Toxocariosis is a neglected zoonotic infection caused by the nematodes Toxocara canis or Toxocara cati. The distribution of the disease is worldwide and mainly affects dogs and cats, and its larval stage can cause human infection with serious repercussions on the health of its hosts. The infection causes a delay in the development, digestive disorders, nonspecific nervous manifestations, and occasionally death of some puppies and kittens associated with hyperparasitosis. In humans, the infection produces clinical syndromes known as visceral larva migrans (VLM), ocular larva migrans (OLM), neurotoxocariosis and covert toxocariosis. The close contact of people with their pets and the environmental conditions that favor the transmission of this diseased place it within the context of one health. The One Health concept is defined as the collaborative efforts of multiple disciplines (medical personnel, veterinarians, researchers, etc.) that work locally, nationally, and globally to achieve optimal health for people, animals, and the environment, from this perspective, toxocariosis is a study model in which classic and recent knowledge of the medical and veterinary area must be combined for its full understanding, with a goal of establishing integrative criteria for its treatment, control, and prevention.
- one health
- visceral larva migrans
- ocular larva migrans
Toxocariosis is a neglected zoonotic disease transmitted from dogs and cats to humans. This is mainly caused by the presence and action of the nematode
2. Biological cycle
In puppies, L3 migrate via blood or lymph to the liver, where they remain for 1 to 2 days. Subsequently, they migrate through blood, pass through the lumen of the atrium and right ventricle of the heart and via the pulmonary artery, reach the lungs, and cross the capillaries to reach the alveoli. The larvae migrate through the lumen of the bronchioles, bronchi, trachea, larynx, and pharynx (tracheal migration), where they are swallowed; during this tracheal migration, the larvae molt to L4. The larvae remain in the stomach for some time (up to Day 10 postinfection), return to the duodenum, and molt to L5 or preadult to finally become adults (19–27 days post-infection). The prepatent period is 4–5 weeks .
In paratenic hosts and adult dogs, L3 larvae migrate through the blood and are distributed throughout the body, mainly to the striated muscle, liver, lungs, kidneys, and brain, where they remain for years in a state of latency or dormancy as infective somatic larvae (dormant larvae) until they die and calcify.
In pregnant bitches, on approximately Day 20 of gestation, many of their dormant larvae are reactivated by the influence of progesterone. Between Days 43 and 47 of gestation, under the influence of progesterone and prolactin, the larvae cross the placenta and infect the fetuses. The larvae remain in the fetal liver until birth; later, by blood, they migrate to the lungs where they remain during the first week of life, molting to L4 occurs during this stage or later when the larva arrives in the stomach by tracheal migration. By the end of the third week, the larvae molt at L5 and develop rapidly into adult worms. After copulation, the females produce eggs that are passed in the feces of the pups at 15 days of age. In recently delivered bitches, some reactivated larvae arrive by the influence of prolactin on the mammary gland and are excreted in the colostrum and milk to be ingested by the puppies, constituting another important source of infection for the litter. The larvae ingested in this way molt at L4 and L5 in the intestinal lumen, where they develop into adult worms without tracheal migration .
In recently delivered bitches, some larvae may reactivate during gestation migrate to the intestine, molt to L4 and L5 and become adult worms. Bitches can remain up to 60 days passing eggs in feces until the adult worms are eliminated spontaneously. This is one of the ways adult worms can develop in adult dogs .
Dormant larvae in the tissues of paratenic hosts can be reactivated when they are predated. If the predator is another paratenic host, the ingested reactivated larvae undergo a new somatic migration and become dormant in this new host. On the other hand, if the predator is an adult dog, the ingested reactivated larvae molt at L4 and L5 and develop into adult worms in the lumen of the small intestine without further somatic migration. In this way, dogs can spend a short time excreting eggs in the feces until the adult worms are eliminated spontaneously. This is another way that adult worms can develop in adult dogs .
The life cycle of
3.1 Dogs and cats
In a second meta-analysis where data from 2,158,069 cats from 51 countries were included, an overall prevalence of
Transplacental transmission from bitches to their puppies is the most important form of
Puppies are the main source of environmental contamination; they can excrete eggs in feces from 15 days of birth, and the greatest egg shedding occurs between 1 and 3 months of age, when they can eliminate more than a million eggs per day. Gradually, the worm burden in the intestine tends to decrease, and they stop shedding eggs before reaching 6 months of age. In addition, the larvae ingested by the lactogenic route gradually increase the worm burden and the elimination of eggs in the puppies. Puppies under three months of age are the only hosts that can develop adult worms in the intestine by ingesting larvated eggs, although apparently, this is not their main route of infection .
