Continuing Education Activity

Toxocariasis is a neglected parasitic infection caused by roundworm larvae that can migrate through multiple organs and produce asymptomatic, ocular, visceral, neurological, or covert disease. Diagnosis remains challenging because symptoms are often nonspecific, serological testing cannot distinguish active from past infection, and severe ocular or neurological complications may occur without peripheral eosinophilia. A measurable practice gap exists in clinicians’ ability to recognize high-risk exposures, select appropriate diagnostic testing, and initiate timely treatment. This activity reviews transmission, clinical syndromes, laboratory and imaging evaluation, anthelmintic therapy, adjunctive corticosteroid use, prevention, and One Health strategies. Participants will gain practical skills to improve diagnostic accuracy, reduce preventable complications, counsel patients and families, and coordinate care with infectious disease specialists, veterinarians, and public health professionals.

Objectives:

• Differentiate ocular toxocariasis, visceral larva migrans, neurotoxocariasis, and covert or common toxocariasis according to characteristic manifestations.
• Select an appropriate treatment regimen based on the patient's age, disease severity, and organ involvement.
• Implement preventive counseling on pet deworming, hygienic disposal of feces, exposure to contaminated soil, and consumption of raw or undercooked meat.
• Implement interprofessional team strategies to improve care coordination and communication and advance the diagnosis, management, and prevention of toxocariasis.

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Introduction

Human toxocariasis is a roundworm infection classified by the World Health Organization as one of the neglected parasitic diseases with significant public health impact.[1][WHO. Global Report on Neglected Tropical Diseases 2024: Executive Summary] The 2 predominant species that cause human infection are Toxocara canis and Toxocara cati. Their life cycles involve a variety of animals that act as definitive hosts, most notably dogs and cats. Humans are accidental hosts and acquire infection by ingesting embryonated eggs from contaminated soil, water, or food or by ingesting larvae in undercooked meat from paratenic animals, such as chickens, rabbits, sheep, and cows. Infection in humans can range from an asymptomatic or mild illness to a life-threatening disease.

Although the highest rates of infection occur in resource-poor parts of the world, toxocariasis occurs worldwide. Toxocariasis remains an understudied and underdiagnosed infectious disease with significant knowledge gaps.[2] Symptoms of infection are often nonspecific and vary depending on the organs involved and the host's immune function. Furthermore, diagnosis is challenging and requires a high index of suspicion. Ocular and central nervous system infections due to Toxocara spp are the most common forms of severe organ involvement, although infection can affect a variety of organs. Exposure to contaminated environments poses a high risk of infection in children. This article will review the etiology, pathophysiology, clinical manifestations, diagnosis, treatment, and prevention of toxocariasis. The article also emphasizes the importance of interprofessional cooperation in treating the disease.

Etiology

Dogs, other canids (eg, foxes, coyotes, and wolves), and felines acquire gastrointestinal tract infections, where the worms complete their life cycle and produce eggs that are excreted in feces (see Image 1. Life Cycle of Toxocara canis). Environmental contamination with embryonated eggs leads to human infection. Humans are considered accidental hosts because ingested eggs in the human gastrointestinal tract release larvae that cannot mature into adult worms. However, the larvae can penetrate the gastrointestinal tract mucosa, enter the circulatory system, and migrate to virtually any organ. Commonly infected organs include the eyes, central nervous system, liver, and lungs. In addition, a covert form of infection without identifiable organ involvement is well recognized.

Toxocara spp eggs in the feces of infected canids and felines are released into the environment, where they can remain infectious for years. In the definitive hosts, the eggs hatch, and the emerging larvae penetrate the intestinal mucosa and migrate via the circulatory system to the liver and lungs. The larvae continue to mature in the lungs, travel to the trachea and oropharynx, are swallowed, enter the intestine, and mature into adult worms, which then reproduce. Female adult worms produce several thousand eggs per day. When accidental hosts ingest embryonated eggs, larvae hatch in the intestine, penetrate the intestinal mucosa, enter the circulation, and migrate to organs. Although the larvae are unable to complete their maturation cycle in an accidental host, they can remain viable in the tissues for many years.

