Tag Archives: C difficile research and development

C. diff. Research and Development Community October 2015

laboratorybeakers3

Here is the latest from the Clostridium difficile research community

 

 

 

Serum 25-hydroxyvitamin D levels are not associated with adverse outcomes in                        Clostridium difficile infection

Clostridium difficile infection (CDI) is a significant source of healthcare-associated morbidity and mortality. This study investigated whether serum 25-hydroxyvitamin D is associated with adverse outcomes from CDI. Patients with CDI were prospectively enrolled. Charts were reviewed and serum 25-hydroxyvitamin D was measured. The primary outcome was a composite definition of severe disease: fever (temperature >38°C), acute organ dysfunction, or serum white blood cell count >15,000 cells/µL within 24-48 hours of diagnosis; lack of response to therapy by day 5; and intensive care unit admission; colectomy; or death within 30 days. Sixty-seven patients were included in the final analysis. Mean (±SD) serum 25-hydroxyvitamin D was 26.1 (±18.54) ng/mL. Severe disease, which occurred in 26 (39%) participants, was not associated with serum 25-hydroxyvitamin D [odds ratio (OR) 1.00; 95% confidence interval (CI) 0.96-1.04]. In the adjusted model for severe disease only serum albumin (OR 0.12; 95%CI 0.02-0.64) and diagnosis by detection of stool toxin (OR 5.87; 95%CI 1.09-31.7) remained independent predictors. We conclude that serum 25-hydroxyvitamin D is not associated with the development of severe disease in patients with CDI.

For full article click on the link below:

http://www.pagepress.org/journals/index.php/idr/article/view/5979

 

Clostridium difficile is a Gram-positive spore-forming pathogen and a leading cause of nosocomial diarrhea. C. difficile infections are transmitted when ingested spores germinate in the gastrointestinal tract and transform into vegetative cells. Germination begins when the germinant receptor CspC detects bile salts in the gut. CspC is a subtilisin-like serine pseudoprotease that activates the related CspB serine protease through an unknown mechanism. Activated CspB cleaves the pro-SleC zymogen, which allows the activated SleC cortex hydrolase to degrade the protective cortex layer. While these regulators are essential for C. difficile spores to outgrow and form toxin-secreting vegetative cells, the mechanisms controlling their function have only been partially characterized. In this study, we identify the lipoprotein GerS as a novel regulator of C. difficile spore germination using targeted mutagenesis. A gerS mutant has a severe germination defect and fails to degrade cortex even though it processes SleC at wildtype levels. Using complementation analyses, we demonstrate that GerS secretion, but not lipidation, is necessary for GerS to activate SleC. Importantly, loss of GerS attenuates the virulence of C. difficile in a hamster model of infection. Since GerS appears to be conserved exclusively in related Peptostreptococcaeace family members, our results contribute to a growing body of work indicating that C. difficile has evolved distinct mechanisms for controlling the exit from dormancy relative to B. subtilis and other spore-forming organisms.

For full article click on the link below:

http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005239

 

XBiotech  the world’s leading developer of next-generation True Human™ therapeutic antibodies, announced today the launch of a research and development program to develop a first-in-class oral monoclonal antibody against Clostridium difficile (C. difficile) infection. Using its proprietary True Human technology, the Company has begun screening human blood samples from donors to identify and clone a therapeutic antibody candidate from individuals with natural immunity to C. difficile infection.

For full article click on the link below:

In a 1-year survey at a university hospital we found that 20·6% (81/392) of patients with antibiotic associated diarrohea where positive for C. difficile. The most common PCR ribotypes were 012 (14·8%), 027 (12·3%), 046 (12·3%) and 014/020 (9·9). The incidence rate was 2·6 cases of C. difficile infection for every 1000 outpatients.
For full article click on the link below:

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=10011117&fileId=S0950268815002459

Microbiota Changes Predict Treatment Failure
Infection with C. difficile is associated with several adverse outcomes including treatment failure (5% to 35%) but researchers do not know what clinical factors can predict this failure.

