Saturday, January 28, 2006
Firm recalls teethers due to bacteria risk
WASHINGTON -- A Massachusetts company recalled 500,000 liquid-filled baby teethers distributed in the U.S. and Canada yesterday.
Possible bacterial contamination could cause serious illness.
Six styles of teethers may be contaminated with the Pseudomonas aeruginosa or the Pseudomonas putida bacteria.
The Disney Days of Hunny Soft Cool Ring Teether, bearing style number Y1447 and the Disney Soft Cool Ring Teether, bearing style number Y1470 or Y1490, feature Winnie-the-Pooh characters. The Sesame Beginnings Chill and Chew Teether, style number Y3095, features Sesame Street characters.
The other teethers recalled are The First Years Cool Animal Teether (style number Y1473) and The First Years Floating Friends Teether (style number Y1474).
Thursday, January 26, 2006
Airborne legionnaires bacteria can travel miles
By Anne Harding
NEW YORK (Reuters Health) - The bacterium responsible for causing legionnaires disease can spread up to 6 kilometers from its source by airborne transmission, French researchers report.
Legionella pneumophila likes to live in hot water, such as in industrial cooling towers or the water systems of large buildings where it can then cause pneumonia-like infections. Now it seems that a wider area may be at risk.
Past studies found airborne legionella spread only a few hundred meters, lead author Dr. Tran Minh Nhu Nguyen, who is currently at the National Public Health Institute in Helsinki, told Reuters Health. If other investigators confirm the new findings, he added, "a number of regulations and guidelines related to this environmental health risk should be revised accordingly."
In the Journal of Infectious Diseases, Nguyen and his team report on their investigation of a 2004 outbreak of legionnaires disease that occurred in Pas-de-Calais in northern France.
They identify a contaminated cooling tower at a petrochemical plant as the source of the outbreak, which killed 21 of the 86 individuals with laboratory-confirmed infection. Most of the victims lived within 6 kilometers of the plant, although one lived 12 kilometers away.
The fatality rate is "striking" when compared with past community-acquired outbreaks, in which fatality rates ranged from1 percent to 11 percent, the researchers note. They think the strain of legionella involved could have been unusually virulent.
The outbreak occurred in two peaks, the first ending after the cooling tower had been shut down and the second beginning during cleaning of the tower and peaking once it had reopened.
The pattern suggests that high-pressure cleaning methods used to decontaminate the towers contributed to the bacterium's spread. "There are measures and guidelines for managing cooling towers contaminated with legionella," Nguyen said. "However, how well they have been adopted and implemented depends on the individual country and setting."
SOURCE: Journal of Infectious Diseases, January 1, 2006.
Wednesday, January 25, 2006
Viable Group A Streptococci In Macrophages During Acute Soft Tissue Infection
Article Date: 17 Jan 2006 - 19:00pm (UK)
This study shows that that group A streptococci survive intracellularly in macrophages during acute invasive infections; the streptococcal pyrogenic exotoxin SpeB may have a role in this survival. Citation: Thulin P, Johansson L, Low DE, Gan BS, Kotb M, et al. (2006) Viable group A streptococci in macrophages during acute soft tissue infection. PLoS Med 3(3): e53.
LINK TO THE PUBLISHED ARTICLE: dx.doi.org/10.1371/journal.pmed.0030053
All works published in PLoS Biology are open access. Everything is immediately available - to read, download, redistribute, include in databases, and otherwise use - without cost to anyone, anywhere, subject only to the condition that the original authorship and source are properly attributed. Copyright is retained by the authors. The Public Library of Science uses the Creative Commons Attribution License.
Tuesday, January 24, 2006
2 million in U.S. may carry staph; infections on the rise
The Dallas Morning NewsPublished on: 01/23/06
DALLAS — The first nationwide statistical snapshot of a worrisome infection estimates at least 2 million people in the country may be silently carrying a potentially dangerous bacterium. And a second study reports that the germ appears to be creeping into hospital patients at a steady pace.
The studies are the latest clues to the behavior of methicillin-resistant Staphylococcus aureus, or MRSA. Since its appearance in the general population in 1999, the infection has already become notorious for illness among inmates, children and professional athletes. Last September, MRSA spread among Katrina evacuees at a shelter in Dallas. The St. Louis Rams battled an outbreak that affected five players, who apparently passed the infection to members of the San Francisco 49ers.
On Friday, the Dallas County Department of Health and Human Services issued a warning about MRSA infections picked up in contaminated whirlpool footbaths at some area nail salons.
Despite high-profile attacks of MRSA, scientists had not been able to say exactly how widespread the bug might be. Most of the time, people carry staph bacteria in their noses without knowing it. Only when it slips through breaks in the skin does MRSA announce itself. It concerns doctors not only because of its potential to cause disease, but also because it resists many traditional treatments.
This month, in the Journal of Infectious Diseases, researchers from the U.S. Centers for Disease Control and Prevention report that about 32 percent of the American population harbors S. aureus. About 1 percent of that staph appears to be MRSA. That would mean between 1.2 million and 3.8 million people carry the more dangerous form.
The most likely staph carriers were children, though the MRSA form was most common among older people, especially women.
"It's become one of the dominant infections of childhood," said Dr. William Schaffner of Vanderbilt University School of Medicine, who wrote a commentary that appears with the study.
Dr. Schaffner also noted that the study was conducted in 2001, just as the organism was getting a foothold in the U.S. population, and later data point to an epidemic that has only grown. For example, about 10 percent of children who come to Vanderbilt are colonized with MRSA.
MRSA has been long known as a hospital menace. In 1999, however, MRSA infections began showing up in otherwise healthy people who had never been near a hospital. The bacterium even got its own acronym: CA-MRSA, for "community acquired" MRSA.
CA-MRSA bears some differences from its hospital-bound cousin. While it appears to be more susceptible to antibiotics, it has at times shown a greater knack for causing some of staph's more terrible consequences, such as a particularly deadly form of pneumonia. Most often, though, CA-MRSA causes skin infections.
The infection is making a renewed name for itself in hospitals. A second study of more than 1,200 intensive care units, to be published in the Feb. 1 issue of Clinical Infectious Diseases, notes that 64 percent of staph infections now appear to be caused by MRSA. In 1992 the number was 36 percent.