Dogs and cats can acquire infection in several ways: transplacental transmission; ingestion of embryonated eggs in contaminated soil; or ingestion of larvae in the tissues of infected paratenic animals, such as fowl, rodents, rabbits, sheep, and cows. Humans acquire infection by accidentally ingesting contaminated soil, water, plants, or undercooked meat from paratenic animals. Children are particularly prone to infection because of their tendency to put infected objects and contaminated fingers in their mouths. In addition, children are frequently exposed to contaminated playground soil and sandboxes. Eggs attached to the fur of dogs and cats can be another source of environmental contamination and accidental ingestion.[3]

Epidemiology

Toxocara organisms are prevalent worldwide. Tropical countries and resource-limited regions tend to have the highest prevalence. Infection with T canis appears more prevalent than with T cati, although definitive evidence is lacking. Results from seroprevalence surveys show infection rates among dogs and cats ranging from less than 7% in Australia and Europe to 50% to 100% in parts of Africa, India, and China.[2] The seroprevalence of Toxocara spp in dogs and cats in the US is not well established. 

Results from seroprevalence surveys of human infection with Toxocara spp showed rates of approximately 14% in the US, 1.5% in Japan, 7% in Sweden, 20% in Malaysia, 22% in Iran, and 81% in Nepal. Seroprevalence rates can vary significantly within countries based on ethnic and socioeconomic factors.[2] In the US, approximately 10,000 clinical cases are diagnosed annually.[4][5] Risk factors for disease include poverty, young age, and a high concentration of dogs and cats in the local environment. Results from environmental sampling identified Toxocara spp eggs in soil samples collected in the US, South America, Europe, Africa, and Asia.[3] Additional sampling would likely identify contaminated soil worldwide.

Pathophysiology

Clinical disease results from the migration of nematode larvae through tissues. The signs and symptoms vary according to the affected organ and the host's inflammatory response. Toxocariasis has been classified into 4 clinical syndromes: ocular toxocariasis, visceral larva migrans, neurotoxocariasis, and covert or common toxocariasis. Covert toxocariasis most often presents with simple, persistent eosinophilia and may be attributed to the continuation of the migratory phase. The classification scheme is based on historical recognition of the most common clinical manifestations of infection. Clinical manifestations may overlap, other organ systems may be involved, and long-term complications remain poorly defined.[2] The larval migratory phase can last for years.[6] Larvae can accumulate in organs and incite localized and systemic type 2 helper T-cell immune responses.[6] 

Histopathology

While histologic demonstration of larvae within tissue is considered definitive evidence of infection, the method is rarely used for the clinical diagnosis of toxocariasis. Histologic evaluation requires an invasive procedure and trained microscopists. Additionally, organisms frequently appear degenerated in microscopic tissue sections and can be difficult to distinguish from other larval parasites.

History and Physical

Key features of the history and physical examination depend on the organ systems involved, the presence of repeated infections, the parasite burden, and the host's inflammatory response. Most Toxocara infections remain asymptomatic. However, a broad range of symptoms can develop because various organ systems may be involved. Table 1 summarizes the different forms of toxocariasis. 

