Methicillin Resistant Staphylococcus Aureus (MRSA)

Full Answer Section

1. Beta-lactam antibiotics (including methicillin) typically inhibit bacterial cell wall synthesis by binding to PBPs.
2. MRSA's mecA protein produces altered PBPs that don't bind to beta-lactam antibiotics, rendering these drugs ineffective against MRSA.

Immune Response:

The human immune system attempts to combat MRSA infection through several mechanisms:

• Phagocytosis: White blood cells engulf and destroy MRSA bacteria. However, protein A can impede this process.
• Antibody-mediated immunity: Antibodies target MRSA, but protein A can interfere with their effectiveness.
• Inflammatory response: Immune cells release inflammatory mediators to isolate and destroy the infection. However, excessive inflammation can damage tissues.

Laboratory Differentiation:

Several laboratory methods can distinguish MRSA from MSSA:

• Oxacillin or cefoxitin disk diffusion test: Antibiotic disks are placed on a culture plate with the bacteria. If the bacteria are susceptible, a clear zone of inhibition (no growth) will surround the disk. MRSA will show no zone of inhibition around the oxacillin or cefoxitin disk.
• Methicillin resistance testing via broth microdilution: This method determines the minimum inhibitory concentration (MIC) of antibiotics needed to inhibit bacterial growth. Higher MICs for methicillin indicate MRSA.
• PCR (polymerase chain reaction) test: This rapid test detects the presence of the mecA gene, confirming MRSA.

Genetic Diversity and Hospital-Acquired Infections:

MRSA strains can acquire new genetic material through horizontal gene transfer (plasmids or bacteriophages), leading to diversity. This diversity allows MRSA to adapt to different environments and develop resistance to additional antibiotics.

Hospital-Acquired MRSA (HA-MRSA):

• Risk Factors: Overuse and misuse of antibiotics in hospitals create a selective pressure, favoring the survival and spread of resistant strains like MRSA. Additionally, factors like catheter use and crowded hospitals can facilitate transmission.
• Risks: HA-MRSA infections are often more severe and challenging to treat due to their multidrug resistance. Increased morbidity, mortality, and healthcare costs are associated with HA-MRSA outbreaks.

Conclusion:

MRSA poses a significant threat due to its virulence factors, antimicrobial resistance, and ability to evolve genetically diverse strains. Continuous surveillance, infection control practices, judicious antibiotic use, and development of new antibiotics are crucial to combat the growing challenge of MRSA, particularly in hospital settings.

Sample Answer

Structure and Virulence:

MRSA, a gram-positive bacterium, shares the same basic structure as Staphylococcus aureus (SA) but harbors additional virulence factors that enhance its ability to cause disease in humans. These factors include:

• Cell wall: Thick peptidoglycan layer provides rigidity and protection against the immune system.
• Protein A: Binds to Fc receptors on immune cells, hindering phagocytosis and antibody-mediated immunity.
• Capsule: Polysaccharide layer helps evade phagocytosis.
• Toxins: Hemolysins lyse red blood cells, while other toxins damage tissues and promote inflammation.

Antimicrobial Resistance Mechanism:

The key factor differentiating MRSA from MSSA is the presence of the mecA gene. This gene encodes an enzyme (mecA protein) that produces penicillin-binding proteins (PBPs) with a low affinity for beta-lactam antibiotics like methicillin. Here's how it works: