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Ribotypes and Prevalence of Clostridium difficile (C. diff) Hypervirulent Strain: NAP1/B1/027

The Hypervirulent Strain of Clostridium Difficile: NAP1/B1/027

– A Brief Overview



Abstract

Clostridium difficile is a gram-positive bacterium notorious for causing epidemic diarrhea globally with a significant health burden. The pathogen is clinically challenging with increasing antibiotic resistance and recurrence rate. We provide here an in-depth review of one particular strain/ribotype 027, commonly known as NAP1/B1/027 or North American pulsed-field gel electrophoresis type 1, restriction endonuclease analysis type B1, polymerase chain reaction ribotype 027, which has shown a much higher recurrence rate than other strains.

Introduction & Background

Clostridium difficile (C. diff) is a gram-positive, anaerobic, motile, spore-forming, rod-shaped bacteria [1-2]. It has been isolated from almost all mammals, including pigs, cows, horses, elephants, and Kodiak bears, as well as in poultry and ostriches. It has also been found in the soil and feces of humans and animals. It is transmitted from person to person by the fecal-oral route. The C. diff isolates found in animals are similar to the ones found in humans, but according to Hensgens et al., this similarity does not mean that interspecies transmission occurs. However, immunocompromised people are still at risk for interspecies transmission [1]. Its pathogenicity is dependent on the two toxins that it produces: enterotoxin A (Toxin A or TcdA) and cytotoxin B (Toxin B or TcdB). Enterotoxin damages the actin in target cells which leads to neutrophil infiltration, inflammation, and necrosis of epithelial cells. Cytotoxin B has been shown to damage tight junctions of epithelial cells, which increases vascular permeability and causes hemorrhage [2-3]. These toxins form the basis of stool analysis when diagnosing people with the suspected infection. Despite all the virulence characters described, C. diff is a poor competitor against other gut flora in the human colon. In a healthy colon, this pathogen is not in sufficient quantity to produce a clinically significant disease. Risk factors that disrupt this balance include antibiotics exposure, health care environment, acid suppressants, and elemental diet. The bacterium can cause severe watery diarrhea that can progress to pseudomembranous colitis [3-8]. It has been named as one of the three microorganisms with an ‘urgent’ threat level by the Centers for Disease Control and Prevention (CDC) based on its public health impact in the United States (US) with an estimated $1.5 billion US in annual health care expenditures [8]. Patients who have more than three episodes of unexplained and new onset unformed stools in 24 hours should be referred for testing for a Clostridium difficile infection (CDI). Also, patients with risk factors described previously should undergo testing for this pathogen [9]. The ribotype 027 strain of C. diff is particularly noteworthy as contradicting evidence in the literature is present regarding the disease severity it causes. We provide here a brief overview of the epidemiology, pathophysiology, and treatment of this particular strain.

Review

Ribotypes and prevalence of Clostridium difficile (C. diff)

Clostridium difficile can be characterized according to its ribotyping which is performed using the polymerase chain reaction. Several different ribotypes have been associated with CDI. The ribotypes 001, 002, 014, 046, 078, 126, and 140 have been found to be prevalent in the Middle East [10-12]. In Asia, ribotypes 001, 002, 014, 017, and 018 are more prevalent [13-15]. The predominant strains in Europe and North America include ribotypes 001, 014, 020, 027, and 078 [6]. The ribotype 027 (also referred to as NAP1/B1/027) has emerged in the last decade. Studies have underlined antimicrobial resistance as one of the causes of its epidemic outbreaks. Capillary electrophoresis (CE) ribotyping is used as the standard for characterization of C. diff isolates. This method relies on the intergeneric region variability between 16S and 23S ribosomal deoxyribonucleic acid (DNA) [16]. Ribotype 027 was found to have reduced susceptibility to metronidazole, rifampicin, moxifloxacin, clindamycin, imipenem, and chloramphenicol [17-18]. It is clinically and financially concerning as it leads to severe disease presentation, as well as antimicrobial resistance with high morbidity and mortality rates as compared to other strains [19]. Strains, such as ribotype 027 (especially its spores), spread more easily within the hospital because they can resist the hospital environment, cleaning, and disinfectants [1]. An observational study conducted on patients admitted with diarrhea in a Veteran Affairs Medical Center showed that around 22% of the patients were positive for the NAP1/B1/027 strain out of all the people who tested positive for CDI. Further, a reduction in the rate of diarrhea caused by the NAP1/B1/027 strain was observed with a prevalence of 16.9% in 2016, down from 26.2% in 2013. An increase in the level of awareness and education was thought to be the reason for this decline [20]. The prevalence of this strain in North America is reportedly around 22% – 36%. Ribotype 027 was identified as the most prevalent strain causing CDI with recent outbreaks in North America [20-22]. The prevalence of this strain was shown to be 48% in hospitals in Poland with an outbreak of CDI during September 2011 to August 2013 [21].

