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        <title>Gut Pathogens - Most accessed articles</title>
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        <description>The most accessed research articles published by Gut Pathogens</description>
        <dc:date>2011-12-23T00:00:00Z</dc:date>
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        <item rdf:about="http://www.gutpathogens.com/content/3/1/1">
        <title>Acne vulgaris, probiotics and the gut-brain-skin axis - back to the future?</title>
        <description>Over 70 years have passed since dermatologists John H. Stokes and Donald M. Pillsbury first proposed a gastrointestinal mechanism for the overlap between depression, anxiety and skin conditions such as acne. Stokes and Pillsbury hypothesized that emotional states might alter the normal intestinal microflora, increase intestinal permeability and contribute to systemic inflammation. Among the remedies advocated by Stokes and Pillsbury were Lactobacillus acidophilus cultures. Many aspects of this gut-brain-skin unifying theory have recently been validated. The ability of the gut microbiota and oral probiotics to influence systemic inflammation, oxidative stress, glycemic control, tissue lipid content and even mood itself, may have important implications in acne. The intestinal microflora may also provide a twist to the developing diet and acne research. Here we provide a historical perspective to the contemporary investigations and clinical implications of the gut-brain-skin connection in acne.</description>
        <link>http://www.gutpathogens.com/content/3/1/1</link>
                <dc:creator>Whitney Bowe</dc:creator>
                <dc:creator>Alan Logan</dc:creator>
                <dc:source>Gut Pathogens 2011, null:1</dc:source>
        <dc:date>2011-01-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-1</dc:identifier>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/15">
        <title>Mycobacterium avium subspecies paratuberculosis, Crohn&apos;s disease 
and the Doomsday Scenario
</title>
        <description>Johne&apos;s disease is chronic inflammation of the intestine caused by Mycobacterium avium subspecies paratuberculosis. Infection and disease are mainly in domestic livestock but can affect many species including primates. Johne&apos;s is a new disease which emerged at the turn of the 19th and 20th centuries and principally involved Europe and North America. It has since spread to former low incidence regions to become a global problem. Crohn&apos;s disease is a chronic inflammation of the intestine in humans which emerged in Europe and North America mid 20th century and increased to become a major healthcare problem. It has now spread to former low incidence regions. Infected animals shed Mycobacterium avium subspecies paratuberculosis in milk and into the environment. Human populations are widely exposed. Outcomes maybe influenced by microbial phenotype. Exposure to extracellular forms of these pathogens may confer some natural protection; exposure to intracellular forms which have passaged through milk macrophages or environmental protists may pose a greater threat to humans particularly individuals with an inherited or acquired susceptibility. Hot spots of human disease such as in Winnipeg which sits on rock at the junction of two rivers may result from local exposure to high levels of waterborne pathogens brought down from farmland. When appropriate methods are used most people with Crohn&apos;s disease are found to be infected. There are no data which demonstrate that these pathogens are harmless to humans. An overwhelming balance of probability and Public health risk favours the conclusion that Mycobacterium avium subspecies paratuberculosis is also pathogenic for people. A two tier co-operative pathogenic mechanism is proposed in Crohn&apos;s disease. Intracellular infection with the primary pathogen widely distributed throughout the gut causes an immune dysregulation and a specific chronic enteric neuropathy with loss of mucosal integrity. Segments of gross inflammatory disease result from the perturbed neuroimmune response to penetration into the gut wall of secondary pathogens from the lumen. These include both normal gut organisms and educated members of the enteric microbiome such as more aggressive E. coli. More new diseases may arise from failure to apply a range of remedial measures to this longstanding zoonotic problem.</description>
        <link>http://www.gutpathogens.com/content/1/1/15</link>
                <dc:creator>John Hermon-Taylor</dc:creator>
                <dc:source>Gut Pathogens 2009, null:15</dc:source>
        <dc:date>2009-07-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-15</dc:identifier>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/19">
        <title>Probiotics and gastrointestinal disease: successes, problems and future prospects</title>
