Haruo Kamiya

Monoclonal IgA antibody-mediated expulsion of Trichinella from the intestine of mice.

To assess the potential role of IgA antibody in expulsion of the nematode of the genus Trichinella from the intestine, a panel of IgA monoclonal antibodies (mAbs) were produced from the mesenteric lymph node cells from BALB/c mice orally vaccinated with irradiated muscle larvae of Trichinella britovi. One IgA mAb, HUSM-Tb1, formed immunoprecipitates on the surface of live muscle larvae, and by immunohistochemistry reacted with their stichocytes and cuticular surface, but not with those tissues of the adult stage or newborn larvae. Intraperitoneal injection of BALB/c mice with this mAb 5 h before challenge conferred a high level of protection (more than 95%) against T. britovi infection, when 2.0 mg of specific IgA/20 g body weight was given to a mouse. The same treatment produced a similar effect in SCID mice lacking functional T- and B-cells, indicating no requirement of synergistc T-cell factors for the effect. Passive transfer of the mAb at the time of challenge or later showed less or no effect upon worm expulsion. It is concluded that the mucosal IgA response, when adequately induced, can impede the establishment of infective Trichinella parasites in the mouse intestine.

Epidemiology of Helicobacter infection in wild rodents in the Xinjiang-Uygur autonomous region of China.

Helicobacter species were detected in the feces of wild rodents captured in Qiemo and Ruoqiang in the Xinjiang-Uygur autonomous region of China by polymerase chain reaction and 16S rRNA partial sequence analysis. Forty-four wild rodents, including one Przewalski’s gerbil (Brachiones przewalskii), three Northern three-toed jerboas (Dipus sagitta), one long-eared jerboa (Euchoreutes naso), 34 midday gerbils (Meriones meridianus), two short-tailed bandicoot rats (Nesokia indica) and three great gerbils (Rhombomys opimus), were examined. Epidemiological studies indicated that Helicobacter spp. were detected in all genera tested; that H. hepaticus, H. apodemus, H. canadensis, and H. winghamensis were widespread in wild rodents; and that the dominant Helicobacter species in rodents differed depending not only on the order or genus of the animal but also on the animal’s habitat. H. bilis, H. pylori, H. rodentium and “H. suncus” were not detected in any animals. It appears that the wild rodents tested in this study are not a reservoir of H. pylori infection.

LARVA MIGRANS BY BAYLISASCARIS TRANSFUGA: FATAL NEUROLOGICAL DISEASES IN MONGOLIAN JIRDS, BUT NOT IN MICE

Raccoon roundworms (Baylisascaris procyonis) and other Baylisascaris species cause patent or latent larva migrans (LM) in a variety of mammals and birds, including humans. It is not clear whether LM by Baylisascaris transfuga, roundworms of bears, is associated with clinical neurological disorders. To clarify this issue, ICR and BALB/c mice as well as Mongolian jirds (Meriones unguiculatus) were orally inoculated with 2,000–5,000 embryonated eggs of B. transfuga. In mice, the ascarid caused symptomatic LM of limited extent and duration, whereas the infection was fatal in jirds; i.e., they exhibited general signs such as severe depression and emaciation on days 8–11 postinfection (PI) and died, or they developed progressive and fatal neurological disorders after day 14 PI. Histological examination showed B. transfuga larvae in the brain of all mice and jirds examined, and the larvae collected from them developed to a size comparable with that of B. procyonis. There existed, however, critical differences in host reactions against larvae localized in the brain of mice and jirds; B. transfuga larvae found in mice were surrounded by granulomatous reactions and immobilized, whereas larvae found in jirds were free from any host reaction and mobile, causing extensive malacia.

Characterization of SSU and LSU rRNA genes of three Trypanosoma (Herpetosoma) grosi isolates maintained in Mongolian jirds.

Trypanosoma (Herpetosoma) grosi, which naturally parasitizes Apodemus spp., can experimentally infect Mongolian jirds (Meriones unguiculatus). Three isolates from A. agrarius, A. peninsulae, and A. speciosus (named SESUJI, HANTO, and AKHA isolates, respectively) of different geographical origin (AKHA from Japan, and the others from Vladivostok), exhibited different durations of parasitaemia in laboratory jirds (2 weeks for HANTO, and 3 weeks for the others). To assess the genetic background of these T. grosi isolates, their small (SSU) and large subunit (LSU) ribosomal RNA genes (rDNA) were sequenced along with those of 2 other Herpetosoma species from squirrels. The SSU rDNA sequences of these 3 species along with available sequences of 3 other Herpetosoma trypanosomes (T. lewisi, T. musculi and T. microti) seemed to reflect well the phylogenetic relationship of their hosts. Three isolates of T. grosi exhibited base changes at 2-6 positions of 2019-base 18S rDNA, at 5-29 positions of 1817/1818-base 28Salpha rDNA, or 1-5 positions of 1557-1559-base 28Sbeta rDNA, and none was separated from the other 2 isolates by rDNA nucleotide sequences. Since base changes of Herpetosoma trypanosomes at the level of inter- and intra-species might occur frequently in specified rDNA regions, the molecular analysis on these regions of rodent trypanosomes could help species/strain differentiation and systematic revision of Herpetosoma trypanosome species, which must be more abundant than presently known.

