# Wound Dressing Materials: Bridging Material Science and Clinical Practice
## 4 Antimicrobial Dressings
### Antibiotics in Wound Dressings  
Antibiotics from various classes, such as aminoglycos, beta-lactams, glycopeptides, quinolones, sulfonamides, and tetracyclines, have been incorporated into wound dressings [88]. Antibiotics can be classified into various classes, each with a distinct mechanism of action that targets specific aspects of bacterial cell function. Beta-lactams and glycopeptides are two prominent classes that interfere with bacterial cell wall synthesis. Beta-lactams, such as penicillin and cephalospor, inhibit the enzymes responsible for cross-linking the peptidoglycan chains in the bacterial cell wall, leading to weakened cell walls and cell lysis. Similarly, glycopeptides like vancomycin bind directly to the peptidoglycan precursors, preventing their incorporation into the cell wall. Both mechanisms ultimately compromise the structural integrity of the bacterial cell wall, causing the bacterium to rupture under osmotic pressure. Another important class of antibiotics includes aminoglycosoides and tetracyclines, which inhibit protein synthesis in bacteria. Aminoglycos, such as gentamicin, bind to the bacterial 30S ribosomal subunit, disrupting the initiation of protein synthesis and causing misreading of mRNA. This results in the production of faulty proteins that cannot function properly, ultimately leading to bacterial cell death. On the other hand, tetracyclines, like doxycycline, bind to the 30S ribosomal subunit as well, but they prevent the attachment of aminoacyl-tRNA to the ribosome, inhibiting the elongation of protein chains. By blocking protein production, these antibiotics effectively prevent bacterial growth and proliferation. Sulfonamides and quinolones target other critical processes in bacterial cells. Sulfonamides, including drugs like sulfamethoxazole, act as competitive inhibitors of dihydropyoate synthase, an enzyme involved in the synthesis of folic acid, which is necessary for nucleic acid synthesis. By inhibiting this enzyme, sulfonamides block the formation of purines and pyrimidines, essential components for DNA and RNA synthesis, thereby preventing bacterial replication. In contrast, quinolones, such as ciprofloxacin, interfere with DNA replication and transcription by inhibiting bacterial DNA gyrase and topoisomerase IV, enzymes responsible for supercoiling and uncoiling DNA. This disruption prevents the bacteria from replicating their DNA and transcribing RNA, leading to bacterial cell death. Each of these antibiotic classes exploits specific vulnerabilities in bacterial metabolism to inhibit growth and combat infections [88]. Specific antibiotics are used based on their effectiveness against certain bacteria. For example, muiprocin is particularly effective against Gram-positive bacteria, including MRSA, while metronidazolezole targets anaerobic bacteria [89]. However, improper or prolonged use of broad-spectrum antibiotic dressings can promote the development of multidrug-resistant bacteria [90]. Studies indicate that more than 70% of bacteria causing wound infections are resistant to at least one commonly used antibiotic [88]. Additionally, the rise of _Staphylococcus aureus_ strains resistant to muiprocin has reduced its efficacy, even though it remains the only approved antibiotic for MRSA decolonization [91]. To optimize treatment, selecting the appropriate antibiotic based on culture and sensitivity testing is essential. Surface swab cultures often have limited reliability due to the presence of transient bacteria on the wound and skin.