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>> [background music] our next speaker isdr. robin jump. dr. jump is a physician scientist with thegeriatric research education and clinical center in the louis stokes cleveland veteransaffairs medical center in cleveland, ohio. she is also an assistant professor of medicinein the division of infectious diseases and hiv medicine at case western reserve. in 2009, dr. jump established an infectiousdisease consultation service for cleveland's va long-term care facility, reducing overallantimicrobial use by 30% over 18 months. building upon the success of this program,she was the principal investigator of a multi-site va grant designed to help providers at longterm care facilities and improve their use
of antimicrobials. after earning her md and phd at case westernreserve through the medical scientist training program, dr. jump completed an internal medicineresidency and infectious disease fellowship at the university hospitals of case medicalcenter. she's certified by the american board of internalmedicine in both specialties. she's presented nationally and internationallyand has numerous publications, serves on a number of national committees including theantimicrobial stewardship subcommittee for the society for the health care epidemiologyof america. please help me welcome dr. robin jump whosetopic just happens to be treatment and prevention
of c. diff. thank you. [ applause ] >> good morning everybody. thank you all of you for being here and foralso to the committee for inviting me to be here. much like argine [assumed spelling], i'm anexpert because i got in a plane to come here and i want to have you also share what yourexperience and stories are because i think this is where we learn a lot more about whathappens in c. diff and you guys can't hear
me. i'm sorry. this always happens. i'm loud in my head but apparently i'm notloud in reality. ok. is that better in the back? all right. fantastic. and i also want to thank so much dr. farah[assumed spelling] and todd and cindy and
peggy for making me feel so welcome and forsuch a red carpet treatment as a speaker. so thank you very much. and also eddie, he has no introduction buteddie also, thank you for inviting me to be so here are my necessary disclosures. and let's talk more about the outline of thetalk which is that we're going to talk about poop, it's all glamour at this point fromhere and out. and they always put me right before lunchalso. and all the way, it gets better. so pathophysiology is what we'll talk aboutfirst and we'll deal with risk factors, talk
about treatment for c. difficile and thenfinally end with infection prevention and control strategies. some of which are evidence-based, some ofwhich are eminence-based and not always just my opinion but other people think it too. but there's a mixture of what is good practiceand what is common sense for how we approach this. so, let me start up by just putting c. difficileon perspective. so i have the pathogens look within the firstcolumn, the number of illnesses per year in the second column and the number of deathsin the third column.
so c. diff causes more infections in the unitedstates than all these other horrible pathogens combined and is actually causing this on theorder of the same number of deaths per year. so, a cilia, that is, it is sometimes to talkabout poop, this is such a big deal. and if my kids know what i did for a living,they would not listen to me when i told them at the dinner table we're not having pottytalk anymore. so let's talk about pathophysiology. so here's a very simplified model of whatit looks like when you get c. diff. there's three different classifications, there'snon-severe, severe and severe complicated. and we'll talk about different treatment approachesfor these.
but, you know, basically non-severe, somebodycan be treated as an outpatient or sometimes in a hospital and sometimes in a nursing homeif that's where they happen to get their c. difficile. severe c. diff means there's a white bloodcell count over 14,000 and basically acute kidney injury. and then severe complicated c. diff, we'renot talking about ileus and trying to get a surgeon involved using an id doc involvedas well. these are the people that are icu bound andmaybe getting colectomies and hail mary treatments. so hopefully, people get better which meansthey become an instamatic carrier for a brief
time and then soon, no c. difficile and that'sthe best way to come out of this. other people don't do so well and that's thenumber of deaths that we have for c. diff. and then there's also the state of recurrentdisease where someone gets better and then it comes back and then we treat them again,they get better, and it comes back and they can go to the cycle many, many times. and at some point, they get-- in all of those,get desperate to try to get them better. so let's talk about how we actually get c.difficile. in all of our intestines, we have a wholeboatload of bacteria in the order of 10 to the 11th to ten to the 13th organisms pergram of stool which is more than i can really
think about well. so there's a lot. and it's a form of host defense. they eat the food that we give them and sothey take up the chemical nutrients. and they can starve out pathogens. they occupy physical locations in the gutthat also keeps other pathogens, or real pathogens were getting a foothold. and so for most of us, when we're exposedto a pathogen that affects the gut, it passes right through.
and for most of us, that's what happens whenwe're exposed to c. diff. it goes in one end and goes out the other. and we don't ever have to really worry aboutit. when someone gets a stomach antibiotic, boththe number of bacteria goes down but also the diversity of species goes away. and so we're going from maybe somewhere inthe order of 500 to 1000 different species to far, far fewer. and also as the numbers go down, so that meansthat they're not eating as much and so there's a lot more nutrients available on the gut.
and that also means they don't take as muchspace and so there's other places for bacteria that it might be pathogens to get in thereand find a home. so when someone who is in this state wherethey've been rendered vulnerable by antibiotics necessary or not, and they got exposed toc. diff spores, they ingest the spores, they find a home, they find food, they germinateand they start making toxin. and the toxin that they make-- the vegetativeform is what's making us sick. so all of this becomes a very fancy way ofme telling you that antibiotics are the most important risk factor of developing c. difficileinfection which everybody here knows otherwise you wouldn't be at the conference.
