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        <title>Gut Pathogens - Latest Articles</title>
        <link>http://www.gutpathogens.com</link>
        <description>The latest research articles published by Gut Pathogens</description>
        <dc:date>2010-07-22T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.gutpathogens.com/content/2/1/8" />
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/8">
        <title>Enteropathogenic Escherichia coli, Samonella, Shigella  and Yersinia:
cellular aspects of host-bacteria interactions in enteric diseases
</title>
        <description>A successful infection of the human intestine by enteropathogenic bacteria depends on the ability of bacteria to attach and colonize the intestinal epithelium and, in some cases, to invade the host cell, survive intracellularly and disseminate from cell to cell. To accomplish these processes bacteria have evolved an arsenal of molecules that are mostly secreted by dedicated type III secretion systems, and that interact with the host, subverting normal cellular functions. Here we overview the most important molecular strategies developed by enteropathogenic Escherichia coli, Salmonella enterica, Shigella flexneri, and Yersinia enterocolitica to cause enteric infections. Despite having evolved different effectors, these four microorganisms share common host cellular targets.</description>
        <link>http://www.gutpathogens.com/content/2/1/8</link>
                <dc:creator>Roberta Reis</dc:creator>
                <dc:creator>Fabiana Horn</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:8</dc:source>
        <dc:date>2010-07-22T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-8</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2010-07-22T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/7">
        <title>Shiga toxin producing Escherichia coli: identification of non-O157:H7-Super-Shedding cows and related risk factors </title>
        <description>Background:
Shiga toxin producing Escherichia coli (STEC) are an important cause of human gastro-enteritis and extraintestinal sequelae, with ruminants, especially cattle, as the major source of infection and reservoir. In this study, the fecal STEC shedding of 133 dairy cows was analyzed over a period of twelve months by monthly sampling with the aim to investigate shedding patterns and risk factors.
Results:
Overall, 24.7% (in total 407) of 1,646 fecal samples were tested positive for stx by PCR with inner-herd prevalences on the different farms of 11.1% to 32.3%. At individual levels, cows were stx-positive on zero to eight consecutive samplings. According to a strictly longitudinal definition of Super-Shedding, in the present study 14 cows were identified as Super-Shedders of non-O157 serotypes.Significant risk factors for the shedding of STEC were the month of sampling, the number of lactations and days in lactation, the nutritional condition, the somatic cell count and the content of protein in milk. Most notably, the presence of STEC Super-Shedding cows in the herd was a significant risk factor, revealing that STEC Super-Shedding is not restricted to STEC O157:H7 alone.
Conclusions:
These data have implications for possible interventions, as removing single non-O157:H7 STEC Super-Shedding cattle from farms would significantly reduce STEC burden.</description>
        <link>http://www.gutpathogens.com/content/2/1/7</link>
                <dc:creator>Andrea Menrath</dc:creator>
                <dc:creator>Lothar Wieler</dc:creator>
                <dc:creator>Katrin Heidemanns</dc:creator>
                <dc:creator>Torsten Semmler</dc:creator>
                <dc:creator>Angelika Fruth</dc:creator>
                <dc:creator>Nicole Kemper</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:7</dc:source>
        <dc:date>2010-07-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-7</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2010-07-09T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/6">
        <title>Genetic affinities of Helicobacter pylori isolates from ethnic Arabs in Kuwait </title>
        <description>Helicobacter pylori is one of the most genetically diverse of bacterial species, and since the 5&apos;-end of cagA gene and the middle allele of vacA gene of H. pylori from different populations exhibit considerable polymorphisms, these sequence diversities were used to gain insights into the genetic affinities of this gastric pathogen from different populations. Because the genetic affinity of Arab strains from the Arabian Gulf is not known, we carried out genetic analysis based on sequence diversities of the cagA and the vacA genes of H. pylori from 9 ethnic Arabs in Kuwait. The analysis showed that the Kuwaiti isolates are closely related to the Indo-European group of strains, although some strains have a tendency to form a separate cluster close to the Indo- European group, but clearly distinct from East Asian strains. However, these results need to be confirmed by analyses of neutral markers (house-keeping genes in a multi-locus sequence typing [MLST]) platform. The profiling of virulence-associated genes may have resulted from ecologically distinct populations due to human migration and geographical separation over long periods of time.</description>
