RxPG News : Bacteriology

Predatory bacteria attack in 'military-style' waves

Sun, 23 Nov 2008 10:54:06 PST

( from http://www.rxpgnews.com ) Washington, Oct 30 - A soil bacteria like M. xanthus executes a wave-like 'military-style' attack in a swarm against their prey, before gobbling them up and moving on.

Despite its deadly role, M. xanthus is harmless to humans and might be used to destroy harmful bacteria on surfaces or in human infections, said John Kirby, associate professor of microbiology at the University of Iowa - Carver College of Medicine.

'When an M. xanthus aggregate is placed inside a colony of E. coli bacteria,' it 'proceeds to eat the colony from the inside out and creates a rippling pattern as the swarm moves through the prey cells,' Kirby said.

'We now know that this rippling pattern is the highly organised behaviour of thousands of cells working in concert to digest the prey.'

'It may be that we can modify this predator-prey relationship or apply it to medically relevant situations,' Kirby said. 'It would be amazing if we could adapt its predatory ability to get rid of harmful bacteria that reside in places we don't want them, including in hospitals or on medical implants.'

The U-I team also showed that the ripple wavelength is adaptable. At high prey density, M. xanthus forms ripples with shorter wavelengths. As prey density decreases, the ripple wavelength gets longer. Eventually, when there is no more prey, the rippling behaviour dissipates.

M. xanthus lives in a multi-cellular unit that can change its structure and behaviour in response to changing availability of prey. This adaptive ability to control movement in response to an environmental stimulus is called chemotaxis, and the research team coined the term predataxis to describe its behaviour in response to prey, said a U-I press release.

These findings were published online in the Proceedings of the National Academy of Sciences - early edition.

In earlier studies, Kirby and James Berleman, postdoctoral fellow in Kirby's lab, showed that the presence of prey causes M. xanthus to form parallel rippling waves that move toward and through prey bacteria.

Now, how the bacteria organise to form these travelling waves in response to the presence of prey is the subject of the study.

The Strange Case of the Radiation-Resistant Bacteria

Mon, 26 Mar 2007 10:54:42 PST

( from http://www.rxpgnews.com ) Fifty years ago, scientists experimenting with gamma radiation to sterilize canned foods were surprised to find spoiled meat in cans zapped with what they thought were lethal levels of ionizing radiation (IR). Inside the bulging cans, they discovered a strain of bacteria now called Deinococcus radiodurans. This extremely resilient microbe can endure 100 times the IR levels that kill other bacteria and levels 2,000 times higher than the lethal human dose.

Researchers investigating the nature of radiation toxicity long ago settled on DNA as its principal target. Within this framework, efforts to understand D. radioduransâs resistance have focused on the mechanisms of DNA repair, with each study revealing seemingly greater levels of efficiency. Surprisingly, this extremophile relies on a set of apparently universal DNA repair proteins, raising an even bigger paradox: DNA repair and synthesis depends on proteins, but these proteins suffer radiation damage, too. And no matter how efficient DNA repair enzymes might be under normal conditions, itâs not clear how they manage to resurrect a radiation-shattered genome if they are also damaged.

Over the past few years, several observations have challenged the DNA-centered view of IR toxicity. For one thing, the D. radiodurans genome, sequenced in 1999, revealed nothing clearly unusual about its DNA repair components. And it appears that bacteria at the opposite ends of resistance sustain about the same amount of DNA damage from a given IR dose, with many bacterial species succumbing to IR doses that cause very little DNA damage. Shewanella oneidensis, for example, cannot survive doses causing less than one double-strand DNA break per genome although it encodes DNA repair systems that appear more complex than those in D. radiodurans, which can weather the 100 double-strand breaks per genome caused by much higher doses just fine.

Might the hypothetical genes identified in the D. radiodurans genome encode proteins with novel repair functions? Or perhaps resistant bacteria can use standard DNA repair equipment in ways other organisms cannot. Or maybe thereâs something special in the way the microbe packages its chromosomes.

A 2004 study by Michael Daly et al. found that IR-resistant and IR-sensitive cells had significantly different mineral concentrations, lending support to a role of manganese and iron in recovery. The researchers showed that the most resistant cells contained about 300 times more manganese and three times less iron than the most sensitive cells. In a new study investigating the functional consequences of this disparity, Daly et al. show that high cytosolic manganese and low iron concentrations facilitate resistance by protecting proteins, but not DNA, from IR-induced oxidative damage. Their findings offer a novel perspective on the long-cryptic nature of D. radiodurans resistance, shifting the focus of toxicity and resistance away from DNA damage and repair toward a potent form of protein protection.

Image overlay of transmission electron microscopy, light microscopy, and X-ray fluorescence microprobe analyses of D. radiodurans. Average abundance of manganese (blue, green, and pink) and iron (red) are shown within a single D. radiodurans diplococcus.

Exposing cells to IR generates a range of potentially harmful molecules called reactive oxygen species (ROS). When ROS accumulate faster than cellular scavengers can neutralize them, they cause oxidative stress and can kill cells. Hydroxyl radicals, one of the primary ROS products of irradiated water (the major component of cells), are particularly toxic to DNA, and can generate other ROS, including hydrogen peroxide and superoxide (a simple peroxyl radical).

High intracellular concentrations of manganese ions are known to alleviate oxidative stress in several bacterial species; these ions can interact with different ROS depending on their oxidation state and their binding with different molecules. Daly et al. reasoned manganese might affect ROS generation during irradiation. They first tested manganeseâs ability to scavenge hydroxyl and superoxide radicals to determine whether its activity protects DNA or proteins. Whereas hydroxyl radicals target both DNA and proteins, superoxide radicals selectively damage proteins. The researchers irradiated DNA and a DNA-modifying enzyme and found that, although manganese ions failed to protect DNA from hydroxyl radicals generated during irradiation, the ions did prevent enzyme damage and preserved enzyme activity.

To understand the nature of manganese protection in cells, the researchers then irradiated IR-sensitive and IR-resistant bacteria and compared their levels of oxidative protein damage. The sensitive cells with the lowest manganese to iron concentration ratios, they found, sustained high levels of protein oxidation; the resistant cells with the highest ratios had no detectable protein oxidation. They showed that proteins purified from D. radiodurans are not inherently oxidation-resistant, and when cells were depleted of manganese, cells were rendered sensitive to IR and protein oxidation. This suggests that the microbe actively offsets the effects of IR by protecting proteins using manganese, specifically with divalent manganese (Mn(II)) ions.

Resistant bacteria, the researchers suspected, might use Mn(II) to transform superoxide radicals, which canât easily cross the cell membrane, into hydrogen peroxide, which can. And thatâs what they found: irradiated D. radiodurans and a second resistant bacteria with high manganese concentrations (Lactobacillus plantarum) released hydrogen peroxide (likely as a product of the âredoxâ reactions that neutralize superoxide radicals), while sensitive and non-irradiated resistant bacteria did not. The researchers went on to show that the resistance of normal D. radiodurans can be controlled externally by inhibiting manganese redox recycling.

Electron micrograph of a cross-section of a D. radiodurans tetracoccus (cluster of four cells).

In the context of previous studies, these results suggest that D. radiodurans relies not on a highly specialized DNA repair machinery, but on a detoxifying mechanism associated with the microbeâs unusual intracellular environment. Most organisms contain near-millimolar concentrations of iron, which under IR will contribute to the formation of hydroxyl radicals and superoxide radicals. In resistant bacteria, millimolar Mn(II) concentrations appear to protect proteins from oxidative damage by eliminating superoxide and its derivatives. This oxidative protection may in turn shield proteins involved in DNA repair, and subsequently allow them to quickly heal DNA lesions, which in sensitive bacteria turn lethal because their repair proteins are ravaged by radiation.

This new model of radiation toxicity opens up novel avenues for radioprotection in diverse settings. Individuals exposed to chronic or acute doses of radiation could potentially benefit from treatments that deliver purified D. radiodurans Mn complexes into their cells. Similarly, the toxic effects of radiation therapy in cancer patients might be ameliorated by antioxidant drugs based on such a protection paradigm. And given that many bacteria, such as S. oneidensis, with favorable bioremediation functions are extremely sensitive to radiation, the new insight on how D. radiodurans survives radiation might prove useful in efforts to contain the toxic runoff from the immense radioactive- and heavy-metal-contaminated waste sites left over from the Cold War.

Evolution of typhoid bacteria

Wed, 29 Nov 2006 10:47:32 PST

( from http://www.rxpgnews.com ) Typhoid fever remains a major health problem in the developing world and continues to cause disease in Europe and on the american continent. The evolutionary history and population structure of Typhi were poorly understood, partly because these bacteria show little genetic diversity. Now a team led by Mark Achtman and Philippe Roumagnac from the Max Planck Institute for Infection Biology, Berlin, has applied population genetic experience from prior work with Yersinia pestis, Escherichia coli, Helicobacter pylori and Neisseria meningitidis to provide novel insights into the evolution of this pathogen.

The team combined its resources to assemble for the first time a globally representative collection of 105 strains of Typhi and investigated the sequence diversity within 90,000 base pairs per strain. Eighty-eight informative sequence differences were detected, showing that the population structure has evolved over the last 10,000 to 43,000 years. Amazingly, the ancestral strain continues to exist today, as do many of its direct descendents, indicating a neutral population structure, whereas normally selective forces lead to extinction of intermediate genotypes. Furthermore, these bacteria are distributed globally, demonstrating that Typhi has spread inter-continentally on multiple occasions.

