Doxycycline inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit, preventing the addition of amino acids to the growing polypeptide chain. This leads to the disruption of bacterial protein synthesis and ultimately, bacterial cell death.
Its antibacterial spectrum is broad, covering Gram-positive and Gram-negative bacteria, as well as some atypical organisms. Specifically, it’s effective against Chlamydia, Rickettsia, Mycoplasma, and certain strains of Borrelia. However, Pseudomonas aeruginosa typically exhibits resistance to doxycycline.
While doxycycline demonstrates activity against some Pseudomonas species under specific conditions in vitro, its clinical use against Pseudomonas aeruginosa infections is generally not recommended due to high rates of resistance. Alternative antibiotics are usually preferred for treating Pseudomonas infections.
Resistance mechanisms in Pseudomonas aeruginosa include efflux pumps and ribosomal protection proteins that decrease doxycycline’s binding affinity and intracellular concentration. These factors contribute to the limited clinical efficacy of doxycycline against this pathogen.
