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Mysterious bacteria without cell walls: How does Mycoplasma pneumoniae escape antibiotic attack?
The scientific community continues to study various microorganisms, among which Mycoplasma pneumoniae is undoubtedly a special one. This very small bacterium, which not only lacks a cell wall, can also cause diseases such as pneumonia in humans. Its unique structure makes it naturally resistant to many antibiotics, making treatment complex and challenging. This article will delve into the characteristics of Mycoplasma pneumoniae, its mechanism of infection, and the way it evades antibiotics.
Mycoplasma pneumoniae is one of the smallest known self-replicating organisms and has a unique evolutionary history and biological characteristics.
Discovery and History
The history of Mycoplasma pneumoniae can be traced back to 1898, when scientists Nocard and Roux first isolated a microorganism related to bovine pneumonia. Over the following decades, the microorganism was gradually characterized and its potential as a pathogen revealed. In 1944, Monroe Eaton first cultured the "Eaton agent" thought to cause "walking pneumonia" in fertilized eggs. This discovery laid the foundation for further research in the future. However, it was not until 1961 that the collaborative research of Robert Chanock and Leonard Hayflick determined the true identity of Eaton agent, namely Mycoplasma pneumoniae.
The discovery of this bacterium changed our understanding of pathogens and established Mycoplasma pneumoniae as one of the major causes of pneumonia.
Biological characteristics
The cells of Mycoplasma pneumoniae have a unique shape, with a width of only 0.1–0.2 microns and a length of one to two microns. Due to its extremely small size, its morphology cannot be clearly observed with a traditional optical microscope, and a stereomicroscope is required. The bacterium's cell membrane contains cholesterol and may have an external capsule structure that allows it to attach to host cells during infection. The genome of this bacterium was sequenced in 1996 and found to consist of 687 coding genes that are critical to its metabolic functions. However, due to the simplification of the genome, Mycoplasma pneumoniae is unable to synthesize most essential biomolecules and therefore relies on the host's resources to survive and reproduce.
Infection mechanism
The pathogenesis of Mycoplasma pneumoniae is complex, and it first relies on attachment organs to attach to human respiratory epithelial cells. In order to evade the host's immune system, the bacterium can also survive by changing the composition of its own cell membrane to mimic the host's membrane. This allows M. pneumoniae to survive within host cells, thus evading most antibiotics. The CARDS toxins it produces also play an important role in causing inflammation and respiratory discomfort. After infection, local tissue and cellular structure destruction due to cell adhesion further exacerbates symptoms and can persist for months.
The main cytotoxic effect of Mycoplasma pneumoniae is its ability to attach to host cells, followed by local destruction of the structure.
Antibiotic treatment and resistance
Currently, for the treatment of Mycoplasma pneumoniae, antibiotics that inhibit protein synthesis, such as macrolides or tetracyclines, are usually chosen. However, as time goes by, especially in Asia, antibiotic resistance has become more and more obvious, with a resistance rate of approximately 100%. In the United States, reports show that the drug resistance rate ranges from 3.5% to 13%. Research in the 2020s pointed out that this resistance is mainly derived from a single basic mutation in the 23S rRNA gene, which makes antibiotics unable to bind effectively and brings great difficulties to medical treatment.
Future research directions
The special properties of Mycoplasma pneumoniae have attracted the attention of many scientists, and future research is expected to provide a deeper understanding of its genome, metabolic pathways and pathogenic mechanisms. This knowledge is not only critical for the development of antibiotics, but may also help us develop new treatments to combat resistance. In the future, the medical community should focus on developing new diagnostic and therapeutic methods to address the challenges posed by Mycoplasma pneumoniae. At the same time, with the advancement of science and technology, can we find the golden key to crack this ancient bacteria?