 Table 1. Characteristics of the Different Clinical Forms of Toxocariasis*

Table

Abbreviations: VLM, visceral larva migrans; OT, ocular toxocariasis; CT, covert or common toxocariasis; NT, neurotoxocariasis*Modified from Chen et al. Infectious Diseases of Poverty (2018) 7:59 http://creativecommons.org/licenses/by/4.0/

Evaluation

Toxocariasis is easily diagnosed in dogs and cats by detecting eggs in their feces. However, the diagnosis of toxocariasis in humans is challenging. Because larvae do not mature into adult worms in humans, eggs are not produced. As mentioned earlier, histologic demonstration of larvae in tissue provides definitive proof of infection, but this method is rarely used in practice.[7] Therefore, diagnosis requires a high index of suspicion. A presumptive diagnosis requires an epidemiological history, a potential exposure history, clinical manifestations, and indirect laboratory test results. The presence of peripheral eosinophilia is often a clue.[8][9] However, patients with ocular toxocariasis and neurotoxocariasis often lack peripheral eosinophilia.[10][11]

Serological tests, notably enzyme-linked immunosorbent assays, are commonly used. However, these tests cannot distinguish acute from chronic infection, and their sensitivity can vary significantly depending on the antigens and antibodies used in the assay.[2] Cross-reactivity with other helminth infections is common. Moreover, serology alone cannot establish a diagnosis of active toxocariasis.[12] The specificity of serological testing ranges from approximately 78% to 92% because of cross-reactivity with other helminth infections.[13] A confirmatory Western blot can increase specificity.

Serology of immigrants with unexplained eosinophilia has proved helpful in identifying individuals with Toxocara spp infection.[14] Enzyme-linked immunosorbent assay analysis of serum, cerebrospinal fluid, and vitreous fluid is used for the presumptive diagnosis of neurotoxocariasis and ocular toxocariasis, respectively. Molecular detection methods for stool and blood samples from dogs and cats are readily available. However, these methods have limited application in humans, because testing requires DNA obtained from infected tissue, cerebrospinal fluid, or ocular material.[15][16][17]

Radiology may provide suggestive evidence of toxocariasis. On ultrasonography and CT scans, eosinophilic granulomas can appear as ill-defined oval lesions.[18][19][20] Imaging of the lungs may show ground-glass opacities and ill-defined nodules.[21] A variety of imaging modalities, including computed tomography, MRI, ultrasonography, and fluorescein angiography, may be used to provide diagnostic clues in patients with ocular toxocariasis.[18][19] Suggestive MRI findings of neurotoxocariasis include hyperintense white matter lesions on fluid-attenuated inversion recovery and T2-weighted images.[22]

A combination of clinical signs and symptoms, eosinophil counts, serologic analysis, and radiographic imaging is the most commonly used method for a presumptive diagnosis of toxocariasis. In patients with presumed ocular toxocariasis and neurotoxocariasis, enzyme-linked immunosorbent assay analysis of ocular fluid and cerebrospinal fluid, respectively, should be obtained. Molecular detection of Toxocara spp DNA in cerebrospinal fluid and ocular material should be sought. Quantitative and serial serologic titers cannot independently establish a definitive diagnosis or response to therapy. A combination of clinical improvement, eosinophil levels, serologic titers, and follow-up radiographic imaging can help assess the response to therapy.[18][23]

Treatment / Management

The approach to treatment depends in part on the classification of toxocariasis being treated. Few large, well-controlled clinical trials have evaluated the efficacy and safety of anthelmintic medications for toxocariasis. The anthelmintic medications albendazole, mebendazole, thiabendazole, and diethylcarbamazine are approved for treatment. Albendazole is considered the drug of choice because it achieves relatively high concentrations in visceral organs, ocular tissues, and the central nervous system. A combination of albendazole and corticosteroids is recommended for the treatment of neurotoxocariasis and ocular toxocariasis.[24][25] In addition, surgical procedures may be necessary to preserve vision in severe cases of ocular toxocariasis. Corticosteroids may also be necessary adjuncts to anthelmintic therapy in cases of pulmonary and cardiac toxocariasis. Finally, results from animal models and case studies evaluating ivermectin for the treatment of toxocariasis were inconclusive regarding efficacy.[26][27][28][29]

