Neurotoxocarosis: marked preference of Toxocara canis for the cerebrum and T. cati for the cerebellum in the paratenic model host mouse - PubMed (original) (raw)

Neurotoxocarosis: marked preference of Toxocara canis for the cerebrum and T. cati for the cerebellum in the paratenic model host mouse

Elisabeth Janecek et al. Parasit Vectors. 2014.

Abstract

Background: Infective larvae of the worldwide occurring zoonotic roundworm T. canis exhibit a marked affinity to the nervous tissues of paratenic hosts. In humans, most cases of neurotoxocarosis are considered to be caused by larvae of T. canis as T. cati larvae have rarely been found in the CNS in previous studies. However, direct comparison of studies is difficult as larval migration depends on a variety of factors including mouse strains and inoculation doses. Therefore, the present study aims to provide a direct comparison of both roundworm species in mice as a model for paratenic hosts with specific focus on the CNS during the acute and chronic phase of disease to provide a basis for further studies dealing with neurotoxocarosis.

Methods: C57Bl/6J mice were infected with 2000 embryonated T. canis and T. cati eggs, respectively as well as Balb/c mice infected with T. cati eggs only. On 8 time points post infection, organs were removed and microscopically examined for respective larvae. Special focus was put on the CNS, including analysis of larval distribution in the cerebrum and cerebellum, right and left hemisphere as well as eyes and spinal cord. Additionally, brains of all infection groups as well as uninfected controls were examined histopathologically to characterize neurostructural damage.

Results: Significant differences in larval distribution were observed between and within the infection groups during the course of infection. As expected, significantly higher recovery rates of T. canis than T. cati larvae were determined in the brain. Surprisingly, significantly more T. canis larvae could be found in cerebra of infected mice whereas T. cati larvae were mainly located in the cerebellum. Structural damage in brain tissue could be observed in all infection groups, being more severe in brains of T. canis infected mice.

Conclusions: The data obtained provides an extensive characterization of migrational routes of T. canis and T. cati in the paratenic host mouse in direct comparison. Even though to a lesser extent, structural damage in the brain was also caused by T. cati larvae and therefore, the potential as pathogenic agents should not be underestimated.

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Figures

Figure 1

Figure 1

Total recovered larvae. Total mean number of T. cati and T. canis larvae recovered from experimentally infected Balb/c and B6 mice during different time points post infection. Error bars indicate standard errors of the mean (SEM).

Figure 2

Figure 2

Larval recovery rates in the brain. Recovery rates in [%] of T. cati and T. canis larvae from the brain based on the total number of recovered larvae in experimentally infected mice during different time points pi. Error bars indicate standard errors of the mean (SEM).

Figure 3

Figure 3

Larval recovery rates in the cerebrum. Recovery rates in [%] of T. cati and T. canis larvae from the cerebrum based on the total larval number found in the brain of experimentally infected mice during different time points pi. Error bars indicate standard errors of the mean (SEM).

Figure 4

Figure 4

Larval recovery rates in the cerebellum. Recovery rates in [%] of T. cati and T. canis larvae from the cerebellum based on the total larval number found in the brain of experimentally infected mice during different time points pi. Error bars indicate standard errors of the mean (SEM).

Figure 5

Figure 5

Macroscopical changes in the brain. Hemorrhagic lesions in brains of a) B6 T. canis infected mice and b) B6 T. cati infected mice on day 7 pi.

Figure 6

Figure 6

Histopathological changes in brain structure. Structural damage observed in brains of experimentally infected B6 mice during the course of infection. a)T. canis and b)T. cati infected mice on day 7 pi. Visible hemorrhages confirm macroscopic observations (cf. Figure 5). c)T. canis and d)T. cati infected mice day 42 pi. In c)T. canis larvae (dashed arrows) are detected in the neuroparenchyma. In d), mild microgliosis is observed. Thin arrows show activated microglia. e)T. canis and f)T. cati infected mice day 98 pi. Structural damage has intensified since day 42 pi. Generally, in T. canis infected mice structural damage was evaluated as more severe than in T. cati infected mice. In e), arrested or migrating T. canis larvae (dashed arrows) can be found. Malacia with demyelination and accumulation of gitter cells (thick arrows) is frequently observed. In f), perivascular lymphocytosis is visualized.

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