Doctors are intensifying efforts to control the spread of MRSA, which thrives in places where people crowd together and which takes advantage of lapses in hygiene.
"It's not fancy drugs that we need in terms of prevention," said Dr. Jane Siegel of Children's Medical Center.
Infectious Diseases Thriving as Human Population Grows
Contact: Jill Stoddard212-854-6465 or firstname.lastname@example.org
Humans have provoked a lot of wobbling in the global food web, and one result is the explosion of infectious diseases.
“All of our infectious diseases are other species making a living off of us,” says Joel Cohen, a populations expert at both Columbia and Rockefeller Universities. “Think of the thousands of bacteria in our gut, the fungi on our skin, the insects that suck our blood, and the diseases those insects inject.”
As a result, new microbes and viruses that prey on humans, such as Ebola and HIV, are burgeoning around the world, and old ones continue to thrive.
“Over the last 10,000 years, the number of humans has increased about 1,000 fold, creating a lot more demand on other species, and providing more available material,” says Cohen.
Of particular interest to Cohen is Chagas’ disease, caused by an insect-borne parasite similar to the one responsible for African sleeping sickness. Cohen’s mathematical model of how the disease spreads has had public health implications for millions of poor Latin Americans.
“The network of infectious disease is incredibly dynamic,” Cohen says.
Because most species rely on other species for their energy, or are consumed by other species in search of energy, the species are all interconnected, forming a network known as the food web.
Cohen himself has kept logs of the species of food he eats, and over time it comes to about 150 different species of plants and animals. Humans collectively consume tens of thousands of other species. “That represents a lot of energy, and a lot of diversity, coming in,” he says.
Cohen's life work is to figure out the dynamics and interactions between the 100 million or so interconnected species on this planet.
The broad reach of his research has earned Cohen not only entrance into expected societies, such as the U.S. National Academy of Sciences, the American Academy of Arts and Sciences, and the American Philosophical Society, but also onto the worldwide Board of Governors of The Nature Conservancy.
Cohen is Abby Rockefeller Mauzé Professor at Rockefeller University and Professor of Populations at the Earth Institute at Columbia University.
In 2002, New York Mayor Michael R. Bloomberg gave Cohen his Award for Excellence in Science and Technology.
This is an edited version of a Rockefeller University article written by Renee Twombly. View full story.
Earth Institute News
Sunday, January 22, 2006
Rare bacteria species found in wounds of tsunami patients. Predominance of gram-negative rods, increased antibiotic resistance
Article in Swedish
[PubMed - indexed for MEDLINE]
Saturday, January 21, 2006
Bacteria in dirt may be "born" resistant to drugs
Thursday, January 19, 2006
By Maggie Fox
WASHINGTON (Reuters) - Bacteria in dirt may be "born" with a resistance to antibiotics, which could help shed light on the problem of drug-defying "superbugs," Canadian researchers said on Thursday.
They tested 480 different bacteria found in soil and discovered that every single one had some resistance to antibiotics, meaning they had evolved a mechanism for evading the effects of the drugs.
The findings, published in the journal Science, could help explain why bacteria so quickly develop resistance to antibiotics, and why drug companies must constantly develop new ones.
"It explains where these things come from in the first place," Gerry Wright, chair of Biochemistry and Biomedical Sciences at Ontario's McMaster University, said in a telephone interview. "This work could prove to be extremely valuable to the drug development process."
Wright's team dug up 480 strains of Streptomyces bacteria and tested them for resistance to various antibiotics.
"Without exception, every strain ... was found to be multi-drug resistant to seven or eight antibiotics on average, with two strains being resistant to 15 of 21 drugs," they wrote in their report.
'A LOGICAL PLACE TO START'
These particular bacteria do not infect people, but Wright believes the findings almost certainly apply to other species of microbes.
"It turns out that Streptomyces make lots of antibiotics," Wright said. "Anything that ends in 'mycin' comes from streptomycin - vancomycin, streptomycin."
That was why they chose this group of bacteria.
"We were curious to see where these things might come from in the first place, so it seemed that was a logical place to start. I expect lots of these (drug-resistant) genes are peppered all over the microbial community," Wright said.
They exposed the bacteria to known antibiotics and then searched for genes that were activated when the microbes survived.
"We found old mechanisms and new mechanisms," Wright said.
"We found a brand-new resistance mechanism to an antibiotic called telithromycin," he said, referring to Aventis' drug Ketek, only approved in 2004.
Ketek was designed to overcome resistance to antibiotics, but one of the bacteria Wright tested evolved a way to prevent it from working.
Almost as soon as penicillin was introduced in the 1940s, bacteria began to develop resistance to its effects, prompting researchers to develop many new generations of antibiotics.
But their overuse and misuse have helped fuel the rise of drug-resistant "superbugs." The U.S. Centers for Disease Control and Prevention says 70 percent of infections that people get while in the hospital are resistant to at least one antibiotic.
Wright said his findings do not get doctors off the hook. He said they still must prescribe antibiotics only when they are needed, and stress to patients the need to use them properly.
Soil bacteria live in a constant kind of arms race, making antibiotics to protect themselves against other bacteria, and then evolving antibiotic resistance to evade the antibiotics made by other bacteria.
"Their coping tactics may be able to give us a glimpse into the future of clinical resistance to antibiotics," Wright said.
Monday, January 16, 2006
A New Way to Stop Food Bacteria??
Researchers believe they may have found a novel way to disrupt bacteria that cause food poisoning.
The US and UK team have uncovered a previously unrecognised mechanism which bacteria use to escape the body's natural defence responses.
Using this mechanism, the pathogens detect a toxic gas produced by the body and turn it into something that is harmless to evade the onslaught.
Interrupting this might be a way to beat these bacteria, they told Nature.
The team from Georgia Institute of Technology in the US, and the John Innes Centre in the UK looked at harmless strains of the bacterium Escherichia coli.
However, they believe their findings will apply to the more harmful strains of E. coli and its close relation salmonella that cause outbreaks of food poisoning around the world.
These bacteria are usually transmitted to humans through undercooked meat, unwashed vegetables and poor food hygiene and can cause diarrhoea and cramps, which usually get better without help.
