Alexsandra Greer

HumBio 153

Parasites Paper





Toxocariasis is a zoonotic disease caused by intestinal roundworms of cats (Toxocara cati) and dogs (Toxocara canis).1,2  Eggs are passed in dog and cat feces and become infectious after an incubation period outside of a host.  If ingested by humans, these eggs can hatch as larvae.  While the larvae cannot develop within a human host, they can cause tissue and organ damage by migrating through the body.2,3  Small children are at the greatest risk of infection, because they are the most likely to come into contact with eggs and ingest them.2,4

Toxocariasis is usually asymptomatic.1,5 However, three syndromes of the disease are recognized: covert toxocariasis, visceral larva migrans (VLM) and ocular larva migrans (OLM).  Symptoms and signs of covert toxocariasis include cough, abdominal pain, headache, changes in behavior, and sleeping issues.4,5  VLM is often characterized by coughing, pneumonia, fever, abdominal pain, and headaches, and is typical of cases with a high parasitic load or repeated infection.1,4 Rare complications with VLM can include seizures, myocarditis, or respiratory failure.1,5,6  OLM is the least common syndrome of toxocariasis and is caused by the parasite entering the host’s eye.  Reduced vision or blindness can result from this form of toxocariasis.1,2,5 


The causative agent of toxocariasis is one of two parasitic roundworms.  Felines are normally the only hosts of Toxocara cati, while Toxocara canis’ life cycle usually only includes canines.1,2



Text Box: Toxonomy7,8:
Kingdom: Animalea
Phylum: Nematoda
Class: Secernentea
Order: Ascaridida
Family: Toxocaridae
Genus: Toxocara
Species: canis, cati











Toxocaral disease and toxocarose are both synonyms for the disease toxocariasis.2,9  The disease is also frequently referenced in terms of its syndromes and their abbreviations: covert toxocariasis, visceral larva migrans (VLM), and ocular larva migrans (OLM).  Finally, the species names of the parasites, Toxocara cati and Toxocara canis, can be used to refer to the disease.9

Synonyms for Toxocariasis2,9:

Toxocaral disease


Covert toxocariasis

Visceral larva migrans (VLM)

Ocular larva migrans (OLM)

Toxocara canis

Toxocara cati














History of Discovery

H.C. Wilder was the first to describe toxocariasis in humans, when he published a paper in 1950 describing ocular granulomas in patients thought to have retinoblastomas. Two years later, Beaver et al. published the presence of Toxocara larvae in granulomas removed from patients with symptoms similar to those in Wilder’s patients.4,10

Clinical Presentation

Physiological reactions to Toxocara infection depend on the host’s immune response and the parasitic load.5  Most cases of Toxocara infection are asymptomatic, especially in adults.1,5,11  When symptoms do occur, they are the result of migration of  second stage Toxocara larvae through the body.2 

Covert toxocariasis is the least serious of the three syndromes and is believed to be due to chronic exposure.  Signs and symptoms of covert toxocariasis are coughing, fever, abdominal pain, headaches, and changes in behavior and ability to sleep.4,5  Upon medical examination, wheezing, hepatomegaly, and lymphadenitis are often noted.5   

Figure 1. T. canis larvae in mouse liver ( 153144).


High parasitic loads or repeated infection can lead to visceral larva migrans (VLM).1  VLM is primarily diagnosed in young children, because they are more prone to exposure and ingestion of infective eggs.2  Toxocara infection commonly resolves itself within weeks, but chronic eosinophilia may result.5,9   In VLM, larvae migration incites inflammation of internal organs and sometimes the central nervous system.1,5  Symptoms depend on the organ(s) affected.5  Patients can present with pallor, fatigue, weight loss, anorexia, fever, headache, rash, cough, asthma, chest tightness, increased irritability, abdominal pain, nausea, and vomiting.2,5  Sometimes the subcutaneous migration tracks of the larvae can be seen.2  Patients are commonly diagnosed with pneumonia, bronchospasms, chronic pulmonary inflammation, hypereosinophilia, hepatomegaly, hypergammaglobulinaemia (IgM, IgG, and IgE classes), leucocytosis, and elevated anti-A and –B isohaemagglutinins.1,2 ,4,10  Severe reactions have occurred in people with atopy; in rare cases, epilepsy, myocarditis, pleural effusion, respiratory failure, and death have resulted from VLM.4,5,9

