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Toxocariasis: Visceral and ocular larva migrans

Toxocariasis: Visceral and ocular larva migrans
Authors:
Peter F Weller, MD, MACP
Karin Leder, MBBS, FRACP, PhD, MPH, DTMH
Section Editor:
Edward T Ryan, MD, DTMH
Deputy Editor:
Elinor L Baron, MD, DTMH
Literature review current through: Apr 2022. | This topic last updated: Dec 21, 2021.

INTRODUCTION — Toxocariasis (also called visceral larva migrans [VLM]) refers to human infection caused by roundworms that are not natural human parasites. Toxocariasis occurs as a result of human infection with the larvae of the dog ascarid, Toxocara canis, or, less commonly, the cat ascarid, Toxocara cati. Another form of VLM is caused by human ingestion of eggs of the pig ascarid, Ascaris suum. Clinical presentations consist of VLM and ocular larva migrans (OLM); infection may also be subclinical.

EPIDEMIOLOGY — Toxocariasis occurs globally; approximately 1.4 billion people are infected worldwide [1,2]. Infection tends to occur more frequently in tropical regions with high humidity than in temperate regions, more frequently among rural populations with inadequate water supply and poor housing than among urban populations, and more commonly in areas affected by poverty [3]. Toxocara larvae can develop at temperatures <50°F, although efficiency decreases as the temperature decreases [3].

One meta-analysis estimated the global seroprevalence of Toxocara to be 19 percent (95% CI 16.6-21.4 percent) [4].

In this study, seroprevalence was highest in the African region, at 37.7 percent (95% CI 25.7-50.6 percent); this finding aligns with another seroprevalence study, which demonstrated antibodies to be common in most African countries [5]. In Southeast Asia, seroprevalence ranges from 3.9 to 84.6 percent [6], with a pooled seroprevalence of 34.1 percent (95% CI 20.2-49.4 percent) [4]. Seroprevalence in the Western Pacific was 24.2 percent (95% CI 6.0-33.5 percent), in the Americas 22.8 percent (95% CI 19.7-26.0 percent), in the European regions 10.5 percent (95% CI 8.5-12.8 percent), and in the Eastern Mediterranean region 8.2 percent (95% CI 5.1-12.0 percent) [4]. In the United States, the seroprevalence of Toxocara was estimated at 13.9 percent based on data from 1988 to 1994 [1]; in a subsequent study based on data from 2011 to 2014, the seroprevalence was estimated to be 5 percent [7]. Rates are increased among individuals living in poverty and among certain under-represented groups (especially African Americans) [7,8].

Life cycle — The life cycle of T. canis occurs in dogs and the life cycle of T. cati occurs in cats; the prevalence of Toxocara infection is highest among puppies and kittens. In North America, it is estimated that about 5 percent of dogs are infected; puppies are more commonly infected than older dogs [9].

Humans acquire the infection as accidental hosts (figure 1). Eggs are shed in the stool of the definitive host. In the environment, eggs embryonate and become infective after about three weeks. Soil contamination with infectious eggs occurs most readily in relatively warm climates, and these embryonated eggs can remain infective in the environment for several years [10]. Following ingestion of infective eggs by dogs or cats, the eggs hatch and larvae (0.5 mm in length) penetrate the gut wall. The larvae then migrate through the lungs, bronchial tree, and enter the esophagus; adult worms develop in the small intestine, where they lay eggs that are shed in the stool.

In most older animals, larvae penetrate the gut wall and, subsequently, larvae encyst in tissues. Encysted larvae can reactivate in female dogs during late pregnancy and infect puppies via transplacental and transmammary routes; adult worms can subsequently become established in the small intestines of puppies.

Toxocara can also be transmitted through ingestion of paratenic hosts (a host that is not required for the parasite life cycle but nonetheless can serve to maintain the life cycle). Eggs ingested by small noncanine mammals (such as rabbits) can hatch and larvae can penetrate the gut wall with subsequent migration into various tissues where they encyst. The life cycle is completed when dogs eat larvae encysted in the tissues of these paratenic 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 food or via ingestion of encysted larvae in the tissues of infected paratenic hosts. Direct contact with infected puppies and kittens is not classically considered to be a risk factor for human infection since the eggs must embryonate before becoming infective, although sometimes pets carry embryonated eggs in their fur. Following ingestion, the eggs hatch and larvae penetrate the intestinal wall and are carried by the circulation to a variety of tissues (liver, heart, lungs, brain, muscle, eyes). The larvae do not undergo any further development in these sites, but the host inflammatory response against the migrating larvae can cause both mechanical and immunopathologic damage to tissues, which leads to local reactions that are the basis of clinical toxocariasis.

Transmission and risk factors — Individuals who ingest embryonated eggs (in soil or on vegetables or fruits) are at risk for developing infection [11]. Infection can also be acquired via ingestion of raw liver or other undercooked meat from an infected intermediate host (rabbit, chicken, cattle, or swine) containing encapsulated larvae [12].

