bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of Shiga/Vero Toxins in Pathogenesis
Authors: Obata Fumiko , Obrig Tom 
Published: October 2014

ABSTRACT

Shiga toxin (Stx) is the primary cause of severe host responses including renal and central nervous system disease in Shiga toxin-producing
Escherichia coli
(STEC) infections. The interaction of Stx with different eukaryotic cell types is described. Host responses to Stx and bacterial lipopolysaccharide are compared as related to the features of the STEC-associated hemolytic-uremic syndrome (HUS). Data derived from animal models of HUS and central nervous system disease in vivo and eukaryotic cells in vitro are evaluated in relation to HUS disease of humans.
Enterohemorrhagic
Escherichia coli
Pathogenesis and the Host Response
Authors: Karpman Diana , Ståhl Anne-Lie 
Published: October 2014

ABSTRACT

Enterohemorrhagic
Escherichia coli
(EHEC) is a highly pathogenic bacterial strain capable of causing watery or bloody diarrhea, the latter termed hemorrhagic colitis, and hemolytic-uremic syndrome (HUS). HUS is defined as the simultaneous development of non-immune hemolytic anemia, thrombocytopenia, and acute renal failure. The mechanism by which EHEC bacteria colonize and cause severe colitis, followed by renal failure with activated blood cells, as well as neurological symptoms, involves the interaction of bacterial virulence factors and specific pathogen-associated molecular patterns with host cells as well as the host response. The innate immune host response comprises the release of antimicrobial peptides as well as cytokines and chemokines in addition to activation and/or injury to leukocytes, platelets, and erythrocytes and activation of the complement system. Some of the bacterial interactions with the host may be protective in nature, but, when excessive, contribute to extensive tissue injury, inflammation, and thrombosis, effects that may worsen the clinical outcome of EHEC infection. This article describes aspects of the host response occurring during EHEC infection and their effects on specific organs.
Shiga Toxin (Verotoxin)-ProducingEscherichia coliin Japan
Authors: Terajima Jun , Iyoda Sunao , Ohnishi Makoto , Watanabe Haruo 
Published: October 2014

ABSTRACTA series of outbreaks of infection with Shiga toxin (verocytotoxin)-producingEscherichia colior enterohemorrhagicE. coli(EHEC) O157:H7 occurred in Japan in 1996, the largest outbreak occurring in primary schools in Sakai City, Osaka Prefecture, where more than 7,500 cases were reported. Although the reason for the sudden increase in the number of reports of EHEC isolates in 1996 is not known, the number of reports has grown to more than 3,000 cases per year since 1996, from an average of 105 reports each year during the previous 5-year period (1991–1995). Despite control measures instituted since 1996, including designating Shiga toxin-producingE. coliinfection as a notifiable disease, and nationwide surveillance effectively monitoring the disease, the number of reports remains high, around 3,800 cases per year. Serogroup O157 predominates over other EHEC serogroups, but isolation frequency of non-O157 EHEC has gone up slightly over the past few years. Non-O157 EHEC has recently caused outbreaks where consumption of a raw beef dish was the source of the infection, and some fatal cases occurred. Laboratory surveillance comprised prefectural and municipal public health institutes, and the National Institute of Infectious Diseases has contributed to finding not only multiprefectural outbreaks but recognizing sporadic cases that could have been missed as an outbreak without the aid of molecular subtyping of EHEC isolates. This short overview presents recent information on the surveillance of EHEC infections in Japan.
Veterinary Public Health Approach to Managing Pathogenic Verocytotoxigenic
Escherichia coli
in the Agri-Food Chain
Authors: Duffy Geraldine , McCabe Evonne 
Published: October 2014

