All bacteriology stories

Discovery could aid fight against cystic fibrosis infection

70652986 — Mon, 26 Mar 2007 06:27:52 -0400

Harvard Medical School researchers have discovered one way that a hardy disease-causing bacteria could be surviving in the lungs of chronically infected cystic fibrosis patients. "This work is important because pathogenic bacteria such as Pseudomonas aeruginosa use protein secretion systems to cause disease in their hosts," said Joseph Mougous, lead author of the study published in the June 9, 2006, issue of Science. "In the case of Pseudomonas aeruginosa, the host may be a cancer patient with a weakened immune system, a burn patient, or a person with cystic fibrosis."

Bacterium present in eyes with 'wet' age-related macular degeneration

70652986 — Mon, 26 Mar 2007 06:23:08 -0400

Age-related macular degeneration (AMD) is the leading cause of blindness in Americans over the age of 55. The majority of vision loss is due to neovascular AMD, the advanced form of the disease characterized by the formation of blood vessels in the macula, the center part of the eye's retina. These blood vessels often leak, thus giving neovascular AMD the name of "wet" AMD.

Researchers at the Massachusetts Eye and Ear Infirmary (MEEI) have found that chlamydia pneumoniae, a bacterium linked to heart disease and capable of causing chronic inflammation, was present in the diseased eye tissue of five out of nine people with "wet" AMD. However, it was not found in the eyes of more than 20 individuals without AMD, providing more evidence that this disease may be caused by inflammation. The study is described in the November 2005 issue of Graefe's Archive for Clinical and Experimental Ophthalmology.

"The paper showed that C. pneumoniae is capable of modifying the function of important cell types involved in regulating normal eye function," said lead author Murat Kalayoglu, MD, PhD. "We found that C. pneumoniae infection led to increased production of vascular endothelial growth factor (VEGF), the key protein involved in wet AMD. That C. pneumoniae infection of human eye cell types increases VEGF production is therefore significant and could explain in part why VEGF levels are increased in many people with wet AMD." Kalayoglu is a Harvard Medical School research fellow in ophthalmology at MEEI.

Sublethal force: New antibiotic aims to tame bacterial toxins

70652986 — Mon, 26 Mar 2007 05:41:29 -0400

Using an innovative screening approach, researchers in the lab of John Mekalanos have identified an entirely new class of antibiotics active against the cholera bacterium. While traditional antibiotics kill bacteria outright by interfering with processes essential for their survival, the new agents block production of bacterial proteins that promote infection and cause cholera symptoms. Tests in animals proved that the new compounds could prevent bacterial colonization.

The work opens up a new world of potential for antibacterial drugs that aim to block the unique disease-causing talents of cholera bacteria, which include the production of cholera toxin. "What we've done is made a custom, organism-specific antibiotic against Vibrio cholerae," said Mekalanos, the Adele Lehman professor of microbiology and molecular genetics and head of that department. Since most bacteria that cause human disease elaborate virulence factors such as toxins, Mekalanos said, "There is no reason our approach can't be replicated for a number of other important pathogens." The research appeared Oct. 13, 2005 in the online edition of Science.

Bacterium proves essential to immune system development

70652986 — Mon, 26 Mar 2007 06:21:13 -0400

In the July 15, 2005 Cell, a team led by Dennis Kasper, the William Ellery Channing Professor of Medicine at Brigham and Women's Hospital and professor of microbiology and molecular genetics at Harvard Medical School (HMS), and Sarkis Mazmanian, HMS instructor in microbiology and molecular genetics, both at the Channing laboratory, reports that Bacteriodes fragilis aids immune system development.

Mammals contain approximately a thousand species, and one trillion cells, of bacteria to every gram of intestinal contents. The team studied germ-free mice and found that these mice have fewer CD4+ T cells in their immune system. When B. fragilis colonized the mice, their CD4+ T cell levels were restored.

Another team in Kasper's lab previously announced that T cells could recognize certain bacterial carbohydrates as antigens. Kasper and Mazmanian found that if the mice were colonized with a strain of B. fragilis that lacked the carbohydrate polysaccharide A (PSA), the bacteria could no longer restore T cell levels in the mice.