Reporting at the American College of Gastroenterology Scientific Meeting in Honolulu, a Mayo Clinic team of researchers looked at which gut microbiota signatures might be useful in determining whether patients will get better.

They defined treatment failure as a non-response to treatment with vancomycin for four days or metronidazole for five days. They looked at 889 patients with primary C. dif in infection (CDI) of whom 60.2% were women and the median age was 54 years. Of these 7% had severe CDI, 70.5% had been treated with metronidazole, 23.8% with vancomycin, and 5.6% with a combination.

Overall 12.5% failed treatment and the rates were similar with each drug.

The researchers looked at clinical factors that might have predicted the failures–age, sex, obesity, prior antibiotic use, and other factors. They found no correlation between having those factors and failing treatment. They did find that patients who responded to treatment had higher quantities of certain bacteria, for instance Faecalibacterium and Bacteroides.

Conversely, the patients who failed treatment had more Streptococcus and Clostridium.

The authors suggest that analyzing these changes in microbiota could be useful. “Gut microbiota signatures may be used to predict treatment response in the absence of reliable clinical predictors,” said Sahil Khanna, MBBS, M S in presenting the study.

For full article click on the link below:

“It Takes A Village” Re: Clostridium difficile (C.diff.) and Healthcare-Associated Infections, By Dr. Rosie D. Lyles, MD,MHA,MSc

“It Takes a Village”
By: Rosie D. Lyles, MD, MHA, MSc, Head of Clinical Affairs for Clorox Healthcare
September 21, 2015

With increasing rates of Clostridium difficile infections (CDI), C. difficile now rivals methicillin-resistance Staphylococcus aureus (MRSA) as the most common organism to cause healthcare-associated infections (HAIs) in the United States. (1) The prevalence of C. difficile infections has more than doubled in U.S. hospitals from 2000 to 2009 (2) and CDI is regarded as one of the serious, expensive, and potentially avoidable consequences of hospitalization. The cost of treating CDI in the hospital is $3427-$9960 (in 2012), and the cost of treating patients with recurrent CDI is $11,631, for a total cost of more than $1.2 billion annually in the United States. (3-4)

In June 2015, the White House spearheaded an executive call to action focused on implementing and improving antibiotic stewardship programs (ASPs) across the continuum of care (acute care facilities, outpatient clinics, doctors’ offices and long-term care facilities). The urgency around this issue stems from the increasing number of antibiotics prescribed, which subsequently breeds multi-drug resistant organisms (MDROs) like C. difficile. Unnecessary or excessive antibiotic use combined with poor infection control practices may increase the spread of C. difficile within a facility and across facilities when infected patients transfer, such as from a hospital to a nursing home. Increasing evidence suggests that contaminated surfaces in healthcare facilities play an important role in the transmission of several key pathogens including C. difficile, vancomycin – resistant enterococci (VRE), MRSA, Acinetobacter baumannii, and norovirus.

In order to reduce HAIs, all hands on deck are required to support a successful infection prevention strategy. In other words, “it takes a village.” Growing up, I remember hearing the phrase, “it takes a village to raise a child,” meaning there is a partnership within a community with several individuals playing a role in the maturation of a youth. Within a hospital, it’s a collaborative team across several departments that implements evidence-based protocols, continues to educate staff and patients, and maintains compliance of infection control strategies/approaches to reduce the risk of a broad range of infections, including CDI. From the C-suite (administrators and senior management) to direct healthcare providers (such as physicians, nurses, aides, and therapists) and environmental staff (EVS); everyone with direct or indirect contact with a patient’s care plays an essential role.

