staphylococcus aureus

ecology

General Epidemiology

ecology

ST398 carriage and infections in farmers, United States

tsmith — Thu, 30 Apr 2015 17:03:15 +0000

ST398 carriage and infections in farmers, United States

I've been working on livestock-associated Staphylococcus aureus and farming now for almost a decade. In that time, work from my lab has shown that, first, the "livestock-associated" strain of methicillin-resistant S. aureus (MRSA) that was found originally in Europe and then in Canada, ST398, is in the United States in pigs and farmers; that it's present here in raw meat products; that "LA" S. aureus can be found not only in the agriculture-intensive Midwest, but also in tiny pig states like Connecticut. With collaborators, we've also shown that ST398 can be found in unexpected places, like Manhattan, and that the ST398 strain appears to have originated as a "human" type of S. aureus which subsequently was transmitted to and evolved in pigs, obtaining additional antibiotic-resistance genes while losing some genes that help the bacterium adapt to its human host. We also found a "human" type of S. aureus, ST5, way more commonly than expected in pigs originating in central Iowa, suggesting that the evolution of S. aureus in livestock is ongoing, and is more complicated than just ST398 = "livestock" Staph.

However, with all of this research, there's been a big missing link that I repeatedly get asked about: what about actual, symptomatic infections in people? How often do S. aureus that farmers might encounter on the farm make them ill? We tried to address this in a retrospective survey we published previously, but that research suffered from all the problems that retrospective surveys do--recall bias, low response rate, and the possibility that those who responded did so *because* they had more experience with S. aureus infections, thus making the question more important to them. Plus, because it was asking about the past, we had no way to know that, even if they did report a prior infection, if it was due to ST398 or another type of S. aureus.

So, in 2011, we started a prospective study that was just published in Clinical Infectious Diseases, enrolling over 1,300 rural Iowans (mostly farmers of some type, though we did include individuals with no farming exposures as well, and spouses and children of farmers) and testing them at enrollment for S. aureus colonization in the nose or throat. Like previous studies done by our group and others in the US, we found that pig farmers were more likely to be carrying S. aureus that were resistant to multiple antibiotics, and especially to tetracycline--a common antibiotic used while raising pigs. Surprisingly, we didn't find any difference in MRSA colonization among groups, but that's likely because we enrolled relatively small-scale farmers, rather than workers in concentrated animal feeding operations (CAFOs) like we had examined in prior research, who are exposed to many more animals living in more crowded conditions (and possibly receiving more antibiotics).

What was unique about this study, besides its large size, was that we then followed participants for 18 months to examine development of S. aureus infections. Participants sent us a monthly questionnaire telling us that they had a possible Staph infection or not; describing the infection if there was one, including physician diagnosis and treatment; and when possible, sending us a sample of the infected area for bacterial isolation and typing. Over the course of the study, which followed people for over 15,ooo "person-months" in epi-speak, 67 of our participants reported developing over 100 skin and soft tissue infections. Some of them were "possibly" S. aureus--sometimes they didn't go to the doctor, but they had a skin infection that matched the handout we had given them that gave pictures of what Staph infections commonly look like. Other times they were cellulitis, which often can't be definitively confirmed as caused by S. aureus without more invasive tests. Forty-two of the infections were confirmed by a physician, or at the lab as S. aureus due to a swab sent by the patient.

Of the swabs we received that were positive, 3/10 were found to be ST398 strains--and all of those were in individuals who had contact with livestock. A fourth individual who also had contact with pigs and cows had an ST15 infection. Individuals lacking livestock contact had infections with more typical "human" strains, such as ST8 and ST5 (usually described as "community-associated" and "hospital-associated" types of Staph). So yes, ST398 is causing infections in farmers in the US--and very likely, these are flying under the radar, because 1) farmers really, really don't like to go to the doctor unless they're practically on their deathbed, and 2) even if they do, and even if the physician diagnoses and cultures S. aureus (which is not incredibly common--many diagnoses are made on appearance alone), there are very limited programs in rural areas to routinely type S. aureus. Even in Iowa, where invasive S. aureus infections were previously state-reportable, we know that fewer than half of the samples even from these infections ever made it to the State lab for testing--and for skin infections? Not even evaluated.

As warnings are sounded all over the world about the looming problem of antibiotic resistance, we need to rein in the denial of antibiotic resistance in the food/meat industry. Some positive steps are being made--just the other day, Tyson foods announced they plan to eliminate human-use antibiotics in their chicken, and places like McDonald's and Chipotle are using antibiotic-free chicken and/or other meat products in response to consumer demand. However, pork and beef still remain more stubborn when it comes to antibiotic use on farms, despite a recent study showing that resistant bacteria generated on cattle feed yards can transmit via the air, and studies by my group and others demonstrating that people who live in proximity to CAFOs or areas where swine waste is deposited are more likely to have MRSA colonization and/or infections--even if it's with the "human" types of S. aureus. The cat is already out of the bag, the genie is out of the bottle, whatever image or metaphor you prefer--we need to increase surveillance to detect and mitigate these issues, better integrate rural hospitals and clinics into our surveillance nets, and work on mitigation of resistance development and on new solutions for treatment cohesively and with all stakeholders at the table. I don't think that's too much to ask, given the stakes.

Reference: Wardyn SE, Forshey BM, Farina S, Kates AE, Nair R, Quick M, Wu J, Hanson BM, O’Malley S, Shows H, Heywood E, Beane-Freeman LE, Lynch CF, Carrel M, Smith TC. Swine farming is a risk factor for infection with and high prevalence of multi-drug resistant Staphylococcus aureus. Clinical Infectious Diseases, in press, 2015. Link to press release.

tsmith Thu, 04/30/2015 - 13:03

Tags

Staphylococcus aureus; antibiotic resistance; farming; agriculture; swine; Iowa;

Various bacteria

I don't get it. We've understood the catastrophic consequences of routine antibiotic use in livestock for decades. How is this still legal? How is this still happening?

Lobbyists? Public health doesn't have the money that the meat and pharmaceutical industry does.

Very, very cool study!

Tangentially, is it ever possible to 'clear' a colonization? I have a friend who, with her two kids, seems to be colonized with a particularly nasty form of strep (everyone constantly has some kind of infection).

Once a person is colonized, are they stuck with that bacteria as a new part of their flora? And, wouldn't we expect their immune system to be very efficient at dealing with it, because of the regular contact?

(Bacteria-immune interaction isn't my forte; I usually do cancer-immune interactions.)

Livestock infections are spreading worldwide. Research have been carried out to cab spread of various infections but still the problem persist .

Superbugs rising

tsmith — Tue, 13 May 2014 10:00:56 +0000

Superbugs rising

It's a parent's worst nightmare. Your healthy child is suddenly ill. The doctors you've trusted to treat him are unable to do anything about it. Drugs that we've relied upon for decades are becoming increasingly useless as bacteria evolve resistance to them. New drugs are few and far between. Old drugs, shelved because of their toxic side-effects, are being brought in as last resorts--kidney failure, after all, is better than certain death.

Unfortunately, this is increasingly the state of medicine today, and people are dying from it. The World Health Organization even recently sounded the alarm, noting that "the world is headed for a post-antibiotic era"--and it takes a lot of consensus to get the WHO to act, so this is a Big Deal.

I was in Washington, DC last week for two days to discuss the issue with other "supermoms" and dads (farmers, physicians, researchers, and parents whose children had experienced antibiotic-resistant infections), and to share information with legislators and government agencies. (I also brought William, 4 months old, for an extra dose of adorableness).

