Version July 2025
INTRODUCTION —
Toxocariasis refers to human infection caused by roundworms that are not natural human parasites, but rather are canine or feline parasites. Toxocariasis occurs as a result of human infection with the larvae of the canid (dog, fox, wolves) ascarid, Toxocara canis, or, less commonly, the cat ascarid, Toxocara cati.
While most infections are asymptomatic or subclinical, infections can cause symptomatic presentations. These include visceral larva migrans (VLM), ocular larva migrans (OLM), or least commonly, neurologic involvement [1].
Another form of VLM is caused by human ingestion of eggs of Ascaris suum [2]. (See "Ascariasis".)
EPIDEMIOLOGY —
Because most infections are subclinical, data on the prevalence of toxocariasis are based on serologic testing.
Toxocariasis occurs globally; approximately 1.4 billion people are infected worldwide [3,4]. 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 [5]. Toxocara larvae can develop at temperatures <50°F, although efficiency decreases as the temperature decreases [5].
One meta-analysis estimated the global seroprevalence of Toxocara to be 19 percent (95% CI 16.6-21.4 percent) [6].
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 [7]. In Southeast Asia, seroprevalence ranges from 3.9 to 84.6 percent [8], with a pooled seroprevalence of 34.1 percent (95% CI 20.2-49.4 percent) [6]. 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) [6]. In the United States, the seroprevalence of Toxocara was estimated at 13.9 percent based on data from 1988 to 1994 [3]; in a subsequent study based on data from 2011 to 2014, the seroprevalence was estimated to be 5 percent [9]. Rates are increased among individuals living in poverty and among certain under-represented groups (especially African Americans) [9,10].
Life cycle — The life cycle of T. canis occurs in dogs, foxes, and wolves; the life cycle of T. cati occurs in cats. The prevalence of Toxocara infection is highest among puppies and kittens.
In the United States, studies of dogs and cats evaluated at veterinary clinics have detected T. canis in 2.5 percent of dogs [11] and T. cati in 4.6 percent of cats [12]. In one study in western Europe, 3.6 percent of dogs were infected with T. canis [13].
Sources of infections include more than domesticated dogs and cats; in a study of feral cats in the United States, 45 percent had fecal exams for T. cati [14]. In a study from Palestine, 46 percent of dogs excreted T. canis eggs; infection rates were higher among stray dogs [15]. A variety of wild canids may be infected with T. canis [16], including red foxes [17]. Infections in canid and felid hosts propagate new infections within non-human hosts as well as excrete eggs infectious for humans.
Humans acquire the infection as accidental hosts (figure 1). Eggs are shed in the stool of the canid or felid 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 [18]. 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 animals that ingest infectious Toxocara eggs, larvae penetrate the gut wall; subsequently, larvae encyst in tissues. In female dogs, encysted larvae can reactivate during late pregnancy and infect their puppies via transplacental and transmammary routes; adult worms can subsequently become established in the small intestines of puppies.
Toxocara can also be transmitted to canid and felid animals via ingestion of paratenic hosts (a host that is not required for the parasite life cycle but nonetheless can serve to maintain the life cycle) (figure 1). Eggs ingested by noncanine mammals 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 (even if not Toxocara infected) or on their paws [19]. 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.
Human transmission and risk factors — Individuals who ingest infectious Toxocara larvae, either from embryonated eggs (in soil or on vegetables or fruits) or less commonly, from animal tissues, are at risk for developing infection [20].
The principal group at risk for acquiring toxocariasis is young children. A review of 65 studies from 22 countries estimated the global seroprevalence for toxocariasis in children to be 25 percent (95% CI 22.0-29.0) with the highest prevalence in Thailand (58.2 percent, 95% CI 50.9-65.5) and the lowest prevalence in Colombia (7.04 percent, 95% CI 3.05-11.3) [21]. There was no difference in risk between rural and urban areas [21].
Among children (but not adults), having a dog is a recognized risk factor [22]. Infections are often acquired outside of the home, such as in public parks and playgrounds, that are widely contaminated with Toxocara eggs [23,24]. Ingestion of infectious eggs derived from Toxocara contaminated soil accounts for most cases of pediatric toxocariasis.
Toxocariasis may be transmitted by two foodborne routes [25]:
●Ground-grown vegetables, including lettuce and spinach, may be contaminated with T. canis and T. cati eggs. In a study of produce samples from four commercial farms in the United Kingdom, 23 percent (95% CI 16.7-31.7) harbored T. canis eggs and 1.7 percent (95% CI 0.5-5.9) bore T. cati eggs [26]. Dogs and foxes were implicated as likely sources of garden contamination. The clinical significance of foodborne transmission to humans is not certain.
●Ingestion of raw liver or other undercooked meat from an infected intermediate host (rabbit, chicken, cattle, or swine) containing encapsulated larvae is another mode of foodborne transmission [25]. Various animal studies have noted that following infection with T. canis, encysted viable larvae may be found in tissues [27]. Infectious larvae of T. canis and T. cati have been detected in various sources, including ostrich, wild boar meat, and free range chickens [28,29]. Human infections have been acquired from eating various tissues, including liver and meat [25,26].
Toxocara infection does occur in travelers, but the incidence is low [30-32].
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 [33].
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 [34]. Most infections are self-limited as larvae become encapsulated (usually in the musculature and liver).
Asymptomatic infection — Many Toxocara infections (as evidenced by anti-Toxocara antibodies) are likely asymptomatic, especially in children. The association with eosinophilia is variable. In a study of migrant children from a pediatric unit in Spain that monitored anti-Toxocara serologies, 65.3 percent were asymptomatic and 57.1 percent had eosinophilia [35].
Signs and symptoms — Two clinical presentations of toxocariasis 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 [36,37].
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/or lymphadenitis associated with high titers of anti-Toxocara antibodies, with or without eosinophilia [38].
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 [39].
Visceral larva migrans
●Transmission via egg ingestion – Classic 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 [40,41]. 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 [40,41]. Computed tomography may demonstrate multifocal subpleural nodules with halo or ground-glass opacities and ill-defined margins [42]. Severe respiratory tract involvement is an uncommon complication of heavy infection.
Migration of larvae through the intestinal wall can cause eosinophilic enteritis and peritonitis [43]. Larvae can also travel via the systemic circulation to muscles, the heart, the eye, or the central nervous system [44,45].
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 [46,47]. (See "Endomyocardial fibrosis", section on 'Eosinophilia'.)
●Transmission via ingestion of animal tissue with encysted Toxocara larvae – Migration of ingested larvae within human tissues can cause multi-organ involvement. Cases of VLM, occurring principally in adults, have been reported following ingestion of raw chicken livers [48] and or raw bovine liver [49]. Cultural preferences in eating animal liver or other organs is reflected in regions where animal foodborne toxocariasis have been documented [27] (notably Korea [50] and other Asian countries). The clinical consequences arise from larval migrations into various organs, including the liver and lung [51].
Toxocariasis can be mistaken for metastatic disease [51-53]; the presence of eosinophilia and radiologic findings may be helpful differentiating features. (See 'Diagnosis' below.)
Ocular larva migrans — OLM involvement may occur as the sole manifestation of toxocariasis; it often presents in individuals without antecedent history of symptomatic VLM [54]. OLM occurs most commonly among older children and adolescents [55]. In one review of ocular toxocariasis in the United States, the median patient age was 8.5 years (range 1 to 60 years) [10]. In a study of 211 patients from Shanghai, China, the median age was 7.7 years [56].
