Writing in the journal Microbiology Today (Society for General Microbiology, UK), Andrew Spiers of the University of Abertay, UK, reviews a new book on Plasmids published by Caister Academic Press. His comments include:

"the very useful guide to bioinformatics (J.E. Grant & P. Stothard), an in-depth description of the molecular machinery of DNA translocation (S. Russi et al.) and a thoroughly excellent discussion of HGT (M. Sota & E.M. Top)"
For full details please visit Plasmids: Current Research and Future Trends

Labels: book review, plasmids

Writing in the journal Microbiology Today (Society for General Microbiology, UK), Paul Hoskisson of the University of Strathclyde, UK, reviews a new book on Corynebacteria published by Caister Academic Press:

"it is not surprising that this book has followed the Handbook of Corynebacterium glutamicum (2005, Eggling & Bott, eds). Obviously there is some overlap in these volumes; however, this one is updated and brings in information relevant to other Corynebacteria ... There is a chapter on plasmids and promoters and their applications that researchers will find very useful in a practical sense ... researchers in the field with find this a useful and up to date addition to their library."
For full details please visit Corynebacteria: Genomics and Molecular Biology

Labels: bacteriology, bacterium, book review, corynebacterium

Writing in the journal Microbiology Today (Society for General Microbiology, UK), John McCarthy of the University of Manchester, UK, reviews a new book on RNA and the Regulation of Gene Expression published by Caister Academic Press:

"the contributions in this book do provide informative and well-structured overviews of current understanding of the roles of non-coding RNAs, short interfering RNAs, microRNAs and retrotransposons in eukaryotic organisms ... cutting edge studies on the potential role of RNA species in the epigenetic regulation of gene expression and on the existence of previously unidentified classes of intergenic and intronic short regulatory RNAs (pyknons) ... a useful purchase for specialist workers in the field as well as for many institutional libraries."
For full details please visit RNA and the Regulation of Gene Expression

Labels: book review, gene expression, regulation, rna

Writing in the journal Microbiology Today (Society for General Microbiology, UK), Madeline Stone & Kathy Bamford from the Imperial College London, UK, review a new book on Staphylococcus published by Caister Academic Press:

"This is an incredibly useful book for anyone with in interest in staphylococci. It provides a broad and in-depth synopsis of up-to-date staphylococcal research. This book is very well suited to its target audiences, researchers who are relatively new to the field and also as a suitable reference for those with greater experience. The first five chapters are particularly informative, providing an excellent overview of the staphylococcal sequencing projects, population structure and evolution of S. aureus, as well as analysis of the methods used ... The chapter on 'Global regulators of Staphylococcus aureus virulence genes' is excellent ... this chapter provides a thorough review of the literature ... We hope that this book will be regularly reviewed and updated in line with this rapidly expanding field."
For full details please visit Staphylococcus: Molecular Genetics

Labels: bacteriology, bacterium, book review, Staphylococcus

Writing in the journal Microbiology Today (Society for General Microbiology, UK), Simon L. Croft of the London School of Hygiene and Tropical Medicine, UK, reviews a new book on Leishmania published by Caister Academic Press:

"The volume is up-to-date; the genome was published in 2005 and the most recent references in the book were published in 2007. There is a richness of information - chapters on gene regulation and the metabolome are particularly engaging ... Let us enjoy a volume that provides a valuable overview of the molecular biology and biochemistry of these fascinating parasites, their metabolic pathways, differentiation process, and their surface molecules"
For full details please visit Leishmania: After The Genome

Labels: bacteriology, bacterium, book review, leishmania

Writing in the journal Microbiology Today (Society for General Microbiology, UK), Edward Bolt of the University of Nottingham, UK, reviews a new book on Archaea published by Caister Academic Press:

"I particularly enjoyed a review on signal transduction in archaea, which captures the frontiersman spirit of some research into Archaea ... The chapter on DNA replication holds it own against several recent review articles in journals ... The book is timely and the publishers promise a 'state-of-the-art overview of Archaea'. In this it mostly works, and its slimness (246 pages) reflects a concise and mostly well-referenced style ... it conveys plenty of the novelty and oddity in Archaea that captures the imagination of students, researchers and PIs."
For full details please visit Archaea: New Models for Prokaryotic Biology