Molecular Phylogeny of the Subfamily Gerbillinae (Muridae, Rodentia) with Emphasis on Species Living in the Xinjiang-Uygur Autonomous Region of China and Based on the Mitochondrial Cytochrome b and Cytochrome c Oxidase Subunit II Genes

Rodents belonging to the subfamily Gerbillinae and living in the Xinjiang-Uygur autonomous region of China were collected in field surveys between 2001 and 2003. We found four Meriones species, including M. chengi M. liycus, M. meridianus, and M. tamariscinus, as well as related species from different genera, Rhombomys opimus and Brachiones przewaliskii For phylogenetic analyses of these gerbilline species, DNA sequences of parts of the mitochondrial cytochrome b (Cytb) and cytochrome c oxidase subunit II (COII) genes were examined with the neighbor Joining, maximum parsimony, maximum likelihood, and Bayesian inference methods. Our phylogenetic analyses suggest that the genus Meriones is not monophyletic and place M. tamaricinus as the sister taxon to a clade comprising Brachiones, Psammomys, Rhombomys, and the other Meriones species. The remaining Meriones species separate into three lineages: M. meridianus (including M. chengi), Meriones unguiculatus, and a clade that includes multiple Meriones species originating from Asia, the Middle East, and Africa. The phylogenetic relationships among the genera Brachines, Meriones, Psammomys, and Rhombomys remain ambiguous, probably due to the saturation of mutations that occurs in fast-evolving mitochondrial DNA. In addition, intraspecific variation was observed for M. meridianus, and this mostly correlated with collection localities, i.e., the northern and southern parts of the Xinjiang region. This variation corresponded to interspecific levels of divergence among other lineages of Meriones. Interestingly, no differences were observed in either the Cytb or COII gene sequences isolated from M. chengi collected from the Turfan Basin in the north and those from M. meridianus in the south, suggesting that M. chengi may be a synonym of M. meridianus.

Persistent infection of Mongolian jirds with a non-pathogenic trypanosome, Trypanosoma (Herpetosoma) grosi.

Non-pathogenic trypanosomes of the subgenus Herpetosoma are normally host specific, and laboratory models include Trypanosoma lewisi in rats and Trypanosoma musculi in mice. Two isolates of Trypanosoma grosi, originating from Apodemus agrarius and Apodemus peninsulae, grew well in Mongolian jirds, Meriones unguiculatus, after intraperitoneal inoculation of 2 x 10(5) or a minimum 500 bloodstream forms. The course of T. grosi infection in jirds resembled T. musculi infection in mice, rather than T. lewisi infection in rats. At week 2 to 3 p.i. trypanosomes disappeared from the bloodstream, and neither prednisolone treatment nor splenectomy prevented parasite elimination from the bloodstream. However, these treatments induced a marked increase in peak parasite counts. Regardless of prednisolone treatment or splenectomy, all jirds after day 21 p.i. became resistant to the reinfection. Although no trypanosomes were detected in the bloodstream of recovered jirds, dividing parasites persisted in the medullary capillaries of the kidney, like T. musculi infection in mice. We propose the T. grosi infection in jirds as an additional laboratory model for the study of non-pathogenic trypanosomes.

Survival of destrobilated adults of Taenia crassiceps in T-cell-depleted Mongolian gerbils.

Abstract In Mongolian gerbils (Meriones unguiculatus), prednisolone treatment induces the survival of strobilated Taenia crassiceps to sexual maturity followed by fecal release of gravid proglottides. The mechanism underlying the effects of prednisolone has not been elucidated in this taeniid/rodent model. Using a novel murine monoclonal antibody specific to a cell-surface determinant of gerbil T-cells (HUSM-M.g.15 of IgG2b isotype) for in vivo depletion of the cells, we examined the T-cell dependence of the following two phenomena: (1) elimination of strobilated T. crassiceps from the intestine of naive gerbils, and (2) depressed egg formation by the cestode in prednisolone-treated gerbils. In T-cell-depleted gerbils, only destrobilated adults were recovered from the intestine, although the recovery rate was comparable with that observed in prednisolone-treated animals. Egg formation by the cestode in T-cell-depleted, prednisone-treated gerbils did not differ from that seen in gerbils treated with prednisolone alone. We conclude that one of main effects of prednisolone can be ascribed to the suppression of T-cell functions that work to eliminate strobilated T. crassiceps from gerbils.