Hemadsorption and Virulence of Mycoplasma Pneumoniae

Abstract

Mycoplasma pneumoniae is a prokaryotic respiratory tract pathogen of man which causes cold agglutinin-associated primary atypical pneumonia. Although relatively little is known about the properties of this organism that endow it with pathogenicity for man, the use of a hamster model system established that the ability of M. pneumoniae to adhere to respiratory tract epithelium is a critical virulence determinant for this pathogen (1,2). Virulent strains of M. pneumoniae, in addition to being capable of adhering to respiratory epithelium, also form colonies on solidified growth medium that readily adsorb erythrocytes of many different species, in a process called hemadsorption (3). It has been established that trypsin treatment of virulent M. pneumoniae colonies eliminated the hemadsorption ability of these colonies (4). Previous studies from our own laboratory have established that trypsin-sensitive proteinaceous structures on the external membrane surface of virulent strain cells of M. pneumoniae are involved in the attachment of this parasite to host respiratory epithelium (5). It has been shown further that a homologous avirulent strain of M. pneumoniae that does not attach to respiratory epithelium in vitro also forms hemadsorption-negative colonies (6). All of these data taken together suggested that M. pneumoniae might utilize the same mechanism(s) for both hemadsorption and attachment to respiratory epithelium. In order to evaluate the relationship of the hemadsorption process to both respiratory epithelium attachment capability and virulence of M. pneumoniae, we employed a mutant analysis approach in conjunction with a hamster model system.