You’d think a super bug with a 50% death rate would get more press. But maybe because KPC is complicated, it doesn’t get the same kind of media frenzy as its far less deadly media rival Ebola. There was one article (in the Australian press) trying to explain KPC.
The problem isn’t helped by a name change. Just call KPC “the superbug formerly known as KPC but now known as CRE.” The first name at least defined a specific bug: Klebsiella pneumoniae carbapenemase, which used to be the major host of antibiotic resistance. But now it’s given its antibiotic resistance to a whole bunch of its friends like e. coli, so together the gang is called: carbapenem-resistant Enterobacteriaceae (CRE). (Here’s a table of the gang members.)
Since it was KPC before it became CRE, let’s follow little KPC. The first sighting was in Japan in 1994, followed by a sighting in North Carolina in 2001. It made some serious inroads in the New York area in 2003-2004 and spread worldwide. By 2009, the CDC recommended CRE as the new name, but nobody has really made the switch, even in the medical literature.
We’re talking about a growing resistance that really puts other antibiotic resistance to shame. And it originated in the U.S., spreading elsewhere from us. “In New York City, the percentage of carbapenem-resistant K pneumoniae rose from 9% in 2002 to 18% in 2004, then further to 38% in 2008. In 2005, the first report of a clinical isolate producing a KPC outside of the US occurred in France from a patient who had recently been hospitalized in New York City.10 The first outbreak outside the US was in Israel,11 and KPCs are now endemic in both Israel and Greece. Enterobacteriaceae-producing KPCs have also been reported in Brazil, China, Colombia, Norway, United Kingdom, India, Sweden,5 and more recently, Italy and Finland.” (study here)
But we haven’t just sent it overseas. “To date, KPC-producing bacteria have been isolated in at least 33 states.” When we say resistant, we don’t mean just to carbapenem antibiotics (hospital use only). “these bacteria had reduced susceptibility or resistance to all beta-lactams including penicillins, cephalosporins, monobactams, and carbapenems. Moreover, in vitro studies of 95 KPC isolates from Brooklyn hospitals during 2003-2004 revealed approximately half to be susceptible to aminoglycosides and very few to be susceptible to fluoroquinolones.” In other words, we’re talking almost global resistance, not just one or two antibiotics. So when you get sick, it’s very possible that they may not have anything to help you. That explains the high death rate.
What makes this worse is that you may not know you’re in trouble even after you know you have an infection: “automated systems will identify seven to eighty-seven percent of KPC-producing K pneumoniae as susceptible to imipenem or meropenem” The computer may not catch that your bacterial infection is resistant until it’s too late to change antibiotics. “A small series of patients with bloodstream infections caused by KPC-producing bacteria from New York City hospitals in 2005 revealed mortality rates of 47% to 66%.” Even when they try to culture out the bacteria, the system may not catch the resistance: “A study of 36 patients in an intensive care unit (ICU) in New York City during a KPC outbreak revealed 39% of all patients had gastrointestinal colonization while only 14% were identified by previous clinical culture.”
So, should we all be terrified? Maybe? We don’t know how far and how fast the problem is spreading because CRE can live happily in your system as long as you don’t get sick. Health care workers exposed to CRE in the hospital can disseminate them out to their entire communities without any ill effects until a community member gets another illness. Given that we have no way to moniter KPC, and that it has transferred incredibly rapidly in less than ten years from New York to worldwide, I would have to agree with the study headline: ”
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