Labels: archaea, bacteriology, bacterium, book review

Writing in the journal International Microbiology, Mercedes Berlanga of the University of Barcelona, Spain, describes a new book on Acinetobacter published by Caister Academic Press as a "useful book ... especially recommended for advanced students in the field, senior researchers, and physicians". She continues to suggest that "all microbiologists will find in the book an exceptional opportunity to extend their understanding of an unusual and unique microbial group."

Other reviewers have also heaped praise on this book, edited by Ulrike Gerischer of the University of Ulm, Germany. It is pleasing that a major new review of Acetinobacter research has been received in such a positive manner by the scientific community. This book will be a major resource for many years to come.

For full details of this book please visit Acinetobacter Molecular Biology

Labels: acinetobacter, bacteriology, bacterium, book review, nosocomial

Mycobacterium tuberculosis, also known as as the "tubercle bacillus" is the bacterium that causes most cases of tuberculosis. The genome has been sequenced and recent research on the genomics and molecular biology of mycobacteria has contributed greatly to our knowledge of this pathogen. Some of the most important recent findings are highlighted here.

Strain Variation and Evolution in Mycobacteria
Mycobacterium tuberculosis appears to be more genetically diverse than generally assumed. There is mounting evidence that this genetic diversity translates into significant phenotypic differences between clinical isolates. M. tuberculosis exhibits a biogeographic population structure and different strain lineages are associated with different geographic regions. Phenotypic studies in the laboratory and in clinical settings suggest that this macro-evolutionary strain variation has implications for the development of new diagnostics and vaccines. Micro-evolutionary variation affects the relative fitness and transmission dynamics of antibiotic-resistant strains. In the light of the emerging epidemic of multidrug-resistant and extensively drug-resistant tuberculosis, there is an urgent need to improve our understanding of the evolution and ecological consequences of strain variation in drug-resistant M. tuberculosis. Further reading: Mycobacterium: Genomics and Molecular Biology

Hypervirulent Mycobacterium tuberculosis
Tuberculosis outbreaks are often caused by hypervirulent strains of Mycobacterium tuberculosis. In experimental animal infections, these clinical isolates elicit unusual immunopathology and may be either hyper- or hypoinflammatory. Similarly, recombinant hypervirulent M. tuberculosis mutants, which exhibit increased bacterial burden or decreased host survival times in model infections, induce a spectrum of inflammatory responses. The majority of hypervirulent mutants identified have deletions in cell wall modifying enzymes or regulators that respond to environmental stimuli. Studies of these mutants have provided insight into the mechanisms that enable M. tuberculosis to mask its full pathogenic potential, inducing a granuloma that provides a protective niche and enables the bacilli to sustain a long-term persistent infection. Further reading: Mycobacterium: Genomics and Molecular Biology

Electron Transport and Respiration in Mycobacteria
Bacteria have evolved a modular respiratory system that enables them to optimize energy production in environments that are variable and may be hostile. By adjusting the composition of the system to suit the specific conditions encountered, the organism is able to thrive in a particular environment. The flexibility conferred by a modular respiratory system is critical to the survival of many bacterial pathogens, including Mycobacterium tuberculosis. The composition of the respiratory systems of sequenced mycobacterial species can be deduced from a comparative analysis of their respiratory gene complements and from the function of specific system components. Common themes have emerged from studies of various models of growth and persistence and can be related to the physiology of this pathogen during infection. Exciting new developments in tuberculosis drug discovery are predicated on targeting respiration and electron transport through inhibition of type II NADH dehydrogenase, ATP synthase, and menaquinone biosynthetic enzymes. Further reading: Mycobacterium: Genomics and Molecular Biology

