Antiinfectives Flashcards
Selective Toxicity
Ability of a drug to injure invading microbes without injuing the cells of the host
Narrow-spectrum Vs. Broad Spectrum
Narrow-spectrum are active against only a few microorganisms.
Broad-spectrum antibiotics are active against a wide array of microbes.
Bactericidal vs Bacteriostatic
Bactericidal drugs kill bacteria
Bacteriostatic drugs only suppress growth
Mechanisms of Resistance
Drug efflux
Altered drug targets
Enzymatic inactivation of drugs
NDM-1 gene
Bacteria with NDM-1 gene are resistant to nearly all available antibiotics
Conjugation
A process in which DNA coding for drug resistance is transferred from one bacterium to another. An important method by which bacteria acquire resistance.
Relationship between antibiotic use and the emergence of drug-resistant microbes
Antibiotics do not cause the genetic changes that underlie resistance. Antibiotics PROMOTE the emergence of drug-resistant organisms by creating selection pressures that favor them.
Broad-spectrum antibiotics promote the emergence of resistance more often than do narrow-spectrum antibiotics.
4 ways to delay the emergence of resistance
1) preventing infections
2) diagnosing and treating infection effectively
3) using antimicrobial drugs wisely
4) preventing patient-to-patient transmission
Major force promoting the emergence of resistance
The food we eat.
Use of antibiotics in livestock.
Minimum inhibitory concentration
Minimum bactericidal concentraion
MIC- The lowest concentration needed to completely suppress bacterial growth. (Less than or equal to 4, lower is better).
MBC0 concentration that reduces the number of bacterial colonies by 99.9%.
Host defenses
Essential to the success of antimicrobial therapy.
Ex) immune system, phagocytic cells
Why do patients need to complete the entire prescribed course of antibiotics?
Symptoms may abate, but reoccurrence can occur.
When do we combine antibiotics?
1) Initial treatment of severe infection
2) Infection with more than one organism
3) treatment of TB
4) Treatment of an infection in which combination therapy can greatly enhance antibacterial effects.
Appropriate use of prophylactic antibiotics
1) Certain surgeries
2) Neutropenia
3) Recurrent UTIs
4) Pts at risk of bacterial endocarditis
Monitoring Antimicrobial Therapy
Clinical response- Frequency of monitoring is directly proportional to the severity of infection.
Reduction of fever, resolution of symptoms.
Lab Results- Drug levels to ensure levels are sufficient but not toxic. Peak and trough.
Success of therapy indicated by the disappearance of infectious organisms from posttreatment cultures. Cultures can become sterile within hours of treatment (UTI) or may take weeks (TB).
Penicillins
Weaken bacterial cell wall, causing cell lysis and death.
Gram-negative bacteria are resistant to penicillins that cannot penetrate the gram-negative cell envelope.
Safest antibiotic available.
Do not combine with aminoglycosides (gentamicin) in the same IV solution.
Beta-lactamases
Enzymes that inactivate penicillins.
Principal Adverse Effect of Penicillins
Allergic reaction- rash to anapylaxis
If patient is allergic to one penicillin they should be considered cross-allergic to all other penicillins. 1% chance of cross-allergy to cephalosporins.
Vancomycin, erythromycin, and clindamycin are safe and effective alternatives to penicillins.
Penicillin metabolism
Eliminated rapidly by the kidneys but can accumulate to harmful levels if renal function is severely impaired.
Penicillin G
Narrow antibacterial spectrum
Unstable in the stomach
Benzathine Penicillin G
Released very slowly after IM injection and thus produces prolonged antibacterial effects.