Recommendations for the duration of anthelmintic therapy vary, and the lack of rigorous clinical trials makes it difficult to specify a duration with a high degree of certainty.[30] Some research findings indicate that a 5-day course of albendazole for visceral larva migrans has a cure rate of 45% to 70%. Recommendations range from 5 to 14 days of therapy for visceral larva migrans. Results from reports indicated similar efficacy with mebendazole and diethylcarbamazine, although both agents have higher rates of adverse effects. Furthermore, prolonged courses of albendazole, ranging from 4 to 8 weeks for the treatment of neurotoxocariasis, were effective in approximately 80% of cases.[3] However, the use and dosage of albendazole remain controversial in children younger than 2 years. The Centers for Disease Control and Prevention recommends the standard 400-mg dose, whereas the World Health Organization recommends a 200-mg dose in children younger than 2 years.[13] Therefore, clinicians should consult infectious disease specialists and state and federal agencies for treatment recommendations.

Differential Diagnosis

The differential diagnosis for visceral larva migrans is extensive, because many infectious and inflammatory diseases may cause eosinophilia, fever, and organ dysfunction. Because toxocariasis occurs worldwide, clinicians should consider local endemicity. Local endemicity should also be considered when evaluating ocular toxocariasis, neurotoxocariasis, and covert or common toxocariasis. Notably, ocular and neural larva migrans due to the helminth Baylisascaris procyonis can be difficult to distinguish from ocular toxocariasis and neurotoxocariasis.[31] Retinoblastoma and ocular infections due to other parasitic, viral, bacterial, and fungal agents are also included in the differential diagnosis of ocular toxocariasis.

Prognosis

Toxocariasis is most often an asymptomatic, mild infectious disease. Disease severity is likely a function of parasite burden, frequency of recurrent infection, and host immune response. Unfortunately, clinicians cannot predict which infected individuals are likely to develop severe complications. Therefore, anthelmintic therapy is recommended for all infected individuals to reduce the risk of complications. The prognosis for patients with ocular toxocariasis and neurotoxocariasis is less certain; the risks of blindness and progressive neurological dysfunction are of great concern. In addition, toxocariasis has been implicated as a possible cause of chronic asthma, neurocognitive disorders, and seizures.[32]

Complications

Toxocariasis can cause numerous complications. The following is a partial list of associated complications:

• Central nervous system diseases
• Ocular diseases
• Eosinophilic hepatitis
• Eosinophilic pneumonia
• Asthma
• Neurocognitive dysfunction
• Fever
• Pruritis
• Seizures
• Neuropsychiatric disorders
• Myocarditis
• Nephritis

Consultations

Consultations should be obtained with infectious disease clinicians and state and federal public health agencies for recommendations regarding optimal approaches to diagnosis and therapy.

Deterrence and Patient Education

Based on currently available tests, clinicians have a limited ability to distinguish between active infection and past inactive infection due to Toxocara spp. Serologic assays can remain positive for years after treatment. The rate of recurrent infection can be high in populations residing in highly endemic regions. Children are at particularly high risk of acquiring and reacquiring toxocariasis because of their exposure to contaminated environments.[33][34] Importantly, certain cultural behaviors, such as consuming raw or undercooked contaminated meat, are difficult to change.[35] Healthcare professionals practicing in many regions with low endemicity are unfamiliar with toxocariasis and may miss opportunities to intervene in individuals with Toxocara infection. The risk is particularly relevant for individuals immigrating from areas of high endemicity.[14]

Preventive efforts should emphasize deworming pets and hygienically disposing of their feces. Few robust clinical studies have assessed the optimal anthelmintic regimen for treating seropositive individuals without symptoms and patients experiencing a variety of Toxocara–associated diseases. Given the worldwide epidemiology and complications resulting from this neglected parasitic disease, greater global efforts are needed to improve prevention, diagnosis, and treatment.

