Mycoplasma is a genus of bacteria responsible for a range of human infections, including respiratory illnesses like “walking pneumonia” (Mycoplasma pneumoniae) and sexually transmitted infections (Mycoplasma genitalium). These organisms are unique because they lack a rigid cell wall structure. This absence presents a significant challenge to treatment, as many standard antibiotics are designed to target and disrupt this bacterial component. Successfully eliminating a Mycoplasma infection requires a specialized approach that bypasses this intrinsic resistance and targets the organism’s internal machinery.
Why Mycoplasma Requires Specialized Treatment
The primary reason Mycoplasma infections require non-standard drug protocols is their distinct cellular anatomy. Unlike most other bacteria, Mycoplasma species do not possess a cell wall made of peptidoglycan, which provides rigidity and protection. This characteristic is an innate feature of the entire class of bacteria known as Mollicutes.
The absence of this structure makes the large and widely used class of beta-lactam antibiotics completely ineffective against Mycoplasma. Antibiotics such as penicillin and cephalosporins work by interfering with cell wall synthesis. Since Mycoplasma lacks this target, these drugs cannot kill the organism.
Because the bacteria exist without a protective cell wall, they rely on a tough cell membrane that incorporates sterols. This unique structural feature is a key factor in their survival. As a result, treatment must focus on processes common to all living cells, such as the mechanisms of protein and DNA replication.
Antibiotic Strategies for Human Infections
Effective treatment strategies for Mycoplasma infections focus on antibiotic classes that interfere with the bacteria’s internal metabolic processes. These drugs must successfully penetrate the bacterial cell membrane to inhibit functions like protein synthesis or DNA replication. The choice of antibiotic depends on the specific species of Mycoplasma, the site of infection, patient age, and potential drug interactions.
Macrolides are frequently the first-line treatment, especially for respiratory infections caused by M. pneumoniae. They include drugs such as azithromycin and clarithromycin. These antibiotics work by binding to the 50S subunit of the bacterial ribosome, which blocks protein synthesis and prevents the bacteria from multiplying. Azithromycin is favored for its convenient dosing regimen and ability to reach high concentrations in the lungs.
Tetracyclines, particularly doxycycline, represent another effective class used for Mycoplasma infections in adults. Doxycycline interferes with protein production by reversibly binding to the 30S ribosomal subunit. This class is often used as a primary alternative to macrolides, especially in cases of macrolide resistance, but is generally avoided in young children due to potential effects on bone and tooth development.
Fluoroquinolones, such as levofloxacin and moxifloxacin, are also highly active against Mycoplasma species. These agents work by inhibiting bacterial DNA gyrase and topoisomerase IV, two enzymes critical for DNA replication and transcription. Fluoroquinolones are typically considered second-line agents due to concerns about potential side effects, and they are generally contraindicated for use in children.
Managing Drug Resistance and Persistent Cases
A significant challenge in treating Mycoplasma infections is the growing prevalence of antibiotic resistance, which can lead to persistent infection or treatment failure. Resistance to macrolides, particularly in M. pneumoniae and M. genitalium, has become a widespread concern globally. This resistance is driven by point mutations in the 23S ribosomal RNA gene, which prevents macrolide drugs from binding effectively to the ribosome.
When a patient fails to improve within 48 to 72 hours of starting macrolide therapy, a persistent infection or macrolide-resistant strain is often suspected. In these instances, clinicians will frequently switch to a second-line agent, such as a tetracycline or a fluoroquinolone, if appropriate for the patient. For macrolide-resistant M. pneumoniae in children, where tetracyclines and fluoroquinolones are restricted, the treatment decision can be complex and may involve extended courses of alternative drugs.
Diagnostic testing is increasingly important for managing resistance, moving beyond initial diagnosis to confirm the eradication of the pathogen or to determine the specific resistance pattern. Molecular tests can detect the mutations associated with macrolide resistance, allowing for a targeted switch to a different class of antibiotic without delay. In some difficult-to-treat cases, particularly those involving M. genitalium, an extended duration of treatment or a sequential combination therapy may be necessary to achieve a complete cure.
Reducing Transmission and Reinfection
Preventing the spread of Mycoplasma involves targeted public health and hygiene measures that address the different routes of transmission for each species. For M. pneumoniae, which causes respiratory infections, simple hygiene practices are a primary defense against infection. This includes regular handwashing, covering coughs and sneezes, and avoiding close contact with individuals who are actively symptomatic.
To prevent reinfection and transmission of sexually transmitted species like M. genitalium, safe sexual practices are necessary. Consistent and correct use of barrier methods, such as condoms, significantly reduces the risk of transmission. After successful treatment, patients should abstain from sexual activity until they and their partners have completed the full course of antibiotics and received a test of cure to confirm the pathogen has been eliminated.