully embryonated and contain infective L3s.
Increasing temperature accelerates the development as well as the degradation of T. canis eggs while temperatures colder than 10 C or warmer (>37 C) are inimical to the maturation or survival of eggs [45]. Embryonation is therefore seasonal in temperate climates but year-round in tropical areas. Eggs are very resistant and survive well over most winters in temperate climates, surviving for 6-12months. Some eggs may be able to survive in moist, cool conditions for 2-4 years or longer [45].
Soil type, pH and percentage of vegetation cover impact upon contamination and viability with clay soils negatively impacting on egg viability [46]. The substrate, light, temperature,  Eggs can be physically dispersed by movements of defi nitive hosts, rainfall, birds, beetles, earthworms, slugs and fl ies. Studies have concentrated on assessing egg contamination of playgrounds, parks, sandpits, and backyards/gardens and have shown contamination to be prevalent [47]. Although such areas seem to provide opportunities for infection, the role of different domestic and wild defi nitive hosts in the contamination of these areas is unclear (McPherson, 2013).

Geographical Distribution
Toxocariasis is found worldwide, although the majority of cases occur where dogs and cats are kept in close proximity to humans (usually household pets). Most cases are reported from the Southeastern United States, Mexico, Hawaii, East and Western Europe, Australia, the Philippines, and South Africa (Fan et al., 2013) (Figure 6).
Within these countries, pet owners (who live in close proximity to infected animals) and children (who are more likely to play in or eat contaminated dirt) are most susceptible to toxocariasis.

Geograph i cal seroprevalence of human infection
Globally, toxocariasis is found in many countries of the world. Seroprevalence is higher in developing countries, but can be considerable in fi rst world countries, as well. In Bali, St. Lucia, Nepal and other countries, seroprevalence is over fi fty percent [9]. Previous to 2007, the U.S. seroprevalence was thought to be around 5% in children [4]. However, Won et al. discovered that U.S. seroprevalence is actually 14% for the population at large [1,48]. In many countries, toxocariasis is considered very rare. Approximately 10,000 clinical cases are seen a year in the U.S., with ten percent being OLM [49].
Permanent vision loss occurs in 700 of these cases (Figure 7).

Risk Factors
There are several factors that have been associated with including parks and playgrounds pose as the main area for risk of human exposure to eggs [58]. Embryonated Toxocara spp. eggs have been recovered from the hair of dogs, which demonstrates that direct human-dog contact could also be a route of infection for humans [59,60]. Consumption of raw or undercooked infected viscera or meat has been incriminated [32].

Humans become infected by ingesting either embryonated
Toxocara eggs from soil [44]; or Toxocara larvae from undercooked giblets (mainly liver) [5]. Humans may also become infected through the ingestion of encapsulated larvae in the raw or undercooked tissues of paratenic hosts such as cows, ostrich, chickens and pigs [61,62], or through unwashed contaminated fruit and vegetables [63]. A new mode of transmission recently proposed is contact with embryonated eggs on a dog's hair coat [59,60].

Incubation Period
In children, the incubation period can be weeks or months  The life cycle is completed when dogs eat these hosts and the larvae develop into egg-laying adult worms in the small intestine. Humans are accidental hosts who become infected by ingesting infective eggs in contaminated soil or infected paratenic hosts. After ingestion, the eggs hatch and larvae penetrate the intestinal wall and are carried by the circulation to a wide variety of tissues (liver, heart, lungs, brain, muscle, eyes). While the larvae do not undergo any further development in these sites, they can cause severe local reactions that are the basis of toxocariasis. The two main clinical presentations of toxocariasis are visceral larva migrans and ocular larva migrans. Diagnosis is usually made by serology or the fi nding of larvae in biopsy or autopsy specimens.

Clinical Signs, Symptoms and Pathology
Symptoms of toxocariasis vary depending on the affected organ, the magnitude of infection and the intensity of the host inflammatory response Pawlowski, 2001 [7]. The broad spectrum of clinical manifestations in toxocariasis varies from asymptomatic to non-specific clinical signs which make it difficult to directly identify clinical cases of toxocariasis. Therefore, patient clinical history regarding risk factors for Toxocara spp. infection such as occupation, residence, travel history, contact with soil, pets and consumption of raw vegetables or undercooked meats should be gathered as additional information for the diagnosis of toxocariasis [15]. The clinical picture of toxocariasis in humans has been systematically classifi ed in four groups: Visceral larva migrans syndrome (VLM), neurological toxocariasis (NT), ocular larva migrans syndrome (OLM) and the more recently described covert toxocariasis [19]. The severity and range of symptoms depends on the tissue invaded, the number of migrating larvae, and the age of the host.

