scholarly journals The O-specific polysaccharide structure and gene cluster of serotype O:12 of the Yersinia pseudotuberculosis complex, and the identification of a novel L-quinovose biosynthesis gene

Glycobiology ◽  
2012 ◽  
Vol 23 (3) ◽  
pp. 346-353 ◽  
Author(s):  
C. De Castro ◽  
J. J. Kenyon ◽  
M. M. Cunneen ◽  
A. Molinaro ◽  
O. Holst ◽  
...  
2009 ◽  
Vol 344 (12) ◽  
pp. 1533-1540 ◽  
Author(s):  
Monica M. Cunneen ◽  
Cristina De Castro ◽  
Johanna Kenyon ◽  
Michelangelo Parrilli ◽  
Peter R. Reeves ◽  
...  

Glycobiology ◽  
2011 ◽  
Vol 21 (9) ◽  
pp. 1131-1139 ◽  
Author(s):  
Johanna J Kenyon ◽  
Cristina De Castro ◽  
Monica M Cunneen ◽  
Peter R Reeves ◽  
Antonio Molinaro ◽  
...  

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 191
Author(s):  
Lucia Rivas ◽  
Hugo Strydom ◽  
Shevaun Paine ◽  
Jing Wang ◽  
Jackie Wright

The rate of yersiniosis in New Zealand (NZ) is high compared with other developed countries, and rates have been increasing over recent years. Typically, >99% of human cases in NZ are attributed to Yersinia enterocolitica (YE), although in 2014, a large outbreak of 220 cases was caused by Yersinia pseudotuberculosis. Up until 2012, the most common NZ strain was YE biotype 4. The emergent strain since this time is YE biotype 2/3 serotype O:9. The pathogenic potential of some YE biotypes remains unclear. Most human cases of yersiniosis are considered sporadic without an identifiable source. Key restrictions in previous investigations included insufficient sensitivity for the isolation of Yersinia spp. from foods, although foodborne transmission is the most likely route of infection. In NZ, YE has been isolated from a variety of sick and healthy domestic and farm animals but the pathways from zoonotic reservoir to human remain unproven. Whole-genome sequencing provides unprecedented discriminatory power for typing Yersinia and is now being applied to NZ epidemiological investigations. A “One-Health” approach is necessary to elucidate the routes of transmission of Yersinia and consequently inform targeted interventions for the prevention and management of yersiniosis in NZ


Microbiology ◽  
2005 ◽  
Vol 151 (12) ◽  
pp. 4093-4102 ◽  
Author(s):  
Saija Kiljunen ◽  
Kristo Hakala ◽  
Elise Pinta ◽  
Suvi Huttunen ◽  
Patrycja Pluta ◽  
...  

Bacteriophage ϕR1-37 was isolated based on its ability to infect strain YeO3-R1, a virulence-plasmid-cured O antigen-negative derivative of Yersinia enterocolitica serotype O : 3. In this study, the phage receptor was found to be a structure in the outer core hexasaccharide of Y. enterocolitica O : 3 LPS. The phage receptor was present in the outer core of strains of many other Y. enterocolitica serotypes, but also in some Yersinia intermedia strains. Surprisingly, the receptor structure resided in the O antigen of Yersinia pseudotuberculosis O : 9. Electron microscopy demonstrated that ϕR1-37 particles have an icosahedral head of 88 nm, a short neck of 10 nm, a long contractile tail of 236 nm, and tail fibres of at least 86 nm. This implies that the phage belongs to the order Caudovirales and the family Myoviridae in the ICTV (International Committee for Taxonomy of Viruses) classification. ϕR1-37 was found to have a lytic life cycle, with eclipse and latent periods of 40 and 50 min, respectively, and a burst size of ∼80 p.f.u. per infected cell. Restriction digestions and PFGE showed that the ϕR1-37 genome was dsDNA and ∼270 kb in size. Enzymically hydrolysed DNA was subjected to HPLC-MS/MS analysis, which demonstrated that the ϕR1-37 genome is composed of DNA in which thymidine (T) is >99 % replaced by deoxyuridine (dU). The only organisms known to have similar DNA are the Bacillus subtilis-specific bacteriophages PBS1 and PBS2. N-terminal amino acid sequences of four major structural proteins did not show any similarity to (viral) protein sequences in databases, indicating that close relatives of ϕR1-37 have not yet been characterized. Genes for two of the structural proteins, p24 and p46, were identified from the partially sequenced ϕR1-37 genome.


1998 ◽  
Vol 66 (2) ◽  
pp. 480-485 ◽  
Author(s):  
S. Schubert ◽  
A. Rakin ◽  
H. Karch ◽  
E. Carniel ◽  
J. Heesemann

ABSTRACT The fyuA-irp gene cluster contributes to the virulence of highly pathogenic Yersinia (Yersinia pestis,Yersinia pseudotuberculosis, and Yersinia enterocolitica 1B). The cluster encodes an iron uptake system mediated by the siderophore yersiniabactin and reveals features of a pathogenicity island. Two evolutionary lineages of this “high pathogenicity island” (HPI) can be distinguished on the basis of DNA sequence comparison: a Y. pestis group and a Y. enterocolitica group. In this study we demonstrate that the HPI of the Y. pestis evolutionary group is disseminated among species of the family Enterobacteriaceae which are pathogenic to humans. It prevails in enteroaggregativeEscherichia coli and in E. coli blood culture isolates (93 and 80%, respectively), but is rarely found in enteropathogenic E. coli, enteroinvasive E. coli, and enterotoxigenic E. coli isolates. In contrast, the HPI was absent from enterohemorrhagic E. coli, Shigella, and Salmonella entericastrains investigated. Polypeptides encoded by the fyuA,irp1, and irp2 genes located on the HPI could be detected in E. coli strains pathogenic to humans. However, these E. coli strains showed a reduced sensitivity to the bacteriocin pesticin, whose uptake is mediated by the FyuA receptor. Escherichia strains do not possess thehms gene locus thought to be a part of the HPI of Y. pestis. Deletions of the fyuA-irp gene cluster affecting solely the fyuA part of the HPI were identified in 3% of the E. coli strains tested. These results suggest horizontal transfer of the HPI between Y. pestis and some pathogenic E. coli strains.


Sign in / Sign up

Export Citation Format

Share Document