Salmonellosis is the second most common cause of food-borne illness worldwide. Contamination of surfaces in food processing environments may result in biofilm formation with a risk of food contamination. Effective decontamination of biofilm-contaminated surfaces is challenging. Using the CDC biofilm reactor, the activities of sodium hypochlorite, sodium hydroxide, and benzalkonium chloride were examined against an early (48-h) and relatively mature (168-h) Salmonella biofilm. All 3 agents result in reduction in viable counts of Salmonella; however, only sodium hydroxide resulted in eradication of the early biofilm. None of the agents achieved eradication of mature biofilm, even at the 90-min contact time. Studies of activity of chemical disinfection against biofilm should include assessment of activity against mature biofilm. The difficulty of eradication of established Salmonella biofilm serves to emphasize the priority of preventing access of Salmonella to postcook areas of food production facilities.
BackgroundAntimicrobial resistance is a major issue in the Shigellae, particularly as a specific multidrug-resistant (MDR) lineage of Shigella sonnei (lineage III) is becoming globally dominant. Ciprofloxacin is a recommended treatment for Shigella infections. However, ciprofloxacin-resistant S. sonnei are being increasingly isolated in Asia and sporadically reported on other continents. We hypothesized that Asia is a primary hub for the recent international spread of ciprofloxacin-resistant S. sonnei.Methods and FindingsWe performed whole-genome sequencing on a collection of 60 contemporaneous ciprofloxacin-resistant S. sonnei isolated in four countries within Asia (Vietnam, n = 11; Bhutan, n = 12; Thailand, n = 1; Cambodia, n = 1) and two outside of Asia (Australia, n = 19; Ireland, n = 16). We reconstructed the recent evolutionary history of these organisms and combined these data with their geographical location of isolation. Placing these sequences into a global phylogeny, we found that all ciprofloxacin-resistant S. sonnei formed a single clade within a Central Asian expansion of lineage III. Furthermore, our data show that resistance to ciprofloxacin within S. sonnei may be globally attributed to a single clonal emergence event, encompassing sequential gyrA-S83L, parC-S80I, and gyrA-D87G mutations. Geographical data predict that South Asia is the likely primary source of these organisms, which are being regularly exported across Asia and intercontinentally into Australia, the United States and Europe. Our analysis was limited by the number of S. sonnei sequences available from diverse geographical areas and time periods, and we cannot discount the potential existence of other unsampled reservoir populations of antimicrobial-resistant S. sonnei.ConclusionsThis study suggests that a single clone, which is widespread in South Asia, is likely driving the current intercontinental surge of ciprofloxacin-resistant S. sonnei and is capable of establishing endemic transmission in new locations. Despite being limited in geographical scope, our work has major implications for understanding the international transfer of antimicrobial-resistant pathogens, with S. sonnei acting as a tractable model for studying how antimicrobial-resistant Gram-negative bacteria spread globally.
Shigella sonnei increasingly dominates the international epidemiological landscape of shigellosis. Treatment options for S. sonnei are dwindling due to resistance to several key antimicrobials, including the fluoroquinolones. Here we analyse nearly 400 S. sonnei whole genome sequences from both endemic and non-endemic regions to delineate the evolutionary history of the recently emergent fluoroquinolone-resistant S. sonnei. We reaffirm that extant resistant organisms belong to a single clonal expansion event. Our results indicate that sequential accumulation of defining mutations (gyrA-S83L, parC-S80I, and gyrA-D87G) led to the emergence of the fluoroquinolone-resistant S. sonnei population around 2007 in South Asia. This clone was then transmitted globally, resulting in establishments in Southeast Asia and Europe. Mutation analysis suggests that the clone became dominant through enhanced adaptation to oxidative stress. Experimental evolution reveals that under fluoroquinolone exposure in vitro, resistant S. sonnei develops further intolerance to the antimicrobial while the susceptible counterpart fails to attain complete resistance.
The 16 Salmonella enterica serovar Enteritidis (S. Enteritidis) typing phages (SETPs) used in the Laboratory of Enteric Pathogens (Health Protection Agency, London, UK) phage-typing scheme have not previously been characterized in detail. We have examined the adsorption properties of the phages with respect to a number of S. enterica serovars and defined phage morphology with electron microscopy. PFGE was used to estimate overall genome size and banding patterns generated by electrophoresis following restriction endonuclease digestion of the genome with HindIII were compared. PCR amplification and sequencing of selected genes was performed. The 16 phages comprise three morphotypes, Podoviridae (SETP1, 8, 10, 14, 15 and 16), Siphoviridae (SETP3, 5, 7, 11, 12 and 13) and Myoviridae (SETP2, 4, 6 and 9). All Podoviridae and Siphoviridae, but not Myoviridae, adsorbed to the O12 lipopolysaccharide antigen of Salmonella serogroups B (4,12) and D 1 (9,12). The genome sizes for the Podoviridae and Siphoviridae (PFGE-A) were approximately 42 kb. The genome size for Myoviridae SETP2, 4 and 9 was 36.5 kb, and for myovirus SETP6 was 27 kb. HindIII digestion of phage DNA produced 9 distinct patterns of 8 to 11 bands. Relationships between phages based on digest patterns were consistent with those defined by morphology. The Podoviridae had homologues of several P22 genes while the Siphoviridae had homologues of several genes present in the sequenced siphovirus SETP3 (EF177456). This study represents an initial step in characterizing the molecular basis that underlies the widely used S. Enteritidis typing scheme.
UWE makes no representation or warranties of commercial utility, title, or fitness for a particular purpose or any other warranty, express or implied in respect of any material deposited. UWE makes no representation that the use of the materials will not infringe any patent, copyright, trademark or other property or proprietary rights.UWE accepts no liability for any infringement of intellectual property rights in any material deposited but will remove such material from public view pending investigation in the event of an allegation of any such infringement. PLEASE SCROLL DOWN FOR TEXT.A new bacteriophage subfamily -"Jerseyvirinae" the family Siphoviridae is proposed, named the "Jerseyvirinae" and consisting of three genera, the 36
Foodborne pathogens can attach to, and survive on, food contact surfaces for long periods by forming a biofilm. Salmonella enterica is the second most common cause of foodborne illness in Ireland. The ability of S. enterica to form a biofilm could contribute to its persistence in food production areas, leading to cross-contamination of products and surfaces. Arising from a large foodborne outbreak of S. enterica serovar Agona associated with a food manufacturing environment, a hypothesis was formulated that the associated Salmonella Agona strain had an enhanced ability to form a biofilm relative to other S. enterica. To investigate this hypothesis, 12 strains of S. enterica, encompassing three S. enterica serovars, were assessed for the ability to form a biofilm on multiple food contact surfaces. All isolates formed a biofilm on the contact surfaces, and there was no consistent trend for the Salmonella Agona outbreak strain to produce a denser biofilm compared with other strains of Salmonella Agona or Salmonella Typhimurium. However, Salmonella Enteritidis biofilm was considerably less dense than Salmonella Typhimurium and Salmonella Agona biofilms. Biofilm density was greater on tile than on concrete, polycarbonate, stainless steel, or glass.
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