NAP1/B1/027 strain

Toxigenicity and Pathogenesis

The North American pulsed-field gel electrophoresis type 1, restriction endonuclease analysis type B1, polymerase chain reaction ribotype 027 (NAP1/B1/027) strain has been shown to contain a gene locus, CdtLoc, that encodes for CD196 ADP-ribosyltransferase (CDT) or binary toxin. The bacterium also produces Toxin A and Toxin B, similar to non-027 ribotypes, through the PaLoc gene locus [23-24]. CDT was first isolated by Popoff et al. [25]. The toxin comprises two separate toxin components: CDTa and CDTb. CDTa, which is an ADP-ribosyltransferase enzyme, modifies actin which results in depolymerization and destruction of the actin cytoskeleton in the gut. CDTb binds to gut cells and increases uptake of CDTa. The destruction caused by CDT favors adherence of bacteria and increased uptake of Toxin A and Toxin B [26].

In addition to the toxins, this strain (along with few others) carries a base pair frameshift deletion at nucleotide 117 of the TcdC gene, which is a negative regulator of Toxins A and B. A mutation in this gene thus causes hyperexpression of toxins by this particular strain. Warny et al. showed that NAP1/B1/027 produces Toxin A approximately 16 times and Toxin B approximately 23 times more than the control strains [27]. One study also proposed that increased sporulation by this strain may also be associated with the increased spread of CDI [28]. The virulent factors associated with NAP1/B1/027 strain have been summarized in Table 1.

Virulent factor Mechanism
1. Toxin A (Enterotoxin A or TcdA) Damages the actin in target cells which leads to neutrophil infiltration, inflammation, and necrosis of epithelial cells [24].
2. Toxin B (Cytotoxin B or TcdB) Damages tight junctions of epithelial cells, which increases vascular permeability and causes hemorrhage [24].
3. CDTa toxin Modification of actin with ADP-ribosylation that results in actin depolymerization and destruction of the cytoskeleton that assists in adherence of bacteria to gut epithelial cells [25-26].
4. CDTb toxin Facilitates uptake of CDTa toxin into the gut epithelial lining [25-26].
5. Hypersporulation Increases reproduction and spread of bacteria [28].
6. TcdC gene mutation (18-bp deletion) Increases the production of Toxin A and Toxin B by down-regulation of feedback inhibitor involved in suppressing toxin production [27].

Previous studies have shown contradicting evidence regarding the severity of disease caused by this particular strain. A recent retrospective analysis by Bauer et al. concluded that NAP1/B1/027 was associated with a decreased odds of severe disease (odds ratio (OR): 0.35, 95% confidence interval (CI) 0.13 – 0.93) and did not increase in-hospital mortality (OR: 1.02, 95% CI 0.53 – 1.96) or recurrence rate (OR: 1.16, 95% CI 0.36 – 3.77) [23]. Several other studies conducted (including cross-sectional, case-control, and cohort studies) did not show any worse outcomes compared to other strains [29-31]. Sirad et al. demonstrated that although NAP1/B1/027 strain may produce more toxins compared to other strains, they produced fewer spores and were not always associated with severe disease [32]. On the contrary, Rao et al. conducted a cohort study and concluded that ribotype 027 was associated with severe CDI (OR: 1.73, 95% CI 1.03 – 2.89; p = 0.037) and increased mortality (OR: 2.02, 95% CI 1.19 – 3.43; p = 0.009) compared to other ribotypes [24]. Another study showed similar results with the North American pulsed-field gel electrophoresis type 1 (NAP1) strain. Multivariate regression analysis exhibited an increase in the severity of CDI with the NAP1 strain (OR: 1.66, 95% CI: 1.90 – 2.54) and increased mortality (OR: 2.12, 95% CI: 1.22 – 3.68) [33]. One study from Quebec labeled this strain to be responsible for severe diseases twice as frequently as compared to other strains [34].