Superbabies against Superbugs

Some of the "super" attendees might be familiar to readers. I had the pleasure of meeting Russ Kremer, who has been profiled in several articles and documentaries. Russ raised pigs in confinement, dosing them with antibiotics from birth to slaughter until he was gored by a boar, resulting in a very difficult-to-treat infection that almost cost him his life. David Ricci was also present. His story was profiled in the Frontline documentary, "Hunting the Nightmare Bacteria." He contracted an infection with bacteria carrying the NDM-1 genes, making them resistant to almost all known antibiotics, and required multiple surgeries and treatment with some of these last-line drugs over many months.

There were also participants you may not have read about previously, like Amanda Hedin and Everly Marcario, who both lost children to antibiotic-resistant infections. I've written before about the immense sadness that comes at times when studying infectious disease, noting that I have a freezer full of bacterial isolates that, while important for study, frequently mark someone's illness or death. It's important work, but heart-wrenching at times.

However, we have very little funding to study such infections. My colleague Eli Perencevich recently estimated the amount of money spent on antibiotic-resistant infections versus HIV/AIDS, and the answer is that it's vastly less. Antibiotic resistance needs to be a priority on many fronts. The FDA has recently made some headway into possibly reducing antibiotic use on farms, though optimism is mixed regarding how much that will actually help things. Hospitals and clinics are working with physicians to encourage and enforce best practices for antibiotic prescribing in these settings.

We need to be responsible with antibiotics. Drugs in development are scarce, and none are ready for prime time. It's almost unimaginable that we may return to a time when an infected scrape could mean the death of a healthy young man, but we're closing in on that every day. The WHO wrote in their report:

“A post-antibiotic era, in which common infections and minor injuries can kill, far from being an apocalyptic fantasy, is instead a very real possibility for the 21st century.”

We need action, not promises. And we need it now.

tsmith Tue, 05/13/2014 - 06:00

Tags

Activism

Various bacteria

Do you have links to studies showing if/how resistance will be reduced as agricultural antibiotic usage drops? How much of a fitness cost do the antibiotic resistance genes carry in the absence of antibiotics? What kind of reductions in usage will we need in order to cut down on antibiotic resistance?

It's complicated and dependent on the species of bacteria and type of antibiotic. When Europe banned the use of avoparcin (a glycopeptide) in poultry, vancomycin-resistant enterococci went down in humans. (see http://jac.oxfordjournals.org/content/46/1/146.full for example). In Quebec, when they stopped using ceftiofur in chickens, they saw a similar decrease in resistance in Salmonella (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874360/). In other cases, yes, resistance can persist even in absence of antibiotics, like fluoroquinolone resistance in Campylobacter (http://www.ncbi.nlm.nih.gov/pubmed/15866763) but even maintaining the status quo and not *increasing* resistance further with continued use would be better than nothing.

Interesting - does the ability to decrease resistance following pulling the antibiotic vary depending in the plasmid that contains the resistance cassettes? One could imagine a'bic resistance genes getting into plasmids that also carry virulence determinants - in that case, I'd predict that the resistance would stick around because of the benefits of the other virulence genes. The bacteria I study (a clinical isolate) has loads of antibiotic resistance determinants but is quite stable in long term animal colonization.

Yep, that's part of it, again, depending on species yada yada. For instance, in Staph aureus I look at methicillin-resistant bugs on the farm, but methicillin itself isn't actually used in farming. So resistance is selected because of penicillin use, and because of other genes which co-localize with the methicillin resistance (mecA) gene. There's also some interesting research suggesting that even zinc use, which has increased in some parts of Europe following a ban on growth-promoter antibiotics, has driven the emergence/persistence of methicillin resistance, again probably due to the resistance genes being on the same cassette.

So basically - we're screwed? Could one develop a compound(s) to encourage plasmid loss? I know there are some topoisomerase inhibitors that can do this - but I wonder about developing ones that are less toxic and that could be used to address the resistance reservoir?

Well, I'm more optimistic than that. I know there is research going on into some of those areas but I have no idea how successful it's been or what the downsides might be. Obviously there's also a lot of research into different compounds--new antibiotics, things like phage lysins, etc. but as mentioned, none of those are ready for prime time.

Have you come across/ Are you familiar with Dr. Martin Blaser at NYU? In his book, he talks about the importance of reducing antibiotic usage and preserving our microbiota from a young age. Its a fascinating read. I'd be curious as to what you think of his work.

Yep. I have his new book and will review it here in the next few weeks.

The human origins of "pig" Staph ST398

tsmith — Tue, 21 Feb 2012 10:40:00 +0000

The human origins of "pig" Staph ST398

I recently gave a talk to a group here in Iowa City, emphasizing just how frequently we share microbes. It was a noontime talk over a nice lunch, and of course I discussed how basically we humans are hosts to all kinds of organisms, and analysis of our "extended microbiome" shows that we share not only with each other, but also with a large number of other species. We certainly do this with my particular organism of interest, Staphylococcus aureus. There are many reports in the literature showing where humans have apparently spread their strains of S. aureus to their pets (dogs, cats, hamsters)--and sometimes the pets have been nice enough to share it right back. My own research looks at S. aureus in pigs and the humans who care for them, and many studies have shown that a "pig" type of MRSA, dubbed sequence type 398 (ST398), can be transmitted from pig carriers to their human caretakers. The assumption has been that this is truly a "pig" strain, originating in swine, and has spread to humans (and other animals, including cattle, poultry, dogs and horses) from pig hosts, either directly or indirectly via contaminated meat products.

According to a new study (open access in mBio), it seems that there has been more sharing of ST398 than we'd realized. Led by Lance Price at TGEN (full disclosure--I'm a coauthor on the paper), his group analyzed 89 ST398 isolates from China, Europe, and North America, including isolates from humans and animals as well as both methicillin-susceptible and -resistant strains. Using whole genomic sequence typing, the evolutionary history of these isolates was reconstructed.

The findings throw the ST398 story a bit on its head. Instead of being a true pig strain, ST398 appears to have originated as a methicillin-susceptible human strain which was transferred into the pig population, picked up antibiotic resistance genes (including resistance to methicillin and tetracyclines), and then has been passed back to farmers as more resistant organisms. Some prophages were also gained or lost along the way, probably due to selection by host factors.

This also suggests that there is still likely a low level of "native human" ST398 circulating in people. There have been a few case reports of ST398 colonization and/or infection in people without any known livestock contact. Some of these have been resistant to methicillin and/or tetracycline, which are more frequently associated with livestock-adapted strains. Are these truly "human" strains which aren't involved in livestock at all, or are these ST398 findings in people lacking livestock contact still due to some livestock exposure along the chain of transmission (farmer neighbors? Transmission via food?) We still don't know, but carrying out more of this WGST will give us better targets in order to be able to differentiate true "human" ST398 strains from those that have been hanging out in animals, and then transmitted back to people.

Now, for long-time science blog readers, this story may sound a bit familiar. Indeed, it looks like ST398 has taken a very similar path to that of another animal-associated S. aureus strain, ST5. As Ed Yong described back in 2009, humans are also the ultimate origin of a "chicken" type of S. aureus ST5, which spread around the world in broiler chicken flocks. In Ed's article, the first author of the chicken ST5 paper, Bethan Lowder, notes that the change in chicken farming from small farms to multinational corporations likely aided the spread of this organism--and the exact same thing has happened with pig farming.

One difference between the two is that ST5 causes disease in chickens, whereas ST398 seems to be a very rare cause of illness in pigs. This is likely one reason that ST398 in pigs went undetected until relatively recently--it's simply not much of an economic issue for pig producers, whereas in chickens, S. aureus can cause several nasty diseases (such as bumblefoot and BCO) leading to animal loss (and thus, less money for the farmer).