Visceral larva migrans (VLM):
The immediate hypersensitivity response to the death of larvae is thought to be the main cause for symptoms of VLM [7]. The fi rst VLM report described a multi-systemic disease with hypereosinophilia and hepatomegaly in three children [16]. Generally young children (<5 years) are most often affected and usually present with fever, abdominal pain, probably due to hepato-and splenomegaly, as well as lower respiratory symptoms such as coughing, bronchospasms and asthma caused by parasitic pneumonia or bronchitis [7,32]. Laboratory diagnosis in these patients commonly reveals leucocytosis, persistent eosinophilia as well as hypergammaglobulinaemia. Other organ involvement such as myocarditis, myalgia with eosinophilic polymyositis, arthritis, and nephritis may also occur. VLM has additionally been associated with dermatological changes such as rash, pruritus, excema, panniculitis, urticara and vasculitis [9]. Although generally most T. canis infections remain unapparent, long-term effects such as development of asthma and promotion of pulmonary fi brosis are suspected to occur [32] (Figure 9).

Neurotoxocariasis:
The number of reported cases of neurotoxocarosis is scarce [65]. In contrast, various animal experiments have indicated frequent CNS involvement in paratenic hosts. Migration of Toxocara spp. larvae to the human brain is most often not associated with clinical central nervous signs, but may in rare cases result in eosinophilic meningitis, encephalitis, myelitis or combined pathological presentations [65,66]. Cerebral lesions are predominantly located in the white matter and additional occlusion of cerebral arterial vessels has been reported. Clinical patients present with a large variety of symptoms according to their individual pathology ranging from headache, fever, photophobia, weakness, dorsalgia, confusion, tiredness, visual impairment to epileptic seizures, neuropsychological disturbances, dementia and depression [67]. Furthermore, motor impairment such as ataxia, rigor, para-or tetraparesis and dysaesthesia as well as urinary retention and faecal incontinence occurred in human cases of toxocarosis [65].

Ocular larva migrans (OLM): Ocular larva migrans syndrome
(OLM) is characterized by an eosinophilic immune response to larval migration into the eye. After formation of an eosinophilic abscess, a granulomatous infl ammatory reaction surrounds the larvae [68]. Histopathological examinations revealed multiple retinal and vitreous haemorrhages, eosinophilic abscesses and granulomatous lesions with or without larvae.
The lack of larvae in some lesions was attributed to destruction of the causative organism and its mobility [68]. OLM occurs predominantly unilaterally. Bilateral ocular involvement has been described but can be considered uncommon [68].
Possible clinical consequences of OLM are blindness and secondary glaucoma [7] (Figures 10-12).  Other clinical manifestations associated with toxocariasis: Toxocara canis infection has also been associated with asthma and may be linked to the rise in asthma observed in inner city children in cities in the USA [70], and other countries

