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- Strains of Yersinia wautersii should continue to be classified as the "Korean Group" of the Yersinia pseudotuberculosis Complex and not as a separate species. [JOURNAL ARTICLE]
- Int J Syst Evol Microbiol 2014 Dec 10.
- Impact of Aeromonas and diarrheagenic Escherichia coli screening in patients with diarrhea in Paraná, southern Brazil. [Journal Article]
- J Infect Dev Ctries 2014; 8(12):1609-14.
A wide diversity of bacterial agents may cause diarrhea, presenting challenges to clinical laboratories to define a diagnosis. Considering that most stool cultures are negative, we screened stool samples from patients with diarrhea for the presence of 14 bacterial enteropathogens, aiming to establish which of them should be included in routine stool analysis.Stool samples from 400 patients with diarrhea were analyzed for the presence of Salmonella, Shigella, Campylobacter, Aeromonas, Plesiomonas shigelloides, Vibrio, Yersinia enterocolitica, and diarrheagenic Escherichia coli using conventional microbiological methods and PCR. Two distinct samples were studied; one included predominantly patients involved in outbreaks, and the other patients of low socioeconomic status presenting sporadic cases of diarrhea.In total, 86 cultures (21.5%) were positive. Mixed infections were found in five patients, leading to recovery of 91 strains of enteropathogenic bacteria: Salmonella Enteritidis (9.2%), Aeromonas (7.2%), diarrheagenic E. coli (5.2%), and C. jejuni (1%). However, Salmonella predominated, with 11.5% frequency in diarrhea outbreaks, while Aeromonas predominated among patients of low socioeconomic status, with 14.6% frequency.Aeromonas and diarrheagenic E. coli, which are not routinely screened for, deserve to be included in laboratory screening panels.
- Phenotypic and genotypic analysis of bio-serotypes of Yersinia enterocolitica from various sources in Brazil. [Journal Article]
- J Infect Dev Ctries 2014; 8(12):1533-40.
Yersinia enterocolitica is a well-known foodborne pathogen widely distributed in nature with high public health relevance, especially in Europe.This study aimed to analyze the pathogenic potential of Y. enterocolitica isolated strains from human, animal, food, and environmental sources and from different regions of Brazil by detecting virulence genes inv, ail, ystA, and virF through polymerase chain reaction (PCR), phenotypic tests, and antimicrobial susceptibility analysis. Pulsed-field gel electrophoresis (PFGE) was used for the assessment of phylogenetic diversity.All virulence genes were detected in 11/60 (18%) strains of serotype O:3, biotype 4 isolated from human and animal sources. Ten human strains (4/O:3) presented three chromosomal virulence genes, and nine strains of biotype 1A presented the inv gene. Six (10%) strains were resistant to sulfamethoxazole-trimethoprim, seven (12%) to tetracycline, and one (2%) to amikacin, all of which are used to treat yersiniosis. AMP-CEF-SXT was the predominant resistance profile. PFGE analysis revealed 36 unique pulsotypes, grouped into nine clusters (A to I) with similarity ≥ 85%, generating a diversity discriminatory index of 0.957. Cluster A comprised all bio-serotype 4/O:3 strains isolated from animal and humans sources.This study shows the existence of strains with the same genotypic profiles, bearing all virulence genes, from human and animal sources, circulating among several Brazilian states. This supports the hypothesis that swine is likely to serve as a main element in Y. enterocolitica transmission to humans in Brazil, and it could become a potential threat to public health as in Europe.
- Prevalence, characterization, and antimicrobial resistance of Yersinia species and Yersinia enterocolitica isolated from raw milk in farm bulk tanks. [JOURNAL ARTICLE]
- J Dairy Sci 2014 Dec 11.
The aims of this study were to investigate the prevalence and to characterize and determine the antibiotic resistance of Yersinia spp. isolates from raw milk. From September 2008 to August 2010, 446 raw milk samples were obtained from farm bulk milk tanks in Varamin, Iran. Yersinia spp. were detected in 29 (6.5%) samples, out of which 23 (79.3%), 5 (17.2%), and 1 (3.4%) were isolated from cow, sheep, and goat raw milk, respectively. The most common species isolated was Yersinia enterocolitica (65.5%), followed by Yersinia frederiksenii (31%), and Yersinia kristensenii (3.4%). Of the 19 Y. enterocolitica isolates, 14 (73.7%) were grouped into bioserotype 1A/O:9, 4 (21.1%) belonged to bioserotype 1B:O8, 1 (5.3%) belonged to bioserotype 4/O:3, and 1 isolate (biotype 1A) was not typable. All the isolates of biotypes 1B and 4 harbored both the ystA and ail genes. However, all the isolates of biotype 1A were only positive for the ystB gene. The tested Yersinia spp. showed the highest percentages of resistance to tetracycline (48.3%), followed by ciprofloxacin and cephalothin (each 17.2%), ampicillin (13.8%), streptomycin (6.9%), and amoxicillin and nalidixic acid (each 3.4%). All of the tested isolates demonstrated significant sensitivity to gentamicin and chloramphenicol. Recovery of potentially pathogenic Y. enterocolitica from raw milk indicates high risks of yersiniosis associated with consumption of raw milk.
