Updated: Jan 27, 2009
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.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).
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%.
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.
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.
No racial predilection has been noted.
Boys usually have higher seroprevalence than girls. This is probably related to differences in play behavior.
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.
The 3 clinical forms of toxocariasis that are traditionally described include the following:
The clinical manifestations of T canis infections depend on the following factors:
| Amebic Meningoencephalitis | Juvenile Rheumatoid Arthritis |
| Ancylostoma Infection | Loffler Syndrome |
| Angioedema | Lymphadenopathy |
| Ascariasis | Lymphoproliferative Disorders |
| Aspergillosis | Meningitis, Aseptic |
| Asthma | Myocarditis, Nonviral |
| Cardiac Tumors | Myocarditis, Viral |
| Cardiomyopathy, Dilated | Naegleria |
| Chorioretinitis | Pericardial Effusion, Malignant |
| Cognitive Deficits | Pericarditis, Bacterial |
| Cutaneous Larva Migrans | Pericarditis, Constrictive |
| Cysticercosis | Pericarditis, Viral |
| Dracunculiasis | Pleural Effusion |
| Echinococcosis | Pneumonia |
| Fascioliasis | Respiratory Failure |
| Fever in the Toddler | Retinoblastoma |
| Fever in the Young Infant | Schistosomiasis |
| Filariasis | Status Asthmaticus |
| Gnathostomiasis | Strongyloidiasis |
| Hookworm Infection | Systemic Lupus Erythematosus |
| Hypereosinophilic Syndrome | Taenia Infection |
| Hypersensitivity Pneumonitis | Trichinosis |
The differential diagnosis of visceral larva migrans (VLM) overlaps that of eosinophilia.
Drug reactions
Capillaria hepatica infection
Eosinophilia-myalgia syndrome
Baylisascaris procyonis infection
Perinatal asphyxia
Most patients with toxocariasis recover without therapy.
Anthelmintic agents are used primarily for severe complications of visceral larva migrans (VLM), such as brain, heart, and lung involvement.
These eradicate the larvae. Parasite biochemical pathways are different from the human host, thus toxicity is directed to the parasite, egg, or larvae. Mechanism of action varies within the drug class. Antiparasitic actions may include the following:
The DOC in most textbooks, but the FDA does not list toxocariasis as an indication. It is obtained only through the manufacturer.
6 mg/kg/d PO divided tid for 10 d
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution to avoid allergic reaction
Broad-spectrum anthelmintic drug; mechanism of action is unclear, but may inhibit the helminth-specific enzyme fumarate reductase.
500 mg PO bid for 7 d; alternatively 50 mg/kg/d PO divided bid, not to exceed 3 g/d
50 mg/kg/d PO divided bid for 7 d; not to exceed 3 g/d
May elevate serum levels of theophylline, increasing toxicity (monitor serum levels and reduce dose prn)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause the parasite to migrate in intestinal infections with Ascaris species; closely monitor in hepatic or renal dysfunction; before initiating therapy, supportive therapy is necessary for anemic, dehydrated, or malnourished patients; use in confirmed worm infestation (not prophylactically); may cause nausea, vomiting, and mild CNS depression
Has poor PO bioavailability; absorption is enhanced by fatty meals; systemic anthelmintic effect is attributed to its sulfoxide metabolite; albendazole may induce its own metabolism.
400 mg PO bid for 5-10 d
10-15 mg/kg/d PO divided bid; not to exceed adult dose
Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue use if LFT results increase significantly (resume when levels decrease to pretest values)
Synthetic broad-spectrum anthelmintic. Likely the drug for which the most experience exists and the safest drug in its class. Inhibits microtubule formation and causes glucose depletion in the worms.
100 mg PO bid for 3 d
<2 years: Not established
>2 years: Administer as in adults
Carbamazepine and phenytoin may decrease effects; cimetidine may increase levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Has increased liver enzyme levels when taken for prolonged periods
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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
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
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.
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.
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
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.
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
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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