The authors propose that the unusual population structure of Typhi reflects long-term carriage by asymptomatic carriers, who reached public notoriety at the beginning of the 20th century with "Mr. N the milker" in England and Typhoid Mary (Mary Mallon) in the U.S.A. These individuals infected 100s of people over the decades while they worked in the food production industry. Healthy carriers may have allowed Typhi to survive in hunter-gatherer populations prior to the Neolithic expansion of city states and facilitated its intercontinental spread. Healthy carriers are also consistent with the observation that individual genotypes of Typhi persist for many decades within each country.

Increasing resistance to antibiotics in recent decades has hampered efforts of clinicians to cure typhoid fever. The indiscriminate use of fluoroquinolones, which is a cost-effective, standard treatment for typhoid fever, has been accompanied by a frightening increase in the numbers of resistant Typhi. Investigations of a large strain collection from southern Asia revealed that many different genotypes independently acquired resistance to nalidixic acid, a quinolone. One of these genotypes, H58, has become predominant throughout southern Asia and has even spread to Africa. In Vietnam, up to 95% of Typhi are now resistant to nalidixic acid and many other antibiotics. Although these cases can still be treated with newer antibiotics, those antibiotics are much more expensive than standard fluoroquinolones, which raises the cost of medical treatment. Furthermore, it is likely that Typhi will develop resistance to these antibiotics as well.

The combination of these investigations raises problems for public health measures. Indiscriminate antibiotic usage results in real-time evolution of bacteria that resist treatment. Furthermore, the healthy carrier state provides a safe reservoir for these bacteria which allows them to evade short-term antibiotic treatment and vaccination, indicating that typhoid fever will remain a major health problem for the foreseeable future.

New Treatment Using Human Antibodies to Target Harmful Toxins May Protect Against C. Difficile

Sun, 19 Nov 2006 04:22:43 PST

( from http://www.rxpgnews.com ) A new therapeutic method using human antibodies to neutralize toxins was found to prevent Clostridium difficile-induced death in hamsters say researchers from New Jersey and Massachusetts. They report their findings in the November 2006 issue of the journal Infection and Immunity.

C. difficile is the leading cause of nosocomial antibiotic-associated diarrhea, often resulting from the administration of antibiotics such as clindamycin, ampicillin, or cephalosporins. C. difficile associated diarrhea (CDAD) effects approximately 300,000 patients per year in the U.S. alone. Treatment available to date includes discontinuation of the antibiotic causing the illness as well as administration of medication such as metronidazole or vancomycin. Although both methods offer initial relief, there is currently a 10 to 20% relapse rate among patients. Due to the recent emergence of more virulent C. difficile strains, in addition to increasing vancomycin resistance, researchers are focusing on new treatments and relapse prevention therapy.

In the study mice were used to isolate human monoclonal antibodies (HuMAbs) capable of neutralizing C. difficile toxins A and B. Researchers then tested anti-toxin A HuMAb CDA1 alone and in conjunction with anti-toxin B HUMAb MDX-1388 for the ability to protect hamsters from C.difficle-induced death and relapse prevention. Results showed that combination therapy reduced mortality from 100% to 45% in the primary disease model and from 78% to 32% in the relapse model.

"These human and animal studies, taken together, demonstrate the relevance of toxin-reactive antibodies in disease outcomes," say the researchers. "Here we describe the characterization of a panel of neutralizing, fully human monoclonal antibodies (HuMAbs) directed against either toxin A or toxin B. HuMAb CDA1 (against toxin A) alone could protect hamsters from mortality, but significantly enhanced protection was observed when the antibodies were administered as a combination therapy."

Guinea Pig Aerosol Challenge Presents New Model for Q Fever Research in Humans

Sun, 19 Nov 2006 04:20:32 PST

( from http://www.rxpgnews.com ) Clinical signs and pathological changes in guinea pigs following an aerosol challenge with acute Q fever were similar to those seen in human acute Q fever indicating an effective animal model of human disease say researchers from Texas A&M University. They report their findings in the November issue of the journal Infection and Immunity.

Q fever, caused by the bacterium Coxiella burnetti, generally infects humans through inhalation with as few as 10 organisms capable of causing disease. C. burnetti has a high degree of resistance to treatment agents and can remain infectious in contaminated soils for years. Due to its highly infectious nature, the Centers for Disease Control and Prevention has listed C. burnetti as a potential weapon of mass destruction reinforcing the need for a safe and effective vaccine. There is currently no licensed vaccine available in the U.S.

In the study select guinea pigs received a killed whole-cell Q fever vaccine after which all were infected with C. burnetti through inhalation of small-particle aerosols and evaluated 28 days postinfection. Noted clinical signs included fever, weight loss, respiratory difficulty and death with the degree and duration of response correlating with the dose of organism delivered. Those guinea pigs vaccinated prior to challenge with the highest dose of C. burnetti did not develop fever and were protected against lethal infection.

"The guinea pig aerosol challenge model presented here mimics both the clinical and pathologic changes seen in human acute Q fever and Q fever pneumonia cases and will provide an accurate and valuable tool for the study of the general pathogenesis of C. burnetti infection, for vaccine assessment, and for evaluations of host immune responses," say the researchers.

Gut Bacteria Cospeciating with Plataspid stinkbug

Wed, 11 Oct 2006 04:56:37 PST

( from http://www.rxpgnews.com ) With some 1 million species and counting, insects may be the most abundant class of animals living today. Their protective exoskeleton, prolific reproductive rate, and wings help their cause, as do the symbiotic bacteria that inhabit their cells, gut, or body cavity. Endocellular symbionts live inside specialized insect cells and provide essential nutrients for their hosts, which in turn provide suitable habitat for the bacteria. Insect mothers transmit endocellular symbionts to their offspring during egg or embryo development, preserving an intimate bond between host and symbiont that is evident in both species' genomes.

Studies that use genome analysis to infer evolutionary relationships (called phylogenetics) show that the history of insect host genes (or phylogeny) often mirrors that of their endocellular symbiontindicating a shared evolutionary history, or cospeciation. Unlike endocellular symbionts, gut or body cavity symbionts are vulnerable to displacement or attack by other microbes and appear to have less-exclusive relationships with their hosts, based on reports that hostsymbiont phylogenies for termites and alydid stinkbugs do not match. But a new study suggests that not all gut symbionts go for the promiscuous lifestyle. Takahiro Hosokawa, Takema Fukatsu, and colleagues provide the first evidence of cospeciation between a group of gut symbionts and their insect hosts, plataspid stinkbugs. Not only do their phylogenies mirror each other, but the gut symbionts share many of the unique genetic traits typical of endocellular symbionts.

A mating pair of the Japanese common plataspid stinkbug Megacopta punctatissima (Image: PLoS Biology)

Plataspid stinkbug symbionts live in the bugs' posterior midgut and are vertically transmitted by the mother in symbiont capsules. When the female lays eggs, small, brown symbiont-filled capsules always appear under the egg mass. Nymph hatchlings ingest symbionts from the capsule.

Hosokawa et al. collected 12 populations of stinkbugs, representing three genera and seven species, from several locations in Japan. (Four species were used in the experiments.) All females had the same three-compartment midgut, which had been previously described in two other species: one section contains the symbionts (called the thin crypt-bearing midgut, or TCM), another secretes webbing that embeds the symbionts into the capsules, and a third produces the shell that encases the capsule. All the females also codeposited capsules and egg masses. (Males have only the TCM.)

After removing the TCM from adult females, the researchers analyzed the DNA of the resident bacteriafocusing on a ribosomal RNA gene called 16S rRNA often used to identify bacteriaand found that each bacterial species was associated with a different stinkbug species. Using the 16S rRNA sequences to infer the bacteria's evolutionary origins, they discovered that the sequences didn't match any other bacterial sequences in the databasesthey fell into their own class of Proteobacteria. Interestingly, however, the symbionts did form a sister groupindicating evolutionary kinshipwith the well-characterized obligate endosymbiont (Buchnera aphidocola) of aphids.

Given the phylogenetic similarity between the stinkbug symbionts and Buchnera, the researchers wondered whether their biology might be similar as well. They divided egg masses into two groups and deprived one group of capsules to generate sibling populations with and without gut symbionts. Adults lacking symbionts showed developmental delays, grew smaller, failed to copulate or reproduce, and died prematurely. Like aphids depend on their endosymbionts, plataspid stinkbugs depend on their gut symbionts to survivehow they do this, however, will be interesting to discover. Like Buchnera, the gut endosymbionts also appear to have co-evolved with their host. The phylogenetic tree of the stinkbugs, the researchers found, perfectly agreed with the phylogenetic relationships of the gut symbionts. Maternal transmission of the symbiont capsule provides a means of stable transmission, but other factors such as physiological compatibility may come into play.

The symbiotic lifestyle appears to have shaped the genome evolution of endocellular symbionts, which have a small genome, a high percentage of A and T nucleotides in their DNA, and accelerated molecular evolution. Whether these genetic traits arose from population genetic forcesfor example, small population size and bottlenecksor from some aspect of the endocellular environment has been a matter of dispute. Hosokawa et al. found the same peculiar genetic patterns in the gut symbionts, lending support to the population genetic hypothesis. They named these gut symbionts Candidatus Ishikawaella capsulata, in honor of Hajime Ishikawa, a pioneer in the molecular study of symbiosis, who recently passed away.

How the symbiont capsule evolved remains an open, and intriguing, question. With some 530 species and 56 genera in the Plataspidae family, researchers have their work cut out for them as they survey the lineages for a stinkbug without a capsule. But with this unique plataspid stinkbug system, they will be well equipped to study insect symbiosis and its influence on genome evolution.