VLM is principally a disease of young children, especially those with exposure to playgrounds and sandboxes contaminated by dog or cat feces [13]. Having a dog as a pet is a recognized risk factor [14]; however, infection is often acquired in settings outside of the home (such as in public parks and playgrounds) [15].

Toxocara infection does occur in travelers, but the incidence is low [16-18].

CLINICAL MANIFESTATIONS — Clinical manifestations range from asymptomatic infection to severe organ injury; they occur as a consequence of damage caused by migrating larvae in addition to the host eosinophilic granulomatous response. Migration of larvae can cause eosinophilic infiltration, granuloma formation, or eosinophilic abscesses [12].

Toxocara spp larvae are unable to grow or replicate in the human host, but parasites can remain viable for at least seven years after infection [19]. Most infections are self-limited as larvae become encapsulated (usually in the musculature and liver).

There are two major categories of clinical manifestations: VLM and OLM. These have also been reported to occur simultaneously [15,20].

Visceral larva migrans — VLM occurs most commonly in young children and results in hepatitis and pneumonitis as the larvae migrate through the liver and lungs, respectively. Heavy infection may result in fever, anorexia, malaise, irritability, hepatomegaly, respiratory symptoms, pruritic urticaria-like cutaneous lesions, and eosinophilia.

Larvae frequently localize in the liver; hepatic manifestations may include hepatomegaly or nodular lesions. Pulmonary involvement may cause dyspnea, wheezing, and a chronic nonproductive cough in 20 to 80 percent of patients [21,22]. Rales are common on physical examination. The chest radiograph demonstrates abnormalities in ≥40 percent of patients with symptomatic illness. Bilateral peribronchial infiltration is most common; parenchymal infiltrates can also occur [21,22]. Computed tomography may demonstrate multifocal subpleural nodules with halo or ground-glass opacities and ill-defined margins [23]. Severe respiratory tract involvement is an uncommon complication of heavy infection. Migration of larvae through the intestinal wall can cause eosinophilic enteritis and peritonitis [24].

Toxocariasis can be mistaken for metastatic disease [25,26]; the presence of eosinophilia and radiologic findings may be helpful differentiating features. (See 'Diagnosis' below.)

Larvae can also travel via the systemic circulation to muscles, the heart, the eye, or the central nervous system (CNS) [27,28]. Cardiac involvement in Toxocara spp infection is a rare but potentially life-threatening complication. The clinical presentation may consist of myocarditis, pericarditis, Loeffler endocarditis (eosinophilic myocarditis), or pericardial effusion; heart failure or cardiac tamponade can occur and can be fatal [29,30]. (See "Endomyocardial fibrosis", section on 'Eosinophilia'.)

CNS manifestations include eosinophilic meningo-encephalitis, space-occupying lesions, myelitis, and cerebral vasculitis causing seizures [31-33]. In a meta-analysis including 11 case-control studies and more than 4700 patients with toxocariasis, an association between epilepsy and Toxocara spp seropositivity was observed (pooled odds ratio [OR] 1.69, 95% CI 1.42-2.01) [34]. Studies have also found an association between infection and cognitive delay, neurodegeneration, or psychiatric illness; however, it is uncertain whether Toxocara infection plays a causal role in pathogenesis [35-37]. Manifestations of the peripheral nervous system include radiculitis, affection of cranial nerves, or musculoskeletal involvement [38]. Death due to myocardial or CNS involvement has been described but is rare.

Ocular larva migrans — OLM involvement may occur as the sole manifestation of VLM; it often presents in individuals without antecedent history of symptomatic VLM [39]. OLM occurs most commonly among older children and adolescents [13]. In one review of ocular toxocariasis in the United States, the median patient age was 8.5 years (range 1 to 60 years) [8].

The ocular lesion is due to larval localization in the eye and the granulomatous response around the larva. Common symptoms are unilateral visual impairment, blurry vision, photophobia, floaters, leukocoria, subsequently causing failing vision and strabismus. The typical lesion is a posterior pole or peripheral whitish elevated granuloma. Occasionally, OLM may present as uveitis (often intermediate and posterior uveitis), papillitis, endophthalmitis, scleritis, or chronic endophthalmitis [40]. Ocular lesions may resemble retinoblastoma (table 1) [41]. The most serious consequence of infection is invasion of the retina with granuloma formation in the periphery or posterior pole, leading to dragging of the retina and eventual retinal detachment, which can lead to blindness [42]. Other complications include ocular hypertension, cataract formation, macular cyst edema, and persistent vitreous opacity [43].

OLM is discussed further separately. (See "Approach to the child with leukocoria", section on 'Ocular toxocariasis'.)

Other presentations — Toxocara can also present with other manifestations. Mild infection may present with eosinophilia only. Other symptoms may include fever, headache, behavioral disturbances, anorexia, abdominal pain, rash, hepatomegaly, nausea, vomiting, as well as wheezing and pulmonary infiltrates [15,44].