so let's do some numbers to back it up. so, besides the individual exposure, it alsoturns out the facility, antibiotic use promotes c. difficile probably through transmissionby promoting transmission. so this is a four-year retrospective cohortstudy that was published in 2015. and the authors examined patient level andward level of risk factors for acquiring c. and what they found is that for every 10%increase in antibiotic use, and this is measured by days of therapy per 1000 patient days ofcare, the relative risk of c. diff went up. and this included people that weren't actuallygetting antibiotics. so the antibiotics that we're giving in thehospital as dr. sebastian said earlier, what
i do as a provider for my patient can affectevery other patient in the ward or in the unit, even those that are actually gettingantimicrobials. and it also turns out that more antibioticsmeans more risk of c. difficile infection. and this goes as we know for length of therapyand it also goes for the number of classes of therapy. so this is a study that was published in 2015also where about 400,000 adults were admitted to 14 hospitals in 2011 and 12. and they had a less than 1% rate of c. difficileinfection which is actually phenomenal. they looked at the relative risk of c. diffbased on the number of classes of antibiotics
that people were exposed to. and for one class of antibiotic, the relativerisk compared to no antibiotic was about two. and then as they got exposed to more thanone class, the risk went up. so there's the vanc and pip-tazo here on number2. and then, there is the changing from vancand pip-tazo to meropenem or to cefepime. and these class changes, and we're bringingin tigecycline. all these switching that we wind up doingas we're chasing either pathogens or ideas can increase risk of c. difficile infection. sometimes this is necessary.
but sometimes it's not. if somebody say, comes in for community acquiredpneumonia and we can deescalate them, maybe they don't need to go out on the floor, comealone when they came in on zithromax and azithro. maybe they can stay on azithro and go on,put out on that. so steps you can take regarding antimicrobialuse to decrease the risk of c. difficile. so, stewardship of course is the mainstayhere. and one of the ideas is to avoid antibioticsimpossible and one thing that i've been trying to talk about a lot with people is to engagewhen you can, when the patient is incredibly ill, and watchful waiting.
now it turns out that families hate that becausewhat they-- and also some nursing staff hates it too because what they hear is, you're notdoing anything. the patient is sick and nothing is happening,you're just watching. and so, what i'm trying to change in the languagethat i use and i invite you to try this too is to say careful observation. we are involved. we are engaged. we are spying the symptoms. we are observing.
we are doing vitals signs. we know what to do if there's a turn for theworse. so we're carefully observing and trying toavoid unnecessary antibiotics or unnecessary medications. and if you throw in powerful in there too,we don't want to expose your family member or you to a medication to a powerful medicationthat may harm you until we're really sure that you need it. so when you do use antibiotics, my suggestionis, when you can go to shorter courses, and i'm thinking now about people that are inout patients in long-term care and on the
regular hospital ward, not necessarily icutype patients, choose narrow-spectrum when possible and also, when you can, choose agentsthat have less excretion of the gi tract. so for example, for treatings, maybe cystitisor uti, a real uti, bactrim is a better choice than a fluoroquinolone because of where itgets excreted. bactrim will concentrate in the bladder. and we all know we all have a sense of whatthese agents are that have to undergo more renal excretion because those are the oneswe have to dose-adjust for people that have renal insufficiency. so that is a reasonable way to think aboutthose differences.
so the other big risk factor for c. difficileis advanced age. and this was demonstrated dramatically withthe outbreak of a hypervirulent strain or the nap1-027, i've forgotten the letters,i just call it hypervirulent or epidemic at this point. so, this is a graph that looks at the epidemiologyfrom 2000 to 2005 when the strain really began to take off in the us. and all-- the entire population together,shown in that black line in the middle is the older adults that already had a much higherrate of c. difficile infection. that's the green and the thick red line ontop.
and they were also the much more affectedby the epidemic strain than other populations were. so c. diff by and large is a disease of olderadults. so why is that? there's a lot of age-related vulnerability. in 2010, greater than 90% of deaths due toc. diff were in people older than five years of age. and this used to be in part because agingleads to immunosenescence. as we age, your immune systems just aren'twhat they were the year previous or the ten
years previous. and that means that there's a poor antibioticresponse and that correlates to an increased risk of difficile infection. and also, older adults have a less diverseand a less resilient gut microbiome. and so when they're exposed to antibiotics,they don't bounce back as quickly in terms of what's happening in their gut microbiome. so what can we do about advanced age? this is all i've got folks. [ laughter ]
if you've got a better idea, please talk tome after we're done. so other risk factors. not surprisingly previous healthcare exposureeither hospitalization or long term care. and by the way, i have-- as i said, i worka lot in long-term care and so, it's-- i hear a lot from long-term care well it's the hospital'sfault, and they hear in the hospital it was long-term care's fault. it's all of us that have to work on this togetherand we are, which is wonderful. so underlying disease severity is also a riskfactor for c. difficile, as is a low albumin which i think really is a reflection of underlyingdisease severity.
