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Toxocariasis

[Toxocara canis] [Toxocara cati]

Causal Agents

Toxocariasis is caused by larvae of Toxocara canis (dog roundworm) and less frequently of T. cati (cat roundworm), two nematode parasites of animals.


Life Cycle

lifecycle

Toxocara canis accomplishes its life cycle in dogs, with humans acquiring the infection as accidental hosts. Unembryonated eggs are shed in the feces of the definitive host the number 1. Eggs embryonate and become infective in the environment the number 2. Following ingestion by dogs the number 3, the infective eggs hatch and larvae penetrate the gut wall. In younger dogs, the larvae migrate through the lungs, bronchial tree, and esophagus; adult worms develop and oviposit in the small intestine the number 4. In older dogs, patent infections can also occur, but larval encystment in tissues is more common. Encysted stages are reactivated in female dogs during late pregnancy and infect by the transplacental and transmammary routes the puppies the number 5, in whose small intestine adult worms become established the number 6. Puppies are a major source of environmental egg contamination. Toxocara canis can also be transmitted through ingestion of paratenic hosts: eggs ingested by small mammals (e.g. rabbits) hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst the number 7. The life cycle is completed when dogs eat these hosts the number 8 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 the number 9 or infected paratenic hosts the number 10. After ingestion, the eggs hatch and larvae penetrate the intestinal wall and are carried by the circulation to a wide variety of tissues (liver, heart, lungs, brain, muscle, eyes) the number 11. While the larvae do not undergo any further development in these sites, they can cause severe local reactions that are the basis of toxocariasis. The two main clinical presentations of toxocariasis are visceral larva migrans and ocular larva migrans. Diagnosis is usually made by serology or the finding of larvae in biopsy or autopsy specimens.

Geographic Distribution

Worldwide.

Clinical Presentation

Many human infections are asymptomatic, with only eosinophilia and positive serology. The two main clinical presentations of toxocariasis are visceral larva migrans (VLM) and ocular larva migrans (OLM). In VLM, which occurs mostly in preschool children, the larvae invade multiple tissues (liver, heart, lungs, brain, muscle) and cause various symptoms including fever, anorexia, weight loss, cough, wheezing, rashes, hepatosplenomegaly, and hypereosinophilia. Death can occur rarely, by severe cardiac, pulmonary or neurologic involvement. In OLM, the larvae produce various ophthalmologic lesions, which in some cases have been misdiagnosed as retinoblastoma, resulting in surgical enucleation. OLM often occurs in older children or young adults, with only rare eosinophilia or visceral manifestations.

Toxocara sp. eggs.

 

Eggs are not clinically diagnostic for human cases. Humans are paratenic hosts for Toxocara spp. and eggs are found only in the feces of definitive hosts (cats and dogs). Toxocara eggs are subspherical, thick-shelled and have a pitted surface. The size range for the three most commonly observed species differs slightly: T. canis measure 80-85 micrometers by 75 micrometers; T. cati measure 65-75 micrometers; and T. leonina measure 75-85 micrometers by 60-75 micrometers.
	Figure A

Figure A: Toxocara sp. egg teased from an adult worm. The worm was never identified, but the egg size is most consistent with T. cati. Image courtesy of the New Jersey State Public Health Laboratory.

	Figure B

Figure B: Toxocara sp. egg teased from an adult worm. The worm was never identified, but the egg size is most consistent with T. cati. Image courtesy of the New Jersey State Public Health Laboratory.

	Figure C

Figure C: Toxocara sp. eggs teased from an adult worm and stained with iodine, magnification at 100×. The adult worm was never identified in this case. Image courtesy of the Alaska State Public Health Laboratory.

	Figure D

Figure D: Egg from same specimen as C but at 400× magnification. Object measured approximately 75 micrometers.

Toxocara canis larva hatching.

	Figure A

Figure A: Toxocara canis larva beginning to hatch.

	Figure B

Figure B: T. canis larva hatching.

	Figure C

Figure C: T. canis larva.

Adult Toxocara sp. worms.

 

Adult Toxocara spp. measure approximately 4-6 cm long (males) and 6-10 cm long (females). Like most ascarids, Toxocara have three “lips” on the anterior end of the worm. They also possess large cervical alae with striations.
	Figure A

Figure A: Toxocara sp. adult female. Stretched out, the worm measured 7.5 cm. Image courtesy of the Alaska State Public Health Laboratory.

	Figure B

Figure B: Close-up of the anterior end of Toxocara sp., showing the three lips characteristic of ascarid worms. Image courtesy of the New Jersey State Public Health Laboratory.

	Figure C

Figure C: Close-up of the anterior end of Toxocara cati, showing the three lips characteristic of ascarid worms.

	Figure D

Figure D: Side view of Image C, showing the broad, arrow-shaped alae with striations, characteristic of T. cati.

	Figure E

Figure E:Close-up of the posterior end of T. cati, showing a prominent point at the end of the “tail.”

	Figure F

Figure F: Close-up of the posterior end of Toxocara sp. Image courtesy of the New Jersey State Public Health Laboratories.

Toxocara sp. in tissue sections stained with hematoxylin and eosin.

 

Toxocara sp. in tissue sections stained with hematoxylin and eosin.
	Figure A

Figure A: Cross-section of Toxocara sp. larvae in liver tissue stained with hematoxylin and eosin (H&E).

	Figure B

Figure B: Longitudinal section of a Toxocara sp. larva in liver tissue stained with H&E.

	Figure C

Figure C: Longitudinal section of a Toxocara sp. larva in lung tissue stained with H&E.

Laboratory Diagnosis

In this parasitic disease the diagnosis does not rest on identification of the parasite. Since the larvae do not develop into adults in humans, a stool examination would not detect any Toxocara eggs. However, the presence of Ascaris and Trichuris eggs in feces, indicating fecal exposure, increases the probability of Toxocara in the tissues. For both VLM and OLM, a presumptive diagnosis rests on clinical signs, history of exposure to puppies, laboratory findings (including eosinophilia), and the detection of antibodies to Toxocara.


Antibody Detection

Antibody detection tests are the only means of confirmation of a clinical diagnosis of visceral larva migrans (VLM), ocular larva migrans (OLM), and covert toxocariasis (CT), the most common clinical syndromes associated with Toxocara infections. The currently recommended serologic test for toxocariasis is enzyme immunoassay (EIA) with larval stage antigens extracted from embryonated eggs or released in vitro by cultured infective larvae. The latter, Toxocara excretory-secretory (TES) antigens, are preferable to larval extracts because they are convenient to produce and because an absorption-purification step is not required for obtaining maximum specificity. Evaluation of the true sensitivity and specificity of serologic tests for toxocariasis in human populations is not possible because of the lack of parasitologic methods to detect Toxocara parasites. These inherent problems result in underestimations of sensitivity and specificity. Evaluation of the Toxocara EIA in groups of patients with presumptive diagnoses of VLM or OLM indicated sensitivity of 78% and 73%, respectively, at a titer of >1:32. When the cutoff titer for OLM cases was lowered to 1:8, sensitivity was increased to 90%. Further confirmation of the specificity of the serologic diagnosis of OLM can be obtained by testing aqueous or vitreous humor samples for antibodies. Specificity has been reported to be >90% at a titer of >1:32. When interpreting the serologic findings, clinicians must be aware that a measurable titer does not necessarily indicate current clinical Toxocara canis infection. In most human populations, a small number of those tested have positive EIA titers that apparently reflect the prevalence of asymptomatic toxocariasis. In the United States The age adjusted seroprevalence rate was estimated to be approximately 14%, using sera from over 20,000 participants in the Third National Health and Nutrition Examination Survey (1988–1994).


