Posted by In the midst of the concern about TEH SWINEY FLOO!, very few people (other than the Mad Biologist), have been discussing the double whammy of influenza followed by bacterial infections. A couple of years ago, I first started describing reports of KPCs:
No, KPC isn’t a new fast food restaurant. It’s short for Klebsiella pneumoniae carbapenemase. The bad news: it’s very hard to treat. The good news: it’s very rare…for now.
Actually, the correct term is KPC-possessing K. pneumoniae [these genes are now showing up in other bacteria], but we’ll just use the slang ‘KPC’–it’s what all the cool microbiologists use (I’ll refer to the carbapenemase gene as the ‘KPC gene’). KPC causes pneumonia, urinary tract infections, and sepsis; the mortality rate from these infections is extremely high.
The KPC gene confers resistance to all cephalosporins and ß-lactam antibiotics: basically, anything named “-cillin”, “-penem”, or “cef-” won’t kill it. Aztreonam doesn’t kill it either. And, of course, it happens to have evolved resistance to most of the other classes of antibiotics, so, like some Acinetobacter, it is only treatable with colistin and tigecycline, which works…except when resistance evolves in the patient, which has been observed multiple times (this is alarming given the relatively few times this therapy has been used).
The KPC gene is found on a highly transmissible plasmid, which means it can be transferred within Klebsiella and can also spread to other Gram-negative bacteria (E. coli, Enterobacter, and others). The good news is that the plasmid is unstable: it doesn’t always manage to wind up in both daughter cells after cell division.
And given that these strains are pan-resistant–not only does the KPC gene provide resistant to all of the derivatives of penicillin, but these strains, and the KPC plasmid, are loaded with other resistance genes–I advocated that this be treated as a serious health threat:
Now is the time to enact national mandatory quarantine and reporting requirements. If KPC becomes prevalent to even a fraction of the extent that MRSA is, we are really in trouble, since MRSA can almost always be treated successfully with vancomycin. KPC is a lot more difficult to treat.
We have a chance to get out in front of a potential public health problem rather than reacting to it once it has already become a severe problem. This one is really scary–if it gets out of control, it will be a lot worse than Acinetobacter ever could be.
Today, in The Wall Street Journal, an op-ed also argues that we need to get out in front of KPC:
Compare this response [to influenza] to the scant media and political attention that have been given to several silent but no less deadly outbreaks of disease in recent years caused by antibiotic-resistant bacteria. Most such outbreaks are treated as the poor stepsisters of pandemic influenza, even while they have killed far more people than swine flu over the same period….
In contrast to the flu, most of these infections receive little or no public attention. The only exception has been methicillin-resistant Staphylococcus aureus (MRSA). This microbe is now receiving significant public attention–but this attention has come some three decades after its spread in the U.S. first began. That delay allowed MRSA to spread uncontrollably, and more than 18,000 people are now estimated to die each year in the U.S. from this bug, according to the Journal of the American Medical Association.
Initially, MRSA was confined to hospital wards and affected primarily the elderly and chronically ill. It therefore remained outside of the headlines and off political agendas. MRSA entered the spotlight only after it began to affect healthy people living outside of hospitals.
But we haven’t learned our lesson:
In the four-month period since it entered the U.S., swine flu has killed 436 people in this country. During this same period, more than 100 people are estimated to have succumbed to carbapenem-resistant Enterobacteriaceae in the New York City area alone, and more have undoubtedly died outside of New York.
Yet the spread of these and other resistant bacteria has met with almost no coordinated effort to fight them in the U.S. Very few resources have been allocated to combat antimicrobial resistance. Last fiscal year, for example, the U.S. government budgeted just $16.9 million for the Centers for Disease Control and Prevention to spend fighting antibiotic resistance, about 1% of the total funding requested for swine flu.
As the authors note, there have been successful prevention–not containment, but prevention–campaigns in Israel and the UK. Yet, outside of New York City, we do nothing. There’s one other point the article doesn’t make: K. pneumoniae cause lung infections.
Why does this matter? Because in 1918, many of the deaths were not directly due to the influenza virus. Instead, they were caused by ‘secondary’ bacterial infections that ordinarily wouldn’t have killed people:
Their findings are striking in the context of modern conceptions of the 1918 pandemic; the great majority of deaths could be attributed to secondary bacterial pneumonia caused by common respiratory pathogens, particularly pneumococci, group A streptococci, and staphylococci, and not to the virus itself. In fact, although evidence of severe viral bronchiolitis was found, often the primary viral insult appeared to be resolving at the time of the secondary infection responsible for the fatality. Their conclusions are strengthened by the remarkable consistency in theme, if not details, displayed across the many studies reviewed and the inclusion in their review of not only gross pathologic findings but blood and lung tissue culture data. In only 4% of the more than 8000 cases reviewed was no bacterial superinfection documented.
The article also reports that K. pneumoniae was implicated in the deaths of these patients (although it was less frequent than the Gram-positives), along with other Gram-negatives, such as E. coli. And if we can’t treat these patients due to antibiotic resistance, the number of deaths which are kicked started by influenza, but utlimately due to bacterial infection, will be higher than anyone is currently thinking about.
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