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Mycoplasma synoviae is a wall-less, Gram-negative bacterium of the class Mollicutes that serves as a significant pathogen in commercial poultry, causing infectious synovitis and chronic respiratory disease [1, 9, 16]. It is characterized by its lack of a cell wall and a reduced genome, which necessitates a parasitic lifestyle and confers intrinsic resistance to beta-lactam antibiotics [7, 8]. The bacterium utilizes specialized surface proteins, such as the variable lipoprotein and haemagglutinin (VlhA), to adhere to host respiratory and synovial epithelia, facilitating colonization and immune evasion [10, 13, 14]. Clinically, infection leads to lameness, swollen joints, and decreased egg production, resulting in substantial economic impact [1, 16, 17]. Therapeutic intervention typically involves the administration of macrolides, tetracyclines, or pleuromutilins, which target the bacterial ribosome to inhibit protein synthesis [8, 17]. While antibiotics can manage clinical symptoms, they often fail to eradicate the pathogen, leading to persistent carrier states and the risk of vertical transmission to progeny [7, 17]. As this entry refers to a whole organism rather than a specific molecule or receptor, it is classified as an incorrect molecular target in this context.
Antibiotics targeting Mycoplasma synoviae primarily act by inhibiting bacterial protein synthesis through binding to the 30S or 50S ribosomal subunits (e.g., tetracyclines, macrolides, pleuromutilins) or by inhibiting DNA replication through the targeting of DNA gyrase (e.g., fluoroquinolones) [8, 17].
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