Wheezing and pulmonary infiltrates, together with eosinophilia, are also the hallmark features of childhood asthma. It has been postulated that the presence of Toxocara larvae in lungs may be an underlying factor in the onset of allergic pulmonary disease, perhaps because of the host response to the parasite. In a meta-analysis including 17 studies (11 case-control studies and six cross-sectional studies), an increased risk for asthma among children with Toxocara infection seropositivity was observed (OR 1.91, 95% CI 1.47-2.47) [45]. However, a causal association remains uncertain, as both positive associations and negative epidemiologic studies have been reported [46,47].

Cutaneous manifestations are relatively common, either alone, together with eosinophilia, and/or in conjunction with other clinical manifestations of toxocariasis. Chronic urticaria is the most dermatologic manifestation; others include chronic pruritus, transient rash, different forms of eczema, hypodermic nodules, eosinophilic panniculitis, and vasculitis [48,49].

Two additional toxocariasis syndromes have been described: "covert toxocariasis" (seen mainly in children) and "common toxocariasis" (seen predominantly in adults); these are probably variations of the same clinical entity with manifestations varying according to the site and intensity of infection and the age of the host [50,51]. Covert toxocariasis refers to nonspecific symptoms and signs including fever, abdominal pain, anorexia, nausea, vomiting, hepatomegaly, cough, headache, lethargy, behavioral and/or sleep disturbances, skin symptoms, limb pains, and lymphadenitis associated with high titers of anti-Toxocara antibodies, with or without eosinophilia [52]. Common toxocariasis refers to a syndrome comprised of chronic weakness, shortness of breath, abdominal pain, rash, itch, urticarial and arthralgia, often with eosinophilia, high immunoglobulin (Ig)E levels, and high titers of Toxocara-specific antibodies [53].

Laboratory tests — In general, VLM should be suspected in the setting of compatible clinical manifestations, together with leukocytosis, eosinophilia, and hypergammaglobulinemia (elevated serum levels of IgE and IgG). Marked leukocytosis with eosinophilia occurs in more than 30 percent of cases of VLM, and elevated titers of anti-A or anti-B isohemagglutinins are commonly observed in about 50 percent of patients [15].

There is no peripheral blood eosinophilia in most cases of OLM, presumably because of the low larval load [54]. Eosinophilia may also be absent in patients with long-standing infection and in those with cutaneous symptoms only [50]. An eosinophilic granulomatous hepatitis may develop, leading to abnormalities in liver function tests including elevated transaminases and/or alkaline phosphatase.

DIAGNOSIS — In general, the diagnosis of toxocariasis should be suspected based on history, clinical examination, and laboratory findings of leukocytosis and eosinophilia; the diagnosis is confirmed via serology (or molecular methods if available) [55].

Laboratory assays — There are several commercial enzyme-linked immunosorbent assay (ELISA) antibody assays that detect human IgG antibodies to Toxocara excretory/secretory antigens of the third-stage larvae of T. canis. The test can detect subclinical or mild infection, though it cannot differentiate between T. canis and T. cati infections. The reliability varies by assay and clinical presentation. As an example, for VLM and some forms of covert toxocariasis, the sensitivity and specificity of the Toxocara enzyme immunoassay (titer 1:32) are estimated at about 78 percent and 92 percent, respectively [13,15,56].

A positive ELISA result does not necessarily demonstrate the presence of active Toxocara infection or prove that clinical symptoms are attributable to toxocariasis; the result must be interpreted in the setting of compatible clinical symptoms and epidemiologic exposure. However, a negative test can help to rule out VLM, although ocular and neurologic toxocariasis can occur with negative serology. Cross-reactivity of the ELISA assay with other parasite antigens is common, and the test may remain positive for several years even following treatment. In some settings, positive ELISA results can be confirmed by western blot [57], which has better sensitivity and specificity compared with ELISA [58] but is also more expensive and labor intensive [59].

Future improvements in Toxocara serodiagnosis will likely include the use of recombinant antigens, simpler assay formats, IgG4 subclass detection, and antigen detection tests [60,61]. Polymerase chain reaction-based methods for detecting Toxocara in clinical samples have been described but are not commercially available [62]. Definitive diagnosis of VLM may also be established via detection of larvae in biopsy tissue, which will show Toxocara larvae within eosinophilic granulomatous lesions. However, biopsy is rarely indicated.

The sensitivity of ELISA for OLM is considerably lower than for VLM; the diagnosis of OLM generally relies on the findings on ophthalmologic examination (picture 1) [63]. Negative serology can occur with a positive vitreous titer [64]. It is possible to compare the antibody levels between the serum and aqueous humour; if the (level of specific IgG in aqueous humour/level of specific IgG in serum)/(total IgG in aqueous humour/total IgG in serum) is greater than 3.0, this can be considered diagnostic [65].

Stool examinations are not helpful since the parasite does not complete a full life cycle involving the human gastrointestinal tract.