and finally, one that we can all do somethingabout is gastric acid suppression. so some data about this, this is a study bymcdonald that came out in 2015 and this is not the first of these, or there's a bodyof literature about proton-pump inhibitor use increase in the risk for c. diff. but this was the one that really, that wentafter-- we had more specifically, i guess. so they looked at risk factor forgetting recurrentc. difficile infection. so which eight grade and 75, it was protonpump inhibitor or ppi use, antibiotic reexposure not surprisingly and then length of stay. so, ppi we definitely all have some influenceand control over.
so they went and looked-- of the 200 peoplethat were in their study, what was the indication for being on a proton-pump inhibitor? and for half of them, there just wasn't one. and so sometimes, [inaudible] for proton pumpinhibitor because they're just-- a patient's coming to the hospital and that's what wedo. that's then that we can try to work on andchange that behavior. other reasons for proton-pump inhibitor wereolder age and with two other risk factors, upper gi bleeding and a history of gerd inthe last 20 days, and those are acceptable. so other steps that we can take to reduceother risk factors are stop ppis unless they
really are needed and avoiding antibioticreexposure. so moving this idea from just in case youhave this, we'll give you antibiotics to a philosophy of we're only going to give antibioticswhen it's necessary. and the worst offenders of the antibioticsare clindamycins, fluoroquinolones and then the later generation cephalosporins. i'm not saying that other antibiotics don'talso lead to c. diff but these are among the worst especially clindamycin. so treatment. there's a lot to be said here and i'm goingstart first with the 2010 guidelines from
the ideas [inaudible]. these are currently undergoing revision. and i feel like everyday, i'm waiting forthe new versions to come out and they're just not there yet. so, soon. but i've been saying that for a year, so soon. so treatment of non severe c. difficile infection. so let's talk about first what the definitionis and is diarrhea, which are three or more unformed stools, excuse me, in less than 24hours.
and then what these diarrheal stools testpositive for c. difficile. and i wanted to mention there, there was actuallya question before i began to talk about what about the stool that's being sent for testing. why does it have to be unformed? so there's about 3% of population that wereasymptomatic carriers of c. diff. we have an inner stool, it doesn't botherso it doesn't make us sick. there's no reason to test or to look for thosepeople. so, the rationale we'll be having when stoolis sent down to the lab for testing to have it conformed with the containers, to makesure the person is actually symptomatic.
so in my hospital, when it takes two daysto get stool ordered and tested down at the lab, it suggests to me that they don't reallyhave c. diff because they don't have a diarrheal sample yet. so that's the rationale behind that. and one of the-- we have the stick test tomy hospital. so if you have a cup of stool in it and youput the stick in and it stays upright, it's not suitable for testing. the stick falls to the side, then it's ok. i live in a simple world you know.
so, for non-severe c difficile infections. it's the first thing, and i think we all overlookedthis. i know, i certainly do, is to stop the antibioticthat got them stick in the first place, if you can. and then other treatments, so the first-lineof agent recommended is still oral metronidazole. and if they're on warfarin, they may go tooral vancomycin. oral metronidazole is as good as oral vancofor non-severe c. difficile infections. and it's only a little bit less good for severec. diff. so, severe c. diff infections the definition--i'm sorry, i slipped that earlier, it's actually
white blood cell count right at 15,000 anda creatinine 1.5 above baseline. i just go with acute kidney injury. the treatment here for severe c. difficileis oral vancomycin 1.25 milligrams p.o. q6 hours. and we'll talk a little bit more about themin a couple of slides. iv metronidazole and oral vanc together areassociated with reduced mortality compared to oral vanc alone. and i see no reason why not to got with theiv metronidazole at this point. so it gets you know, it goes in through thearm and goes-- it undergoes first pass metabolism
in the liver. some of it gets in the gi tract, but it also,from liver metabolism, but it also gets in the leaky gut and then gets into the lumenof the intestine where it needs to go to actually fight the c. difficile. so in a way, it's self-tapering medicationwhen people are having-- getting it as an iv form. and this was one center study but it clinically,it makes sense to me. so treatment of severe c. diff infectionsthat are complicated, so these are unstable patients that are having ileus or toxic megacolonthat are bound for the or.
so here's where the evidence is not so good. and there's a lot of, what's the word, witchcraftthat goes in to trying to figure out how we're going to treat these folks. things are getting better but it still-- it'sa carrot and stick approach sometimes. so oral vanc high dose, the recommendationsis 500 milligrams p.o. q6 or per rectum q6. i don't like the idea of sitting in rectaltubes in the people that already have a friable gut, but that's just me, i'm not a surgeon. five hundred milligrams isn't really betterthan 125, but i think it makes us all feel better.
but what that 500 milligrams of p.o. vancdoes and this doesn't make sense to me but i've seen the data. it kills off a gram-native organism calledbacteroides fragilis which is actually a big a big good part of our gut microbiome. so by giving more of the vanc, we're actuallymaybe not doing such good things for those patients. so treatment here, iv metronidazole of reasonabledose of oral vancomycin, and then people at one point, we're doing iv ig that's fallenout of favor. tigecycline has to be a hail mary approach.