As a healthcare professional, it’s very important for hospitals to focus on the bigger picture when it comes to infection prevention strategy and control. Prioritizing infection control measures for just one or two pathogens of concern is insufficient. At the end of the day, one pathogen doesn’t trump another because patients don’t want an HAI from ANY pathogen! The horizontal approaches aim to reduce the risk of infections due to a broad array of pathogens through implementation of standardized practices that do not depend on patient-specific conditions:

• Proper hand hygiene
Hand hygiene practices in compliance with the Centers for Disease Control and Prevention (CDC) or World Health Organization (WHO) guidelines are a key component in preventing and controlling C. difficile, in addition to many other HAI-causing pathogens.
• Universal use of gloves or gloves and gowns
Donning the correct protective equipment minimizes contact with pathogens. It is also important to follow protocols for properly discarding this equipment.
• Universal decolonization (daily optimal bathing with chlorhexidine gluconate (CHG))
CHG bathing has been shown to decrease the bioburden of microorganisms on the patient, the environment, and the hands of healthcare personnel.
• Antimicrobial stewardship program
Ensuring every patient receives an antibiotic only when needed: the right agent, at the right dose, for the right duration.
• Evidence-based environmental cleaning and disinfection products
At a minimum, effective environmental cleaning involves using cleaners & disinfectants that are registered by the Environmental Protection Agency (EPA). Supplementing manual cleaning with new technology like ultraviolet (UV) light provides an extra layer of protection and the most comprehensive approach. UV has the highest-energy form that can inactivate dangerous and persistent pathogens by eradicating microorganism deoxyribonucleic acid (DNA) that may be left on surfaces, which can be missed with traditional cleaning. Finally, because C. difficile has been found in non-CDI patient rooms, using an EPA-registered sporicidal surface disinfectant to clean all patient rooms (daily and terminal) is great strategy to prevent the spread of the bacteria.

I had the pleasure of attending the CDC’s Environmental Hygiene for Ebola and Other Emerging Pathogens meeting on September 14, 2015, with attendees from academia, private industry, federal employees and health organizations, participated in a roundtable discussion on the research framework needed to determine the public health significance of non-critical environmental surface contamination and provide guidance to healthcare facilities about the methods to reduce the contamination of non-critical environmental surfaces reliably in order to improve patient safety. Every participant present at the meeting agreed that, due to the challenges/barriers that hospitals face with preventing HAIs (both from emerging pathogens and more common pathogens like C. difficile), it takes a village to successfully implement evidence-based protocols, continue to educate and maintain compliance with infection prevention protocols.

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About Rosie D. Lyles, MD, MHA, MSc, Head of Clinical Affairs for Clorox Healthcare

Rosie D. Lyles, MD, MHA, MSc is the Head of Clinical Affairs for the Clorox Professional Products Company where she serves as a research fellow and primary medical science liaison for the healthcare business, supporting all scientific research as well as clinical and product intervention design and development.
Dr. Lyles previously served as a physician researcher and study director for multiple epidemiologic research initiatives in the Division of Infectious Diseases at the Cook County Health and Hospitals System, investigating healthcare-associated infections with a particular focus on the epidemiology and prevention of multidrug-resistant organisms and infections in intensive care units and in long-term acute care hospitals. She has directed numerous clinical studies and interventions for the Centers for Disease Control and Prevention (CDC) and the Chicago Antimicrobial Resistance and Infection Prevention Epicenter.
During her nine years as a study director and physician researcher at Hektoen Institute for Medical Research, Dr. Lyles’ work included CDC Epicenters Prevention program studies on bloodstream infections, Clostridium difficile infections and case-control studies of community-acquired Methicillin-resistant Staphylococcus aureus (MRSA). She also performed surveillance studies of Klebsiella pneumoniae carbapenemase (KPC) positive patients, examining universal contact isolation and patient skin antisepsis protocols to identify ways to optimize standard infection control measures.
Dr. Lyles received her medical degree from St. Matthew’s University School of Medicine and holds a Master of Health Service Administration from St. Joseph College. She also recently completed a Master of Science in Clinical Research and Translational Sciences through the University of Illinois at Chicago. She is an active member of the Association of Professionals in Infection Control and Epidemiology, the Infectious Disease Society of America, the Society for Healthcare Epidemiology of America and has served as a peer reviewer for the National Institutes of Health, New England Journal of Medicine, and American Journal of Infection Control.
References:
1. Dubberke, ER, et al. Strategies to Prevent Clostridium difficile Infections in Acute Care Hospitals: 2014 Update. Infect Control Hosp Epidemiol. 2014, V35:S48-S65
2. Tabak et al., Predicting the Risk for Hospital-onset Clostridium difficile Infection (HO-CDI) at the Time if Inpatient Admission: HO-CDI Risk Score. Infect Control Hosp Epidemiol. 2015, 36: 6; 695-701
3. Magill, SS. et al. “Multistate Point-Prevalence Survey of Health Care-Associated Infections.” The New England Journal of Medicine 370.13 (2014): 1198–1208.
4. Dubberke, ER, and Olsen, MA. “Burden of Clostridium Difficile on the Healthcare System.” Clinical infectious diseases 55 Suppl. 2 (2012): S88–92.
5. Septimus, E., et al. “Approaches for preventing Healthcare-associated Infections: Go Long or Go Wide?” Infect Control Hosp Epidemiol. 2014. 35: 7; 797-801