Lipid biosynthetic machinery of Mycobacterium tuberculosis
Mycobacterium tuberculosis posseses a repertoire of complex lipids. Many of these lipids are crucial to its survival and virulence. Fatty-acyl components of the mycobacterial lipids are synthesised by the concerted action of fatty acid synthases (FASs) and polyketide synthases (PKSs). While the single multifunctional type I FAS carries out de novo biosynthesis from acetyl-CoA, the multicomponent type II FAS generates the very long acyl chains from type I FAS products. Polyketide synthases take over from FAS to complete the biosynthesis of the unusual acyl chains of many exotic lipids like mycolic acids, phthioceroldimycocerosate ester, sulfolipids and mannosyl-beta-1-phophomycoketides. The novel family of fatty acyl-adenylate ligases (FAALs) is crucial to this intricate enzymatic network. FAALs mediate the crosstalk between FAS and PKS by activating long-chain fatty acids to fatty acyl-adenylates which are transacylated onto the PKSs. Further reading: Mycobacterium: Genomics and Molecular Biology

DNA Repair in Mycobacteria
Sequence comparisons indicate that mycobacteria possess the majority of the key DNA repair pathways identified in other bacterial species, including base excision repair, nucleotide excision repair, recombination repair and non-homologous end-joining. However, there are some notable differences such as the absence of a mismatch repair system, as well as variations in the components of other repair pathways. Currently functional studies of DNA repair within mycobacterial species are limited, but this is an expanding area of research. It has been demonstrated that DNA-damage induced mutagenesis is mediated by a different class of DNA polymerase to that used in Escherichia coli. Although the classical SOS system of gene regulation in response to DNA damage is conserved and functional in mycobacteria, many of the DNA repair genes whose expression increases following DNA damage are controlled by an alternative system or systems that are yet to be characterised. The increase in expression observed for a number of Mycobacterium tuberculosis DNA repair genes in infection models suggests that DNA repair might be particularly important during pathogenesis. Further reading: Mycobacterium: Genomics and Molecular Biology

Oxygen, Nitric Oxide, and Carbon Monoxide Signaling in Mycobacteria
Mycobacterium tuberculosis is an aerobe that can survive extended periods of anaerobiosis. The bacillus responds to inhibition of respiration during hypoxic conditions as well as exposure to NO and CO by the induction of over 60 genes, referred to as the "dormancy regulon". Control of the dormancy regulon by NO and CO, not just hypoxia, is mediated by a three component regulatory system composed of two sensors, DosT and DosS and a transcriptional regulator DosR. The dormancy proteins are part of a programmed strategy employed by the bacilli to survive in the absence of aerobic respiration. Further reading: Mycobacterium: Genomics and Molecular Biology

Sulphur Metabolism in Mycobacteria
Sulphur is a key life-supporting element. The recent combined efforts of genomic analysis and laboratory studies have greatly clarified the mycobacterial sulphur metabolic pathways. Sulphur metabolism contributes to intracellular survival and virulence of Mycobacterium tuberculosis. Several enzymes in the sulphur metabolic pathways are essential for mycobacterial survival. Further reading: Mycobacterium: Genomics and Molecular Biology

The Eukaryotic-like Serine/Threonine Protein Kinase Family in Mycobacteria
Mycobacteria have a complex life style comprising different environments and developmental stages. Signal sensing and transduction leading to cellular responses must be tightly regulated to allow survival under variable conditions. Prokaryotes normally regulate their signal transduction processes through two-component systems, however, the genome sequence of Mycobacterium tuberculosis revealed a large number of eukaryotic-like serine/threonine kinases. It is becoming clear that in M. tuberculosis, many of these kinases are involved in the regulation of metabolic processes, transport of metabolites, cell division and virulence. Further reading: Mycobacterium: Genomics and Molecular Biology

Protein Secretion Systems of Mycobacteria
Mycobacteria have a highly complex cell wall. Specialised secretion systems are therefore required to transport proteins across this cell wall. However, genome analysis shows that, apart from the omnipresent Sec and Tat systems, all of the known secretion pathways of other bacteria are absent. Mycobacteria do have a second SecA protein (SecA2) that is involved in the extracellular accumulation of a specific protein subset. In addition, a new secretion pathway was recently identified that is responsible for the secretion of various proteins into the culture supernatant. This pathway is present in multiple copies in the mycobacteria and has been named the type VII secretion pathway. Further reading: Mycobacterium: Genomics and Molecular Biology