The basis for these contradictory findings can be explained by several reasons, including study design, study population, sample size, the method of detection for C. diff, study setting, and unmeasured confounders. Given these contradictory results, healthcare providers should focus on treating this infection based on their clinical judgment and markers of severe infection, including the number of diarrheal episodes, signs of dehydration, creatinine level, albumin level, white blood cell count, associated co-morbidities, immunocompromised state, etc.

Prevention

Preventive strategies employed for NAP1/B1/027 strain are similar to strategies taken for other strains. These include barrier methods (gloves and gown while examining patient), use of disposable equipment, handwashing with soap and water, disinfecting the environment, and antimicrobial stewardship [35]. Further vaccines are being developed targeting the toxins, including TcdA and TcdB, for simultaneous prevention and treatment of CDI. Actoxumab and bezlotoxumab, which are monoclonal antibodies against TcdA and TcdB, are being investigated for this purpose. A combined Phase III trial (MODIFY I (NCT01241552) and MODIFY II (NCT01513239)) showed benefit from bezlotoxumab, but the combination of actoxumab and bezlotoxumab did not yield any further benefit [36]. Bezlotoxumab has received Food and Drug Administration (FDA) approval in October 2016 and is to be used in patients more than 18 years of age, who are at high risk of recurrence from CDI, and are receiving antibiotics [37]. A novel tetravalent vaccine against TcdA, TcdB, CDTa, and CDTb has been proposed by Secore et al. using a hamster model which has shown promising results [38].

A novel drug, SYN-004 (ribaxamase), is under investigation that has shown promising results for preventing CDI. This drug, which is a β-lactamase, is excreted into the gut and degrades the excess antibiotic that prevents disruption of normal gut flora, ultimately preventing CDI [39]. The Phase IIa clinical trial of this drug showed that ribaxamase at a dose of 150 mg every six hours results in an undetectable concentration of ceftriaxone in the intestine which can potentially decrease the likelihood of a C. diff infection, given the less probability of disruption of the gut bacteria.

Resistance to Antibiotics and Treatment

Cases of NAP1/B1/027 reported in Panama were found to be highly resistant to clindamycin, moxifloxacin, levofloxacin, ciprofloxacin, and rifampin but were susceptible to metronidazole and vancomycin [40]. Susceptibility of ribotype 027 and non-027 ribotypes to different antibiotics was tested in a study in Canada. Ribotype 027 showed a resistance of 92.2% to moxifloxacin compared to 11.2% for other strains. Similarly, 78.2% of ribotype 027 strains were resistant to ceftriaxone compared to 15.7% of other strains. Ribotype 027 demonstrated a greater than four-fold higher minimum inhibitory concentration (MIC) to metronidazole (4 vs. 1 μg/ml) and two-fold higher MIC for fidaxomicin (1 vs. 2 μg/ml). For clindamycin and vancomycin, the resistance was similar in both groups [41].