However, in those who are particularly vulnerable, such as people with weakened immune systems, the consequences can be particularly serious and may require hospital treatment.
Food poisoning bacteria
About six million people in the UK - 10% of the population - have a case of food poisoning each year. More than half of these are caused by bacteria such as E. coli and salmonella.
There are drugs available to treat complicated infections but the bacteria are learning how to dodge these and are becoming resistant.
Ultimately, Professor Ray Dixon and colleagues hope their discovery will help scientists find new ways to treat such infections.
They found E. coli was able to recognise and rid itself of the poisonous nitric oxide that the body produced to fight infection.
The bacterium has a protein called NorR that once activated controls the expressions of genes. These genes hold the code for an enzyme that removes the nitric oxide, allowing the bug to fend off the body's defences.
Colleague Professor Stephen Spiro explained: "It turns out that the protein NorR contains a single molecule of iron. Our study found that the nitric oxide binds to the iron, which activates the protein.
"If we can interfere with the mechanism, it could lead to better antibiotics and treatments," he said.
Professor Dixon stressed that this would be some years away.
Professor Jay Hinton, head of molecular microbiology at the Institute of Food Research, said:
"Antibiotic resistance is increasing. We do need alternatives.
"What they have found is interesting and unexpected. This, coupled with other work, could lead to new treatments in the future."
He recommended more studies to determine whether the same mechanism was apparent in pathogenic strains of Salmonella, E. coli and other food poisoning bugs.
BBC Health News
Sunday, January 15, 2006
Stomach bacteria linked to iron deficiency
Thursday, January 12, 2006
By Anthony J. Brown, MD
NEW YORK (Reuters Health) - Helicobacter pylori infection, which affects about one third of adults in the US, is associated with an increased risk of iron deficiency and related anemia, according to the results of a new study.
Moreover, this relationship holds true even in the absence of peptic ulcer disease, which can cause iron-deficiency anemia through hemorrhage, the researchers report in the American Journal of Epidemiology.
"For the first time in a national sample of the US population, we found an apparent link between H. pylori infection and iron deficiency" and iron-deficiency anemia, lead author Dr. Victor M. Cardenas, from the University of Texas at Houston, told Reuters Health.
H. pylori infection has previously been found to cause stomach inflammation and most ulcers. The bacterium also increases the risk of stomach cancer.
The researchers identified this new relationship based on an analysis of data from the current National Health and Nutrition Examination Survey (1999-2000). Data on 7,462 subjects who were at least three years of age were included in the analysis.
The presence of H. pylori infection raised the risk of iron deficiency and iron-deficiency anemia by 1.4- and 2.6-fold, respectively. H. pylori infection was also tied to other types of anemia, but to a much lesser extent.
How might H. pylori infection promote iron deficiency short of causing a bleeding ulcer? "The rapid turnover of H. pylori, which seems to sequester iron, is one possible mechanism," Cardenas said.
He added that his group is now seeking funding for a randomized trial to see if eradication of H. pylori can improve iron deficiency in children.
SOURCE: American Journal of Epidemiology, January 15, 2006.
Saturday, January 14, 2006
Lyme Disease Prevention and ControlReducing exposure to ticks is the best defense against Lyme disease and other tick-borne infections. There are several approaches you and your family can use to prevent and control Lyme disease.
Use repellent, tick checks, and other simple measures to prevent tick bites
Control ticks around your home and in your community
Ask your doctor if taking antibiotics after tick bite is right for you
Learn the early signs of tick-borne illness
A Lyme disease vaccine is no longer available. The vaccine manufacturer discontinued production in 2002, citing insufficient consumer demand. Protection provided by this vaccine diminishes over time. Therefore, if you received the Lyme disease vaccine before 2002, you are probably no longer protected against Lyme disease.
Ticks Transmit Lyme Disease
The Lyme disease bacterium, Borrelia burgdorferi, normally lives in mice, squirrels and other small animals. It is transmitted among these animals – and to humans -- through the bites of certain species of ticks.
In the northeastern and north-central United States, the blacklegged tick (or deer tick, Ixodes scapularis) transmits Lyme disease. In the Pacific coastal United States, the disease is spread by the western blacklegged tick (Ixodes pacificus). Other tick species found in the United States have not been shown to transmit Borrelia burgdorferi. Blacklegged ticks live for two years and have three feeding stages: larvae, nymph, and adult. When a young tick feeds on an infected animal, the tick takes the bacterium into its body along with the blood meal. The bacterium then lives in the gut of the tick. If the tick feeds again, it can transmit the bacterium to its new host. Usually the new host is another small rodent, but sometimes the new host is a human. Most cases of human illness occur in the late spring and summer when the tiny nymphs are most active and human outdoor activity is greatest.Although adult ticks often feed on deer, these animals do not become infected. Deer are nevertheless important in transporting ticks and maintaining tick populations.
Other Modes of Transmission
There is no evidence that Lyme disease is transmitted from person-to-person. For example, a person cannot get infected from touching, kissing or having sex with a person who has Lyme disease.
During Pregnancy & While Breastfeeding
Lyme disease acquired during pregnancy may lead to infection of the placenta and possible stillbirth, however, no negative effects on the fetus have been found when the mother receives appropriate antibiotic treatment. There are no reports of Lyme disease transmission from breast milk.
Although no cases of Lyme disease have been linked to blood transfusion, scientists have found that the Lyme disease bacteria can live in blood that is stored for donation. As a precaution, the American Red Cross and the US Food and Drug Administration ask that persons with chronic illness due to Lyme disease do not donate blood. Lyme disease patients who have been treated with antibiotics and have recovered can donate blood beginning 12 months after the last dose of antibiotics was taken.
Although dogs and cats can get Lyme disease, there is no evidence that they spread the disease directly to their owners. However, pets can bring infected ticks into your home or yard. Consider protecting your pet, and possibly yourself, through the use of tick control products for animals.
You will not get Lyme disease from eating venison or squirrel meat, but in keeping with general food safety principles meat should always be cooked thoroughly. Note that hunting and dressing deer or squirrels may bring you into close contact with infected ticks.