Labels: bacillus, bacteriology, bacterium, mycobacteria, mycobacterium, tuberculosis

The genus Clostridium represents a heterogeneous group of anaerobic spore-forming bacteria, comprising prominent toxin-producing species, such as C. difficile, C. botulinum, C. tetani and C. perfringens, in addition to well-known non-pathogens like solventogenic C. acetobutylicum. In the last decade several clostridial genomes have been deciphered and post-genomic studies are currently underway. The advent of newly developed, genetic manipulation tools have permitted functional-based and systems biology analyses of several clostridial strains. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Botulinum and Tetanus Neurotoxins
Botulinum neurotoxins (BoNT) and tetanus toxin (TeNT) are potent toxins which are responsible for severe diseases, botulism and tetanus, in men and animals. BoNTs induce a flaccid paralysis, whereas TeNT causes a spastic paralysis. Both toxins are zinc-dependent metalloproteases, which specifically cleave one of the three proteins (VAMP, SNAP25, and syntaxin) forming the SNARE complex within target neuronal cells which have a critical function in the release of neurotransmitter. BoNTs inhibit the release of acetylcholine at peripheral cholinergic nerve terminals, whereas TeNT blocks neurotransmitter release at central inhibitory interneurons. Only a single form of TeNT is known, but BoNTs are divided in 7 toxinotypes and various subtypes, which differ in amino acid sequences and immunological properties. In contrast to TeNT, BoNTs are associated to non-toxic proteins (ANTPs) to form highly stable botulinum complexes. TeNT is produced by Clostridium tetani, and BoNTs by Clostridium botulinum and atypical strains of Clostridium barati and Clostridium butyricum. The genes encoding the neurotoxin and ANTPs are clustered in a DNA segment, called botulinum locus, which is located on chromosome, plasmid or phage. Neurotoxin synthesis is a highly regulated process, which occurs in late exponential growth phase and beginning of stationary phase, and which is dependent of alternative sigma factors (BotR or TetR). BotR and TetR are related to other clostridial sigma factors, TcdR and UviA, which are involved in the control of Clostridium difficile toxins A and B, and Clostridium perfringens bacteriocin, respectively. BotR, TetR, TcdR and UviA form a new subgroup of RNA polymerase sigma factors. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Clostridium perfringens Enterotoxin
Clostridium perfringens enterotoxin (CPE) causes the intestinal symptoms of a common food-borne illness and ~5-15% of all antibiotic-associated diarrhea cases. In food poisoning isolates, the enterotoxin gene (cpe) is usually present on the chromosome, while cpe is carried by conjugative plasmids in antibiotic-associated diarrhea isolates. CPE action involves its binding to claudin receptors, oligomerization/prepore formation, and prepore insertion to form a functional pore that kills cells by apoptosis or oncosis. The C-terminal half of CPE mediates receptor binding, while its N-terminal half is required for oligomerization. CPE/CPE derivatives are being explored for cancer therapy/diagnosis and improved drug delivery. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