An infectious agent of deception, exposed through proteomics

Sun, 01 Oct 2006 22:55:37 PST

( from http://www.rxpgnews.com ) Salmonella bacteria, infamous for food poisoning that kills hundreds of thousands worldwide, infect by stealth. They slip unnoticed into and multiply inside macrophages, the very immune system cells the body relies on to seek and destroy invading microbes.

Just how Salmonella escapes detection by macrophages, turning predator cells to prey complicit in promoting infection, has seemed impossibly complicated, a needle-in-a-haystack proposition involving thousands of proteins, the building blocks that carry out cells' vital functions.

Applying the high-volume sorting and analytical power of proteomics--a detailed survey of microbial proteins present in the 24 hours that follow mouse-macrophage infection--a team led by Liang Shi of the Department of Energy's Pacific Northwest National Laboratory has turned up a suspect protein.

PNNL scientists have identified a protein in Salmonella bacteria that enables it to infect immune cells called macrophages. Seen here: Salmonella, isolated from infected macrophrages. (Mildly color-enhanced. Photo credit: Pacific Northwest National Laboratory.)

The discovery of the protein, dubbed STM3117, is detailed today (Sept. 29) in The Journal of Biological Chemistry. Knocking out the gene that codes for STM3117, the researchers subsequently crippled the microbe's ability to multiply inside macrophages. Shi and colleagues say the protein and two closely related proteins discovered in the study are similar in genetic sequence to those known to make and modify chemicals in the microbe's cell wall called peptidoglycan.

Drug and vaccine designers armed with this mouse-model information can target chemicals or immune responses that disrupt peptidoglycan synthesis and other processes linked to Salmonella's colonization of macrophages in humans, said Joshua Adkins, a co-author on Shi's paper and lead author of a related study in Molecular & Cellular Proteomics last month. A quick identification of these proteins, Adkins added, could help physicians assess the virulence of a given strain.

The candidate proteins were winnowed from among 315 possibilities that emerged through a combination of techniques, culminating in measurements by Fourier-transform mass spectrometry, or FT-MS. A suite of FT-MS instruments customized by co-author and PNNL-based Battelle Fellow Richard D. Smith enabled the team to rapidly separate and identify many proteins at once even as macrophages were being infected.

Most of the initial candidates were designated "house-keeping" proteins, or those whose numbers relative to other proteins remained more or less constant during the course of infection. But 39 proteins shot up in number during bacterial colonization of macrophages, and of those, a handful or so--including STM3117--responded specifically to a macrophage protein associated with resistance to microbial infection. A standard assay called Western blot confirmed the abundance increases of that small group of proteins during infection.

Gram positive bacterial membrane mystery solved

Fri, 01 Sep 2006 17:55:37 PST

( from http://www.rxpgnews.com ) A 25-year quest to identify the first biochemical step that many disease-causing bacteria use to build their membranes has led to a discovery that holds promise for effective, new antibiotics against these bacteria, according to investigators at St. Jude Children's Research Hospital. The finding is significant because the biochemical step the antibiotic would block is not used by humans. Therefore, such a drug would not cause dangerous side effects.

A report on this finding appears in the September 1 issue of Molecular Cell.

The discovery also demonstrated that current textbooks use the wrong type of bacterium as a model to explain a critical biochemical step that most disease-causing bacteria use to make their membranes, according to Charles Rock, Ph.D., a member of the St. Jude Department of Infectious Diseases and senior author of the paper. As bacteria grow in size or divide, they must make additional membrane using a series of biochemical reactions. The first step in this process is the transfer of a fatty acid to a molecule called G3P. Bacteria then convert this molecule into a variety of other molecules called phospholipids, which are the building blocks of membranes.

"We identified a biochemical process that uses a previously unrecognized molecule as a raw material to make phospholipid," Rock said. "That discovery solved a mystery that has puzzled researchers for 25 years."

Scientists have used E. coli bacteria for many years as a model to understand how disease-causing bacteria make membrane phospholipids, but E. coli is an unsuitable model for most pathogens (disease-causing bacteria), according to Rock.

First, E. coli is a so-called gram-negative bacterium, while many of the pathogens researchers are interested in are gram-positive, Rock noted. Among those gram-positive organisms are Staphylococcus aureus, which causes skin infections and serious blood infections, and Streptococcus pneumoniae, which causes pneumonia. The terms "gram-positive" and "gram-negative" refer to the response of bacteria to a standard laboratory process by which they are stained as a first step in identification.

Laboratory strains of E. coli do not cause disease; and the enzyme E. coli uses during the first step in making membranes does not exist in most other bacteria, including gram-positive pathogens. Therefore, the way gram-positive bacteria make phospholipid building blocks remained a mystery for over more than two decades. Now, however, the St. Jude team reports that the gram-positive pathogens use two enzymes, called PlsX and PlsY, to kick off phospholipid synthesis.

"In fact, the biochemical pathway that uses PlsX and PlsY is the most widely distributed bacterial pathway for initiating the production of phospholipids," explained the study's first author, Ying-Jie Lu, Ph.D., of the St. Jude Department of Infectious Diseases. "It turns out that E. coli is more of an oddball rather than in the mainstream when it comes to how it makes membranes."

E. coli fuses a molecule called G3P with a fatty acid in a single step. Rock's team showed that gram-positive pathogens first use PlsX to synthesize a compound called fatty acyl-phosphate, then use PlsY to transfer the fatty acid to G3P. These steps initiate membrane phospholipid formation required for cell growth.

"Our discovery of PlsX and PlsY not only solved a troublesome mystery," Rock said. "It's also important because identifying the essential components required for disease-causing bacteria to grow and multiply is a key part of developing new strategies for controlling infections."

Salmonella bacteria use RNA to assess and adjust magnesium levels

Fri, 07 Apr 2006 03:46:37 PST

( from http://www.rxpgnews.com ) Researchers at Washington University School of Medicine in St. Louis have added a gene in the bacterium Salmonella to the short list of genes regulated by a new mechanism known as the riboswitch.

The Salmonella riboswitch is the first to sense and respond to a metal ion, substantially expanding the types of molecules that riboswitches can detect to help cells assess and react to their environment.

First identified in 2002, riboswitches sense when a protein is needed and stop the creation of the protein if it isn't. That in itself isn't remarkable--scientists have been aware for decades of sensors in the cell that can cause molecules to bind to DNA to turn protein production on and off.

A riboswitch, however, doesn't rely on anything binding to DNA; instead, the switch is incorporated into messages for construction of proteins. These messages are protein-building instructions copied from DNA into strands of RNA. The riboswitch is a sensor within the RNA that can twist it into different configurations that block or facilitate the production of the protein encoded in the message.

Previously identified riboswitches respond to organic compounds such as nucleotides and sugars. The Salmonella riboswitch, reported in the April 7 issue of the journal Cell, responds to magnesium ions, key elements in the stability of cell membranes and reactants in an energy-making process that fuels most cells.

"Magnesium ions are essential to the stability of several different critical processes and structures in the cell, so there has to be a fairly intricate set of regulators to maintain consistent levels of it," says senior investigator Eduardo A. Groisman, Ph.D., professor of molecular microbiology. "To approach such a complex system, we study it in a simpler organism, the Salmonella bacterium."

Groisman and his colleagues uncovered the magnesium riboswitch while they were investigating the MgtA gene, which is controlled by the major regulator of Salmonella virulence, the phoP/phoQ system. The MgtA gene codes for a protein that can transport magnesium across the bacterium's cell membrane. Groisman's group showed 10 years ago that the phoP/phoQ system controls when Salmonella makes MgtA.

When Salmonella experiences a low-magnesium environment, phoQ chemically modifies phoP. The changed phoP binds to DNA, increasing the number of times instructions for making MgtA and over 100 other proteins are copied from DNA. But when Salmonella encounters a high-magnesium environment, phoQ deactivates phoP, and fewer copies of the instructions for making MgtA are made.

When Groisman and his colleagues created a mutant strain lacking the phoQ gene, though, they were surprised to find that production of the instructions to make the MgtA protein could still somehow respond to magnesium, producing less of its protein at high magnesium levels.

Researchers used a computer program to determine how RNA copied from the MgtA gene might be folding up. The program predicted RNA copied from the gene could have two significantly different configurations. Because of the significant differences between these configurations, Groisman, who is also a Howard Hughes Medical Institute investigator, became interested in a region at the beginning of the RNA strand that contains no protein-building instructions. He theorized that it might be a riboswitch that responded to high magnesium levels by twisting the RNA into a configuration where its protein-building instructions somehow could not be used or were invalidated.

"One of our tests to see if this was something more than a computer fantasy was to take this segment that contains no protein-building instructions off the MgtA gene and paste it into another genetic configuration," Groisman says. "We wanted to see if it conferred sensitivity to magnesium levels, which it did."

In addition, Groisman's group showed that one RNA configuration was common in low magnesium levels while another was common in high magnesium levels.

They also searched the genomes of other bacteria with MgtA genes to see if their DNA included a sequence similar to the riboswitch in Salmonella. In six other bacteria, a similar sequence precedes the MgtA gene and can twist RNA copied from it into different configurations.

"Normally you would expect to find that a DNA sequence that is conserved among different species is encoding part of a protein," Groisman says. "But here we're talking about a part of a message that does not encode a protein. So why would it be conserved? There must be some important role that the sequence is fulfilling that is leading to its conservation, such as giving the cell expanded ability to sense and respond to magnesium levels."

Follow-up inquiries are already underway to locate the riboswitch's "brain"--the section of the RNA strand that responds to magnesium; and to learn how the high-magnesium configuration of the RNA disrupts final production of the protein.

