The global dissemination of the multiply-antibiotic-resistant Salmonella enterica serovar Typhimurium DT104 clone with the resistance genes located in a class 1 integron, here designated In104, within genomic island SGI1 is a significant public health issue. Here, we have shown that SGI1 and variants of it carrying different combinations of resistance genes are found in several Salmonella enterica serovars. These are serovars Cerro, Derby, Dusseldorf, Infantis, Kiambu, and Paratyphi B dT ؉ isolated from human infections and serovar Emek from sewage effluent. Two new variants, SGI1-I and SGI1-J, both of which include the dfrA1-orfC cassette array, were identified.
High-throughput epidemiological typing systems that provide phylogenetic and genotypic information are beneficial for tracking bacterial pathogens in the field. The incidence of Salmonella enterica serovar Typhi infection in Indonesia is high and is associated with atypical phenotypic traits such as expression of the j and the z66 flagellum antigens. Utilizing a high-throughput genotyping platform to investigate known nucleotide polymorphisms dispersed around the genome, we determined the haplotypes of 140 serovar Typhi isolates associated with Indonesia. We identified nine distinct serovar Typhi haplotypes circulating in Indonesia for more than 30 years, with eight of these present in a single Jakarta suburb within a 2-year period. One dominant haplotype, H59, is associated with j and z66 flagellum expression, representing a potential pathotype unique to Indonesia. Phylogenetic analysis suggests that H59 z66 ؉ , j ؉ isolates emerged relatively recently in terms of the origin of serovar Typhi and are geographically restricted. These data demonstrate the potential of high-throughput genotyping platforms for analyzing serovar Typhi populations in the field. The study also provides insight into the evolution of serovar Typhi and demonstrates the value of a molecular epidemiological technique that is exchangeable, that is internet friendly, and that has global utility.
Although four of the five Salmonella pathogenicity islands (SPIs) have been characterized in detail for Salmonella enterica serovar Typhimurium, and the fifth has been characterized for Salmonella enterica serovar Dublin, there have been limited studies to examine them in detail in a range of pathogenic serovars of S. enterica. The aim of this study was to examine these regions, shown to be crucial in virulence, in pathogenic serovars to identify any major deletions or insertions that may explain variation in virulence and provide further understanding of the elements involved in the evolution of these regions. Multiple strains of each of the 13 serovars were compared by Southern blot hybridization using a series of probes that together encompassed the full length of all five SPIs. With the exception of serovar Typhimurium, all strains of the same serovar were identical in all five SPIs. Those serovars that differed from serovar Typhimurium in SPI-1 to SPI-4 and from serovar Dublin in SPI-5 were examined in more detail in the variant regions by PCR, and restriction endonuclease digestion and/or DNA sequencing. While most variation in hybridization patterns was attributable to loss or gain of single restriction endonuclease cleavage sites, three regions, in SPI-1, SPI-3, and SPI-5, had differences due to major insertions or deletions. In SPI-1 the avrA gene was replaced by a 200-base fragment in three serovars, as reported previously. In SPI-5, two serovars had acquired an insertion with similarity to the pagJ and pagK genes between pipC and pipD. In SPI-3 the genes sugR and rhuM were deleted in most serovars and in some were replaced by sequences that were very similar to either the Escherichia coli fimbrial operon, flanked by two distinct insertion sequence elements, or to the E. coli retron phage ⌽R73. The distribution of these differences suggests that there have been a number of relatively recent horizontal transfers of genes into S. enterica and that in some cases the same event has occurred in multiple lineages of S. enterica. Thus, it seems that insertion sequences and retron phages are likely to be involved in continuing evolution of the pathogenicity islands of pathogenic Salmonella serovars.
Salmonellosis is a global problem caused by the international movement of foods and high incidence in exporting countries. In September 2001, in an outbreak investigation Australia isolated Salmonella Stanley from imported peanuts, which resulted in a wider investigation in Canada, England & Wales and Scotland. Patients infected with Salmonella serotypes known to be isolated from peanuts and reported to surveillance systems were interviewed to determine exposure histories. Tagged image file format (TIFF) images of pulsed-field gel electrophoresis (PFGE) patterns of Salmonella isolates were shared electronically amongst laboratories. Laboratories tested packets of 'Brand X' peanuts from various lots and product lines. In total, 97 cases of S. Stanley and 12 cases of S. Newport infection were found. Seventy-three per cent (71/97) of S. Stanley cases were in persons of Asian ethnicity. Twenty-eight per cent of cases recalled eating Brand X peanuts and a further 13% had peanuts in their house in the previous month or had eaten Asian-style peanuts. Laboratories isolated S. Stanley, S. Newport, S. Kottbus, S. Lexington and S. Unnamed from Brand X peanuts. Isolates of S. Stanley from peanuts and human patients were indistinguishable by PFGE. This international outbreak resulted from a product originating from one country affecting several others. Rapid sharing of electronic DNA images was a crucial factor in delineating the outbreak; multinational investigations would benefit from a harmonized approach.
A 6-week-old child with acute urinary tract infection caused by Shiga toxin -producing Escherichia coli (STEC) O5:H0 developed hemolytic-uremic syndrome (HUS). Molecular and phenotypic analysis of the urinary isolate indicated that it lacked uropathic properties and that it was probably of intestinal origin. Nevertheless, the patient did not experience a diarrheal prodrome, nor was STEC or Shiga toxin detected in his feces at any time. Examination of the patient's serum pointed to recent infection with E. coli O5, with no evidence of exposure to E. coli O157, O111, or O26. A review of 13 previously reported cases of HUS associated with acute urinary tract infection indicated that this was the first case of nondiarrheal HUS in which infection with the most common STEC serogroups was specifically excluded. This case illustrates the need to investigate patients with nondiarrheal HUS for infection with STEC.
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