Dr Klaus Aktories and Dr Panagiotis Papatheodorou from the University of Freiburg have identified the molecular docking site of a bacterial toxin

The pharmacologists and toxicologists Prof./ Dr. Klaus Aktories
and Dr. Panagiotis Papatheodorou from the University of Freiburg have identified the molecular docking site that is responsible for the C. difficile toxin’s being able to bind to its receptor on the membrane of the intestinal epithelium.

 IMAGE

Caption:  Bacterial toxins usually exert their full deadly effect in the host cell’s interior. The toxins overcome the cell membrane by binding to a surface receptor, which conveys them into the cell’s interior.

Credit© Panagiotis Papatheodorou

Clostridium difficile is a dangerous intestinal bacterium that can cause severe diarrhoea and life-threatening intestinal infections after long-term treatment with antibiotics. The pharmacologists and toxicologists Prof. Dr. Dr. Klaus Aktories and Dr. Panagiotis Papatheodorou from the University of Freiburg have identified the molecular docking site that is responsible for the C. difficile toxin’s being able to bind to its receptor on the membrane of the intestinal epithelium. This docking site functions like an elevator, transporting the toxins into the cell’s interior. By binding to the surface receptor, the toxins are able to overcome the cell membrane. Once inside the cell, C. difficile exerts its full lethal effect. “Bacteria are becoming increasingly resistant to antibiotics. That’s why new types of therapy that aren’t based primarily on bacteria are necessary,” Aktories said. “Our goal in the future should be to reduce the toxicological potential of toxins as well,” he added. The team of researchers has recently published their results in the Journal of Biological Chemistry.

The intestinal pathogen C. difficile is most commonly found in hospitals and is often acquired by older people and people with weakened immune systems. In Western countries, infections with so-called hypervirulent strains of C. difficile are rapidly increasing and are much more dangerous and more difficult to treat. The pathology of C. difficile infections is primarily triggered by two toxins released by the pathogen, which then damage the intestinal epithelium. Particularly dangerous hypervirulent strains produce a third toxin, C. difficile transferase (CDT). This CDT toxin modifies the cytoskeleton, causing the host cells to collapse and die. Aktories and Papatheodorou identified the surface protein LSR (lipolysis-stimulated lipoprotein receptor) as the receptor for the CDT toxin already in 2011. It is through the LSR that CDT enters the host cell.

Papatheodorou, Aktories and their team of researchers have now identified the regions in the CDT toxin and the LSR receptor that interact with one another. In order to achieve this, the scientists genetically designed truncations of the toxin and the LSR receptor as well as cells without LSR. They then tested whether or not the CDT toxin could bind to its receptor and be absorbed in the cell. They discovered that the parts of the toxin that interact with the receptor are much smaller than previously believed. All that is necessary for toxin absorption is the part of the receptor outside of the cell. “In the future, it should be possible to block these areas in the toxin and receptor in order to prevent the toxin from entering the host cell,” Papatheodorou explained.

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Papatheodorou and Aktories are researchers at the Institute of Experimental and Clinical Pharmacology and Toxicology at the University of Freiburg. Aktories is also a member of the cluster of excellence BIOSS Centre for Biological Signalling Studies at the University of Freiburg.

