Mycoplasma pneumoniae is major cause of respiratory infections including community acquired pneumonia, and the organism is an established cause of extrapulmonary complications such as encephalitis. At present three classes of drugs are used to treat M. pneumoniae infections: macrolides, tetracyclines, and fluoroquinolones. Of these only macrolides are generally considered acceptable for use in children under the age of 8 years. Recent epidemiologic data from Europe and Asia have documented the rapid and extensive emergence of macrolide resistance in M. pneumoniae. However, there is at present no surveillance of antibiotic resistance in M. pneumoniae in the United States to give physicians an idea of the scope of this problem. We propose to conduct a surveillance study of macrolide resistance in children in Alabama using traditional culture and molecular-based methods for detection of M. pneumoniae respiratory infections and to evaluate a PCR-based assay that will detect macrolide resistance directly in clinical specimens. We also plan to sub-type M. pneumoniae isolates to determine whether resistance is occurring frequently throughout the population or if clonal spread of resistant strains is occurring. The application of molecular methods to detect macrolide resistance in clinical specimens is essential for physicians to adequately treat serious infections cause by this organism.
Mycoplasma pneumoniae is a major cause of respiratory infections in humans. Recent reports from Europe and Asia have documented a rapid and extensive rise in resistance to macrolide antibiotics such as azithromycin, but there is no knowledge about the extent of this problem in the United States and no prospective studies to provide any surveillance data. We propose to conduct a prospective study in children using traditional culture and molecular-based methods to test for antibiotic resistance in M. pneumoniae.
| Lai, Jen-Feng; Zindl, Carlene L; Duffy, Lynn B et al. (2010) Critical role of macrophages and their activation via MyD88-NF?B signaling in lung innate immunity to Mycoplasma pneumoniae. PLoS One 5:e14417 |