There is no credible evidence that Lyme disease can be transmitted through air, food, water, or from the bites of mosquitoes, flies, fleas, or lice.
Lyme Disease Transmission
Lyme Disease Symptoms
The Lyme disease bacterium can infect several parts of the body, producing different symptoms at different times. Not all patients with Lyme disease will have all symptoms, and many of the symptoms can occur with other diseases as well. If you believe you may have Lyme disease, it is important that you consult your health care provider for proper diagnosis.
The first sign of infection is usually a circular rash called erythema migrans or EM. This rash occurs in approximately 70-80% of infected persons and begins at the site of a tick bite after a delay of 3-30 days. A distinctive feature of the rash is that it gradually expands over a period of several days, reaching up to 12 inches (30 cm) across. The center of the rash may clear as it enlarges, resulting in a bull’s-eye appearance. It may be warm but is not usually painful. Some patients develop additional EM lesions in other areas of the body after several days. Patients also experience symptoms of fatigue, chills, fever, headache, and muscle and joint aches, and swollen lymph nodes. In some cases, these may be the only symptoms of infection.
Untreated, the infection may spread to other parts of the body within a few days to weeks, producing an array of discrete symptoms. These include loss of muscle tone on one or both sides of the face (called facial or “Bell’s palsy), severe headaches and neck stiffness due to meningitis, shooting pains that may interfere with sleep, heart palpitations and dizziness due to changes in heartbeat, and pain that moves from joint to joint. Many of these symptoms will resolve, even without treatment.
After several months, approximately 60% of patients with untreated infection will begin to have intermittent bouts of arthritis, with severe joint pain and swelling. Large joints are most often effected, particularly the knees. In addition, up to 5% of untreated patients may develop chronic neurological complaints months to years after infection. These include shooting pains, numbness or tingling in the hands or feet, and problems with concentration and short term memory.
Most cases of Lyme disease can be cured with antibiotics, especially if treatment is begun early in the course of illness. However, a small percentage of patients with Lyme disease have symptoms that last months to years after treatment with antibiotics. These symptoms can include muscle and joint pains, arthritis, cognitive defects, sleep disturbance, or fatigue. The cause of these symptoms is not known. There is some evidence that they result from an autoimmune response, in which a person’s immune system continues to respond even after the infection has been cleared.
Lyme Disease Symptoms
Lyme Disease Diagnosis
Lyme disease is diagnosed based on symptoms, objective physical findings (such as erythema migrans, facial palsy, or arthritis), and a history of possible exposure to infected ticks. Validated laboratory tests can be very helpful but are not generally recommended when a patient has erythema migrans. For detailed recommendations on serologic testing, click here.
When making a diagnosis of Lyme disease, health care providers should consider other diseases that may cause similar illness. Not all patients with Lyme disease will develop the characteristic bulls-eye rash, and many may not recall a tick bite. Laboratory testing is not recommended for persons who do not have symptoms of Lyme disease.
Laboratory Testing Several forms of laboratory testing for Lyme disease are available, some of which have not been adequately validated. Most recommended tests are blood tests that measure antibodies made in response to the infection. These tests may be falsely negative in patients with early disease, but they are quite reliable for diagnosing later stages of disease.
CDC recommends a two-step process when testing blood for evidence of Lyme disease. Both steps can be done using the same blood sample.
1) The first step uses an ELISA or IFA test. These tests are designed to be very “sensitive,” meaning that almost everyone with Lyme disease, and some people who don’t have Lyme disease, will test positive. If the ELISA or IFA is negative, it is highly unlikely that the person has Lyme disease, and no further testing is recommended. If the ELISA or IFA is positive or indeterminate (sometimes called "equivocal"), a second step should be performed to confirm the results.
2) The second step uses a Western blot test. Used appropriately, this test is designed to be “specific,” meaning that it will usually be positive only if a person has been truly infected. If the Western blot is negative, it suggests that the first test was a false positive, which can occur for several reasons. Sometimes two types of Western blot are performed, “IgM” and “IgG.” Patients who are positive by IgM but not IgG should have the test repeated a few weeks later if they remain ill. If they are still positive only by IgM and have been ill longer than one month, this is likely a false positive.
CDC does not recommend testing blood by Western blot without first testing it by ELISA or IFA. Doing so increases the potential for false positive results. Such results may lead to patients being treated for Lyme disease when they don’t have it and not getting appropriate treatment for the true cause of their illness. For detailed recommendations for test performance and interpretation of serologic tests for Lyme disease, click here.
Other Types of Laboratory Testing
Some laboratories offer Lyme disease testing using assays whose accuracy and clinical usefulness have not been adequately established. These tests include urine antigen tests, immunofluorescent staining for cell wall-deficient forms of Borrelia burgdorferi, and lymphocyte transformation tests. In general, CDC does not recommend these tests. Click here for more information. Patients are encouraged to ask their physicians whether their testing for Lyme disease was performed using validated methods and whether results were interpreted using appropriate guidelines.
Patients who have removed a tick often wonder if they should have it tested. In general, the identification and testing of individual ticks is not useful for deciding if a person should get antibiotics following a tick bite. Nevertheless, some state or local health departments offer tick identification and testing as a community service or for research purposes. Check with your health department; the phone number is usually found in the government pages of the telephone book.
Lyme Disease Diagnosis
Lyme Disease Treatment and Prognosis
The National Institutes of Health (NIH) has funded several studies on the treatment of Lyme disease. These studies have shown that most patients can be cured with a few weeks of antibiotics taken by mouth. Antibiotics commonly used for oral treatment include doxycycline, amoxicillin, or cefuroxime axetil. Patients with certain neurological or cardiac forms of illness may require intravenous treatment with drugs such as ceftriaxone or penicillin.
Patients treated with antibiotics in the early stages of the infection usually recover rapidly and completely. A few patients, particularly those diagnosed with later stages of disease, may have persistent or recurrent symptoms. These patients may benefit from a second 4-week course of therapy. Longer courses of antibiotic treatment have not been shown to be beneficial and have been linked to serious complications, including death.
Studies of women infected during pregnancy have found that there are no negative effects on the fetus if the mother receives appropriate antibiotic treatment for her Lyme disease. In general, treatment for pregnant women is similar to that for non-pregnant persons, although certain antibiotics are not used because they may affect the fetus. If in doubt, discuss treatment options with your health care provider.