So, where do we go from here? Clearly studies like this show the utility of using WGST to examine the evolution and spread of these strains. If you look at how spa types are distributed throughout the tree, you can see that those alone don't tell you much about where the strain came from, or if it's fully "human" or a pig-adapted lineage. Ideally, a set of simple markers could be found to distinguish ancestral human strains from livestock strains (as methicillin-sensitive ST398 can also be found in pigs, so methicillin resistance alone isn't enough of an indicator that it's a "pig" strain). We'll be working on this in ST398 and other strains we see being shared between animals and humans, in order to better understand this generous sharing we're doing amongst species.

Reference:

Lance B. Price, Marc Stegger, Henrik Hasman, Maliha Aziz, Jesper Larsen, Paal Skytt Andersen, Talima Pearson, Andrew E. Waters, Jeffrey T. Foster, James Schupp, John Gillece, Elizabeth Driebe, Cindy M. Liua, Burkhard Springer, Irena Zdovc, Antonio Battisti, Alessia Franco, Jacek Å»mudzki, Stefan Schwarz, Patrick Butayej, Eric Jouy, Constanca Pomba, M. ConcepciÃ³n Porrero, Raymond Ruimy, Tara C. Smith, D. Ashley Robinson, J. Scott Weese, Carmen Sofia Arriola, Fangyou Yu, Frederic Laurent, Paul Keima,, Robert Skov, & Frank M. Aarestrup (2012). Staphylococcus aureus CC398: Host Adaptation and Emergence of Methicillin Resistance in Livestock mBio, 3 (1), 305-311 : 10.1128/mBio.00305-11

tsmith Tue, 02/21/2012 - 05:40

Tags

http://www.cbc.ca/quirks/episode/2012/03/03/march-3-2012/

Great article! New research says you can't simply say: MRSA or "Pig MRSA" is caused by the overuse of antibiotics in the pig industry. It seems to be more complicated.

Well, not exactly. Yes, it is more complicated, but note that resistance to several classes of antibiotics were acquired in pigs--so I think the overuse of antibiotics in ag is certainly a large factor in strains of ST398 that are antibiotic-resistant.

Hi Tara, I saw this yesterday and forwarded it to my EID editor in hopes of replacing ref. #10. I see now why one of the reviewers suggested referencing it. It would appear that the MSSA ST398 strains described in the EID paper may be 'ancestral', circulating at low levels in humans as you describe...

Tara, I was reading, "We Beasties," and Kevin was talking about nominations for some sort of science blogging award. He does have some writing I'd like to vote for/nominate. But, I'd like to point out this piece seems pretty solid to me. As well as the one on MRSA in pork products and "antibiotic" free label.

Was just listening to the Quirks & Quarks podcast. Heard this familiar story. Didn't hear Bob say "Tara Smith" until the end. It's your 9:06 of fame?

Very fluent.

I enjoyed the interview on Quirks & Quarks. Sounds like very promising research.
You mentioned animal husbandry practices in Europe but have you seen some of the innovations at places like Polyface Farms in Virginia? They combine animals like pigs and cows or chickens and rabbits to help create less mono-culture environments that help reduce disease. They also move the pens around to spread out the manure around the land and keep a healthier environment for the animals.
http://mulefootpigs.tripod.com/id21.html
http://www.polyfacefarms.com/story/

MRSA in pork products: does the "antibiotic-free" label make a difference?

tsmith — Thu, 19 Jan 2012 16:35:00 +0000

MRSA in pork products: does the "antibiotic-free" label make a difference?

Back in November, I blogged about one of our studies, examining methicillin-resistant Staphylococcus aureus (MRSA) in Iowa meat products. In that post, I mentioned that it was one of two studies we'd finished on the subject. Well, today the second study is out in PLoS ONE (freely available to all). In this study, we focused only on pork products, and included 395 samples from Iowa, Minnesota, and New Jersey. We also looked at not only conventional meats, but also "alternative" meat products. Most of the latter were products labeled "raised without antibiotics" or "raised without antibiotic growth promotants"--in the markets we tested, very few USDA-certified organic products were available unfrozen, and we were looking for fresh meat products.

In our previous paper, we found MRSA on 1.2% of 165 meat samples. In the current study, we found a higher prevalence--6.6% of 395 samples were contaminated with MRSA. (More about the differences in methods between our two studies later). Interestingly, we didn't find a statistically significant difference in MRSA prevalence on conventional versus alternative pork products--a finding that surprised me, as it contradicts what we've found to date looking at the sources of this meat--conventional versus "alternative" pig farms. Other groups have also found differences on-farm versus on-meat: a 2011 study looking at feedlot cattle didn't find any MRSA in animal samples, though the same group found MRSA in beef products. So, our disparate findings between farms and meat samples are not unheard-of. However, even though our sample size was larger than other U.S. studies to date, it was still fairly small overall--300 conventional and 95 alternative pork samples over a 4-week sampling period from 3 states, so larger multi-state studies are needed to further examine this angle.

It also suggests that we need processing plants and packing companies to work with us to determine where products are being contaminated--because while there may be arguments about the public health importance of MRSA on meats (or lack thereof), it's very likely that if S. aureus are ending up on meat products, other pathogens are as well.

What does the molecular typing tell us, speaking of contamination source? We carried out analyses on all the MRSA and found that the most common type of MRSA was ST398, the "livestock" strain that we previously found on pig farms in the U.S. We also found two "human" types were common: USA300 (a "community-associated" strain) and USA100 (typically considered a "hospital-associated" strain). In the simplest analysis of these findings, these molecular types (a combination of "human" and "pig" strains) suggests that MRSA on raw pork products may be coming both from farms and from food handlers. However, in real life, it's not quite so straightforward. USA100 types have also been found in live pigs. So has USA300. As such, the source of contamination and relative contributions of live pigs versus human meat handlers currently isn't certain.

Within the MRSA strains, we found high levels of antibiotic resistance, similar to what was reported in the recent Waters et al. study. In ours, 76.9% were resistant to two or more antibiotics and 38.5% were resistant to three or more antibiotics tested. (I'll note that we only had funding to test the MRSA--we weren't able to do these tests on all the methiciin-susceptible strains).

Did MRSA prevalence increase in the period between our first study (spring 2009) and this one (late summer/fall 2010)? I doubt it. For this paper, we used a different sampling method, adding the samples to a sterile stomacher bag so that the entire sample was immersed in the culture medium; for the first paper we used external swabbing and so likely didn't capture as many bacteria. This current study more likely represents the "true" MRSA prevalence. But--all isolates were only called as positive/negative, and we didn't measure the number of bacteria on each piece of meat. So, there theoretically could have been just a few colonies of MRSA on the entire piece of meat, and that would have been called a positive sample, while another meat product covered with hundreds of MRSA would have been put in the same category. Therefore, more subtle differences may exist that we didn't pick up in this study, but we will examine in other ongoing studies.

So--what's the take-home here? Don't assume that any meat product is contamination-free, and always use good food handling/cooking practices when dealing with raw meats. As far as the titular question, well, we're still hashing that one out.

References

Hanson et al. Prevalence of Staphylococcus aureus and methicillin-resistant Staphylococcus aureus (MRSA) on retail meat in Iowa.

Waters et al. Multidrug-Resistant Staphylococcus aureus in US Meat and Poultry.

O'Brien et al. MRSA in conventional and alternative retail pork products.

Lin et al. Evidence of multiple virulence subtypes in nosocomial and community-associated MRSA genotypes in companion animals from the upper midwestern and northeastern United States.