        <link>http://www.gutpathogens.com/content/2/1/6</link>
                <dc:creator>M. John Albert</dc:creator>
                <dc:creator>Hanan Al-Akbal</dc:creator>
                <dc:creator>Rita Dhar</dc:creator>
                <dc:creator>Ronita De</dc:creator>
                <dc:creator>Asish Mukhopadhyay</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:6</dc:source>
        <dc:date>2010-07-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-6</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2010-07-05T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/5">
        <title>Probiotic therapy - recruiting old friends to fight new foes</title>
        <description>Against a backdrop of increasing antibiotic resistance, and the emergence of new and evolving pathogens, clinicians are increasingly forced to consider alternative therapies - probiotics are one such alternative.</description>
        <link>http://www.gutpathogens.com/content/2/1/5</link>
                <dc:creator>Roy Sleator</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:5</dc:source>
        <dc:date>2010-06-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-5</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2010-06-25T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/4">
        <title>Emerging trends in the etiology of enteric pathogens as evidenced from an active surveillance of hospitalized diarrhoeal patients in Kolkata, India</title>
        <description>Background:
This study was conducted to determine the etiology of diarrhoea in a hospital setting in Kolkata. Active surveillance was conducted for 2 years on two random days per week by enrolling every fifth diarrhoeal patient admitted to the Infectious Diseases and Beliaghata General Hospital in Kolkata.
Results:
Most of the patients (76.1%) had acute watery diarrhoea in association with vomiting (77.7%) and some dehydration (92%). Vibrio cholerae O1, Rotavirus and Giardia lamblia were the important causes of diarrhoea. Among Shigella spp, S. flexneri 2a and 3a serotypes were most predominantly isolated. Enteric viruses, EPEC and EAEC were common in children &lt;5 year age group. Atypical EPEC was comparatively higher than the typical EPEC. Multidrug resistance was common among V. cholerae O1 and Shigella spp including tetracycline and ciprofloxacin. Polymicrobial infections were common in all age groups and 27.9% of the diarrhoea patients had no potential pathogen.
Conclusions:
Increase in V. cholerae O1 infection among &lt;2 years age group, resistance of V. cholerae O1 to tetracycline, rise of untypable S. flexnerii, higher proportion of atypical EPEC and G. lamblia and polymicrobial etiology are some of the emerging trends observed in this diarrhoeal disease surveillance.</description>
        <link>http://www.gutpathogens.com/content/2/1/4</link>
                <dc:creator>Gopinath Nair</dc:creator>
                <dc:creator>Thandavarayan Ramamurthy</dc:creator>
                <dc:creator>Mihir Bhattacharya</dc:creator>
                <dc:creator>Triveni Krishnan</dc:creator>
                <dc:creator>Sandipan Ganguly</dc:creator>
                <dc:creator>Dhira Saha</dc:creator>
                <dc:creator>Krishnan Rajendran</dc:creator>
                <dc:creator>Byomkesh Manna</dc:creator>
                <dc:creator>Mrinmoy Ghosh</dc:creator>
                <dc:creator>Keinosuke Okamoto</dc:creator>
                <dc:creator>Yoshifumi Takeda</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:4</dc:source>
        <dc:date>2010-06-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-4</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2010-06-05T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/3">
        <title>Current insights in to the pathophysiology of 	
Irritable Bowel Syndrome 
</title>
        <description>Irritable Bowel Syndrome (IBS) represents a functional disorder of gastrointestinal tract without the presence of an anatomic defect, in which abdominal pain is relieved with defecation and is associated with altered bowel habits.IBS includes a wide range of symptoms while its pathophysiology is very complicated. Recent studies indicate that the most important mechanisms include visceral sensitivity, abnormal gut motility and autonomous nervous system dysfunction. The interactions between these three mechanisms make bowel&apos;s function susceptible to many exogenous and endogenous factors like gastrointestinal flora, feeding and psychosocial factors. Recent data indicate that according to the above mechanisms, the influence of genetic factors and polymorphisms of human DNA in the development of IBS is equally important.</description>
        <link>http://www.gutpathogens.com/content/2/1/3</link>
                <dc:creator>Theodoros Karantanos</dc:creator>
