Anti-M. pneumoniae P1 monoclonal antibody, clone C2059N

Mycoplasma pneumoniae (Mp) is the causative agent of mycoplasmal pneumonia in humans. Mycoplasma pneumonia accounts for more than 1/3 of all atypical pneumonias and its pathological changes are mainly interstitial pneumonia. The source of infection is the patient or carrier, mainly through droplet transmission, and most patients are children and adolescents. Mycoplasma pneumoniae mainly invades the respiratory tract and causes primary atypical pneumonia. It has an incubation period of 2-3 weeks and causes upper respiratory tract infection, followed by tracheitis, bronchitis, bronchiolitis and pneumonia. Latent and mild infections are more common and may also lead to severe pneumonia or associated extrapulmonary tissue and organ lesions such as maculopapular rashes of the skin and mucous membranes, haemolytic anaemia, myocarditis, meningitis or encephalitis. Pathogenicity is also associated with delayed hypersensitivity. Mycoplasma pneumoniae has no cell wall and the outermost layer is the cell membrane, which is highly polymorphic, mainly filamentous, 2 to 5 um long. There is a special spherical structure at the tip of the filament and sometimes spherical or bi-spherical bacteria can be seen. Gram stain is negative under the microscope, but it is not easy to stain. The Giemsa stain is lavender. It is sensitive to low osmotic pressure. Nutritional requirements are higher than for normal bacteria. 10% to 20% human or animal serum must be added to the culture medium. 10% fresh yeast extract must be added during initial isolation and culture. The optimum pH is 7.8 to 8.0, and a pH below 7.0 may cause death. It grows best under 5% CO₂ conditions and the optimum growth temperature is 36-37°C. Mycoplasma grows slowly with very little turbidity in liquid culture medium, and colonies appear after 5-7 days of incubation on solid culture medium. Mycoplasma pneumoniae colonies are large, 10-100 μm in diameter. When first isolated, they are small granular colonies. After several passages, they form typical "fried egg" colonies. The centre of the colony is thicker and grows downward into the culture medium, and the surrounding area is a thin and transparent granular area. The colony can absorb guinea pig red blood cells; it can produce haemolysin, which can rapidly and completely dissolve mammalian red blood cells. Small granular colonies visible to the naked eye appear in semi-solid culture medium.

Figure 1. A longitudinal schematic depicting the cellular architecture of Mycoplasma pneumoniae. (Sources: Parrott GL, et al. 2016)

Since the discovery of Mycoplasma pneumoniae in 1962, scientists have done a lot of research on it and its true appearance has gradually emerged. As we all know, bacteria in general have a typical structure of cell wall, cell membrane and nucleus. But surprisingly, although Mycoplasma pneumoniae is also a bacterium, it does not have the structure of the outermost cell wall. And its cell size is only 0.1-0.2um, which is one six-hundredth of the diameter of a human hair. Because its size is much smaller than that of normal bacteria, it is difficult to observe with a conventional light microscope. When it is examined under an electron microscope, this pathogen is found to have a typical tip-like structure called an "adhesion organelle". Don't underestimate this structure, it is an important weapon for Mycoplasma pneumoniae to cause disease. It uses this suction cup-like tip-like structure to adhere firmly to the surface of the human respiratory tract, and can also slide like an earthworm on the surface of respiratory cells, extracting nutrients from the cells and damaging the respiratory cells, making it difficult to remove, leading to chronic infection. Therefore, Mycoplasma pneumoniae is usually transmitted by "respiratory droplets" after close contact with symptomatic patients. Mycoplasma pneumoniae can cause infection in people of all ages and is a major cause of community-acquired pneumonia in children. Pathogens must grow and multiply in order to continue to grow and spread, and Mycoplasma pneumoniae is no exception. In 1996, researchers completed the sequencing of the genome of Mycoplasma pneumoniae and found that its genome is only one-fifth the size of that of E. coli. In the process of evolution, Mycoplasma pneumoniae has streamlined its genome to the extreme, retaining only the genes needed to maintain basic metabolism. This also means that this small pathogen cannot survive independently outside the body and must live as a parasite on our cells. Scientists have to provide a very nutrient-rich medium to grow it in vitro, which is why Mycoplasma pneumoniae grows extremely slowly in vitro. Normal bacteria can reproduce one generation in 15 minutes, but Mycoplasma pneumoniae can reproduce one generation in 1-6 hours.

Each pathogen has its own 'weapon' to attack. After attaching to human respiratory epithelial cells, Mycoplasma pneumoniae first fuses with the respiratory epithelial cell membrane and damages the cells using its own various hydrolases and nucleases. At the same time, Mycoplasma pneumoniae can produce some toxin proteins or cytokines, such as a community-acquired respiratory distress syndrome toxin called CARDS, which directly damage cells. Due to the late start of Mycoplasma pneumoniae research, there are still many potential pathogenic mechanisms to be explored. As mentioned earlier, Mycoplasma pneumoniae lacks cell wall components, which renders the current therapeutic drugs on the market that target the cell wall, such as beta-lactam antibiotics, ineffective. Therefore, only macrolides, tetracyclines and quinolones can be used for treatment. Laboratory tests can help to determine whether there is a Mycoplasma pneumoniae infection. For bacteria, the culture method is the 'gold standard' for detection and the ability to see colonies on the culture medium is the most direct evidence. However, as mentioned above, the growth rate of Mycoplasma pneumoniae is extremely slow. It usually takes 2-3 weeks or even longer for clinical samples to go from culture to bacterial growth. Therefore, although this method is the gold standard, it cannot be used in clinical testing. Currently, most detection methods for Mycoplasma pneumoniae are serological. This detection method mainly detects antibodies produced after Mycoplasma pneumoniae infection. Because it is simple to use, it can be detected by taking blood from the fingertip. It is currently the main detection method for Mycoplasma pneumoniae.

P1 Adhesin
P1 Protein
P1 Surface Protein
Adhesin P1
P1 Attachment Protein
M. pneumoniae Adhesion Protein P1
M. pneumoniae P1 Major Adhesin