Plasmid characterization and pulsed‐field electrophoretic analysis demonstrate that ampicillin‐resistant strains of Salmonella enteritidis phage type 6a are derived from Salm. enteritidis phage type 4

Ridley, Anne; Punia, Parul; Ward, L. R.; Rowe, B.; Threlfall, E. J.

doi:10.1111/j.1365-2672.1996.tb03555.x

Cited by 18 publications

(17 citation statements)

References 12 publications

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“…Changes of phage type could be due to phage type conversion among the Papua New Guinea serovar Typhi strains. Phage conversion is a well-documented phenomenon associated with the loss or acquisition of plasmids, phage conversion by temperate phages, and loss of lipopolysaccharide (2,4,17,18,26). It remains possible that the replacement of serovar Typhi strains of phage type D2 by strains of phage type D1, UVS, VNS, and UVS1 may represent a posttreatment effect and that strains have been selected following eradication of other competing strains.…”

Section: Discussionmentioning

confidence: 99%

Increasing Genetic Diversity of Salmonella enterica Serovar Typhi Isolates from Papua New Guinea over the Period from 1992 to 1999

et al. 2002

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Pulsed-field gel electrophoresis (PFGE) of XbaI-digested chromosomal DNA was performed on 133 strains of Salmonella enterica serovar Typhi obtained from Papua New Guinea, with the objective of assessing the temporal variation of these strains. Fifty-two strains that were isolated in 1992 and 1994 were of one phage type, D2, and only two predominant PFGE profiles, X1 and X2, were present. Another 81 strains isolated between 1997 and 1999 have shown divergence, with four new phage types, UVS I (n ‫؍‬ 63), UVS (n ‫؍‬ 5), VNS (n ‫؍‬ 4), and D1 (n ‫؍‬ 9), and more genetic variability as evidenced by the multiple and new PFGE XbaI profiles (21 profiles; Dice coefficient, F ‫؍‬ 0.71 to 0.97). The two profiles X1 and X2 have remained the stable, dominant subtypes since 1992. Cluster analysis based on the unweighted pair group method using arithmetic averages algorithm identifies two main clusters (at 87% similarity), indicating that the divergence of the PFGE subtypes was probably derived from some genomic mutations of the X1 and X2 subtypes. The majority of isolates were from patients with mild and moderate typhoid fever and had various XbaI profiles. A single isolate from a patient with fatal typhoid fever had a unique X11 profile, while four of six isolates from patients with severe typhoid fever had the X1 pattern. In addition, 12 paired serovar Typhi isolates recovered from the blood and fecal swabs of individual patients exhibited similar PFGE patterns, while in another 11 individuals paired isolates exhibited different PFGE patterns. Three pairs of isolates recovered from three individuals had different phage types and PFGE patterns, indicating infection with multiple strains. The study reiterates the usefulness of PFGE in assessing the genetic diversity of S. enterica serovar Typhi for both long-term epidemiology and in vivo stability and instability within an individual patient.

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Section: Discussionmentioning

confidence: 99%

Increasing Genetic Diversity of Salmonella enterica Serovar Typhi Isolates from Papua New Guinea over the Period from 1992 to 1999

et al. 2002

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“…However, a lifestyle where little opportunity for horizontal exchange should exist is apparently not limiting for vectors of such exchange, because individual haplotypes of the host-restricted and invasive serovar Typhi have acquired a variety of plasmids and/or lysogenic prophages (40). Alternatively, different lineages might differ in their propensities for importing DNA via transduction or conjugation due to lineage-specific differences in immunity to bacteriophages, such as are due to CRISPRs (4), or patterns of susceptibility to bacteriophages, such as are encoded by certain plasmids (52). A further mechanism that could affect the frequency of homologous recombination is the existence of lineage-specific differences for defense mechanisms against genetic exchange, such as restriction-modification systems (R-M systems).…”

Section: Smentioning

confidence: 99%

Evolution and Population Structure of Salmonella enterica Serovar Newport

et al. 2010

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Salmonellosis caused by Salmonella enterica serovar Newport is a major global public health concern, particularly because S. Newport isolates that are resistant to multiple drugs (MDR), including thirdgeneration cephalosporins (MDR-AmpC phenotype), have been commonly isolated from food animals. We analyzed 384 S. Newport isolates from various sources by a multilocus sequence typing (MLST) scheme to study the evolution and population structure of the serovar. These were compared to the population structure of S. enterica serovars Enteritidis, Kentucky, Paratyphi B, and Typhimurium. Our S. Newport collection fell into three lineages, Newport-I, Newport-II, and Newport-III, each of which contained multiple sequence types (STs). Newport-I has only a few STs, unlike Newport-II or Newport-III, and has possibly emerged recently. Newport-I is more prevalent among humans in Europe than in North America, whereas Newport-II is preferentially associated with animals. Two STs of Newport-II encompassed all MDR-AmpC isolates, suggesting recent global spread after the acquisition of the bla CMY-2 gene. In contrast, most Newport-III isolates were from humans in North America and were pansusceptible to antibiotics. Newport was intermediate in population structure to the other serovars, which varied from a single monophyletic lineage in S. Enteritidis or S. Typhimurium to four discrete lineages within S. Paratyphi B. Both mutation and homologous recombination are responsible for diversification within each of these lineages, but the relative frequencies differed with the lineage. We conclude that serovars of S. enterica provide a variety of different population structures.Salmonellosis is a major global cause of diarrheal and extraintestinal disease in humans and animals (66). Salmonella enterica subspecies enterica (referred to herein as S. enterica) has been subdivided serologically into Ͼ1,500 serovars (35), but we focus on S. enterica serovar Newport (S. Newport) here because over the last decade it has been a very common cause of human salmonellosis in both the United States and Europe (13,16,27). Furthermore, multidrug-resistant S. Newport isolates that are also resistant to extended-spectrum cephalosporins (MDR-AmpC) have now been reported from several countries (3,24,36) and are a serious problem among both food animals and humans (17,25,36,48,67). MDR-AmpC isolates are resistant to ␤-lactams, including third-generation cephalosporins, aminoglycosides, tetracyclines, sulfonamides and chloramphenicol (12, 36). Resistance to ␤-lactams is caused by plasmids carrying the ampC gene bla CMY-2 , which encodes the CMY-2 ␤-lactamase (11,65).Most of our current understanding of the population structure of S. enterica relies on a series of seminal publications from R. K. Selander's group in the 1990s. These publications showed that some serovars consisted of monophyletic groups-so-called clonal groupings-but many other serovars confounded isolates from multiple lineages and were therefore polyphyletic (5,51,55,56). More recent studie...

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“…Some plasmids are responsible for the phage conversion, which permits bacteria to resist phage infection. For example, the pOG670 plasmid of 54 kb, belonging to the group of incompatibility X (IncX), present in S. enteritidis, is capable of converting phages types 1 and 4 into type 6a, and phage 8 into type 13 (Ridley et al, 1996). In S. abortus-equi, a plasmid of 85 kb that codifies resistance to toxic heavy metals (chromium, arsenic, cadmium, and mercury) was described.…”

Section: Epidemiologymentioning

confidence: 99%