eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Toxocariasis

Author: Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Coauthor(s): Marcelo Laufer, MD, Division of Pediatric Infectious Diseases, Attending, Miami Children's Hospital
Contributor Information and Disclosures

Updated: Jan 27, 2009

Introduction

Background

Toxocariasis is caused by Toxocara canis and, less frequently, Toxocara catis, which are intestinal nematodes (roundworms) found in dogs and cats, respectively. In humans, toxocariasis is considered an aberrant infection because humans are incidental hosts, and the parasites cannot completely mature in the human body. Instead, the invasive larvae migrate for months through different organs until they are overcome by the human inflammatory reaction and die. The larvae can survive in tissues for at least 9 years and, possibly, for the life of the host.

Three clinical forms of toxocariasis are traditionally described; these include visceral larva migrans (VLM), ocular larva migrans (OLM), and covert toxocariasis. Numerous disease manifestations have also been attributed to these parasites.

Diagnosis is based on serologic findings. Polymerase chain reaction (PCR) has been introduced as a diagnostic tool. Examination of stools has no role in the evaluation of toxocariasis. Whether or not the infection should be treated and, if so, when and how it should be treated is controversial. Mebendazole, thiabendazole, albendazole, and diethylcarbamazine, among others, are agents used in the treatment. Corticosteroids also have a significant role in therapy.

Pathophysiology

Most frequently, human toxocariasis is caused by T canis, a canine roundworm. Adult T canis female worms are usually found in young puppies and lactating female dogs. The adult T canis female worms can excrete as many as 200,000 eggs per day. These eggs need several weeks of optimal environmental conditions (10-35°C, high soil humidity) to develop from noninfective unembryonated forms to infective embryonated eggs. The embryonated eggs are resistant to freezing, moisture, and extreme pH levels.

When a dog ingests the infective eggs, the larvae hatch in the small intestine, penetrate the intestinal wall, and gain access to the blood and lymphatic circulation. The larvae invade the liver, lungs, and other tissues. In most dogs, the larval maturation process is arrested in most tissues, but in a pregnant female, T canis resumes development and migrates across the placenta, infecting the fetus. After the birth of the puppies, the larvae continue their maturation process, migrating from the lungs to the GI tract via the trachea; they achieve their mature forms in the puppies' intestinal tracts. Female dogs then become reinfected while caring for their puppies. The main sources of eggs, therefore, are puppies younger than 3 months and lactating female dogs.

Humans are paratenic hosts for T canis. Paratenic hosts are transport hosts in which the larvae never develop into adult worms. The infection is acquired by ingesting T canis embryonated eggs. Sources of these eggs include areas where dogs defecate, such as parks. As much as 20-30% of soil samples from public parks and children's sandboxes are contaminated with Toxocara eggs. Infections acquired by ingestion of raw snails and raw lamb have also been reported.

The cat roundworm, T catis, has a life cycle similar to that of T canis except that vertical transmission is due to lactation more than transplacental transmission. One report documents 4 cases of adult T catis intestinal infection in children. However, in most cases, humans are paratenic hosts. T catis causes fewer cases of human infection than T canis, probably because of the defecation patterns of cats, which make environmental infestation less frequent.

Tissue damage is due to the host inflammatory reaction more than the infection itself. The larvae produce glycosylated proteins, usually referred to as Toxocara excretory secretory antigens. These antigens induce a Th2-type CD4+ cellular immune response characterized by the production of interleukin 4 that promotes the switching of B-cell isotypes to the production of immunoglobulin E (IgE) and interleukin 5. These, in turn, promote eosinophil differentiation and vascular adhesion.

Although Toxocara organisms are the most common causes of VLM, case reports have noted other zoonotic nematodes that cause VLM, including Ascaris suum,1 Baylisascaris procyonis (raccoon ascarid), and Lagochilascaris minor (opossum ascarid).