Pulmonary involvement may result in eosinophilia that is detectable in bronchoalveolar lavage (BAL) fluid. One case of marked pulmonary infiltration demonstrated 64 percent eosinophils in the BAL analysis [58].

In the setting of central nervous system involvement, the cerebrospinal fluid may show eosinophils [66]. (See "Eosinophilic meningitis".)

Imaging studies — Hepatic and cerebral lesions may be observed with ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) [67,68]. In one review of radiographic changes associated with hepatic VLM, CT and MRI showed multiple, ill-defined lesions, usually measuring 1.0 to 1.5 cm in diameter, scattered throughout the liver parenchyma [12]. Lesions are usually oval but may be angular or trapezoid. The lesions differ from metastatic nodules in that they are usually uniform in size, nonspherical in shape, and are best seen on portal venous phase (image 1). Pulmonary VLM appear on CT as multifocal subpleural nodules with halo or ground-glass opacities (GGOs) and ill-defined margins (image 2) [23].

In one review of radiographic changes associated with pulmonary VLM, four patterns were observed: GGOs, solid nodules, consolidation, and linear opacities; lower lung involvement was predominant [69].

Ultrasound biomicroscopy has been used as a diagnostic technique for the evaluation of patients with ocular toxocariasis [70].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of VLM includes:

Strongyloidiasis – Transpulmonary migration of Strongyloides larvae can produce dry cough, throat irritation, dyspnea, wheezing, and hemoptysis. Similarly, pulmonary involvement of toxocariasis may cause dyspnea, wheezing, and a chronic, nonproductive cough. Strongyloides larvae may be detected in stool, sputum, bronchoalveolar lavage fluid, or pleural fluid. (See "Strongyloidiasis".)

Schistosomiasis – Schistosomiasis can cause periportal fibrosis and eosinophilia; in general, there are no apparent signs of liver dysfunction. This is in contrast with VLM, which may be associated with abnormal liver function tests including elevated transaminases and/or alkaline phosphatase. The diagnosis of schistosomiasis is established with stool microscopy and/or serologic testing. (See "Schistosomiasis: Epidemiology and clinical manifestations" and "Schistosomiasis: Diagnosis".)

Ascariasis – Ascariasis may be associated with pneumonitis (known as Loeffler syndrome) in sensitized individuals during larval migration through the lungs. Pulmonary symptoms are less common in regions with continuous transmission of Ascaris lumbricoides. Ascariasis may also involve the biliary tree but is not associated with hepatitis as with VLM. The diagnosis of ascariasis is usually established via stool microscopy. (See "Ascariasis".)

EchinococcusEchinococcus is associated with cystic lesions in the liver and lung that may be demonstrated with ultrasonography or computed tomography; VLM may be appreciated on computed tomography as nodular lesions. The diagnosis of Echinococcus is established with a combination of imaging and serology. (See "Echinococcosis: Clinical manifestations and diagnosis".)

Allergic bronchopulmonary aspergillosis – Allergic bronchopulmonary aspergillosis is a complex hypersensitivity reaction that occurs when bronchi become colonized by Aspergillus species. Clinical manifestations include recurrent episodes of bronchial obstruction, fever, malaise, cough, and peripheral blood eosinophilia. Chest radiography may demonstrate parenchymal infiltrates and bronchiectasis. (See "Clinical manifestations and diagnosis of allergic bronchopulmonary aspergillosis".)

The differential diagnosis of OLM includes:

Retinoblastoma – Both retinoblastoma and OLM may present with strabismus, poor vision, and leukocoria ("white pupil") (table 1). The diagnosis of retinoblastoma can usually be made with dilated ophthalmoscopic examination. Pathology is necessary to confirm the diagnosis. (See "Retinoblastoma: Clinical presentation, evaluation, and diagnosis".)

Toxoplasmosis – Toxoplasmosis can cause chorioretinitis (a posterior uveitis). It is suspected based on a characteristic scarring appearance (picture 2); the diagnosis is supported by serology. (See "Toxoplasmosis: Ocular disease".)

Ocular tuberculosis – Ocular tuberculosis may be presumed in the presence of suggestive ocular findings (such as choroidal granuloma, broad-based posterior synechiae, retinal vasculitis with or without choroiditis, or serpiginous-like choroiditis) in combination with systemic findings consistent with tuberculosis.

Other parasitic infections can cause eosinophilia in the setting of focal lesions; examples include capillariasis (liver lesions) and gnathostomiasis (brain lesions).

TREATMENT — The treatment approach varies according to symptoms and location of the larvae; data are limited. Treatment is generally based on clinical experience and expert opinion. Most individuals with mild symptoms due to toxocariasis do not require anthelminthic therapy; symptoms are usually self-limited and resolve within a few weeks [71]. Eosinophilia may resolve much more slowly over many months, likely due to ongoing antigenic stimulation from dead larvae. In the setting of protracted symptoms, the possibility of reinfection (such as from continued ingestion of contaminated soil) should be considered.

