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Patent Toxocara canis infections in previously exposed and in helminth-free dogs after infection with low numbers of embryonated eggs


Fahrion, A S; Staebler, S; Deplazes, P (2008). Patent Toxocara canis infections in previously exposed and in helminth-free dogs after infection with low numbers of embryonated eggs. Veterinary Parasitology, 152(1-2):108-115.

Abstract

The outcome of Toxocara canis infections in the canine host depends on the migratory pathway of parasite larvae (somatic or tracheal) which is considered to be related to the host's age and its immune status. However, field studies attest high prevalences of patent T. canis infections in adult animals. The controlled induction of patent infections with low doses of embryonated eggs was investigated in 18 beagles in a 7-month study until their 16th life month. The animals were assigned to three groups, each consisting of three vertically infected dogs (with a short patent infection as pups before anthelmintic treatment) and three helminth-free dogs. At study days 10 and 40, the animals of groups 1 and 3 were given each 100 embryonated T. canis eggs. In each case, group 1 was treated 10 days post-infection with Milbemax, while dogs of group 3 remained untreated. Control group 2 was not experimentally infected but treated as group 1. Two weeks after first egg administration, a sharp increase of specific antibody reactions in ELISA and increased eosinophilic counts indicated larval invasion in all infected dogs. 42-56 days following first infection, patent infections were detected coproscopically in all animals of group 3, but in none of the uninfected dogs (group 2) or the infected and treated dogs (group 1). Following a 3-month observation period, all animals of the three groups were treated with piperazine citrate to eliminate intestinal infections and all were administered 100 embryonated eggs. Subsequently, patent infections developed in animals of all groups: in one of the infected and treated animals of group 1, in five of the so far not infected control group 2 and in four of the dogs with previous patent infections (group 3). Susceptibility to patent infections was not significantly altered in T. canis-free dogs compared to dogs with previous patent infection (vertically acquired or experimentally induced). However, dogs of group 1 treated with Milbemax after repeated egg administration developed a significantly increased resistance to patent infections as compared to control dogs (group 2). Observed prepatency periods were between 40 and 56 days and did not differ in the three groups. Even in urban areas, facing high infection pressure with Toxocara eggs maintained by a high dog and fox population, dogs of all ages are at risk to develop patent T. canis infections.

The outcome of Toxocara canis infections in the canine host depends on the migratory pathway of parasite larvae (somatic or tracheal) which is considered to be related to the host's age and its immune status. However, field studies attest high prevalences of patent T. canis infections in adult animals. The controlled induction of patent infections with low doses of embryonated eggs was investigated in 18 beagles in a 7-month study until their 16th life month. The animals were assigned to three groups, each consisting of three vertically infected dogs (with a short patent infection as pups before anthelmintic treatment) and three helminth-free dogs. At study days 10 and 40, the animals of groups 1 and 3 were given each 100 embryonated T. canis eggs. In each case, group 1 was treated 10 days post-infection with Milbemax, while dogs of group 3 remained untreated. Control group 2 was not experimentally infected but treated as group 1. Two weeks after first egg administration, a sharp increase of specific antibody reactions in ELISA and increased eosinophilic counts indicated larval invasion in all infected dogs. 42-56 days following first infection, patent infections were detected coproscopically in all animals of group 3, but in none of the uninfected dogs (group 2) or the infected and treated dogs (group 1). Following a 3-month observation period, all animals of the three groups were treated with piperazine citrate to eliminate intestinal infections and all were administered 100 embryonated eggs. Subsequently, patent infections developed in animals of all groups: in one of the infected and treated animals of group 1, in five of the so far not infected control group 2 and in four of the dogs with previous patent infections (group 3). Susceptibility to patent infections was not significantly altered in T. canis-free dogs compared to dogs with previous patent infection (vertically acquired or experimentally induced). However, dogs of group 1 treated with Milbemax after repeated egg administration developed a significantly increased resistance to patent infections as compared to control dogs (group 2). Observed prepatency periods were between 40 and 56 days and did not differ in the three groups. Even in urban areas, facing high infection pressure with Toxocara eggs maintained by a high dog and fox population, dogs of all ages are at risk to develop patent T. canis infections.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:05 Vetsuisse Faculty > Institute of Parasitology
04 Faculty of Medicine > Institute of Parasitology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
600 Technology
Language:English
Date:25 March 2008
Deposited On:03 Dec 2008 07:15
Last Modified:05 Apr 2016 12:32
Publisher:Elsevier
ISSN:0304-4017
Publisher DOI:10.1016/j.vetpar.2007.11.022
PubMed ID:18201825
Permanent URL: http://doi.org/10.5167/uzh-4857

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