Paratenic hosts infected by ingesting larvated eggs present in soil, food or water accumulate L3 in their tissues. If these are predated, they can be a source of infection for adult dogs. If predated by another paratenic host, the larvae can infect the new host, bypassing a definitive host.
Due to the great difficulty of identifying the physical presence of somatic larvae, the most common way to identify
The seroprevalence of
The most common way of infection in humans occurs through the accidental ingestion of
There are multiple reports of the presence of
4. Canine and feline toxocariosis
4.1 Pathogenesis and clinical picture
The adult worms of
Larval migration in mild or moderate infections in puppies generally does not produce obvious clinical signs; however, larval migration in severe infections produces respiratory signs such as tachypnea, cough, and runny nose. Nervous signs such as incoordination or convulsions are occasionally observed in puppies due to the passage of the larvae through the brain. In puppies with intense prenatal infection, the lesions produced by the passage of the larvae in the liver, lungs, or central nervous system can cause the death of the puppies in the first 2 weeks of life .
Mild to moderate adult worm infections in puppies are usually asymptomatic or cause mild digestive symptoms and growth retardation. In severe infections, dirty-looking bristly hair, rough skin, painful intestinal distention, vomiting (frequently with adult worms), bulging abdomen (mainly when they have just eaten), presence of large amounts of gas produced by intestinal dysbiosis, alternating periods of constipation and diarrhea with profuse mucus, decreased appetite and growth retardation, can be observed. The blood count shows eosinophilia and anemia. Occasionally, there may be the death of puppies due to aspiration of vomit and intestinal obstruction or rupture. The presence of large numbers of adult worms as a result of massive prenatal infections in puppies can cause complete obstruction of the intestinal lumen, intussusception of the small intestine, and death of the entire litter [9, 29, 30].
In kittens, there is no transplacental transmission; therefore, the development of adult worms occurs until almost 30 days of age and the beginning of the elimination of eggs at approximately 50 days of age. The clinical picture is similar to that described in dogs but less severe, diarrhea, vomiting, and loss of appetite predominate, and deaths are very rare. The highest incidence of
4.2 Diagnosis of toxocariosis in dogs and cats
Sporadically, shed adult worms can be observed macroscopically in the vomit or feces of puppies. The detection of
In adult dogs and paratenic hosts, infection by somatic larvae can be demonstrated by the detection of specific antibodies against excretion-secretion antigens using immunological techniques such as ELISA or Western blot; however, due to their cost, difficulty in obtaining the antigens, and their difficult implementation, these techniques are not widely used in the veterinary field .
5. Human toxocariosis
Human toxocariosis is a neglected worldwide zoonosis caused by nematodes of the genus
5.1 VLM syndrome
In the 1950s, second-stage larvae of
In humans, after ingestion of infective eggs, the larvae hatch in the small intestine and penetrate the intestinal wall, from which they are transported by the blood circulation to various organs, mainly the liver, heart, lungs, brain, muscle, and eyes . In these organs, the larvae actively migrate, aided by proteases with which they cause tissue damage and exert a histophagous spoliating action (traumatic action). The migrating larvae do not continue their development; however, they remain dormant for several years, but they continue to secrete excretion-secretion antigens that induce an inflammatory response in some organs, such as the liver and spleen (hepatosplenomegaly), or are mediators of immunopathological alterations in other organs, such as the lung, where they produce eosinophilic pulmonary infiltration related to cough and persistent secretion .
Given the impossibility of carrying out studies in humans, experimental models have been developed in different species of paratenic hosts, such as primates , rabbits , rats , mice , and gerbils , where the sequence of pathophysiological and immunological events of VML have been studied. In these models, it has been observed that organ injuries can be acute or chronic. The acute phase is characterized by a severe inflammatory response that causes multifocal lesions with necrosis and vacuolization with polymorphonuclear infiltrate, mainly neutrophils with the presence of eosinophils in the liver and lungs. The chronic phase is characterized by the presence of granulomatous lesions with infiltrates of mononuclear cells, fibroblasts, and eosinophils, as well as the presence of fibrosis around the lesion with traces of calcification in the center of the lesions, which in some cases can be extensive. The main organs affected are the liver, lung, kidney, and brain (Figure 2). These lesions can be seen with or without the presence of the larva, which suggests the importance of the antigenic excretion-secretion products released by the larva in the tissues.
The clinical picture of VLM includes hyperleukocytosis (30,000–60,000 cells/mm3), eosinophilia (14–90%), abdominal pain, enlargement of lymph nodes, hepatomegaly, splenomegaly, increased ishemagglutinins and liver enzymes, intermittent fever, cough, and bronchospasm, among others [44, 45, 46, 47]. The severity of the condition depends on the number of eggs ingested and the presence of larvae in critical places; although most patients recover and the signs subside with anthelmintic treatment, deaths from this infection have been reported [48, 49].
