Salmonella enterica serovar Agona strains isolated from human cases were compared to strains that were derived from a clone caused a serovar shift in broilers. Pulsed field gel electrophoresis (PFGE) analysis with XbaI or BlnI digestion showed that three of seven strains from human case strains and most of the 81 strains from broilers were clustered in single complex in a minimum spanning tree (MST) reconstructed from the PFGE data. All the strains from human cases and 22 randomly selected strains from broilers were also analyzed by whole genome sequencing (WGS). Analysis of single nucleotide polymorphism (SNP) in the S. Agona core genes showed that four strains from human cases and all the strains from broilers were clustered in a maximum likelihood phylogenetic tree (ML tree) and an MST. These results indicated that the strains derived from the clone caused the serovar shift had already spread to humans. PFGE analysis with XbaI showed that four strains from broilers did not cluster with the other strains in an MST, though all those strains clustered in an ML tree and an MST reconstructed from SNP data. Moreover, three strains from broilers did not cluster in an MST reconstructed from PFGE with BlnI digestion, though those strains clustered in an ML tree and an MST reconstructed from SNP data. Therefore, it was suggested that S. Agona strains derived from a particular clone could not be traced by PFGE analysis but can be investigated by WGS analysis.

Various antibacterial agents have been developed and used for the treatment and prevention of infectious diseases. These drugs show antibacterial activity by inhibiting growth or directly killing bacteria. This antibacterial activity induces the microbial substitution and the emergence of drug-resistant bacteria.1) Therefore, improper use of antibacterial agents selects for drug-resistant bacteria and increases their prevalence. To prevent this problem, it is necessary to develop therapeutic agents that are fundamentally different from current antibacterial agents.2) It is possible that prevention or blockage of bacterial infections could be achieved by interfering with the adherence and/or the invasion of bacteria in host cells. The type III secretion apparatus, one of the virulence factors in bacteria, is necessary for the invasion of pathogenic bacteria into host cells. [3][4][5] Preventing the function of the type III secretion apparatus can attenuate the infectious capacity of pathogenic bacteria, including Yersinia 6) and Chlamydia, 7) without actually killing of the bacteria. Therefore, the type III apparatus has been considered a candidate target site for the development of new antibacterial agents. 8,9) Actin-like protein, MreB, which serves a cytoskeletal function, is necessary for maintenance of the rod-shape of bacteria, including Escherichia coli and Bacillus subtilis. [10][11][12] Furthermore, MreB is associated with chromosome segregation and protein localization to the cell poles.13-15) S-(3,4-Dichlorobenzyl)isothiourea (A22), which was discovered as an inhibitor of replication in E. coli, inhibits the function of MreB by binding to MreB and transforming rod-shaped bacterial cells into coccoid forms. 13,16) A22 has a bacteriostatic effect on certain Gram-negative bacilli, including E. coli. 16)Shigella spp., which are Gram-negative rod-shaped bacteria, are some of the causative agents of bacillary dysentery. 17)Via oral ingestion, Shigella reaches the colon and invades the intestinal epithelial cells, causing destruction of the epithelial layer. The type III secretion system is necessary for the invasion of Shigella into epithelial cells and it delivers effectors directly into host cells. 17,18) The secreted effectors identified in S. flexneri are virulence factors for host cells and various type III effectors, including IpaA, IpaB, IpaC, IpaD, IpgD, and VirA. [18][19][20] Type III secretion systems are not found in non-pathogens. Furthermore, in addition to the type III secretion system, the rod-shape of Shigella seems likely to be necessary for the invasion of host cells because the shape of the cells is linked to the polar localization of certain proteins, including IcsA. 15,21) In this study, the antibacterial activity of A22 was determined, in addition to its coccoid form-inducing effects. Furthermore, the infectious capacity and effector secretion of A22-induced coccoid Shigella cells were examined. We suggest the utility of A22 as a lead compound for generating new anti-infectious drugs an...

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Clostridium perfringens is an important pathogen that is responsible for gastroenteritis; the causative agent for the symptoms is C. perfringens enterotoxin (CPE), which is mainly produced by type F C. perfringens. Since shellfishes may gather C. perfringens in the water environment, this study estimated the potential circulation of type F C. perfringens among humans, sewage, and Ruditapes philippinarum (asari clams) as a result of sewage pollution. A comparison of the characteristics among the isolates from 86 sewage influents, 36 effluents, 76 asari clams, and 37 humans was conducted. Serotyping, cpe genotyping, and toxin genotyping showed that C. perfringens with a plasmid IS1151 sequence downstream of cpe was predominant among sewage influents, effluents, humans, and asari clams. Multilocus sequence typing suggested that some isolates from a human, sewage influents, effluents, and asari clams were linked to each other. These results demonstrated that asari clams are the necessary infection sources of C. perfringens responsible for carriers and foodborne diseases, and that these pathogens from humans infected by asari clams can pollute the water environment. It is useful to assess bacteria such as C. perfringens isolates from sewage to estimate the trend of those from the community.