Resistance to erythromycin is linked to mutations in the ribosomal methylase genes, whereas resistance to fluoroquinolones is due to a mutation in DNA gyrase. Resistance to rifamycin and fidaxomicin is attributed to ribonucleic acid (RNA) polymerase methylation. The presence of phenicol and lincosamide genes has been shown to cause resistance to linezolid. A study conducted in hospitals of Mexico showed some isolates of ribotype 027 to have reduced susceptibility to fidaxomicin despite the unavailability of this drug in Mexico and the patients being unexposed to it [42]. Antibiotics form the basis of treatment for the NAP1/B1/027 strain. Currently, no specific Infectious Diseases Society of America (IDSA) guidelines are available to guide treatment for this particular strain, and hence, the treatment is similar to a non-NAP1/B1/027 strain [9]. Based on the current guidelines for treating CDI overall, we propose the following table for treating infection caused by the NAP1/B1/027 strain (Table 2).

First line treatment Alternative treatment
Initial non-severe infection Oral vancomycin, 125 mg four times daily for 10 days Fidaxomicin, 200 mg twice daily for 10 days; If neither is available, then use metronidazole, 500 mg three times daily for 10 days
First non-severe recurrence Repeat oral vancomycin, 125 mg four times daily for 10 days Fidaxomicin, 200 mg twice daily for 10 days
Second non-severe recurrence Oral vancomycin taper as follow: 125 mg four times daily for seven to 14 days, 125 mg twice daily for seven days, 125 mg twice once daily for seven days, 125 mg once every other day for seven days, 125 mg once every three days for 14 days Fidaxomicin, 200 mg orally twice daily for 10 days, or a fecal microbiota transplant
Subsequent non-severe recurrence Fecal microbiota transplant Tapering oral vancomycin with probiotics, IVIG, fidaxomicin
Severe disease Oral vancomycin, 125 mg four times daily, increase to 500 mg four times daily if no improvement noted in 24-48 hours or associated complications, including renal failure, ileus, etc. Fidaxomicin if the patient cannot tolerate oral vancomycin for any reason
Ileus Add IV metronidazole, 500 mg every eight hours, to oral vancomycin or fidaxomicin therapy; consider general surgery consult as needed Intracolonic vancomycin, IVIG

This strain has not shown any resistance to fidaxomicin, but there has been some contradicting evidence to this. A case report was published in 2017 in which the NAP1 C. diff infection, resistant to treatment with fidaxomicin and fecal transplants, was effectively treated with intravenous immunoglobulin (IVIG) [43]. Given the emerging threat of antibiotic resistance, increasing awareness, controlling infections, and antimicrobial stewardship can be effective measures to reduce this threat [17].

Currently, several novel antibiotics are under investigation which have gone through various randomized controlled trials for CDI treatment. Ridinilazole and cadazolid have completed Phase II trials, while surotomycin has completed two Phase III trials which have shown promising results [44-47].

Conclusions

The data regarding the NAP1/B1/027 strain is inconclusive with ongoing debates whether this particular strain is associated with severe disease. Further research, including meta-analyses, are needed to solve this enigma. Clinicians should guide treatment based on their judgment and objective evidence of disease severity.


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Ferring Pharmaceuticals Acquires Rebiotix, Inc.

Ferring acquires innovative biotechnology company and microbiome pioneer Rebiotix Inc.

  • Rebiotix’s RBX2660 is a non-antibiotic treatment in Phase 3 development for the prevention of recurrent Clostridium difficile infection (CDI) and has the potential to be the world’s first approved human microbiome product
  • CDI is one of the most common healthcare-associated infections in the US, affecting more than 500,000 people and causing approximately 29,000 deaths each year.1
  • Ferring’s global capabilities ensure broader patient access to any future approved human microbiome treatments derived from Rebiotix’s Microbiota Restoration Therapy™ (MRT™) drug platform

Saint-Prex, Switzerland & Roseville, MN, US – 05 April, 2018 — Ferring Pharmaceuticals* and Rebiotix Inc.  announce that they have agreed to the acquisition of Rebiotix by Ferring. This acquisition brings together two innovative healthcare companies that share a common commitment to exploring and understanding the human microbiome to develop new solutions for patients.

The most advanced investigational microbiome treatment from Rebiotix is RBX2660, a non-antibiotic treatment currently in Phase 3 development for the prevention of recurrent CDI. RBX2660 has the potential to be the first human microbiome product approved anywhere in the world. In the US, RBX2660 has received FDA Fast Track, Breakthrough Therapy and Orphan Drug Designations, which means the FDA considers it eligible for Expedited Review, once the submission has been made.

