Gut Pathogens

Publisher: International Society for Genomic and Evolutionary Microbiology, BioMed Central

Current impact factor: 2.28

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 2.281
2013 Impact Factor 2.07
2012 Impact Factor 2.738
2011 Impact Factor 2.109

Impact factor over time

Impact factor

Additional details

5-year impact 2.61
Cited half-life 3.40
Immediacy index 0.26
Eigenfactor 0.00
Article influence 0.64
ISSN 1757-4749
OCLC 318907797
Material type Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

BioMed Central

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  • Conditions
    • Publisher's version/PDF may be used
    • Eligible UK authors may deposit in OpenDepot
    • Creative Commons Attribution License
    • Copy of License must accompany any deposit.
    • All titles are open access journals
    • 'BioMed Central' is an imprint of 'Springer Verlag (Germany)'
  • Classification

Publications in this journal

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    ABSTRACT: Pneumocystis carinii pneumonia occasionally appears in immunodeficient patients. While several reports have shown that Pneumocystis carinii pneumonia occurred in the early phase of starting infliximab treatment in patients with Crohn’s disease (CD), the present case suggests for the first time that an increased dosage of infliximab may also lead to pneumonia. A 51-year-old male had been taking 5 mg of infliximab for the treatment of CD for 10 years with no adverse events. Beginning in September 2013, the dose of infliximab had to be increased to 10 mg/kg because his status worsened. Thereafter, he complained of a fever and cough, and a CT scan revealed ground-glass opacities in the lower lobes of the bilateral lung with a crazy-paving pattern. Bronchoscopy detected swelling of the tracheal mucosa with obvious dilations of the vessels. A polymerase chain reaction using a bronchoalveolar lavage fluid sample detected specific sequences for Pneumocystis jirovecii; thus he was diagnosed with Pneumocystis carinii (jirovecii) pneumonia. After discontinuing infliximab and starting antibiotic treatment, his symptoms and CT findings were dramatically improved. The administration of an increased dosage of infliximab can cause Pneumocystis carinii pneumonia in CD patients.
    Preview · Article · Dec 2016 · Gut Pathogens
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    ABSTRACT: Background: Recent research suggests integration of the intestinal microbiota in gut-brain communication which could lead to new approaches to treat neurological disorders. The highly social prairie voles are an excellent model system to study the effects of environmental factors on social behavior. For future studies on the role of probiotics in ameliorating disorders with social withdrawal symptoms, we report the characterization of intestinal Lactobacillus isolates with probiotic potential from voles. Methods and results: 30 bacterial strains were isolated from the vole intestine and found to be distinct but closely related to Lactobacillus johnsonii using 16S rRNA gene sequencing and Random Amplification of Polymorphic DNA fingerprinting. In vitro characterizations including acid and bile tolerance, antimicrobial effects, antibiotic susceptibility, and adherence to intestinal epithelial cells were performed to assess the probiotic potential of selected strains. Since previous studies revealed that mercury ingestion triggers social deficits in voles, mercury resistance of the probiotic candidates was evaluated which could be an important factor in preventing/treating these behavioral changes. Conclusions: This study demonstrates that lactobacilli with probiotic potential are present in the vole intestine. The Lactobacillus isolates identified in this study will provide a basis for the investigation of probiotic effects in the vole behavioral model system.
    Preview · Article · Dec 2015 · Gut Pathogens
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    ABSTRACT: Escherichia coli is a normal inhabitant of the gut which upon acquiring virulence factors becomes potentially able to cause diseases. Although E. coli population augments in Crohn's disease (CD), the reason of this proliferation is not yet clear. CD associated E. coli shows features of extraintestinal pathogenic categories (ExPEC), and eventually the ability to invade cultured epithelial cells, a property observed among diarrheagenic E. coli (DEC). In this work, data on the characterization of an E. coli isolate from a CD patient reveal that, besides invasiveness, CD associated E. coli may harbor other typical DEC markers, namely those defining enterohemorragic (EHEC) and enteroaggregative (EAEC) pathotypes. The studied strain, detected both in an ileum biopsy and stools, belonged to the B2 E. coli reference collection (EcoR) phylogroup and harbored the intimin, Shiga