The ocular lesion is due to larval localization in the eye and the granulomatous response around the larva. Presentations of OLM include [57]:
●Posterior granuloma, typically submacular or peripapillary often with prominent retinal striae or folds
●Peripheral granuloma with vitreoretinal traction extending toward the posterior pole
●Unilateral or panuveitis
Common symptoms are unilateral visual impairment, blurry vision, photophobia, floaters, leukocoria, subsequently causing failing vision and strabismus. A typical lesion is a posterior pole or peripheral whitish elevated granuloma. OLM may present as uveitis (often intermediate and posterior uveitis), papillitis, endophthalmitis, scleritis, or chronic endophthalmitis [56,58]. Ocular lesions may resemble retinoblastoma (table 1) [59].
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 [60]. Other complications include ocular hypertension, cataract formation, macular cyst edema, and persistent vitreous opacity [61].
Neural toxocariasis — The migrations of Toxocara larvae within neural tissues are recognized, although uncommon, and may cause varied manifestations depending on the presumed site of larval localization and any attendant inflammation. Larvae are rarely documented within lesions, so the presumptive diagnosis rests on positive anti-Toxocara serologies and attendant blood and/or CSF eosinophilia. While neural involvement may arise from classic pediatric VLM, many infections are likely acquired in adults due to food-borne acquisition.
The most common presentation of neural toxocariasis is myelitis [62]. Of note, 2 of 28 European travelers seen in Antwerp, Belgium, with toxocariasis presented with transverse myelitis [31]. In a review of 104 patients with neurotoxocariasis, 70 presented with myelitis. Males accounted for 87 percent and the mean age was 42.3 +/- 15.2 years. Sensory and motor deficits often with autonomic dysfunction were common. Concomitant liver or lung involvement compatible with larval migrations were found in approximately 13 percent [62].
Neural toxocariasis may also present with cerebral involvement. In the review of 104 patients, 34 patients (18 males, mean age 33.5 +/- 21.3 years) had cerebral involvement [62]. Cerebral manifestations include encephalitis, eosinophilic meningo-encephalitis, space-occupying lesions, and cerebral vasculitis [62-65]. Less common manifestations in the peripheral nervous system include radiculitis, affection of cranial nerves, or musculoskeletal involvement [66].
In addition to myelitis and cerebral presentations of neurotoxocariasis, sero-epidemiologic studies, based on positive Toxocara serologies, have associated infections with epilepsy and altered cognitive function. 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) [67]. An analysis of the United States National Health and Nutrition Examination Survey (NHANES) from 2011 to 2015 reported that among 3188 United States adults aged 60 and above, seropositive toxocariasis was associated with worse working memory, sustained attention, processing speed and global cognition [68]. Other studies have also found an association between infection and cognitive delay, neurodegeneration, or psychiatric illness. [69,70]. However, in part recognizing issues on the specificity and chronicity of assayed anti-Toxocara antibodies, it is uncertain whether Toxocara infection plays a causal role in such pathogenesis.
Other presentations — Toxocariasis in its covert/common forms can present with varied 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 [71,72]. 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) [73]. However, a causal association remains uncertain, as both positive associations and negative epidemiologic studies have been reported [74-76].
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 common dermatologic manifestation; others include chronic pruritus, transient rash, different forms of eczema, hypodermic nodules, eosinophilic panniculitis, and vasculitis [77,78].
Laboratory findings — 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 [71].
There is no peripheral blood eosinophilia in most cases of OLM, presumably because of the low larval load [79]. Eosinophilia may also be absent in patients with long-standing infection and in those with cutaneous symptoms only [36].
DIAGNOSIS
Clinical suspicion — 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) [80].
Laboratory assays — Antibody assays to detect infections with the T. canis and T cati ascarids can be confounded by cross-reactivity with other ascarid and other helminth parasites [4]. In addition, available assays cannot differentiate between recent and prior infection, and often remain positive for decades in the absence of disease [34].
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 [1]. 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 [55,71,81].
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 toxocariasis, 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 [82], which has better sensitivity and specificity compared with ELISA [34,83] but is also more expensive and labor intensive [84].