“The scientific advances Rebiotix has made add significant strategic value to Ferring’s leadership in gastroenterology,” said Michel Pettigrew, President of the Executive Board and Chief Operating Officer, Ferring Pharmaceuticals. “Therapies targeted towards the microbiome have the potential to transform healthcare. Together, we have a unique opportunity to help people living with debilitating and life-threatening conditions like Clostridium difficile infection.”

Rebiotix’s proprietary MRT drug platform delivers healthy, live, human-derived microbes into the gastrointestinal tract. It provides a standardised, stabilised product that is ready-to-use in an easy-to-administer format. The MRT pipeline consists of a number of investigational treatments including RBX7455, a non-frozen, lyophilised oral capsule formulation, in development for the prevention of recurrent CDI.

“Ferring shares our passion for understanding the role the microbiome plays in human health and has global capabilities that offer huge potential for the investigational therapies that we have in development,” said Lee Jones, Founder, President and Chief Executive Officer, Rebiotix, Inc. “Rebiotix was founded to revolutionise healthcare by harnessing the power of the human microbiome and this is a significant milestone in achieving that goal.”

“This acquisition strengthens our innovation pipeline and complements our own ongoing microbiome research as well as our partnerships with world-leading organisations in this area,” said Per Falk, Chief Science Officer, Ferring Pharmaceuticals. “Rebiotix’s culture and passion for high quality, innovative research fits with our own and complements our existing R&D capabilities.”

In addition to the acquisition of Rebiotix, Ferring, as a leader in gastroenterology, is supported by ongoing partnerships with world-leading research organisations in the field of microbiome research including the Karolinska Institutet and Science for Life Laboratory, the Centre for Translational Microbiome Research, Intralytix, The Institut Pasteur, the University of Lille, MyBiotics Pharma, March of Dimes and Metabogen.


About Ferring Pharmaceuticals

Ferring Pharmaceuticals is a research-driven, specialty biopharmaceutical group committed to helping people around the world build families and live better lives. Headquartered in Saint-Prex, Switzerland, Ferring is a leader in reproductive medicine and women’s health, and in specialty areas within gastroenterology and urology. Ferring has been developing treatments for mothers and babies for over 50 years. Today, over one third of the company’s research and development investment goes towards finding innovative and personalised healthcare solutions to help mothers and babies, from conception to birth. Founded in 1950, Ferring now employs approximately 6,500 people worldwide, has its own operating subsidiaries in nearly 60 countries and markets its products in 110 countries.

Learn more at www.ferring.com, or connect with us on Twitter, Facebook, Instagram, LinkedIn and YouTube.

About Rebiotix Inc.

Rebiotix Inc. is a late-stage clinical microbiome company focused on harnessing the power of the human microbiome to revolutionise the treatment of challenging diseases. Rebiotix possesses a deep and diverse clinical pipeline targeting several other disease states with drug products built on its pioneering MRT platform. The MRT platform is a standardised, stabilised drug technology that is designed to rehabilitate the human microbiome by delivering a broad consortium of live microbes into a patient’s intestinal tract via a ready-to-use and easy-to-administer format. For more information on Rebiotix and its pipeline of human microbiome-directed therapies, visit www.rebiotix.com.

About RBX2660

RBX2660 is the most advanced product utilising Rebiotix’s proprietary MRT drug platform. RBX2660 is in Phase 3 development for the prevention of recurrent CDI and has the potential to be the first human microbiome product approved anywhere in the world. It consists of a microbiota suspension of intestinal microbes and is administered via enema.

*Ferring Holding Inc. signed the agreement as part of Ferring Pharmaceuticals Group

“What is C. diff.?” One Woman Walked Up To Us And Asked – Then the Crowd Followed

Heather and Kimberly III 7.23.16

The C Diff Foundation Volunteer Patient Advocates; Heather Clark and
her sister, Kimberly Reilly participated at local events over the summer season  to educate and advocate
for C. diff. infection prevention, treatments, and environmental safety within the local communities raising C. diff. awareness and saving lives.