- Isolation and characterization of Yersinia-specific bacteriophages from pig stools in Finland. [JOURNAL ARTICLE]
- J Appl Microbiol 2014 Dec 11.
Bacteriophages infect bacteria and they are present everywhere in the world including the intestinal tracts of animals. Yersiniosis is a common foodborne infection caused by Yersinia enterocolitica and Yersinia pseudotuberculosis. As these bacteria are frequently isolated from pigs we wanted to know whether Yersinia-specific bacteriophages are also present in the pig stools, and, if so, whether there is a positive or negative association between the prevalence of the Yersinia-phages and the pathogenic Yersinia in the stool samples.Altogether 793 pig stool samples collected between November 2010 and March 2012 from 14 Finnish pig farms were screened for the presence of bacteriophages able to infect Y. enterocolitica serotype O:3, O:5,27 or O:9 strains, or Y. pseudotuberculosis serotype O:1a, O:1b or O:3 strains. Yersinia phages were isolated from 90 samples from eight farms. Y. enterocolitica O:3 was infected by 59 phages, 21 phages infected serotypes O:3 and O:5,27, and two phages infected serotypes O:3, O:5,27 and O:9, and Y. pseudotuberculosis O:1a by 8 phages. Many phages originating from pigs in the same farm were identical based on their restriction enzyme digestion patterns; 20 clearly different phages were selected for further characterization. Host ranges of these phages were tested with 94 Yersinia strains. Six of the phages infected eight strains, 13 phages infected three strains, and one phage infected only one strain, indicating that the phages had a relatively narrow host range.There was a clear association between the presence of the host bacteria and specific phages in the stools.The isolated bacteriophages may have potential as biocontrol agents for yersiniosis in both humans and pigs in future, and as alternatives or in addition to antibiotics. To our knowledge, this is the first reported isolation of Yersinia-specific phages from pig stool samples. This article is protected by copyright. All rights reserved.
- Anti-PcrV antibody strategies against virulent Pseudomonas aeruginosa. [JOURNAL ARTICLE]
- Hum Vaccin Immunother 2014 Oct 1.:0.
Abstract Pseudomonas aeruginosa is an opportunistic bacterial pathogen that causes fatal acute lung infections in critically ill individuals. Its pathogenesis is associated with bacterial virulence conferred by the type III secretion system (TTSS), through which P. aeruginosa causes necrosis of the lung epithelium and disseminates into the circulation, resulting in bacteremia, sepsis, and mortality. TTSS allows P. aeruginosa to directly translocate cytotoxins into eukaryotic cells, inducing cell death. The P. aeruginosa V-antigen PcrV, a homolog of the Yersinia V-antigen LcrV, is an indispensable contributor to TTS toxin translocation. Vaccination against PcrV ensures the survival of challenged mice and decreases lung inflammation and injury. Both the rabbit polyclonal anti-PcrV antibody and the murine monoclonal anti-PcrV antibody, mAb166, inhibit TTS toxin translocation. mAb166 IgG was cloned, and a molecular engineered humanized anti-PcrV IgG antigen-binding fragment, KB001, was developed for clinical use. KB001 is currently undergoing Phase-II clinical trials for ventilator-associated pneumonia in France and chronic pneumonia in cystic fibrosis in USA. In these studies, KB001 has demonstrated its safety, a favorable pharmacokinetic profile, and promising potential as a nonantibiotic strategy to reduce airway inflammation and damage in P. aeruginosa pneumonia.
- The role of pgaC in Klebsiella pneumoniae virulence and biofilm formation. [Journal Article]
- Microb Pathog 2014 Dec.:89-99.
