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        <title>Editor's picks</title>
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        <description>The editor's pick of recent articles published by BMC Microbiology</description>
        <dc:date>2012-05-06T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2180/12/67" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2180/12/65" />
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        <title>The nucleotide excision repair (NER) system of Helicobacter pylori: Role in mutation prevention and chromosomal import patterns after natural transformation</title>
        <description>Background:
Extensive genetic diversity and rapid allelic diversification are characteristics of the human gastric pathogen Helicobacter pylori, and are believed to contribute to its ability to cause chronic infections. Both a high mutation rate and frequent imports of short fragments of exogenous DNA during mixed infections play important roles in generating this allelic diversity. In this study, we used a genetic approach to investigate the roles of nucleotide excision repair (NER) pathway components in H. pylori mutation and recombination.
Results:
Inactivation of any of the four uvr genes strongly increased the susceptibility of H. pylori to DNA damage by ultraviolet light. Inactivation of uvrA and uvrB significantly decreased mutation frequencies whereas only the uvrA deficient mutant exhibited a significant decrease of the recombination frequency after natural transformation. A uvrC mutant did not show significant changes in mutation or recombination rates; however, inactivation of uvrC promoted the incorporation of significantly longer fragments of donor DNA (2.2-fold increase) into the recipient chromosome. A deletion of uvrD induced a hyper-recombinational phenotype.
Conclusions:
Our data suggest that the NER system has multiple functions in the genetic diversification of H. pylori, by contributing to its high mutation rate, and by controlling the incorporation of imported DNA fragments after natural transformation.</description>
        <link>http://www.biomedcentral.com/1471-2180/12/67</link>
                <dc:creator>Claudia Moccia</dc:creator>
                <dc:creator>Juliane Krebes</dc:creator>
                <dc:creator>Stefan Kulick</dc:creator>
                <dc:creator>Xavier Didelot</dc:creator>
                <dc:creator>Christian Kraft</dc:creator>
                <dc:creator>Christelle Bahlawane</dc:creator>
                <dc:creator>Sebastian Suerbaum</dc:creator>
                <dc:source>BMC Microbiology 2012, 12:67</dc:source>
        <dc:date>2012-05-06T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2180-12-67</dc:identifier>
                            <dc:title>NER contributes to H. pylori diversity</dc:title>
                            <dc:description>Genetic diversification of Helicobacter pylori is controlled, in part, by the nucleotide excision repair system (NER) which contributes to both the bacteria?s high mutation rate and control of the incorporation of imported DNA fragments after natural transformation.</dc:description>
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                <prism:publicationName>BMC Microbiology</prism:publicationName>
        <prism:issn>1471-2180</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>67</prism:startingPage>
        <prism:publicationDate>2012-05-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1471-2180/12/65">
        <title>Allelic sequence heterozygosity in single Giardia parasites</title>
        <description>Background:
Genetic heterogeneity has become a major inconvenience in the genotyping and molecular epidemiology of the intestinal protozoan parasite Giardia intestinalis, in particular for the major human infecting genotype, assemblage B. Sequence-based genotyping of assemblage B Giardia from patient fecal samples, where one or several of the commonly used genotyping loci (beta-giardin, triosephosphate isomerase and glutamate dehydrogenase) are implemented, is often hampered due to the presence of sequence heterogeneity in the sequencing chromatograms. This can be due to allelic sequence heterozygosity (ASH) and /or co-infections with parasites of different assemblage B sub-genotypes. Thus, two important questions have arisen; i) does ASH occur at the single cell level, and/or ii) do multiple sub-genotype infections commonly occur in patients infected with assemblage B, G. intestinalis isolates?
Results:
We used micromanipulation in order to isolate single Giardia intestinalis, assemblage B trophozoites (GS isolate) and cysts from human patients. Molecular analysis at the tpi loci of trophozoites from the GS lineage indicated that ASH is present at the single cell level. Analyses of assemblage B Giardia cysts from clinical samples at the bg and tpi loci also indicated ASH at the single cell level. Additionally, alignment of sequence data from several different cysts that originated from the same patient yielded different sequence patterns, thus suggesting the presence of multiple sub-assemblage infections in congruence with ASH within the same patient.