 

On behalf of the C Diff Foundation , we sincerely thank you Heather and Kimberly for your dedication, your time, and for joining the
C Diff Foundation partnering and sharing our global mission.

We are truly grateful to the many special Volunteer Patient Advocates, the special individuals donating their time in “Raising C. diff. Awareness within their communities” around the globe.  Thank You!

Heather and Kimberly lost their dear Father from C.diff. involvement.  Shortly after his passing,  Heather and Kimberly took a stand with the C Diff Foundation and dedicated their time and efforts in  “Raising C. diff. Awareness” to help educate, and advocate for this life-threatening infection that played a big part in their Father’s passing.

To listen to Heather’s journey, with fellow C. diff. survivors,  – please click on the podcast link below:

http://www.voiceamerica.com/episode/85287/c-diff-survivors-share-their-unique-journey-through-a-c-diff-infection-and-how-it-changed-their

“What is C. diff.?”

Clostridium difficile (C.diff.) is gram-positive, anaerobic, and a spore, rod/spindle-shape,
a common bacterium of the human intestine in 2 – 5%. C diff. becomes a serious gastrointestinal infection when individuals have been exposed to antibiotic therapy, and/or have experienced a long-term hospitalization, and/or have had an extended stay in a long-term care facility. However; the risk of acquiring a C diff. infection (CDI) has increased as it is in the community (Community Acquired CDI) and found in outpatient settings.

There are significant risk factors in patients who are immunosuppressant, ones who have been on antibiotic therapy, and the elderly population.

How do Antibiotics cause C diff.? The antibiotics cause a disruption in the normal intestinal flora which leads to an over growth of C difficile bacteria in the colon. The leading antibiotics known to disrupt the normal intestinal flora, yet not limited to, are Ampicillin, Amoxicillin, Cephalosporins, Clindamycin, and the broad spectrum antibiotics.

Since  November 2012 the CDC has shared public announcements regarding antibiotic use: Colds and many ear and sinus infections are caused by viruses, not bacteria. Taking antibiotics to treat a “virus” can make those drugs less effective when you and your family really need them. Limiting the usage of antibiotics will also help limit new cases of CDI.
*Always discuss the symptoms and medications with the treating Physician.

What are C.diff. Symptoms? Symptoms of Clostridium difficile (C.diff.)
C.diff. strains produce several toxins; the most popular are enterotoxin – Clostridium difficile toxin A and cytotoxin – Clostridium difficile toxin B.  Both strains are responsible for the symptoms of diarrhea, abdominal pain, fever, fatigue, and can advance to a complication of a severe inflammation of the colon; pseudomembranous colitis, which can also lead to further complications of toxic megacolon.

How is C.diff. Transmitted? Mode of transmission of CDI can be either directly or indirectly, hospital acquired (nosocomial) or community – acquired; Ingesting C.diff spores transmitted from others and patients by hands, or altered normal intestinal flora by antibiotic therapy allowing proliferation of C.diff.  in the colon.  Coming in contact with surfaces, devices, or material with Clostridium difficile spores can easily be transferred to individuals by hands that have touched a contaminated surface or item. Examples of surfaces, devices, and materials contaminated with C.diff. spores in hospital and community/outpatient settings: commodes, bath tubs, showers, hand rails, bed rails, counter tops, handles, clothing, medical equipment, and electronic rectal thermometers.

The C Diff Foundation provide a wide range of programs, such as education, and advocacy for C. diff. infection prevention, treatments, support, and environmental safety worldwide, training of volunteer patient advocates (VPA’s) across the globe to provide educational workshops, supplying life-saving medications for those afflicted with this infection from young children to seniors, building satellite branches across the globe, presenting educational workshops in educational programs, improving and expanding the C. difficile infection awareness, providing global tele-conferencing support sessions in mental health counseling, long-term illnesses, the prevention, treatments, environmental safety with nutritional education for patients, and families suffering through a C. difficile infection
and so much more.