References:
  1. Won KY, Kruszon-Moran D, Schantz PM, and Jones JL. 2006. National Seroprevalence and Risk Factors for Zoonotic Toxocara spp. Infection. Am. J. Trop. Med. Hyg. 79: 552–557.
  2. Smith HV. Antibody reactivity in human toxocariasis. In: Lewis JW, Maizels RM, editors. Toxocara and toxocariasis: clinical, epidemiological, and molecular perspectives. London, UK: Institute of Biology and the British Society for Parasitology; 1993. p. 91-109.

Treatment Information

Treatment with albendazole or mebendazole is indicated for visceral toxocariasis, although optimal duration of treatment is undefined. Both drugs are metabolized in the liver; prolonged use of albendazole (weeks to months) has led to development of pancytopenia in some patients with compromised liver function. Patients on long term treatment should be monitored by serial blood cell counts. However, albendazole has been used to treat millions of patients worldwide and in mass drug administration campaigns, and it is considered to be a safe drug with low toxicity record. In addition to antiparasitic therapy, symptomatic therapy including steroid treatment to control inflammation may be indicated.

Drug Dose and duration
Albendazole 400 mg by mouth twice a day for five days (both adult and pediatric dosage)
Mebendazole 100-200 mg by mouth twice a day for five days (both adult and pediatric dosage)

Albendazole

Oral albendazole is available for human use in the United States.

Albendazole is pregnancy category C. Data on the use of albendazole in pregnant women are limited, though the available evidence suggests no difference in congenital abnormalities in the children of women who were accidentally treated with albendazole during mass prevention campaigns compared with those who were not. In mass prevention campaigns for which the World Health Organization (WHO) has determined that the benefit of treatment outweighs the risk, WHO allows use of albendazole in the 2nd and 3rd trimesters of pregnancy. However, the risk of treatment in pregnant women who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.

Pregnancy Category C: Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal, or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus.

It is not known whether albendazole is excreted in human milk. Albendazole should be used with caution in breastfeeding women.

The safety of albendazole in children less than 6 years old is not certain. Studies of the use of albendazole in children as young as one year old suggest that its use is safe. According to WHO guidelines for mass prevention campaigns, albendazole can be used in children as young as 1 year old. Many children less than 6 years old have been treated in these campaigns with albendazole, albeit at a reduced dose.

Mebendazole

Mebendazole is available in the United States only through compounding pharmacies.

Mebendazole is in pregnancy category C. Data on the use of mebendazole in pregnant women are limited. The available evidence suggests no difference in congenital anomalies in the children of women who were treated with mebendazole during mass treatment programs compared with those who were not. In mass treatment programs for which the World Health Organization (WHO) has determined that the benefit of treatment outweighs the risk, WHO allows use of mebendazole in the 2nd and 3rd trimesters of pregnancy. The risk of treatment in pregnant women who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.

Pregnancy Category C: Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal, or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus.

It is not known whether mebendazole is excreted in breast milk. The WHO classifies mebendazole as compatible with breastfeeding and allows the use of mebendazole in lactating women.

The safety of mebendazole in children has not been established. There is limited data in children age 2 years and younger. Mebendazole is listed as an intestinal antihelminthic medicine on the WHO Model List of Essential Medicines for Children, intended for the use of children up to 12 years of age.

For ocular toxocariasis, the goal of treatment is to minimize damage to the eye. Systemic antiparasitic treatment with albendazole or mebendazole at the same doses as for visceral disease may be beneficial for active disease. Attempts to surgically remove the larva may be unsuccessful. Control of inflammation in the eye by use of topical or systemic steroids may be indicated. For patients with quiescent disease, improved outcomes may result from surgical intervention to prevent further damage due to chronic inflammation.

DPDx is an education resource designed for health professionals and laboratory scientists. For an overview including prevention and control visit www.cdc.gov/parasites/.

  • Page last reviewed: May 3, 2016
  • Page last updated: May 3, 2016
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