Neuropathological studies of experimental toxocariasis in lead exposed mice

Summers, B. A.; Cypess, Raymond H.; Dolinsky, Zelig S.; Burright, Richard G.; Donovick, Peter J.

doi:10.1016/0361-9230(83)90153-3

Cited by 18 publications

(10 citation statements)

References 5 publications

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“…Several studies (Burren 1972;Dunsmore et al 1983;Summers et al 1983) recorded non-random distribution of the larvae in the brain; the larvae were detected from myelinated tracts of the corpus callosum, internal and external fornix capsules, cerebral peduncles and the cerebral medulla (Summers et al 1983). Due to low number of experimental mice, we do not present data on the distribution of larvae in particular areas of the organ; nevertheless, we confirmed the presence of larvae in different brain areas in which white matter the most affected part.…”

Section: Discussionmentioning

confidence: 99%

Imaging of Toxocara canis larvae labelled by CFSE in BALB/c mice

et al. 2010

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Mice are used most often as a model for human toxocariasis caused by Toxocara canis larvae. Variety of symptoms developing during the infection reflects behaviour of the larvae, which are able to escape from the intestine and further invade and damage various host organs. In order to find an approach enabling observation on parasite behaviour in mouse in vivo, we used an epifluorescence method and a small animal imaging system (SAIS). Larvae of T. canis were labelled by carboxyfluorescein succinimidyl ester (CFSE) which incorporated on the parasite gastrointestinal tract. Following infection of BALB/c mice by CFSE-labelled larvae it has been observed that staining had no influence on viability and further migratory activity of the parasites through the host organs (the intestine, liver, lungs and brain) where they were detected by SAIS until day 17 p.i. In addition, the dye did not affect larval antigenic activity as well as the development of related immune response. Imaging of parasites labelled by CFSE, therefore, may represent a promising way to study behaviour of T. canis larvae in a paratenic host.

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Section: Discussionmentioning

confidence: 99%

Imaging of Toxocara canis larvae labelled by CFSE in BALB/c mice

et al. 2010

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“…Summers et al . (40) recorded larvae from the cerebrum including heavily myelinated tracts of the corpus callosum and internal and external fornix capsules, as well as the cerebellum including the cerebellar peduncles and cerebellar medulla in Binghamton Heterogeneous stock mice. Good et al .…”

Section: Discussionmentioning

confidence: 99%

Blood–brain barrier impairment with enhanced SP, NK‐1R, GFAP and Claudin‐5 expressions in experimental cerebral toxocariasis

Liao

Cho²,

Kao

et al. 2008

Parasite Immunology

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SUMMARY Infection by Toxocara canis in humans may cause cerebral toxocariasis (CT). Appreciable numbers of T. canis larvae cross the blood–brain barrier (BBB) to invade the brain thus causing CT. In the present studies, we evaluated the BBB permeability and BBB injury as assessed by the cerebral Evans blue (EB) concentration as well as by pathological changes and glial fibrillary acidic protein (GFAP) expression in T. canis‐infected mice monitored from 3 days (dpi) to 8 weeks post‐infection (wpi). The vasodilation neuropeptides, the expressions of substance P (SP) and its preferred binding neurokinin‐1 receptor (NK‐1R) as well as claudin‐5 of tight‐junction proteins associated with BBB impairment were also assessed by Western blotting and reverse‐transcriptase polymerase chain reaction. Results revealed that BBB permeability increased as evidenced by a significantly elevated EB concentration in brains of infected mice. BBB injury appeared due to enhanced GFAP protein and mRNA expressions from 4 to 8 wpi. Leukocytes might have been unrelated to BBB impairment because there was no inflammatory cell infiltration despite T. canis larvae having invaded the brain; whereas markedly elevated SP protein and NK‐1R mRNA expressions concomitant with enhanced claudin‐5 expression seemed to be associated with persistent BBB impairment in this experimental CT model.

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“…That is, infected mice which were exposed either simultaneously (18,19) or previously (20) to lead showed less dramatic changes in behavior than infected animals without such exposure to a toxicant. Interestingly, the neuropathology observed using light microscopic techniques was confined primarily to large myelinated fiber tracts, but was not different between animals exposed to parasite alone or in combination with lead (5). These data suggest that evidence for both the pattern of specific behavioral deficits and instances of resistance may occur depending on the regime ofinfection and exposure to other environmental toxins.…”

Section: Immunological Considerationmentioning

confidence: 76%

“…"Parasites, with their bizarre pathology, often cause confusion in diagnosis, especially in countries where they are uncommon" (3). Part of the problem may lie in the fact that many of the pathological changes found associated with parasitic infection may be caused by inflammation or immunopathological reactions, with eosinophilia as a characteristic accompaniment (3)(4)(5).…”

Section: Scope Of the Problemmentioning

confidence: 99%

“…These T. canis larvae, which are less than 0.5 mm long (9) and 0.02 mm in width 1 week after infection (22), migrate through various organs of the aberrant host, including liver, lung, muscle, retina, and brain (5,7,(23)(24)(25)(26). The larvae may continue to circulate until they reach the brain, where, unlike other sites in which they may be sequestered, they are not encapsulated (5,24) and can remain viable for many years, allowing for continuing damage to the central nervous system (CNS). T. canis may be transmitted to humans and other unnatural hosts by direct contact with infected puppies as well as by ingestion of contaminated food, water, and soil.…”

Section: T Canis: Brain and Behaviormentioning

confidence: 99%

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