Weese et al. The Prevalence of Methicillin-Resistant Staphylococcus aureus Colonization in Feedlot Cattle.

Weese et al. Detection and quantification of methicillin-resistant Staphylococcus aureus (MRSA) clones in retail meat products.

tsmith Thu, 01/19/2012 - 11:35

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Huh. That is interesting, that there's little difference in the sources.

I don't eat much meat, but of course it could still get to me with bad handling practices. I really wish people weren't so opposed to irradiation or other possible non-antibiotic methods of reducing these.

Is there any evidence of MRSA hanging out in the food processing plants nooks and crannies?
I know we're thinking of Listeria as kind of hanging out in the plants in a semi-permanent (i.e. not anything that can be cleaned out) sort of way. But we have no real clue if it's hiding in drains in biofilms or if there are asymptomatic carriers among the workers, or what.

I haven't seen any studies of that and we've not been able to get into any plants, but I find it hard to imagine it *wouldn't* be there. I'd love to check on environmental surfaces, in the air, and in workers' noses.

Are the animals on whom you find MRSA sick? If you are finding the bugs on the meat, this means they have breached the skin barrier and are not commensal per se. DO you find more MRSA on hides and hair?

Are titers ever determined for these studies, or is it a PCR yes/no?

Susan, MRSA rarely causes actual disease in pigs--it's typically commensal. Finding it on the meat doesn't mean it's necessarily *in* the muscle--many ways it can become contaminated during processing, and with ground products, obviously anything that was external means it can go anywhere. When we do animal MRSA sampling, we usually check the nose as that's the main reservoir, though it can also be found on skin.

hibob, these are using pure cultures, and no blood/serology. So we isolate first, and then use PCR for the variety of molecular genetic testing we carry out.

Or are you asking for quantitation of microbial counts on the meat products? As mentioned, that wasn't done for this particular study.

When we do animal MRSA sampling, we usually check the nose as that's the main reservoir, though it can also be found on skin.

Even if you bought a pig, and feed it yourself, with vegetables that you buy in your local grocery.. it still wouldn't be really 'clear' meat. Nowadays literally everything is polluted.

Lately I've been seeing more articles talking about MRSA contamination of meat, and other than as a marker for the prevalence of antibiotic overuse, I'm not sure this is a real problem. Maybe it's my constant exposure to MRSA in the hospital that has led to me to be less worried about it, because so many people are carriers, but it's really not that big a deal outside the ICU. Further, with meat, staph contamination in general will be inevitable with time. I see it as less of a slaughterhouse problem and more of an issue for the local health department checking the fridge temperatures in restaurants, and being sure to sear the outsides of your steak. I think we have to just accept that our general pattern of antibiotic overuse has made this a ubiquitous bacterium, and we just have to get used to it now. In terms of food contaminants I'd be much more bothered by campylobacter, enterotoxigenic e. coli, etc.

I had no idea MRSA was killing so many people (and how gross it looked): http://nutritionfacts.org/videos/toxic-megacolon-superbug/

Mark, I guess we differ on "not that big of a deal." As far as death, I agree with you that the ICU will be the worst cases, but we still see and hear stories from many people with recurrent infections that really impact their quality of life.

For food, I differ with you that I don't see it as much of a cooking issue (searing the outsides of your steak), but an environmental contamination issue (eg Grandma handling meat products and then touching her nose, or not wiping everything down carefully after having meat packages on the countertops, etc.) I agree that campy etc. cause more nasty disease directly attributable to food contamination, but we're really just starting to scratch the surface as far as understanding what, if any, role that meat products play in the ecology and transmission of S. aureus.

RE: Post #11 "...but we're really just starting to scratch the surface as far as understanding what, if any, role that meat products play in the ecology and transmission of S. aureus." In your line of research, I'd be careful what surfaces you're scratching :-)

I was reading an article in Science about finding MRSA in non-farm soil samples. I assume that these are totally different strains. (Around here, there are pigs rooting around in the fields, but I gather most pigs are born and die indoors.)

For food, I differ with you that I don't see it as much of a cooking issue (searing the outsides of your steak), but an environmental contamination issue (eg Grandma handling

Trioxidane is the key in fighting infection and superbugs. A new technology is tackling just that with the use of ozone and hydrogen peroxide.

I buy "raised without antibiotics" or "raised without antibiotic growth promotants" meats because it's a better way to raise animals and for the health of various critters living in and around the pig farms and the in waterways effected by run-off, not for my own health.

And then I eat at Taco Bell and have beef that was probably raised by Zombies and then processed by even more evil Zombies using hacksaws with blades dipped in Hep C.

Does this count as middle ground?

What three states did you perform the study?

Tara, you said in a comment, "we've not been able to get into any plants" Have you not been able to because the plants won't let you or you just decided not to?

Re #17, we haven't found any that will let us in. The 3 states were mentioned in the first paragraph--Minnesota, Iowa and New Jersey.

Thanks for answering the second question and sorry about the first question. I'm surprised at myself that I missed it in the first paragraph.

There is little evidence that LA-MRSA strains are being able to colonize either the slaughterhouse environment (each slaughterhouse tends to have it's own established "flora" or humans. Hospital associated strains are by far, the isolates mostly associated with Human infections of MRSA.
In terms of food safety, MRSA behaves pretty much in the same way as MSSA when ingested by the gastro-intestinal route, and, like MSSA is rarelly treated. Even because foodborne outbreaks with S. Aureus are not really ususally associated with the organism it self but rather the toxins it produces, it really tends much more to be a foodborn intoxication rather than a foodborne infection.
That said, what mostly concerns me are the latest findings of hospital associated strains colonizing pets.
Happy to discuss.

There has been very little examination of MRSA in slaughterhouses here in the US--and note that the meat was found to be contaminated with a mix of LA, CA, and even HA strains. You note that "Hospital associated strains are by far, the isolates mostly associated with Human infections of MRSA"--but this is a bit misleading. Certainly for invasive infections, absolutely. But for skin and soft tissue infections, CA seem to be more important--and remember that MRSA are only the tip of the iceberg, as MSSA are out there causing infections as well but don't get any respect.

Finally, as noted we're not looking at it as a food-borne illness, per se, but another vehicle for introducing S. aureus into homes and colonizing their inhabitants.

Thank you for your stimulating reply.
You are not looking at it as food-borne illness, correct. However you mention in this blog entry you have found it in pork without qualifying the finding, therefore misleading the reader. In my opinion which is why I made the note.
Worse than that in my opinion is the omission that current consensus is that MRSA transmission and colonization is thought to occur mostly from living host to living host. Not through animal products. Fomites in general may play a smaller part.
In Europe, environmental sampling of slaughterhouse environment has not revealed colonization of the slaughterhouse environment. In fact carcasse sampling at slaughterhouse level indicates that MRSA strains seem unable to pass beyond the lairage. Why this happens is unclear. Could be the way carcasses are dressed, could be C&D procedures or simple competition with pre-existing slaughterhouse flora.
Your results are interesting, however, from the entry in the blog I infer that samples were taken of pork in shelf at retailer - correct? If so, there are plenty of steps in the supply chain from slaughterhouse to cutting plant, transport and final retailer where humans could have contaminated your samples with CA and HA strains. The LA strains however are harder to explain.
Finally, my note about Hospital associated strains is certainly not misleading, at least in the European context..
The focus in MRSA rather than MSSA is most justified. One is very resilient to our tools combat it, while the other still has quite a bit still to go.
Happy to discuss.

I do discuss those issues both in the post I linked to from my previous MRSA/food post, as well as in the paper, which is open access and freely available to anyone with an internet connection. I'm not sure what you expect in a blog post--I'm certainly not going to repeat every finding and caveat from the paper verbatim--hence the linking.