To read the article in its entirety click on the link below:

http://www.eurekalert.org/pub_releases/2015-06/b-cf-mds060915.php

Scientific research demonstrates new evidence supporting Fecal Microbiota Transplant successful in treating C. difficile infections

Research published in the open access journal Microbiome offers new evidence for the success of fecal microbial transplantation (FMT) in treating severe Clostridium difficile infection (CDI), a growing problem worldwide that leads to thousands of fatalities every year.

Research led by Michael Sadowsky, Alex Khoruts, and colleagues at the University of Minnesota in collaboration with the Rob Knight Lab at the University of Colorado, Boulder, reveals that healthy changes to a patient’s microbiome are sustained for up to 21 weeks after transplant, and has implications for the regulation of the treatment. Findings also demonstrate the dynamic nature of fecal microbiota in FMT donors and recipients.

In FMT, fecal matter is collected from a donor, purified, mixed with a saline solution and placed in a patient, usually by colonoscopy. In contrast to standard antibiotic therapies                                (e.g., Vancomycin)  which further disrupt intestinal microflora and may contribute to the recurrence of CDI, FMT restores the intestinal microbiome and healthy gut function.

Using DNA samples of healthy individuals from the Human Microbiome Project (HMP) as a baseline, Sadowsky and his team compared changes in fecal microbial communities of recipients over time to the changes observed within samples from the donor. Significantly, the composition of gut microbes in the both donor and recipient groups varied over the course of the study, but remained within the normal range when compared to hundreds of samples collected by the HMP.

According to Sadowsky, the findings have important implications for a range of diseases associated with microbial imbalance, or dysbiosis, and could influence the regulatory regime surrounding FMT, currently treated as a drug by the U.S. Food and Drug Administration (USFDA).

“The dynamic nature of fecal microbiota in both the donor and recipients suggests that the current framework of regulation, requiring consistent composition, may need to be reexamined for fecal transplantations,” says Michael Sadowsky. “Change in fecal microbial composition is consistent with normal responsiveness to shifts in the diet and other environment factors. Variability should be taken into account when comparing microbial composition in normal individuals to those with dysbiosis characteristic of disease states, especially when assessing clinical interventions and outcomes.

Also discovered in the research, the performance of frozen and fresh preparations of fecal material was indistinguishable. Though the sample was limited and warrants further study with a larger cohort, it has several implications for the widespread adoption of FMT. The frozen preparation greatly simplifies the standardization and distribution of the fecal material. It also facilitates long-term storage of donor material for future study and makes FMT accessible to a greater number of physicians and patients. Finally, it offers advantages over fresh material in the testing of fecal samples for pathogens, which in some cases can take several weeks to complete.

While FMT is particularly successful in patients who suffer from recurrent CDI, University of Minnesota researchers led by Sadowsky and Dr. Alex Khoruts are currently preparing for a clinical trial using FMT to improve insulin sensitivity in pre-diabetic patients and to treat metabolic syndrome.

 

To read the article in its entirety please click on the following link:

http://www.eurekalert.org/pub_releases/2015-04/uom-nes040915.php

C. diff. and Healthcare-Associated Infections Discussed Live on C. diff. Radio

CdiffRadioPost

#CdiffRadio

C Diff Foundation, Sponsor, with Founder            Nancy C. Caralla, Executive Director and               Dr. Chandrabali Ghose, Chairperson of the Research and Development Community will be broadcasting live on Tuesdays delivering the most up-to-date information pertaining to a leading super-bug/ Healthcare Associated Infection (HAI),  C. difficile, with additional HAI’s, and a variety of related healthcare topics.

Topic experts will be joining your hosts to discuss prevention, treatments, clinical trials, and environmental safety products on a global level.

Tune in Tuesdays beginning March 3rd at 11 AM Pacific Time (2 PM Eastern Time, 7 PM UK) on the VoiceAmerica network  http://www.voiceamerica.com/show/2441/c-diff-spores-and-more

 

C. difficile (C.diff.) News – University of Michigan Scientists discover how C. diff. wreaks havoc in the gastrointestinal system

Study in mice could lead to better treatment and prevention for humans

Sometimes, science means staying awake for two days straight.