Figures 2, 3.  Ocular granulomas caused by deceased, second stage larvae in children diagnosed with OLM (http://www.pubmedcentral.; Bassukas et al.).


Ocular larva migrans (OLM) is rare compared with VLM.2,12  A light Toxocara burden is thought to induce a low immune response, allowing a larva to enter the host’s eye.4  Although there have been cases of concurrent OLM and VLM, these are extremely exceptional.4  OLM is often unilateral and from a single larva migrating into and encysting within the orbit.2,13  Loss of vision occurs over days or weeks.4  Other signs and symptoms are red eye, leukokoria, fixed pupil, retinal fibrosis, retinal detachment, chorioretinitis, chronic endophthalmitis, uveitis, vitritis, neuroretinitis, papillitis, retinal granulomas, and strabismus.2,4,13,14  Ocular granulomas resulting from OLM are frequently misdiagnosed as retinoblastomas.2  Toxocara damage in the eye is permanent and can result in blindness.1,5,13

A case study published in 2008 supported the hypothesis that eosinophilic cellulitis may also be caused by infection with Toxocara.  In this study, the adult patient presented with eosinophilic cellulitis, hepatosplenomegaly, anemia, and a positive ELISA for T. canis.15


Transmission of Toxocara to humans is primarily through ingestion of infective eggs.1,3  The eggs are passed in feline or canine feces, but the defecation habits of dogs cause T. canis transmission to be more prevalent than that of T. cati.2,3  Both Toxocara canis and Toxocara cati eggs require a several week incubation period outside of the host before becoming infective, so fresh eggs cannot cause toxocariasis.2,3,5 

Young children who put contaminated objects in their mouths or exhibit pica are most at risk of developing symptoms.2,4,10  Flies that feed on feces can act as mechanical vectors and contaminate surfaces or foods.4  Humans can also contaminate foods by not washing their hands before eating.1,5

Humans are not the only accidental hosts of Toxocara.  Consumption of undercooked rabbit, chicken, and sheep can lead to infection; encysted larvae in the meat can become reactivated and migrate through a human host.  Special attention should be paid to thoroughly cooking giblets and liver to avoid transmission.2,4 


Dogs are the reservoir for Toxocara canis, but puppies pose the greatest risk of spreading the infection to humans.1,5  Infection in most adult dogs is characterized by encysted second stage larvae.  However, these larvae can become reactivated in pregnant females and cross the placental barrier to infect the pups.  Vertical transmission can also occur through breastmilk.2,3,16  Infectious mothers, and puppies under five weeks old, shed eggs in their feces. 3,16  Approximately fifty percent of  puppies and twenty percent of adult dogs are infect with T. canis.2

            Cats are the reservoir for Toxocara cati.1,5  As with T. canis, encysted second stage larvae in pregnant or lactating females can become reactivated.  However, vertical transmission can only occur through breastfeeding. Although kittens are more of a risk for human infection than adult cats, the defecation habits of cats reduce the chances of human infection with T. cati.3


Flies can act as mechanical vectors for Toxocara, but most infections occur without a vector.4

Incubation Period

The incubation period for Toxocara canis and cati eggs depends on temperature and humidity.2,3  Under ideal summer conditions, eggs can mature to the infective stage after two weeks outside of a host.3,4,5  Toxocara eggs can remain infectious for years, as they are very resistant to the affects of chemicals and temperature changes.5,7,17 






Figures 3, 4.   T. canis adults and an embryonated T. canis egg ( Nematodes /nems_top.htm; artid=153144).


