Taxonomy and morphological features
Mycoplasmas belong to the class Mollicutes (soft-skinned) of the phylum Tenericutes. This is a vast group including 4 families, 6 genera, and about 150 species of microorganisms, of which 15 species are isolated from humans. Key human pathogens belong to the genera Mycoplasma and Ureaplasma.
Their main anatomical feature is the complete absence of a cell wall. The cell is covered exclusively by a cytoplasmic membrane, which contains sterols to compensate for strength. Sometimes a microcapsule is found externally. Due to the lack of a rigid framework, these bacteria are characterized by high osmotic sensitivity and extreme polymorphism (pleomorphism). In smears, they may appear as filamentous, flask-shaped, or coccoid forms.
Externally, mycoplasmas morphologically resemble L-forms of bacteria when examined under a phase-contrast microscope. They do not form spores, are Gram-negative (stain negatively), and are easily filtered through bacterial filters.
Cultural properties and biochemical activity
By type of respiration, mycoplasmas are facultative anaerobes with an optimal temperature of 37 °C. These are extremely "fastidious" microorganisms: for growth, they require complex media based on heart, brain, serum, and yeast extracts.
An obligatory component of the nutrient medium is cholesterol, which mycoplasmas need to build their own membrane. Urea is additionally required for the cultivation of ureaplasmas. Alternative methods of cultivation include chicken embryos and cell cultures.
Mycoplasmas grow slowly — from 49 to 96 hours.
- On solid media, they form small "fried egg"-like colonies: their opaque center grows deeply into the agar, while the periphery remains round and translucent.
- In liquid media, growth often occurs without visible turbidity, so it is detected either by subculturing or by sediment microscopy.
Biochemical activity in the group is low. Most utilize glucose with acid production. A differential feature of the genus Ureaplasma is the presence of urease — they utilize urea. Mycoplasma growth is inhibited by specific immune sera.
Pathogenicity factors and mechanism of infection
Pathogenic forms of mycoplasmas are most often flask-shaped or filamentous. A specific terminal structure, critical for virulence, is located at the cell pole. It consists of a complex of adhesin proteins and auxiliary (accessory) proteins. Accessory proteins are rich in proline, which ensures proper folding of adhesins.
Mechanism of host cell damage:
- Attachment (adhesion) to species-specific glycolipid receptors on the human cell membrane.
- The bacterium begins to produce hydrogen peroxide ($H_2O_2$), peroxide radicals, and hemolysins.
- Damage to the host membrane occurs, followed by closer fusion of the microbial and host cell membranes.
- As a result, the metabolism of the infected cell is disrupted, and the defensive function of the ciliated epithelium is suppressed.
Ecology, resistance, and clinical significance
The antigenic structure of mycoplasmas is represented by species-specific glycolipid and protein antigens. In the environment, bacteria demonstrate relatively high resistance, often inhabiting soil and standing water. However, they are sensitive to disinfectants and antiseptics at standard concentrations.
Many species are part of the normal human microflora. For example, M. salivarium and M. orale colonize the oral cavity, while M. hominis and U. urealyticum are detected in the urogenital system (including in 30–70% of healthy women and 40–80% of sexually active people).
Main diseases caused by mycoplasmas (anthroponotic infections):
- Respiratory mycoplasmosis: pathogen M. pneumoniae (atypical pneumonia).
- Urogenital infections: pathogens M. hominis, M. genitalium, U. urealyticum.
- Neonatal pathology: premature infants are especially susceptible (more often infected with M. hominis and U. urealyticum).
Only short-lived immunity is formed after the infection.
Briefly: answers to topical questions
Which antibiotic groups are used to treat mycoplasma infections, given their natural resistance to beta-lactams?
Antibiotics that act intracellularly or disrupt protein and DNA synthesis are used to treat mycoplasma infections.
- Macrolides are first-line drugs (azithromycin, clarithromycin, erythromycin).
- Tetracyclines are alternative drugs (doxycycline), effective due to intracellular penetration.
- Fluoroquinolones are alternative agents (ofloxacin, ciprofloxacin).
- Lincosamides are used for etiotropic therapy in pregnant women.
What is the peculiarity of the antigenic structure of mycoplasmas, and what autoimmune reactions (cross-reactivity) can it cause?
The antigenic structure of mycoplasmas is represented by species-specific glycolipid and protein antigens. As triggers of autoimmune reactions, mycoplasmas are capable of causing nonspecific polyclonal stimulation of B-lymphocytes. This leads to the activation of polyclonal lymphocytes by infectious agents, which serves as one of the mechanisms for breaking autoimmune tolerance and may provoke the development of autoimmune diseases.
What laboratory diagnostic methods are used to detect mycoplasmoses in modern practice?
Bacteriological, immunological, and molecular-genetic methods are used to detect mycoplasmoses.
- Bacteriological method — inoculation of material first into liquid media, followed by subculturing onto solid media or using biphasic media.
- Rapid diagnostics — direct immunofluorescence assay (DFA) for direct antigen detection.
- Molecular-genetic methods — PCR and DNA hybridization to confirm the diagnosis.
The mycoplasma class is named Mollicutes, derived from the Latin mollis (soft) and cutis (skin). Remember: they have "soft skin" because they completely lack a rigid cell wall. This explains both their pleomorphism (shape shifting) and resistance to antibiotics acting on the cell wall.
Class and exam questions
Why is it useless to prescribe penicillins or cephalosporins for mycoplasma infections?
These antibiotics work by destroying the bacterial cell wall. Since mycoplasmas genetically lack one, they exhibit natural (absolute) resistance to drugs of this group.
Why is cholesterol added to nutrient media for mycoplasmas?
Cholesterol is vital for mycoplasmas because they incorporate it into their cytoplasmic membrane to ensure its strength and compensate for the absent cell wall.
How to detect mycoplasma growth in a liquid nutrient medium?
Since mycoplasmas multiply in liquid media without visible turbidity, their growth is confirmed either by sediment microscopy after centrifugation or by subculturing onto solid media (looking for "fried egg" colonies).
What else to study on this topic
- Cytotoxic and cytolytic effect of mycoplasma peroxide radicals on the host cell
- Mechanisms of long-term persistence of "membrane parasites" in the body
- The role of proline-rich accessory proteins in adhesin folding
- Alternative cultivation methods (chicken embryos and cell cultures)
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