surgically removed, or laser photocoagulation and cryoretinopexy can be used to destroy ocular granulomas. 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. treatment of ocular toxocariasis is more difficult 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. seroprevalence is higher in developing countries, but can be considerable in first world countries, as well. in bali, st. lucia, nepal and other countries, seroprevalence is over fifty percent. previous to 2007, the u.s. seroprevalence was thought to be around 5% in children. however, won et al. discovered that u.s. seroprevalence is actually 14% for the population at large. in many countries, toxocariasis is considered very rare. approximately 10,000 clinical cases are seen a year in the u.s., with ten percent being olm. permanent vision loss occurs in 700 of these cases. young children are at the greatest risk of infection because they play outside and tend to place contaminated objects and dirt in their mouths. dog ownership is another known risk factor for transmission. there is also a significant correlation between high toxocara antibody titers and epilepsy in children. parasitic loads as high as 300 larvae in a single gram of liver have been noted in humans. the "excretory–secretory antigens of larvae ... released from their outer epicuticle coat ... readily sloughed off when bound by specific antibodies" incite the host's immune response. the tipping point between development of vlm and olm is believed to be between 100 and 200 larvae. 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. ocular granulomas that form around a larva typically are peripheral in the retina or optic disc. visceral larva migrans seems to affect children aged 1–4 more often while ocular larva migrans more frequently affects children aged 7–8. between 4.6% and 23% of us children have been infected with the dog roundworm egg. this number is much higher in other parts of the world, in tropical countries there is seroprevalence of up to 80–90%, such as colombia, where up to 81% of children have been infected, or honduras where seroprevalence among school-age children was reported to be 88%. 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. in 1950, campbell-wilder was the first to describe toxocariasis in humans; she published a paper describing ocular granulomas in patients with endophthalmitis, coat's disease, or pseudoglioma. 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. the dangers of toxocariasis were first raised in britain in the 1970s, leading to a public health scare. 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, in order 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 if 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.