The diagnosis of VLM is based on the initial detection of antibodies against excretion-secretion antigens of
5.2 OLM syndrome
This syndrome was first described by Wilder in 1950, who found nematode larvae (unidentified at the time) in 24 of 46 pseudogliomas in eyes enucleated for endophthalmitis with apparent retinoblastoma . Nichols later identified the larvae as
OLM is a disease that generally occurs in young patients. In a systematic review and meta-analysis of studies published internationally, it was observed that the highest infection rate was detected in the 1–25 mean age group; within this range, the highest prevalence occurred between 11 and 20 years of age and was higher in men than in women . It has been shown that having contact with dogs, ownership of dogs or cats, exposure to soil, and consuming raw/undercooked meat can be risk factors for OLM [12, 26, 34, 60].
OLM is generally observed in the absence of clinical signs and symptoms of VLM; it is considered to occur in people initially exposed to a small number of larvae, so they do not mount a significant immune response (many patients with a clinical diagnosis of OLM are seronegative to
The lesions detected in the eyes of patients diagnosed with OLM have been granulomas located near the optic disc or intraretinal (see Figure 2C), posterior and peripheral retinochoroiditis, panuveitis, optic papillitis, uveitis, retinal deformation or detachment, idiopathic epiretinal membranes, infiltration of inflammatory cells in the humor vitreous, hemorrhagic lesions and neuroretinitis as a sequel to migration of larvae in the retina [60, 67, 68, 69]. The main clinical manifestations include poor visual acuity, vision loss, strabismus, leukorrhea, eye irritation, and endophthalmitis [58, 70]. In most cases, lesions occur in only one eye, although there are reports of bilateral conditions .
The initial diagnosis of OLM is based on clinical signs and observation of lesions with an ophthalmoscope in the fundus examination. Confirmation of the diagnosis can be made by the detection of antibodies against excretion-secretion antigens of
The first report of the presence of an encapsulated larva of
In humans, many
In experimental models, it has been shown that
The clinical pictures of neurotoxocariosis in humans rarely occur simultaneously with signs of VLM. Most clinical manifestations occur in adult men with an average age of 35–42 years. Clinical signs associated with neurotoxocariosis may be indicators of different neurological disorders, such as myelitis (sensation disorders such as tingling sensation or hypoesthesia to specific dermatomes; motor disorders such as sphincter disturbances and conus medullaris syndrome; autonomic disturbances such as bladder and bowel dysfunction, and erectile failure), encephalitis (focal deficits, confused state, seizure and cognitive disorders) or meningitis (headaches, stiff neck/neck pain, nausea or vomiting, and Kernig’s/Brudzinski’s sign). Fever may occur on some occasions, although this is not a constant sign [76, 78].
The association between
In this context, Walsh and Haseeb , conducted one of the most conclusive studies; they analyzed a sample of 3,949 children representative of the US child population. Seropositive to
The diagnosis of neurotoxocariosis is difficult because there is no characteristic clinical syndrome. Due to the lack of confirmatory diagnostic tests and the nonspecific nature of its symptoms, neurotoxocariosis is probably underdiagnosed. As there is no universally accepted criterion for the diagnosis of this syndrome, a comprehensive diagnosis must be considered that must include the broad spectrum of neurological manifestations (signs of meningitis, encephalitis, myelitis, and/or cerebral vasculitis), together with high titers of antibodies against
5.4 Covert toxocariosis
Taylor et al.  proposed the term covert toxocariosis to describe a new clinical entity of human toxocariosis. It is currently considered that covert toxocariosis is characterized by nonspecific symptoms and signs that are not associated with the VLM, OLM,or neurotoxocariosis. Clinical manifestations include asthma, acute bronchitis, pneumonia, wheezing with or without Loeffler’s syndrome, chronic urticaria or eczema, lymphadenopathy, myositis, and pseudorheumatoid syndrome, with or without eosinophilia.