Pearls and Other Issues

The following are pearls regarding toxocariasis:

• Toxocariasis is caused by roundworm parasites.
• Dogs and cats are definitive hosts.
• Toxocara canis and Toxocara cati are the predominant species causing human infection.
• Infection with T canis is thought to be more common, but this has not been definitively established.
• Both T canis and T cati have similar life cycles and cause the same disease manifestations.
• Toxocariasis has a worldwide distribution and affects several billion people.

  • Tropical and resource-limited regions have the highest prevalence.
  • Children are at high risk of acquiring an infection.
• Adult worms reside in the intestines of dogs and cats and produce several hundred thousand eggs daily.
• Infected dogs and cats contaminate the environment through fecal excretion of Toxocara eggs.
• Humans and other animals are accidental hosts.

  • Eggs are accidentally ingested from contaminated soil, water, and plants.
  • Ingestion of larvae contained in raw or undercooked meat from paratenic animals is another source of human infection.
  • Eggs give rise to larvae in the human intestine.
  • Larvae penetrate the intestine and migrate to various organs.
  • A high inoculum of ingested eggs and larvae, along with repeated infections, can result in a high parasite burden.
  • Larvae can remain viable in organs for many years.
  • Most infections remain asymptomatic.
  • The liver, lungs, eyes, and central nervous system are the most commonly infected organs.
• Symptomatic disease can take many forms and present with nonspecific symptoms and signs.
• Severe disease often involves the eyes and the central nervous system.
• Eosinophilia is commonly associated with infection.

  • Chronic inflammation and allergic reactions are common complications.
• Diagnosis is challenging and requires a high index of suspicion.

  • Serological assays are most commonly used to make a presumptive diagnosis.

    • Serological assays do not distinguish acute from chronic infection.
    • These assays cross-react with other helminth infections.
    • A Western blot is required to confirm a diagnosis, but is not readily available.
  • Microscopic evaluation requires an invasive procedure and experienced microscopists.
  • Tissue microscopy can be used to definitively establish a diagnosis. Consequently, it is not often performed.
  • Radiographs can be helpful as an adjunct to diagnosis.
• In clinical practice, the diagnosis is presumptive and often based on a combination of clinical symptoms, eosinophilia, serology, and radiographic imaging.
• The anthelmintic medications albendazole, mebendazole, thiabendazole, and diethylcarbamazine are approved for treatment.

  • Albendazole is the drug of choice because of its pharmacokinetic and adverse effect profile.
  • Dosage and duration of therapy depend on the patient's age, disease extent, and the organ system involved.

    • Robust clinical trials assessing optimal therapy are lacking.
  • Adjunct corticosteroids are administered to treat inflammation in patients with ocular and central nervous system disease.
  • Patients with asymptomatic Toxocara spp infection should be treated to reduce the risk of ocular and central nervous system disease.
• Prevention is difficult to achieve due to large populations of feral canids and cats.

  • Young children's behavior places them at risk of ingesting contaminated soil.
  • Household pets should be dewormed.
  • Pet feces should be disposed of hygienically.
  • Consumption of raw or undercooked animal meat should be avoided.

Enhancing Healthcare Team Outcomes

The treatment and prevention of Toxocara infection are complex because toxocariasis is not solely a human disease and requires a One Health approach. Domestic animal carrier rates directly affect the risk of acquisition; vertical transmission is common in dogs and cats, and no vaccine exists. Therefore, interprofessional collaboration is necessary for adequate control. The first challenge is increasing awareness. Toxocariasis is considered a neglected tropical infection, given the limited research, funding, and publicity it receives despite its significant disease burden. The roles of the primary care clinician, public health practitioner, infectious disease specialist, and veterinarian are invaluable in educating patients about preventing this parasitic infection.

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Disclosure: Ellis Tobin declares no relevant financial relationships with ineligible companies.

Disclosure: Claire Milam declares no relevant financial relationships with ineligible companies.

Disclosure: Lacey Menkin-Smith declares no relevant financial relationships with ineligible companies.