The Cholesterol-dependent Cytolysins and Clostridium septicum α-Toxin
Two classes of pore-forming toxins of the clostridia are represented by the cholesterol-dependent cytolysins (CDCs) and the Clostridium septicum α-toxin. The CDCs are found in a wide variety of clostridial species, but are also found in many species from other Gram-positive genera. As a result, various CDCs have evolved specific traits that appear to enhance their ability to complement the pathogenic mechanism of a specific bacterial species. In contrast, closely related toxins to C. septicum α-toxin (AT) have not been found in other species of the clostridia, although C. perfringens epsilon toxin appears to be distantly related. Remarkably, distant relatives of AT have been found in species of Gram-negative bacteria as well as certain species of mushrooms and the enterolobin tree seed. Although the CDCs appear to be restricted to Gram-positive bacterial pathogens it has recently been shown that the unusual protein fold of their membrane-penetrating domain is present in proteins of the eukaryotic complement membrane attack complex. Both toxins penetrate the membrane by the use of a β-barrel pore but differ significantly in their pore-forming mechanisms. The contribution of both classes of toxins to disease is not yet well understood for the clostridia. It is clear that they play important, but likely different roles in clostridial disease. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Binary Bacterial Toxins
Several proteins from Gram-positive, spore-forming bacilli use a synergistic binary mechanism for intoxicating eukaryotic cells. These toxins include Clostridium botulinum C2 toxin, Clostridium difficile toxin (CDT), Clostridium perfringens iota (ι) toxin, and Clostridium spiroforme toxin (CST). Furthermore, closely related Bacillus species such as Bacillus anthracis, Bacillus cereus, and Bacillus thuringiensis produce strikingly similar binary toxins. As per existing literature, these latter proteins have provided a "model" for the clostridial binary toxins. Each of these clostridial and bacillus binary toxins consists of distinct enzymatic "A" and binding "B" proteins that work in concert. Conservation of a basic intoxication theme between different genera clearly suggests retention of an evolutionarily successful mechanism promoting bacterial survival and dissemination throughout Nature. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Group I and II Clostridium botulinum
Clostridium botulinum, producing highly potent botulinum neurotoxin, is a diverse species consisting of four genetically and physiologically distinct groups (Groups I-IV) of organisms. Groups I and II C. botulinum produce A, B, E, and/or F toxins which cause human botulism. In addition, some strains of Clostridium butyricum and Clostridium barati produce type E and F toxins, respectively, and have thus been related to human illness. Human botulism appears in five different forms, such as the classical food botulism, infant botulism, wound botulism, adult infectious botulism, and iatrogenic botulism. Typical of all forms of human botulism is descending flaccid paralysis which may lead to death upon respiratory muscle failure. While the research and diagnostics of botulinum neurotoxigenic clostridia and botulism were based on toxin detection by the mouse bioassay until mid 1990¹s, the subsequent development of molecular detection and typing assays enabled rapid, sensitive, specific, and ethically acceptable molecular epidemiological detection, identification and strain characterization of these organisms, increasing our understanding of the epidemiology of botulinum neurotoxigenic clostridia and botulism. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