Diagnosis of Human Toxocariasis
Diagnosis and treatment of patients with toxocariasis have been associated with diffi culty [5]. is about one-third of the total body length [75]. On pathological examinations, the cuticle presents two characteristic lateral alae [76]. T. cati larvae have a similar morphology with T. canis [75]. The morphological identifi cation of Toxocara infection by species eggs has been documented to give minor differences. Scanning electron microscopic observation was able to differentiate T. canis eggs from T. cati eggs based on their respective characteristic surface structures. Both species have subspherical eggs with marked pitted surfaces, but the surface pitting of T. canis is coarser than that in T. cati [77].
Immunodiagnosis: Development of serological methods was prompted by the diffi culties and uncertainties of direct visual diagnosis [74]. To confi rm suspected toxocariasis, it is recommended that patients should always be examined with serodiagnostic tests using at least two consecutive serum samples taken approximately 2 weeks apart [15]. An ELISA detecting IgG antibodies against Toxocara Excretory-Secretory There is great interest in this combined diagnostic procedure because TES-ELISA provides fast and relatively inexpensive negative results. The only current concern is the diagnostic value of a positive result, which is constantly obscured by the presence of a more or less elevated seroprevalence rate.
Common/ covert toxocariasis is mostly a benign infection, so a large majority of infected subjects are asymptomatic or have very few symptoms and go undiagnosed. In this form, this helminthiasis is often self-limiting and leaves residual specifi c  antibodies. On average, the duration of a positive TES-ELISA result would be 2.7 years, and over 5 years for WB [19]. A positive serodiagnostic caused by residual antibodies that do not have any diagnostic signifi cance can therefore be associated with any infectious or non-infectious disease. If separated from the ongoing clinical and laboratory context, such a positive result has no diagnostic value and should be only taken into account after the possible etiologies of the observed syndromes -including blood eosinophilias-have been ruled out [74].
Immunodiagnosis of ocular and neurological compartmentalized forms represents a diffi cult problem. The parasite burden is always tiny and often reduced to one larva; thus an immunodiagnostic test carried out on serum usually is negative [78]. For ocular toxocariasis, immunodiagnosis is made possible using Aqueous Humor (AH) in a TES-ELISA [79] or WB [80]. Both methods detect specifi c IgG. For neurological toxocariasis, immunodiagnosis can be carried out on CSF [78].
Immunodiagnosis on AH or CSF should be always coupled with serum testing. If the results are discordant namely negative on serum but positive AH or CSF, this fi nding indicates intraocular or intrathecal synthesis of specifi c anti-ES Ag IgG. When serum and any aspirated fl uid are simultaneously positive, synthesis of specifi c IgG in the eye or CNS should be assessed using Reiber's formula [81].

Treatment
Albendazole is the treatment of choice for toxocariasis.
Patients receiving a 5-day treatment course of albendazole For the eradication of eggs in the soil, it had been reported to be impractical [15]. However, the following soil treatment procedures worthy of note include rigorous faecal removal practices, regularly replacing sand or sterilizing it, and eliminating sandpits or sandcastles altogether in public areas [82].

Prevention and Con trol
Pet owners need to involve veterinarians in controlling the transmission of Toxocara from pets to humans. Since pregnant or lactating dogs and cats and their offspring have the highest, active parasitic load, these animals should be placed on a deworming program (Holland et al., 2006;CDC, 2014). Regular anthelmintic treatment, particularly in puppies and kittens, will reduce the number of infectious eggs in the environment [25].
Reduce contact with contaminated soil. When working with soil (through gardening or other activities), it is important to wear gloves [56]. Pet faeces should be picked up and disposed of or buried, as they may contain Toxocara eggs (CDC, 2009).
Practicing this measure in public areas, such as parks and beaches, is especially essential for decreasing transmission [7]. Also, sandboxes should be covered when not in use to prevent cats from using them as litter boxes. Hand washing after working on contaminated soil [15], before eating and after playing with pets, as well as after handling dirt will reduce the chances of ingesting Toxocara eggs.
Washing all fruits and vegetables [9,63], keeping pets out of gardens and thoroughly cooking meats can also prevent transmission. Finally, teaching children not to place nonfood items, especially dirt, in their mouths will drastically reduce the chances of infection. Toxocara spp. eggs are very resistant to adverse environmental conditions and remain infective for years. Since no practical methods exist for reducing environmental egg burdens, prevention of initial contamination of the environment is the most important tool [15]. In order to increase awareness of the potential zoonotic hazards, veterinary practitioners, general practitioners and public health agencies should provide suffi cient information and advice for minimizing the risk of infection. Health education and discouraging geophagia in children are fundamental [82].
Continuous education with emphasis on zoonotic risks is strongly recommended.

Conclusion
Toxocariasis remains a problem throughout the world, causing multisystem disease, especially in young people.
Prevalence of parasite infection in dogs with importance for human health is usually high, resulting in risk of zoonotic transmission from dogs to humans [83][84][85][86][87][88][89][90][91][92][93][94][95][96]. Co-habitation of human with dog and cat pets enhances transmission of Toxocara. Contact with infected dog, especially pups, is a risk factor for infection, which is a reason for concern in term of public health because the presence of dogs in urban areas is becoming increasingly frequent. Researches on the prevalence of toxocariasis in Nigeria are limited and the high seroprevalence revealed in recent studies is of great public health importance. Several individuals are exposed to various risks associated with toxocariasis while some apparently