                <dc:creator>Theofano Markoutsaki</dc:creator>
                <dc:creator>Maria Gazouli</dc:creator>
                <dc:creator>Nicholas Anagnou</dc:creator>
                <dc:creator>Dimitrios Karamanolis</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:3</dc:source>
        <dc:date>2010-05-13T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-3</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2010-05-13T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/2">
        <title>Helicobacter pylori: a poor man&apos;s gut pathogen?</title>
        <description>Helicobacter pylori is one of the human pathogens with highest prevalence around the world; yet, its principal mode of transmission remains largely unknown. The role of H. pylori in gastric disease and cancer has not been established until the end of the 20th century. Since then, its epidemiology has been extensively studied, and an accruing body of literature suggests that not all humans are equally at risk of infection by this gut pathogen. Here, we briefly review the different epidemiological aspects of H. pylori infection with emphasis on those factors related to human poverty. The epidemiology of H. pylori infection is characterized by marked differences between developing and developed countries, notably among children. In addition, congruent lines of evidence point out to socioeconomic factors and living standards as main determinants of the age-dependent acquisition rate of H. pylori, and consequently its prevalence. These data are alarming in the light of the changing global climate and birth rate, which are expected to change the demography of our planet, putting more children at risk of H. pylori and its complications for years to come.</description>
        <link>http://www.gutpathogens.com/content/2/1/2</link>
                <dc:creator>Mohammed Mahdy Khalifa</dc:creator>
                <dc:creator>Radwa Sharaf</dc:creator>
                <dc:creator>Ramy Aziz</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:2</dc:source>
        <dc:date>2010-03-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-2</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2010-03-31T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/1">
        <title>Mycobacterium avium subsp. paratuberculosis as a trigger of type-1 diabetes: destination Sardinia, or beyond?</title>
        <description>Type 1 diabetes mellitus (T1DM) is a multifactorial autoimmune disease in which the insulin producing &#946; cell population is destroyed by the infiltrated T lymphocytes. Even though the exact cause of T1DM is yet to be ascertained, varying degree of genetic susceptibility and environmental factors have been linked to the disease progress and outcome. Mycobacterium avium subsp. paratuberculosis (MAP) is an obligate zoonotic pathogen that causes chronic infection of intestines in ruminants, the Johne&apos;s disease. MAP that can even survive pasteurization and chlorination has also been implicated to cause similar type of enteritis in humans called Crohn&apos;s disease. With the increasing recognition of the link between MAP and Crohn&apos;s disease, it has been postulated that MAP is an occult antigen which besides Crohn&apos;s could as well be thought to trigger T1DM. Epitope homologies between mycobacterial proteins (Hsp 65) and pancreatic glutamic acid decarboxylase (GAD 65) and infant nutrition studies implicate MAP as one of the triggers for T1DM. PCR and ELISA analyses in diabetic patients from Sardinia suggest that MAP acts as a possible trigger for T1DM. Systematic mechanistic insights are needed to prove this link. Unfortunately, no easy animal model(s) or in-vitro systems are available to decipher the complex immunological network that is triggered in MAP infection leading to T1DM.</description>
        <link>http://www.gutpathogens.com/content/2/1/1</link>
                <dc:creator>Pittu Rani</dc:creator>
                <dc:creator>Leonardo Sechi</dc:creator>
                <dc:creator>Niyaz Ahmed</dc:creator>
                <dc:source>Gut Pathogens 2010, 2:1</dc:source>
        <dc:date>2010-03-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-1</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2010-03-29T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/25">
        <title>A rhodanine agent active against non-replicating intracellular Mycobacterium avium subspecies paratuberculosis</title>
        <description>Background:
Antibiotic therapy targeting chronic mycobacterial disease is often ineffective due to problems with the emergence of drug resistance and non-replicating persistent intracellular antibiotic resistant phenotypes. Strategies which include agents able to enhance host cell killing mechanisms could represent an alternative to conventional methods with the potential for host clearance if active against dormant phenotypes. Investigations of agents with potential activity against non-replicating mycobacteria however are restricted due to a need for assays that can assess bacterial viability without having to culture.