Conclusions:
Our results conclusively show that ASH does occur at the single cell level in assemblage B Giardia. Furthermore, sequence heterogeneity generated during sequence-based genotyping of assemblage B isolates may possess the complexity of single cell ASH in concurrence with co-infections of different assemblage B sub-genotypes. These findings explain the high abundance of sequence heterogeneity commonly found when performing sequence based genotyping of assemblage B Giardia, and illuminates the necessity of developing new G. intestinalis genotyping tools.</description>
        <link>http://www.biomedcentral.com/1471-2180/12/65</link>
                <dc:creator>Johan Ankarklev</dc:creator>
                <dc:creator>Staffan G Svärd</dc:creator>
                <dc:creator>Marianne Lebbad</dc:creator>
                <dc:source>BMC Microbiology 2012, 12:65</dc:source>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2180-12-65</dc:identifier>
                            <dc:title>Heterozygosity in single Giardia parasites</dc:title>
                            <dc:description>Different alleles are present in the nuclei of a single Giardia trophozoite, which explains the high abundance of sequence heterogeneity commonly found when performing sequence based genotyping.</dc:description>
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                <prism:publicationName>BMC Microbiology</prism:publicationName>
        <prism:issn>1471-2180</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>65</prism:startingPage>
        <prism:publicationDate>2012-05-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <title>Thin-film fixed-bed reactor (TFFBR) for solar photocatalytic inactivation of aquaculture pathogen &lt;it&gt;Aeromonas hydrophila&lt;/it&gt;</title>
        <description>Background:
Outbreaks of infectious diseases by microbial pathogens can cause substantial losses of stock in aquaculture systems. There are several ways to eliminate these pathogens including the use of antibiotics, biocides and conventional disinfectants, but these leave undesirable chemical residues. Conversely, using sunlight for disinfection has the advantage of leaving no chemical residue and is particularly suited to countries with sunny climates. Titanium dioxide (TiO2) is a photocatalyst that increases the effectiveness of solar disinfection. In recent years, several different types of solar photocatalytic reactors coated with TiO2 have been developed for waste water and drinking water treatment. In this study a thin-film fixed-bed reactor (TFFBR), designed as a sloping flat plate reactor coated with P25 DEGUSSA TiO2, was used.
Results:
The level of inactivation of the aquaculture pathogen Aeromonas hydrophila ATCC 35654 was determined after travelling across the TFFBR under various natural sunlight conditions (300-1200 W m-2), at 3 different flow rates (4.8, 8.4 and 16.8 L h-1). Bacterial numbers were determined by conventional plate counting using selective agar media, cultured (i) under conventional aerobic conditions to detect healthy cells and (ii) under conditions designed to neutralise reactive oxygen species (agar medium supplemented with the peroxide scavenger sodium pyruvate at 0.05% w/v, incubated under anaerobic conditions), to detect both healthy and sub-lethally injured (oxygen-sensitive) cells. The results clearly demonstrate that high sunlight intensities (&#8805; 600 W m-2) and low flow rates (4.8 L h-1) provided optimum conditions for inactivation of A. hydrophila ATCC 3564, with greater overall inactivation and fewer sub-lethally injured cells than at low sunlight intensities or high flow rates. Low sunlight intensities resulted in reduced overall inactivation and greater sub-lethal injury at all flow rates.
Conclusions:
This is the first demonstration of the effectiveness of the TFFBR in the inactivation of Aeromonas hydrophila at high sunlight intensities, providing proof-of-concept for the application of solar photocatalysis in aquaculture systems.</description>
        <link>http://www.biomedcentral.com/1471-2180/12/5</link>
                <dc:creator>Sadia J Khan</dc:creator>
                <dc:creator>Robert H Reed</dc:creator>
                <dc:creator>Mohammad G Rasul</dc:creator>
                <dc:source>BMC Microbiology 2012, 12:5</dc:source>
        <dc:date>2012-01-13T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2180-12-5</dc:identifier>
                            <dc:title>Sunny prospects for aquaculture purification</dc:title>
                            <dc:description>Aeromonas hydrophila, an important pathogen in aquaculture systems, can be inactivated using a photocatalytic reactor coated with a thin film of titanium dioxide which increases the effectiveness of solar disinfection, demonstrating the application of solar photocatalysis in purification of aquaculture systems.</dc:description>
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                <prism:publicationName>BMC Microbiology</prism:publicationName>
        <prism:issn>1471-2180</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2012-01-13T00:00:00Z</prism:publicationDate>
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