Are outbreaks and sporadic respiratory infections by Mycoplasma pneumoniae due to two distinct subtypes?

Abstract

Thirty-seven clinical isolates of Mycoplasma pneumoniae, cultured from patients' respiratory material between 1986 and 1994, were typed by immunological methods and by polymerase chain reaction (PCR). For immunological typing two monoclonal antibodies (mAb) were used that recognized the P1 adhesion of Mycoplasma pneumoniae strain FH but differed in their ability to inhibit the adherence of Mycoplasma pneumoniae to erythrocytes. The mAb P1.58, which was not able to inhibit adherence, showed reactions with all patients' isolates in immunoblots, whereas the adherence-inhibiting mAb P1.62 reacted with only seven patients' isolates. Due to variations within the P1-adhesin genome of Mycoplasma pneumoniae group 1 (Mycoplasma pneumoniae type strain M129) and group 2 (Mycoplasma pneumoniae type strain FH), two primer sets were designed. According to the size of the PCR-amplification products, all clinical isolates that showed no mAb P1.62 reactivity belonged to Mycoplasma pneumoniae group 1, whereas mAb P1.62-positive-reacting mycoplasma isolates were characterized as group 2 strains. During an outbreak of Mycoplasma pneumoniae diseases in 1992, all 19 clinical isolates showed no cross-reactivity in immunoblots with the mAb P1.62 and were typed by PCR as Mycoplasma pneumoniae group 1 strains. Furthermore, 206 Mycoplasma pneumoniae complement fixation test-positive patient sera (titer > 1:40) from the study period were tested for adherence-inhibiting antibodies towards both type strains. Thirty-two sera showed adherence-inhibiting antibodies towards group 1 and 22 towards group 2 mycoplasmas. In only seven sera were adherence-inhibiting antibodies directed to both Mycoplasma pneumoniae groups. The serological data of the outbreak in 1992 revealed that patients with Mycoplasma pneumoniae group 1 infections developed adherence-inhibiting antibodies more frequently than did patients infected with group 2, which might have implications for the pathogenesis of Mycoplasma pneumoniae diseases and subsequent infections.