You keep suggesting the European studies and that I'm misleading, but from research in my lab and others, the situation with swine-associated S. aureus here in the US is quite different from that in Europe. As such, you can't directly extrapolate from their findings to our issues here in the US--meaning we still have a lot of unanswered questions. The strains we see even in live animals in the US are much more diverse than those seen in Europe--we see HA and CA even in our live pigs, so it's unclear whether when we see those in meat samples if it's coming from people or animals (again, as we discuss in the paper). And I disagree that it's a settled matter that meat isn't a risk--so does the USDA, who has funded me to investigate that very question. In this case, meats are acting as essentially a moving fomite, which can possibly contaminate kitchens and meat handlers. There are some interesting environmental sampling papers which show lots of SA associated with kitchen sinks, wastebaskets, etc., and meat products are one (of several) places those could come from.

I have not read the paper nor followed the links, just the post and the comment section from readers. The comments from some readers appear to show this misunderstanding of nature of the hazards between invasive MRSA and general foodborne toxinfection from MRSA/MSSA. I do apologise if the comment about that topic is unfair.
By the way, I have just discovered this blog and am just now going through the older entries. Very interesting, stimulating and very good information to the public. So please do not take my comments as criticism for the sake of it but rather as true discussion and debate of ideas.
I am mentioning European studies and the European context simply because it is the one I know better. I am not suggesting that your study is misleading, I am suggesting that while interesting it does not really fundamentally challenge EFSA's opinion on risk of Human infection with MRSA. being:
1 - HA strains are the largest contributors to human infections
2 - Human colonization with MRSA in a determined geographical area tends to follow the strains in the local hospital
3 - CA is a recognized issue in the US but much much less so in Europe.
4 - LA strains tend to circulate amongst livestock and colonize specific groups of people, constituting an occupational hazard
5 - Within LA's equine LA's appear to be expanding and horses are starting to show the same pattern as Human, i.e. MRSA strains in horses tend to be regionally clustered and related with equine veterinary hospitals

Regarding your disagreement. First I did not say that pork or fomites in general are not a risk, just that epidemiologically, it is not as significant as live host to live host transmission. Second your postulated route contamination of kitchens is, in my opinion, unnecessary to explain what we observe, I am not discarding it, do not take me wrong, I just find it a weaker, less probable explanation. SA likes moist warm mucosas to live and multiply. It survives in fomites and can even multiply given certain right conditions but it mostly survives, not thrives in fomites, I think that your most obvious source of SA in a determined environment has to be a living host the majority of times, so in a kitchen I would look at the inhabitants first: habitants, people visiting, pets and only then pork products.

Of much more importance, I think, are findings of HA and CA strains colonizing living livestock and, I stress again pets. Because they can serve as secondary sources for further re-infection in a community, in the particular case of livestock, where on top of it you apply extra selective pressure due to a different range of antibiotics being used on those strains you can end up with a brand new strain (in fact given enough time that is an inevitability!) or transfer of resistance genes between LA and CA and HA strains which later find their way back to a hospital.
In the case of pets it is extremely worrying because they tend to have a much more intimate contact with people and secondly because you also risk that they go on to contaminate small animal veterinary hospitals where selective pressure will just compound your problem.
Very happy with this debate.

MRSA found in Iowa meat

tsmith — Wed, 09 Nov 2011 08:00:00 +0000

MRSA found in Iowa meat

I've blogged previously on a few U.S. studies which investigated methicillin-resistant Staphylococcus aureus in raw meat products (including chicken, beef, turkey, and pork). This isn't just a casual observation as one who eats food--I follow this area closely as we also have done our own pair of food sampling investigations here in Iowa, and will be doing a much larger, USDA-funded investigation of the issue over the next 5 years.

Let me sum up where the field currently stands. There have been a number of studies looking at S. aureus on raw meat products, carried out both here in North American and in Europe. In a study from the Netherlands, a large percentage of samples were found to harbor MRSA (11.9% overall, but it varied by meat type--35.3% of turkey samples were positive, for example). Most of there were a type called ST398, the "livestock" strain. This was also found in one Canadian study (5.5% MRSA prevalence, and 32% of those were ST398), but no ST398 were found in a second study by the same group.

Here in the US, prevalence has found to be lower than in that Dutch study (from no MRSA found, up to 5% of samples positive). Furthermore, in the previously-published studies, no MRSA ST398 was found in samples of US meat, though this paper did find plenty of methicillin-sensitive S. aureus (MSSA) ST398 strains. Instead, most of the MRSA isolates have been seemingly "human" MRSA types, like USA100 (a common hospital-associated strain) and USA300 (a leading community-acquired strain).

Why am I rehashing all of this? We have a new paper out examining S. aureus in Iowa meats--and did find for the first time MRSA ST398, as well as MRSA USA300 and MSSA strains including both presumptive "human" and "animal" types. This was just a pilot study and numbers are still fairly small, but enough to say that yes, this is here in the heart of flyover country as well as in the other areas already examined.

As I mentioned, this is one of two studies we've completed examining MRSA on meat; the other is still under review and much more controversial, but I will share that as soon as I'm able. And with the USDA grant, we'll be working on better understanding the role that contaminated meats play in the epidemiology and transmission of S. aureus for the next several years, so expect to see more posts on this topic...

References

Hanson et al. Prevalence of Staphylococcus aureus and methicillin-resistant Staphylococcus aureus (MRSA) on retail meat in Iowa. J Infect Public Health. 2011 Sep;4(4):169-74. Link.

Waters et al. Multidrug-Resistant Staphylococcus aureus in US Meat and Poultry . Clin Infect Dis. 2011 May;52(10):1227-30. Link.

Weese et al. Methicillin-resistant Staphylococcus aureus (MRSA) contamination of retail pork. Can Vet J. 2010 July; 51(7): 749-752. Link.

De Boer et al. Prevalence of methicillin-resistant Staphylococcus aureus in meat. Int J Food Microbiol. 2009 Aug 31;134(1-2):52-6. Link.

Pu et al. Isolation and characterization of methicillin-resistant Staphylococcus aureus strains from Louisiana retail meats. Appl Environ Microbiol. 2009 Jan;75(1):265-7. Link.

Bhargava et al. Methicillin-resistant Staphylococcus aureus in retail meat, Detroit, Michigan, USA. Emerg Infect Dis. 2011 Jun;17(6):1135-7. Link.

tsmith Wed, 11/09/2011 - 03:00

Tags

http://www.cbsnews.com/stories/2011/04/15/health/main20054211.shtml

Dr. Smith,

Thanks for the great blog.

Do you plan to look at MRSA infections among people who handle meat as part of their job (who either acquired MRSA from the meat and/or who have transmitted MRSA to the meat)?

Ken

Very good post I very much enjoyed reading it, keep at it as I hope to read more.

That does it. I'm having tofurkey surprise for dinner tonight.

Ken, no plans to look at that currently, but perhaps toward the end of the grant. I'm more interested in consumers right now. Plus, there are pros and cons of looking at those who work in meat handling. Pros--obviously lots of meat contact, BUT con--in theory are also trained to handle properly, use gloves and handwashing, etc. There was one previous study (here) that looked at that population for colonization, and found a low level.

MRSA enters the tiniest micro crack in the skin, people touch their noses after handling meat. Cutting up and preparing raw meat is no different than putting your hands on MRSA wounds of infected humans. Expect the USDA to cover up these facts because the meat industry is a multi-billion dollar business and for every single representative in Congress Senate and House the meat industry hires 100 lobbyists so to pay these law makers, so the meat industry can do whatever they like without any regard to the consequences of human safety. We are NOW entering into a new age where antibiotics are becoming ineffective. Antibiotic abuse on farm factories is the cause of that since most people do handle raw meat.