The excretion-secretion antigens produced by
Asthma is a lung disease characterized by an exacerbation of the immune response in the airways to a variety of external stimuli, which produces inflammation, bronchospasm, and obstruction of the airways, which are reversible spontaneously or with treatment. Since years ago, several epidemiological and experimental studies have shown a significant relationship between
The exact mechanisms by which
6. Comprehensive control of toxocariosis
The main role in the control of toxocariosis falls on the veterinarian, who is responsible for the diagnosis and deworming programs in dogs and cats, as well as the awareness and health education of pet owners so that they are aware of the threat of this and other infectious diseases from pets to humans. Periodic deworming of dogs and cats is an effective strategy to reduce the worm burden and, therefore, the number of eggs in the environment . Puppies and kittens must be dewormed (piperazine, ivermectin, mebendazole, pyrantel, and febantel, among others) at one month of age, and the treatment should be repeated at least twice in 15 days. In adult dogs, coproparasitoscopic examinations (Faust technique) should be carried out every 6 months, and positive dogs should be dewormed, with special care for dogs with known predatory habits. There are no effective antiparasitic agents against somatic larvae of
The main way of infection in humans is the ingestion of infective eggs (L3 passive) that contaminate their environment. The fecal of dogs and, to a lesser extent, of cats in the soil of public parks, gardens, ridges, and rural areas, among others, is the cause of the gradual accumulation of infective eggs of
One of the risk factors most frequently associated with human toxocariosis is ownership of dogs or cats. For this reason, it is necessary to wash the floors daily with soap and water inside the houses or patios where the dogs live and defecate to detach the infective eggs from the surfaces and achieve their mechanical dragging to the drainage, considering that the infective eggs resist most commercial disinfectants. In addition, due to the possible presence of infective eggs attached to pet hair, it is necessary to periodically bathe and brush dogs and cats to avoid the presence of
Drainage water contaminated with
7. Health professionals involved
In summary, toxocariosis is a complex disease that, for its comprehensive control from a one health perspective, requires the knowledge of researchers and different health professionals. The veterinarian is the professional responsible for the diagnosis, control, and prevention of toxocariosis in pets that act as definitive hosts of the parasite (dogs and cats), as well as in domestic species that can act as paratenic hosts (chickens, pigs, beef, rabbits, etc.).
From the perspective of human health, the joint work of a very wide variety of health professionals is required to achieve an early and accurate diagnosis of the disease or at least a firm suspicion of the condition. Among these are parasitologists, infectologists, pediatricians, allergists, ophthalmologists, neurologists, dermatologists, imaging specialists, and epidemiologists, who are sensitized and trained to cover the entire clinical spectrum that human toxocariosis can produce. In addition, highly trained laboratory personnel are required for the parasitological, immunological, and molecular diagnosis of toxocariosis in animals and humans.
This chapter was funded by grants from PAPIIT/UNAM (No. IN210322 and IN211222). We deeply thank César Cuenca-Verde from FESC-UNAM for their technical assistance.
Conflict of interest
The authors declare no conflict of interest.
Deplazes P, Eckert J, Mathis A, Samson-Himmelstjerna GV, Zahner H. Parasitology in Veterinary Medicine. Wageningen Academic Publishers: Wageningen; 2016. p. 652
González-García T, Muñoz-Guzmán MA, Sánchez-Arroyo H, Prado-Ochoa MG, Cuéllar-Ordaz JA, Alba-Hurtado F. Experimental transmission of Toxocara canisfrom Blattella germanicaand Periplaneta americanacockroaches to a paratenic host. Veterinary Parasitology. 2017; 246:5-10
Alba-Hurtado F. Parasitología Veterinaria. Ciudad de México: UNAM; 2020. p. 184
Schnieder T, Laabs EM, Welz C. Larval development of Toxocara canisin dogs. Veterinary Parasitology. 2011; 175:193-206