        <description>Gastrointestinal disease is a major cause of morbidity and mortality worldwide each year. Treatment of chronic inflammatory gastrointestinal conditions such as ulcerative colitis and Crohn&apos;s disease is difficult due to the ambiguity surrounding their precise aetiology. Infectious gastrointestinal diseases, such as various types of diarrheal disease are also becoming increasingly difficult to treat due to the increasing dissemination of antibiotic resistance among microorganisms and the emergence of the so-called &apos;superbugs&apos;. Taking into consideration these problems, the need for novel therapeutics is essential. Although described for over a century probiotics have only been extensively researched in recent years. Their use in the treatment and prevention of disease, particularly gastrointestinal disease, has yielded many successful results, some of which we outline in this review. Although promising, many probiotics are hindered by inherent physiological and technological weaknesses and often the most clinically promising strains are unusable. Consequently we discuss various strategies whereby probiotics may be engineered to create designer probiotics. Such innovative approaches include; a receptor mimicry strategy to create probiotics that target specific pathogens and toxins, a patho-biotechnology approach using pathogen-derived genes to create more robust probiotic stains with increased host and processing-associated stress tolerance profiles and meta-biotechnology, whereby, functional metagenomics may be used to identify novel genes from diverse and vastly unexplored environments, such as the human gut, for use in biotechnology and medicine.</description>
        <link>http://www.gutpathogens.com/content/1/1/19</link>
                <dc:creator>Eamonn Culligan</dc:creator>
                <dc:creator>Colin Hill</dc:creator>
                <dc:creator>Roy Sleator</dc:creator>
                <dc:source>Gut Pathogens 2009, null:19</dc:source>
        <dc:date>2009-11-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-19</dc:identifier>
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        <item rdf:about="http://www.gutpathogens.com/content/3/1/16">
        <title>Bacillus Coagulans GBI-30 (BC30) improves Indices of Clostridium difficile-Induced Colitis in Mice
</title>
        <description>Background:
Probiotics have beneficial effects in rodent models of Clostridium difficile (C. diffiicle)-induced colitis. The spore forming probiotic strain Bacillus Coagulans GBI-30, 6086 (BC30) has demonstrated anti-inflammatory and immune-modulating effects in vitro. Our goal was to determine if BC30 improved C. difficile-induced colitis in mice. Starting on study day 0, female C57BL/6 mice were dosed by oro-gastric gavage for 15 days with vehicle (saline) or BC30 (2 &#215; 109 CFU per day). Mice in the C. difficile groups received an antibiotic mixture (study days 5 to 8 in the drinking water), and clindamycin (10 mg/kg, i.p., on study day 10). The C. difficile strain VPI 10463 was given by gavage at 104 CFU to induce colitis on day 11. On day 16, stools and colons were collected for further analyses.
Results:
All mice treated with BC30 survived on study day 13, while two mice treated with vehicle did not survive. On day 12, a significant difference (p = 0.0002) in the percentage of mice with normal stools (66.7%) was found in the BC30/C. difficile group, as compared to the vehicle/C. diffcile group (13.0%). On study day 16, 23.8% of mice treated with BC30 had normal stools, while this value was 0% with vehicle treatment (p value = 0.0187). On this day, the stool consistency score for the BC30/C. difficile group (1.1 &#177; 0.2) was significantly lower (p &lt; 0.05) than for the vehicle/C. difficile cohort (1.9 &#177; 0.2). BC30 modestly attenuated the colonic pathology (crypt damage, edema, leukocyte influx) that was present following C. difficile infection. Colonic MIP-2 chemokine contents (pg/2 cm colon) were: 10.2 &#177; 0.5 (vehicle/no C. difficile), 24.6 &#177; 9.5 (vehicle/C. difficile) and 16.3 &#177; 4.3 (BC30/C. difficle).
Conclusion:
The probiotic BC30 improved some parameters of C. difficile-induced colitis in mice. BC30 prolonged the survival of C. diffiicle infected mice. Particularly, this probiotic improved the stool consistency of mice, in this infectious colitis model.</description>
        <link>http://www.gutpathogens.com/content/3/1/16</link>
                <dc:creator>Leo Fitzpatrick</dc:creator>
                <dc:creator>Jeffrey Small</dc:creator>
                <dc:creator>Wallace Greene</dc:creator>
                <dc:creator>Kelly Karpa</dc:creator>
                <dc:creator>David Keller</dc:creator>
                <dc:source>Gut Pathogens 2011, null:16</dc:source>
        <dc:date>2011-10-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-16</dc:identifier>
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        <item rdf:about="http://www.gutpathogens.com/content/2/1/21">
        <title>Ulcerative colitis and Crohn&apos;s disease: is Mycobacterium avium subspecies paratuberculosis the common villain?</title>
        <description>Mycobacterium avium, subspecies paratuberculosis (MAP) causes a chronic disease of the intestines in dairy cows and a wide range of other animals, including nonhuman primates, called Johne&apos;s (&quot;Yo-knee&apos;s&quot;) disease. MAP has been consistently identified by a variety of techniques in humans with Crohn&apos;s disease. The research investigating the presence of MAP in patients with Crohn&apos;s disease has often identified MAP in the &quot;negative&quot; ulcerative colitis controls as well, suggesting that ulcerative colitis is also caused by MAP. Like other infectious diseases, dose, route of infection, age, sex and genes influence whether an individual infected with MAP develops ulcerative colitis or Crohn&apos;s disease. The apparently opposite role of smoking, increasing the risk of Crohn&apos;s disease while decreasing the risk of ulcerative colitis, is explained by a more careful review of the literature that reveals smoking causes an increase in both diseases but switches the phenotype from ulcerative colitis to Crohn&apos;s disease. MAP as the sole etiologic agent of both ulcerative colitis and Crohn&apos;s disease explains their common epidemiology, geographic distribution and familial and sporadic clusters, providing a unified hypothesis for the prevention and cure of the no longer &quot;idiopathic&quot; inflammatory bowel diseases.</description>