CBS news reported about half the meat sold in America is infected with superbugs like MRSA

Luke, the USDA has no ability to review/censor what our findings are, and they were very interested in our proposed research. You might be surprised at what goes on behind the scenes. We've even had funding from the National Pork Board to do some of these studies.

And the CBS story refers to the Waters paper which I cited above.

It's not a freaking spider bite

tsmith — Thu, 11 Aug 2011 07:00:00 +0000

It's not a freaking spider bite

Over at White Coat Underground, Pal has the post that I've been meaning to write. Earlier this summer, a family member posted on Facebook that a friend of her daughter was nursing a "nasty spider bite" that she got while camping in Michigan. Her post claimed it was a Brown Recluse bite. Being my usually buttinski self, I posted and told her that it was really, really unlikely to be a brown recluse bite, and that the friend-of-the-daughter-of-the-relative should hie thee to her physician and get the "bite" checked out. I told her that rather than a spider bite, it could be a Staph infection and may require antibiotics.

Now, I should note that few people in my family really "get" just what it is that I do, and even fewer of them realize that I spend my days researching bacterial infections, and that Staph in particular is my specialty. So I didn't take it personally when she pooh-poohed my suggestion and told me I had no idea what I was talking about, and that FOTDOTR's doctor had already seen the bite and proclaimed it to be due to a brown recluse. Okay, whatever, northern Michigan is completely the wrong place to get a bite from one of these critters and many research papers say the same thing--that "spider bites" usually aren't bites at all. I pointed this out (and linked some Google images of supposed spider bites in comparison to Staph infection images) and then left the conversation.

A day later, relative posted an update in the thread--FOTDOTR ended up going back to the doctor as the "bite" was getting worse. As I suspected, she had now officially been diagnosed with a staph infection--and yet they were still trying to determine "what kind of spider bit her." A few hours later, relative asked "What is MRSA? FOTDOTR was just diagnosed with that from the spider bite."

This is when I started pulling out my hair, since I'd linked info about MRSA several days prior by this point. There was no spider bite, damn it!

Anyway, FOTDOTR got treatment (though relative probably still believes it's from a spider bite) and I know at least a few people on the thread now may at least think "staph" when someone says "spider bite"--so overall, a good ending.

Pal notes:

Despite this widespread belief, most "spider bites" in my part of the country [Michigan, ahem--TS] aren't caused by spiders, and probably aren't bites at all. (The feared "brown recluse" does not live naturally in my part of the country, although importations have been reported. They do not generally survive through the winter.) The distinction is important for a few reasons. First, many of us are guilty of wanton arachnicide propelled by our unwarranted fears. Second, many "bites" are probably bacterial infections and should be treated properly. Finally, there's my own bias that we shouldn't assume things that aren't so.

Indeed.

tsmith Thu, 08/11/2011 - 03:00

Tags

infection

MRSA

spider bite

Brava (and PAL too). You would not believe how many times I have had this exact conversation. Well, actually, OK, you probably would...

Indeed. I have my own little rant on the subject near the end of this article. The only reason I can figure for spiders getting blamed for so many of these skin lesions, is that people see a skin lesion, and jump to the conclusion that because it is small, circular, and red, it must be a bite. They then bound ahead to the assumption that they must have been bitten while sleeping, so they check in the bedroom and find spiders. Which they immediately blame.

For the record, I have captured, poked, prodded, and otherwise harassed a lot of spiders of many different species over the years while trying to get pictures. And not one of them has ever bitten me, or even shown any interest in trying. Not *one*. *Ever*. I am therefore *very* skeptical of people who claim spider bites unless they actually saw the spider do it.

Still makes my skin crawl... But not as much as bed bugs.

@Tim

I managed to harass a jumping spider into biting me once. It felt like a brief sharp pinch. However, there was no persistant welt or redness. And I agree. I am highly dubious of claims of spider bites. It's not as if a spider could possibly feed off a human. (Unlike the very many insects - and microbes - that do exactly that.

I have the same reaction when people tell me they killed a water moccasin or a copperhead in their back yard. Most of the time, they've merely killed some unfortunate nonvenomous snake.

iiiinteresting. Now I'm going through the various spots-on-skin things I've had over the years and wondering how many were actually bites of any type of critter at all. There's really only one time that I was fairly sure it was a spider - three marks in an uneven line that were "speckle-y" and itched like crazy for a couple of days. The spider caught in the blanket nearby made it seem like a good indicator, but that was years ago and I've never had anything similar again. And, now I think I could have been entirely wrong. Made for a good story to creep out my friends though.

Being bitten by things is annoying, and people are quite often afraid of spiders. Maybe they just seem like a convenient target for the blame. The idea that scary things can get you without your knowledge tends to kick in people's imagination. (and, in the case of your friend, her doctor's imagination apparently) Personally, spiders bug me far, far less than mosquitoes. I'd love to have spider webs all around my house if it would result in fewer frickin' mosquitoes.

In my experience, spider bites are usually characterized by a row of bites. The spider takes a chomp, walks a few paces, then takes another. Fortunately, the only spiders that have tasted my flesh have been pretty innocuous. No worse than mosquito bites.
But yeah, I've been through crawlspaces teeming with black widows and never gotten a bite from them. I have a couple big, fat harvestmen in cobwebs in my kitchen, happily keeping down the summer influx of fruit flies. They are welcome in my space as long as they stay out of my bed.

Boy, does this hit home. Several years ago I purchased a classic car for restoration. It had been sitting in a garage for several years with all of the various parts inside the car. I had it towed home and stuck it in my garage and eventually did an inventory of just exactly what I had bought. Several days after this exercize I developed a small, circular red patch on my right elbow. Now mind you, I never saw a spider or felt anything like a bite, but combined with a low-grade fever and flu-like symptoms, my wife eventually brought me to the emergency room. By this time the red patch had spread almost all of the way down from my right elbow to the wrist. Every one of my family members was telling every one within earshot, "Brown Recluse!, Brown Recluse!!" Seeing as how this was Arizona, it made some sense, but I was never convinced. Anyhow, I spent 6 days in the hospital being pumped with antibiotics before the infection would clear. Now, thanks to your post, my mind is now clear that the cause was not due to an insect bite, but probably a staf infection unrelated to the car, insects, my wife (well, maybe her..) or my family.

I used to have a tarantula that was quite aggressive, and would have bitten me given the chance, but to the best of my knowledge I've never been bitten by a spider. I have woken up in the morning with a dead spider in the sheets, and remembered that something was tickling my legs at night. Poor thing must have wandered into my bed thinking it was a safe place to hide, only to be squished as I rolled around at night. It didn't bite me, or at least there was no noticeable effect if it did.

I also had a jumping spider in my truck while I was camping in it near Moab. It jumped from a pile of clothes to the ceiling in the truck when I moved, so I raised a stainless steel plate up underneath it, which it obligingly dropped onto, so I could then let it out.

And I definitely agree with kickabout that "spiders bug me far, far less than mosquitoes". Those nasty little things have bitten me thousands of times, and they do carry some pretty nasty diseases (West Nile virus up here, malaria and other horrible diseases elsewhere).

-mark.

Peter Parker actually had a staph infection?

How would the victim get the MRSA infection? Just pricking herself on something and either having the Staph already on her skin or exposing the broken skin afterward? Or is it possible to get the MRSA infection without a break in the skin?