and there's all sorts of other things thatwe're doing now. and i'll get to those. also monitoring serum lactate in white bloodcell count is an important part of managing someone with severe and complicated c. diffas is consulting a surgeon and getting an id doc involved. a key for all of us is to not do test of curewhen someone is better from c. diff than just let them be better, where we don't need tomake it go away every time we reexpose them to try to treat an asymptomatic person, wherewe're actually messing up their gut floral again.
so let's just leave them alone. and then for treating recurrent disease, stopthe inciting antibiotic which i still forget to do. the first recurrence, we still repeat metronidazole. the second recurrence is oral vancomycin andthen the third recurrence or the-- sorry, yeah, the third recurrence and more. people are doing oral vanco or the oral vancomycintaper or we have lots of other options now. so, fidaxomicin, which joe mentioned earlierand i agree is not a first-line therapy. this isn't an agent that's anti [inaudible]c. difficile but spares other members of the
gut microbiome. the treatment outcomes for recurrent c. difficileare equivalent of that of oral vancomycin. and it does appear to reduce the risk of recurrentdisease. and this was trialed in older adults in somelarge clinical trials. and i just wanted to show you fidaxomicinhere. so the-- this little molecule on the bottom,that's penicillin-- i'm sorry that's metronidazole, excuse me. this one is penicillin. so you've got the house in the garage in thedriveway and the play ground in the back which
is the other r group where people have fun. this is-- sorry it's a little id humor. and then this is fidaxomicin. so it's called a macrocyclic antibiotic. so there's one, two, three rings and thenthere's this thing in the middle. i don't-- it's like a super ring. it's like a knuckle ring, right? so, i don't know how this works but it seemsto not affect a lot of the gut microbiome and only get c. diff.
but you can see why it's called a macrocyclic,three rings and the thing in the middle. all right, so let's talk more about why itshould not be first-line therapy. it's just too expensive right now. a 10-day course of fidaxomicin and these are$2013, it's $3300. and i don't know many people that can affordthat. vancomycin capsules for a 14-day course areactually $2000. so, a little bit of cost savings there, butnot much. so what we do at my pharmacy at the va, andnot all vas do this but mine does in cleveland, and we compound vanc.
so we take a bag of iv vancomycin, reconstituteit into 100 mls of d5ws, my guess, and divide that into 8 syringes. and that becomes something that goes withthe patient's mouth, squirt four times a day. and it's about 40 bucks for the entire 14-daycourse. and this-- there's so much cost savings that--if that-- we'll actually fedex the vanco to somebody's house if they've gone home on anoral vanco, rather than gives in the capsules. so it's a huge cost-saving. it works as-- i think it's not all that challengeto do. it depends on what the regulatory bodies arefor your hospital or your pharmacy is to what
they're allowed to do for the compounding. and then of course, metronidazole is $30 fora course. this is part of why it's first line therapy,is also effective and even when we're talking about severe c. difficile, the effectivenessof oral metronidazole is just a little bit less than that of oral vancomycin. and so, if we're talking about a situationwhere it's $2000 or just $30 and now your really robust patient, they didn't get better,i tend to go with the oral metronidazole still. so, there's a whole bunch of other therapiesout there now. and fecal microbiota transplant assures thatyou've all heard about, though maybe not with
a great deal of welcoming to it. so the bottom line here is that this administrationof feces from a healthy donor into someone that's got c. difficile infection. it works. people get better in one or two days. they get better with one or two treatments. and i can't think of anything else that wedo in medicine that does involve a scalpel where we do it once or twice and we'd-- we'vemade you better unlike, most people stay better. and this works in older adults as well asyounger adults in the series of 10 people
or the 80-- 8 of 10 has some [inaudible] resolution. and this keeps going. it gets better and better the more that wedo this. they are beginning to see-- we're all beginningto see reports of complications. but in general, poop transfer works and itworks well. and i know it's not glamorous but this iswhat-- this is where we are. and by the way, so this is why they put mebefore lunch. this is a glass of chocolate milk. it doesn't look this bad.
but wait, it gets better. so, yeah. now we can do frozen poop transplants. this is a randomized, non inferiority studyof 232 adults that all have refractory c. difficile infection. so they had instead of using fresh poop, theyuse frozen poop that was thawed and then underwent, then had the fecal microbiota transplant. and it worked as well as the fresh stuff did. so now, we can have a freezer full of poop.
we can have preferred poop donors, which iknow sounds silly but it make sense because they can be screened for things like hiv andhepatitis ab before they do their donation. and so that, that works out well. and it's actually-- it's a cost-effectiveand well-tolerated strategy. so rather that have someone come back in thehospital for a third or fourth sixth time for their c. diff, or have to stay in nursinghome or have to be in isolation. if on their second or third recurrence they'rewilling and we're willing to offer and they're willing to accept fmt, if i failed oral metronidazole,i'd go for it. so, there're maybe people that are interestedin starting your own center of poop excellence
which i think would be a fantastic thing todo. and there's actually some guidelines aboutthis now and that's in your slides. and i had to say it so-- i get to-- i getto stay up here and joke about it because i don't actually have to do it. the gastroenterologist in my hospital, theyactually do the fecal microbiota transplant and that is under id, in partnership withid. but they are the ones that do it because they'redoing this by colonoscopy, which means they can bill for it, which is why the id doctorsdon't because we don't know how to [inaudible] for things like this.
we don't do procedures other than a chartbiopsy. so-- and it gets better. so if i didn't ruin ice cream and chocolatemilk now, i can at least attack easter eggs. so now, we've got poop pills. this is oral, capsulized, frozen fecal microbiotatransplantation. the capsules are stored at minus 8 degrees. the treatment is made from a single donor. there's a trial in 20 patients for the wideage range. and they take 15 capsules a day over a two-dayperiod, is really well-encapsulated in lots
and lots of the gelatin. so it doesn't-- it's not as unpalatable asyou might think, and it worked. and again honestly, i do it if metronidazoledidn't work first. this is still somewhat experimental. people are still kind of learning how to dothis, but it's getting more and more acceptance. and here's part of why it works. so this was a study that came out of i thinkit was china. and it was just-- it was a case report. yes, freeze dry.
so they used freeze dried poop pills. and the first two bars on the left-hand sideof your graph are showing the donor stool and then the donor feces after it was freezedried. so, what you can see is that it's really differentfrom that third bar, which is the woman that had crohn's disease and refractory c. difficileinfections. so they've got microbiome as very differentbetween the two people. and when she received the freeze-dried pooppills, got better. and her gut microbiome changed dramaticallyand her c. diff went away. so this is how it works.
this is why the fecal microbiota transplantworks is because all at once, we're repopulating the gut with all those lovely, diverse andincreased numbers of bacteria. they get back and then they eat up the food,they occupy the physical locations and then they can chase the c. diff out. so with the freeze dried poop pills, now actuallymy mentor curtis donskey is doing this-- they whole send the freeze dried pills to the patientsby mail, which i think is fantastic. so they can do their prep at home. they can take their pills at home. and that leads me to the question of a famouscompany.
so i think that's the worst of it. so let's move on to infection control andprevention. so, c. difficile lives out in outside of ourbodies as spores. and the spores can be recovered after monthsof being left in the surface, at least five months is what-- people have [inaudible] inthe literature. it's really difficult to kill using routinecleaning agents which is why now i love the smell of bleach. and the spores are shed into this-- onto theskin of our patients and also into the environment. and this hand print here was from one of ourid fellows years ago.
she put on a glove. she touched the hand-- or she touched herhand to the belly of a patient, pretty much like i'm doing to my own belly now, becauseif there were skin to blood contact and then she put her hand on the plate. and c. diff. not all of it, the bigger, yellow, flocculentcolors of the c. diff. i don't know what the smaller, white thingsare. but to get the idea, it's all over a patient'sskin. so when i see-- and if it's all over the skin,you also know it's all over the environment.
and maybe you've never had this experienceat your hospital, but i sure had that in mine. i'm the id doctor or the id fellow at thetime sitting up, so i have [inaudible] i see the surgeon go in, and talk to the patient. you know, and lay on the bed, or stand overby the sink or whatever it is. and i say, you know, you really need to havea gown and glove on if you're going to be in there. but we're not touching the patient, so it'sok. how are you going to tell them that you'rea testament to medical care? yeah.
but i'm sure that only happens where i practice. so, let's talk about asymptomatic carriersas well. so this is some work that was done also bycurtis donskey and it we-- we compared the rate of c. difficile spores that were foundin the environment. and it compares people with actual c difficileinfection or c difficile such as disease, they can tell us in all their paper. in asymptomatic carriers and non-carriersand they swabbed the call button, the bed rail, the table, the telephone. and basically, for people that actually havec difficile, there was an 80% detection of
spore somewhere in the environment. for people that were symptomatic carriers,it was 60%. and people that really doesn't have c. diff,it was about 20%. so, as many of you have heard before, andwas-- i was reminded of this morning by alex, we all live in a world that has a think veneerof poop everywhere we go, especially on the hospital. and there's c. diff there too. so for nursing home-onset c difficile, thisis another study that was done by dr. donskey but also we look at-- there's other peoplethat have found this to be true.
so, this graph compares the number of patientsthat were admitted and that's still on the y-axis, the x-axis is weeks after admissionto a long-term care facility. and it's a different way to think about wherethe c. diff is being acquired and this is, you know, a part of what we're being judgedon now and from a regulatory standpoint. so hospital-associated c difficile in long-termcare onset was happening within the first five weeks of transfer from the hospital tothe long-term care facility. and then later on after that-- that kind oftime point there, that break point, then they're classified as being long-term care associatedwithout antibiotic exposure or with antibiotic exposure, but a long-term care, playing thefinger at long term care for the onset.