ABSTRACT

Verocytoxigenic
Escherichia coli
(VTEC) comprises many diverse serogroups, but seven serogroups, O157, O26, O103, O145, O111, O21, and O45, have been most commonly linked to severe human infections, though illness has also been reported from a range of other VTEC serogroups. This poses challenges in assessing the risk to humans from the diverse range of VTEC strains that may be recovered from animals, the environment, or food. For routine assessment of risk posed by VTEC recovered from the agri-food chain, the concept of seropathotype can be used to rank the human risk potential from a particular VTEC serogroup on the basis of both serotype (top seven serogroups) and the presence of particular virulence genes (
vt
in combination with
eae
, or
aaiC
plus
aggR
). But for other VTEC serogroups or virulence gene combinations, it is not currently possible to fully assess the risk posed. VTEC is shed in animal feces and can persist in the farm environment for extended periods ranging from several weeks to many months, posing an ongoing reservoir of contamination for grazing animals, water courses, and fresh produce and for people using farmland for recreational purposes. Appropriate handling and treatment of stored animal waste (slurries and manures) will reduce risk from VTEC in the farm environment. Foods of animal origin such as milk and dairy products and meat may be contaminated with VTEC during production and processing, and the pathogen may survive or grow during processing operations, highlighting the need for well-designed and validated Hazard Analysis Critical Control Point management systems. This article focuses on a veterinary public health approach to managing VTEC, highlighting the various routes in the agri-food chain for transmission of human pathogenic VTEC and general approaches to managing the risk.
Shiga Toxin/Verocytotoxin-Producing
Escherichia coli
Infections: Practical Clinical Perspectives
Authors: Davis T. Keefe , Van De Kar Nicole C. A. J. , Tarr Phillip I. 
Published: October 2014

ABSTRACT

Escherichia coli
strains that produce Shiga toxins/verotoxins are rare, but important, causes of human disease. They are responsible for a spectrum of illnesses that range from the asymptomatic to the life-threatening hemolytic-uremic syndrome; diseases caused by
E. coli
belonging to serotype O157:H7 are exceptionally severe. Each illness has a fairly predictable trajectory, and good clinical practice at one phase can be inappropriate at other phases. Early recognition, rapid and definitive microbiology, and strategic selection of tests increase the likelihood of good outcomes. The best management of these infections consists of avoiding antibiotics, antimotility agents, and narcotics and implementing aggressive intravenous volume expansion, especially in the early phases of illness.
Tn7
Authors: Peters Joseph E. 
Published: October 2014

ABSTRACT

The bacterial transposon Tn7 is distinguished by the levels of control it displays over transposition and its capacity to utilize different kinds of target sites. Transposition is carried out using five transposon-encoded proteins, TnsA, TnsB, TnsC, TnsD, and TnsE, which facilitate transfer of the element while minimizing the chances of inactivating host genes by using two pathways of transposition. One of these pathways utilizes TnsD, which targets transposition into a single site found in bacteria (
attTn7
), and a second utilizes TnsE, which preferentially directs transposition into plasmids capable of moving between bacteria. Control of transposition involves a heteromeric transposase that consists of two proteins, TnsA and TnsB, and a regulator protein TnsC. Tn7 also has the ability to inhibit transposition into a region already occupied by the element in a process called target immunity. Considerable information is available about the functional interactions of the Tn7 proteins and many of the protein–DNA complexes involved in transposition. Tn7-like elements that encode homologs of all five of the proteins found in Tn7 are common in diverse bacteria, but a newly appreciated larger family of elements appears to use the same core TnsA, TnsB, and TnsC proteins with other putative target site selector proteins allowing different targeting pathways.
The Molecular Genetics of Fluoroquinolone Resistance in
Mycobacterium tuberculosis
Authors: Mayer Claudine , Takiff Howard 
Published: October 2014

