The Zoonotic and Animal Pathogens Research Laboratory at the University of Edinburgh has worked with a UK-based animation company to produce a full-length animation representing the key stages of E. coli O157:H7 interaction within the gastrointestinal tract. This movie was featured in the August 2004 issue of Microbiology Today, published by the Society for General Microbiology.
Prion diseases are fatal and at present there are neither cures nor therapies available to delay disease onset or progression in humans. Inspired in part by therapeutic approaches in the fields of Alzheimer’s disease and amyotrophic lateral sclerosis, researchers tested five different drugs which are known to efficiently pass through the blood-brain barrier in a mouse prion system. Groups of intracerebrally prion-challenged mice were treated with the drugs curcumin, dapsone, ibuprofen, memantine and minocycline. Treatment with antibiotics dapsone and minocycline had no therapeutic benefit. Ibuprofen-treated mice showed severe adverse effects, which prevented assessment of therapeutic efficacy. Mice treated with low- but not high-dose curcumin and mice treated with memantine survived infections significantly longer than untreated controls. These results encourage further research efforts to improve the therapeutic effect of these drugs.
The peptidoglycan layer is a unique and essential structural element in the cell wall of most bacteria (Peptidoglycan structure and architecture. FEMS Microbiology Reviews, 08 Jan 2008). Made of glycan strands cross-linked by short peptides, the so-called peptidoglycan sacculus forms a closed, bag-shaped structure surrounding the cytoplasmic membrane. Peptidoglycan sacculi have the strength to withstand the cell’s turgor pressure of up to 25 atmospheres. On the other hand, the sacculi are not rigid walls but are flexible structures, allowing reversible expansion under pressure, and they have relatively wide pores, enabling diffusion of large molecules such as proteins. Because the peptidoglycan completely surrounds the cytoplasmic membrane, the sacculus has a similar size and shape as the bacterial cells from which it was isolated.
The main function of peptidoglycan is to preserve cell integrity by withstanding the turgor pressure inside the cell. Inhibition of peptidoglycan biosynthesis (e.g. by mutations or antibiotics such as penicillin) or degradation (e.g. by lysozyme) in growing cells results in cell lysis. Peptidoglycan contributes to the maintenance of a defined cell shape (e.g. rod or sphere) and serves as a scaffold for anchoring other cell envelope components such as proteins and teichoic acids. It is intimately involved in the processes of cell growth and cell division. However, peptidoglycan is absent in some bacteria such as Mycoplasma species, Planctomyces, Rickettsia and Chlamidiae.
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Peptidoglycan is composed of an overlapping lattice of two sugars, N-acetyl glucosamine (NAG) and N-acetyl muramic acid (NAM) cross-linked by amino acid bridges. The exact molecular makeup of these cross-bridges is species-specific. NAM is only found in the cell walls of bacteria and nowhere else. Attached to NAM is a side chain generally composed of four amino acids. In the best-studied bacterial cell wall (that of Esccherichia coli) the cross-bridge is most commonly composed of L-alanine, D-alanine, D-glutamic acid and diaminopimelic acid. In Staphylococcus aureus, the pentapeptide coming off the NAM is composed of the amino acids L-alanine, D-glutamine, L-lysine, and two D-alanines.
There is a two-layered organization of the bacterial cell wall, with a zone of low density next to the plasma membrane. This “inner wall zone” or “periplasmic space” has a thickness between 16 nm (in Staphylococcus aureus) and 22 nm (in Bacillus subtilis). The “outer wall zone” of higher density is the polymeric peptidoglycan–teichoic acid complex with its attached surface proteins. The thickness of the outer zone varies with the species, growth phase of the cells and growth conditions, but is in the range of 15–30 nm. Unravelling the molecular architecture of the bacterial cell wall has been a constant aspiration for microbiologists, but is proving to be a frustrating topic. In particular, the architecture of the cell wall of Gram-positive bacteria is far from being understood. Gram-positive species not only have a thick, multi-layered peptidoglycan but other major surface polymers linked to it.
