I've previously mentioned a bacterial pathogen called Acinetobacter baumannii (a bit more information here), and Mike has discussed it rather frequently. A. baumannii is ordinarilly a commensal bacterium--one that may live on the skin of healthy people for many years without ever causing disease. It becomes a problem when one is immunocompromised in some manner, and unable to keep growth of the bacterium in check. Once this happens, it's difficult to reverse, as the bacterium brings new meaning to the term "antibiotic resistant." As Mike blogged previously, a genomic analysis revealed that the bacterium has 52 resistance genes--it's no wonder it shrugs off everything doctors throw at it. And now, it seems that we're importing additonal cases of A. baumannii infections from Iraq, which are entering the country as soldiers are transported from hospital to hospital along the evacuation chain. More below the fold.
First, it should be noted that Acinetobacter itself isn't exactly new:
Forerunners of the bug causing the military infections have been making deadly incursions into civilian hospitals for more than a decade. In the early 1990s, 1,400 people were infected or colonized at a single facility in Spain. A few years later, particularly virulent strains of the bacteria spread through three Israeli hospitals, killing half of the infected patients. Death by acinetobacter can take many forms: catastrophic fevers, pneumonia, meningitis, infections of the spine, and sepsis of the blood. Patients who survive face longer hospital stays, more surgery, and severe complications.
What's novel is the frequency with which this bacterium is infecting (and killing) soldiers and civilians in Iraq (due largely to the evolution of resistance to multiple antibiotics), and the sheer magnitude of its presence in medical facilities there:
The investigators did find acinetobacter in Iraq. It wasn't in the dirt - except for a few bugs under a dripping air conditioner outside a health care facility in Mosul - or in the fresh wounds, either. But multidrug - resistant Acinetobacter baumannii was thriving in the emergency rooms, ICUs, and operating rooms of the combat support hospitals. As Paul Scott, one of the lead investigators, told a meeting of civilian epidemiologists in Chicago last spring, "This appeared to be a hospital-associated outbreak throughout our entire health care system."
The wounded soldiers were not smuggling bacteria from the desert into military hospitals after all. Instead, they were picking it up there. The evacuation chain itself had become the primary source of infection. By creating the most heroic and efficient means of saving lives in the history of warfare, the Pentagon had accidentally invented a machine for accelerating bacterial evolution and was airlifting the pathogens halfway around the world. (Emphasis mine)
Um, oops.
There is a bit of a bright side here. The absence of the bacterium in the soil means it doesn't appear to have a natural environmental reservoir there. Therefore, if the hospital contamination can be cleaned up and contained (a very difficult task even in a well-equipped hospital, admittedly, and even more difficult in a temporary combat support hospital that's short on even basic supplies), transmission could be minimzed or eliminated.
However, that doesn't mean that we'll see the last of drug-resistant A. baumannii. The bacterium has also spread in several hospitals in the United States, as noted in the article, and was the cause of a rather large outbreak (236 cases over 2 months' time) in Arizona as well. And as the author of the Wired story, Steve Silberman, emphasizes, it's not over:
Acinetobacter is now a difficult part of daily life in many military hospitals, as it is in civilian ICUs and burn wards worldwide. And the rise of many other types of multidrug-resistant bacteria will make things even more difficult in the next few years, because there are few new antibiotics coming down the pipeline.
"The bugs are outpacing us, and these drugs are not the kind that bring in incredible profits," says Robert Guidos, director of public policy for the Infectious Diseases Society of America. "We're planning for bioterrorism and pandemic influenza, but what about the hundreds of thousands of people dying each year from nontheoretical situations? We need to think in longer terms."
One of the most unsettling long-term questions about the military outbreak is how far the bugs of war will proliferate now that thousands of Iraq veterans have entered the VA hospital system. Many of the older vets who are already there - struggling with chronic conditions for decades, in and out of nursing homes - fall into the bacteria's target demographic.
We've watched MRSA (methicillin-resistant Staphylococcus aureus) go from being a nosocomial (hospital-based) worry to becoming a real problem in the community. We can't say that Acinetobacter would follow the same path. However, we already know that it's good at co-opting genes from other bacteria (many of its resistance genes came from Pseudomonas, Salmonella, and E. coli), and these resistant strains don't appear to have a genetic disadvantage compared to susceptible strains (from anything I've read, at least). So if it does jump in the community, I'd guess that we're in trouble.
For more information:
Multidrug-Resistant Acinetobacter Extremity Infections in Soldiers (EID, 2005)
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I've worked micro at one of the hospitals in Europe (where most Iraq related casualties get sent), right up until a few months ago. I've seen it come through, and it's scary to see the resistances. The scariest part for me was how quickly they developed. When it first came up, you could kill it by looking at it crosseyed. Suddenly, we had to skip the primary antibiotics because they didn't work anymore. Then the next level, and the next. Of all the questions the docs would ask, the one I hated answering the most was "What am I supposed to do with a bug that's resistant to EVERYTHING?"
