Plasmids
milhayser | June 14, 2016The first observation of a bacterial gene called MCR-1 in the United States has scientists worried, if not surprised. The gene provides resistance to colistin, an antibiotic with nasty side effects used to combat multidrug-resistant bacteria. On Aetiology, Tara C. Smith writes "colistin has seen a new life in the last decade or so as a last line of defense against some of these almost-untreatable infections." But now, bacteria wielding MCR-1 threaten to leave humans defenseless. On The Pump Handle, Liz Borkowski explains "MCR-1 is of particular concern because it’s carried on a plasmid, a…
mikethemadbiologist | June 6, 2011After Friday's post, I've held off on writing much about the German E. coli outbreak, often referred to by its serotype, O104:H4, or as HUSEC041 (HUS stands for hemolytic uremic syndrome). Having had the weekend to digest some of the ongoing analysis and news reports, here are some additional thoughts:
1) The multilocus sequence type (MLST) of this outbreak is definitely ST678. This means this outbreak strain is related to an older strain found in 2001 that caused disease. A new, improved assembly released by BGI yields a perfect match to ST678. In addition, there is independent…
mikethemadbiologist | March 4, 2011I haven't gone after creationists in quite a while, because it just starts to feel like picking on the slow kid. Both PZ Myers and Kele Cable attended a seminar by Answers in Genesis High Wackaloon Terry Mortenson. I don't think you could pay me enough to wade through that morass of unadulterated bullshit, but they've filed some reports (there's a Twitter feed here). But what burned me up was seeing this come across the Twitter transom:
Antibiotic resistance always evolves from a loss of information. [PZ:] Not true!
Sweet Baby Intelligent Designer, Mortenson is stupid.
Let's leave aside…
mikethemadbiologist | January 28, 2010Over at The Tree of Life, Jonathan Eisen asks:
What do people think are the potential benefits that could come from finishing?
For those who don't know what genome finishing is, I'll let Eisen give the short summary:
Finishing: Using any combination of laboratory, computational and other analyses one can both fill in gaps in the assembly and improve the quality of the assembly. This can generally be called "finishing"
In the context of microbial genomes, here are some of my thoughts about finishing (italics orignal; boldface mine):
Whole genomes don't come flying out of the sequencing…
mikethemadbiologist | December 4, 2009Yesterday, four people emailed me, asking about Brian Palmer's Slate article about antibiotic resistance. Since I'll probably get more such emails (and thank you for sending them), I'll offer my thoughts below:
1) Palmer's basic point about antibiotic development not being the answer is right. All a new drug does is kick the can down the road, since resistance will evolve to the new drug. Having said that, we currently do need new drugs, so we shouldn't stop developing them.
2) Palmer is not correct about plasmid curing as being a solution to antibiotic resistance. If we come up with a…
mikethemadbiologist | August 12, 2009In 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…
mikethemadbiologist | June 2, 2009A recent post about the looming specter of bioterrorism by William Lind due to 'biohacking' seems overblown to me. But before I get Lind, what I find particularly disturbing about hyping a non-existent bioterror threat is that it makes combating infectious disease--the stuff that kills millions worldwide--much harder due to unnecessary regulations and restrictions. Onto Lind:
For years, I have warned in these columns and elsewhere that the future weapon of mass destruction we should most fear is not a nuke. Rather, it is a genetically engineered plague, a plague no one has ever seen before…
mikethemadbiologist | May 21, 2009...the signal peptide? Interesting. I'll start at the beginning.
One of the few bright spots regarding the problem of antibiotic resistance is that resistance typically infers a fitness cost to the bacterium, at least initially. In other words, the resistant strain usually grows slower than a nearly identical sensitive strain*. While compensatory mutations can lower or eradicate this 'cost of resistance', it is thought that resistance can't increase initially without favorable selective conditions--antibiotic use--due to the cost of resistance.
We'll need a little background about…
mikethemadbiologist | May 20, 2009While I'm away at ASM, here's something from the archives for you
When I read Olivia Judson's post about hopeful monsters, I didn't think she used the term correctly (here are some good explanations why), but I was surprised by Jerry Coyne's response.
First, the personal attack on Judson is unwarranted: when we reach the point where the serious challenge to evolutionary biology is the misuse of a discredited decades-old idea, as opposed to the politically powerful anti-science creationist movement, we're in a pretty good place. She made a mistake--I don't think her motives were self-…
mikethemadbiologist | October 30, 2008ScienceBlogling Revere links to a news article about high levels of VRE, vancomycin resistant enterococci in beach sand. While Revere and the article both describe how this indicates that VRE are established in the community, I think a far more chilling problem isn't mentioned at all: VMRSA.
What's VMRSA? Vancomycin resistant MRSA (methicillin resistant Staphylococcus aureus).
