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Delftia acidovorans is a Gram-negative, non-fermenting aerobic bacillus that belongs to the Comamonadaceae family, previously classified under the genera Pseudomonas and Comamonas (1, 6). While it is primarily an environmental saprophyte found in soil and water, it has emerged as an opportunistic human pathogen capable of causing serious infections such as bacteremia, infective endocarditis, and pneumonia, particularly in immunocompromised individuals or those with indwelling medical devices (2, 4). A unique biological feature of this organism is its ability to biomineralize gold; it secretes the non-ribosomal peptide delftibactin, which protects the bacterium by precipitating toxic gold ions into harmless metallic gold nuggets (6, 13). Clinically, D. acidovorans is notable for its intrinsic resistance to aminoglycosides, which complicates empirical treatment strategies for Gram-negative infections (2, 8). Effective therapeutic options generally include carbapenems, piperacillin-tazobactam, and trimethoprim-sulfamethoxazole, though susceptibility can vary among clinical isolates (1, 3, 15). (1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214660/ (2) https://pubmed.ncbi.nlm.nih.gov/22130722/ (3) https://microbiologyopen.onlinelibrary.wiley.com/doi/full/10.1002/mbo3.1311 (4) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4629471/ (6) https://en.wikipedia.org/wiki/Delftia_acidovorans (8) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11444101/ (13) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253457/ (15) https://pubmed.ncbi.nlm.nih.gov/35835222/
Antibacterial agents targeting this organism act through various mechanisms: inhibition of bacterial cell wall synthesis (beta-lactams), inhibition of protein synthesis (tigecycline), inhibition of folate metabolism (trimethoprim-sulfamethoxazole), or inhibition of DNA gyrase/topoisomerase (fluoroquinolones) (1, 2, 8).
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