Question

Which antibiotic is active against some strains of vancomycin-resistant E. faecium? (A) azithromycin (B) doxycycline (C) chloramphenicol (D) clindamycin (E) quinupristin-dalfopristin

Short answer

Quinupristin-dalfopristin is active against some strains of vancomycin-resistant E. faecium.

Step-by-step solution

Understanding the Problem

We need to identify which antibiotic is effective against some strains of vancomycin-resistant Enterococcus faecium (VRE). VRE is a type of bacteria that has developed resistance to vancomycin, and we must choose an antibiotic that can combat this resistant strain.

Options Evaluation

Let's evaluate each of the given antibiotics: - **Azithromycin, Doxycycline, and Clindamycin**: These antibiotics are not typically effective against VRE due to the different mechanisms of resistance and action they exhibit. - **Chloramphenicol**: While chloramphenicol has a broad spectrum of activity, its effectiveness against VRE is limited and not reliable. - **Quinupristin-dalfopristin**: This is an antibiotic known to be effective against some strains of VRE, particularly when the strain is resistant to vancomycin but susceptible to quinupristin-dalfopristin.

Conclusion

After evaluating the options, the antibiotic quinupristin-dalfopristin is recognized as active against some strains of vancomycin-resistant Enterococcus faecium. This antibiotic combination can inhibit bacterial growth in strains resistant to other treatments.

Key concepts

vancomycin-resistant Enterococcus faecium

Vancomycin-resistant Enterococcus faecium (VRE) is a type of bacteria that poses a significant challenge in the healthcare setting due to its resistance to vancomycin, which is often used as a last-resort antibiotic. This resistant strain has emerged as a major concern, particularly in hospitals, because it can lead to severe infections that are difficult to treat. Resistance in VRE is primarily due to genetic mutations that alter the target site of the antibiotic, making it ineffective.
VRE can cause various infections, such as urinary tract infections, bloodstream infections, and wound infections, which require careful management. Treating infections caused by VRE is complicated because the options for effective antibiotics are limited. Therefore, it is critical to identify antibiotics that can still target these resistant strains, ensuring they are used appropriately to limit further resistance.

quinupristin-dalfopristin

Quinupristin-dalfopristin is a combination of two antibiotics that work together to combat bacterial infections, including those caused by some strains of vancomycin-resistant Enterococcus faecium. This antibiotic duo is part of a group known as streptogramins, which are designed to inhibit bacterial protein synthesis.
Quinupristin and dalfopristin each have distinct but complementary actions. Dalfopristin binds to a specific part of the bacterial ribosome, which enhances the binding of quinupristin and results in a potent synergistic effect. This dual-action maximizes the efficacy against bacteria that may have developed resistance to other antibiotics. Users must be aware that while effective, quinupristin-dalfopristin is not a first-line treatment and is typically reserved for cases where other antibiotics fail, keeping the focus on managing antibiotic resistance efficiently.

antibiotic mechanisms

Understanding how antibiotics work is crucial in dealing with resistant strains like vancomycin-resistant Enterococcus faecium. Most antibiotics can be grouped based on their mechanisms of action, which include:

• Inhibiting cell wall synthesis, which is the basis for the function of beta-lactams like penicillin.
• Disrupting protein synthesis, a strategy employed by antibiotics like quinupristin-dalfopristin and macrolides.
• Altering nucleic acid synthesis, as done by fluoroquinolones.
• Interfering with metabolic pathways, a method used by sulfonamides.

Each mechanism targets a vital part of bacterial growth or replication, although bacterial resistance can occur through genetic mutations or acquiring resistance genes from other bacteria. Ensuring the correct use of antibiotics based on these mechanisms is key not only to treat infections effectively but also to prevent the development and spread of antibiotic-resistant bacteria.