ABSTRACT

The fluoroquinolones (FQs) are synthetic antibiotics effectively used for curing patients with multidrug-resistant tuberculosis (TB). When a multidrug-resistant strain develops resistance to the FQs, as in extensively drug-resistant strains, obtaining a cure is much more difficult, and molecular methods can help by rapidly identifying resistance-causing mutations. The only mutations proven to confer FQ resistance in
M. tuberculosis
occur in the FQ target, the DNA gyrase, at critical amino acids from both the gyrase A and B subunits that form the FQ binding pocket. GyrA substitutions are much more common and generally confer higher levels of resistance than those in GyrB. Molecular techniques to detect resistance mutations have suboptimal sensitivity because gyrase mutations are not detected in a variable percentage of phenotypically resistant strains. The inability to find gyrase mutations may be explained by heteroresistance: bacilli with a resistance-conferring mutation are present only in a minority of the bacterial population (>1%) and are therefore detected by the proportion method, but not in a sufficient percentage to be reliably detected by molecular techniques. Alternative FQ resistance mechanisms in other bacteria—efflux pumps, pentapeptide proteins, or enzymes that inactivate the FQs—have not yet been demonstrated in FQ-resistant
M. tuberculosis
but may contribute to intrinsic levels of resistance to the FQs or induced tolerance leading to more frequent gyrase mutations. Moxifloxacin is currently the best anti-TB FQ and is being tested for use with other new drugs in shorter first-line regimens to cure drug-susceptible TB.
Genetics of Mycobacterial Arabinogalactan and Lipoarabinomannan Assembly
Authors: Jankute Monika , Grover Shipra , Birch Helen L. , Besra Gurdyal S. 
Published: October 2014

ABSTRACT

The cell wall of
Mycobacterium tuberculosis
is unique in that it differs significantly from those of both Gram-negative and Gram-positive bacteria. The thick, carbohydrate- and lipid-rich cell wall with distinct lipoglycans enables mycobacteria to survive under hostile conditions such as shortage of nutrients and antimicrobial exposure. The key features of this highly complex cell wall are the mycolyl-arabinogalactan-peptidoglycan (mAGP)–based and phosphatidyl-
myo
-inositol–based macromolecular structures, with the latter possessing potent immunomodulatory properties. These structures are crucial for the growth, viability, and virulence of
M. tuberculosis
and therefore are often the targets of effective chemotherapeutic agents against tuberculosis. Over the past decade, sophisticated genomic and molecular tools have advanced our understanding of the primary structure and biosynthesis of these macromolecules. The availability of the full genome sequences of various mycobacterial species, including
M. tuberculosis
,
Mycobacterium marinum
, and
Mycobacterium bovis
BCG, have greatly facilitated the identification of large numbers of drug targets and antigens specific to tuberculosis. Techniques to manipulate mycobacteria have also improved extensively; the conditional expression-specialized transduction essentiality test (CESTET) is currently used to determine the essentiality of individual genes. Finally, various biosynthetic assays using either purified proteins or synthetic cell wall acceptors have been developed to study enzyme function. This article focuses on the recent advances in determining the structural details and biosynthesis of arabinogalactan, lipoarabinomannan, and related glycoconjugates.
The Sculpting of theMycobacterium tuberculosisGenome by Host Cell–Derived Pressures
Authors: Russell David G. , Lee Wonsik , Tan Shumin , Sukumar Neelima , Podinovskaia Maria , Fahey Ruth J. , Vanderven Brian C. 
Published: October 2014

ABSTRACTMycobacterium tuberculosisis an incredibly successful pathogen with an extraordinary penetrance of its target host population. The ability to infect many yet cause disease in few is undoubtedly central to this success. This ability relies on sensing and responding to the changing environments encountered during the course of disease in the human host. This article discusses these environmental cues and stresses and explores how the genome ofM. tuberculosishas evolved under the purifying selections that they exert. In analyzing the response ofM. tuberculosisto a broad range of intracellular pressures, it is clear that, despite genome downsizing,M. tuberculosishas retained an extraordinary flexibility in central carbon metabolism. We believe that it is this metabolic plasticity, more than any of the virulence factors, that is the foundation forM. tuberculosis’s qualities of endurance.
The Physiology and Genetics of Oxidative Stress in Mycobacteria
Authors: Cumming Bridgette M. , Lamprecht Dirk A. , Wells Ryan M. , Saini Vikram , Mazorodze James H. , Steyn Adrie J. C. 
Published: October 2014