For details on long term treatment trials sponsored by NIH visit the NIH Lyme Disease web site.
To read treatment guidelines developed by the Infectious Disease Society of America, click here (IDSA Guidelines for Treatment of Lyme Disease/PDF 120KB, 114 pages).
Lyme Disease Treatment and Prognosis
Lyme Disease Statistics
Lyme Disease Resources
Other tick-borne diseases
Tuesday, January 10, 2006
New warning signs for child meningitis
• Research has highlighted three new earlier symptoms of meningitis
• New signs include cold hands and feet, mottled skin colour and leg pain
• Meningitis Trust estimates 3,000 people a year in the UK become infected
"Early diagnosis and treatment is crucial to increase the likelihood of patient survival," - Harry Burns, the chief medical officer for Scotland
Story in full THOUSANDS of children's lives will be saved after meningitis researchers identified new early-warning signs for parents.
Until now, parents have been warned to look out for their child having a headache, stiff neck, sensitivity to light and a pinprick rash as signs of meningitis. But these symptoms can occur as little as two hours from the child becoming critically ill or even dying, leaving little time for treatment.
Now research has highlighted three new earlier symptoms of the infection - leg pain, cold hands and feet, and an abnormally pale, mottled skin colour - which together, or separately with other signs such as fever, can be indicators of the condition.
Doctors said the findings could speed up diagnosis and treatment of the disease, which the Meningitis Trust estimates infects 3,000 people a year in the UK, killing 300 - mostly children. Worldwide, the figure runs into thousands.
Dr Matthew Thomson, from Oxford University, who led the research, agreed that spotting the signs of the disease earlier could save thousands of lives.
"This disease develops so quickly in children - from the child becoming ill to being dead within 24 hours," he said. "The sooner a child can be spotted and admitted to hospital, the more likely they are to survive and do well."
Dr Thompson led a team investigating children who contracted the most dangerous, bacterial form of meningitis.
Most had only non-specific symptoms in the first four to six hours, but were close to death 24 hours after infection. Classic symptoms developed late, after an average of 13 to 22 hours. However, 72 per cent of the children developed identifiable early sepsis (infection) symptoms in just eight hours on average.
Almost three out of four parents noticed the onset of symptoms such as cold hands and feet, leg pain, and abnormal pallor up to 19 hours before their children were admitted to hospital.
In an online edition of the medical journal, The Lancet, published today, the researchers wrote: "
Although we must avoid undermining the importance of classic symptoms, we could substantially speed up diagnosis if the emphasis was shifted to early recognition of sepsis."
The researchers analysed patient questionnaires and scoured medical records.
Of the 448 children surveyed, all aged 16 or younger, 103 died and 345 survived. Only half the children were sent to hospital the first time they saw a doctor. In many cases, children were admitted to hospital only after an initial misdiagnosis, the research found. Generally, doctors look for the classic symptoms of rash, headaches, stiff neck, light sensitivity and impaired consciousness.
"We believe that primary-care clinicians are over-reliant on using these three symptoms to diagnose meningococcal disease in children, and that parents may be influenced by doctors or public health campaigns to seek medical advice only on the appearance of features such as a rapidly evolving rash," said Dr Thompson's team. "Moreover, clinicians and parents may be falsely reassured by the absence of these features."
Often children were seen by a local GP who had never encountered a case of meningitis outside hospital.
Dr Thompson warned that the research was in the early stages, but recommended that all parents be informed of the new warning signs.
The new warnings relate to the early signs of meningococcal disease, which can lead to meningitis as well as septicaemia and blood poisoning.
Vaccination can protect children against meningitis C, but other strains, most commonly meningitis B, kill children and adults indiscriminately.
In developed countries, meningitis, with its associated illnesses, are the leading infectious causes of death in children. At least four in 100,000 British children will at some time become ill with meningococcal disease.
Harry Burns, the chief medical officer for Scotland, promised to examine the research. "Early diagnosis and treatment is crucial to increase the likelihood of patient survival," he said. "We will look closely at the findings and consider carefully our advice to parents and doctors."
Olivia Giles, an Edinburgh lawyer who lost her limbs to meningococcal septicaemia in 2002, said the symptoms of blood poisoning, such as the pallor caused by blood rushing to protect vital organs, were well known.
But she said the fact it occurs earlier than classic symptoms should be stressed to all parents.
"You should be on the alert and have the information in the house or your purse so if you feel something is not normal you can look at the information and monitor the symptoms."
Ms Giles suffered from the early symptoms. "My hands and feet felt like blocks of ice and I had a horrible pallor from very early on," she said.
But it was not until 24 hours later, when the classic symptoms of meningococcal septicaemia emerged, that she was rushed to hospital. Doctors were left with no option but to amputate her hands and feet.
"Every second counts," says Ms Giles. "The minute it gets into your blood, it spreads rapidly. The sooner they give you the antibiotics, the less damage it will do."
Miss Giles, 40, who married this summer, added: "Listen to your instincts, be armed and ready to act quickly. You do not wait for a rash. The cold hands and feet is quite a warning."
Beverley Corbett, of the Meningitis Trust, which funded the research, also welcomed the research."Diagnosis of meningococcal disease is extremely difficult in the early stages, especially when classic symptoms are not present," she said. "This is why we emphasise the importance of early symptoms and remaining vigilant."
How the disease strikes
‘Classic’ symptoms: Red rash Headache Stiff neck Sensitivity to light Impaired consciousness
‘New’ symptoms: Leg pain Cold hands and feet Abnormally pale or mottled skin colour
Monday, January 09, 2006
New Angiotech product designed to fight infections
By LEONARD ZEHR
Thursday, January 5, 2006 Page B2
Moving to shed its image of a one-product company, Angiotech Pharmaceuticals Inc. is expanding its line of biomaterials with a drug-coated catheter designed to reduce hospital infections.
Best known for its drug-coated stents, which prop open blocked coronary arteries, Angiotech is expected to announce today that it has begun a pivotal clinical trial in the United States of a central venous catheter (CVC) coated with the chemotherapy drug 5-Flourouracil (5-FU).