Robert, it is possible to get an infection even without broken skin, though they're much more commonly associated with pre-existing wounds.

I recently was bitten by a spider in my sleep. And if it wasn't a spider, I'm not so sure I want to know what it was. There were two puncture wounds that eventually ended up blistering and swelling something awful. It hurt a little bit, but the worst part was the intolerable itching. I don't know if that was a direct result of the bite or if my hyperactive immune system identified it as an allergen, but ugh....I'm glad it's gone now, save for a fading scar. It took about a month to go away and that was with keeping it very clean and in a healing environment.

The only spiders that I've seen around where I sleep are jumping spiders, orb weavers, and those long skinny spindly ones that like to hang out in basements (not sure what they're called). I know the orb weavers are pretty docile, but I've read that the varieties of the latter two can give nasty bites sometimes, though nothing requiring medical intervention except occasionally in vulnerable individuals (e.g. infants)

I was pretty surprised when researching my awful spider bite to find out what you just posted above though. It turns out all those painful "bites" on me throughout the years were probably not from spiders at all, though I do suspect some sort of insect for the majority.

When I tell people that say they have a spider bite that it's probably something else, they seem offended....

The "spider bite" of Baltimore is even less likely to be a spider and we basically translate it straight into "skin-popping" for the chart.

I suspect that in some communities doctors call any small red, inflamed spot that won't heal a 'spider bite'. Far less likely to cause a panic than telling them it's MRSA that might, with a heaping help of bad luck, cause their limb to liquefy and fall off. Standard treatment for these 'spider bites' is the same as treating a MRSA infection. Minus the panic.

Back in the 60s people felt roughly the way they panicked when they heard the diagnosis of cancer. There were all sorts of euphemisms used to avoid telling people they had the big-C. A popular one was their having an 'abnormal growth'.

I was reading a blog dealing with field medicine in remote locations and the medic claimed the standard treatment for such things, because antibiotics are extremely hard to get, was to rig a dilute chlorine bleach drip to irrigate the area and keep it saturated until the infection clears. Once cleared standard wound management was started. He claimed it worked well as lion as the patient was otherwise healthy.

I'm no expert but assuming your standard festering third-world hole and a chronic shortage of hygiene and medicine it sounded like a plan. I realize you can't make medical calls but it would be great to hear what an expert on staph has to say about what strikes me as a unconventional treatment plan.

Tim: I believed I had spider bites for the reasons you claim plus one more -- when I got rid of the spiders behind my bed, the recurrent bites stopped cold. It's not a lock-solid case, but it does seem logical.

Those of you who reported multiple bites in the night that were intensely itchy thereafter were bitten by the dread "kissing bug" Triatoma sanguisuga, a fit subject for the next blockbuster horror movie!

In my twenties, I once put on a spring dress that had been hanging in my closet in Oregon all winter, and went to work. Shortly after I sat down at my desk, I felt a sharp sting on my thigh. I ran into the bathroom and lifted up my skirt and found a five inch circular bruise on my leg. I took off my dress and shook it, not finding any spider, and went back to work. Within an hour I started to feel a edgy and feverish and slightly dizzy. I worked all day and went home and never went to see a doctor. I felt sick for a day or two and then recovered. The bruise, however, lasted two or three months, gradually changing colors and finally clearing up. Based on the suddenness of the attack, and my feeling of having been poisoned, I am pretty sure it was a spider bite.

Better than waking up out of a sound sleep after a wasp sting. We commonly have Polistes wasps come in the house in the fall to overwinter and ending up crawling under the covers with you or dropping off the ceiling onto the bed in the middle of the night. Talk about jumping out of your skin!

I've spent years trying to convince friends that the red bump on them wasn't really a spider bite. Then my MIL got bit by something large enough to leave two visible fang marks on her leg and cause a huge nasty necrotizing reaction. It's the one and only time I've argued for a spider bite - she ended up going to the ER that day as the swelling spread more than 1 inch an hour. The doctor agreed, and guessed brown recluse. But we'll never know, because we never saw the beast.

I wonder what nasties may be transmitted from the surface of the fangs by even non poisonous spiders.

I was bitten by a brown recluse while sleeping. After extensive research I found out that they carry the flesh eating disease and have migrated to almost all parts of the U.S. These spiders live for 7 years and are resistant to most pesticides.

I know roaches can bite you and it looks like spider bites. I saw it on the show "Billy The Exterminator". There was a house that was so infested with roaches that there was a mouse that died and you could see the roaches eating it to the point where it was nothing but bones. They are especially dangerous to people with diabetes because most people don't feel them biting their legs, which get infected. Fleas bite too and sometimes the bites look like spider bites. All people have staph on their skin, it just takes a poke or scratch to open the skin and let the infection in.The spiders with the really long legs are what we call daddy longlegs and are not poisonious to humans because our skin is too thick for their fangs to puncture, but they are deadly to roaches and other bugs, so I don't mind them in the house.

I am quite confused by the ignorance of so many MI residents and doctors related to the diagnosis of brown recluse spider bites. I currently have a roommate that rents my basement. My home is only 17 yrs old and has a very nice finished basement area. The roommate is a veteran around 60 yrs old and not in the best of health. About one month ago, the roomate advised he had a spider bite on his rt forearm and it was very infected. He saw a doctor and was treated with antibiotics and it healed after a couple weeks. The roommate used a spider 'bomb' in the basement to kill any spiders hanging around. A couple days ago this roommate advised of another spider bite. The location was exactly the same as the first but on the lt forearm this time. Roommate was started on antibiotics again and was scheduled to return to VA in a couple days to have the 'bite' lanced. At his appt he was told he was definitely bit by a brown recluse spider. The doctor cut out a decent size area of his forearm and sent him home with more anti optics and bandages. When my roommate starting telling me about the extent of the infection I asked if it was MRSA. He of course said the doctors confirmed it was a brown recluse spider bite and pulled up pictures on the Internet to show him proof. I WAS SHOCKEd!! I can't imagine how a doctor could determine that a patient was bit by a brown recluse, in Michigan, twice in a month, in the same exact location but opposite sides of the body, without any signs of a spider, ever!!!! Now I am tiptoeing around my own house sanitizing everything!! How does a medical professional not know about the non-existence of brown recluse in MI and the rarity of a spider bite to begin with?? This roomate works in a bar and is always leaning his forearms on the bar as he stands. His skin is very thin and I can only surmise he had a tear in his skin and MRSA entered. How do I convince my roommate to address this further with his doctor? And how do I suggest he take extreme precautions not to spread the infection to the rest of the household without treating him like a leper?? Panic has taken me over!!

I had a deer tick removed on my upper left shoulder close to the neck within 8-12 hours, washed it, put iodine and anti-bacterial cream on it. This was on the 4th. On the 17th or 18th, about two weeks out, I had what appeared to be a bite surrounded by a very dark red rash, no bullseye, on my inner left thigh, which developed on the 19th through the 24th into light red splotches of rash all over my body. I froze the small deer tick and saved it for analysis. On my visit to the doctors they indicated that it probably was the deer tick bite that caused the rash, not a spider bite, and they took blood samples and put me on the antibiotic used for treating Lyme disease for 21 days. I am still on it and the rash is disappearing after the 3rd or 4th day so far. I have not received the report on the Lyme disease sample and will on July 1 - 27 days out from the tick bite; however, the test may no0t show positive until several weeks after the bite and this sample was taken almost 3 weeks - 20 days - after the bite.
I observed a puncture "bite" in the center of the dark red rash. Why could this have not been an insect? What else could cause a puncture mark that itched? None of the other light red rashes - some semi-circular with light "bullseyes" with no puncture marks itch. The nurse asked me if I ever had MRSA. I have not. Could this be a staph infection of some type coincidental with the tick or "spider" bite?

