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Toxocara
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
As accidental host, humans (especially young children) may acquire T. canis through ingestion of infective eggs (containing L2 larvae) from soil (playgrounds, sandpits, and gardens), the hair of pet dog and cat, and unwashed vegetables; or ingestion of encapsulated larvae contained in raw or undercooked meat (pig, chicken, rabbit, or lamb). L2 larvae penetrate the gut wall, travel with the blood and lymph to any tissue in the body (e.g., the lungs, heart, liver, eyes, brain, and muscles), in which they do not develop further but can cause severe local reactions, commonly referred to as VLM, ocular larva migrans (OLM) (with one or more larvae migrating to the eye through the central retinal artery or the short posterior ciliary artery), or NT. It may take between 1 week and 2 years for the disease to be apparent.
Thiabendazole and Flubendazole
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Thiabendazole has demonstrated efficacy in patients with visceral larva migrans (VLM), administered as 25 mg/kg p.o. bid (maximum, 3 g/day) for 7 days. It has been replaced by albendazole (Magnaval and Charlet, 1987) for the treatment of VLM owing to treatment-limiting side effects. Furthermore, in a small study of 34 patients with either VLM or ocular larva migrans, albendazole appeared to be of superior efficacy (Sturchler et al., 1989).
Ocular Toxocariasis
Published in Ocular Immunology and Inflammation, 2021
Emmett T. Cunningham, Manfred Zierhut
While many Toxocara infections are asymptomatic, moderate to severe systemic, neurologic, and/or ocular infections can occur. These are referred to respectively as visceral (VLM), neurologic (NVM), and ocular larva migrans (OLM; also known as ocular toxocariasis OT).1,2 Three classic patterns or OT have been described, including posterior granuloma – typically submacular or peripapillary and with pronounced retinal striae or folds; peripheral granuloma, often with a vitreoretinal traction band extending toward the posterior pole; and severe, unilateral intermediate or panuveitis referred to as nematode or Toxocara endophthalmitis. Atypical presentations of OT also exist.5–8 One metanalysis,9 three original articles,10−12 and one letter10 in this issue of Ocular Immunology & Inflammation (OII) address aspects of the prevalence, presentation, treatment and outcome of OT.
Pediatric Ocular Toxocariasis in Costa Rica: 1998-2018 Experience
Published in Ocular Immunology and Inflammation, 2021
Joaquin Martinez, Gabriela Ivankovich-Escoto, Lihteh Wu
Currently, there are no treatment guidelines for the treatment of ocular toxocariasis. Our treatment decisions have evolved over the experience gained in the past two decades. In general, if the patient presented acutely and there was a chance that the Toxocara larva was still alive, thiabendazole was prescribed either alone or in combination with corticosteroids to decrease the inflammatory reaction. The role of anti-helminthic drugs remains unclear.19,20 Combination therapy of anti-helminthic and corticosteroids may be of use in specific cases.21 In a very small comparative trial, albendazole appeared to be more effective than thiabendazole in the treatment of patients with visceral or ocular larva migrans secondary to toxocariasis.20 In a slightly larger trial, mebendazole and diethylcarbamazine had similar therapeutic efficacy but mebendazole had a lower rate of adverse events. Despite these reports, it is unclear if these anti-helminthic drugs kill intraocular Toxocara larvae. A case report looked at the thiabendazole concentration in ocular fluids following oral administration of the drug. According to Maguire and collegues,22 anti-parasitic levels of the medication can be achieved intraocularly after oral ingestion. Our impression is that anti-helminthic drugs could have some use only in very acute cases, because once the granuloma is formed, or even before, the larva is already dead.
Keys to Unlock the Enigma of Ocular Toxocariasis: A Systematic Review and Meta-analysis
Published in Ocular Immunology and Inflammation, 2021
Milad Badri, Aida Vafae Eslahi, Meysam Olfatifar, Sahar Dalvand, Elham Houshmand, Amir Abdoli, Hamidreza Majidiani, Ali Eslami, Mohammad Zibaei, Morteza Ghanbari Johkool, Ali Taghipour, Sima Hashemipour
A broad range of zoonotic parasitic diseases are transmitted by animals, especially cats and dogs.1,2 Toxocariasis is an important neglected tropical disease with a worldwide distribution mainly caused by larvae of the Toxocara canis or Toxocara cati, which are intestinal ascarid nematodes of canids and felids, respectively.3–5 It is estimated that 19.0% (95%CI, 16.6–21.4%) of people worldwide is seropositive regarding Toxocara spp. infection.6 The eggs are excreted in the feces and they become infective after passing their incubation period in the soil under the favorable circumstances of humid temperate climate,5,6 which can ensure their survival for up to one year.7 Both definitive and paratenic hosts (chickens, ruminants, pigs, etc.) can be infected via swallowing embryonated eggs in soil or raw vegetables contaminated with the feces of dogs and cats.8,9 Humans also get infected via close contact with contaminated soil or consumption of raw/undercooked meat prepared from tissues of paratenic hosts.10–12 Humans act as an accidental host and larvae do not develop into adult worms. Ingested larvae penetrate the intestinal mucosa and migrate to various organs, such as liver, lungs, heart, brain, eyes, and skeletal muscle.13–15 There are different clinical types of human toxocariasis including visceral larva migrans (VLM), ocular larva migrans (OLM), neurotoxocariasis (NT), and covert toxocariasis (CT).15