The essential functions of peptidoglycan and its confinement to bacteria make it a perfect target for attacking these organisms. β-lactams and glycopeptides, powerful bactericidal antibiotics, interfere with the last steps of peptidoglycan synthesis. Glycopeptides such as vancomycin bind the C-terminal end of the peptidoglycan disaccharide-pentapeptide precursor, preventing its incorporation into peptidoglycan. The targets of β-lactams were identified as penicillin-binding proteins (PBPs), and multiple PBPs with different affinities for β-lactams are generally present in the cell envelope. Resistance to β-lactams and glycopeptides is of major concern in the treatment of bacterial infections. Frequently, bacteria produce enzymes (β-lactamases) that inactivate these antibiotics. Gram-negative cells can reduce the permeability of their outer membrane and many bacteria lower the antibiotic concentration near the targets using efflux proteins. However, bacteria are also able to modify one or more important PBPs such that their affinity for the antibiotic is reduced, as is the case in peumococci. Methicillin resistant Staphylococcus aureus (MRSA) and Enterococci possess low affinity PBPs that replace the other PBPs in the presence of antibiotics. Resistance to glycopeptides was reported for the first time in enterococci in the 1980s. It results from the acquisition of genetic elements that allow the synthesis of modified peptidoglycan precursors showing a reduced binding capacity for the antibiotics. More recently, it was demonstrated that peptidoglycan has a role in innate immunity in mammals and insects and could contribute to bacterial pathogenesis.
In the last two decades, the improvement of analytical methods has shown that within a particular species, variations in peptidoglycan structure occur as a function of aging, growth medium, pathogenesis, or in the presence of antibiotics. This type of research has implications not only in the field of bacterial physiology, but also in those of innate immunity, pathogenicity, and antibacterial therapy.
A previous study indicated that approximately 30% of cultivable soil bacteria may contain inducible prophage; however, the degree to which this cultivation-based estimate applies to indigenous soil bacteria is unknown. To estimate the prevalence of lysogeny within soil bacterial communities, induction assays were carried out by extracting bacteria from soil and subsequently exposing extracts to mitomycin C, or by exposing bacteria to mitomycin C through direct addition to soil slurries. Induction was assessed as an increase in viral direct counts relative to those obtained in controls, as detected by epifluorescence microscopy. Extracting bacteria from soils followed by 18 hours mitomycin C exposure generated significantly higher prophage induction than all other treatments. For three Antarctic soil samples, estimates of inducible fraction were statistically indistinguishable across two independent assays, indicating that this approach is highly reproducible. Although the inducible fraction was lower in Antarctic soils and higher in temperate Delaware soils (22-68%), no clear correlations were found between lysogeny and soil physical properties. For Delaware soils, inducible fraction estimates were similar between whole soil assays (44%) and cultivation-based approaches (30%). While these data suggest that lysogeny is common among soil bacteria, the specific factors which promote temperate interactions remain unclear.