The only answer we could give: Throw everything you've got at it, quarantine the patient, and pray that the god that supposedly created the bug to do this will for some reason take pity on this guy.
That powerless feeling is one of the worst. It's stuff like this that makes me fear bacteria more than viruses. We may someday come up with a way to cure viral diseases via gene therapy or something, but bacteria just stays 3 steps ahead of us.
The hospitals are keeping a very close eye on it, but that doesn't mean we can do anything bout it other than try to prevent spread. I expect this to just become a bigger and bigger issue, like MRSA.
I've been following this since my husband came back with it in July 2003.
It was December 2003, about the time we figured out it was leishmaniasis attacking his reconstructed leg and not the AB, before I could get anyone in the DOD or the CDC to answer my repeated questions regarding it. After I threatened to go to the news I received a telephone call from the acting Army Surgeon General. He told me that this AB was in the soil in Iraq and that it was the same AB that they had found in victims of the earthquakes in Turkey. He referred to it as Acinetobacter Baumannii Valmari. Even spelled it for me.
This leaves me skeptical that we have the whole story.
Thank you for the very informative posts on this. Those of us who are not scientists appreciate the explanations.
It appears that this bacterium does have a natural reservoir in soil. Were you refering to this strain only? I suppose that this isolate may not be selected for in a normal environment and could disappear if dealt with severely? So many questions, so little time!
Yes, I'm referring to the multi-resistant strain.
AB's just one of those difficult oppurtunistic pathogens that can get into the system when the immune system is very weak (immunosuppressed, or critically ill) or when the oppurtunity arises (traumatic injuries or in the lungs of cystic fibrosis patients)
Moreover, AB is one of the toughest environmental bacteria (especially for a Gram negative), reported as surviving up to 25 days on dry surfaces. Look up
Fournier, P. & Richet, H. (2006). The epidemiology and control of Acinetobacter baumannii in health care facilities. Clin Infect Dis 42, 692-699.
And even more shocking, it has reportedly one of the largest "collection" or "islands" of resistance genes reported to date in the bacteria
Fournier et al. (2006). Comparative Genomics of Multidrug Resistance in Acinetobacter baumannii. PLoS Genet 2, e7
..
Not surprisingly, A. baumannii clinical strains either intermediate or resistant to a full range of anti-pseudomonal antibiotics, and only the 1950s drug colistin retain some consistent activity
McGowan, J. & John E. (2006). Resistance in Nonfermenting Gram-Negative Bacteria: Multidrug Resistance to the Maximum. The American Journal of Medicine
Antimicrobial Resistance Prevention Initiative: Proceedings of an Expert Panel on Resistance 119, S29-S36.
Even new drugs seem to be losing activity or not as efficient as they're supposed to be ... example tigecycline
Peleg, A. Y., et al. (2007). Acinetobacter baumannii bloodstream infection while receiving tigecycline: a cautionary report
10.1093/jac/dkl441. J. Antimicrob. Chemother. 59, 128-131.
I have been working with multi-drug resistant stains of Ab for the past year, and the bad news is that I am detecting polymyxin resistant AB (colistin resistant strains) after they are challenged with colistin/polymyxins in in vitro and animal models of infection as well (manuscript submitted)
Some in vitro indicators of colistin resistance has already been published
Li, J., et al. (2006). Colistin: the re-emerging antibiotic for multidrug-resistant Gram-negative bacterial infections. The Lancet Infectious Diseases 6, 589-601.
Li, J., et al. (2006). Heteroresistance to Colistin in Multidrug-Resistant Acinetobacter baumannii. Antimicrob. Agents Chemother. 50, 2946-2950
Currently, there is no compounds in the drug development pipeline against this bacteria, and polymyxins (e.g. colistin, CMS, polymyxin B) remains the last line antibiotic for this bug
Well, thats why we need to be careful when using the antibiotics we have available against this particular bug which (as Tara has mentioned) have a penchant for co-opting resistance genes. Especially worrying is the current widespread use or misuse of polymyxin monotherapy(despite currently having little or no solid PK/PD data to guide appropriate use of polymyxins)
Currently, there is no compounds in the drug development pipeline against this bacteria, and polymyxins (e.g. colistin, CMS, polymyxin B) remains the last line antibiotic for this bug
Reference
Talbot, Get al. (2006). Bad Bugs Need Drugs: An Update on the Development Pipeline from the Antimicrobial Availability Task Force of the Infectious Diseases Society of America. Clin Infect Dis 42, 657-668.