and it seems what's happening for these patientsthat leave from the hospital vulnerable, and get to the nursing home are then-- when they'reexposed to c. diff spores is that we create between two locations. we create the perfect storm so people candevelop c difficile. so this is part of why it's all of us workingtogether, hospitals and nursing homes to try to reduce what's-- reduce the rates of c difficile. so, in terms of infection prevention and control,one way that we can try to improve how we deal with c. diff is to extend isolation. so this graph looks at the proportion of peoplethat have c. diff contamination on their skin,
in the time of the resolution of their diarrheaalong the x axis. and so even a week after their diarrhea hasresolved, about half of the patients or residents still have c difficile spores on their skin. we'd suggest that this idea of letting themout of isolation in their contact precaution is two days after the diarrhea resolved, maybe too quick. they may need to extend that and go longer. if it's working in your institution, stickwith it. if it's not, maybe seven days or ten daysor in total, are discharged if you are in a hospital is another way to think about this.
this hasn't worked well in long-term carebecause in long term care, it's supposed to be a home-like environment and you can't tellsomebody you have to stay [inaudible]. you can't stay, you have to stay in your roomfor the next two weeks. so that leads to problems of disinfection. so, this is the home-like environment thatwe have at a couple of the rooms in our va long-term care facility. and then the question is how do you cleanthis? how do we clean all the surfaces? we can't wipe down teddy.
we can always get though all the stuff that'son the-- on the rack on the walls. and also, in our institution, environmentalservices as well, we can't touch patient's possessions. that's nurse's jobs. and the nurses said, "you've got to be kiddingme" well, i don't have time for that either. so, then also it became a problem in that--and i wonder how widespread that is. if those conversations have taken place whereyou are. so one of the things that we do in situationslike this is that we have in our facility, one of the ultraviolet devices.
and this is a standalone unit, you put itin the room, you shut the door, you leave and come back an hour later. and the c. diff spores have been fried bythe uv light. and it seems to work very well. and so we do this for [inaudible] things inthe hospital and we do this for our long-term care facility residents when it's time forthem to come out of contact precautions. and so they have to be out of the room foran hour, not a problem. we do it over lunch or over dinner, or whenthey're on occupational therapy. and it's easy as well.
it's expensive to buy the machine but it'seasy to do. so things that we can do for infection control,to minimize transmission by patients or residents is to of course put people on a private roomif we know they have c. difficile or if we suspect they have c. difficile. in usually, from a hospital perspective, youknow, the person with the disease or the person who is complaining is the one that has toleave. i don't think for c. diff there's always goodpolicy. if i have c. diff, and i leave, and poor alexwas left in the room, he's still going to be exposed to the spores that are left behind.
so it doesn't make more sense to have alexgo to the clean room and leave me behind in my own fecal veneer? not that alex is my roommate, he was justthe first guy that i saw that you'd pick on here on the audience. we're very liberal on cleveland you know. so encouraging hand hygiene among all staffand among the patients and the residents, depending or-- or the resident-- when i sayresident, please forgive me, i'm thinking about long-term care. but we should encourage our resident physicianto also to wash their hands.
so hand hygiene with soap and water. soap and water, it actually is the water andwashing under the faucet that gets the spores to come off the hands. they're very sticky, they really like yourskin a lot, more so than many other germs. and if you can't do soap and water, then alcoholhand rub isn't a bad thing to do. it's not as effective, but there's some evidenceto say that it's ok. i would still choose soap and water any day. but if you-- all you can get is hand rub thenthe-- it's ok. it's in the insolation, we talked about--and so this isn't evidence-based, but it sure
made sense. having people that are using common equipment,go to use that common equipment at the end of the day, and then thinking now about long-termcare facility and rehab and occupational therapy and physical therapy. this was something that was implemented ata nursing home in the-- in my region. c. diff patients go last. and then they can wipe in the equipment withbleach. in the next morning, the room is ready togo for the people that don't have contagious diseases.
other things that we can do, did i miss one? ok, sorry i think i jumped ahead of myselfto minimize transmission by staff with soap and water. single use in disposable equipment, so norectal thermometers is a big one here. we do single use or-- i'm sorry, assignedthing like assign blood pressure cuffs per room or the hoyer lifts, they get the onebed or one lift per patient. and then those get to laundry before theycome back into circulation. sorry, that's a dedicated equipment. and then also, a lot of education to the staffannually is the minimal that should be happening
and especially for high turnover of staff,i'm thinking here about nurses aids where they're in a job for three months, six monthsbefore they move on. there's-- they don't get institutional memoryas a group, as a work force. so we have to keep giving them education ona very regular basis like every three months or six months. and also including environmental servicesin this education as well. they had-- they don't often understand howcritical their role is in preventing transmission. they'd often don't get rewarded for what they'redoing when they're doing a good job but they sure do hear when things don't go well.
so i think rewarding them for good cleaningis important. contact precautions with downing gloves atmy facility. for a long time, we didn't have these thingsavailable at the door, i had to go down the hall and then come back and get them. and so, i would carry them in my pocket. i'm only seeing one patient at a time, ourpoor nurses are seeing you know, four or five patients a time. that really comes-- it's a work burden, there'sa workflow burden. so now, everything is available at the doorfor us.