Both species produce eggs that are brown and pitted.7,12,17  T. canis eggs measure 75-90mm and are spherical in shape, where as the eggs of T. cati are 65-70mm in diameter and oblong.2,7,17 Second stage larvae hatch from these eggs and are approximately 0.5mm long and 0.02mm wide.5  Adults of both species have complete digestive systems and three lips, each composed of a dentigerous ridge.7,17 Adult T. canis are found only within dogs and the males are 4-6cm in length with a curved posterior end.7,10  The males each have spicules and one “tubular tesis.”7 Females can be as long as 15cm, with the vulva stretching one third of their bodylength.7 The females do not curve at the posterior end.7,10  T. cati adult females are approximately 10cm long, while males are typically 6cm or less.  The adults only occur within felines, and male T. cati are curved at the posterior end.17

Life Cycle

            Both cats and dogs can become infected with Toxocara through ingestion of eggs or by vertical transmission of the larvae.3,16  Transmission to the definitive hosts can occur by ingestion of infected accidental hosts, such as earthworms, cockroaches, rodents, rabbits, chickens, or sheep, as well.2,4,17 

Figure 5. Life cycle of T. canis in canines.  The life cycle of T. cati is similar to that of T. canis, except that kittens cannot be infected while in the uterus ( 


Eggs hatch as second stage larvae in the intestines of the definitive host (for consistency, this paper will assume that second stage larvae emerge from Toxocara eggs, although there is debate as to whether larvae are truly in their second or third stage of development).4,10 Larvae enter the bloodstream and migrate to the lungs, where they are coughed up and swallowed.  The larvae mature into adults within the small intestine, where copulation and ovaposition of 100,000-200,000 eggs a day occurs.3,4,7,13  Eggs are passed in the feces and only become infective after an incubation period outside the host.  During this incubation period, molting from first to second (and possibly third) stage larva takes place within the egg.4,17  In most adult canines and felines, the full lifecycle does not occur, but instead second stage larvae encyst after a period of migration through the body.  Reactivation of the larvae is common only in pregnant and lactating females of the definitive host.  The full lifecycle usually only occurs in these females and their offspring.3,16

Figure 6. Diagram of transmission and pathology of Toxocara. Since larvae cannot mature within a human host they will eventually encyst and be encapsulated in a granuloma by the host’s immune system (


Second stage larvae will also hatch in the small intestine of an accidental host, such as a human, after ingestion of infective eggs.  The larvae will then migrate through the organs and tissues of the accidental host, most commonly the lungs, liver, eyes, and brain.  After this period of migration, Toxocara will encyst as second stage larvae.2,3,5  No further development occurs within accidental hosts.2,16


Demonstration of Toxocara larvae would constitute a definitive diagnosis for toxocariasis, however biopsies to look for second stage larvae in human hosts are generally not very effective.4,5  PCR, ELISA, and serological testing are more commonly used to diagnose Toxocara infection.4,5,9  Serological tests are dependant on parasitic burden, and are unfortunately not very specific.4  ELISAs are much more reliable and currently have a 78% sensitivity and a 90% specificity.6   A 2007 study announced an ELISA specific to Toxocara canis, which will minimize false positives from cross reactions with similar roundworms and will help distinguish if a patient is infected with T. canis or T. cati.18  OLM is often diagnosed after a clinical examination.6  Granulomas can be found throughout the body and can be visualized using ultrasound, MRI, and CT technologies.4

Management and Therapy

Toxocariasis is a self-limiting disease in humans, because the Toxocara larvae cannot mature within human hosts.2  Corticosteroids are prescribed in severe cases of VLM or if the patient is diagnosed with OLM.  Either 400mg albendazole (preferred) or 100-200mg mebendazole (“second line therapy”) twice a day for five days can be prescribed as an antihelminthic.2,5,6,13  Granulomas can be surgically removed, or laser photocoagulation and cryoretinopexy can be used to destroy ocular granulomas. 4, 6,13,19