C. difficile large clostridial toxins
Clostridium difficile, as all clostridia, is a toxin producing microorganism and the toxins are the main virulence factors. In the early eighties it was clear that two large toxins are produced by the bacterium and epidemiological studies have indicated that strains either produce both toxins (toxin A, TcdA, and toxin B, TcdB) or none of them. Toxigenic strains were usualy associated with the disease, while nontoxigenic were not. This simple situation changed as strains producing only TcdB or strains producing an additional toxin (binary toxin CDT) were described. Such strains with unusual toxin production pattern were subsequently found to have changes in the genomic PaLoc region encoding the toxins TcdA and TcdB. These changes are the basis for a method that distinguish C. difficile strains into toxinotypes. The variability of genes coding for large clostridial toxins (LCTs) has consequences in laboratory diagnosis, changes in understanding of the role of both toxins in pathogenesis, in structure function relationships and in the understanding of the evolutions of LCTs. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Comparative Genomics of Clostridium difficile
The recent emergence of hypervirulent strains of Clostridium difficile and their ability to spread across continents, has caused alarm in both hospitals and the community. This has drawn attention away from other important pathogenic C. difficile strains, which are responsible for significant morbidity and mortality. Little is known about the genetic diversity of these strains and their less pathogenic counterparts. The recent publication of the genome sequence of strain 630 and advances in both microarray and mutagenesis technologies promises to revolutionise our understanding of the pathogenesis and population dynamics of C. difficile. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Surface Structures of Clostridia
The cell wall of Clostridium difficile has an architecture typical of other Gram-positive bacteria. A thick peptidoglycan layer lies external to the cell membrane with many associated cell wall proteins. In C. difficile two major cell wall proteins constitute the S-layer, a paracrystalline two-dimensional array surrounding the entire cell. The sequences of these S layer proteins (SLPs) are variable between strains, perhaps reflecting immunological pressures on the cell. The genome sequence reveals a family of proteins with homology to the high molecular weight SLP; each of these proteins have a second unique domain but their functions remain largely uncharacterised. This family of cell wall proteins is also found in some other species, for example C. botulinum and C. tetani, but not in others such as C. perfringens. Some cell wall proteins of C. difficile, including the SLPs, have properties that imply an involvement in pathogenesis, particularly in binding to host cell tissues. The cell wall proteins of C. difficile may also act as immunogens to induce a partially protective immune response to infection, and may be considered as components of future vaccines against C. difficile associated disease. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Antibiotic resistance determinants in Clostridium difficile
Clostridium difficile, the well known nosocomial pathogen responsible for the majority of antibiotic associated diseases, is increasingly recognised also as the cause of community-associated disease and of enteric disease in animals. The organism is resistant to several antibiotics and can survive disruption of the normal intestinal flora after antibiotic treatment exploiting this advantage to colonize and cause disease. The study of the mechanisms responsible for resistance have highlighted the presence of mobile genetic elements in the C. difficile genome, potentially acquired from other microorganisms. C. difficile might be able to disseminate resistance determinants to other species, thus collaborating to the evolution of the antibiotic resistant patterns that characterise the bacteria circulating worldwide. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Genetic Knock-out Systems for Clostridia
Despite the medical and industrial importance of the genus Clostridium our understanding of their basic biology lags behind that of their more illustrious counterpart, Bacillus. The advent of the genomics era has provided new insights, but full exploitation of the data becoming available is being hindered by a lack of mutational tools for functional genomic studies. Thus, in the preceding decades the number of clostridial mutants generated has been disappointingly low. On the one hand, the absence of effective transposon elements has stymied random mutant generation. On the other hand, the construction of directed mutants using classical methods of recombination-based, allelic exchange has met with only limited success. Indeed, in the majority of clostridial species mutants are largely based on integration of plasmids by a Campbell-like mechanism. Such single crossover mutants are unstable. As an alternative, recombination-independent strategies have been developed that are reliant on retargeted group II intron. One element in particular, the ClosTron, has been devised which provides the facility for the positive selection of mutants. ClosTron-mediate mutant generation is extremely rapid, highly efficient and reproducible. Moreover the mutants made are extremely stable. Its deployment considerably expands current options for functional genomic studies in clostridia. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Clostridia in Anti-tumor Therapy
Although traditional anticancer therapies are effective in the management of many patients, there are a variety of factors that limit their effectiveness in controlling some tumors. These observations have led to interest in alternative strategies to selectively target and destroy cancer cells. In that context, Clostridium-based tumor targeted therapy holds promise for the treatment of solid tumors. Upon systemic administration, various strains of non-pathogenic clostridia have been shown to infiltrate and selectively replicate within solid tumors. This specificity is based upon the unique physiology of solid tumors, which is often characterized by regions of hypoxia and necrosis. Clostridial vectors can be safely administered and their potential to deliver therapeutic proteins has been demonstrated in a variety of preclinical models. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Metabolic Networks in Clostridium acetobutylicum
Clostridia belong to the few bacterial genera able to undergo cell differentiation. They can either grow vegetatively or form endospores, the most resistant survival form of all living organisms. Some species, e. g. Clostridium acetobutylicum, link the metabolic network of sporulation to that of solventogenesis (formation of acetone and butanol). This gives them an ecological advantage by preventing toxic effects of acidic end products from the fermentation and allows them to stay longer metabolically active. In other clostridia, even toxin formation is coupled to sporulation. The key component for these links at the molecular level is the response regulator Spo0A in its phosphorylated form. In contrast to bacilli, clostridia do not possess a phosphorelay for Spo0A activation. Instead, phosphorylation is catalyzed directly by still unknown kinases or by butyryl phosphate. In addition to Spo0A~P, various other regulators are required to control the different metabolic networks. Systems biology is a new approach to understand these processes and their interaction at the molecular level and to adapt them for biotechnological use. Further reading: Clostridia: Molecular Biology in the Post-genomic Era