The team found that PSA induces the Th1 subset of T cells. The immune system relies on a balance between these cell-mediated responses and antibody-mediated, or Th2, responses. Kasper said that mice and humans raised in sterile environments have immune systems skewed toward Th2 responses. If bacterial factors like PSA are necessary for development of the Th1 arm of the immune system, it would reinforce that bacteria is essential for immune function.

Risk of becoming resistant to antibiotics may be lower than expected for chronic sinus infection sufferers

70652986 — Mon, 26 Mar 2007 05:39:22 -0400

"This study was designed to help determine how great a risk antibiotic resistance was among chronic sinus patients to determine if there is a need to re-evaluate how we diagnose and treat the condition. Interestingly, our research shows that patients suffering from chronic sinus infections may be able to lower their rate and likelihood of antibiotic resistance if a careful and strict approach to care is followed," said Neil Bhattacharyya, M.D., an otolaryngologist at BWH and the study's lead author.

In this study, Bhattacharyya and co-author Lynn J. Kepnes, R.N.P., followed 90 CRS patients over a seven-year period. Bacteria cultures were analyzed for changes in each patient's level of antibiotic resistance over the course of his or her treatment.

Hold that penicillin

70652986 — Mon, 26 Mar 2007 05:31:53 -0400

“The threat of resistance to antibiotics by bacteria increased so dramatically from the 1970s to the mid-1990s that the Centers for Disease Control and Prevention (CDC) labeled it a national public health crisis,” said Jonathan Finkelstein of the Harvard Medical School and Harvard Pilgrim Health Care in Boston. The CDC has called on doctors to be sure their patients' conditions really warrant use of the drugs, and to resist parental pressure to prescribe antibiotics for their children's colds or flu. This attention by public health agencies, the news media, and others appears to be working. Finkelstein and his colleagues did a study that reveals a steep drop in prescriptions written for children from 1996 to 2000. The researchers checked information on 225,000 patients ages 3 months to 18 years in nine health plans in various parts of the United States. They found a 24 percent drop for kids ages 3 months to 3 years, 25 percent for those 3 to 6 years, and 16 percent for the 6- to 18-year group. The results were published in the September 2003 issue of the journal Pediatrics.

Dual action anthrax vaccine more effective than current vaccine in early tests

70652986 — Mon, 26 Mar 2007 05:31:35 -0400

A new vaccine prods the immune system to attack both the anthrax bacterium ( Bacillus anthracis ) and the toxins it makes. This dual action represents an improvement over the currently available vaccine, which targets only the toxins. In a test of the vaccine using mice, animals were injected first with the vaccine, then 10 days later with anthrax toxin. All the vaccinated mice survived the toxic challenge, while unvaccinated mice exposed to the toxin died within 24 hours. "It worked like a charm," said Julia Wang, Harvard Medical School assistant professor at Brigham and Women's Hospital, who led the study. "Clearly, there is a need for a better anthrax vaccine," she added. The researchers suggest that the new vaccine will also be an important tool for treating those already infected with anthrax as a so-called therapeutic vaccine.

Enzyme pair joins fight against drug-resistant bacteria

70652986 — Mon, 26 Mar 2007 05:27:58 -0400

Scientists have been striving to develop antibiotics against drug-resistant bacterial strains. Most attempts have been plagued by a lack of molecular tools for manipulating -- and ultimately improving -- the structure of naturally occurring antibiotics. Harvard Medical School researchers Heather Losey, Christopher T. Walsh, and their colleagues reported in the Dec. 16, 2002 issue of the journal Chemistry & Biology that they harnessed two enzymes, which work by adding sugars to a central molecular core, and used them to create new versions of two potent antibiotics, vancomycin and teicoplanin. It is not clear if the new versions are effective against drug-resistant bacterial strains.

Bacterial construct makes for elegant vaccine

70652986 — Mon, 26 Mar 2007 05:24:39 -0400

Investigators from Harvard Medical School and London's Hammersmith Hospital have found a way to use the bacterium Listeria along with Escherichia coli to fight disease instead of causing it. In the November 2001 issue of Gene Therapy, Darren Higgins, Harvard Medical School assistant professor of microbiology, and Hammersmith co-authors report that by modifying E. coli to express a Listeria protein, they have created a vaccine that protects mice against melanoma. The study, conducted at the Molecular Oncology Unit of Cancer Research UK at Hammersmith, is the first in vivo test of this new vaccine approach developed by Higgins and colleagues.