We are working together and dedicated at raising C. diff. awareness to witness a decrease in newly diagnosed C. difficile infections worldwide and through dedication and efforts of the
C Diff Foundation Volunteers – we will meet our goals.

Lycoming Fair 7.16.16

 

 

 

 

 

 

Treatments For CDI?   Treating C diff is becoming more challenging to physicians, frustrating to patients, and costly to the health care industry. To date there are three antibiotics effective at treating C diff: Metronidazole is prescribed to treat mild to moderate symptoms and is cost effective (8). Vancomycin is prescribed for moderate to severe symptoms via: oral route as intravenous administration does not achieve gut lumen therapeutic levels. Vancomycin is prescribed to patients with unsuccessful results from the Metronidazole, or the patient is allergic, or pregnant, breastfeeding, or younger than ten years of age.

The most recent antibiotic, Dificid (fidaxomicin) http://www.dificid.com is the first medication approved by FDA to treat C diff. Associated-Diarrhea CDAD in over twenty five years with superiority in sustained clinical response (5) Loperamide, diphenoxylate and bismuth medications are contraindicated as they slow the fecal transit time which extends the toxins in the gastrointestinal system.

The use of Cholestyramine has demonstrated positive results as toxins A and B bind to the resin as it passes through the intestines aiding in slowing bowel motility and assists in decreasing dehydration (9).

C.diff. spores are able to live outside of the body for a very long period of time and are resistant to most routine cleaning agents. It has also been proven that alcohol based hand sanitizers remain ineffective in eradicating C. diff. spores. In 2009 Clorox Commercial Solutions Ultra Clorox Germicidal Bleach ® was named the first and only product to obtain Federal EPA registration for killing C. diff. spores on hard, non porous surfaces when used as directed (1).

Please visit the following Page for additional information:

https://cdifffoundation.org/c-diff-infection-%e2%99%a5-home-care/

 

The CDC also recommends a 1:10 ( 1 cup bleach to 9 cups of water) dilution of bleach and water for cleaning hard non-porous surfaces keeping areas covered with solution for 10 minutes and the solution is to be mixed fresh daily.

Hand hygiene following the guidelines in HAND WASING; it is important to wash hands before entering and exiting a patient’s room (4). The spores are difficult to remove from hands; Universal Contact Precautions remain best practice for healthcare personnel and Contact Precautions for patients with a confirmed diagnosis of CDI. Prevention through education about CDI has proven effective and beneficial to environmental housekeeping departments, health care professionals, administration, patients, and their families (2)

https://cdifffoundation.org/hand-washing-updates/

 

To Join The C Diff Foundation Volunteer Patient Advocate Program, please contact us by email info@cdifffoundation.org  or call us toll-free 1-844-FOR-CDIF

 

 

References:

(1) Clorox registered EPA
http://www.ahe.org/ahe/learn/press-releases/2009/20090402_clorox_epa_cdiff.shtml

(2) Clostridium difficile (CDI) Infections thttp://www.cdc.gov/hai/pdfs/toolkits/CDItoolkitwhite_clearance_edits.pdf
(3) Lab Tests and Diagnosis Mayo Clinichttp://www.mayoclinic.com/health/c-difficile/DS00736/DSECTION=tests-and-diagnosis
(4) CDC Hand washing
http://www.cdc.gov/Features/HandWashing/

(5) FDA announcement Dificid
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm257024.htm

(5) Dificid.com
http://www.dificid.com

(6) Probiotics in the prevention of antibiotic-associated diarrhea
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3105609/

(6) Danimals PRNewswire8/Jan2012;
http://www.prnewswire.com/news-releases/dannonr-danimalsr-adds-proven-benefits-of-probiotics-53347947.html

(7) Get smart antibiotics week CDC
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6144a7.htm

(8) Metronidazole
http://www.everydayhealth.com/drugs/flagyl

(9) Cholestyranine
http://www.globalrph.com/cholestyramine.htm