For individuals with moderate to severe symptoms due to VLM, treatment consists of albendazole (400 mg orally with fatty meal twice daily for five days) [72]. In cases of severe respiratory, myocardial, or central nervous system involvement, concomitant prednisone (0.5 to 1 mg/kg/day) is warranted. Some favor treatment in the setting of moderate eosinophilia and positive serology even in the setting of minimal symptoms, given risk of larval localization to the brain during the course of infection [50,54].

For treatment of OLM topical or systemic corticosteroids are used to control intraocular inflammation. If there is sight-threatening ocular inflammation, we favor treatment with anti-inflammatory therapy with corticosteroids (eg, prednisone 0.5 to 1 mg/kg/day with slow taper). The extent of benefit on initial clinical symptoms achieved by adding in albendazole therapy is uncertain but recurrences are reduced [73,74]. In addition to prednisolone, we therefore recommend albendazole 400 mg orally twice daily for two weeks, given with a fatty meal. The optimal dosing for albendazole is uncertain; data are limited to retrospective studies [75]. In complicated cases, surgical intervention may be warranted [76].

Mebendazole (100 to 200 mg orally twice daily for five days) is an alternative to albendazole [77], but albendazole is preferred (particularly in OLM and neurologic disease) since it crosses the blood-brain barrier. Ivermectin does not appear to be effective for toxocariasis [78]. Diethylcarbamazine (3 to 4 mg/kg/day for 21 days, starting at 25 mg/day for adults) has been found to be effective in a small number of cases but has greater side effects than albendazole so it is rarely used.

Follow-up consists of monitoring the eosinophil count, which usually decreases within one month of treatment [79]. Serology is not a good follow-up tool because IgG decreases very slowly. Studies have suggested that IgE decreases after therapy [80], but this is not reliable [59].

PREVENTION — Good hygiene practices, timely disposal of pet feces, and routine deworming of pets are important strategies for prevention of toxocariasis in humans [8]. Hand washing should be encouraged after contact with pets or areas at high risk for soil contamination, such as playgrounds and sandboxes [8]. Education regarding behaviors that increase risk for infection is also important, including geophagia and consumption of raw or undercooked meat (particularly liver). Consuming raw vegetables that have been irrigated by contaminated wastewater or grown in soil contaminated with Toxocara eggs is also a risk factor for infection; cooking or thorough rinsing in clean water will render foods safe [81].

SUMMARY AND RECOMMENDATIONS

Toxocariasis (also called visceral larva migrans [VLM]) refers to human infection caused by helminths that are not natural human parasites. Toxocariasis occurs as a result of human infection with the larvae of the dog ascarid, Toxocara canis, or, less commonly, the cat ascarid, Toxocara cati. VLM is principally a disease of young children, especially those with exposure to playgrounds and sandboxes contaminated by dog or cat feces. (See 'Introduction' above.)

The life cycle of T. canis occurs in dogs (figure 1). Puppies are a major source of environmental egg contamination. Humans are accidental hosts who become infected by ingesting eggs in contaminated soil or encysted larvae in the tissues of infected paratenic hosts. Ingested eggs mature into larvae which penetrate the intestinal wall and are carried by the circulation to a variety of tissues (liver, heart, lungs, brain, muscle, eyes). The larvae can cause severe local reactions at these sites. (See 'Life cycle' above.)

Larvae frequently localize in the liver; hepatic manifestations may include hepatomegaly or nodular lesions. Mild infection may be asymptomatic and only suspected by the finding of elevated blood eosinophilia. Heavy infection may result in fever, anorexia, malaise, irritability, hepatomegaly, and pruritic urticaria-like cutaneous lesions. Ocular larva migrans (OLM) is due to larval localization in the eye and the granulomatous response around the larva. Common symptoms are unilateral visual impairment and subsequent strabismus; complete visual loss can occur. (See 'Clinical manifestations' above.)

VLM should be suspected in the setting of compatible clinical manifestations together with leukocytosis, eosinophilia, and hypergammaglobulinemia (elevated serum levels of immunoglobulin [Ig]E and IgG). In the appropriate clinical scenario, the diagnosis can be confirmed by enzyme-linked immunosorbent assay antibody assay, which detects human IgG antibodies to Toxocara excretory/secretory antigens. (See 'Laboratory tests' above.)

In general, individuals with mild symptoms may not require anthelminthic therapy as symptoms are usually self-limited. For individuals with moderate to severe symptoms, we suggest treatment with albendazole (Grade 2C). In cases of severe respiratory, myocardial, or central nervous system involvement, we suggest concomitant treatment with prednisone (Grade 2C). (See 'Treatment' above.)

Good hygiene practices, timely disposal of pet feces, and routine deworming of pets are important strategies for prevention of toxocariasis in humans. Hand washing should be encouraged after contact with pets or areas at high risk for soil contamination, such as playgrounds and sandboxes. (See 'Prevention' above.)

