Toxocariasis

Physiological reactions to Toxocara infection depend on the host's immune response and the parasitic load. Most cases of Toxocara infection are asymptomatic, especially in adults. When symptoms do occur, they are the result of migration of second-stage Toxocara larvae through the body. Covert toxocariasis 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. Upon medical examination, wheezing, hepatomegaly, and lymphadenitis are often noted. A light Toxocara burden is thought to induce a low immune response, allowing a larva to enter the host's eye. Loss of vision occurs over days or weeks. Ocular granulomas resulting from OLM are frequently misdiagnosed as retinoblastomas. A case study published in 2008 supported the hypothesis that eosinophilic cellulitis may also be caused by infection with Toxocara: the adult patient presented with eosinophilic cellulitis, hepatosplenomegaly, anemia, and a positive ELISA for T. canis. ==Cause==

Transmission Toxocara is usually transmitted to humans through ingestion of infective eggs. T. canis can lay around 200,000 eggs per day. Eating undercooked rabbit, chicken, or sheep can lead to infection; encysted larvae in the meat can become reactivated and migrate through a human host, causing toxocariasis. Under ideal summer conditions, eggs can mature to the infective stage after two weeks outside of a host. However, as identified in a case study presented within the journal of helminthology, the second stage of larvae development poses strict vulnerabilities to certain environmental elements. High temperatures and low moisture levels will quickly degrade the larvae during this developmental stage. Infectious mothers, and puppies under five weeks old, pass eggs in their feces. Morphology Both species produce eggs that are brown and pitted. During this incubation period, molting from first to second (and possibly third) stage larva takes place within the egg. The larvae will then migrate through the organs and tissues of the accidental host, most commonly the lungs, liver, eyes, and brain. Since L2 larvae cannot mature in accidental hosts, after this period of migration, Toxocara larvae will encyst as second stage larvae. ==Diagnosis==

Finding Toxocara larvae within a patient is the only definitive diagnosis for toxocariasis; however, biopsies to look for second-stage larvae in humans are generally not very effective. 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. OLM is often diagnosed after a clinical examination. Granulomas can be found throughout the body and can be visualized using ultrasound, MRI, and CT technologies. ==Prevention==

Actively involving veterinarians and pet owners is important for controlling the transmission of Toxocara from pets to humans. A group very actively involved in promoting a reduction of infections in dogs in the United States is the Companion Animal Parasite Council -- CAPC. Since pregnant or lactating dogs and cats and their offspring have the highest, active parasitic load, these animals should be placed on a deworming program. Also, sandboxes should be covered when not in use to prevent cats from using them as litter boxes. Hand washing before eating and after playing with pets, as well as after handling dirt will reduce the chances of ingesting Toxocara eggs. There is currently no vaccine available or under development. ==Treatment==

Toxocariasis will often resolve itself because the Toxocara larvae cannot mature within human hosts. Visceral toxocariasis in humans can be treated with antiparasitic drugs such as albendazole or mebendazole, tiabendazole or diethylcarbamazine usually in combination with anti-inflammatory medications. Steroids have been utilized with some positive results. Anti-helminthic therapy is reserved for severe infections (lungs, brain) because therapy may induce, due to massive larval killing, a strong inflammatory response. Ocular toxocariasis is more difficult to treat and usually consists of measures to prevent progressive damage to the eye. ==Epidemiology==

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. Parasitic loads as high as 300 larvae in a single gram of liver have been noted in humans. In the western part of the world, seroprevalence is lower, around 35–42%. ==History==

Werner described a parasitic nematode in dogs in 1782 which he named Ascaris canis. Johnston determined that what Werner had described was actually a member of the genus Toxocara established by Stiles in 1905. Fülleborn speculated that T canis larvae might cause granulomatous nodules in humans. In 1947 Perlingiero and Gyorgy described the first case of what was probably toxocariasis. Their patient was a 2-year-old boy from Florida who had classical symptoms and eosinophilic necrotizing granulomas. ==Other animals==

Cats Some treatments for infection with Toxocara cati include drugs designed to cause the adult worms to become partially anaesthetized and detach from the intestinal lining, allowing them to be excreted live in the feces. Such medications include piperazine and pyrantel. These are frequently combined with the drug praziquantel which appears to cause the worm to lose its resistance to being digested by the host animal. Other effective treatments include ivermectin, milbemycin, and selamectin. Dichlorvos has also been proven to be effective as a poison, though moves to ban it over concerns about its toxicity have made it unavailable in some areas. Treatment for wild felids, however, is difficult for this parasite, as detection is the best way to find which individuals have the parasite. This can be difficult as infected species are hard to detect. Once detected, the infected individuals would have to be removed from the population, to lower the risk of continual exposure to the parasites. A primary method that has been used to lower the amount of infection is removal through hunting. Removal can also occur through landowners, as Dare and Watkins (2012) discovered through their research on cougars. Both hunters and landowners can provide samples that can be used to detect the presence of feline roundworm in the area, as well as help remove it from the population. This method is more practical than administering medications to wild populations, as wild animals, as mentioned before, are harder to find in order to administer medicinal care. Medicinal care, however, is also another method used in roundworm studies; such as the experiment on managing raccoon roundworm done by Smyser et al. (2013) in which they implemented medical baiting. However, medicine is often expensive and the success of the baiting depends on whether the infected individuals consume the bait. Additionally, it can be costly (in time and resources) to check on baited areas. Removal by hunting allows agencies to reduce costs and gives agencies a more improved chance of removing infected individuals. ==References==