Frequency

United States

Toxocariasis is a public health problem. The prevalence of infection in different communities is directly proportional to the infection rates among canines and the free access of dogs to public places. Obviously, the higher the rate of infected dogs and the easier their access to public places, the more easily humans are exposed to infective eggs. Because eggs need weeks in the soil to become infective, direct contact with young puppies is not a risk factor for acquiring disease. Young children are at higher risk because of their play habits and tendency to place their fingers in their mouths. Children with pica (geophagia) and children who have contact with puppy litters are particularly at risk, as are children with mental retardation. In tropical climates, the high temperature and humidity favor the embryonization of eggs.

The prevalence of seropositivity varies not only from country to country but also in different regions within a country. The real prevalence of toxocariasis is difficult to estimate because tests are performed only when the diagnosis is suspected, and most infections are asymptomatic. The seroprevalence of children, as measured with enzyme-linked immunosorbent assay (ELISA), varies from 4-8%. Seroprevalence is higher in the southeastern United States and Puerto Rico. Minorities, such as black and Hispanic groups, have rates as high as 16-30%.

International

The prevalence of human toxocariasis in tropical regions is higher than that in the United States. The highest seroprevalence ever recorded was in a village of Santa Lucia, West Indies, where the prevalence was 86% in children aged 6 months to 6 years. This community had an extraordinarily high rate of canine T canis infection combined with peridomestic areas contaminated with canine waste and pica habits among the children. Serologic surveys in different countries reveal seropositivity rates of 19% in the Netherlands, 2.5% in Germany, 39% in Brazil, 5.8-36% in the Czech Republic, 0-37% in Spain, 5.2% in Cuba, 10.9 % in Jordan, 47.5% in Colombia, 81% in Nepal, and 13% in the Slovak Republic.

An interesting study in Venezuela stresses the higher risk of the disadvantaged sectors of society for acquiring the infection.2 In this study, only 1.8% of middle-class urban subjects had positive findings, compared with 20% of urban-slum dwellers, 25% of rural farmers, and 35% of Amazon Indians. In Bolivia, toxocariasis was thought to be one of the causes of the higher prevalence of epilepsy, particularly partial epilepsy.

Mortality/Morbidity

Although sudden death due to T canis infestation has been reported, mortality is unusual. The major morbid condition is decreased visual acuity caused by OLM. Evidence suggests that toxocariasis may be one of the causative factors of allergic asthma.

Race

No racial predilection has been noted.

Sex

Boys usually have higher seroprevalence than girls. This is probably related to differences in play behavior.

Age

Individuals of all ages are at risk. Although the seroprevalence increases with age, VLM with more severe symptoms occurs mainly in young children. VLM is diagnosed mainly in children aged 1-7 years. OLM is more common in older children and young adults.

Clinical

History

The 3 clinical forms of toxocariasis that are traditionally described include the following:

  • Visceral larva migrans (VLM)
    • General: The classic VLM syndrome consists of episodes of fever, coughing and wheezing, anemia, eosinophilia, hepatomegaly, and positive Toxocara titers. The patient usually has malaise, asthenia, and vague abdominal symptoms. VLM is diagnosed mainly in children aged 1-7 years. Systemic disease rarely results in ocular disease. Many organs can be involved in VLM.
    • Dermatologic
      • Skin lesions, such as urticaria and nodules, have been described. Toxocariasis can cause chronic idiopathic urticaria, especially when it is associated with eosinophilia.
      • Well syndrome is an eosinophilic cellulitis of unknown origin. A report described 2 cases with clinical and histologic features of Well syndrome with positive anti-Toxocara titers.3 Not only did the symptoms respond to treatment with albendazole, but the antibody titer also normalized. However, studies of toxocariasis as the cause of chronic urticaria are inconsistent.
      • After an initial study demonstrating T canis antibodies in 65% of patients with chronic urticaria (n=51), compared with 21% in controls (n=81), others found a seroprevalence of 20% in chronic urticaria (n=128) versus 13% in controls (n=236), a seroprevalence of 8% in chronic urticaria (n=110), a seroprevalence of 13% in children with the condition, and a seroprevalence of 30% in controls.4
    • Pulmonary: Wheezing is a common sign of VLM. Progression to eosinophilic pneumonia and respiratory failure has been reported. Isolated reports describe diffuse noncavitating pulmonary nodules and pleural effusions. A case report that described a 65-year-old previously healthy male with a 2-week history of fever and night sweats; weight loss; eosinophilia; high erythrocyte sedimentation rate; and abnormal chest radiograph findings that revealed bilateral hilar and mediastinal lymphadenopathy and discrete bilateral pleurisy demonstrates that, in its acute presentation, VLM can be confused with lymphoma.5
    • Hepatic and lymphatic: VLM is usually associated with hepatomegaly. When histologic results are available, they usually reveal granulomatous hepatitis. Pyogenic liver abscess concomitant with Toxocara hepatitis has also been reported. The spleen is enlarged less often than is the liver. Generalized lymphadenopathy is an infrequent manifestation of toxocariasis. A 24-month-old boy in whom lymphedema was the main clinical manifestation of toxocariasis has been reported.6 Two cases of isolated eosinophilic ascites due to Toxocara have been reported.7
    • Rheumatologic: Frequently, manifestations such as arthralgias, monoarthritis, migratory cutaneous lesions, and small-vessel vasculitis coincidentally occur with VLM. One case report describes Henoch-Schönlein purpura in a 17-year-old male in association with anti-Toxocara immunoglobulin G (IgG) and IgE that spontaneously resolved.8
    • Cardiac: Although infrequently involved, all layers of the heart can be affected. The most common presentation is myocarditis. Among the unusual manifestations described in the literature are Loeffler endomyocarditis9 and pericardial tamponade.10
    • CNS: Toxocariasis is one of the causes of eosinophilic meningitis, a form of aseptic meningitis in which the WBCs in the cerebrospinal fluid mainly consist of eosinophils. Other less common entities described in association with VLM are encephalitis, larval invasion of the brain parenchyma, solitary mass lesions that cause seizures, static encephalopathy, arachnoiditis, and spinal cord lesions. 
  • Ocular larva migrans (OLM)
    • This refers to eye (usually retinal) involvement during Toxocara infection. By chance, the larvae migrate to the eyes, where they induce an eosinophilic inflammatory reaction. Most of the time, it is unilateral.
    • Ocular toxocariasis is an uncommon disease that occurs primarily in young patients. It affects females and males with approximately equal frequency. Most patients report a history of recent exposure to puppies or kittens. The disease is unilateral in most cases, with mild-to-moderate intermediate or diffuse inflammation. Patients with OLM are older than those with VLM. They lack systemic symptoms, such as fever, cough, and abdominal pain, and do not have significant eosinophilia.
    • OLM manifests as a loss of visual acuity, leukocoria, strabismus, and eye pain. It can be confused with a retinoblastoma.
    • Other presentations of OLM include endophthalmitis with secondary retinal detachment, uveitis, vitreous abscess, and optic neuritis.
    • Among patients with uveitis, toxocariasis is relatively uncommon. In a review of 2,185 patients with uveitis, toxocariasis was the etiology in 22 patients (1%).11 The mean patient age was 16.5 years. Inflammation was unilateral in 90.9%. The most common symptoms caused by Toxocara uveitis were blurred vision in 18 eyes (75%), pain or photophobia in 8 eyes (33.3%), and floaters in 4 eyes (16.7%). The presentation was of a granuloma in the peripheral retina in 50% of cases, granuloma in the macula in 25% of cases, and moderate-to-severe vitreous inflammation, mimicking endophthalmitis in 25% of cases. Serum ELISA for antibodies to Toxocara was positive in 11 patients (50%), negative in 8 patients (36.4%), and unknown in 3 patients (13.6%). The 4 patients tested for vitreous or aqueous ELISA showed positive titers (2 had negative serologic titers), confirming that seronegativity does not exclude the diagnosis. The primary causes of vision loss were vitreitis, cystoid macular edema, andtraction retinal detachment.
  • Covert toxocariasis
    • Most cases of toxocariasis are asymptomatic. The term covert toxocariasis refers to a less specific syndrome that was recognized with the wider use of serodiagnostic assays for Toxocara infection.
    • Usual symptoms are chronic or recurrent abdominal pain, hepatomegaly, coughing, wheezing, sleep disturbances, headache, malaise, anorexia, and failure to thrive, among others. Eosinophilia is less frequent and less pronounced with this form than with VLM and Toxocara antibody titers are lower. 

The clinical manifestations of T canis infections depend on the following factors:

  • Number of infective eggs
  • Duration of infection
  • Anatomic location of the larvae
  • Host immune response

Physical

  • VLM
    • General: The classic VLM syndrome consists of wheezing, hepatomegaly, and, occasionally, minimal abdominal tenderness.
    • Dermatologic: Urticaria and nodules are common. Cellulitis may occur in Well syndrome.
    • Pulmonary: Wheezing is typical. Evidence of pleural effusions is rarely noted.
    • Hepatic and lymphatic: VLM is usually associated with hepatomegaly. Generalized lymphadenopathy is an infrequent manifestation.
    • Rheumatologic: Monoarthritis, migratory cutaneous lesions, and evidence of small-vessel vasculitis may be present.
    • Cardiac: Findings suggestive of myocarditis are the most common.
    • CNS: A stiff neck and focal neurologic signs may be present.
  • OLM
    • Loss of visual acuity
    • Leukocoria
    • Strabismus
    • Secondary retinal detachment
    • Uveitis
    • Vitreous abscess
    • Optic neuritis
  • Covert toxocariasis
    • Wheezing
    • Hepatomegaly
    • Abdominal tenderness
    • Failure to thrive

Causes

  • The primary causes of toxocariasis are T canis and T catis.
  • Toxocara species are not the only causes of OLM and VLM; others include Baylisascaris procyonis, Gnathostoma spinigerum, Trichinella spiralis, and Angiostrongylus and Anisakis species. Other causes include A suum (especially in Japan); Angiostrongylus cantonensis or Angiostrongylus costaricensis; and, much less commonly, ascarids from salt-water fishes, such as members of the genera Phocanema, Anisakis, and Contracaecum.
  • Cutaneous larva migrans is caused by Ancylostoma duodenale.

More on Toxocariasis

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Differential Diagnoses & Workup: Toxocariasis
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Follow-up: Toxocariasis
Multimedia: Toxocariasis
References

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Further Reading

Keywords

toxocariasis, allergic asthma, anemia, arthralgia, aseptic meningitis, chronic idiopathic urticaria, covert toxocariasis, cystoid macular edema, encephalitis, eosinophilia, eosinophilic cellulitis, eosinophilic meningitis, eosinophilic pneumonia, epilepsy, granulomatous hepatitis, Henoch-Schönlein purpura, hepatomegaly, Loeffler endomyocarditis, lymphadenopathy, lymphedema, lymphoma, migratory cutaneous lesions, monoarthritis, myocarditis, ocular larva migrans, OLM, parasitic infection, pericardial tamponade, pica, pleural effusions, pyogenic liver abscess, respiratory failure, small-vessel vasculitis, Toxocara canis, T canis, Toxocara catis, T catis, toxocarosis, traction retinal detachment, uveitis, visceral larva migrans, VLM, vitreitis, Well syndrome

Contributor Information and Disclosures

Author

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Coauthor(s)

Marcelo Laufer, MD, Division of Pediatric Infectious Diseases, Attending, Miami Children's Hospital
Marcelo Laufer, MD is a member of the following medical societies: American Academy of Pediatrics and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Medical Editor

Ashir Kumar, MBBS, MD, FAAP, Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University; Consulting Staff, Department of Pediatrics, EW Sparrow Hospital
Ashir Kumar, MBBS, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association of Physicians of Indian Origin, American Federation for Clinical Research, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine
Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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