Patients who harbor the highly contagious bacterium causing staph infections can develop serious and sometimes deadly symptoms a year or longer after initial detection, a UC Irvine infectious disease researcher has found. A study led by Dr. Susan Huang shows that almost one-quarter of the patients who acquire the antibiotic-resistant bacterium MRSA (Methicillin-resistant Staphylococcus aureus) developed staph infections at least a year after initial detection. The infections included pneumonia and blood diseases, some of which were linked to deaths. The most serious staph infections begin in hospitals or other healthcare settings, such as nursing homes and dialysis centers. The study is the first to show such long-term risk of these infections and point to the need for new treatment approaches.

An international team of researchers supported by the National Institutes of Health (NIH) has blocked staph infections in mice using a drug previously tested in clinical trials as a cholesterol-lowering agent. The novel approach, described in the February 14 online edition of Science, could offer a new direction for therapies against a bacterium that�s becoming increasingly resistant to antibiotics. A pigment similar to the one that gives carrots their color turns Staphylococcus aureus (�staph�) golden. In the bacterium, this pigment acts as an antioxidant to block the reactive oxygen molecules the immune system uses to kill bacteria. Researchers had speculated that blocking pigment formation in staph could restore the immune system�s ability to thwart infection. While perusing a magazine on microbial research, Eric Oldfield, Ph.D., of the University of Illinois at Urbana-Champaign read how in 2005 University of California, San Diego researchers knocked out a gene in staph�s pigment-making pathway to create colorless�and less pathogenic�bacteria. �I looked at the metabolic pathway and noticed that it was similar to the one for the production of cholesterol in humans,� said Oldfield, senior author of the Science paper, who had spent decades studying this pathway. With numerous cholesterol-lowering drugs already on the market and in development, he wondered if any could turn staph colorless and make them once again susceptible to the immune system.

In hopes of combating the growing scourge of antibiotic-resistant bacteria, in particular drug-resistant staph bacteria, a team of scientists from the Scripps Research Institute has designed a new type of vaccine that could one day be used in humans to block the onset of infection. The advantage of the new vaccine is that it would work not only on current bacterial resistant stains but also would not induce the potential for new bacterial resistance because, rather than killing bacterial cells, it blocks their communication system, preventing the shift from harmless to virulent, thus allowing the body’s natural defenses to combat the bacteria. The bacterial infection process is dependent on a sort of chemical conversation between individual bacterial cells, referred to as quorum sensing. In their free-living state, bacteria are typically easy to kill and non-virulent. The shift to virulence is dependent on small molecules emitted by bacteria known as autoinducers, because bacteria sense when concentrations of these autoinducers are high enough to suggest a large number of other bacteria are present.

As many as 1.2 million U.S. hospital patients may be infected each year with a virulent staph infection that's resistant to antibiotics -- a rate almost 10 times greater than previous estimates, a new study finds.

A dangerous, drug-resistant staph germ may be infecting as many as 5 percent of hospital and nursing home patients, according to a comprehensive study.

Researchers at the National Institute of Allergy and Infectious Diseases (NIAID), a component of the National Institutes of Health, have discovered a survival mechanism in a common type of bacteria that can cause illness. The mechanism lets the bacteria protect itself by warding off attacks from antimicrobial peptides (AMPs), which are defense molecules sent by the body to kill bacteria. Led by Michael Otto, Ph.D., of NIAID’s Rocky Mountain Laboratories (RML), the scientists used the gram-positive bacterium Staphylococcus epidermidis to study its response to a specific human AMP, human beta defensin 3. S. epidermidis is one of several hard-to-treat infectious agents that can be transmitted to patients in hospitals via contaminated medical implants. In gram-negative bacteria—such as those that cause plague and salmonellosis—a sensory and gene regulation system named PhoP/PhoQ protects invading bacteria, and scientists believe if they develop a better understanding of this system they could develop new drugs that are more effective at protecting people from infection. Likewise, now Dr. Otto and his research group are hoping for similar possibilities for gram-positive bacteria with their discovery of “aps,” which stands for antimicrobial peptide sensor. Aps has three parts: apsS, the sensor region; apsR, the gene regulation region; and apsX, which has an unknown function that Dr. Otto’s group is investigating. Studies show that all three components of aps must be present for the system to function and effectively protect bacteria from AMPs.