Muñoz-Guzmán MA, Alba-Hurtado F. Progesterone and prolactin: Hormones important for the reactivation of Toxocara canislarvae in bitches. Advances in Neuroimmune Biology. 2018; 7:67-78
Coati N, Schnieder T, Epe C. Vertical transmission of Toxocara catiSchrank 1788 (Anisakidae) in the cat. Parasitology Research. 2004; 92:142-146
Rostami A, Riahi SM, Hofmann A, Ma G, Wang T, Behniafar H, et al. Global prevalence of Toxocarainfection in dogs. Advances in Parasitology. 2020; 109:561-583
Rostami A, Sepidarkish M, Ma G, Wang T, Ebrahimi M, Fakhri Y, et al. Global prevalence of Toxocarainfection in cats. Advances in Parasitology. 2020; 109:615-639
Overgaauw PA, Nederland V. Aspects of Toxocaraepidemiology: Toxocarosis in dogs and cats. Critical Reviews in Microbiology. 1997; 23:233-251
Fakhri Y, Gasser RB, Rostami A, Fan CK, Ghasemi SM, Javanian M, et al. Toxocaraeggs in public places worldwide-A systematic review and meta-analysis. Environmental Pollution. 2018; 242:1467-1475
Fisher M. Toxocara cati: An underestimated zoonotic agent. Trends in Parasitology. 2003; 19:167-170
Rostami A, Riahi SM, Holland CV, Taghipour A, Khalili-Fomeshi M, Fakhri Y, et al. Seroprevalence estimates for toxocariasis in people worldwide: A systematic review and metaanalysis. PLoS Neglected Tropical Diseases. 2019; 13:e0007809
Gyang PV, Akinwale OP, Lee YL, Chuang TW, Orok AB, Ajibaye O, et al. Seroprevalence, disease awareness, and risk factors for Toxocara canisinfection among primary schoolchildren in Makoko, an urban slum community in Nigeria. Acta Tropica. 2015; 46:135-140
Holland CV. Knowledge gaps in the epidemiology of Toxocara: The enigma remains. Parasitology. 2017; 144:81-94
Hotez PJ, Wilkins PP. Toxocariasis: America’s most common neglected infection of poverty and a helminthiasis of global importance? PLoS Neglected Tropical Diseases. 2009; 3:e400
Manini MP, Marchioro AA, Colli CM, Nishi L, Falavigna-Guilherme AL. Association between contamination of public squares and seropositivity for Toxocaraspp. in children. Veterinary Parasitology. 2012; 188:48-52
Hernández SA, Gabrie JA, Rodríguez CA, Matamoros G, Rueda MM, Canales M, et al. An integrated study of Toxocarainfection in Honduran children: Human seroepidemiology and environmental contamination in a coastal community. Tropical Medicine and Infectious Disease. 2020; 5:135
Wang S, Li H, Yao Z, Li P, Wang D, Zhang H, et al. Toxocarainfection: Seroprevalence and associated risk factors among primary school children in central China. Parasite. 2020; 27:30. DOI: 10.1051/parasite/2020028
Hoffmeister B, Glaeser S, Flick H, Pornschlegel S, Suttorp N, Bergmann F. Cerebral toxocariasis after consumption of raw duck liver. The American Journal of Tropical Medicine and Hygiene. 2007; 76:600-602. DOI: 10.1.1.318.4997&rep=rep1&type=pdf
Yoshikawa M, Nishiofuku M, Moriya K, Ouji Y, Ishizaka S, Kasahara K, et al. A familial case of visceral toxocariasis due to consumption of raw bovine liver. Parasitology International. 2008; 57:525-529
Choi D, Lim JH, Choi DC, Lee KS, Paik SW, Kim SH, et al. Transmission of Toxocara canisvia ingestion of raw cow liver: A cross-sectional study in healthy adults. The Korean Journal of Parasitology. 2012; 50:23-27. DOI: 10.3347/kjp.2012.50.1.23
Karaca I, Menteş J, Nalçacı S. Toxocaraneuroretinitis associated with raw meat consumption. Turkish Journal of Ophthalmology. 2018; 48:258. DOI: 10.4274/tjo.27085
Roddie G, Holland C, Stafford P, Wolfe A. Contamination of fox hair with eggs of Toxocara canis. Journal of Helminthology. 2008; 82:293-296
da Cunha-Amaral HL, Rassier GL, Pepe MS, Gallina T, Villela MM, de Oliveira-Nobre M, et al. Presence of Toxocara caniseggs on the hair of dogs: A risk factor for visceral larva migrans. Veterinary Parasitology. 2010; 174:115-118
Bakhshani A, Maleki M, Haghparast A, Shirvan SP, Borji H. A survey on Toxocara catieggs on the hair of stray cats: A potential risk factor for human toxocariasis in Northeastern Iran. Comparative Immunology, Microbiology and Infectious Diseases. 2019; 64:10-13
Maurelli MP, Santaniello A, Fioretti A, Cringoli G, Rinaldi L, Menna LF. The presence of Toxocaraeggs on dog’s fur as potential zoonotic risk in animal-assisted interventions: A systematic review. Animals. 2019; 9:827. DOI: 10.3390/ani9100827
