Resistant 'Superbugs' Create Need for Novel Antibiotics

Teri Capriotti, DO, MSN, CRNP

Disclosures

Dermatology Nursing. 2007;19(1):65-70. 

In This Article

A wide number of "smart" bacteria in the environment have "learned" how to resist the arsenal of antibiotics. Decades of overuse and misuse of antibiotics have caused this crisis: overzealous antibiotic prescribing by clinicians, excess use of antibacterial household products by the public, and widespread use of antibiotics in livestock. Antibiotics are ubiquitous within the environment. Bacteria are highly adaptable organisms which have an extraordinary ability to mutate in response to their environmental conditions. The widespread use of antibiotics has provided the conditions needed for bacteria to mutate genetically and develop resistance to these drugs.

How Bacteria Become ‘Superbugs'

Each time a new antibiotic is introduced and used widely, a small number of bacterial organisms decipher how to resist the drug's bactericidal effects. The bacteria that survive the effects of antibiotics are the most adaptable organisms which develop genome mutations or resistance genes. These genetically changed bacteria multiply to produce a population of antibiotic-resistant organisms. The resistant bacteria also can transfer their newly acquired resistance genes to other species of bacteria through the process of conjugation (a reproductive interaction). As bacteria reproduce and transfer resistance to other bacterial species, new strains develop which can resist the effects of existing antibiotics. Lethal and contagious, these antibiotic-resistant organisms have been termed superbugs. Staphylococci, enterococci, and pneumococci have proven the ability to develop superbug status (Rybak, 2004).

Methicillin-resistant staphylococcus aureus (MRSA) is probably the best known superbug. First observed in 1960, MRSA continued to increase slowly in the bacterial population, until clinicians realized its significant virulence in the 1980s-1990s. MRSA was once eradicated reliably by vancomycin (VancocinAE), an antibiotic of the glycopeptide class. With time, the MRSA bacteria became resistant to vancomycin and vancomycin-resistant staphylococcus aureus (VRSA) soon arose.

To add to the challenge, MRSA infection, once confined to clinical settings as a nosocomial problem, recently became a community-acquired infection. Its spread into the population at large has required a dual classification for MRSA infection: either community-associated MRSA (CA-MRSA) or health care-associated MRSA (HA-MRSA). CA-MRSA infection has involved the skin and soft tissue most commonly, with cases increasing worldwide. However, a specific strain of CA-MRSA has been the cause of a severe necrotizing pneumonia in otherwise healthy individuals. This virulent strain of MRSA has been under intense investigation since the first cases were diagnosed in 2002 (Francis et al., 2004).

The increasing incidence of community-acquired MRSA infection has created an urgent need for antibiotics with unique mechanisms of action. Most of the current available antibiotics are chemical modifications of existing agents with similar mechanisms. According to a study of emergency room patients in the Los Angeles area, skin and soft tissue infections caused by CA-MRSA have increased in incidence from 29% in 2001 to 64% in 2004 (Moran, Amii, Abrahamian, & Talan, 2005). Although nosocomial MRSA infections have been challenging clinicians since the early 1990s, CA-MRSA infection is a more ominous threat to the population as a whole and is increasing rapidly in incidence.

In 2003, 60% of infections due to S. aureus in intensive care patients were resistant to methicillin (National Nosocomial In fections Surveillance, 2004). HA-MRSA frequently causes bacteremia, sepsis, or pneumonia in clinical settings. HA-MRSA has been responsible for surgical site and wound infection, ventilator-associated pneumonia, and central line bacteremia.

In addition, MRSA has been successful in transmitting resistance genes to a completely different species of bacteria, enterococcus faecalis. MRSA has transmitted its gene for vancomycin resistance to enterococcus. This has led to the strain identified as vancomycin-resistant enterococcus (VRE) or glycopeptide-resistant enterococcus (GRE). VRE has created its own set of treatment challenges for clinicians (Pfeltz & Wilkinson, 2004).

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