Labels: bacillus, bacteriology, bacterium, clostridia, clostridium

from Gerard Carter in Aus. J. Med. Sci. (2008) 29: 63-64

Pathogenic Treponema, edited by Radolf and Lukehart, is a comprehensive update of the current state of knowledge of the Treponemes and other spirochaetes ... Thirty five scientists who specialise in molecular biology, epidemiology, entomology and microbiology have pooled their findings of their more recent research efforts to produce an up-to-date account of Treponemal biology ... This hardback text is sturdily bound (less and less common these days) and beautifully printed on very high quality paper. It will make a welcome and useful addition to the libraries of any microbiological research laboratory and pathology establishment.

Further reading: Pathogenic Treponema

Labels: bacteriology, bacterium, book review, treponema

from Paul H. Edelstein in Legionella: Molecular Microbiology

The history of Legionnaires' disease began at least 33 years before the 1976 Philadelphia epidemic, when Legionella micdadei was isolated from human blood. Multiple isolations of several different Legionella spp. were made prior to 1976, and it was known by 1968 that tetracycline therapy prevented deaths in L. pneumophila-infected chicken embryos. The 1976 epidemic provided the scientific focus and resources necessary to determine that L. pneumophila caused epidemic pneumonia and to show that epidemics of Legionnaires' disease had occurred worldwide many years before 1976. Despite a surfeit of available resources and expertise, the effort to isolate the etiologic agent succeeded solely on the basis of one person's determination to solve a scientific problem and his willingness to reexamine his assumptions about prior laboratory results. Pontiac fever, a disease of unknown etiology, is a self-limiting and short duration febrile illness that has been associated with exposure to L. pneumophila. Because of non-specific clinical findings that overlap with other diseases, accurate diagnosis of Pontiac fever in non-outbreak settings is impossible. Legionnaires' disease can be diagnosed specifically through specialized laboratory tests, but not by clinical findings alone. This is because the clinical findings of Legionnaires' disease overlap with those of other more common causes of community acquired pneumonia. Antimicrobial therapy of Legionnaires' disease requires the use of drugs that are active against intracellular Legionellaspp., such as tetracyclines, macrolides, azalides and antibacterial quinolones.

Further reading: Legionella: Molecular Microbiology

Labels: bacteriology, bacterium, legionella

from Anke Becker and Frank-Jörg Vorhölter in Microbial Production of Biopolymers

Plant-pathogenic bacteria of the genus Xanthomonas are able to produce the acidic exopolysaccharide xanthan gum. Because of its physical properties, it is widely used as a viscosifer, thickener, emulsifier or stabilizer in both food and non-food industries. Xanthan consists of pentasaccharide repeat units composed of D-glucosyl, D-mannosyl, and D-glucuronyl acid residues in a molar ratio of 2:2:1 and variable proportions of O-acetyl and pyruvyl residues. The xanthan polymer has a branched structure with a cellulose-like backbone. Synthesis originates from glucose as substrate for synthesis of the sugar nucleotides precursors UDP-glucose, UDP-glucuronate, and GDP-mannose that are required for building the pentasaccharide repeat unit. This links the synthesis of xanthan to the central carbohydrate metabolism. The repeat units are built up at undecaprenylphosphate lipid carriers that are anchored in the cytoplasmic membrane. Specific glycosyltransferases sequentially transfer the sugar moieties of the nucleotide sugar xanthan precursors to the lipid carriers. Acetyl and pyruvyl residues are added as non-carbohydrate decorations. Mature repeat units are polymerized and exported in a way resembling the Wzy-dependent polysaccharide synthesis mechanism of Enterobacteriaceae. Products of the gum gene cluster drive synthesis, polymerization, and export of the repeat unit.

Further reading:
1. Microbial Production of Biopolymers
2. Plant Pathogenic Bacteria

Labels: bacterium, biopolymers, biotechnology, genetic engineering, xanthan, xanthomonas