        <link>http://www.gutpathogens.com/content/2/1/21</link>
                <dc:creator>Ellen Pierce</dc:creator>
                <dc:source>Gut Pathogens 2010, null:21</dc:source>
        <dc:date>2010-12-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-21</dc:identifier>
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        <prism:startingPage>21</prism:startingPage>
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        <item rdf:about="http://www.gutpathogens.com/content/3/1/2">
        <title>Treating critically ill patients with probiotics: beneficial or dangerous?</title>
        <description>Probiotic bacteria are live microorganisms which confer to health benefits of the host. They help to maintain the integrity of the intestinal barrier function by modulating the mucosal and systemic immune response of the host. These bacteria have proven their beneficial effect in several conditions of ulcerative colitis. More recently probiotics/synbiotics have been included in the treatment of critically ill patients. However to date it remains uncertain whether probiotics/synbiotics are beneficial or even dangerous to the clinical outcome of this patient group. This article reviews the current evidence of the use of bacteria in critically ill patients in intensive care settings.</description>
        <link>http://www.gutpathogens.com/content/3/1/2</link>
                <dc:creator>Christoph Jacobi</dc:creator>
                <dc:creator>Christian Schulz</dc:creator>
                <dc:creator>Peter Malfertheiner</dc:creator>
                <dc:source>Gut Pathogens 2011, null:2</dc:source>
        <dc:date>2011-02-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-2</dc:identifier>
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        <prism:startingPage>2</prism:startingPage>
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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, null:2</dc:source>
        <dc:date>2010-03-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-2</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
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        <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/3/1/20">
        <title>The Broad Street pump revisited: dairy farms and an ongoing outbreak of inflammatory bowel disease in Forest, Virginia</title>
        <description>We report an ongoing outbreak of ulcerative colitis and Crohn&apos;s disease in Forest, Virginia involving 15 unrelated children and teenagers who resided in close proximity to dairy farms. Some of our cases demonstrated serologic evidence of Mycobacterium avium subspecies paratuberculosis infection, suggesting its potential role as an etiologic agent.</description>
        <link>http://www.gutpathogens.com/content/3/1/20</link>
                <dc:creator>Ellen Pierce</dc:creator>
                <dc:creator>Stephen Borowitz</dc:creator>
                <dc:creator>Saleh Naser</dc:creator>
                <dc:source>Gut Pathogens 2011, null:20</dc:source>
        <dc:date>2011-12-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-3-20</dc:identifier>
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        <prism:startingPage>20</prism:startingPage>
        <prism:publicationDate>2011-12-23T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.gutpathogens.com/content/1/1/6">
        <title>A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndrome.</title>
        <description>Chronic fatigue syndrome (CFS) is complex illness of unknown etiology. Among the broad range of symptoms, many patients report disturbances in the emotional realm, the most frequent of which is anxiety. Research shows that patients with CFS and other so-called functional somatic disorders have alterations in the intestinal microbial flora. Emerging studies have suggested that pathogenic and non-pathogenic gut bacteria might influence mood-related symptoms and even behavior in animals and humans. In this pilot study, 39 CFS patients were randomized to receive either 24 billion colony forming units of Lactobacillus casei strain Shirota (LcS) or a placebo daily for two months. Patients provided stool samples and completed the Beck Depression and Beck Anxiety Inventories before and after the intervention. We found a significant rise in both Lactobacillus and Bifidobacteria in those taking the LcS, and there was also a significant decrease in anxiety symptoms among those taking the probiotic vs controls (p = 0.01). These results lend further support to the presence of a gut-brain interface, one that may be mediated by microbes that reside or pass through the intestinal tract.</description>
        <link>http://www.gutpathogens.com/content/1/1/6</link>
                <dc:creator>A Venket Rao</dc:creator>
                <dc:creator>Alison Bested</dc:creator>
                <dc:creator>Tracey Beaulne</dc:creator>
                <dc:creator>Martin Katzman</dc:creator>
                <dc:creator>Christina Iorio</dc:creator>
                <dc:creator>John Berardi</dc:creator>
                <dc:creator>Alan Logan</dc:creator>
                <dc:source>Gut Pathogens 2009, null:6</dc:source>
        <dc:date>2009-03-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-1-6</dc:identifier>
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                <prism:publicationName>Gut Pathogens</prism:publicationName>
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        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2009-03-19T00:00:00Z</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, null:4</dc:source>
        <dc:date>2010-06-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1757-4749-2-4</dc:identifier>
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