  1. Won KY, Kruszon-Moran D, Schantz PM, Jones JL. National seroprevalence and risk factors for Zoonotic Toxocara spp. infection. Am J Trop Med Hyg 2008; 79:552.
  2. Ma G, Rostami A, Wang T, et al. Global and regional seroprevalence estimates for human toxocariasis: A call for action. Adv Parasitol 2020; 109:275.
  3. Azam D, Ukpai OM, Said A, et al. Temperature and the development and survival of infective Toxocara canis larvae. Parasitol Res 2012; 110:649.
  4. Rostami A, Riahi SM, Holland CV, et al. Seroprevalence estimates for toxocariasis in people worldwide: A systematic review and meta-analysis. PLoS Negl Trop Dis 2019; 13:e0007809.
  5. Lötsch F, Grobusch MP. Seroprevalence of Toxocara spp. antibodies in humans in Africa: A review. Adv Parasitol 2020; 109:483.
  6. Chou CM, Fan CK. Seroprevalence of Toxocara spp. infection in Southeast Asia and Taiwan. Adv Parasitol 2020; 109:449.
  7. Liu EW, Chastain HM, Shin SH, et al. Seroprevalence of Antibodies to Toxocara Species in the United States and Associated Risk Factors, 2011-2014. Clin Infect Dis 2018; 66:206.
  8. Centers for Disease Control and Prevention (CDC). Ocular toxocariasis--United States, 2009-2010. MMWR Morb Mortal Wkly Rep 2011; 60:734.
  9. Mohamed AS, Moore GE, Glickman LT. Prevalence of intestinal nematode parasitism among pet dogs in the United States (2003-2006). J Am Vet Med Assoc 2009; 234:631.
  10. Despommier D. Toxocariasis: clinical aspects, epidemiology, medical ecology, and molecular aspects. Clin Microbiol Rev 2003; 16:265.
  11. Glickman LT, Cypess RH. Toxocara infection in animal hospital employees. Am J Public Health 1977; 67:1193.
  12. Lim JH. Toxocariasis of the liver: visceral larva migrans. Abdom Imaging 2008; 33:151.
  13. Hotez PJ, Wilkins PP. Toxocariasis: America's most common neglected infection of poverty and a helminthiasis of global importance? PLoS Negl Trop Dis 2009; 3:e400.
  14. Carvalho EA, Rocha RL. Toxocariasis: visceral larva migrans in children. J Pediatr (Rio J) 2011; 87:100.
  15. Rubinsky-Elefant G, Hirata CE, Yamamoto JH, Ferreira MU. Human toxocariasis: diagnosis, worldwide seroprevalences and clinical expression of the systemic and ocular forms. Ann Trop Med Parasitol 2010; 104:3.
  16. Baaten GG, Sonder GJ, van Gool T, et al. Travel-related schistosomiasis, strongyloidiasis, filariasis, and toxocariasis: the risk of infection and the diagnostic relevance of blood eosinophilia. BMC Infect Dis 2011; 11:84.
  17. Van Den Broucke S, Kanobana K, Polman K, et al. Toxocariasis diagnosed in international travelers at the Institute of Tropical Medicine, Antwerp, Belgium, from 2000 to 2013. PLoS Negl Trop Dis 2015; 9:e0003559.
  18. Overbosch FW, van Gool T, Matser A, Sonder GJB. Low incidence of helminth infections (schistosomiasis, strongyloidiasis, filariasis, toxocariasis) among Dutch long-term travelers: A prospective study, 2008-2011. PLoS One 2018; 13:e0197770.
  19. Smith H, Holland C, Taylor M, et al. How common is human toxocariasis? Towards standardizing our knowledge. Trends Parasitol 2009; 25:182.
  20. Paul M, Stefaniak J, Twardosz-Pawlik H, Pecold K. The co-occurrence of Toxocara ocular and visceral larva migrans syndrome: a case series. Cases J 2009; 2:6881.
  21. Huntley CC, Costas MC, Lyerly A. Visceral larva migrans syndrome: clinical characteristics and immunologic studies in 51 patients. Pediatrics 1965; 36:523.
  22. Snyder C. Visceral larva migrans — ten years' experience. Pediatrics 1961; 28:85.
  23. Sakai S, Shida Y, Takahashi N, et al. Pulmonary lesions associated with visceral larva migrans due to Ascaris suum or Toxocara canis: imaging of six cases. AJR Am J Roentgenol 2006; 186:1697.
  24. Arslan F, Baysal NB, Aslan A, et al. Toxocara related peritonitis: A case report and review of literature. Parasitol Int 2019; 73:101950.
  25. Ota KV, Dimaras H, Héon E, et al. Toxocariasis mimicking liver, lung, and spinal cord metastases from retinoblastoma. Pediatr Infect Dis J 2009; 28:252.
