antibiotics
mikethemadbiologist | June 16, 2008
I've been saying for a while now that the 'piggy MRSA*', known as ST398, is going to be a problem. Always listen to the Mad Biologist.
Last week, I was talking to someone who is monitoring MRSA in the New York area, and they've seen two cases of ST398 MRSA in hospitals. This really shouldn't come as a surprise since ST398 is sweeping through the swine population. The only question now is will ST398 simply replace the predominant MRSA strains, or will it add to the total number of MRSA infections and deaths.
Of course, those aren't mutually exclusive possibilities...
*MRSA is methicillin…
mikethemadbiologist | June 6, 2008
So while I was at the American Society for Microbiology meeting this week (and my talk went fine, thanks for asking), I saw a poster by one of ScienceBlogling Tara's students, Abby Harper, about MRSA (methicillin resistant Staphylococcus aureus) in pigs.
In the past, I've talked about how, in Europe, there is a strain of MRSA that is sweeping through pigs in Europe, ST398. Essentially, this is a silent epidemic sweeping through pigs (it doesn't seem to cause that much disease is pigs; it's primarily a commensal). In agricultural communities, it seems to be spreading from pigs to people.…
mikethemadbiologist | May 8, 2008
Over at Shakespeare's Sister, I came across this link to an announcement of a new Chlorox disinfectant that is "a one-step, labor-saving solution for killing both strains of MRSA."
There seems to be some confusion here.
Let's start with the basics. MRSA is the bacterium methicillin resistant Staphylococcus aureus. Traditionally, MRSA has been classified into two kinds: CA-MRSA, community-acquired MRSA, and HA-MRSA, hospital-acquired MRSA*. A CA-MRSA infection is defined as an infection that occurs in a patient who has been in the hospital for less than 48 hours; in other words, they…
mikethemadbiologist | April 30, 2008A recent article by National Institute of Allergy and Infectious Diseases (NIAID) staff emphasized that NIAID funds over $800 million annually to study antimicrobial resistance. I've heard this same argument many times, and, every time, people always grumble about how that money includes all microorganisms, as opposed to bacterial antibiotic resistance (NIAID never breaks the money down by organism). In particular, the ESKAPE organisms (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumanni, Pseudomonas aeruginosa, and Enterobacter species), most of which…
mikethemadbiologist | April 27, 2008I originally posted this over two years ago. Moral of the story--don't believe every breathless medical breakthrough drug development story you read. (and if it were really good, they wouldn't be telling anyone about it):
From Chemical and Engineering News:
Enter The Mannopeptimycins: New class of antibiotics offers hope in treating resistant infections by Bethany Halford
Mannopeptimycins, a family of antibiotics recently mined from a decades-old research effort, could give doctors the weapon they've been looking for in the fight against antibiotic-resistant infections. The compounds…
mikethemadbiologist | April 24, 2008An outbreak of vancomycin resistant MRSA, or VMRSA, would be the 'perfect microbiological storm', even worse than vancomycin resistant Staphylococcus aureus (VRSA). The only currently available antibiotics that would be effective against it would have to be used off-label, and are not very effective against sepsis (bloodstream) infections. Fortunately, VRSA is observed only anecdotally: a single patient, usually on long-term vancomycin therapy, is infected with it, and it is not spread to other patients or healthy people.
One reason is that most patients with VRSA are already in hospitals…
sporte | April 17, 2008In the class that I'm teaching, we found that several PCR products, amplified from the 16S ribosomal RNA genes from bacterial isolates, contain a mixed base in one or more positions.
We picked samples where the mixed bases were located in high quality regions of the sequence (Q >40), and determined that the mixed bases mostly likely come from different ribosomal RNA genes. Many species of bacteria have multiple copies of 16S ribosomal RNA genes and the copies can differ from each other within a single genome and between genomes.
Now, in one of our last projects we are determining where…
sporte | April 16, 2008Ribosomes are molecular machines that build new proteins. This process of synthesizing a protein is also known as translation.
Many antibiotics prevent translation by binding to ribosomal RNA. In the class that I'm teaching, we're going to be looking at ribosome structures to see if the polymorphisms that we find in the sequences of 16S ribosomal RNA are related antibiotic resistance.
This is related to our metagenomics project where we investigate the polymorphisms we find in 16S ribosomal RNAs.
This 6 minute video introduces ribosomes, discusses where they're found, what they're made of,…
mikethemadbiologist | April 15, 2008Well, it's a better title than "Duration of Stool Colonization in Patients Infected with Extended-Spectrum Beta-Lactamase-Producing Escherichia coli and Klebsiella pneumoniae." What the authors were looking at is how long E. coli and K pneumoniae (another opportunistic commensal that is found in people at low densities) that carry resistance genes that encode enzymes known as ESBLs (extended-spectrum beta-lactamases).
ESBLs confer resistance to many of the antibiotics that start with "cef-" (or "ceph-") or that end in "-cillin" making these drugs ineffective at treating these infections.