Future improvements in Toxocara serodiagnosis will likely include the use of recombinant antigens, simpler assay formats, IgG4 subclass detection, and antigen detection tests [85,86]. Polymerase chain reaction-based methods for detecting Toxocara in clinical samples have been described but are not commercially available [87]. Definitive diagnosis of toxocariasis 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) [88]. Negative serology can occur with a positive vitreous titer [89]. It is possible to compare the antibody levels between the serum and aqueous humor; if the (level of specific IgG in aqueous humor/level of specific IgG in serum)/(total IgG in aqueous humor/total IgG in serum) is greater than 3.0, this can be considered diagnostic [90].
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 [83].
In the setting of central nervous system involvement, the cerebrospinal fluid may show eosinophils [91]. (See "Eosinophilic meningitis".)
Imaging studies — Hepatic and cerebral lesions may be observed with ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) [92,93]. 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 [33]. 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) [42].
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 [94].
Ultrasound biomicroscopy has been used as a diagnostic technique for the evaluation of patients with ocular toxocariasis [95].
DIFFERENTIAL DIAGNOSIS —
The differential diagnosis of toxocariasis 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 due to Ascaris lumbricoides may be associated with pneumonitis (known as Loeffler syndrome) in sensitized individuals during larval migration through the lungs. The diagnosis of ascariasis is usually established via stool microscopy. Infections with the porcine Ascaris suum may cause a VLM syndrome. (See "Ascariasis".)
●Echinococcus – Echinococcus 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
Preferred approach
Visceral larva migrans — 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.
●Antihelminthic therapy
•Mild symptoms – Most individuals with mild symptoms due to toxocariasis do not require anthelminthic therapy; symptoms are usually self-limited and resolve within a few weeks [96]. Eosinophilia may or may not 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 or foods) should be considered.
•Moderate to severe symptoms – For individuals with moderate to severe symptoms due to toxocariasis, treatment consists of albendazole (400 mg orally with fatty meal twice daily for five days) [97].
For individuals in East Asia (where toxocariasis in adults is largely food-borne and relapse with new liver or lung lesions has been described), treatment consists of albendazole (400 mg orally with fatty meal twice daily) for four weeks [98]. If new liver or lung lesions develop, a repeat course of albendazole (same dose) for eight weeks is warranted.
●Role of steroids – 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 [36,79].
Ocular larva migrans — 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 [99,100]. In addition to prednisone, 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 [101]. In complicated cases, surgical intervention and larval extraction may be required [102,103].
Alternative agents — Mebendazole (100 to 200 mg orally twice daily for five days) is an alternative to albendazole [104], but albendazole is preferred (particularly in OLM and neurologic disease) since it is better absorbed and crosses the blood-brain barrier. Ivermectin does not appear to be effective for toxocariasis [105].
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 — Follow-up consists of monitoring the eosinophil count, which variably decreases after treatment. Serology is not a good follow-up tool because IgG decreases very slowly. Studies have suggested that IgE decreases after therapy [106], but this is not reliable [84].
PREVENTION —
Good hygiene practices, timely disposal of pet feces, and routine deworming of pets are important strategies for prevention of toxocariasis in humans [10]. Hand washing should be encouraged after contact with pets or areas at high risk for soil contamination, such as playgrounds and sandboxes [10]. 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 [107].
SUMMARY AND RECOMMENDATIONS
●General principles – Toxocariasis 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 canine ascarid, Toxocara canis, or, less commonly, the cat ascarid, Toxocara cati. Toxocariasis is often a disease of young children, especially those with exposure to playgrounds and sandboxes contaminated by dog or cat feces. Toxocariasis can develop in adults following consumption of raw liver and tissues from animals. (See 'Introduction' above.)
●Life cycle – The life cycle of T. canis occurs in dogs, foxes, and wolves (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 inflammatory reactions at these sites. (See 'Life cycle' above.)
●Clinical manifestations – 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.)
●Diagnosis – The syndrome of 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 findings' above.)
●Treatment – 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.)
●Prevention – 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. In addition, the consumption of raw liver and meat from Toxocara infected animals should be avoided. (See 'Prevention' above.)