Every instance of VMRSA has involved an MRSA strain acquiring a plasmid (mini-chromosome) from a VRE strain. So far, most of these cases have occurred in Michigan. Apparently, the VRE strain that carries this…
mikethemadbiologist | August 18, 2008
This is not good. A recent article in Emerging Infectious Diseases describes two separate cases of community-acquired ST398 MRSA--and neither case was associated with agriculture. Let me explain what this means and why this is really bad news.
MRSA--methicillin resistant Staphylococcus aureus--is a serious problem: in the U.S., it kills more people annually than AIDS. Typically, the therapy used to treat MRSA is vancomycin, and strains resistant to vancomycin can't be treated on-label with any commercial antibiotics*. ST398 is a new clone of MRSA that is thought to be associated with…
mikethemadbiologist | August 7, 2008Yesterday, I mentioned my doubts about there being two anthrax strains used in the 2001 attacks. Thanks to an article identified by reader TomJoe, I'm convinced that there was only one anthrax strain involved, if the only evidence for the existence of two strains is that there is a DNA inversion.
Just to remind everyone, this is what I mean by a DNA inversion:
In many bacteria, inversions are used as regulatory mechanisms--when the DNA is in one direction, nearby genes are turned on, and when in the other, they're turned off. Like so (this is a made up example for illustrative purposes only…
mikethemadbiologist | March 12, 2008I've written before about CTX-M-15 beta-lactamases which make bacteria resistant to most cephalosporin antibiotics--those antibiotics that begin with cef- (or ceph-) or end with -cillin. I've also discussed the role of clonal spread in the rise of antibiotic resistance: most (but obviously not all) resistant infections are not the result of a sensitive strain evolving resistance during the course of infections, but rather due to colonization by a previously resistant strain. A recent article in Emerging Infectious Diseases discusses the role of clonal spread in the dissemination of CTX-M-…
mikethemadbiologist | January 28, 2008When I read Olivia Judson's post about hopeful monsters, I didn't think she used the term correctly (here are some good explanations why), but I was surprised by Jerry Coyne's response.
First, the personal attack on Judson is unwarranted: when we reach the point where the serious challenge to evolutionary biology is the misuse of a discredited decades-old idea, as opposed to the politically powerful anti-science creationist movement, we're in a pretty good place. She made a mistake--I don't think her motives were self-aggrandizing. Second, if you're going to launch an ad homeniem attack,…
mikethemadbiologist | August 9, 2007...the signal peptide? Interesting. I'll start at the beginning.
One of the few bright spots regarding the problem of antibiotic resistance is that resistance typically infers a fitness cost to the bacterium, at least initially. In other words, the resistant strain usually grows slower than a nearly identical sensitive strain*. While compensatory mutations can lower or eradicate this 'cost of resistance', it is thought that resistance can't increase initially without favorable selective conditions--antibiotic use--due to the cost of resistance.
We'll need a little background about…
mikethemadbiologist | May 27, 2007From Monday to Friday, I attended the American Society for Microbiology meeting held in Toronto. Before I get to some of the interesting science, my apologies to all of the people who suggested we meet up. Unfortunately, I never look at the blog (or almost never) while I'm on the road, so I missed your messages (it's best to email me directly). Anyway, here's the list of random things:
The E. coli responsible for the spinach outbreak is found in many feral swine. Hence, feral swine are a possible reservoir of E. coli O157:H7. Of course, feral pigs roaming around California in significant…
mikethemadbiologist | May 4, 2007No, 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*, 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 Ã-lactam antibiotics: basically,…
mikethemadbiologist | March 7, 2007Or maybe terrifying is a better word. I just returned from the Network on Antimicrobial Resistance in Staphylococcus aureus meeting, where I learned some very interesting things about S. aureus (since I'm going to refer to MRSA, methicillin resistant S. aureus repeatedly, go check this link if you want to know more about MRSA):
1) 43% of all skin infections in the U.S. are the result of one strain of MRSA. Not 43% of staphylococcal infections. All skin infections.
2) According to the NHANES study, the number of people who carry S. aureus asymptomatically (in other words, it lives up your…
mikethemadbiologist | January 4, 2007A while back I posted about how awful it would be for the FDA to approve the use of cefquinome, an antibiotic similar to the medically important drug cefepime. I even coauthored a letter about it. Well, it turns out the IDSA wrote a letter about cefquinome too (the whole letter, in pdf). There's good and bad things about the letter. First, the bad--the IDSA proposals about what to do if cefquinome is approved:
1. Limit the marketing status to prescription only.
2. Prohibit extra-label use of the product.
3. Limit the extent of use to "low," meaning that the drug will be administered…
mikethemadbiologist | December 24, 2006...so no blogging. Instead, I'll leave you with a "make sexy time" photo (to steal Borat's phrase):
It's E. coli having sex. Well, actually it's conjugation. Many bacteria have plasmids which are 'mini-chromosomes' (antibiotic resistance genes are often found on plasmids). The bacteria are able to build protein tubes ("pili") and send copies of plasmids to another cell.