cytotoxin 1, and AggR transcriptional activator encoding genes (eae, stx1, aggR, respectively); displayed aggregative adherence to Hep-2 cells and an ability to enter Caco-2 cells four times as high as that of EIEC reference strain and half of invasiveness of AIEC LF82. It was able to enter and replicate in J774 macrophages with invasiveness 85 times as high as that of LF82, but with only one sixth of the intracellular proliferation ability of the later. Extracellular products with cytotoxic activity on Vero cells were detected in strain's cultures. Preliminary analysis indicated similarity of this strain's genome with that of O104:H4/2011C-3493. Following its isolation from a resected CD patient, the strain was characterized by in vitro adhesion and invasion assays to Hep-2, invasion to Caco-2 cells and to J774 macrophages and tested for the ability to form biofilm and to produce Shiga cytotoxins. PCRs were carried out to identify virulence genetic markers and for EcoR phylogrouping. The strain's genome was sequenced by means of Ion torrent PGM platform. The detection, in a CD patient, of an E. coli combining virulence features of multiple DEC pathotypes seems not only to stress the relevance of E. coli to CD etiopathogenesis but also to indicate the existence of new and potentially more virulent strains putatively associated with this disease.
    Full-text · Article · Dec 2015 · Gut Pathogens
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    ABSTRACT: The worldwide increase of food-borne infections with antibiotic resistant pathogens constitutes a major public health problem. Therefore, this study aimed to determine the prevalence, antibiogram, virulence genes profiles and integron characteristics of non-typhoidal Salmonella spp. isolated from poultry meat and diarrhoeic patients in Egypt. A total of 150 samples comprising (100 poultry meat and 50 diarrhoeic patients’ stool) were examined for the presence of Salmonella spp. using culture methods followed by biochemical and serological identification of the isolates. All Salmonella strains were tested for their susceptibility to the antibiotics using disk diffusion method and screened for the presence of virulence genes and class I integrons using PCR. The overall prevalence of Salmonella spp. in poultry meat samples was 10 % compared to 4 % in diarrhoeic patients. All the isolates were serologically identified into Salmonella Typhimurium (seven isolates), S. Derby, S. Kiel, S. Rubislaw (one isolate, each) and untypable strains (two isolates). Antibiotic susceptibility testing showed a higher resistance of the total isolates to erythromycin and tetracycline (100 %, each), followed by amoxicillin-clavulanic acid (91.7 %), trimethoprim-sulfamethoxazole (83.3 %), streptomycin, nalidixic acid, ampicillin-sulbactam (75 %, each), gentamycin, ampicillin (66.7 %, each), chloramphenicol (58.3 %), ciprofloxacin (25 %) and ceftriaxone (16.7 %). Virulence genes profiles revealed the presence of sopB gene in five Salmonella strains isolated from poultry meat (n = 3) and humans (n = 2). Moreover, pefA was only identified in three isolates from poultry meat. On the other hand, S. Kiel and S. Typhimurium (one isolate, each) were harboring hilA and stn genes, respectively. Class 1 integrons were detected in all Salmonella spp. with variable amplicon sizes ranged from 650–3000 bp. Sequencing of these amplicons revealed the presence of gene cassettes harboring aac(3)-Id, aadA2, aadA4, aadA7, sat, dfrA15, lnuF and estX resistance genes. Nucleotide sequence analysis showed point mutations in the aac(3)-Id of S. Derby, aadA2, estX-sat genes of S. Typhimurium. Meanwhile, frame shift mutation was observed in aadA7 genes of S. Typhimurium. Increasing rate of antimicrobial resistance and class 1 integrons among multidrug resistant Salmonella spp. has prompted calls for the reduction of antimicrobial use in livestock to prevent future emergence of resistance.
    Preview · Article · Dec 2015 · Gut Pathogens
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    ABSTRACT: How host cell glycosylation affects EPEC or EHEC O157:H7 invasion is unclear. This study investigated whether and how O-glycans were involved in EPEC or EHEC O157:H7 invasion into HT-29 cells. Lectin histochemical staining confirmed stronger staining with PNA, which labeled Galβ1, 3 GalNAc (core 1 structure) in HT-29-Gal-OBN and C2GnT2-sh2/HT-29 cells, compared with control cells. EPEC or EHEC O157:H7 invasion into HT-29 and its derived cells was based on the intracellular presence of GFP-labeled bacteria. The differentiation of HT-29 cells led to a reduction in EPEC internalization compared with HT-29 cells (p < 0.01). EPEC or EHEC O157:H7 invasion into HT-29-OBN and HT-29-Gal-OBN cells increased compared with HT-29 and HT-29-Gal cells (p < 0.05 and p < 0.01). Core 2 O-glycan-deficient HT-29 cells underwent a significant increase in EPEC (p < 0.01) or EHEC O157:H7 (p < 0.05) invasion compared with control cells. Bacterial invasion into cultured cells was determined by a gentamicin protection assay and a GFP-labeled bacteria invasion assay. O-glycans biosynthesis was inhibited by benzyl-α-GalNAc, and core 2 O-glycan-deficient HT-29 cells were induced by C2GnT2 interference. These data indicated that EPEC or EHEC O157:H7 invasion into HT-29 cells was related to their O-glycosylation status. This study provided the first evidence of carbohydrate-dependent EPEC or EHEC O157:H7 invasion into host cells.