Staphylococcus aureus gets bad press. But most of us carry it at some point and in this article in Microbiology Today (February 2008), Simon Foster says this is not as bad as we think:
It is all too easy to fear and loathe S. aureus and with such antipathy, to gloss over the special relationship which has evolved between us and one of our most faithful microbes. We all have a high titre of circulating antibodies against S. aureus and so we must be challenged subclinically on a regular basis. Getting a serious S. aureus infection is actually remarkably difficult and mostly requires immense effort on our part via injury, surgery, indwelling medical devices, etc. S. aureus is an opportunist pathogen for which many of the diseases it causes are distinctly inopportune for the bacterium. Endocarditis and other deep-seated infections give little chance for reintroduction into the environment. Superficial and minor skin lesions are the primary infections caused by S. aureus and the flow of golden pus gives relief to the host and the prospect of dispersal to the pathogen…
Being a teenager can be so horrible that many adults (especially teachers and parents) have wiped its ghastly memories from their minds. It is easy to feel lonely and isolated, but don’t worry, you are not alone: there are over 10 times the numbers of microbes living in and on you than there are human cells in your body. You are home to a complex community of bugs such as bacteria, viruses, fungi and protozoa. They live in your gut, mouth, skin, vagina, upper respiratory tract and urethra, and each of us has our own unique collection. They help digestion, synthesize vitamins, boost immunity and occupy niches that would otherwise be filled by pathogens. Puberty is a time of change, both physically and emotionally, and this affects your microbes too…
Otitis media is inflammation of the middle ear: the small space between the ear drum and the inner ear. Diagnostic criteria include rapid onset of symptoms, middle ear effusion, and signs and symptoms of middle ear inflammation. Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis are the most common bacterial isolates from the middle ear fluid of children with acute otitis media. Fever, otalgia, headache, irritability, cough, rhinitis, listlessness, anorexia, vomiting, diarrhea, and pulling at the ears are common, but nonspecific symptoms. Detection of middle ear effusion by pneumatic otoscopy is key in establishing the diagnosis. Observation is an acceptable option in healthy children with mild symptoms. Antibiotics are recommended in all children younger than six months, in those between six months and two years if the diagnosis is certain, and in children with severe infection. High-dosage amoxicillin (80 to 90 mg per kg per day) is recommended as first-line therapy. Macrolide antibiotics, clindamycin, and cephalosporins are alternatives in penicillin-sensitive children and in those with resistant infections. Patients who do not respond to treatment should be reassessed. Hearing and language testing is recommended in children with suspected hearing loss or persistent effusion for at least three months, and in those with developmental problems.
The incidence of antimicrobial resistance and expressed and unexpressed resistance genes among commensal Escherichia coli isolated from healthy farm animals at slaughter in Great Britain in 1999 was investigated. The prevalence of antimicrobial resistance among the isolates varied according to the animal species. Of 836 isolates from cattle tested only 5.7% were resistant to one or more antimicrobials, while only 3.0% of 836 isolates from sheep were resistant to one or more agents. However, 92.1% of 2480 isolates from pigs were resistant to at least one antimicrobial. Among isolates from pigs, resistance to some antimicrobials such as tetracycline (78.7%), sulphonamide (66.9%) and streptomycin (37.5%) was found to be common, but relatively rare to other agents. The isolates had a diverse range of resistance gene profiles, with tet(B), sul2 and strAB identified most frequently. Seven out of 615 isolates investigated carried unexpressed resistance genes. One trimethoprim-susceptible isolate carried a complete dfrA17 gene but lacked a promoter for it. However, in the remaining six streptomycin-susceptible isolates, one of which carried strAB while the others carried aadA, no mutations or deletions in gene or promoter sequences were identified to account for susceptibility. The data indicate that antimicrobial resistance in E. coli of animal origin is due to a broad range of acquired genes. A high prevalence of antimicrobial resistant Escherichia coli isolated from pigs and a low prevalence of antimicrobial resistant E. coli from cattle and sheep in Great Britain at slaughter. FEMS Microbiology Letters (OnlineEarly Articles).
Why does it matter?
Historically, antimicrobials have been used in animal production for both therapeutic and growth promotion purposes. The European Union has gradually banned the use of all growth-promoting antimicrobials. However, antimicrobials are still used as therapeutic agents in food production. In the UK, veterinary antimicrobial use ranges between 440 and 480 tonnes annually, over 80% of which are used in food-producing animals. The tetracyclines account for approximately half of this amount, with significant use also recorded for trimethoprim/sulphonamides, -lactams, aminoglycosides, macrolides and fluoroquinolones.
