Klebsiella pneumoniae is a member of the Enterobacteriaceae family. It and E. coli account for the vast majority of hospital- and community-acquired urinary tract infections (UTIs), and it can cause a particularly deadly form of community-acquired pneumonia among alcoholics. Hospital outbreaks leading to respiratory, bloodstream, and wound infections are common, spreading contact with personnel or medical devices like catheters and ventilators.

This video shows the trends in inpatient K. pneumoniae resistance to imipenem, one of four closely related carbapenems—the newest and most potent class in the large family of beta-lactam antibiotics, which includes penicillins and cephalosporins. Because of the similarities in resistance profiles among the four carbapenems, the current series represents the epidemiology of carbapenem-resistant K. pneumoniae (CRKP) isolates, a pathogen that is drawing considerable attention.

The map shows that levels of CRKP did not become significant until 2002 and were initially concentrated in the Mid-Atlantic census division, with sporadic occurrences in South Atlantic and other states. Between 2004 and 2006, rates above 1% were prevalent in only one region, but after 2007, resistance spread nationally to all but the East South Central region. In the end of the period, the trend was most pronounced in the Mid- and South Atlantic, East North Central, and Mountain divisions.

The national rate of resistant isolates we report is lower than the 3.6%–10.1% ranges documented by the 2006–2007 National Healthcare Safety Network (NHSN), which surveys only infected patients from fewer facilities. CRKP is still a regionalized but rapidly spreading phenomenon. Its emergence relates to the production of an enzyme that disables imipenem. Known as K. pneumoniae carbapenemase (KPC), this enzyme was discovered in 2001 and soon after became endemic in several New York hospitals. The trend was alarming because East Coast hospitals were already facing a wave of resistant infections that could only be treated with carbapenems. In addition to KPC, other enzymes, such as the New-Delhi metallo-betalactamase (NDM-1), are spreading globally (mostly outside the United States) and rendering gram-negative bacterial infections virtually untreatable.

The observed rise of CRKP causes concern for several reasons. First, KPC infection is associated with a fatal outcome in 47%–57% of cases. Second, treatment is limited to either collistin (an old antibiotic rarely used because of its kidney toxicity) or tigecycline (which fails to clear bloodstream infections)—a limitation that highlights the urgent need to develop drugs active against gram-negative bacteria. Third, the ability of carbapenemase-encoding genes to spread through plasmid transfer enables the spread of resistance to related species like E. coli, a transfer that may occur even in the same patient. Finally, the presence of KPC is difficult to detect in routine laboratory testing. The epidemiology of carbapenem-resistant bacteria may therefore follow the endemic spread of MRSA beyond hospitals and into the community.

The national average resistance level for the sample was 0.07%, rising from 0% in 2000 to 2.65% in 2009.

The sample consists of 229,702 inpatient isolates tested for imipenem resistance. Data are not available from the following states: AR (2008–2009), CO (2006–2009), GA (2007–2009), IA (2000–2003), IN (2007–2009), KY (2007–2009), MA (2000–2003), NE (2003–2004), NV (2009), RI (2000–2004), UT (2007–2009), CT, MS, MT, NH, SD, and WY.