    Full-text · Article · Dec 2015 · Gut Pathogens
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    ABSTRACT: Although Crohn's disease (CD) etiology remains unclear, a growing body of evidence suggests that CD may include an infectious component, with Mycobacterium avium subsp. paratuberculosis (MAP) being the most likely candidate for this role. However, the molecular mechanism of the MAP involvement in CD pathogenesis remains unclear. The polymorphism of the NOD2 gene, coding for an intracellular pattern recognition receptor, is a factor of predisposition to mycobacterial infections and CD. Recent findings on NOD2 interactions and functions provide the missing pieces in the puzzle of a NOD2-mediated mechanism common for mycobacterial infections and CD. Implications of these new findings for the development of a better understanding and treatments of CD and mycobacterial infections are discussed.
    Full-text · Article · Dec 2015 · Gut Pathogens
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    ABSTRACT: Acute and chronic inflammatory diseases of the intestine impart a significant and negative impact on the health and well-being of human and non-human mammalian animals. Understanding the underlying mechanisms of inflammatory disease is mandatory to develop effective treatment and prevention strategies. As inflammatory disease etiologies are multifactorial, the use of appropriate animal models and associated metrics of disease are essential. In this regard, animal models used alone or in combination to study acute and chronic inflammatory disease of the mammalian intestine paired with commonly used inflammation-inducing agents are reviewed. This includes both chemical and biological incitants of inflammation, and both non-mammalian (i.e. nematodes, insects, and fish) and mammalian (i.e. rodents, rabbits, pigs, ruminants, dogs, and non-human primates) models of intestinal inflammation including germ-free, gnotobiotic, as well as surgical, and genetically modified animals. Importantly, chemical and biological incitants induce inflammation via a multitude of mechanisms, and intestinal inflammation and injury can vary greatly according to the incitant and animal model used, allowing studies to ascertain both long-term and short-term effects of inflammation. Thus, researchers and clinicians should be aware of the relative strengths and limitations of the various animal models used to study acute and chronic inflammatory diseases of the mammalian intestine, and the scope and relevance of outcomes achievable based on this knowledge. The ability to induce inflammation to mimic common human diseases is an important factor of a successful animal model, however other mechanisms of disease such as the amount of infective agent to induce disease, invasion mechanisms, and the effect various physiologic changes can have on inducing damage are also important features. In many cases, the use of multiple animal models in combination with both chemical and biological incitants is necessary to answer the specific question being addressed regarding intestinal disease. Some incitants can induce acute responses in certain animal models while others can be used to induce chronic responses; this review aims to illustrate the strengths and weaknesses in each animal model and to guide the choice of an appropriate acute or chronic incitant to facilitate intestinal disease.
    Preview · Article · Nov 2015 · Gut Pathogens
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    ABSTRACT: To assess the prevalence of gastrointestinal neoplasia in patients with Streptococcus bovis infectious endocarditis we performed a retrospective cohort analysis of all episodes of S. bovis infectious endocarditis treated at our institution between January 2000 through December 2014. Twenty-five patients were identified for this purpose. 12/25 patients received colonoscopy and 1/25 of the patients was assessed with CT colonography. Of the 13 who underwent colonic assessment, 11 were diagnosed with colonic neoplasms at different stages of development. In the absence of any strong contraindication, gastroenteroscopic evaluation in all patients diagnosed with S. bovis infectious endocarditis should be pursued.
    Full-text · Article · Oct 2015 · Gut Pathogens