Klebsiella pneumoniae has emerged as one of the major pathogens for community-acquired and nosocomial infections. A four-gene locus that had a high degree similarity with Escherichia coli pgaABCD and Yersinia pestis hmsHFRS was identified in K. pneumoniae genomes. The pgaABCD in E. coli encodes the envelope-spanning Pga machinery for the synthesis and secretion of poly-β-linked N-acetylglucosamine (PNAG). In a limited number of phylogenetically diverse bacteria, PNAG was demonstrated to mediate biofilm formation and had a role in the host-bacteria interactions. The presence of conserved pgaABCD locus among various K. pneumoniae strains suggested a putative requirement of PNAG for this bacterium.In this study, an in-frame deletion of pgaC was generated in K. pneumoniae CG43 and named ΔpgaC. The loss of pgaC affected the production of PNAG and attenuated the enhancement of in vitro biofilm formation upon the addition of bile salts mixture. In mouse models, ΔpgaC exhibited a weakened ability to colonize the intestine, to disseminate extraintestinally, and to induce a systemic infection when compared to K. pneumoniae CG43.Our study demonstrated that pgaC participated in the bile salts induced biofilm formation and was required for K. pneumoniae virulence in vivo.
- Detection of Yersinia enterocolitica in food: an overview. [JOURNAL ARTICLE]
- Eur J Clin Microbiol Infect Dis 2014 Nov 20.
Yersinia enterocolitica is a gastrointestinal pathogen which causes yersiniosis, an illness characterized by diarrhea, ileitis, and mesenteric lymphadenitis. Y. enterocolitica is transmitted via the feco-oral route by the consumption of contaminated food or water. Several phenotypic and genotypic methods have been developed to reliably detect Y. enterocolitica in food. However, the source of infection of many recently reported foodborne outbreaks remains obscure. The detection of this pathogen in food is a challenging task, since it shares similarities with other enteric bacteria. The presence of other microorganisms in the food samples makes it even more difficult to identify this slow-growing pathogen. Therefore, the present-day emphasis is on the development of sensitive, easily automated methods suitable for in-situ detection, allowing quick and cost-effective characterization of food samples. This review summarizes and compares the currently available cultural, immunological, and molecular methods, particularly in relation to their specific merits or demerits when implemented for the detection of Y. enterocolitica in food.
- Serological characterization of the enterobacterial common antigen substitution of the lipopolysaccharide of Yersinia enterocolitica O:3. [JOURNAL ARTICLE]
- Microbiology 2014 Nov 18.
Enterobacterial common antigen (ECA) is a polysaccharide present in all members of Enterobacteriaceae anchored either via phosphatidylglycerol (PG) or lipopolysaccharide (LPS) to the outer leaflet of outer membrane (ECAPG and ECALPS, respectively). Only the latter form is ECA-immunogenic. We earlier demonstrated that Yersinia enterocolitica O:3 and its rough (O-specific polysaccharide-negative) mutants were ECA-immunogenic implicating that they contained ECALPS however, it was not known which part of the LPS core region was involved in ECA binding. To address this, we used a set of three deep-rough LPS mutants for rabbit immunizations. The obtained polyvalent antisera were: (i) analyzed for the presence of anti-LPS and anti-ECA antibodies; (ii) treated with caprylic acid (CA) to precipitate IgM antibodies and protein aggregates; and (iii) adsorbed with live ECA-negative bacteria to obtain specific anti-ECA antisera. We could demonstrate the presence of antibodies specific for both ECAPG and ECALPS in all antisera obtained. Both CA treatment and adsorption with ECA-negative bacteria efficiently removed anti-LPS antibodies resulting in specific anti-ECA sera. The LPS of the ECALPS positive deepest-rough mutant contained only lipid A and 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo) residues of the inner core suggesting that ECALPS was linked to the Kdo-region of LPS in Y. enterocolitica O:3.
- Bacterial programming of host responses: coordination between type I interferon and cell death. [Journal Article, Review]
- Front Microbiol 2014.:545.
During mammalian infection, bacteria induce cell death from an extracellular or intracellular niche that can protect or hurt the host. Data is accumulating that associate type I interferon (IFN) signaling activated by intracellular bacteria with programmed death of immune effector cells and enhanced virulence. Multiple pathways leading to IFN-dependent host cell death have been described, and in some cases it is becoming clear how these mechanisms contribute to virulence. Yet common mechanisms of IFN-enhanced bacterial pathogenesis are not obvious and no specific interferon stimulated genes have yet been identified that cause sensitivity to pathogen-induced cell death. In this review, we will summarize some bacterial infections caused by facultative intracellular pathogens and what is known about how type I IFN signaling may promote the replication of extracellular bacteria rather than stimulate protection. Each of these pathogens can survive phagocytosis but their intracellular life cycles are very different, they express distinct virulence factors and trigger different pathways of immune activation and crosstalk. These differences likely lead to widely varying amounts of type I IFN expression and a different inflammatory environment, but these may not be important to the pathologic effects on the host. Instead, each pathogen induces programmed cell death of key immune cells that have been sensitized by the activation of the type I IFN response. We will discuss how IFN-dependent host cell death may increase host susceptibility and try to understand common pathways of pathogenesis that lead to IFN-enhanced bacterial virulence.