CVCs are inserted into very ill patients to administer fluids, drugs and nutrients and withdraw blood, but they pose a risk of infection by bacteria contaminating the surface of the catheter.
Infections that reach the bloodstream can become life threatening.
According to industry estimates, there are about 3.5 million CVC procedures in the United States each year, resulting in up to 250,000 related infections and 40,000 deaths.
"This is a really big market," said Rui Avelar, a doctor and Angiotech's chief medical officer. "Infections can be devastating if they happen with hip and knee replacement surgery and implanting a pacemaker."
The company figures the annual cost of caring for patients with CVC-associated infections in the United States is about $2.3-billion (U.S.).
He said minute quantities of 5-FU can be an effective anti-bacterial agent.
"We think [this product] kills a wide variety of bugs. Because it isn't an antibiotic, we are not contributing to an increase of antibiotic resistant bacteria and we have shown that it blocks creation of biofilm."
Biofilms are an important survival tool for bacteria and are associated with antibiotic resistance in some bacterial infections.
Dr. Avelar said some CVCs are now coated with antibiotics. "If you can come up with an anti-infective that isn't an antibiotic, you are head and shoulders above everybody else."
Angiotech's one-year CVC study will enroll 600 patients at 20 clinics in the United States.
"The use of 5-FU as an anti-infective coating to prevent catheter-related bloodstream infections is innovative and unique," said Dr. Stephen Heard, lead investigator for the trial and chairman of the department of anesthesiology at the University of Massachusetts Memorial Medical Center.
For Angiotech, anti-infective products represent another step in diversifying the company's revenue base.
The company derives about 90 per cent of its revenue -- estimated at $200-million in 2005 -- from royalties on the sale of the Taxus drug-coated stent, which shaped a $5-billion-a-year industry.
"People can't see beyond the Taxus stent, even though we're doing a lot of other things," Dr. Avelar said.
It has commercialized surgical sealants to control bleeding and adhesive gels to prevent tissue adhesion after surgery.
Besides biomaterials, such as stents, to prevent scarring and a vascular wrap in clinical testing to prevent the narrowing of blood vessels, the company is developing products to accelerate healing and treat localized tumours from recurring after surgery with a drug-coated biomaterial.
"New competitors in drug-coated stents are not likely before 2008 and our initiatives will hit in 2007 and 2008," he said.
Friday, January 06, 2006
Scientists in move over MRSA
The bug not only costs lives - the health service spends thousands of pounds on trying to keep it out of hospitals.
Pharmacists at Queen's University in Belfast say they have developed a new way of killing MRSA.
It is due to be tried out on patients as early as next year.
For many years antibiotics have been used to kill bacteria, but bugs like MRSA are resistant to antibiotics, so now scientists are turning the clock back.
Dr Ryan Donnelly of Queen's School of Pharmacy
Dr Ryan Donnelly, of Queen's School of Pharmacy, said: "The ability of light to kill bacteria was first discovered about 100 ago, but because of the antibiotic era it was largely forgotten.
"It is only recently with the emergence of antibiotic-resistant bacteria that this has come to the fore again and many different groups involved in treating the likes of MRSA are trying to use this technology now."
A new gel is used to put a drug where it is needed.
Dr Paul McCarron, also of Queen's, said: "I saw my son, Niall, who was playing with kiddies' slime and I was just looking at the way it flowed between his fingers.
Dr Paul McCarron got inspiration from kiddies' play slime
"I thought it had the correct flow properties, to press into a leg ulcer for example. In other words, it can be pressed in and it will slowly flow to fill the cavity.
"More importantly, whenever you remove it, it can be removed all in one go."
The gel deposits a drug into the wound or ulcer and then it is lifted out, leaving behind the drug.
The drug makes MRSA and other bugs sensitive to light - much more so than the human cells, so when a powerful light is shone on the wound, it is the bugs like MRSA that will be killed.
Dr Donnelly said: "Certainly, from the work we have done so far, we would like to think that this technology could be successful in eradicating MRSA from wounds and burns in patients in the clinical situation."
BBC Northern Ireland health correspondent Dot Kirby said tests were due to begin on patients in Belfast City Hospital in the next 12 to 18 weeks.
"If this technique does work, its cost is likely to be small," she said.
"The drugs are cheap and the light units are expected to cost around £15,000. Each light unit could serve a whole hospital."
BBC Health News
Wednesday, January 04, 2006
Mycobacterium Avium Complex (MAC)
Mycobacterium Avium Complex (MAC) is a serious illness caused by common bacteria. MAC is also known as MAI (Mycobacterium Avium Intracellulare). MAC infection can be localized (limited to one part of your body) or disseminated (spread through your whole body, sometimes called DMAC). MAC infection often occurs in the lungs, intestines, bone marrow, liver and spleen.
The bacteria that cause MAC are very common. They are found in water, soil, dust and food. Almost everyone has them in their body. A healthy immune system will control MAC, but people with weakened immune systems can develop MAC disease.Up to 50% of people with AIDS may develop MAC, especially if their CD4 cell count is below 50. MAC almost never causes disease in people with more than 100 CD4 cells.HOW DO I KNOW IF I HAVE MAC?
The symptoms of MAC can include high fevers, chills, diarrhea, weight loss, stomach aches, fatigue, and anemia (low numbers of red blood cells). When MAC spreads in the body, it can cause blood infections, hepatitis, pneumonia, and other serious problems.
Many different opportunistic infections can cause these symptoms. Therefore, your doctor will probably check your blood, urine, or saliva to look for the bacteria that causes MAC. The sample will be tested to see what bacteria are growing in it. This process, called culturing, can take several weeks. Even if you are infected with MAC, it can be hard to find the MAC bacteria.If your CD4 cell count is less than 50, your doctor might treat you for MAC, even without a definite diagnosis. This is because MAC infection is very common but can be difficult to diagnose.
HOW IS MAC TREATED?
The MAC bacteria can mutate and develop resistance to some of the drugs used to fight it. Doctors use a combination of antibacterial drugs (antibiotics) to treat MAC. At least two drugs are used: usually azithromycin or clarithromycin plus up to three other drugs. MAC treatment must continue for life, or else the disease will return.