On…
mikethemadbiologist | April 9, 2008While many laboratory experiments have shown that antibiotic resistance imposes a fitness cost on resistant bacteria, it's far less clear if this is the case in natural populations. In Europe, the phasing out of a vancomycin analogue, avoparicin, resulted in a dramatic decrease in vancomycin resistance in enterococci bacteria, from roughly seven percent to about three percent. However, the drop doesn't appear to have continued further (although the economic and health burdens of treating vancomycin resistant enterococci make this decrease a good thing).
One of the problems with most studies…
edyong | April 3, 2008Antibiotics are meant to kill bacteria, so it might be disheartening to learn that some bacteria can literally eat antibiotics for breakfast. In fact, some species can thrive quite happily on nothing but antibiotics, even at high concentrations.
The rise of drug-resistant bacteria poses a significant threat to public health and many dangerous bugs seem to be developing resistance at an alarming rate. The headline-grabbing MRSA may be getting piggybacks from livestock to humans, while several strains of tuberculosis are virtually untreatable by standard drugs.
But a startling new study…
mikethemadbiologist | April 2, 2008Over at denialism blog, PalMD has two posts which, to me anyway, are related. The first has describes how sexually transmitted diseases (STDs) are actually treated with antibiotics:
After hours, we see walk-ins, and that's where the STD fun really begins. For whatever reason, I see STDs daily at the walk-in clinic, but almost never in my private practice. Most commonly, we see only one partner, and, at least in my state, treatment of the absent partner is prohibited. Basically, we only get one shot at folks, and we don't have access to rapid tests. So what do we do? We order a lot of "…
mikethemadbiologist | March 20, 2008OK, last post about this bozo, and then I'm done (famous last words...). In the previous post, I dealt with Egnor's claim that the evolution of antibiotic resistance by selection of resistant genotypes is obvious, and not germane (namely, that it wasn't obvious at one point in time). What bothered me with not just Egnor's claim (which I'll get to a minute) and ScienceBlogling Mike's response is that evolutionary biology does have a significant role to play in combating the evolution and spread of antibiotic resistance.
First, what Egnor said:
The important medical research on antibiotic…
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 | March 10, 2008
ScienceBlogling Mike Dunford reminds us that Michael Egnor's creationist stupidity, like Camus' plague, never disappears, but only wanes. Egnor has unleashed his formidable stupidity on the concepts of artificial and natural selection.
So many fucking morons, so little Mad Biologist. Fortunately, I've written about this before:
The difference between artificial selection and natural selection isn't that the selective agent (e.g., pesticides) is a result of human activity. The difference is in what determines what is the 'fittest': a person's decision as to what traits are preferable, or…
mikethemadbiologist | March 7, 2008There's not much to add in terms of rebutting intelligent design creationist Jonathan Wells' latest misappropriation of science that Larry Moran, Orac, and Ian Musgrave didn't already write. But Wells' latest screed demonstrates just how pathetically low intelligent design creationism has sunk. An argument that stupid is a tacit admission of defeat.
Essentially, Wells' argument can be summarized as "if evolutionary biology isn't cited in every single biology paper EVAH!, then evolutionary biology isn't relevant to biology." Never mind that every step in genomic biology involves…
mikethemadbiologist | March 5, 2008Yes, this is O157:H7, not ExPEC. Bully for you.
One thing regarding popular accounts of antibiotic resistance I've noticed is that there is an overemphasis on the evolution of resistance, and an underemphasis on the spread of resistant bacteria. While the evolution of resistance is important, most of what we see in a hospital is not the de novo change of a sensitive strain into a resistant one (i.e., evolution), but, instead, the survival and spread of already resistant bacteria in this antibiotic-laden environment.
What this means is that changes in the frequency of resistant organisms,…
mikethemadbiologist | February 29, 2008One piece of infection control legislation moving (slowly) through Congress is the Healthy Hospitals Act, H.R. 1174 (it's so slow that it's, erm, an act of 2007). H.R. 1174 would amend "the Social Security Act to require public reporting of health care-associated infections data by hospitals and ambulatory surgical centers and to permit the Secretary of Health and Human Services to establish a pilot program to provide incentives to hospitals and ambulatory surgical centers to eliminate the rate of occurrence of such infections."
There are many good provisions in this legislation:
Hospitals…
mikethemadbiologist | February 27, 2008And that includes the pets. Since I saw the 'TV version' while at the gym yesterday, that spurred me to get around to discussing this article about the transmission of E. coli within families.
In the article, the authors sampled at least seven isolates* of E. coli from 152 people and 76 pets, and then genetically typed them. Within households, pets were most likely to share genetically identical E. coli (58% of possible 'pet-pet' pairs), followed by adult-child (34%), child-child (33%), adult-adult (24%), adult-pet (18%), and child-pet (15%). What's interesting is that only 12% of shared…
mikethemadbiologist | February 13, 2008How antibiotic resistant your E. coli are has to do with where you've been, not what you eat.
A recent study isolated E. coli from 567 newly hospitalized patients and 100 vegetarians (one E. coli isolate per person), and screened them for resistance to X antibiotics, including ciprofloxacin, nalidixic acid, trimethoprim-sulfamethoxazole (the primary treatment for E. coli-related urinary tract infections), ceftriaxone, and ceftazidime (the last two indicate the presence of an extended-spectrum beta-lactamase, and can only be reliably treated with carbapenems).
The only significant risk factors…