But losing sleep is a small sacrifice to make, if you want to learn more about tiny bacteria that sicken half a million Americans each year, kill more than 14,000 of them, and rack up $4.8 billion in health care costs.

That’s what drove a team of University of Michigan scientists to work around the clock to study the bacterium called Clostridium difficile, C. difficile (C.diff.), the bane of hospitals and nursing homes. Many patients can develop it after taking antibiotics to treat infections.

In a new paper in the journal Infection and Immunity, the researchers lay out for the first time exactly how C. difficile wreaks havoc on the guts of animals in a short time, and causes severe diarrhea and life-threatening disease in humans.

Despite the heavy toll the organism takes, no team had ever been able to measure C. difficile activity over time in this way. Their findings could help lead to better prevention and treatment of C. difficile infections.

A fast track to disease

The researchers started by introducing C. difficile spores into mice via their mouths – similar to what might happen in a hospital environment where spores from past patients’ infections abound. Then, they studied what happened after the spores entered the body, by taking gut samples at regular intervals and studying them under special conditions. The animals had all received antibiotics.

Through their hours-long surveillance, the researchers found that it took C. difficile only about 24 hours to go from hard spores to toxin-producing, diarrhea-inducing cells all the way at the other end of the digestive tract, in the large intestine.

The researchers also show that bile acids in the gut “woke up” the dormant bacteria spores, and that they grow into cells in the small intestine within 24 hours of exposure.

C difficile microbiome

Because antibiotic have the ability to disrupt the gut’s normal community of other bacteria – called the gut microbiome — C. difficile cells could continue down to the large intestine and start their toxic effects on the cells that line the colon.

When they tested the contents of the small intestine separately, they also showed this happens whether or not the animals have received antibiotics.

In the large intestine, they even saw how C. difficile cells formed spores  – allowing them to survive the exit from the body in feces and go on to infect a new host.

“If we can understand the process that specific bacteria use to germinate and get established, we may be able to intervene more effectively,” says Vincent Young, M.D., Ph.D., the senior author of the new study, a professor at the U-M Medical School and co-leader of the school’s Host Microbiome Initiative. “We assume that antibiotics change the gut microbiome, but we haven’t known how that allows C. difficile to gain a foothold and begin to ramp up growth.”

First author Mark Koenigsknecht, Ph.D., a postdoctoral fellow in Young’s lab who is now continuing his research at the U-M College of Pharmacy, was one of the researchers who was up all night to get data for the experiment.

“We introduced 100 spores through the mouth, and within six hours we could find 1,000 cells in the intestinal tract,” he notes. “We chose this strain of C. difficile because of its rapid ability to cause disease in animals, but we didn’t think it would happen that quickly.”

Tracking C. difficile’s effect on the gut

 

Effect of C Diff on gut cells

Click the image to see it larger

The U-M team used a mouse model they developed, and a common antibiotic in the cephalosporin class. The strain of C. difficile used in the experiment originated with a patient years ago, but is available for purchase as a laboratory culture.

Anaerobic chambers

Special oxygen-free chambers were
used in the research,
 giving researchers
the ability to study the gut microbiome

in the anaerobic environment that’s present
inside the body.

Working in facilities made possible by the Host Microbiome Initiative, they took samples at regular intervals from seven different areas of the digestive tracts of the mice. They then whisked the samples into special oxygen-free facilities, called anaerobic chambers, that allowed them to see the amount and forms of C. difficile present in each gut region.

With the help of Patrick Schloss, Ph.D., a professor in the Department of Microbiology & Immunology, the researchers used DNA analysis to see what the entire gut microbiome looked like in antibiotic-treated animals and those that hadn’t been treated. The antibiotics really disrupted the community of bacteria in the small intestine, and C. difficile came to dominate in 36 hours.