  26. Anderson A, Fordham LA, Bula ML, Blatt J. Visceral larval migrans masquerading as metastatic disease in a toddler with Wilms tumor. Pediatr Radiol 2006; 36:265.
  27. Marx C, Lin J, Masruha MR, et al. Toxocariasis of the CNS simulating acute disseminated encephalomyelitis. Neurology 2007; 69:806.
  28. Enko K, Tada T, Ohgo KO, et al. Fulminant eosinophilic myocarditis associated with visceral larva migrans caused by Toxocara canis infection. Circ J 2009; 73:1344.
  29. Kuenzli E, Neumayr A, Chaney M, Blum J. Toxocariasis-associated cardiac diseases--A systematic review of the literature. Acta Trop 2016; 154:107.
  30. Park SJ, Jang CW, Kim YK, et al. Toxocariasis-Associated Acute Perimyocarditis with Cardiogenic Shock: A Case Report. Am J Case Rep 2021; 22:e930573.
  31. Dzikowiec M, Góralska K, Błaszkowska J. Neuroinvasions caused by parasites. Ann Parasitol 2017; 63:243–253.
  32. Deshayes S, Bonhomme J, de La Blanchardière A. Neurotoxocariasis: a systematic literature review. Infection 2016; 44:565.
  33. Bossi G, Bruno R, Novati S, et al. Cerebral Toxocariasis as a Cause of Epilepsy: A Pediatric Case. Neuropediatrics 2021; 52:142.
  34. Luna J, Cicero CE, Rateau G, et al. Updated evidence of the association between toxocariasis and epilepsy: Systematic review and meta-analysis. PLoS Negl Trop Dis 2018; 12:e0006665.
  35. Hotez PJ. Toxocariasis: A neglected infection for the Anthropocene epoch. Adv Parasitol 2020; 109:879.
  36. Nicoletti A. Neurotoxocariasis. Adv Parasitol 2020; 109:219.
  37. Gale SD, Hedges DW. Neurocognitive and neuropsychiatric effects of toxocariasis. Adv Parasitol 2020; 109:261.
  38. Jabbour RA, Kanj SS, Sawaya RA, et al. Toxocara canis myelitis: clinical features, magnetic resonance imaging (MRI) findings, and treatment outcome in 17 patients. Medicine (Baltimore) 2011; 90:337.
  39. Good B, Holland CV, Taylor MR, et al. Ocular toxocariasis in schoolchildren. Clin Infect Dis 2004; 39:173.
  40. Stewart JM, Cubillan LD, Cunningham ET Jr. Prevalence, clinical features, and causes of vision loss among patients with ocular toxocariasis. Retina 2005; 25:1005.
  41. Chuah CT, Lim MC, Seah LL, et al. Pseudoretinoblastoma in enucleated eyes of Asian patients. Singapore Med J 2006; 47:617.
  42. Suh LH, Sweeney DA, Jun AS. A 33-year-old man with a white pupil. Clin Infect Dis 2006; 43:1043.
  43. Boye B, Wayne M, Sukumaran S, Vijayan V. Blurry Vision and Irregularly Shaped Pupil in a 3-Year-Old Female. Clin Pediatr (Phila) 2019; 58:1038.
  44. Fan CK, Holland CV, Loxton K, Barghouth U. Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders? Clin Microbiol Rev 2015; 28:663.
  45. Aghaei S, Riahi SM, Rostami A, et al. Toxocara spp. infection and risk of childhood asthma: A systematic review and meta-analysis. Acta Trop 2018; 182:298.
  46. Cooper PJ. Interactions between helminth parasites and allergy. Curr Opin Allergy Clin Immunol 2009; 9:29.
  47. Li L, Gao W, Yang X, et al. Asthma and toxocariasis. Ann Allergy Asthma Immunol 2014; 113:187.
  48. Gavignet B, Piarroux R, Aubin F, et al. Cutaneous manifestations of human toxocariasis. J Am Acad Dermatol 2008; 59:1031.
  49. Recuero JK, Binda G, Kiszewski AE. Eosinophilic panniculitis associated with toxocariasis in a child. An Bras Dermatol 2019; 94:250.
  50. McGuinness SL, Leder K. Global burden of toxocariasis: A common neglected infection of poverty. Curr Trop Med Rep 2014; 1:52.
  51. Mazur-Melewska K, Mania A, Sluzewski W, Figlerowicz M. Clinical pathology of larval toxocariasis. Adv Parasitol 2020; 109:153.
  52. Taylor MR, Keane CT, O'Connor P, et al. Clinical features of covert toxocariasis. Scand J Infect Dis 1987; 19:693.
  53. Glickman LT, Magnaval JF, Domanski LM, et al. Visceral larva migrans in French adults: a new disease syndrome? Am J Epidemiol 1987; 125:1019.
  54. Pawlowski Z. Toxocariasis in humans: clinical expression and treatment dilemma. J Helminthol 2001; 75:299.