also, designating someone on every shift toreplenish supplies, and make sure they're there. how many times have that-- well, i can countfrom the last time i was on rounding which is last week or this week. and at least four patient out of the 20 thati saw, i had to go find the equipment. i had to go find the gown and glove becauseit wasn't available at the door. the gloves are there but the gowns weren't. so having somebody replenish that on everyshift just make it their job to go around once in eight hours.
so that it minimizes again the-- it makesit easier, reduces the barrier of getting a gown on. and then also disinfectant wipes bleach, apparently,it's a regulatory mandate that we can't have liquid bleach around anymore because someonemight drink it. i know. so, we have wipes, we've got bleach containingwipes and those bleach containing wipes, need to smell like bleach. it can't just say clorox in the outside becauseclorox sells some non-bleach things so you're not going to save money by going to say, costcoand getting a great, big box of them.
it really does have to have bleach in there. so, having those in the door makes it easyto wipe down equipment, to wipe down my stethoscope for example, to wipe down the blood pressurecuff or the bar code scanner that may have gone in the room with the person giving themedicine. and then finally, infection control, so, involving,educating housekeeping staff, as we're minimizing environmental reservoirs. daily dose infection of high-touch surfacesis where the bleach wipes also come into play. we started doing this once a day for patient'srooms when we know they have c. difficile. and then twice a day at nursing stations,and it helped reduce some of the rates of
c. difficile on a couple the wards that wereaffected. also, assessing the adequacy of cleaning beforechanging to a new product. it may be that their product works just fine,but it's not being used correctly or enough by the cleaning staff. they may not know for example that after usinga bleach solution, it has to be made up once every 24 hours, it's no good after that. so, they have-- they may not have been educatedabout that specific application. and then also making sure that the cleaningand disinfection agents being used, rnds, sporicidal, i have to say it's sporicidal.
the-- it's hard on hospitals because it makesthe equipment disintegrate more quickly. it wears and tears in the equipment. so this is-- it's a challenge. it's always this balance that we have to gothrough. one of the products that people are usingto assess the adequacy of cleaning is to put an agent that fluoresces under black lights,or uv lights on to different parts of patient's rooms. and then going after environment serviceshave been there and see if the spots are still there or not.
if you do this, tide works well, it glowsin the dark and it's relatively inexpensive compared to something else that might be outthere. and also, if you try to do this, one, tryyourself to go in and wipe off the tides that you know are agents so that you know whatkind of pressure and force is required to make this happen. so that you know, what you're asking or lettinghousekeeping staff to do isn't realistic for the surface. and then also, once they catch on, housekeepingstaff may also go out by their own black lights and they'll look around for the spots to seeif they've been cleaning well enough or not.
which is good and you know, they might beplaying with the test and move your spots around. so this is where, you know, it's not evidence-basedbut you know, these are lessons learned. all right, so active surveillance. this is a relatively new idea for c. diff. and it was done in a hospital over a periodof i for-- i'm sorry, i forgot how many-- about a two or three-year period. so they did rectal swabs upon hospital admissionto detect c. difficile by looking for toxin b. and if the resident or the [inaudible]the patient coming less passive they want
to contact precaution for the durations ofhospitalization. and of nearly 7600 admissions, about 5% ofthe people coming in were identified as carriers. so here's the exception to that stick testthat i told you because we're doing rectal swabs here. so it doesn't matter if they did or did nothave diarrhea. there was a high rate of asymptomatic carriage. so, when the study was done, during the epidemicperiod, their rate of c. difficile healthcare requires, so c. difficile was about 11%. it went-- i'm hoping that that presents theright value there, i'm sorry.
oh, a number of infections for 10,000 patientdays, i did put it in there, that's good. so the-- in their pre-intervention period,it was about seven healthcare acquired infections per 10,000 patient days. and during the intervention period when theyactually put people on isolation base on the positive c-difficile screen, the rate cutin half. so it does seem to be effective. how this plays into cost, i don't know, butit seems like a very cost-effective thing to try. how this plays into what patients will acceptto be willing to put up with, i also don't
know. the idea of doing a rectal swab on a 14-yearold boy, or an 80-year old woman, it's caused consequences to it. and these are some of the unattended consequencesof what we have to deal now with healthcare-acquired infection prevention. i get an awesome lot about probiotics. can we use probiotics to prevent c. difficile? there's a metaanalysis that slightly favorsthe use the probiotics for preventing c difficile. and the probiotics in use, specifically werelactobacillus kci, acidophilus and rhamnosus
in varying combinations and also saccharomycesboulardii. these were all done as part of clinical trialsand i have a clear bias where i don't really care for probiotics in general. because when someone says i'm going to giveprobiotics, i feel like i'm saying i'm going to go backpack in europe. so, are you going to paris or prague? or portugal which is a country so that's differentfrom going to the city. and we don't know what's really in probiotics. they're not fda-regulated or approved.
