Enterotoxigenic Escherichia coli (ETEC) serotype O169:H41 organisms have become the most prevalent ETEC in Japan since the first outbreak in 1991. It was assumed that the outbreaks were due to clonal spread of this new ETEC serotype. The relationship of 32 strains isolated from 6 outbreaks were examined for biotype, antibiotic susceptibility, enterotoxigenicity, protein banding pattern, lipopolysaccharide banding pattern, plasmid analysis, and ribotyping. Further, the strains were examined by haemagglutination, surface hydrophobicity, and the ability to adhere to HEp-2 cells. The present study suggests that the outbreaks were caused by multiple clones of STp-producing O169:H41 since they showed differences in ribotype and outer membrane protein banding patterns. The strains did not agglutinate human or bovine red blood cells in a mannose-resistant manner. They adhered to HEp-2 cells in a manner resembling enteroaggregative E. coli. Five strains were examined by dot-blot tests for the colonization factor antigens CFA/I, CS1, CS2, CS3, CS4, CS5, CS6, CS7, PCFO159, PCFO166 and CFA/III. Although four strains expressed CS6, no structure for CS6 was identified. A strain that the anti-CS6 MAbs did not react with could adhere to HEp-2 cells in mannose resistant manner; thus, it is unlikely that CS6 play an important role in the adhesion to the cells. Electron microscopy studies of the O169:H41 strains suggested that curly fimbriae, a possible new colonization factor, may be playing an important role in the adhesion of the bacteria to HEp-2 cells. In conclusion, outbreaks due to ETEC O169:H41 were caused by multiple clones, and the strains should be examined in detail for a possible new colonization factor.

The cecal content of rats administered dimethylarsinic acid for 6 months via drinking water was cultured in GAM medium with 10 mg l À1 of dimethylarsinic acid. Arsenic compounds in the culture were analyzed by ion chromatography with inductively coupled plasma mass spectrometry (IC-ICP-MS). Dimethylarsinic acid was metabolized. Two bacterial Escherichia coli strains, A3-4 and A3-6, were isolated from the culture. These strains metabolized dimethylarsinic acid and yielded two unidentified arsenic compounds, M-2 and M-3. A3-6 methylated dimethylarsinic acid to trimethylarsine oxide. Both strains metabolized trimethylarsine oxide and yielded an unidentified arsenic compound, M-1. These unknown arsenic compounds were the same compounds as detected in the urine and the feces of rats administered dimethylarsinic acid. The strains reduced arsenate to arsenite efficiently. Cysteine was required for metabolism of dimethylarsinic acid by these bacteria, but glutathione was not required. These results strongly suggested that the intestinal bacteria have a different arsenic metabolism from that in mammals and that they may play a possible role in mammalian arsenic metabolism. Copyright INTRODUCTIONEpidemiological studies have indicated that arsenic is carcinogenic.1 However, the mechanism of induction of carcinogenesis by arsenic and the chemical form of the ultimate carcinogen is still unclear. The metabolism of arsenic in mammals is well known. When inorganic arsenic is introduced into the mammalian body, it is reduced to trivalent arsenic, and is methylated to monomethylarsonic acid (MMA), dimethylarsinic acid (DMA) or trimethylarsine oxide (TMAO).2,3 Since DMA is the principal metabolite of inorganic arsenic in rat 4 and is supposed to be a carcinogen or a promoter, 5,6 it is important to study the metabolism of DMA.Some researchers have suggested the possibility of contribution of intestinal bacteria to the metabolism of arsenic in mammals. Intestinal bacteria of experimental animals are able to methylate inorganic and organic arsenic.7-9 On the other hand, it appears that bacterial metabolism of arsenic differs from mammalian metabolism. Cullen et al. 10 reported that intestinal bacteria in ceca of rats demethylate a methylated arsenic compound. Yoshida et al. 11,12 detected three unknown arsenic compounds in the urine and feces of rats administered DMA, TMAO or MMA. They suggested that these unknown arsenic compounds might be produced by intestinal bacteria, since elimination of the unknown compounds is greater in rats administered arsenics orally than in those administered it intraperitoneally. It is possible that these compounds are produced by intestinal bacteria and are related to the toxic effects of DMA in mammals.We examined the ability of culture of rat cecal content to yield unknown arsenic compounds from DMA, and attempted to isolate the bacteria metabolizing DMA.

ABSTRACT. Toxocara spp. eggs were detected from 30 (75%) out of 40 sandpits of parks, in Osaka city. This prevalence was higher compared to those reported other areas of Japan. Since we examined a large quantity of sample, this could have resulted to higher prevalence. The number of eggs recovered decreased following fence construction around sandpits, but it did not sufficiently prevent the contamination of eggs. Improvement of fence design and education of sandpit users are necessary when contemplating fence construction around sandpits as a measure against contamination with Toxocara spp. eggs. -KEY WORDS: fence construction, Osaka city , Toxocara egg.

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