Skin and soft tissue infections are treated best with local wound care with or without topical antibiotics (e.g., neomycin). Spontaneous or surgical drainage of pus and debride-ment of necrotic tissue is an effective mode for treatment of staphylococcal abscess. Systemic antibiotics are necessary for deep-seated and systemic infections.
◗ Penicillin resistance in staphylococci
Penicillin resistance in the bacteria is increasingly recognized since 1945. Nearly 80% or more strains of S. aureus are resistant to penicillin. It is of three types:
1. Plasmid-mediated resistance: This type of resistance may bedue to the production of enzyme penicillinase (beta-lactamase), which is plasmid mediated. This enzyme inactivates penicillin by splitting the beta-lactam rings. Staphylococci produce four types of penicillinases (A, B, C, and D). Penicillinase plasmids are transmitted to the staphylococci by both transduction and con-jugation. The plasmids also carry markers of resistance to heavy metals, such as arsenic, cadmium, mercury, lead, and bismuth as well as to other antibiotics, such as erythromycin and fusidic acid.
2. Chromosomal-mediated resistance: This type of resis-tance has also been documented. Reduction in the affinity of the penicillin-binding proteins (PBPs; present on the cell wall of the staphylococci) to the beta-lactam antibiotics also con-tributes to the resistance of the bacteria to penicillins and other beta-lactam antibiotics.
3. Tolerance to penicillin: Staphylococci developing toleranceto penicillin are only inhibited but not killed. Penicillin-resistant strains can be treated with beta-lactamase-resistant penicillins, e.g., oxacillin, flucloxacillin, cloxacillin, methicillin, or vancomycin.
◗ Methicillin-resistant staphylococci
Methicillin-resistant S. aureus (MRSA) denotes resistance of S. aureus to penicillin, as well as to all other beta-lactam anti-biotics including the third-generation cephalosporins and car-bapenems. Resistance to methicillin is due to the production of a novel PBP, designated as PBP 2a. PBPs are the targets of beta-lactam antibiotics.
Infections caused by MRSA are being increasingly reported worldwide since 1980. The infection is also being increasingly reported now, from different hospitals. MRSA usually colo-nizes the broken skin and can cause a wide range of local and systemic staphylococcal infections.
Hospital staffs harboring MRSA are the chief source of infection for the patients. These strains can cause a wide range of infections including bacteremia, endocarditis, and pneu-monia. These strains are increasingly recognized as important agents of hospital-acquired infection in hospitalized patients undergoing prosthetic heart valve surgery.
MRSA strains can be treated with glycopeptide antibiot-ics, such as vancomycin and teicoplanin in serious systemic infections, such as pneumonia, bacteremia, and endocarditis. MRSA are sensitive to one or more of the second-line drugs, which include erythromycin, clindamycin, quinolones, fusidic acid, trimethoprim, chloramphenicol, tetracycline, and rifampi-cin. However, ciprofloxacin, rifampicin, and fusidic acid are not used simply because of the possibility of emergence of resistance.
Proper hand-washing and use of topical agents, such as mupirocin and chlorhexidine on skin and nose to eradicate the agents are effective to prevent and control nosocomial infections caused by MRSA.