Keegan JD, Holland CV. A comparison of Toxocara canisembryonation under controlled conditions in soil and hair. Journal of Helminthology. 2013; 87:78-84
Miller AD. Pathology of larvae and adults in dogs and cats. Advances in Parasitology. 2020; 109:537-544
Parsons JC. Ascarid infections of cats and dogs. The Veterinary Clinics of North America: Small Animal Practice. 1987; 17:1307-1339
Epe C. Intestinal nematodes: Biology and control. Veterinary Clinics of North America: Small Animal Practice. 2009; 39:1091-1107. DOI: 10.1016/j.cvsm.2009.07.002
Ursache AL, Györke A, Mircean V, Dumitrache MO, Codea AR, Cozma V. Toxocara catiand other parasitic enteropathogens: More commonly found in owned cats with gastrointestinal signs than in clinically healthy ones. Pathogens. 2021; 10:198
Muñoz-Guzmán MA, Alba-Hurtado F. Secretory-excretory antigens of Toxocara canisrecognized by puppies of the Mexico City metropolitan area. Vet Méx. 2010; 41:59-64
Ma G, Holland CV, Wang T, Hofmann A, Fan CK, Maizels RM, et al. Human toxocariasis. The Lancet Infectious Diseases. 2018; 18:14-24
Badri M, Eslahi AV, Olfatifar M, Dalvand S, Houshmand E, Abdoli A, et al. Keys to unlock the enigma of ocular toxocariasis: A systematic review and meta-analysis. Ocular Immunology and Inflammation. 2021; 29:1-12
Beaver PC, Snyder CH, Carrera GM, Dent JH, Lafferty JW. Chronic eosinophilia due to visceral larva migrans: Report of three cases. Pediatrics. 1952; 9:7-19
Carvalho EA, Rocha RL. Toxocariasis: Visceral larva migrans in children. The Journal of Pediatrics. 2012; 87:100-110
Lim JH. Toxocariasis of the liver: Visceral larva migrans. Abdominal Imaging. 2008; 33:151-156
Morsy TA. Toxocariasis: Visceral and ocular larva migrans. Journal of the Egyptian Society of Parasitology. 2020; 50:41-48
Aljeboori TI, Ivey MH. Toxocara canisinfection in baboons. The American Journal of Tropical Medicine and Hygiene. 1970; 19:249-254
Morales OL, Lopez MC, Nicholls RS, Agudelo C. Identification of Toxocara canisantigens by Western blot in experimentally infected rabbits. Revista do Instituto de Medicina Tropical de São Paulo. 2002; 44:213-216
Del Río-Araiza VH, Nava-Castro KE, Alba-Hurtado F, Quintanar-Stephano A, Muñoz-Guzmán MA, Cuenca-Micò O, et al. Endocrine immune interactions during chronic toxocariasis caused by Toxocara canisin a murine model: New insights into the pathophysiology of an old infection. Veterinary Parasitology. 2018; 252:173-179
Kavitha KT, Sreekumar C, Latha BR, Gowri AM, Nagarajan B, Azhahianambi P, et al. Migratory behaviour and pathological changes of Toxocara canisin organs and tissues of experimentally infected Balb/c mice. J Entomol Zool St. 2018; 6:2388-2392
Alba-Hurtado F, Muñoz-Guzmán MA, Valdivia-Anda G, Tórtora JL, Ortega-Pierres MG. Toxocara canis: Larval migration dynamics, detection of antibody reactivity to larval excretory–secretory antigens and clinical findings during experimental infection of gerbils ( Meriones unguiculatus). Experimental Parasitology. 2009; 122:1-5
Snyder CH. Visceral larva migrans Ten years’experience. Pediatrics. 1961; 28:85-91
Baldisserotto M, Conchin CF, Soares MDG, Araujo MA, Kramer B. Ultrasound findings in children with toxocariasis: Report on 18 cases. Pediatric Radiology. 1999; 29:316-319. DOI: 10.1007/s002470050596.pdf
Wiśniewska-Ligier M, Woźniakowska-Gęsicka T, Sobolewska-Dryjańska J, Markiewicz-Jóźwiak A, Wieczorek M. Analysis of the course and treatment of toxocariasis in children-a long-term observation. Parasitology Research. 2012; 110:2363-2371. DOI: 10.1007/s00436-011-2772-y
Desai SN, Pargewar SS, Agrawal N, Bihari C, Rajesh S. Hepatic visceral larva migrans with atypical manifestations: A report of three cases. Tropical Gastroenterology. 2020; 39:211-221. DOI: 10.7869/tg.507
Rugiero E, Cabera ME, Ducach G, Noemi I, Viovy A. Systemic toxocariasis in the adult patient. Revista Médica de Chile. 1995; 40:1097-1099
Kuenzli E, Neumayr A, Chaney M, Blum J. Toxocariasis-associated cardiac diseases—A systematic review of the literature. Acta Tropica. 2016; 154:107-120
Mohamad S, Azmi N, Noordin R. Development and evaluation of a sensitive and specific assay for diagnosis of human toxocariasis by use of three recombinant antigens (TES-26, TES-30USM, and TES-120). Journal of Clinical Microbiology. 2009; 47:1712-1717. DOI: 10.1128/JCM.00001-09