ABSTRACTDuring infection,Mycobacterium tuberculosisis exposed to a diverse array of microenvironments in the human host, each with its own unique set of redox conditions. Imbalances in the redox environment of the bacillus or the host environment serve as stimuli, which could regulate virulence. The ability ofM. tuberculosisto evade the host immune response and cause disease is largely owing to the capacity of the mycobacterium to sense changes in its environment, such as host-generated gases, carbon sources, and pathological conditions, and alter its metabolism and redox balance accordingly for survival. In this article we discuss the redox sensors that are, to date, known to be present inM. tuberculosis, such as the Dos dormancy regulon, WhiB family, anti-σ factors, and MosR, in addition to the strategies present in the bacillus to neutralize free radicals, such as superoxide dismutases, catalase-peroxidase, thioredoxins, and methionine sulfoxide reductases, among others.M. tuberculosisis peculiar in that it appears to have a hierarchy of redox buffers, namely, mycothiol and ergothioneine. We discuss the current knowledge of their biosynthesis, function, and regulation. Ergothioneine is still an enigma, although it appears to have distinct and overlapping functions with mycothiol, which enable it to protect against a wide range of toxic metabolites and free radicals generated by the host. Developing approaches to quantify the intracellular redox status of the mycobacterium will enable us to determine how the redox balance is altered in response to signals and environments that mimic those encountered in the host.
Mechanisms of Pyrazinamide Action and Resistance
Authors: Zhang Ying , Shi Wanliang , Zhang Wenhong , Mitchison Denis 
Published: October 2014

ABSTRACT

Pyrazinamide (PZA) is a unique antituberculosis (anti-TB) drug that plays a key role in shortening TB therapy. PZA kills nonreplicating persisters that other TB drugs fail to kill, which makes it an essential drug for inclusion in any drug combinations for treating drug-susceptible and drug-resistant TB such as multidrug-resistant TB. PZA acts differently from common antibiotics by inhibiting multiple targets such as energy production, trans-translation, and perhaps pantothenate/coenzyme A required for persister survival. Resistance to PZA is mostly caused by mutations in the
pncA
gene encoding pyrazinamidase, which is involved in conversion of the prodrug PZA to the active form pyrazinoic acid. Mutations in the drug target ribosomal protein S1 (RpsA) are also found in some PZA-resistant strains. The recent finding that
panD
mutations are found in some PZA-resistant strains without
pncA
or
rpsA
mutations may suggest a third PZA resistance gene and a potential new target of PZA. Current phenotype-based PZA susceptibility testing is not reliable due to false resistance; sequencing of the
pncA
gene represents a more rapid, cost-effective, and reliable molecular test for PZA susceptibility testing and should be used for guiding improved treatment of multidrug-resistant and extensively multidrug-resistant TB. Finally, the story of PZA has important implications for not only TB therapy but also chemotherapy in general. PZA serves as a model prototype persister drug and hopefully a “tipping point” that inspires new efforts at developing a new type of antibiotic or drug that targets nonreplicating persisters for improved treatment of not only TB but also other persistent bacterial infections.
Double-Strand DNA Break Repair in Mycobacteria
Authors: Glickman Michael S. 
Published: October 2014

ABSTRACT

Discontinuity of both strands of the chromosome is a lethal event in all living organisms because it compromises chromosome replication. As such, a diversity of DNA repair systems has evolved to repair double-strand DNA breaks (DSBs). In part, this diversity of DSB repair systems has evolved to repair breaks that arise in diverse physiologic circumstances or sequence contexts, including cellular states of nonreplication or breaks that arise between repeats. Mycobacteria elaborate a set of three genetically distinct DNA repair pathways: homologous recombination, nonhomologous end joining, and single-strand annealing. As such, mycobacterial DSB repair diverges substantially from the standard model of prokaryotic DSB repair and represents an attractive new model system. In addition, the presence in mycobacteria of a DSB repair system that can repair DSBs in nonreplicating cells (nonhomologous end joining) or when DSBs arise between repeats (single-strand annealing) has clear potential relevance to
Mycobacterium tuberculosis
pathogenesis, although the exact role of these systems in
M. tuberculosis
pathogenesis is still being elucidated. In this article we will review the genetics of mycobacterial DSB repair systems, focusing on recent insights.
Plasmid Replication Control by Antisense RNAs
Authors: Brantl Sabine 
Published: October 2014