How deadly toxin botulinum neurotoxin A hijacks cells

Fri, 17 Mar 2006 14:01:37 PST

( from http://www.rxpgnews.com ) Scientists have pinpointed exactly how botulinum neurotoxin A - a potential agent of biological warfare and one of the most lethal toxins known to man - is able to sneak into cells.

The finding is crucial for the development of new treatments against botulism, a paralytic illness caused by the toxin more commonly known as botox. As small amounts of botox are also known to alleviate many medical problems, the recent work could help to quell any risks associated with the toxin's clinical use.

Writing in the current online edition of Science, a team of researchers at the University of Wisconsin-Madison and the University of Texas report that botox latches onto a protein known as SV2 to gain entry into neurons.

"Our work shows that botox is really smart and clever," says senior author Edwin Chapman, a UW-Madison professor of physiology and an investigator of the Howard Hughes Medical Institute. "It uses SV2 to sneak into nerves like a Trojan horse."

"Botulinum neurotoxins are among the six most dangerous bioterrorism threats," adds lead author Min Dong, a UW-Madison postdoctoral researcher in the department of physiology. "Knowing the protein receptor for [botulinum toxins] can pave the way for developing anti-toxin reagents which may block the entry of toxins into cells."

The botulinum toxins, of which there are seven types, are made by a bacterium commonly found in soil, known as Clostridium botulinum. Of the seven-identified by the letters A through G--botox A lasts a particularly long time in neurons. While that feature makes it especially useful in the clinic, it also means that botox A may pose a particularly dangerous threat as a biological weapon.

The toxin enters neurons by binding to nerve endings and preventing the release of crucial chemical messengers, known as neurotransmitters, that communicate with muscles. When enough nerve endings are invaded, botox can lead to paralysis and death.

By capitalizing on the ability of botox to act on a localized group of muscles, doctors have strategically used the toxin to treat an array of medical troubles, including migraine headaches, chronic inflammation and even stuttering. "I don't think there's a neuromuscular junction that hasn't been inhibited by injecting with botox A," says Chapman.

Chapman and his team located the exact molecular gateway through which botox penetrates cells by gathering clues from earlier research that pointed to the potential importance of tiny neural storage bins known as "synaptic vesicles." Situated at nerve endings, synaptic vesicles continually work to store and release neurotransmitters.

Dozens of proteins, including SV2, work to ensure that vesicles function properly. With standard screening experiments known as "entry assays," the scientists were able to zero in on SV2. To confirm that result, they acquired mice that were genetically engineered to carry reduced amounts of SV2. Without that protein around, the researchers found that botox was unable to wreak havoc.

String Test: Effective and Inexpensive Method for Detecting Helicobacter pylori

Sat, 11 Mar 2006 20:36:37 PST

( from http://www.rxpgnews.com ) Swallowing a string may offer a simple and effective alternative to costly and invasive techniques used for detecting Helicobacter pylori in patients say researchers from the U.S. and abroad. They report their findings in the March 2006 issue of the Journal of Clinical Microbiology.

Helicobacter pylori is a gram negative bacterium known for causing chronic gastric distress in individuals worldwide and can lead to the development of peptic ulcers and early onset of gastric cancer. Current methods for detecting H. pylori infection do provide highly sensitive and specific results, but they can be costly, invasive, and uncomfortable.

In the study 35 patients with gastric complaints were administered the string test (or Entero test) which involves swallowing a capsule with a protruding absorbent string whose end is held outside the mouth. The ingested string is then retrieved and microbes from the gastrointestinal tract are recovered and studied. H. pylori was cultured from 80% of the strings of those patients who had also undergone extensive biopsy procedures and received positive results. No organisms were found on strings taken from patients whose biopsy results were negative.

"Our study shows that the string test, which is minimally invasive, inexpensive, and not dependent on sophisticated or costly equipment or radioactivity, allows culture of H. pylori from infected persons about 80% as efficiently as endoscopic gastric biopsies," say the researchers. "We suggest that the H. pylori string test assays will be of increasing importance in a public health context."

Scientists develop biosensor to detect E. Coli bacteria

Sat, 25 Feb 2006 10:02:37 PST

( from http://www.rxpgnews.com ) Scientists have developed a fast working biosensor that can accurately and rapidly detect an infectious agent that causes food borne illness, including the dangerous E. Coli bacteria.

The unique technology developed by the University of Rochester Medical Centre uses a protein from the suspect bacteria as part of the sensing system that includes a silicon chip and a digital camera.

"Traditional methods of detection of bacteria can take days but the biosensor developed by them could take as much time as it takes for a snapshot," said lead researcher Benjamin Miller.

The Rochester team called the technology "arrayed imaging reflectometry".

The system utilises a silicon chip that is made in a manner so that laser light reflected off the chip is invisible unless the target bacteria are present.

A protein from the bacteria, Translocated Intimin Receptor or Tir, is placed on the chip. The Tir can be seen as a "molecular harpoon", Miller said.

The E. Coli sends out the harpoon into a cell. Once it is in, the Tir binds with an E. Coli protein called Intimin. A similar process occurs between the Tir placed on the chip and any E. Coli in the sample.

The binding of the probed sample and the bacteria alters the surface of the chip. A digital camera image of the chip captures the changes for analysis and confirmation of detection.

Describing the new technology as inexpensive, Miller said that a physician some day could use it in his office to confirm a streptococcal infection in a patient with a sore throat.

Found - bacteria with strange magnetic personality

Fri, 24 Feb 2006 02:25:37 PST

( from http://www.rxpgnews.com ) Researchers have reported the discovery of a bacterium with strange magnetic properties - it tends to swim towards south magnetic pole while being in the northern hemisphere.

While 'Magnetotactic bacteria' are known to swim toward geomagnetic north in the northern hemisphere and geomagnetic south in the southern hemisphere, researchers from the Massachusetts Institute of Technology (MIT), the Woods Hole Oceanographic Institution (WHOI) and Iowa State University have found a bacterium in New England that does just the opposite: a northern hemisphere creature that swims south.

Because this behaviour doesn't make sense in the natural environment of the bacteria, where swimming south would take them away from areas with their preferred oxygen level, the researchers believe there must be other explanations for why some magnetotactic bacteria swim in particular directions, notes an MIT release.

The team dubbed the bacterium the barbell for its appearance. In a study reported in a recent issue of Science, they describe how they used genetic sequencing and other laboratory techniques to identify the barbell, which was found coexisting with other previously described magnetotactic bacteria in Salt Pond on Cape Cod.

Magnetotactic bacteria are found throughout the world in chemically stratified marine and freshwater environments, said lead author Sheri Simmons, a graduate student of the MIT.

Simmons and colleagues studied the bacterium under laboratory conditions and say the behaviour in natural environment could be different from its laboratory behaviour. Their results, however, suggest new models are needed to explain how these magnetotactic bacteria behave in the environment.

Student discovers protein in yoghurt that fights E. coli

Fri, 24 Feb 2006 02:22:37 PST

( from http://www.rxpgnews.com ) A high school student in the US has discovered a protein in yoghurt that has the potential to fight E.coli, the leading cause of diarrhoea in the world.

The yet to be named protein was discovered by 16-year-old Serena Fasano, a junior at Glenelg High School, after three years of research at the University Of Maryland School Of Medicine. Her father is director of the Mucosal Biology Research Center.

Fasano has been awarded a patent for the protein, although it is officially owned by the University of Maryland, reported the online edition of Baltimore Sun.

The student happened to notice an unusual ingredient lactobacillus in yoghurt. She obtained - through her father - specimens of E.coli 042, added varying amounts of yoghurt to it and chronicled the results.

The dish with the most yoghurt had the least E. coli, so Fasano was able to say that yoghurt kills E.coli, which kills six million people annually in the world, mostly children in Third World nations.

Slugs May Spread E. coli to Salad Vegetables

Fri, 20 Jan 2006 14:00:37 PST

( from http://www.rxpgnews.com ) A new study suggests that slugs have the potential to transmit E. coli to salad vegetables. Researchers from the University of Aberdeen, United Kingdom, report their findings in the January 2006 issue of the journal Applied and Environmental Microbiology.

Escherichia coli O157, an emerging zoonoses in many countries including the U.S. and U.K., has a 3 to 5 percent mortality rate in humans. Farm animals such as cattle and sheep have been previously identified as major reservoirs of this strain of E. coli by passing it through manure which is then used to fertilize crops. Slugs are widespread agricultural pests that continuously ingest bacteria from the soil and their environment. Their tendency to contaminate leafy vegetables often targeted for human consumption identifies them as likely source for E. coli transmission.

Laboratory testing found E. coli O157 in 0.21 % of field slugs on a sheep farm in the UK. Further studies revealed that the slug species, Deroceras reticulatum, could maintain viable E. coli on its external surface for 14 days and slugs that were fed E. coli shed viable bacteria in their feces persisting for up to 3 weeks.

"This study provides evidence that slugs can act as vectors of E. coli O157 from an environmental source to fruit or vegetables," say the researchers. "The research demonstrates that E. coli in D. reticulatum has a relatively long external and internal survival time and also shows that ability of E. coli to persist at length in excreted slug feces."

Escherichia coli doesnt gamble with its metabolism

Sat, 17 Dec 2005 15:57:38 PST

( from http://www.rxpgnews.com ) The ubiquitous and usually harmless E. coli bacterium, which has one-seventh the number of genes as a human, has more than 1,000 of them involved in metabolism and metabolic regulation. Activation of random combinations of these genes would theoretically be capable of generating a huge variety of internal states; however, researchers at UCSD will report in the Dec. 27 issue of Proceedings of the National Academy of Sciences (PNAS) that Escherichia coli doesnt gamble with its metabolism. In a surprise about E. coli that may offer clues about how human cells operate, the PNAS paper reports that only a handful of dominant metabolic states are found in E. coli when it is grown in 15,580 different environments in computer simulations.