People react differently to anti-MAC drugs. You and your doctor may have to try different combinations before you find one that works for you with the fewest side effects.
The most common MAC drugs and their side effects are:
Amikacin (Amkin®): kidney and ear problems; taken as an injection.
Azithromycin (Zithromax®): nausea, headaches, vomiting, diarrhea; taken as capsules or intravenously.
Ciprofloxacin (Cipro® or Ciloxan®): nausea, vomiting, diarrhea; taken as tablets or intravenously.
Clarithromycin (Biaxin®): nausea, headaches, vomiting, diarrhea; taken as capsules or intravenously. Note: The maximum dose of Biaxin is 500 milligrams twice a day.
Ethambutol (Myambutol®): nausea, vomiting, vision problems.
Rifabutin (Mycobutin®): rashes, nausea, anemia. Many drug interactions.
Rifampin (Rifampicin®, Rifadin®, Rimactane®): fever, chills, muscle or bone pain; can turn urine, sweat, and saliva red-orange (may stain contact lenses); can interfere with birth control pills. Many drug interactions.
CAN MAC BE PREVENTED?
The bacteria that cause MAC are very common. It is not possible to avoid being exposed. The best way to prevent MAC is to take strong anti-HIV medications. Even if your CD4 cell count drops very low, there are drugs that can stop MAC disease from developing in up to 50% of people.
The antibiotic drugs azithromycin and clarithromycin have been used to prevent MAC. These drugs are usually prescribed for people with less than 75 CD4 cells.Combination antiretroviral therapy can make your CD4 cell count go up. If it goes over 100 and stays there for 3 months, it may be safe to stop taking medications to prevent MAC. Be sure to talk with your doctor before you stop taking any of your prescribed medications.
DRUG INTERACTION PROBLEMS
Several of the drugs used to treat MAC interact with many other drugs, including antiretroviral drugs, antifungal drugs, and birth control pills. This is especially true for rifampin, rifabutin and rifapentine. Be sure your doctor knows about all the medications that you are taking so that all possible interactions can be considered.
THE BOTTOM LINE
MAC is a serious disease caused by common bacteria. MAC can cause serious weight loss, diarrhea, and other symptoms.
If you develop MAC, you will probably be treated with azithromycin or clarithromycin plus one to three other antibiotics. You will have to continue taking these drugs for life to avoid a recurrence of MAC.People with 75 CD4 cells or less should talk with their doctors about taking drugs to prevent MAC.
Mycobacterium avium complex
Mycobacterium avium complex, or MAC, is a serious bacterial infection that HIV+ people can get. MAC is related to tuberculosis. MAC is also sometimes called MAI, which stands for Mycobacterium avium intracellulare.
MAC infection is usually found only in people with under 50 T4 cells. The symptoms of MAC can include weight loss, fevers, chills, night sweats, swollen glands, abdominal pains, diarrhea and overall weakness. MAC usually affects the intestines and inner organs first, causing liver tests to be high. Swelling and inflammation also occur.
Preventing MAC: A multi-center trial has shown that rifabutin, or Mycobutin, can nearly cut in half the rate at which people develop MAC. The drug is approved for prevention of MAC. Recent information from studies of rifabutin show that the drug may also help people live longer. Taking the drug for MAC prevention reduced the risk of dying by 14% in these studies. The most serious side effects of rifabutin are low white blood-cell counts and elevated liver enzymes. Very few people in trials had to discontinue the drug because of toxicity.
Clarithromycin (Biaxin) is the second drug to be approved for the prevention of MAC. In studies, it reduced the number of MAC infections by 69%, or over two-thirds. In a recent study people taking this drug to prevent MAC lived longer on average than those receiving placebo (a fake or dummy pill used in clinical trials to see if a treatment really works).
A third drug called azithromycin has now also been approved for preventing MAC. This drug can be taken once a week. A recent study found that azithromycin was better at preventing MAC than rifabutin. Azithromycin has not been directly compared to clarithromycin for preventing MAC.
A recent study comparing rifabutin, clarithromycin and a combination of the two drugs found clarithromycin to be clearly superior to rifabutin for the prevention of MAC.
However, clarithromycin is also thought to be the most effective treatment for MAC. Some doctors are concerned that if a person develops MAC while taking clarithromycin, the MAC infection will be resistant to the effects of the drug. This would make the infection much harder to treat. In studies, half the people that developed MAC while taking clarithromycin turned out to have MAC infections that were resistant to the drug. This might have been due to their having an undetected active MAC infection before starting preventive treatment. It is very important that you are properly tested for both active MAC and tuberculosis (TB) infection before starting any preventive treatment.
Treating MAC: The recommendations of the US Public Health Task Force on MAC are that treatment for disseminated MAC should include at least 2 drugs, one of which should be clarithromycin or azithromycin. Effective treatment should continue for life.
The Task Force also noted that many doctors use ethambutol as the second drug, and that other second, third or fourth drug(s) include: rifabutin, rifampin, ciprofloxacin and amikacin. Due to a recent study, clofazimine (trade name Lamprene) is no longer recommended as a part of MAC treatment. The study found that poor survival was associated with adding clofazimine to MAC treatment. The recommendations do not support the use of isoniazid (INH) or pyrazinamide for MAC therapy.
A recent alert from the National Institutes of Health also notes that the drug clarithromycin (Biaxin) should never be used at dose higher than the approved dose of 500 mg twice a day.
Some cautions: If you're taking AZT, rifabutin can reduce the amount of AZT in your blood. Lower amounts of AZT would make the AZT less effective against HIV. Rifabutin also lowers the amount of clarithromycin in the blood.
The anti-fungal drug fluconazole (Diflucan) can increase the amount of rifabutin in the blood by up to 80%. Increased levels of drug in the blood may lead to greater risk of side effects.
Side effects of rifabutin can be kidney and liver damage, bone marrow suppression, rash, fever, gastrointestinal distress, and uveitis (a swelling of the eye). Early warning signs of kidney problems are decreased urination, increased thirst, or light-headedness after you stand up. Uveitis can cause eye pain, light sensitivity, redness and blurred vision. A harmless side effect of rifabutin can be an orange color that appears in the urine and other body fluids, and sometimes on the skin, too. Soft contact lenses can become permanently discolored. Side effects of clarithromycin can be diarrhea, nausea, and abnormal or metallic taste. Clarithromycin may cause severe abdominal pain at high doses. Side effects of azithromycin include mild GI symptoms such as nausea and diarrhea, dizziness, sensitivity to sunlight, and rare cases of hearing loss.