Okay... but every one of my "spider bites" is in pairs. Two bumps, not just one. And in various places -- my hand, my foot, my back, my stomach. All in pairs. Uneven pairs, like one fang had a lot more poison than the other, but still. I can't think of why staph or some other bacterial infection would consistently come in pairs like that, even if that would otherwise be a more likely explanation for the blisters that have formed a couple days after the itching and redness started.

ASM-ESCMID conference on methicillin-resistant Staph in animals

tsmith — Fri, 17 Jun 2011 11:30:00 +0000

ASM-ESCMID conference on methicillin-resistant Staph in animals

As I mentioned previously, I'm heading up organization of this conference, which will take place September 8-11 in Washington, DC. The abstract submission deadline has just been extended another week until next Friday, the 24th, so there's still time to send in an abstract. Hope to see many of you in September!

tsmith Fri, 06/17/2011 - 07:30

Tags

Conferences and meetings

animals

conference

MRSA

Nick Kristof on our food supply

tsmith — Sun, 12 Jun 2011 08:00:00 +0000

Nick Kristof on our food supply

Nick Kristof has an op/ed in today's NY Times noting some sober statistics about the food we eat: that it puts 350,00 people in the hospital and kills 5,000 in the U.S. every year. He also cites three of our papers examining MRSA and swine/swine facilities.

tsmith Sun, 06/12/2011 - 04:00

Tags

Policy

For those of us who like to eat raw veggies and salads, there is a simple way to almost-guarantee safety: soak the food for 20 minutes in diluted dish soap or dilute chlorinated water. Rinse thoroughly, and enjoy.

p.s. the dish soap taste DOES rinse off

When is MRSA not MRSA?

tsmith — Fri, 03 Jun 2011 07:00:00 +0000

When is MRSA not MRSA?

...when it contains a weird gene conferring methicillin resistance that many tests miss.

Methicillin-resistant Staphylococcus aureus (MRSA) has become a big issue in the past 15 years or so, as it turned up outside of its old haunts (typically hospitals and other medical facilities) and started causing infections--sometimes very serious--in people who haven't been in a hospital before. Typically MRSA is diagnosed using basic old-school microbiology techniques: growing the bacteria on an agar plate, and then testing to see what antibiotics it's resistant to. This can be done in a number of ways--sometimes you can put a little paper disc containing antibiotics right onto a plate where you've already spread out a bacterial solution and see which discs inhibit growth, or sometimes you can grow the bacteria in a plate with increasing concentrations of antibiotics, to see when the drugs are high enough to stop growth. Both look at the phenotype of these bacteria--the proteins they're expressing which lead to the bacteria's drug resistance.

However, these culture-based methods are slow--they can take days between when the patient first is seen by a doctor and the time the results come back from the clinical lab. For this reason, increasingly labs are moving to molecular methods, which are much quicker than the culture-based methods. Indeed, detection of the gene responsible for methicillin resistance, mecA, has been the gold standard for *really* identifying MRSA, even beyond phenotypic methods.

A new pair of papers demonstrate the limitations of this reliance. Like many science discoveries, this one started with a "huh, weird" moment. Investigators noticed that a number of their S. aureus samples were categorized as MRSA using the traditional phenotypic methods, but were negative when it came to the mecA DNA test. Genetic analysis showed that these isolates carried a different mecA gene, dubbed mecALGA251. The investigators searched their isolate collection in England, and also worked with collaborators in Scotland and Denmark to search through their banks for additional mecA-negative MRSA, and found almost 70 isolates, including one dating back to 1975. (A second paper by a different group examined two isolates in Ireland).

Now is when it starts to get really interesting. (Continued below)

Many of the isolates from England were of cattle origin--from milk samples. When these were typed, most of them were the same spa type (a way to type S. aureus, sequencing a repetitive region of the Protein A gene, which encodes a surface protein). These were t843. Why is this interesting? Because t843 is considered to be a "cattle" type of S. aureus. So sure, it makes sense that you'd find it in milk samples--that's a no-brainer. But it was also found in human samples in England, Scotland, and Denmark (including that previously-mentioned human isolate from 1975). A second paper also found t843 in a patient from Ireland, along with a closely-related spa type in a second patient (t373). What is this "cattle" strain doing infecting humans? The authors draw parallels to the emergence of the "pig" strain of S. aureus, ST398, that has also been found in humans and other animals (including dogs, horses, rats, and chickens). Is this another "animal" strain that's emerging in humans? Or is it a human strain that we've given to cattle, like we did with chickens? The types found in humans and milk samples in the same areas match pretty nicely between humans and cattle (shown below, Figure 2 in the manuscript), suggesting local interspecies transmission.

Looking over time, they also noted that the prevalence of this odd mecA gene increased over time in their database (2007-2010). It's still low--less than 1% of the samples--but what was also unique was that it was in other lineages besides the t843 strains. As in, at least 3 different lineages besides the one containing t843. So, it looks like this weird mecALGA251 gene is jumping around, inserting itself into all kinds of methicillin-susceptible S. aureus. ("Regular" mecA does this too so that wasn't completely shocking, but it was a surprise that it's had enough time to spread to 4 different lineages without ever being detected).

Where does this leave us? We have to be careful and make sure we don't outsmart ourselves with our technology. For now, the benefits of using DNA-based identification methods still outweigh risks of missing weird MRSA since its prevalence is fairly low, but we need to be cognizant of the potential to miss isolates, and keep backing up our molecular methods with old-school cultures. We also need to periodically adjust our "gold standard" molecular tests to include novel findings like this new mecA. The authors note that in addition to their new findings, they also found several isolates "that had an MRSA phenotype but no mecA gene that could be detected by PCR (polymerase chain reaction)"--so there might be other unique mecA genes (or other resistance mechanisms) that remain undiscovered.

Finally, this paper again makes me ever so jealous of the surveillance systems in other countries. In Denmark, for example, all MRSA are to be submitted to the Statens Serum Institut, where they type all of them. Now sure, Denmark is much smaller than the U.S., but even to have this type of surveillance state-wide is incredibly difficult here. Trying to compare between states? Even harder. So--do we have these strains here? Probably so, but it will be more hit-or-miss to find them.

Edited to add: Scientific American has an article on this as well, where I weigh in.

Citations

Laura GarcÃa-Ãlvarez, Matthew TG Holden, Heather Lindsay, Cerian R Webb, Derek FJ Brown, Martin D Curran, Enid Walpole, Karen Brooks, Derek J Pickard, Christopher Teale, Prof Julian Parkhill, Stephen D Bentley, Giles F Edwards, E Kirsty Girvan, Angela M Kearns, Bruno Pichon, Robert LR Hill, Anders Rhod Larsen, Robert L Skov, Sharon J Peacock, Duncan J Maskell, & Mark A Holmes (2011). Meticillin-resistant Staphylococcus aureus with a novel mecA homologue in human and bovine populations in the UK and Denmark: a descriptive study Lancet Infectious Diseases Link

Anna C. Shore1, Emily C. Deasy, Peter Slickers, Grainne Brennan, Brian O'Connell, Stefan Monecke, Ralf Ehricht, & David C. Coleman (2011). Detection of Staphylococcal Cassette Chromosome mec Type XI Encoding Highly Divergent mecA, mecI, mecR1, blaZ and ccr Genes in Human Clinical Clonal Complex 130 Methicillin-Resistant Staphylococcus aureus Antimicrobial Agents and Chemotherapy Link

tsmith Fri, 06/03/2011 - 03:00

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