Antibacterial Drugs General Terminology Mindy Valenti Resistance Bacterial growth continues despite use of antibacterials. Natural or inherent resistance: no prior exposure to the antibacterial drug being used. Acquired resistance: prior exposure to the antibacterial drug being used causes the bacteria to evolve and become resilient. Bacteria evolve as minor mutations occur. Eventually the bacteria to become resistant to antibiotics that normally killed them. The bacteria can produce an enzyme which will destroy an antibiotic. The bacterial cell wall receptor binding sites can modify so the antibiotic no longer recognizes the cell. The bacterial cell wall can evolve to inhibit the action of the antibiotic even if it reaches the binding sites. The bacteria can adapt to push out antibiotic that reaches the cell through efflux resistance, preventing adequate MEC. Bacteria are able to transmit genetic material to other species of bacteria causing them to become resistant. Methicillin-resistant-staphylococcus aureus (MRSA) is bacteria resistant to methicillin, penicillin, and cephalosporins. Vancomycin (Vancocin) is most often used as treatment. Vancomycin-resistant enterococci faecium (VREF) is on the rise and may cause death in immunocompromised clients. Linezolid (Zyvox) can be used for treatment. Antibacterials/Antimicrobials and Antibiotics Antibacterials and antimicrobials inhibit the growth of or kill bacteria. Antibiotics are substances produced by a particular type of microorganism that inhibit growth of or kill a different microorganism. Bacteriostatic: inhibit bacterial growth. Bactericidal: kill bacteria. Natural or manufactured substances work with normal body defenses and medical procedures to treat infections. Pharmacokinetics and Pharmacodynamics Antibiotics have high affinity to bacterial cell wall binding sites. Absorption, distribution, metabolism, and excretion will over all determine how long an antibiotic is bound to the bacterial cell wall receptor sites. The longer the half-life the longer the drug remains on the binding sites. This means less frequent dosing. Minimum effective concentration (MEC) is needed for an antibacterial to be effective. Antibiotic dosing intervals depends on pathogen type, location of the infection, severity of the infection, and immunocompetence of the client. Peak and trough levels may be require in drugs with a narrow therapeutic index. Mechanism of Action The antibacterial prevents cell wall synthesis of the bacteria by enzyme breakdown. Cell wall damage will cause the cell to fill with water eventually rupturing, which kills the bacterial cell. Inhibition of enzyme synthesis causes the bacterial cell membrane to become more permeable causing loss of cellular substance and cell lysis. Protein synthesis is inhibited in the bacteria without affecting normal cells. Protein production is needed for cell structure and enzyme action in order for the bacteria to survive. The antibacterial binds with nucleic acid and enzymes required for nucleic acid synthesis to stop the formation of ribonucleic acid (RNA) and deoxyribonucleic acid (DNA). The antibiotic then interferes with steps of cell metabolism. Nursing Implications Ensure C & S samples are obtained properly and timely before antibiotics are started. Assess patient for effectiveness of treatment. Ensure peak and trough levels are drawn at correct time intervals. Teach clients to take antibiotic until it is completely gone. Encourage the client to increase fluid intake. Preventing further resistance New drugs are being developed that will disable the antibiotic resistant action in the bacteria when taken with an antibiotic. Bacterial vaccinations. Studies have revealed inappropriate use of antibiotics in 50% of hospitalized clients. Frequent and improper use of antibiotics can cause resistance to occur more rapidly. Cross-resistance: Resistance that occurs in antibiotics with similar properties of action. Culture and sensitivity (C & S) testing is done to identify the infecting bacteria and which antibiotic will be best to kill it. Broad-spectrum antibiotics are effective against gram-positive and gram- negative bacteria. Narrow-spectrum antibiotics are effective against a specific type of bacteria. References Aziz, A. (2013). The role of healthcare strategies in controlling antibiotic resistance. British Journal Of Nursing, 22(18), 1066-1074. Kaufman, G. (2011). Antibiotics: mode of action and mechanisms of resistance. Nursing Standard, 25(42), 49-55. Kee, J.L., Hayes, E.R., & McCuistion, L.E. (2012). Pharmacology: A nursing process approach. St. Louis: Elsevier Saunders. Body Defenses Client age, immunoglobulins, white blood cells (WBCs), nutrition, organ function, and circulation will affect the body’s ability to combat infection.