They also examined the intestinal tract under a microscope. The toxin produced by C. difficile cells in their vegetative, or growing, state causes an effect on the cells that line the digestive tract, causing them to become “leaky”, raising the alarm among nearby immune system cells, and leading to diarrhea. The cell changes were seen in the large intestine about 30 hours after spore introduction.

Next steps

C difficile graphs

Three graphs showing how quickly
C. difficile took over the guts of
antibiotic-treated mice.

Koenigsknecht notes that this is the first time researchers have seen in a living animal that toxin production, and production of new spores of C. difficile capable of surviving outside the body, occur at the same time. This indication that the two processes are linked, and that they are switched on by some factor in the body, is intriguing, he says.

Now, the effort to figure out what that signal is, whether different strains of C. difficile act differently, and who is most vulnerable to its effects, will continue.

Koenigsknecht has teamed with College of Pharmacy professors to test the use of a seven-foot-long tube that can be threaded down the human digestive tract and used to retrieve samples at different locations along the way. Originally developed for testing how drugs are broken down and used by the body, it could provide an entirely new window into the human microbiome.

“Now that we understand what C. difficile is doing, we can also go and ask more questions about how the machinery inside the cell is turning on,” he says. “We have to know how to study it before we can cure it.” Animal-based research is vital to this effort.

Young notes that there are many ways C. difficile could take over an antibiotic-decimated gut. “Does it prevent other bacteria from growing, or out-compete them by eating faster? Does it communicate with the cells of the gut lining? We’re trying to figure out the interaction between the ‘good bugs’ and the ‘bad bugs’, and the lining of the gut.” Young is an associate professor of infectious diseases and of microbiology and immunology.

In addition to Young, Schloss and Koenigsknecht, the study’s authors are Casey Theriot, Ingrid Bergin and Cassie Schumacher.

The research was funded by the National Institutes of Health grants U19AI090871, K01GM109236 and 5R01GM099514. It used the U-M Metabolomics Core, funded by NIH grant U24 DK097153. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health

For entire article please click on the link below:

http://www.uofmhealth.org/news/archive/201502/stalking-wily-foe-u-m-scientists-figure-out-how-c-difficile

Rebiotix, Inc. PUNCH CD 2 Study – Second Clinical Trial Initiated

Update

24 November 2014

Rebiotix has initiated our second clinical trial (PUNCH CD 2) focusing on the treatment of recurrent C. difficile infection!

REBIOTIX, INC.

The PUNCH CD 2 study is a Phase 2B randomized controlled trial to assess the effectiveness and safety of RBX2660 (microbiota suspension) for the treatment of recurrent               Clostridium difficile (C. diff.)  infection.

About the Study   The PUNCH CD 2 study is the first multicenter prospective, multicenter, randomized, placebo-controlled, double-blind study of a microbiota restoration therapy. It has been designed to provide the highest quality of evidence to-date about this non-antibiotic approach to treating recurrent C. diff. infection.

Approximately 117 patients at over 20 sites in the US and Canada are expected to be enrolled in study.

Patients will be randomized into three different study groups: one group will receive two enemas containing RBX2660; another group will receive two enemas without the active drug; and the third group will receive one enema with RBX2660 and one without.  If a patient’s C. diff. infection reoccurs before 8 weeks after treatment, he or she may be eligible to crossover to receive active treatment with RBX2660.

All patients will be followed for 24 months after treatment.

Further Study Details

For more information on the study you may:

Find Out if You Could be Eligible

A physician participating in the PUNCH CD 2 study will determine if you are eligible to participate in the study. However, you can take a brief survey (less than 1 ½ minutes to complete) to learn if you meet the major study eligibility criteria.

How to Enroll as a Participant

If a study physician thinks you may be a good candidate, you will be given complete information about the study including the responsibilities for participation. You can find out if there is a study site near you by reviewing the clinical study site locations for PUNCH CD 2.


Caution: New Drug – Limited by Federal (or United States) law to investigational use.

 

*Please note – The C Diff Foundation does not endorse this product or any product and this posting is strictly for informational purposes only.