so we don't know how many myocultures thereare. we don't know the number-- we don't know whatthe species are. because it's often proprietary, and when we'retalking on mixture species, we don't even know if there's kind of species control. it's what they started off with you know,10,000 half-lives that go over the bacteria and what they're actually putting in theirpackaging now. and so there's no oversight, there's no wayof knowing what is actually going in, in their probiotics. so this is my problem with probiotics.
there are two fda-approved probiotics, yogurtand kefir. does it work? i have no idea. i hear anecdotes that yes, it does. does it hurt? absolutely not. all of us can have yogurt. it can even go [inaudible] right? it's all right.
so, other infection prevention steps thatwe can take for facility-wide measures, antimicrobial stewardship, which we're hearing about here. surveillance for c. difficile infection andalso for surveillance of the environment, avoiding test of cure, so that we're not borrowingfrom, we're not looking for people to have-- to have gotten over their c. diff by a labtest but rather we go by symptoms. and finding a lab-based alert system, so thatwhen someone has a positive c. diff test that gets common to their providers, so they'renot waiting until monday morning to find out that the person should have been in isolationor on treatment from a couple days ago. and i'd also like to advocate for early responseto potential c. difficile infection.
so define criteria to suspect c. difficilelike a rate of three unformed stools in a day. and engage in preemptive contact isolation. i would much rather have someone in isolationfor two days when they didn't need it than have them with c. diff and spreading poopall over their room and elsewhere when they should have been-- when they could have beenin contact precautions. and finally, standing orders to test for c.difficile when criteria are met. so we're not waiting to go, like joe talkedabout it earlier going out through the chain of who does and who does not want it to happen.
but just letting us-- letting even nursesjust do the c diff testing. nurses giving flu shots, nurses can figureout when to order a c difficile test, no problem. so let's empower them to do that. on the horizon, there're vaccines. so, these have been-- these are undergoingclinical trial now. and vaccines are being tested in older adults,specifically in older adults. the one that i'm aware of now is a three-doseregimen at zero, one or six months, a lot like hepatitis a and b vaccine. and that works to generate antibodies againsttoxin a and b and they last at least through
6 months after the vaccine has been given. and it seemed to be well-tolerated in termsof the actual injection. efficacy studies are pending. so we'll know in a year or two how well thisis going to work. i'm very excited about this. i would much rather do a vaccine and preventinfection than do a fecal microbiota transplant even though as you know, i'm a proponent ofit. so, some take home messages. antibiotic exposures are the main risk factorfor c. difficile infection.
metronidazole and oral vanco are still themainstays of treatment. fecal microbiota transplant is safe and effectiveand infection control is especially challenging in post-acute and long-term care settingsbecause we're trying to balance between a home-like environment and infection controlpractices and principles. and i'd like to end with this message of hope. and i'd be happy to take your question. thank you very, very much. >i'd-- i have a couple of questions. thank you so much for your presentation.
i do have a couple of questions. one pertaining to pediatric patients, sometimesi get calls from the pediatric providers, community providers about kids that are testedand oftentimes, you don't have that history of the three stools or these are kids whoare in promotility agents. can you comment on how to address that? oftentimes, the questions revolve around thepalatability of metronidazole and kids now tolerating so three days into the cause. they're not tolerating the medications butthey're better-- do you have any comments to that?
and my second question is healthcare workersin test of cure. there are some institutions that do requiretest of cure for certain things. but when it comes to c difficile infection,what do you recommend? >> so for the pediatric question, i have toconfess that i don't have a lot of experience working with children in terms of medicalcare. so my approach to this would be why were theytested for c. diff in the first place, especially if they're on a promotility agent, just becausethey-- and we see this a lot in older adults too where they-- gets put on laxatives ortwo-piece and they've got diarrhea and they get tested for c. diff and they get treatedfor c. diff and they really just had started
something that makes their-- have in diarrheaand have diarrhea that might be part of what's happening with the pediatric population. if they're not tolerating the metronidazoleand they're better, my id got sense [inaudible] to stop the poison, stop the metronidazoleand let them be. that's not evidence-based, it's just you know,practical, we just don't always have a good place in this. in terms of test of cure before someone--if you're talking about transferring from one institution to another, they want to seesomeone who's negative for c difficile. i don't-- i've heard this before and i'veencountered this.
and this is extraordinarily frustrating becauseyou can tell them about the evidence, but we can't always decide what policies theirinstitution will have. so it's a lot of education. it's talking with their infection controlpractitioner. sometimes you know, well you may not get thispatient and we'll have to think twice about whether not your-- and this institution canhandle some of their other patient, their complex problems. sometimes that convey threat of no businesscan be helpful as well. and i think that we also have to maybe askour regulatory partners to help assist with
this, that you can't refuse a patient intoyour facility based on history of c. difficile. if they're having-- if they're able to controltheir secretions basically, they should be allowed to go. but saying it and doing it are two differentthings. all right, if there's no other questions,i will leave you to enjoy lunch which we'll have chocolate ice cream and chocolate milk. i'll be happy to take question outside, thankyou. [ music ]
