The emergence of methicillin resistance in Staphylococcus aureus is similar to that of penicillin resistance seen in the 1960s.
As indicated in my previous article MRSA Superbug, the emergence of methicillin resistance is similar to the emergence of penicillin resistance in staphylococcus. Staphylococcus aureus, commonly referred to as “staph”, is a common commensal carried on the skin and in the nose. The moist squamous epithelium of the nasal passages provide an optimal environment for Staphylococcus aureus. Approximately 25-30% of the population are colonized with the organism (normally carry), and a further 60% carry Staphylococcus aureus intermittently (transient carriage).
Staphylococcus aureus is one of the most common causes of skin infection in North America, causing pimples, boils and carbuncles and impetigo?. Staph is opportunistic: if the normal barrier defense provided by our skin becomes damaged, staph may take advantage of the situation and cause infection. Cuts, bites, and abrasions provide opportunities for staph to invade and cause infection, and no doubt most of us have had a staph infection at some time in our lives. These minor infections are often treated without antibiotics.
Staphylococcus aureus can also cause more serious invasive infections such as surgical wound infections, abscesses, pneumonia, and septicemia (bloodstream infection). Many hospital-acquired (nosocomial) infections are caused by S. aureus. Whereas healthy individuals have a small risk of invasive infection, hospitalized patients, whose normal defenses may be compromised by illness, invasive surgical procedures, indwelling devices such as intravenous or urinary catheters, and various ventilating devices, have a significantly higher risk of infection. And because antibiotics are heavily used in hospital environments, the risk of acquiring infection from organisms with resistance to antibiotics is also significantly higher. Methicillin-resistant S. aureus is one of these organisms, although there are other antibiotic-resistant organisms that threaten hospitalized patients.
S. aureus has a number of virulence factors (ability to cause disease) that enable it to cause infection:
- Proteins on the organism’s surface promote adherence to damaged tissues, increasing its ability to cause skin and invasive infections.
- Mechanisms to bind proteins in the bloodstream allow it to escape detection and attack by antibodies produced by our immune system.
- Expression of membrane-damaging toxins and superantigen toxins that cause tissue damage and toxic shock symptoms.
The occurrence and severity of infection depends on which particular virulence factors are carried. For instance, one of the toxins produced by some strains of S. aureus - Panton-Valentine leukocidin (PVL) – is toxic to human white blood cells, and strains expressing PVL have been associated with severe skin infections and necrotizing pneumonia, a severe form of pneumonia associated with extensive tissue damage.
Some of the virulence factors of S. aureus are expressed by genes that are located on mobile genetic structures that can be transferred from one organism to another. Factors resulting in antibiotic resistance can also be transferred among strains on mobile genetic elements. The gene coding for methicillin resistance is one of these. Watch for my article on the relationship between staph and MRSA.