When it comes to genomes, a great deal of complexity boils down to just a few simple themes, said Bernhard Palsson, a professor of bioengineering at UCSDs Jacobs School of Engineering and co-author of the study, which was made available online Dec. 15. Researchers have confirmed the complexity of individual parts of biochemical networks in E. coli and other model organisms, but our large-scale reconstruction of regulatory and metabolic networks involving hundreds of these parts has shown that all this genetic complexity yields surprisingly few physiological functions. This is possibly a general principal in many, if not all, species.

Palsson and his colleagues at UCSD, postdoctoral fellows Christian L. Barrett and Christopher D. Herring, and Ph.D. candidate Jennifer L. Reed, created a computer model of an E. coli cell based on the experimental results of thousands of previous experiments, some of which were completed decades ago. The goal of this study was to comprehensively simulate all the possible molecular interactions in a well studied strain of E. coli to gain a global view of the range of functional network states, said Barrett. Complex cellular networks can potentially generate lots of different behaviors, but we find that cells utilize only a few of them.

Barrett, Palsson, Herring, and Reed simulated the behavior of 1,010 of E. colis 4,200 genes. This particular subset of the bacteriums genome is tightly organized into interacting networks involved in metabolism or regulation of gene activation, or transcription. These linked networks are devoted to sensing, ingesting, and degrading potential food in the form of sugars and other energy-rich organic molecules.

E. coli must also have an efficient way to eliminate waste products. It, like all living things, generates energy in a process that involves the removal of electrons from food molecules and attaching them to acceptor molecules. For aerobic organisms, the final electron acceptor is usually oxygen, which is converted into water in the process.

E. coli can grow with or without oxygen, using nitrate or other molecules as its final electron acceptor. We found that the type of terminal electron acceptor in the growth environment and the presence or absence of glucose is very important to E. coli, said Barrett. Our simulations show that these two factors are key determinants of how the bacterium organizes itself.

This statistical projection of E. coli's computation-based activity profiles permits researchers to visualize the "space" of transcriptional regulation of genes involved in metablism and metabolic regulation. The clusters' positions are a function of the available electron acceptor, indicated by the ellipses, the carbon "food" source, and to a lesser degree by the source of nitrogen. (The number in parenthesis by each of the 13 clusters is the numbers of different activity profiles in the cluster.) (Image Courtesy: UCSD)

Barrett, Palsson, and their colleagues simulated the functional states of E. colis metabolic and transcriptional regulatory networks in the 15,580 environments of food sources and electron acceptors. To their surprise, no matter what carbon source it ingests or electron acceptor used, E. coli exhibits only six distinct functional states.

This study gives a systems biology view of how a phenotype, or a network state advantageous to a microorganism is comprised of a tiny subset of a much larger universe of possibilities as provided for in the genome, said Palsson. On a high level we can say that E. coli is obsessed with how it breathes and whether or not glucose is available to eat. All of its genetic complexity basically enables it to generate a nice steady state for itself regardless of what it has to live on.

Higher organisms have larger genomes and much more complexity, but Palsson noted that several theoretical studies predict that even eukaryotic cells will exhibit a relatively small number of functional states. When we uncover the regulatory networks in eukaryotes, including human, we will most likely be able to use computer simulations to uncover the different possible cell types in a manner similar to what was done in our work with E. coli, said Palsson.

Understanding how Rickettsia conorii interacts with host cells

Sat, 17 Dec 2005 15:40:38 PST

( from http://www.rxpgnews.com ) New research by a team of scientists in France and the United States has identified both the bacterial and host receptor proteins that enable Rickettsia conorii, the Mediterranean spotted fever pathogen to enter cells. Understanding how this bacterium interacts with the cells of its host could lead to new therapeutic strategies for diseases caused by related pathogens, including Rocky Mountain spotted fever and typhus.

Pascale Cossart, an HHMI international research scholar at the Pasteur Institute in Paris, together with her postdoctoral fellow Juan Martinez and collaborators in Paris and at Case Western Reserve University in Cleveland, Ohio, has identified the first receptor for a Rickettsial bacterium. Their findings will be reported in the December 16, 2005, issue of the journal Cell.

Rickettsial bacteria are transmitted by fleas, ticks, and lice to humans and other mammals, where they can cause dangerous and sometimes fatal infections. There are two types of Rickettsial pathogensthe spotted fever group, which includes the Rickettsia conorii bacteria studied by Cossart and her colleagues, and the typhus group. Both must live inside cells to survive. Rickettsia have been classified by the National Institute of Allergy and Infectious Diseases (NIAID) as agents with potential for use as tools for bioterrorism.

Mediterranean spotted fever is transmitted by a dog tick. The symptoms are generally mild and respond to antibiotics that shorten the course of the disease. But serious complications occur as much as 10 percent of the time, usually in patients who are elderly or who have some other underlying disease. Left untreated, Mediterranean spotted fever can be deadly.

Cossart and her team demonstrated that the Ku70 protein on the surface of host cells is critical for R. conorii to enter the cell, making it the first Rickettsial receptor ever identified. This receptor is a subunit of a protein complex present mainly in the nucleus, but also in the cell cytoplasm and at the cell membrane, said Cossart. We have thus used several approaches to establish our findings definitively. Ku70 is probably not the only receptor involved in bacterial entry, she noted.

The researchers found that R. conorii specifically binds to Ku70, and that binding and recruitment of Ku70 at the surface of the host cell are important events in R. conorii's invasion of mammalian cells. In addition, since Ku70 has previously been shown to control cell death, the new findings suggest that Rickettsia, whichlike several other intracellular parasitesprevent cell death in order to multiply inside living cells, may also use this property of their receptor for a succesful infection.

We found that Ku70 interacts with a bacterial protein called rOmpB, which is present on the surface of Rickettsia bacteria, Cossart said. The mechanism underlying this interaction remains unclear, so we are now investigating how rOmpB, expressed by R. conorii, interacts with Ku70 and allows bacterial entry.

Her team has already shown that Ku70 has to be present in certain well-organized regions of the cell membrane called rafts, and that the protein modifier called ubiquitin modifies Ku70 as soon as the bacteria interact with it. This step is critical for cell entry. Whether other Rickettsia and other pathogens use Ku70 as a receptor is still unknown, Cossart said.

Rapid tests for meningitis and MRSA are being developed

Mon, 17 Oct 2005 19:20:38 PST

( from http://www.rxpgnews.com ) Rapid tests for serious disease such as meningitis, chlamydia and the hospital superbug MRSA are being developed by a new company, Atlas Genetics Ltd, which is being launched using £500,000 funding and the expertise of academics at the University of Bath.

Current hospital tests take up to 72 hours, by which time the patients may have become seriously ill and may have spread the disease.

Patents have been filed in relation to Atlass key technology and it is expected that it will enable hospitals and eventually GPs to perform tests on the spot and make decisions about treatment within 20 minutes. The potential market for Atlass products is valued at over $3 billion (£1.7 billion) and is growing rapidly.

The company is working on a product that will analyse a clinical sample of blood, urine or saliva using a test cartridge inserted into a small, portable instrument.

The basis of this sensitive and specific test is an electronic tag developed by the company that automatically indicates the presence of DNA from the bacteria causing the disease.

This innovative technology has been developed over the last three years with a team of leading scientists from the Department of Chemistry at the University of Bath, including Professor Laurie Peter, Dr Toby Jenkins, Dr Chris Frost and Dr Stephen Flower. This was in collaboration with companies now acquired by Osmetech Plc, which is also a party to the current joint venture.

The commercial and technical management team of Dr John Clarkson, Dr Gordon Forrest, Dr Russ Keay, Alison Kibble and Karen Yates is highly experienced and have held senior positions in medical diagnostics, health care marketing, product development and finance.

The £500,000 already raised came in part from the Sulis Seedcorn Fund, which provides support for the new businesses set up using research carried out by the Universities of Bath, Bristol and Southampton. The Sulis institutional investment matched a £250,000 investment from a private investor who was introduced by the South West Angel and Investor Network (SWAIN), which brings together investors and companies seeking equity funding in the South West region.

Atlas was set up with the guidance and support of the University's Research and Innovation Services, which markets the University's resources of people, facilities and intellectual property to generate funds in support of research and teaching.

E.colis Defense Mechanism Uncovered

Thu, 29 Sep 2005 21:27:38 PST

( from http://www.rxpgnews.com ) Researchers at the Georgia Institute of Technology and the John Innes Centre in the United Kingdom have uncovered a mechanism with which disease-causing bacteria may thwart the bodys natural defense responses. The findings, which could ultimately lead to the development of more effective antibiotics, appear in the September 29, 2005 issue of the journal Nature.

Nitric oxide is produced by the body to fight infections. We discovered a mechanism that allows bacterial cells to detect nitric oxide and turn it into something thats harmless to the cell, said Stephen Spiro, associate professor in the School of Biology at Georgia Tech.

Spiro, along with colleagues Benoît D'Autréauz, Nicholas Tucker and Ray Dixon from the John Innes Centre, studied a non-pathogenic strain of Escherichia coli, which is very closely related to salmonella bacteria.

The pathogenic forms of E. coli and salmonella are usually transmitted to humans through undercooked meat, unwashed vegetables and cross contamination from surfaces on which these foods were prepared. Infections from either of these organisms can cause diarrhea, abdominal cramps and sometimes more serious illnesses that require hospitalization. E.coli doesnt respond well to antibiotics, while salmonella has developed several drug-resistant strains. Learning how the bacteria handle the bodys immune response is the first step in developing more effective medicines.

Spiro and colleagues focused their study on the NorR protein and the role it plays in reducing the levels of nitric oxide. In response to nitric oxide, NorR binds to DNA in order to regulate expression of an enzyme that reduces the amount of nitric oxide in the bacteria. Since nitric oxide binds to metals, the researchers suspected that there might be a metal in the protein.

Escherichia coli O157:H7 strain

It turns out that the protein NorR contains a single molecule of iron, said Spiro. Our study found that the nitric oxide binds to the iron, which in turn activates the protein.

Once activated, the protein controls expression of the norVW genes. These genes encode an enzyme that removes the nitric oxide, allowing the bacteria to fend off the bodys defenses.

The discovery of this mechanism is just the first step in what Spiro hopes will be a line of research aimed at disrupting the mechanism by which the bacteria rids itself of the poisonous nitric oxide.

If we can interfere with the mechanism, it could lead to better antibiotics and better treatments, said Spiro.

The research was funded by a grant from the Biotechnology and Biological Sciences Research Council.

A fat-sugar complex that anchors LTA could be target to block bacterial CNS infection

Tue, 06 Sep 2005 20:21:38 PST

( from http://www.rxpgnews.com ) A single molecular anchor that allows bacteria to invade the nervous system may hold the key to treating many types of bacterial meningitis, a UCSD School of Medicine study has found.

By blocking the molecules anchoring ability, researchers may be able to find a way to stave off the most common serious infection of the central nervous system and a major cause of childhood death and disability. The researchers findings appear in the September 2005 issue of the Journal of Clinical Investigation.

Kelly Doran, Ph.D, assistant professor of pediatrics, Victor Nizet, M.D., associate professor of pediatrics, and their colleagues have identified a gene that produces a fat-sugar complex, which in turn anchors a molecule called LTA (short for lipoteichoic acid), found on the bacterial cell wall. This anchoring is a necessary first step for bacteria to cross from the bloodstream into the central nervous system through an anatomical obstacle called the blood-brain barrier.

Streptococcus, which can cause meningitis, has to penetrate the normally impermeable blood-brain barrier in order to enter the central nervous system and cause disease, said Doran. How this happens is not well known for bacteria. We wanted to see how bacteria interact with blood-brain barrier cells to begin the process of crossing over into the nervous system.

The team began by looking for new bacterial genes that allowed them to penetrate the barrier. Through a process that involved generating and screening thousands of Streptococcus mutants in a laboratory model of the human blood-brain barrier, the researchers found that a gene called iagA (short for invasion association gene-A) played a central role.

By producing a fat-sugar complex that anchors LTA, iagA establishes a link that allows bacteria to begin making its way into the nervous system. The researchers found that removing the iagA gene from the Streptococcus inhibited bacterial interactions with the blood-brain barrier, reducing mortality rates up to 90 percent in mice.

Mice that were infected with the normal, or wild-type, Streptococcus bacteria containing iagA died within days showing evidence of bacterial meningitis. In contrast, most of the mice survived when infected with bacteria missing the single iagA gene, Doran said. Blocking the anchoring of LTA on the bacterial cell surface could become new a therapeutic target for preventing bacterial meningitis.

Doran and Nizet noted that the study focused on how bacteria can begin the invasion process, and that additional Streptococcus toxins and the bodys own immune response also contribute to the development of meningitis. In their ongoing efforts, the researchers are looking at all of these factors in order to paint a complete picture of how the bacteria invade the brain and spinal cord to produce this potentially devastating infection.

Bacterial meningitis must be treated quickly and aggressively with antibiotics, since up to 25 percent of affected children may die or suffer permanent cognitive deficits, cerebral palsy, blindness, deafness or seizures. Therefore, an early acting treatment would help reduce the high rates of disability and death.

Previous studies have found that Streptococcus bacteria from infants with serious disease have significantly higher levels of LTA than bacterial strains in infants without symptoms, Nizet said. This underscores the importance of this anchor-LTA interaction, as well as its potential importance as a drug target.

Listeria monocytogenes uses receptor-mediated endocytosis to infect hosts

Mon, 22 Aug 2005 15:23:38 PST

( from http://www.rxpgnews.com ) French scientists have learned how Listeria monocytogenes, which causes a major food-borne illness, commandeers cellular transport machinery to invade cells and hide from the body's immune system. They believe that other infectious organisms may use the same mechanism.

The Listeria bacterium, found in soil and water, can be transmitted to humans via undercooked and unpasteurized food, causing flu-like symptoms or gastrointestinal distress. For individuals with weakened immune systems, listeriosis can be fatal, and infections during pregnancy can lead to miscarriage, stillbirth, premature delivery, or infection of the newborn.

The research was conducted by Pascale Cossart, a Howard Hughes Medical Institute international research scholar, and her colleague Esteban Veiga at the Institut Pasteur in Paris, and will be published in the August 21, 2005, issue of Nature Cell Biology. Cossart and Veiga detailed how Listeria invades cells by activating cellular machinery that transports viruses, small molecules, and proteins. Once it has safely entered a cell, the microbe can replicate and continue the process of infection.

The body usually deals with bacteria and other large, foreign microbes through a process called phagocytosis. Specialized cells engulf the invading microbe and destroy it. Scientists long believed that cells use a second process, called endocytosis, to deal with smaller molecules or viruses. In endocytsosis, a cell's outer membrane pinches inward around the target to form a pocket that's brought inside the cell, creating a structure called a vesicle.

"Phagocytosis and endocytosis may, in fact, be more similar than past research suggests. This is a totally new concept," Cossart says.

Cossart's lab had observed that Listeria which is 20 times the size of the largest particle scientists believed a cell could take in by endocytosis could invade non-phagocytic cells. Other labs had made similar observations with other bacteria. Cossart and Veiga investigated the underlying machinery behind this uncommon invasion strategy, which they knew depended on an interaction between a protein on the surface of the bacteria, known as InlB, and a protein called Met on the surface of the cell it was invading.

They discovered that when InlB interacts with Met, the cell responds by adding a chemical tag to Met that flags it for protein recycling or degradation. Since Met is on the outside surface of the cell and the recycling and degradation machineries are inside, the cell must bring Met inside through endocytosis in order to dispose of it. As the cell creates the vesicle that will transport tagged Met, Listeria stows away and invades the cell.

By manipulating the gene expression of the cells Listeria was invading, the researchers showed that specific molecules known to be involved in endocytosis were essential for successful invasion by Listeria. Similarly, they found that an enzyme that tags proteins for recycling was also required.

Listeria's use of receptor-mediated endocytosis to infect hosts, according to Cossart, suggests that other bacteria may exploit the same mechanism to gain entry into non-phagocytic cells. "This mechanism of cell entry may be used by several different kinds of bacteria, which is a major deviation from the belief that endocytosis is strictly for importing small molecules into cells," she says.

One bacterial cell can stop the growth of another on physical contact

Fri, 19 Aug 2005 22:28:38 PST

( from http://www.rxpgnews.com ) Scientists have discovered a new phenomenon in which one bacterial cell can stop the growth of another on physical contact. The bacteria that stop growing may go into a dormant state, rather than dying. The findings have implications for management of chronic diseases, such as urinary tract infections.

The discovery by a team of scientists working in the laboratory of David Low, professor of biology at the University of California, Santa Barbara, is reported in the August 19 issue of the journal Science. The findings indicate that Escherichia coli, one culprit in urinary tract infections, contains genes that when turned on block the growth of other E. coli bacteria that they touch. The finding was a complete surprise to the scientists, said Low.

The discovery may eventually lead to new antimicrobial agents to halt bacterial growth which would be an entirely new system to shut bacteria down, according to the scientists. "This has potential implications for new antibiotics," said Low. "If bacteria can do this, then maybe we can do it."

Doctoral student and first author Stephanie Aoki, and a team of scientists working in the Low lab, made the discovery while studying other aspects of E. coli. After working for two years, the team identified two genes required for this "stop on contact" phenomenon.

"We don't know if these 'stopped' cells are dead or alive," said Low. "They don't grow after they've been touched. They don't grow on plates, but laboratory stains show they may be alive. You might call them dead, but they don't break apart the way dead cells do. These cells appear to stay intact, perhaps in a quiescent mode, or dormant state."

Aoki explained, "We are currently exploring how contact between bacteria can inhibit cell growth and determining what this contact-dependent inhibition of growth (CDI) system is used for. These genes are present in E. coli, including uropathogenic E. coli that cause urinary tract infections, and similar genes may be present in other pathogens such as the plague bacillus, Yersinia pestis."

Low said that one possible interpretation is that bacteria use this system to eliminate competition in the environments they grow in. "Another possibility is that the bacteria use the CDI system to shut themselves off inside a host, going into a dormant state where they may go undetected by the immune system," he said.

Thousands of women in this country have chronic urinary tract infections, noted the scientists. The disease seems to go away for awhile, then something triggers recurrence of the disease.

Work by Scott Hultrgen at Washington University has indicated that E. coli cells may hide in the walls of the bladder and urinary tract in a dormant state, explained Low. It is possible that the newly discovered CDI system contributes to this process.

"By studying the CDI system, we hope to understand more about how bacteria interact with each other and with their hosts, and how these interactions contribute to disease," said Aoki.

The findings may have repercussions outside of better understanding of urinary tract infections. Other diseases may have similar mechanisms, according to the scientists. "This research is in its infancy, but opens the door for exploration of the roles of contact-dependent growth inhibition in urinary tract infections and possibly other diseases," said Low.

"Aoki has discovered an entirely new phenomenon," explained Low, who has studied E. coli for over 20 years. "It is fascinating that bacteria have developed a system by which one cell can contact another and inhibit its growth."