ABSTRACT

Plasmids are selfish genetic elements that normally constitute a burden for the bacterial host cell. This burden is expected to favor plasmid loss. Therefore, plasmids have evolved mechanisms to control their replication and ensure their stable maintenance. Replication control can be either mediated by iterons or by antisense RNAs. Antisense RNAs work through a negative control circuit. They are constitutively synthesized and metabolically unstable. They act both as a measuring device and a regulator, and regulation occurs by inhibition. Increased plasmid copy numbers lead to increasing antisense-RNA concentrations, which, in turn, result in the inhibition of a function essential for replication. On the other hand, decreased plasmid copy numbers entail decreasing concentrations of the inhibiting antisense RNA, thereby increasing the replication frequency. Inhibition is achieved by a variety of mechanisms, which are discussed in detail. The most trivial case is the inhibition of translation of an essential replication initiator protein (Rep) by blockage of the
rep
-ribosome binding site. Alternatively, ribosome binding to a leader peptide mRNA whose translation is required for efficient Rep translation can be prevented by antisense-RNA binding. In 2004, translational attenuation was discovered. Antisense-RNA-mediated transcriptional attenuation is another mechanism that has, so far, only been detected in plasmids of Gram-positive bacteria. ColE1, a plasmid that does not need a plasmid-encoded replication initiator protein, uses the inhibition of primer formation. In other cases, antisense RNAs inhibit the formation of an activator pseudoknot that is required for efficient Rep translation.
Historical Events That Spawned the Field of Plasmid Biology
Authors: Kado Clarence I. 
Published: October 2014

ABSTRACTThis chapter revisits the historical development and outcome of studies focused on the transmissible, extrachromosomal genetic elements called plasmids. Early work on plasmids involved structural and genetic mapping of these molecules, followed by the development of an understanding of how plasmids replicate and segregate during cell division. The intriguing property of plasmid transmission between bacteria and between bacteria and higher cells has received considerable attention. The utilitarian aspects of plasmids are described, including examples of various plasmid vector systems. This chapter also discusses the functional attributes of plasmids needed for their persistence and survival in nature and in man-made environments. The termplasmid biologywas first conceived at the Fallen Leaf Lake Conference on Promiscuous Plasmids, 1990, Lake Tahoe, California. The International Society for Plasmid Biology was established in 2004 (www.ISPB.org).
Spore Surface Display
Authors: Isticato Rachele , Ricca Ezio 
Published: October 2014

ABSTRACT

A variety of bioactive peptides and proteins have been successfully displayed on the surface of recombinant spores of
Bacillus subtilis
and other sporeformers. In most cases, spore display has been achieved by stably anchoring the foreign molecules to endogenous surface proteins or parts of them. Recombinant spores have been proposed for a large number of potential applications ranging from oral vaccine vehicles to bioremediation tools, and including biocatalysts, probiotics for animal or human use, as well as the generation and screening of mutagenesis libraries. In addition, a nonrecombinant approach has been recently developed to adsorb antigens and enzymes on the spore surface. This nonrecombinant approach appears particularly well suited for applications involving the delivery of active molecules to human or animal mucosal surfaces. Both the recombinant and nonrecombinant spore display systems have a number of advantages over cell- or phage-based systems. The stability, safety of spores of several bacterial species, and amenability to laboratory manipulations, together with the lack of some constraints limiting the use of other systems, make the spore a highly efficient platform to display heterologous proteins.
Evolution in the
Bacillaceae
Authors: Fajardo-Cavazos Patricia , Maughan Heather , Nicholson Wayne L. 
Published: October 2014

ABSTRACT

The family
Bacillaceae
constitutes a phenotypically diverse and globally ubiquitous assemblage of bacteria. Investigation into how evolution has shaped, and continues to shape, this family has relied on several widely ranging approaches from classical taxonomy, ecological field studies, and evolution in soil microcosms to genomic-scale phylogenetics, laboratory, and directed evolution experiments. One unifying characteristic of the
Bacillaceae
, the endospore, poses unique challenges to answering questions regarding both the calculation of evolutionary rates and claims of extreme longevity in ancient environmental samples.