Publications by authors named "Hana Tlapak"

Numbers of infections with Neisseria gonorrhoeae are among the top three sexually transmitted infections (STI) worldwide. In addition, the emergence and spread of antimicrobial resistance (AMR) in Neisseria gonorrhoeae pose an important public-health issue. The integration of genomic, phenotypic and epidemiological data to monitor Neisseria gonorrhoeae fosters our understanding of the emergence and spread of AMR in Neisseria gonorrhoeae and helps to inform therapy guidelines and intervention strategies.

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We have extended previously published sets of simple sequence repeat markers for selected to be polymorphic for the German-standard isolates of pathotypes P1, P2, P6, P8, and P18. These markers also complement the extensive published information on DNA polymorphisms for the mitogenomes of . This extended set of 35 markers representing 73 alleles differentiated 51 isolates from Europe and North America into three large, well-separated clusters and subclusters using dendrogram analysis, principal coordinates analysis (PCoA), and population substructure analysis using STRUCTURE 2.

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Here we present the characterization of a bacteriophage (vB__KIRK) including the morphology, the genome sequence and the induction of the prophage. The prophage sequence (FhaGI-1) has previously been identified in strain 3523. UV radiation induced the prophage to assemble phage particles consisting of an icosahedral head (~52 nm in diameter), a tail of up to 97 nm in length and a mean width of 9 nm.

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We recently identified and described a putative prophage on the genomic island FhaGI-1 located within the genome of AS02-814 ( subsp. -like 3523). In this study, we constructed two variants of a phage integration vector, called pFIV1-Val and pFIV2-Val ( Integration Vector-tRNA-specific), using the sites and the site-specific integrase (FN3523_1033) of FhaGI-1, a chloramphenicol resistance cassette and a gene for counter selection of transformants against the vector backbone.

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causes Legionnaires' disease but is known to be less virulent than is one of the species that is nonflagellated. The genes of the flagellar regulon are absent, except those encoding the alternative sigma-28 factor (FliA) and its anti-sigma-28 factor (FlgM). Similar to , and , located in the same phylogenetic clade, have no flagellar regulon, although both are positive for and Here, we investigated the role and function of both genes to better understand the role of FliA, the positive regulator of flagellin expression, in nonflagellated strains.

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Legionella pneumophila, the causative agent of Legionnaires disease, has a biphasic life cycle with a switch from a replicative to a transmissive phenotype. During the replicative phase, the bacteria grow within host cells in Legionella-containing vacuoles. During the transmissive phenotype and the postexponential (PE) growth phase, the pathogens express virulence factors, become flagellated, and leave the Legionella-containing vacuoles.

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Recently, we identified a putative prophage on a genomic island (GI) within the genome sequence of Francisella hispaniensis isolate AS0-814 (Francisella tularensis subsp. novicida-like 3523) by the analysis of the CRISPR-Cas systems of Francisella. Various spacer DNAs within the CRISPR region of different F.

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