This study demonstrated that antimicrobial resistance is common among E. coli from healthy pigs in Great Britain, but relatively rare among E. coli from sheep and cattle. Resistance phenotypes among E. coli of animal origin are extremely diverse and are mediated by a wide range of different resistance genes, suggesting the presence of a large population of resistant E. coli, particularly among pigs. This resistance is of concern as it can potentially spread to humans, either via direct colonization of the human gut by animal strains of E. coli or through transmission of resistance genes to resident bacteria in the human gut.
You probably know that bacteria come in a range of different shapes. Rod-shaped cells are called bacilli (as in Bacillus anthracis), spherical cells are called cocci (as in Staphylococcus aureus), and helical bacteria come in three forms, vibrio - curved or comma-shaped rods (such as Vibrio cholerae), spirilla - thick, rigid helices (such as Rhodospirillum rubrum) and spirochetes - thin, flexible helices (such as Treponema pallidum). A few rare bacteria (such as Haloquadratum walsbyi) are even cubic. So we know bacteria have different shapes. This article is about why and how.
The shapes of bacterial cells do not occur randomly, but have arisen over millions of years of evolution because each shape confers some selective advantage on the species in the environment in which it lives. Bacteria are very small, so they have a large surface-to-volume ratio. This allows rapid uptake of nutrients and gasses and supports a highly active internal biochemistry. Some bacteria expand their surface area even further by surface features such as filaments and stalks.
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For optimum motility, there is a fairly narrow range of optimum sizes and shapes. The fastest swimmers are medium-length rods with a particular length-to-width ratio, since this is the most efficient shape for swimming. A typical bacterium can move at about 100 times its body length in a second (e.g. about 50 µm/sec), whereas the fastest swimming fish such as tuna can move only about 10 body lengths per second, and the fastest land animal, the cheetah, can only manage 25 body lengths per second. Bacteria which live in highly viscous environments use their helical shape to great advantage, literally corkscrewing their way though the medium.
Cell size and shape may also be a defence against predation in some cases, with certain bacteria making themselves too large, too small or too awkwardly shaped (e.g. with surface projections) to be consumed by planktonic feeders, which often have a relatively narrow range of acceptable prey size.
So if there is an optimum size and shape for bacterial cells in a particular environment, how is cell morphology produced? With no control over shape, all cells would be spherical, a shape produced by the turgor pressure of the cytoplasm on the outer membrane, rather like blowing up a balloon. In most (but not all) bacteria, shape is maintained by the cell wall, specifically the peptidoglycan layer, which has the approximate strength of strong, stiff fabric. Digest the peptidoglycan with lysozyme or inhibit its deposition using antibiotics such as penicillin and the cells become spherical protoplasts or spheroplasts. The shape of the wall is determined by the way it is deposited, and this is controlled by a cytoskeleton. In bacteria, the cytoskeleton is made up of two types of proteins. Tubulin-like proteins are responsible for the construction of the septum and the poles of the cell. Actin-like proteins localize peptidoglycan synthesis in the lateral walls of rod-shaped cells. As in eukaryotes, the cytoskeleton is produced by self-organized assembly, although the details of the processes involved are only just becoming clear.
Beneficial bacteria that live on salamander skins have the ability to inhibit pathogenic fungi. Our study aimed to identify the specific chemical agents of this process and asked if any of the antifungal compounds known to operate in analogous plant-bacteria-fungi systems were present. Crude extracts of bacteria isolated from salamander skin were analyzed. These investigations show that 2,4-diacetylphloroglucinol is produced by the bacteria isolate Lysobacter gummosus, which was found on the red-backed salamander, Plethodon cinereus. Furthermore, exposure of the amphibian fungal pathogen, Batrachochytrium dendrobatidis, to different concentrations of 2,4-diacetylphloroglucinol resulted in an IC50 value comparable to crude extract concentrations. This study is the first to show that an epibiotic bacterium on an amphibian species produces a chemical that inhibits pathogenic fungi.
A previous study indicated that approximately 30% of cultivable soil bacteria may contain 
