scholarly journals Yersiniophage ϕR1-37 is a tailed bacteriophage having a 270 kb DNA genome with thymidine replaced by deoxyuridine

Microbiology ◽  
2005 ◽  
Vol 151 (12) ◽  
pp. 4093-4102 ◽  
Author(s):  
Saija Kiljunen ◽  
Kristo Hakala ◽  
Elise Pinta ◽  
Suvi Huttunen ◽  
Patrycja Pluta ◽  
...  
Keyword(s):  
Yersinia Pseudotuberculosis ◽  
Burst Size ◽  
Outer Core ◽  
International Committee ◽  
Amino Acid Sequences ◽  
Structural Proteins ◽  
Virulence Plasmid ◽  
O Antigen ◽  
Serotype O ◽  
Phage Receptor

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.

scholarly journals Bacteriophage φYeO3-12, Specific forYersinia enterocolitica Serotype O:3, Is Related to Coliphages T3 and T7

2000 ◽  
Vol 182 (18) ◽  
pp. 5114-5120 ◽  
Author(s):  
Maria Pajunen ◽  
Saija Kiljunen ◽  
Mikael Skurnik
Keyword(s):  
Physical Map ◽  
Burst Size ◽  
Restriction Enzymes ◽  
Structural Proteins ◽  
Close Relative ◽  
Lytic Phage ◽  
Serotype O ◽  
One Step ◽  
Phage Capsid ◽  
Phage Receptor

Bacteriophage φYeO3-12 is a lytic phage of Yersinia enterocolitica serotype O:3. The phage receptor is the lipopolysaccharide O chain of this serotype that consists of the rare sugar 6-deoxy-l-altropyranose. A one-step growth curve of φYeO3-12 revealed eclipse and latent periods of 15 and 25 min, respectively, with a burst size of about 120 PFU per infected cell. In electron microscopy φYeO3-12 virions showed pentagonal outlines, indicating their icosahedral nature. The phage capsid was shown to be composed of at least 10 structural proteins, of which a protein of 43 kDa was predominant. N-terminal sequences of three structural proteins were determined, two of them showing strong homology to structural proteins of coliphages T3 and T7. The phage genome was found to consist of a double-stranded DNA molecule of 40 kb without cohesive ends. A physical map of the phage DNA was constructed using five restriction enzymes. The phage infection could be effectively neutralized using serum from a rabbit immunized with whole φYeO3-12 particles. The antiserum also neutralized T3 infection, although not as efficiently as that of φYeO3-12. φYeO3-12 was found to share, in addition to the N-terminal sequence homology, several common features with T3, including morphology and nonsubjectibility to F exclusion. The evidence conclusively indicated that φYeO3-12 is the first close relative of phage T3 to be described.

scholarly journals Role of YadA, Ail, and Lipopolysaccharide in Serum Resistance of Yersinia enterocolitica Serotype O:3

2005 ◽  
Vol 73 (4) ◽  
pp. 2232-2244 ◽  
Author(s):  
Marta Biedzka-Sarek ◽  
Reija Venho ◽  
Mikael Skurnik
Keyword(s):  
Yersinia Enterocolitica ◽  
Alternative Pathway ◽  
Outer Membrane Proteins ◽  
Outer Core ◽  
Normal Serum ◽  
Serum Resistance ◽  
Bacterial Killing ◽  
Term Survival ◽  
O Antigen ◽  
Serotype O

ABSTRACT Complement attack is a host strategy leading to elimination of pathogens. Yersinia enterocolitica expresses several potential complement resistance factors: the outer membrane proteins YadA and Ail as well as lipopolysaccharide (LPS). To study the contribution of these factors to the survival of Y. enterocolitica serotype O:3 in nonimmune human serum, we constructed 23 mutant strains of Y. enterocolitica O:3 expressing different combinations of YadA, Ail, LPS O antigen, and LPS outer core. Survival of bacteria was analyzed in normal serum (with functional classical, lectin, and alternative complement activation pathways) and EGTA-Mg-treated serum (only alternative pathway functional). Kinetic killing tests revealed that the most potent single-serum resistance factor needed for long-term survival was YadA; Ail was also indispensable, but it provided short-term survival and delayed the bacterial killing. On the contrary, the LPS O antigen and outer core, when in combination with YadA, Ail, or both, had a minor and often negative effect on serum resistance. Bacteria in the exponential phase of growth were more resistant to serum killing than stationary-phase bacteria. After exposing bacteria to EGTA-Mg-treated serum, O antigen could prevent deposition of covalently bound C3b on bacteria at 3 min of incubation, even as a single factor. At later time points (15 and 30 min) it had to be accompanied by YadA, Ail, and outer core. In normal serum, the bacteria were less resistant to C3b deposition. However, no direct correlation between the C3 deposition pattern and bacterial resistance was observed.

scholarly journals Pathogenic Yersinia enterocolitica Strains Increase the Outer Membrane Permeability in Response to Environmental Stimuli by Modulating Lipopolysaccharide Fluidity and Lipid A Structure

2003 ◽  
Vol 71 (4) ◽  
pp. 2014-2021 ◽  
Author(s):  
J. A. Bengoechea ◽  
K. Brandenburg ◽  
M. D. Arraiza ◽  
U. Seydel ◽  
M. Skurnik ◽  
...  
Keyword(s):  
Membrane Permeability ◽  
Outer Membrane ◽  
Yersinia Enterocolitica ◽  
Lipid A ◽  
Yersinia Pseudotuberculosis ◽  
Acyl Chain ◽  
Growth Conditions ◽  
Virulence Plasmid ◽  
Serotype O ◽  
Outer Membrane Permeability

ABSTRACT Pathogenic biotypes of Yersinia enterocolitica (serotypes O:3, O:8, O:9, and O:13), but not environmental biotypes (serotypes O:5, O:6, O:7,8, and O:7,8,13,19), increased their permeability to hydrophobic probes when they were grown at pH 5.5 or in EGTA-supplemented (Ca2+-restricted) media at 37°C. A similar observation was also made when representative strains of serotypes O:8 and O:5 were tested after brief contact with human monocytes. The increase in permeability was independent of the virulence plasmid. The role of lipopolysaccharide (LPS) in this phenomenon was examined by using Y. enterocolitica serotype O:8. LPS aggregates of bacteria grown in acidic or EGTA-supplemented broth took up more N-phenylnaphthylamine than LPS aggregates of bacteria grown in standard broth and also showed a marked increase in acyl chain fluidity which correlated with permeability, as determined by measurements obtained in the presence of hydrophobic dyes. No significant changes in O-antigen polymerization were observed, but lipid A acylation changed depending on the growth conditions. In standard medium at 37°C, there were hexa-, penta-, and tetraacyl lipid A forms, and the pentaacyl form was dominant. The amount of tetraacyl lipid A increased in EGTA-supplemented and acidic media, and hexaacyl lipid A almost disappeared under the latter conditions. Our results suggest that pathogenic Y. enterocolitica strains modulate lipid A acylation coordinately with expression of virulence proteins, thus reducing LPS packing and increasing outer membrane permeability. The changes in permeability, LPS acyl chain fluidity, and lipid A acylation in pathogenic Y. enterocolitica strains approximate the characteristics in Yersinia pseudotuberculosis and Yersinia pestis and suggest that there is a common outer membrane pattern associated with pathogenicity.

scholarly journals Yersiniosis in New Zealand

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 191
Author(s):  
Lucia Rivas ◽  
Hugo Strydom ◽  
Shevaun Paine ◽  
Jing Wang ◽  
Jackie Wright
Keyword(s):  
New Zealand ◽  
One Health ◽  
Yersinia Pseudotuberculosis ◽  
Developed Countries ◽  
Farm Animals ◽  
Pathogenic Potential ◽  
Targeted Interventions ◽  
Serotype O ◽  
Large Outbreak ◽  
Insufficient Sensitivity

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

scholarly journals Contribution of the Major Secreted Yops of Yersinia enterocolitica O:8 to Pathogenicity in the Mouse Infection Model

2004 ◽  
Vol 72 (9) ◽  
pp. 5227-5234 ◽  
Author(s):  
Konrad Trülzsch ◽  
Thorsten Sporleder ◽  
Emeka I. Igwe ◽  
Holger Rüssmann ◽  
Jürgen Heesemann
Keyword(s):  
Small Intestine ◽  
Systemic Infection ◽  
Effector Proteins ◽  
Infection Model ◽  
Virulence Plasmid ◽  
The Novel ◽  
Serotype O ◽  
Mouse Infection Model ◽  
Mouse Tissues ◽  
First Time

ABSTRACT Pathogenic yersiniae (Yersinia pestis, Y. pseudotuberculosis, and Y. enterocolitica) harbor a 70-kb virulence plasmid (pYV) that encodes a type III secretion system and a set of at least six effector proteins (YopH, YopO, YopP, YopE, YopM, and YopT) that are injected into the host cell cytoplasm. Yops (Yersinia outer proteins) disturb the dynamics of the cytoskeleton, inhibit phagocytosis by macrophages, and downregulate the production of proinflammatory cytokines, which makes it possible for yersiniae to multiply extracellularly in lymphoid tissue. Y. enterocolitica serotype O:8 belongs to the highly mouse-pathogenic group of yersiniae in contrast to Y. enterocolitica serotype O:9. However, there has been no systematic study of the contribution of Yops to the pathogenicity of Y. enterocolitica O:8 in mice. We generated a set of yop gene deletion mutants of Y. enterocolitica O:8 by using the novel Red cloning procedure. We subsequently analyzed the contribution of yopH, -O, -P, -E, -M, -T, and -Q deletions to pathogenicity after oral and intravenous infection of mice. Here we showed for the first time that a ΔyopT deletion mutant colonizes mouse tissues to a greater extent than the parental strain. The ΔyopO, ΔyopP, and ΔyopE mutants were only slightly attenuated after oral infection since they were still able to colonize the spleen and liver and cause systemic infection. The ΔyopO mutant was lethal for mice, whereas ΔyopP and ΔyopE mutants were successfully eliminated from the spleen and liver 2 weeks after infection. In contrast the ΔyopH, ΔyopM, and ΔyopQ mutants were highly attenuated and not able to colonize the spleen and liver on any of the days tested. The ΔyopH, ΔyopO, ΔyopP, ΔyopE, ΔyopM, and ΔyopQ mutants had only modest defects in the colonization of the small intestine and Peyer's patches. The ΔyopE mutant was eliminated from the small intestine 3 weeks after infection, whereas the ΔyopH, ΔyopP, ΔyopM, and ΔyopQ mutants continued to colonize the small intestine at this time.

Sign in / Sign up

Export Citation Format

Share Document