Humans are accidental hosts of Toxocara, yet toxocariasis is seen throughout the world.  Most cases of toxocariasis are seen in people under the age of twenty.11  Seroprevalence is higher in developing countries, but can be considerable in first world countries, as well.4 In Bali, St. Lucia, Nepal and other countries, seroprevalence is over fifty percent.4  Previous to 2007, the U.S. seroprevalence was thought to be around 5% in children.2  However, Won et al. discovered that U.S. seroprevalence is actually 14% for the population at large.5,11  Approximately 100,000 clinical cases are seen a year in the U.S., with ten percent being OLM.11,13  Permanent vision loss occurs in 700 of these cases.13 

Young children are most at risk of infection from playing outside and placing contaminated objects and dirt in their mouths.2,4,10  Dog ownership is another known risk factor for transmission.10  Sadly, there is also a significant correlation between high Toxocara antibody titers and epilepsy in children.2

Parasitic loads as high as 300 larvae in a single gram of human liver have been noted.4  The “excretory-secretory antigens of larvae… released from their outer epicuticle coat [and]… readily sloughed off when bound by specific antibodies” incite the host’s immune response.5  The tipping point between development of VLM and OLM is believed to be between 100 and 200 larvae.4  The lighter infection in OLM is believed to stimulate a lower immune response and allow for migration of a larva into the eye.  Larvae are thought to enter the eye through the optic nerve, central retinal artery, short posterior ciliary arteries, soft tissues, or cerebrospinal fluid.4,13  Ocular granulomas that form around a larva typically are peripheral in the retina or optic disc.13

Public Health and Prevention Strategies/Vaccines

Active involvement of veterinarians and pet owners is important for controlling transmission of Toxocara from pets to humans.  Since pregnant/lactating dogs and cats and their offspring have the highest, active parasitic load, these animals should be placed on a deworming program.1,3,4  Pet feces should be picked up and disposed of or buried, as they may contain Toxocara eggs.1  Practicing this measure in public areas, such as parks and beaches, is especially essential for decreasing transmission.2,10  Also, sandboxes should be covered when not in use to prevent cats from using them as litter boxes.  Hands should be washed after touching cats or dogs, as well as after handling dirt to avoid ingestion of eggs.1,2,4 

Hand washing before eating will also reduce the risk of ingesting infectious eggs.1  Washing all fruits and vegetables, keeping pets out of gardens and thoroughly cooking meats can prevent transmission by food.4  Finally, teaching children not to place nonfood items, especially dirt, in their mouths will drastically reduce the chances of oral transmission.1 

Toxocariasis has been named one of the neglected diseases of U.S. poverty, because of its prevalence in Appalachia, the southern U.S., inner city settings, and minority populatons.20  Unfortunately, there is no vaccine available or currently under development.11,20  However, the mitochondrial genomes of both T. cati and T. canis have recently been sequence, which could lead to breakthroughs in treatment and prevention.21


Useful Web Links

Center for Disease Control, Division of Parasitic Diseases:

GIDEON. "Toxocariasis:”

Despommier, D. Toxocariasis: Clinical Aspects, Epidemiology, Medical Ecology, and Molecular Aspects. Clin Microbiol Rev. 2003;16:265–272.





1. Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, Division of Parasitic diseases. "Fact Sheet: Toxocariasis." 5 Nov. 2007. 19 Jan. 2009. < dpd/parasites/toxocara/factsht_toxocara.htm>.

2. Markell, Edward K. and Marietta Voge. Markell and Voge’s Medical Parasitology.  9th ed. St. Louis: Saunders Elsevier, 2006.

3. Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, Division of Parasitic diseases. "Guidelines for Veterinarians: Prevention of Zoonotic Transmission of Ascarids and Hookworms of Dogs and Cats." 27 Sept. 2004 19 Jan. 2009 < /ascaris/prevention.htm>.

4. Holland, Celia and H.V. Smith. Toxocara: The Enigmatic Parasite. Wallingford, UK and Cambridge, MA: CABI Publishing, 2006. 26 Jan. 2009 < 10157926>.

5. Huh, Sun and Sooung Lee. eMedicine from WebMD. “Toxocariasis.” 20 Aug. 2008. 26 Jan. 2009. <>.


6. Auweerter, Paul. Johns Hopkins. Point-of-Care Information Technology Center: ABX Guide. “Toxocariasis.”  8 Jan. 2008. 19 Feb. 2009 < /toxocariasis.html?contentInstanceId=425999&siteId=153>.

7. Harris-Linton, Megan. The University of Michigan Museum of Zoology: Animal Diversity Web. “Toxocara canis.” 2001. 26 Jan. 2009 < /information/Toxo cara_canis.html>.

8. Johnstone, Colin. University of Pennsylvania. The Nematodes.24 Jan. 2000. 26 Jan. 2009 <>.

9. GIDEON. "Toxocariasis". 2009. 26 Jan. 2009. < index.php>.

10. Despommier, D. Toxocariasis: clinical aspects, epidemiology, medical ecology, and molecular aspects. Clin Microbiol Rev. 2003;16:265–272. 26  Jan. 2009



11. Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, Division of Parasitic diseases. “New CDC study results show Toxocara infection more common than previously thought.” 19 Jan. 2009 <>.


12. The Merck Veterinary Manual. “Roundworm.” 2008. 26 Jan. 2009 <http://www.merckvetmanual. com/mvm/index.jsp?cfile=htm/bc/23505.htm>.

13. Review of Optometry Online: Handbook of Ocular Disease Management. "Toxocariasis: Ocular Larva Migrans". 26 Jan. 2009 <>.

14. Stewart, JM, LD Cubillan, and ET Cunningham, Jr. Prevalence, clinical features, and causes of vision loss among patients with ocular Toxocariasis. Retina. 2005 Dec;25(8):1005-13


15. Bassukas, Ioannis D., Georgios Gaitanis, Aikaterini Zioga, Christina Boboyianni, and Christina Stergiopoulou. Febrile “migrating” eosinophilic cellulitis with hepatosplenomegaly: adult Toxocariasis – a case report. Cases Journal 2008, 1:356.

16. Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, DPDx: Parasites and Health.  “Toxocariasis.” 19 Jan. 2009 



17, Soskolne, Gayle. The University of Michigan Museum of Zoology: Animal Diversity Web. “Toxocara cati.” 2001. 26 Jan. 2009



18. Iddawela, R.D., R.P.V.J. Rajapakse, N.A.N.D. Perera and Takeshi Agatsuma. Characterization of a Toxocara canis species-specific excretory-secretory antigen (TcES-57) and development of a double sandwich ELISA for diagnosis of visceral larva migrans. Korean Journal of Parasitology. Vol. 45, No. 1: 19-26, March 2007.

19. Werner, Jane C., Robin D. Ross, W. Richard Green and John C. Watts. Pars Plana Vitrectomy and Subretinal Surgery for Ocular Toxocariasis. Arch Ophthalmol. Vol. 117, Apr 1999.

20. Hotez, Peter J. Neglected Infections of Poverty in the United States of America. PLOS: Neglected Tropical Diseases. 2008 June;2(6):e256.

21. Li, Ming-Wei, Rui-Qing Lin, Hui-Qun Song, Xiang-Yun Wu and Xing-Quan Zhu. The complete mitochondrial genomes for three Toxocara species of human and animal health significance. BMC Genomics 2008, 9:224.

Other Useful Information

Center for Disease Control, Division of Parasitic diseases. "What Every Pet Owner Should Know About Roundworms and Hookworms."