1. 
   

   What are the most frequent types of antibiotic resistance?

   
   
2. 
   

   Which patients are at risk for infections with antibiotic-resistant organisms?

   
   
3. 
   

   How are antibiotic-resistant organisms transmitted among patients?

   
   
4. 
   

   What types of genes confer antibiotic resistance?

   
   
5. 
   

   What types of isolation precautions exist, and when are they indicated?

Antibiotic resistance was described at the dawn of the antibiotic era. In Alexander Fleming’s initial report of the antibacterial action of penicillin in 1929, he noted that it was usually inactive against enteric Gram-negative bacteria. In 1940, while engaged in isolating and purifying penicillin, Edward Abraham and Ernst Chain incidentally discovered that Escherichia coli produced penicillinase. While the global explosion and dissemination of antibiotic resistance in recent decades is alarming, perhaps it should not be too surprising. As most antibiotics are derived from substances produced by molds and bacteria to inhibit the growth of rival microorganisms, mechanisms of antibacterial resistance evolved before humans harnessed these compounds for medicinal use.

When antibiotics reduce populations of non-resistant organisms, resistant organisms are able to proliferate. Rates of invasive infections with drug-resistant bacteria increase after recent antibiotic exposure. Conversely, reduced use of antibiotics has been shown to decrease the prevalence of antibiotic-resistant organisms. Certain bacterial infections are now resistant to all antibiotics, with a limited number of promising antibiotics in the developmental pipeline.

Highly antibiotic-resistant organisms are usually thought of as exclusively hospital-acquired pathogens. However, community acquisition of resistant pathogens is on the rise, including methicillin-resistant Staphylococcus aureus (MRSA) and extended-spectrum beta-lactamase-producing Escherichia coli. This chapter reviews resistant bacteria of importance to the hospitalist, including the ESKAPE pathogens, for which there may be no effective drug therapy in the near future (Table 186-1).

The medically important staphylococci may be divided into two main groups based on the rapid coagulase test, a measure of the ability of a staphylococcal colony to produce a clot in a tube of rabbit serum. Coagulase-negative staphylococci (principally Staphylococcus epidermidis) have little virulence aside from biofilm production, and generally only cause infections of medical devices, such as central venous catheters and joint prostheses. By contrast, Staphylococcus aureus (coagulase-positive) is innately pathogenic, and is one of the few bacteria that cause severe infection in both community and health care settings.

Although methicillin is no longer used in clinical practice, methicillin-resistance is still used as marker of staphylococcal resistance to beta-lactams. Methicillin-resistant Staphylococcus aureus (MRSA) isolates are also resistant to oxacillin, nafcillin, cefazolin, and all other beta-lactams. Contact precautions are required for hospitalized patients with MRSA (Table 186-2). While many clinical isolates of coagulase-negative staphylococci are methicillin-resistant, contact precautions are not required for these organisms because of their minor clinical and epidemiological implications.