Fillaux J, Magnaval JF. Laboratory diagnosis of human toxocariasis. Veterinary Parasitology. 2013; 193:327-336
Mazur-Melewska K, Mania A, Sluzewski W, Figlerowicz M. Clinical pathology of larval toxocariasis. Advances in Parasitology. 2020; 109:153-163
Özbakış G, Doğanay A. Visceral larva migrans detection using PCR–RFLP in BALB/c mice infected with Toxocara canis. Journal of Helminthology. 2020; 94:1-8
Dietrich CF, Cretu C, Dong Y. Imaging of toxocariasis. Advances in Parasitology. 2020; 109:165-187
Wilder HC. Nematode endophthalmitis. Transactions of the American Academy of Ophthalmology and Otolaryngology. 1950; 55:99-109
Nichols RL. The etiology of visceral larva migrans: I. Diagnostic morphology of infective second-stage Toxocaralarvae. Journal of Parasitology. 1956; 42:349. DOI: 10.2307/3274518
MRH T. Ocular toxocariasis. In: Holland CV, Smith HV, editors. Toxocara: The Enigmatic Parasite. Pondicherry: Cromwell Press Ltd; 2006. pp. 127-144
Pivetti-Pezzi P. Ocular toxocariasis. International Journal of Medical Sciences. 2009; 6:129-130. DOI: 10.7150/ijms.6.129
Zibaei M, Sadjjadi SM, Jahadi-Hosseini SH. Toxocara catilarvae in the eye of a child: A case report. Asian Pacific Journal of Tropical Biomedicine. 2014; 4:S53-S55. DOI: 10.12980/APJTB.4.2014C1281
Ahn SJ, Woo SJ, Jin Y, Jin Y, Chang YS, Kim TW, et al. Clinical features and course of ocular Toxocariasis in adults. PLoS Neglected Tropical Diseases. 2014; 8:e2938. DOI: 10.1371/journal.pntd.0002938
Sharkey JA, McKay PS. Ocular toxocariasis in a patient with repeatedly negative ELISA titre to Toxocara canis. The British Journal of Ophthalmology. 1993; 77:253-254. DOI: 10.1136/bjo.77.4.253
Fata A, Hosseini SM, Woo SJ, Zibaei M, Berenji F, Farash BRH, et al. Frequency of Toxocaraantibodies in patients clinically suspected to ocular toxocariasis in the northeast of Iran. Iranian Journal of Parasitology. 2020; 16:305-311
Alba-Hurtado F, Tortora PJL, Tsutsumi V, Ortega-Pierres MG. Histopathological investigation of experimental ocular toxocariasis in gerbils. International Journal for Parasitology. 2000; 30:143-147
Taylor MRH. The epidemiology of ocular toxocariasis. Journal of Helminthology. 2001; 75:109-118
Hayashi E, Akao N, Fujita K. Evidence for the involvement of the optic nerve as a migration route for larvae in ocular toxocariasis of Mongolian gerbils. Journal of Helminthology. 2003; 77:311-315
Choi KD, Choi JH, Choi SY, Jung JH. Toxocaraoptic neuropathy: Clinical features and ocular findings. International Journal of Ophthalmology. 2018; 11:520-523
Yokoi K, Goto H, Sakai JI, Usui M. Clinical features of ocular toxocariasis in Japan. Ocular Immunology and Inflammation. 2003; 11:269-275
Stewart JM, Cubillan LD, Cunningham JR, Emmett T. Prevalence, clinical features, and causes of vision loss among patients with ocular toxocariasis. Retina. 2005; 25:1005-1013. DOI: 10.1097/00006982-200512000-00009
Bae KW, Ahn SJ, Park KH, Woo SJ. Diagnostic value of the serum anti-toxocara IgG titer for ocular toxocariasis in patients with uveitis at a tertiary hospital in Korea. Korean Journal of Ophthalmology. 2016; 30:258-264
Shields JA. Ocular toxocariasis. A review. Survey of Ophthalmology. 1984; 28:361-381
Campbell JP, Wilkinson CP. Imaging in the diagnosis and management of ocular toxocariasis. International Ophthalmology Clinics. 2012; 52:145-153
Inchauspe S, Echandi LV, Dodds EM. Diagnosis of ocular toxocariasis by detecting antibodies in the vitreous humor. Archivos de la Sociedad Española de Oftalmología. 2018; 93:220-224
Beautyman W, Woolf AL. An Ascarislarva in the brain in association with acute anterior poliomyelitis. The Journal of Pathology and Bacteriology. 1951; 63:635-647
Beautyman W, Beaver PC, Buckley JJ, Woolf AL. Review of a case previously reported as showing an ascarid larva in the brain. The Journal of Pathology and Bacteriology. 1966; 91:271-273
Springer A, Heuer L, Janecek-Erfurth E, Beineke A, Strube C. Histopathological characterization of Toxocara canis-and T. cati-induced neurotoxocarosis in the mouse model. Parasitology Research. 2019; 118:2591-2600
Meliou M, Mavridis IN, Pyrgelis ES, Agapiou E. Toxocariasis of the nervous system. Acta Parasitologica. 2020; 65:291-299
Cardillo N, Rosa A, Ribicich M, López C, Sommerfelt I. Experimental infection with Toxocara catiin BALB/c mice, migratory behaviour and pathological changes. Zoonoses and Public Health. 2009; 56:198-205
Deshayes S, Bonhomme J, de La Blanchardière A. Neurotoxocariasis: A systematic literature review. Infection. 2016; 44:565-574. DOI: 10.1007/s15010-016-0889-8
Magnaval JF, Galindo V, Glickman LT, Clanet M. Human Toxocarainfection of the central nervous system and neurological disorders: A case control study. Parasitology. 1997; 115:537-543
Worley G, Green JA, Frothingham TE, Sturner RA, Walls KW, Pakalnis VA, et al. Toxocaracanis infection: Clinical and epidemiological associations with seropositivity in kindergarten children. The Journal of Infectious Diseases. 1984; 149:591-597
Jarosz W, Mizgajska-Wiktor H, Kirwan P, Konarski J, Rychlicki W, Wawrzyniak G. Developmental age, physical fitness and Toxocaraseroprevalence amongst lower secondary students living in rural areas contaminated with Toxocaraeggs. Parasitology. 2010; 137:53-63
Marmor M, Glickman L, Shofer F, Faich LA, Rosenberg C, Cornblatt B, et al. Toxocara canisinfection of children: Epidemiologic and neuropsychologic findings. American Journal of Public Health. 1987; 77:554-559. DOI: 10.2105/AJPH.77.5.554
Nelson S, Greene T, Ernhart CB. Toxocara canisinfection in preschool age children: Risk factors and the cognitive development of preschool children. Neurotoxicology and Teratology. 1996; 18:167-174
Walsh MG, Haseeb MA. Reduced cognitive function in children with toxocariosis in a nationally representative sample of the United States. International Journal for Parasitology. 2012; 42:1159-1163
Fan CK. Pathogenesis of cerebral toxocariasis and neurodegenerative diseases. Advances in Parasitology. 2020; 109:233-259
Taylor MR, Keane CT, O'connor P, Girdwood ARW, Smith H. Clinical features of covert toxocariasis. Scandinavian Journal of Infectious Diseases. 1987; 19:693-696
Aghaei S, Riahi SM, Rostami A, Mohammadzadeh I, Javanian M, Tohidi E, et al. Toxocaraspp. infection and risk of childhood asthma: A systematic review and meta-analysis. Acta Tropica. 2018; 182:298-304
Maizels RM. Toxocara canis: Molecular basis of immune recognition and evasion. Veterinary Parasitology. 2013; 193:365-374
Mazur-Melewska K, Figlerowicz M, Cwalińska A, Mikoś H, Jończyk-Potoczna K, Lewandowska-Stachowiak M, et al. Production of interleukins 4 and 10 in children with hepatic involvement in the course of Toxocaraspp. infection. Parasite Immunology. 2016; 38:101-107. DOI: 10.1111/pim.12303
Hakim SL, Thadasavanth M, Shamilah RR, Yogeswari S. Prevalence of Toxocara canisantibody among children with bronchial asthma in Klang Hospital, Malaysia. Transactions of the Royal Society of Tropical Medical and Hygiene. 1997; 91:528-528
Muñoz-Guzmán MA, del Río-Navarro BE, Valdivia-Anda G, Alba-Hurtado F. The increase in seroprevalence to Toxocara canisin asthmatic children is related to cross-reaction with Ascaris suumantigens. Allergologia et Immunopathologia. 2010; 38:115-121
Pinelli E, Brandes S, Dormans J, Gremmer E, Van Loveren H. Infection with the roundworm Toxocara canisleads to exacerbation of experimental allergic airway inflammation. Clinical and Experimental Allergy. 2008; 38:649-658
Li L, Gao W, Yang X, Wu D, Bi H, Zhang S, et al. Asthma and toxocariasis. Annals of Allergy, Asthma & Immunology. 2014; 113:187-192
Cooper PJ. Toxocara canisinfection: An important and neglected environmental risk factor for asthma? Clinical and Experimental Allergy. 2008; 38:551-553
Gavignet B, Piarroux R, Aubin F. Millon L, Humbert P. Cutaneous manifestations of human toxocariasis. Journal of the American Academy of Dermatology 2008;59:1031-1042
Wolfrom E, Chene G, Boisseau H, Beylot C, Geniaux M, Taieb A. Chronic urticaria and Toxocara canis. Lancet. 1995; 345:196
Wolfrom E, Chene G, Lejoly-Boisseau H, Beylot C, Geniaux M, Taieb A. Chronic urticaria and toxocara canis infection. A case-control study. Annales de Dermatologie et de Venereologie. 1996, January; 123(4):240-246
Palmer CS, Thompson RA, Traub RJ, Rees R, Robertson ID. National study of the gastrointestinal parasites of dogs and cats in Australia. Veterinary Parasitology. 2008; 151:181-190
Lee AC, Schantz PM, Kazacos KR, Montgomery SP, Bowman DD. Epidemiologic and zoonotic aspects of ascarid infections in dogs and cats. Trends in Parasitology. 2010; 26:155-161