Monday, January 02, 2006
Bacterial Protein Mimics Host to Cripple Defenses
Like a wolf in sheep’s clothing, a protein from a disease-causing bacterium slips into plant cells and imitates a key host protein in order to cripple the plant’s defenses. This discovery, reported in this week’s Science Express by researchers at the Boyce Thompson Institute (BTI) for Plant Research, advances the understanding of a disease mechanism common to plants, animals, and people.
That mechanism, called programmed cell death (PCD), causes a cell to commit suicide. PCD helps organisms contain infections, nip potential cancers in the bud, and get rid of old or unneeded cells. However, runaway PCD leads to everything from unseemly spots on tomatoes to Parkinson’s and Alzheimer’s diseases.
BTI Scientist and Cornell University Professor of Plant Pathology Gregory Martin studies the interaction of Pseudomonas syringae bacteria with plants to find what determines whether a host succumbs to disease. Martin and graduate student Robert Abramovitch previously found that AvrPtoB, a protein Pseudomonas injects into plants, disables PCD in a variety of susceptible plants and in yeast (a single-celled ancestor of both plants and animals). Abramovitch and Martin compared AvrPtoB’s amino acid sequence to known proteins in other microbes and in higher organisms, but found no matches that might hint at how the protein works at the molecular level.
“We had some biochemical clues to what AvrPtoB was doing, but getting the three-dimensional crystal structure was really key,” Martin explained. To find that structure, Martin and Abramovitch worked with collaborators at Rockefeller University. The structure of AvrPtoB revealed that the protein looks very much like a ubiquitin ligase, an enzyme plant and animal cells use to attach the small protein ubiquitin to unneeded or defective proteins. Other enzymes then chew up and “recycle” the ubiquitin-tagged proteins.
To confirm that AvrPtoB was a molecular mimic, Martin and Abramovitch altered parts of the protein that correspond to crucial sites on ubiquitin ligase. These changes rendered Pseudomonas harmless to susceptible tomato plants, and made the purified protein inactive. AvrPtoB’s function is remarkable not only because its amino acid sequence is so different from other ubiquitin ligases, but also because bacteria don’t use ubiquitin to recycle their own proteins.
“An interesting question is where this protein came from,” Martin noted. “Did the bacteria steal it from a host and modify it over time, or did it evolve independently? We don’t know.”
Regardless, the discovery “helps us understand how organisms regulate cell death on a fundamental level,” Martin said. AvrPtoB provides a sophisticated tool researchers can use to knock out PCD brought on by a variety of conditions, shedding light on immunity. The protein itself or a derivative might one day be applied to control disease in crops or in people. For now, Martin and Abramovitch are working to find which proteins AvrPtoB acts on, and what role those proteins play in host PCD.
Sunday, January 01, 2006
High Level Of Antibiotic Resistance In Bacteria That Cause Food Poisoning
The bacteria, Campylobacter, causes between 5 and 14 percent of all diarrhoeal illness worldwide. The most common sources of infection are inadequately cooked meat, particularly poultry, unpasteurised milk and contaminated drinking water. The illness normally clears up after a week, without treatment. But small children and people with a weakened immune system often take antibiotics to prevent the infection from spreading to the bloodstream – and causing life threatening septicaemia.
Researchers from the Swiss Federal Veterinary Office collected raw poultry meat samples from 122 retail outlets across Switzerland and Liechtenstein, and tested their antibiotic resistance. From 415 meat samples, they isolated 91 strains of Campylobacter, 59% of which were sensitive to all the antibiotics tested.
19 strains (22%) were resistant to one antibiotic, 9 strains (10%) to two antibiotics, and 8 strains (9%) were resistant to at least three antibiotics. Two strains were resistant to five antibiotics. One of these showed resistance to ciprofloxacin, tetracycline and erythromycin – the most important antibiotics for treating Campylobacter infection in humans.
Meat was more likely to be infected with Campylobacter if it was kept chilled, rather than frozen. However, the storage conditions did not affect the frequency of antibiotic resistance in the bacteria.
Although the frequency of antibiotic resistance in Switzerland may seem high, meat produced in the country was, in fact, less likely to be infected with antibiotic resistant Campylobacter than meat produced elsewhere. Jürg Danuser commented: "The level of antibiotic resistance in Campylobacter depends on the amount of antibiotics that the chickens received. Maybe in Switzerland antibiotics were used less, so there is less resistance"
Initially, the researchers thought that poultry was more likely to be infected with antibiotic resistant bacteria if it was raised using conventional indoor farming methods rather than in an animal-friendly way. However, the majority of meat produced in an animal friendly way came from Switzerland, and this skewed the results. The researchers therefore concluded that only the country of origin and not the farming methods were likely to influence the level of antibiotic resistance in the bacteria.
Jürg Danuser discussed this: "It's possible that chickens raised in an animal-friendly way are more healthy, so they need less treatment with antibiotics and so their Campylobacter are less resistant to antibiotics. But the other side of the story is that these chickens go outside more often, so they are in more contact with wild birds, which is the reservoir of Campylobacter."
These findings are of concern for Swiss consumers, but, as mentioned above, the picture for other countries is even bleaker. The researchers wrote: "The high prevalence of Campylobacter in raw poultry meat samples found in this study agrees with data from other studies." In the USA, 90% of Campylobacter strains isolated from poultry meat had resistance to at least one, and 45% to at least two antibiotics.
Worries over antibiotic resistant bacteria led the EU to ban the use of four antibiotics as growth promoters in chickens, in 1999. The US Food and Drugs administration (FDA) followed their lead in late 2000, by banning the use of a particular class of antibiotics called fluorquinolones in poultry farming.
Food poisoning caused by eating Campylobacter infected poultry is on the increase. In Switzerland, 1 in 1,086 people suffer from Campylobacter infection every year; the number is approximately ten times higher in the US.