Loren Miller, M.D., M.P.H. has found no reliable epidemiological or clinical risk factors that could distinguish patients with CA-MRSA infection from patients with CA-MSSA infection. “What this means,” says Dr. Miller, “is that the average Joe or Jane can get CA-MRSA.”
In a continuing effort to improve the clinical management of community-acquired methicillin-resistant staphylococcus aureas (CA-MRSA), Loren Miller, M.D., M.P.H. and colleagues at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) found no reliable epidemiological or clinical risk factors that could distinguish patients with CA-MRSA infection from patients with CA-MSSA infection. They suggest that, in settings where CA-MRSA is common, all patients with suspected CA S. aureus infection be placed in contact isolation and given appropriate therapy until the pathogens are identified. “What this means”, says Dr. Miller, “is that the average Joe or Jane can get CA-MRSA. A person doesn’t have to be special to get CA-MRSA. So a physician who thinks their patient with a skin infection is unlikely to have CA-MRSA because they haven’t been to jail or use illicit drugs is apt to be wrong over half of the time.” The research findings appear in the February 15, 2007 edition of Clinical Infectious Diseases.
In a separate article published in the same journal, Miller ands his colleagues investigated the outcomes for patients with either CA-MRSA or CA-MSSA skin infection 30 and 120 days after diagnosis. Despite the common belief that patients with CA-MRSA skin infection have more-serious outcomes than do patients with CA-MSSA infection, the authors found similar outcomes in the two groups. However, CA-MRSA infections are widely believed to be more transmissible than CA-MSSA infection. The authors also found data that close contacts of persons with CA-MRSA infection may have a higher likelihood of acquiring an infection than those with CA-MSSA. This observation supports the notion that CA-MRSA strains are more highly transmissible than the “old-fashioned” S. aureus, or CA-MSSA, strains.
CA-MRSA is a methicillin-resistant Staphylococcus aureus infection, first recognized in the 1980s. Traditionally MRSA infections have been associated with hospitalization or other healthcare-associated risk factors, but in recent years, physicians and other healthcare providers have observed an increasing number of people with MRSA infections who lack traditional healthcare-associated risk factors. These people appear to have community-associated infections. Most infections caused by Staphylococcus aureus are skin and soft tissue infections such as abscesses or cellulitis. CA-MRSA is the most common cause of skin infection in many locales in the U.S., including Southern California. CA-MRSA strains are notable for their ability to spread in closed settings and cause recurrent infections among healthy persons.
These findings continue a series of investigations and research into CA-MRSA with data from the Los Angeles area. In findings published in February 2005 in The New England Journal of Medicine, Dr. Miller reviewed records of more than 800 patients whose wound cultures grew MRSA in the Los Angeles area from January 2003 to April 2004. 14 people were identified with necrotizing fasciitis, informally known as “flesh-eating bacteria,” over a 14-month stretch through April 2004. As a result, physicians have been instructed that if they see cases of necrotizing fasciitis, they are to treat for the resistant bug in addition to the other known causes until they know the causative bacterial.
Dr. Miller and his colleagues in LA BioMed’s Division of Infectious Disease have a reputation for examining cutting-edge issues. For example:
In a seminal article titled “Trends in Antimicrobial Drug Development: Implications for the Future” published in 2004, Brad Spellberg, MD and his colleagues reported that the need for new antimicrobial agents is greater than ever because of the emergence of multidrug resistance in common pathogens, the rapid emergence of new infections, and the potential for use of multidrug-resistant agents in bioweapons. They determined that FDA approval of new antibacterial agents decreased by 56% from 1998 to 2002. Spellberg’s article became the basis of a July 2004 report by The Infectious Diseases Society of America (IDSA) titled “Bad Bugs, No Drugs: As Antibiotic Discovery Stagnates, a Public Health Crisis Brews.” Many if not all of the frightening conclusions in that report continue to be valid today.
Candida albicans and its related candidal species have emerged as the fourth most common organism recovered in blood cultures in hospitalized patients and carry an attributable mortality rate of 38%, even when treatment with currently available antifungals is used. Dr. John E. Edwards, Jr. and colleagues at LA BioMed have determined that the gene ALS1 in Candida encodes a protein (A1s1p), an important cell surface adhesion responsible for the attachment of the organism to human cells. The Edwards team has found that vaccination of mice with A1s1p protein protects against intravenous inoculations of C. albicans. They have developed a molecular biological approach to efficiently discover new cell wall proteins that may be adhesions and become future vaccine candidates. They have also developed the technology to couple selected proteins of interest to selected carbohydrate antigens in the candidal cell wall. The combined protein/carbohydrate antigens may have enhanced antigenicity.
Michael Yeaman, MSc, PhD, Professor of Medicine with the Department of Medicine/Infectious Diseases, has been appointed to serve as a member of the Host Interactions with Bacterial Pathogens Study Section (HIBP), Center for Scientific Review (CSR). The HIBP reviews applications involving studies that focus on bacterial factors that alter/affect host cells, or the host aspect of the host pathogen interaction. Dr. Yeaman’s appointment to the study section is an indication of how highly his research is regarded by his peers in the field of infectious diseases. Dr. Yeaman has focused his research on the relationship between microbial pathogenesis and host defense. He has studied the mechanisms of intracellular killing of microbial pathogens by macrophages and neutrophils, the structures and mechanisms of action of antibiotics and antimicrobial peptides, the role of virulence factors in pathogenesis of infections, and the interactions between bacterial and fungal pathogens with eukaryotic cells.