  55. Chen J, Liu Q, Liu GH, et al. Toxocariasis: a silent threat with a progressive public health impact. Infect Dis Poverty 2018; 7:59.
  56. Jones JL, Kruszon-Moran D, Won K, et al. Toxoplasma gondii and Toxocara spp. co-infection. Am J Trop Med Hyg 2008; 78:35.
  57. Magnaval JF, Fabre R, Maurières P, et al. Application of the western blotting procedure for the immunodiagnosis of human toxocariasis. Parasitol Res 1991; 77:697.
  58. Roig J, Romeu J, Riera C, et al. Acute eosinophilic pneumonia due to toxocariasis with bronchoalveolar lavage findings. Chest 1992; 102:294.
  59. Fillaux J, Magnaval JF. Laboratory diagnosis of human toxocariasis. Vet Parasitol 2013; 193:327.
  60. Rodríguez-Caballero A, Martínez-Gordillo MN, Medina-Flores Y, et al. Successful capture of Toxocara canis larva antigens from human serum samples. Parasit Vectors 2015; 8:264.
  61. Noordin R, Yunus MH, Tan Farrizam SN, Arifin N. Serodiagnostic methods for diagnosing larval toxocariasis. Adv Parasitol 2020; 109:131.
  62. Fogt-Wyrwas R, Jarosz W, Mizgajska-Wiktor H. Utilizing a polymerase chain reaction method for the detection of Toxocara canis and T. cati eggs in soil. J Helminthol 2007; 81:75.
  63. Despommier D. Toxocariasis: clinical aspects, epidemiology, medical ecology, and molecular aspects. Clin Microbiol Rev 2003; 16:265.
  64. Inchauspe S, Echandi LV, Dodds EM. Diagnosis of ocular toxocariasis by detecting antibodies in the vitreous humor. Arch Soc Esp Oftalmol (Engl Ed) 2018; 93:220.
  65. de Visser L, Rothova A, de Boer JH, et al. Diagnosis of ocular toxocariasis by establishing intraocular antibody production. Am J Ophthalmol 2008; 145:369.
  66. Eberhardt O, Bialek R, Nägele T, Dichgans J. Eosinophilic meningomyelitis in toxocariasis: case report and review of the literature. Clin Neurol Neurosurg 2005; 107:432.
  67. Jain R, Sawhney S, Bhargava DK, et al. Hepatic granulomas due to visceral larva migrans in adults: appearance on US and MRI. Abdom Imaging 1994; 19:253.
  68. Zachariah SB, Zachariah B, Varghese R. Neuroimaging studies of cerebral "visceral larva migrans" syndrome. J Neuroimaging 1994; 4:39.
  69. Lee KH, Kim TJ, Lee KW. Pulmonary Toxocariasis: Initial and Follow-Up CT Findings in 63 Patients. AJR Am J Roentgenol 2015; 204:1203.
  70. Liu J, Li S, Deng G, et al. Ultrasound biomicroscopic imaging in paediatric ocular toxocariasis. Br J Ophthalmol 2017; 101:1514.
  71. Schantz PM, Glickman LT. Toxocaral visceral larva migrans. N Engl J Med 1978; 298:436.
  72. Drugs for Parasitic Infections, 3rd ed, The Medical Letter, New Rochelle, NY 2013.
  73. Woodhall D, Starr MC, Montgomery SP, et al. Ocular toxocariasis: epidemiologic, anatomic, and therapeutic variations based on a survey of ophthalmic subspecialists. Ophthalmology 2012; 119:1211.
  74. Barisani-Asenbauer T, Maca SM, Hauff W, et al. Treatment of ocular toxocariasis with albendazole. J Ocul Pharmacol Ther 2001; 17:287.
  75. Jee D, Kim KS, Lee WK, et al. Clinical Features of Ocular Toxocariasis in Adult Korean Patients. Ocul Immunol Inflamm 2016; 24:207.
  76. Giuliari GP, Ramirez G, Cortez RT. Surgical treatment of ocular toxocariasis: anatomic and functional results in 45 patients. Eur J Ophthalmol 2011; 21:490.
  77. Magnaval JF. Comparative efficacy of diethylcarbamazine and mebendazole for the treatment of human toxocariasis. Parasitology 1995; 110 ( Pt 5):529.
  78. Magnaval JF. Apparent weak efficacy of ivermectin for treatment of human toxocariasis. Antimicrob Agents Chemother 1998; 42:2770.
  79. Magnaval JF, Glickman LT, Dorchies P, Morassin B. Highlights of human toxocariasis. Korean J Parasitol 2001; 39:1.
  80. Elefant GR, Shimizu SH, Sanchez MC, et al. A serological follow-up of toxocariasis patients after chemotherapy based on the detection of IgG, IgA, and IgE antibodies by enzyme-linked immunosorbent assay. J Clin Lab Anal 2006; 20:164.
  81. Bowman DD. Ascaris and Toxocara as foodborne and waterborne pathogens. Res Vet Sci 2021; 135:1.
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