Results:
This study describes the development and use of a pre16S ribosomal gene RNA/DNA ratio viability assay which is independent of the need for culture, supported by a novel thin layer accelerated mycobacterial colony forming method for determining viability and culturability of MAP in intracellular environments. We describe the use of these tools to demonstrate intracellular killing activity of a novel rhodanine agent (D157070) against the intracellular pathogen Mycobacterium avium subspecies paratuberculosis (MAP) and show that the culturability of MAP decreases relative to its viability on intracellular entry suggesting the induction of a non-culturable phenotype. We further demonstrate that D157070, although having no direct activity against the culturability of extracellular MAP, can bind to cultured MAP cells and has significant influence on the MAP transcriptome, particularly with respect of &#948;L associated genes. D157070 is shown to be taken up by bovine and human cells and able to enhance host cell killing, as measured by significant decreases in both culturability and viability of intracellular MAP.
Conclusions:
This work suggests that pre16srRNA gene ratios represent a viable method for studying MAP viability. In addition, the rhodanine agent D157070 tested is non-toxic and enhances cell killing activity against both growing and latent MAP phenotypes.</description>
        <link>http://www.gutpathogens.com/content/1/1/25</link>
                <dc:creator>Tim Bull</dc:creator>
                <dc:creator>Richard Linedale</dc:creator>
                <dc:creator>Jason Hinds</dc:creator>
                <dc:creator>John Hermon-Taylor</dc:creator>
                <dc:source>Gut Pathogens 2009, 1:25</dc:source>
        <dc:date>2009-12-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-25</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>25</prism:startingPage>
        <prism:publicationDate>2009-12-23T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/24">
        <title>Helicobacter pylori - a seasoned pathogen by any other name</title>
        <description>Helicobacter pylori is a well known inhabitant of human stomach which is linked to peptic ulcer disease and gastric adenocarcinoma. It was recently shown in several studies that H. pylori can be harnessed as a surrogate marker of human migration and that its population structure and stratification patterns exactly juxtapose to those of Homo sapiens. This is enough a testimony to convey that H. pylori may have coevolved with their host. Several protective effects of H. pylori colonization have been considered as evidence of a presumed symbiotic relationship. Contrary to this assumption is the presence of a strong virulence apparatus within H. pylori; why a co-evolved parasite would try inflicting its host with serious infection and even causing cancer? The answer is perhaps embedded in the evolutionary history of both the bacterium and the host. We discuss a hypothetical scenario wherein H. pylori may have acquired virulence genes from donors within its environment that varied with change in human history and ecology. The H. pylori genomes sequenced to date portray fairly high abundance of such laterally acquired genes which have no assigned functions but could be linked to inflammatory responses or other pathogenic attributes. Therefore, the powerful virulence properties and survival strategies of Helicobacter make it a seasoned pathogen; thus the efforts to portray it as a commensal or a (harmless) &apos;bacterial parasite&apos; need rethinking.</description>
        <link>http://www.gutpathogens.com/content/1/1/24</link>
                <dc:creator>Niyaz Ahmed</dc:creator>
                <dc:creator>Shivendra Tenguria</dc:creator>
                <dc:creator>Nishant Nandanwar</dc:creator>
                <dc:source>Gut Pathogens 2009, 1:24</dc:source>
        <dc:date>2009-12-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-24</dc:identifier>
        <prism:publicationName>Gut Pathogens</prism:publicationName>
        <prism:issn>1757-4749</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>24</prism:startingPage>
        <prism:publicationDate>2009-12-23T00:00:00Z</prism:publicationDate>
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