Putting bacteria to work

70652986 — Mon, 26 Mar 2007 05:24:01 -0400

A nautical group of bacteria known as Prochlorococcus removes carbon dioxide from air and fixes it into the carbon content of their own tiny bodies. The more carbon dioxide they take from the air, the less is available to capture the heat that is causing the warm-up of our planet. That adds up to a lot of carbon. "Prochlorococcus is a major ocean sink for carbon," says George Church, professor of genetics at Harvard Medical School and a faculty member of the Harvard-M.I.T. Division of Health Sciences and Technology. "It is responsible for 40 percent of the photosynthesis (carbon dioxide removal) on Earth." A quart of ocean water often contains 100 million Prochlorococcus cells. Its population in the global ocean could be as high as 10 trillion trillion.

Discovering what lives in your mouth

70652986 — Mon, 26 Mar 2007 05:23:35 -0400

Your mouth is a great place for micropests to dwell. Glistening white plateaus, dark crevices, and slimy surfaces boast steamy temperatures of 95 degrees Fahrenheit. The microbes bathe in a saliva-induced humidity of 100 percent, and eat a lavish diet of sugar and other carbohydrates. It's so lush and varied, researcher Donna Mager refers to it as a mini-jungle. Mager is a fellow in oral medicine at the Forsyth Institute, an independent research institution in Boston. Forsyth scientists, most of whom are on the faculty of the Harvard School of Dental Medicine, have found 615 different species of bacteria - and they're still counting.

Staying healthy amidst bacterial "Overkill"

70652986 — Mon, 26 Mar 2007 05:21:18 -0400

A new book by Harvard School of Public Health Assistant Professor of Risk Analysis and Decision Science Kimberly Thompson takes a look at how the way we live is causing the rise of drug-resistant germs that are threatening an abrupt end to "The Age of Miracles" and bringing us all into "The Age of Risk Management." The book is called "Overkill: How Our Nation's Abuse of Antibiotics and Other Germ Killers is Hurting Your Health and What You Can Do About It" and published by Rodale Press. Thompson wrote it with health writer Debra Bruce. The Age of Miracles arose in the last century as new medicines and vaccines, coupled with a new understanding of the causes of disease, ended the everyday sway of scourges such as polio, diphtheria, measles, and rubella.

Novel anthrax treatments explored

70652986 — Mon, 26 Mar 2007 05:16:32 -0400

R. John Collier, Presley Professor of Microbiology and Molecular Genetics at Harvard Medical School, has been working on anthrax toxin for 15 years. He started his research because he found the workings of the anthrax bacterium interesting from a biological point of view. The events of the fall of 2001, when anthrax-laced letters killed several people in the United States and scared millions more, suddenly made his work of vital importance to the world. Working with several different research teams, Collier and colleagues have made several discoveries that could lead to new anti-anthrax treatments. The most interesting discovery involves the way that anthrax attacks healthy cells.

A strategy to neutralize anthrax toxin in the body

70652986 — Mon, 26 Mar 2007 05:16:12 -0400

A Harvard Medical School research team has developed a strategy to neutralize anthrax toxin in the body. So far they have tried the treatment in rats. Normally, rats die within hours after being injected with anthrax toxin. But when the toxin was followed minutes later with an injection of an inhibiting agent known as a polyvalent ligand -- itself completely innocuous -- the rats were protected from the toxin's effects. Asked if the polyvalent ligand can be tested in humans, research team leader R.

Resistance to antibodies is reversed

70652986 — Mon, 26 Mar 2007 05:13:12 -0400

It's a frightening -- and increasingly common -- problem. A patient seeks treatment for a particular ailment in a hospital and develops an entirely different disease: a bacterial infection that is resistant to antibiotics. Researchers have worked to come up with better and more powerful antibiotics, but even an antibiotic such as vancomycin, which used to be the last line of defense against bacterial infections, has been beaten by bacteria. Harvard researchers came up with a way to treat a bacterium called Enterococcus faecalis, which has recently emerged as a major source of infection in hospitals in the United States and other developed countries. By replacing one of its genes, the research team was able to render the bacterium susceptible to vancomycin once again.