Oral Vaccine from Bacterial Ghosts May Protect Against E. coli

Thu, 18 Aug 2005 02:44:38 PST

( from http://www.rxpgnews.com ) Researchers from Austria and Russia have developed an oral vaccine comprised of bacterial ghosts, or empty bacterial envelopes, which may protect against E. coli in animals and humans. Their findings appear in the August 2005 issue of the journal Infection and Immunity.

Enterohemorrhagic Escherichia coli (EHEC) is a bacterial pathogen associated with several life threatening diseases in humans. O157:H7, one of the most harmful and frequently studied strains of the bacteria can cause intestinal inflammation ranging from diarrhea to hemorrhagic colitis, with more severe cases afflicting children and the elderly. EHEC O157:H7 has also been identified as a bioterrorism agent. There is currently no specific treatment against EHEC infection and antibiotics are not recommended as they prompt the liberation of toxins which can worsen the clinical course of the disease.

Because the major reservoir for EHEC O157:H7 is cattle, researchers are focusing on a vaccine that will prevent infection in both humans and animals. In order to mimic the bacteria's natural route of infection they developed an oral vaccine in hopes of eliciting local immunity in the gut.

In the study production of the protein E-mediated lysis was controlled to produce EHEC bacterial ghosts, or non-living bacterial cell envelopes. They have the same surface components of live cells and are capable of inducing strong immune responses, but the lack of genetic material inhibits transfer of resistance genes. An oral vaccine containing the bacterial ghosts was administered to mice that were challenged with a lethal dose of the EHEC strain 55 days later. A single dose of the vaccine resulted in an 86 percent protection rate and mice receiving a booster after 28 days showed a 93 percent survival rate. Non-immunized mice challenged with the bacteria had a 26 to 30 percent rate of survival.

"Bacterial ghosts as candidate vaccines and carriers of foreign viral and/or bacterial antigens are under development as multivalent vaccines against diarrheal diseases of humans and might represent new, improved nonliving bacterial vaccines with excellent safety properties and high immunological potential," say the researchers.

Olives May Successfully Transmit Beneficial Bacteria to Humans

Thu, 18 Aug 2005 02:42:38 PST

( from http://www.rxpgnews.com ) Table olives may serve as a carrier for delivering beneficial bacteria to humans, according to researchers from Italy. Their findings appear in the August 2005 issue of the journal Applied and Environmental Microbiology.

Probiotic foods contain healthy bacteria intended to promote microbial balance, inhibit pathogens and protect humans from gastrointestinal diseases. Researchers are also investigating their role in reducing risk of cancer, preventing food allergies, and alleviating symptoms of lactose intolerance.

The researchers studied survival rates of various strains of four probiotic bacteria, Lactobacillus rhamnosus, Lactobacillus paracasei, Bifidobacterium bifidum, and Bifidobacterium longum, on table olives at room temperature. L. paracasei was noted for its survival on olives throughout the three month experiment and was recovered from fecal samples in four out of five volunteers who consumed 10 to 15 olives per day for 10 days.

"The results reported here suggest that table olives are a suitable substrate for delivering probiotic species, since populations of L. paracasei, a strain selected for its potential probiotic characteristics assessed in vitro and for its lengthy survival on olives, were detected in the feces of human volunteers," say the researchers. "This result meets one of the aims of the current research, that of finding new delivery systems ensuring the stability and viability of strains."

Phages Affect Gene Expression and Fitness in E. coli

Wed, 22 Jun 2005 13:04:38 PST

( from http://www.rxpgnews.com ) Life is hard for bacteria. Not only must they constantly compete against their comrades for resources and living space, theyre also subject to infection by pathogensviruses called bacteriophageswhich can affect their ability to survive and prosper. Two types of bacteriophages threaten bacteria: lytic phages and lysogenic (or temperate) phages.

Acquisition of a lytic phage (for example, T2, T4, or T6) is an immediate death sentence for the bacterium; upon infection, a lytic phage subverts the bacteriums biochemical machinery to make copy after copy of itself until the bacterium bursts, or lyses, from the burden. In contrast, a temperate phage (for example, λ phage) can lie dormant for many generations before it co-opts the bacteriums machinery to reproduce, but eventually it, too, lyses the bacterial cell as it releases a host of new phages. From the perspective of the bacterium, it is better to be infected by a temperate phage than a lytic phage because infection with a lytic phage means instant death, while a temperate phage may lie dormant long enough for the bacterium to reproduce.

Temperate phages achieve dormancy by producing a phage gene product (in the case of λ phage, called cI) that represses the production of other phage genes; phage reproduction ceases as long as this repressor is produced. Once infected by a temperate phage, bacteria are protected from secondary infections by various other phages, because the temperate phage prevents the others from becoming established in the cell. But might temperate phage infection confer other advantages on bacterial survival?

Edward Coxs group at Princeton University examined this question by looking for evidence that temperate phage infection triggers changes in bacterial behavior. Working with λ phages, the authors studied how phage infection affects the regulation of genes that might impact the bacteriums survival by comparing the constellation of genes expressed in uninfected E. coli bacteria to those in E. coli carrying a dormant λ phage.

They found that λ phage caused reduced expression of the bacterial gene pckA, which codes for an enzyme that helps bacteria grow on carbon sources (fuels) other than glucose; without functioning pckA, bacteria grow normally in an environment containing glucose, but grow only slowly in an environment containing alternative carbon sources such as succinate. E. coli carrying λ phage fail to make the pckA gene product because the pckA gene is turned off by the virally encoded repressor cI. Interestingly, the researchers found evidence that the repressors made by other temperate phages may also be able to turn off pckA expression, and that the pckA genes of other bacteria related to E. coli might also be regulated by temperate phage repressors.

The fact that this relationship between temperate phage repressors and regulation of the pckA gene is so well conserved argues that the ability to turn off this gene might be positively selected; therefore, pckA repression must confer some sort of survival benefit to the bacterium. Its not clear what this benefit might be, but one explanation is that slowing bacterial growth in glucose-poor environments might help the bacterium elude detection by the immune system of any animal it invades, increasing its chances of survival. Alternatively, slower bacterial growth might slow down the onset of viral reproduction and eventual lysis. Regardless, it is clear that there is a strong relationship between the temperate phages and the bacteria they colonize. These results have significant implications for the evolution of fitness in these bacterial populations.

Three New Phases of Repairing DNA Damage in E. coli

Wed, 22 Jun 2005 13:04:38 PST

( from http://www.rxpgnews.com ) Any cell that receives a dose of radiation is placed in a dangerous situation. The DNA damage resulting from exposure to such radiation (or any other mutagen) can cause massive rearrangements to genetic information and potentially kill the cell. Bacteria have learned to cope with this threat by activating genes that repair DNA damage and by preventing a cell from dividing before these repairs are completed. In the bacteria Escherichia coli, these repair genes form what is known as the SOS response.

The E. coli SOS response has been used to study DNA repair for decades, and a great deal is known about how the more than 30 genes involved in the response function. Two proteins figure prominently in this response. The LexA protein acts as a repressor and inhibits the expression of SOS genes under normal conditions; in the event of DNA damage, the protein RecA inactivates the LexA repressor by enhancing its autocleavage into two fragments, which initiates the SOS response. While these initial stages are well understood, how all the SOS genes are coordinated, and ultimately turned off, is only beginning to be explored.

In a new study, Joel Stavans, Uri Alon, and colleagues have closely followed the SOS response in individual E. coli cells to investigate its dynamics. Previous studies, which monitored the temporal pattern of activation of entire populations of cells, found that SOS genes turned on in one peak upon DNA damage. But Friedman et al. found that SOS genes in individual bacteria respond to DNA damage in three precisely timed phases. This observation reveals the importance of examining complex processes at the level of single cells, while furthering our understanding of how the SOS response is structured in E. coli.

Friedman et al. monitored the SOS response by attaching a green fluorescent protein (GFP) to the promoters (the section of DNA responsible for activating a gene) of three SOS genes (lexA, recA, and umuDC). Bacteria expressing these promoter-GFP fusions became fluorescent within minutes of being exposed to UV radiation, visualized using time-lapse fluorescence microscopy. Since GFP fluorescence is directly correlated with the expression of each of the chosen genes (i.e., their promoter activity), the authors could gauge the SOS response rate upon DNA damage.

To induce the SOS response, the authors exposed E. coli cells to UV radiation. By monitoring individual cells at two-minute intervals after this dose, Friedman et al. found up to three peaks of promoter activity at roughly 30, 60, and 100 minutes. Although the amount of this activity and the average number of peaks varied between cells, the timing was always similar in different cells, suggesting a highly structured, timed response. When the authors averaged this response over the population, it washed out into a single peakwhich explains why the three peaks of expression were not previously detected.

A deeper look into the dynamics of the SOS response in single E. coli cells showed that it did not correlate with cell size, suggesting the SOS response is not synchronized with the cell cycle. In addition, Friedman et al. repeated their experiments in a bacterial strain lacking the SOS response gene umuDC. The peak pattern was altered in this mutant strain, and the precision in the appearance of the peaks was reduced. By re-examining the SOS response in single cells, Friedman et al. have visualized an accurately timed and synchronized DNA repair process. Modulations in response to DNA damage have also been observed recently in individual mammalian cells. Future experiments in E. colione of the most genetically tractable model systemsshould help explain how this timed response is related to the different pathways of DNA repair and shutoff of the response.

