It is one of the smallest self-replicating organisms and its discovery traces back to 1898 when Nocard and Roux isolated a microorganism linked to cattle pneumonia.

This agent was classified as a bacteria due to its cultivation method and because antibiotics were effective in treating the infection, questioning its viral nature.

Pathogenic mechanisms of M. pneumoniae involve host cell adhesion and cytotoxic effects, including cilia loss and hydrogen peroxide release, which lead to respiratory symptoms and complications such as bronchial asthma and chronic obstructive pulmonary disease.

Treatment of M. pneumoniae infections typically involves macrolides or tetracyclines, as these antibiotics inhibit protein synthesis, though resistance has been increasing, particularly in Asia.

This resistance predominantly arises from mutations in the 23S rRNA gene, which interfere with macrolide binding, complicating management and necessitating alternative treatment strategies.

[6][24] Mycoplasmas, which are among the smallest self-replicating organisms, are parasitic species that lack a cell wall and periplasmic space, have reduced genomes, and limited metabolic activity.

The extremely small cell size means they are incapable of being examined by light microscopy; a stereomicroscope is required for viewing the morphology of M. pneumoniae colonies, which are usually less than 100 μm in length.

[6] The inability to synthesize a peptidoglycan cell wall is due to the absence of genes encoding its formation and results in an increased importance in maintenance of osmotic stability to avoid desiccation.

[24] The genome contains 687 genes that encode for proteins, of which about 56.6% code for essential metabolic enzymes; notably those involved in glycolysis and organic acid fermentation.

[6][25][27] These limitations make M. pneumoniae dependent upon import systems to acquire essential building blocks from their host or the environment that cannot be obtained through glycolytic pathways.

[28][29] Since Mycoplasma pneumoniae has a reduced genome, it has a smaller number of overall paths and metabolic enzymes, which contributes to its more linear metabolome.

[28] In summary, the linear topology of Mycoplasma pneumoniae's metabolome leads to reduced efficiency in its metabolic reactions, but still maintains similar levels of metabolite concentrations, cellular energetics, adaptability, and global gene expression.

Mycoplasma pneumoniae, on average, has a high number of reactions per path within its metabolome in comparison to other model bacterial species.

According to Waites and Talkington, specialized reproduction occurs by “binary fission, temporally linked with duplication of its attachment organelle, which migrates to the opposite pole of the cell during replication and before nucleoid separation”.

[6][25] It is composed of a central filament surrounded by an intracytoplasmic space, along with a number of adhesins and structural and accessory proteins localized at the tip of the organelle.

[6] Loss of proteins in the cytoskeleton involved in the localization of P1 in the tip structure, such as HMW1–HMW3, also cause avirulence due to the lack of adhesin clustering.

[25][34] P30 mutants also display distinct morphological features such as multiple lobes and a rounded shape as opposed to elongated, which suggests P30 may interact with the cytoskeleton during formation of the attachment organelle.

Internal localization may produce chronic or latent infections as M. pneumoniae is capable of persisting, synthesizing DNA, and replicating within the host cell even after treatment with antibiotics.

[26] The exact mechanism of intracellular localization is unknown, however the potential for cytoplasmic sequestration within the host explains the difficulty in completely eliminating M. pneumoniae infections in afflicted individuals.

[6] Local damage may also be a result of lactoferrin acquisition and subsequent hydroxyl radical, superoxide anion and peroxide formation.

[6] Secondly, M. pneumoniae produces a unique virulence factor known as Community Acquired Respiratory Distress Syndrome (CARDS) toxin.

Local inflammation and hyperresponsiveness by infection induced cytokine production has been associated with chronic conditions such as bronchial asthma and has also been linked to progression of symptoms in individuals with cystic fibrosis and COPD.

As first choice, azithromycin or clarithromycin are used, as they have more convenient pharmacokinetics than erythromycin : they only need to be taken once or twice and not four times a day and they have fewer side effects.

Alternatively, tetracyclines (eg, doxycycline), and respiratory fluoroquinolones (eg, levofloxacin or moxifloxacin) can be used; they have an undesirable side effect profile in children.

[39] Since routine culture and susceptibility testing is not performed, as M. pneumoniae is difficult to grow, clinicians will select an antibiotic based on an estimate of local resistance, on treatment response and on other factors.[which?