Clues to a Parasitic Nematodes Bacterial Partnership

Tue, 29 Mar 2005 16:31:38 PST

( from http://www.rxpgnews.com ) More than a billion people are at risk for infection with filarial nematodes, parasites that cause elephantiasis, African river blindness, and other debilitating diseases in more than 150 million people worldwide. The nematodes themselves play host to bacteria that live within their cells, but in this case, the relationship is classic mutualism, with each benefiting from the other. Indeed, the Wolbachia bacterium is so crucial to its host nematode that apparently eradicating it with antibiotics severely compromises the nematodes ability to complete its life cycle within its human host. Thus, understanding the details of this symbiosis may help identify new strategies for controlling diseases caused by filarial nematodes. In a new study, Barton Slatko and colleagues present the complete DNA sequence of the Wolbachia pipientis strain within Brugia malayi, a parasitic nematode responsible for lymphatic filariasis, and analyze its genome for clues to the interdependence of the two species.

This Wolbachia genome is small, only about a million base pairs, and many metabolically critical genes have degraded through mutation to the point of uselessness. This phenomenon, called reductive evolution, is typical of long-term symbioses, as the two partners increasingly complement one anothers biochemical activities, reducing the selection pressure on otherwise lethal mutations. Wolbachias translational machinery and DNA repair equipment are largely intact. The bacterium appears to supply nucleotides to its host, as it contains complete pathways for biosynthesis of both purine and pyrimidine nucleotides. This is in contrast to Rickettsia, a close relative of Wolbachia and a mammalian parasite. Slatko and colleagues enumerate a variety of other pathways that have either been degraded or preserved, and highlight patterns in the genome structure through comparisons with both Rickettsia and another Wolbachia strain, found in fruit flies. For example, the two Wolbachia strains appear to have different membrane structures, possibly reflecting their different lifestyles (mutualistic versus parasitic).

Wolbachia can manufacture riboflavin and FAD, which are essential metabolic coenzymes and which do not appear to be made by its host. Conversely, it cannot synthesize amino acids and a variety of other vitamins and cofactors, and probably depends on the nematode to supply them. One discovery of possible significance is the presence in the bacterium of the synthetic pathway for hemethe oxygen-carrying iron component of hemoglobin. The nematode may require heme for synthesis of developmental hormones, so Wolbachias heme pathway may be an inviting target for therapy against nematode infection. Since no new antifilarial has been developed in two decades, these results may quickly lead to new therapeutic strategies against these parasites.

The Bacterias Guide to Survival

Tue, 22 Mar 2005 20:50:38 PST

( from http://www.rxpgnews.com ) From The Worst Case Scenario Survival Handbookwith handy entries like How to escape from killer bees and How to escape from quicksandto The Zombie Survival Guide: Complete Protection from the Living Dead, survival guides are one of the latest publishing fads.

If there was a market for it, a survival guide for bacteria might include topics like How to use your pili to keep your host from going apoptotic. A hosts cells can respond to a bacterial infection with apoptosis, or programmed cell death. For bacteria that pass directly from host to host, this can pose a problem. If the bacteria are highly virulent and induce too much cell death, they could take down their host before theyre able to jump ship, thus hurting the bacterias chances of survival in the long run.

Earlier studies suggested that bacteria can use their pili, finger-like appendages that many bear on their surface, to pull on a hosts cell membranes and thus influence the cells behavior. But these studies, which looked at mutant bacteria that could not retract their pili, did not examine the matter of how the bacteria coax their hosts to stay alive.

Now, in PLoS Biology, a group of researchers present more direct evidence that bacteria can induce changes in hosts gene expressionand possibly keep the host cells alive longerthrough tiny tugs on cell membranes. The study, led by Magdalene So, examined gene activity in human epithelial cells infected with Neisseria gonorrhoeae, the bacteria responsible for the sexually transmitted disease gonorrhea.

By comparing cells infected with normal N. gonorrhoeae to those infected with a mutant strain with defective pili, the researchers found a subset of 52 host genes that had higher activity when the host was infected with the normal bacteria, suggesting that the pulls of the pili were responsible. They also ran a key control experiment with an artificial mechanical pull on the host cell membrane. By coating magnetic beads with a preparation of bacterial pili, the beads attached themselves to the cell membranes. Then, in the presence of a magnetic field, the beads tugged on the cell membrane, approximating the effects on gene expression during infection with normal bacteria.

Thus, the mechanical tugs seem responsible for triggering a signaling cascade in the host cells, which ultimately affects the hosts gene expression. Many of the genes that increased in activity due to the tugs were already known to regulate apoptosis and cellular response to stress, including mechanical strain on the membrane. Also, a majority of these genes were known to be induced by a family of proteins called mitogen-activated protein kinases, or MAPKs. The researchers showed that blocking MAPKs reduced the activity of several of the genes that are usually enhanced by infection with the normal bacteria. Also, they found that cells infected with the bacteria tended to survive treatment with staurosporine, a chemical that normally induces apoptosis.

Overall, the groups findings support previous speculations that some bacteria influence gene expression and the fate of cells in their hosts by tugging on the host cells membranes with their pili. For bacteria like N. gonorrhoeae that pass directly from host to host, the researchers argue, it would be in a bacteriums interest to help keep its host alive. And bacteria appear to do this with the help of their pili.

Host Cell Lipids Facilitate Listeria monocytogenes Movement

Tue, 22 Mar 2005 20:44:38 PST

( from http://www.rxpgnews.com ) When the bacterium Listeria monocytogenes invades the body, it commandeers its host cell's actin cytoskeleton to invade other cells. In a report published in the Journal of Biological Chemistry, a group of scientists provide insight into the molecular mechanisms behind this infection technique.

Listeria causes a variety of diseases, the most severe being meningoencephalitis, an inflammation of the brain and the membranes that envelop the brain and spinal cord. Infection begins when the bacterium binds to a receptor on the surface of a cell, causing the cell to ingest it. The bacterium multiplies inside the cell and then uses a cellular protein called ActA to stimulate the host cell's actin to form filaments at one end of the bacterium.

"As these filaments lengthen, they drive the bacterium through the cell until it reaches the peripheral or outer cell membrane," explains Dr. Frederick Southwick of the University of Florida College of Medicine. "Here the growing actin filaments push the bacterium against the membrane, forming long membrane projections called filopodia. These filopodia push into adjacent cells and are ingested by them. The bacteria then enter the new cell and begin the cycle anew. Essentially Listeria takes over or hijacks the host cell's actin cytoskeleton to move within cells, and to spread from cell to cell."

In most cells, two membrane lipids, PIP2 and PIP3, are associated with the formation of new actin filaments. PIP3 is synthesized from PIP2 by an enzyme called PI3-kinase. The lipids attract and modify the functions of proteins involved in regulating actin assembly. PIP2 and PIP3 also prevent capping proteins from binding to the ends of actin filaments, allowing new actin filament assembly.

Because Listeria is capable of stimulating actin assembly and PIP2 and PIP3 are known to localize to regions of new actin assembly, Dr. Southwick and his colleagues decided to explore the roles these lipids play in Listeria infection.

"We had expected to see PIP2 and PIP3 only at the very back of Listeria where new actin assembly was taking place," recalls Dr. Southwick. "To our surprise these lipids also localized to the front of the moving bacteria." The researchers also noticed that Listeria movement slowed down when the bacteria were treated with molecules that inhibited PI3-kinase, proving that Listeria depend on PI3-kinase to move.

"Our studies show that Listeria is capable of inside-out signaling," explains Dr. Southwick. "Most signals arise from molecules binding receptors on the outside of the cell. In the case of Listeria, we find that this intracellular pathogen can harness signals from the inner rather than the outer surface of the cell membrane.

"The most exciting and surprising finding is that an intracellular bacteria is able to attract host cell membrane lipids to its surface and these membrane lipids facilitate the ability of the bacterium to move within cells. This capability is unique to Listeria and is not found in another intracellular bacteria, Shigella. Our experiments show that Listeria is a simplified model system for studying how phosphoinositides regulate the actin cytoskeleton, and this model promises to yield additional insights into how these phospholipids control the cell's actin cytoskeleton. Our discoveries provide additional fundamental clues as how cells move."

These findings may also open the door to using PI3-kinase inhibitors or other agents that lower PIP2 and PIP3 levels to slow the spread of Listeria and control infection in patients who are not responding to antibiotics, although that application is a long way off, says Dr. Southwick.

Oysters in US showed high prevalence of Salmonella

Fri, 18 Feb 2005 16:38:38 PST

( from http://www.rxpgnews.com ) Oysters harvested from thirty-six bays around the United States showed high prevalence of Salmonella according to a report that appears in the February 2005 journal Applied and Environmental Microbiology.

Known carriers of viral and bacterial pathogens, seafood and shellfish accounted for 7.42% of food poisoning related deaths attributed to Salmonella between 1990 and 1998. Characterized by fever, abdominal cramps, and diarrhea, salmonellosis is responsible for approximately 500 deaths annually in the U.S. alone. Current guidelines require the shellfish industry to test for evidence of bacterial contamination, however previous studies indicate that Salmonella could be present in oysters appearing otherwise healthy, indicating the need for testing specific to Salmonella.

"There are no current requirements for U.S. states to test harvesting waters for the presence of human pathogens, such as Salmonella spp.," say the researchers.

In the study oysters were harvested from thirty-six U.S. bays, twelve from the West, East, and Gulf coasts during the summer of 2002 and four bays per coast in the winter of 2002, and tested for the presence of Salmonella. Results showed that 7.4% of the oysters tested were positive for Salmonella and they came from all three U.S. coasts.

"Potential pathogenic serotypes of Salmonella were isolated from oysters harvested on all three U.S. coasts," say the researchers. "The testing of the oyster meat specifically for Salmonella spp. on a regular basis throughout the year, in each bay open for harvesting, would appear to be the only mechanism to remedy this oversight."

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