Objectives Describe the incidence of C difficile in the US Review - - PDF document

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C difficile – What’s New?

Linda R.Greene,RN,MPS,CIC,FAPIC linda_greene@urmc.rochester.edu Manager, Infection Prevention UR Highland Hospital Rochester, NY linda_greene@urmc.rochester.edu

Objectives

 Describe the incidence of C difficile in the US  Review epidemiology and pathogenesis of C. difficile  Discuss recent literature to risk factors and prevention

strategies

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Burden of C. difficile in the US

Estimated that C. difficile caused approximately 453,000 incident infections and was associated with approximately 29,000 deaths in the United States in 2011 on the basis of data from active population- and laboratory-based surveillance across diverse geographic locations in the United States Only an estimated 24% of cases occurred in hospital settings

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C difficile

Of the estimated community onset cases 82% were estimated to be associated with outpatient health care exposure

swallow spore or vegetative form (stomach acid does not kill) small intestine vegetative form large intestine disease happens if normal flora disrupted toxins released inflammation

Acquiring C difficile

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Pseudomembranous colitis

An inflammatory process that can lead to formation of pseudo membranes; a mixture of inflammatory cells, fibrin, bacteria and cellular components, which exude from the bowel mucosa.

Ingested Normal flora interrupted Small Intestine Spores Germinate Pseudomembrane C Difficile toxins monocytes Neutrophils Toxin A attracts neutrophils and monocytes, and toxin B degrades the colonic epithelial cells, both leading to colitis, pseudomembrane formation, and watery diarrhea C difficile reproduces in the intestinal crypts, releasing toxins A and B, causing severe inflammation. Mucous and cellular debrisare expelled, leading to the formation of pseudomembranes

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Toxic megacolon

Toxic megacolon is characterized by extreme inflammation and distention of the colon. Common symptoms are pain, distention of the abdomen, fever, rapid heart rate, and dehydration. This is a life-threatening complication that requires immediate medical treatment.

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Transmission

 C diff is shed in feces  The transmission is

fecal -> oral

 C. diff spores can live

for months on contaminated surfaces.

Prevention

Judicious use of antibiotics

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Risk Factors

Conclusions:

• The risk of HA-CDI remains greatest for cephalosporins and clindamycin, and their

importance as inciting agents should not be minimized.

• The importance of fluoroquinolones should not be overemphasized,

particularly if fluoroquinolone-resistant epidemic strains of C. difficile are absent.

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Other Risk Factors

 C difficile occurrence could increase with moderate to high opioid

administration ( delayed passage of intestinal contents allows closer contact with the mucosa and increases chance of infection)

 Corticosteroid use – 1.5 to 3 fold increase

Other Risk Factors

Chemotherapy hypothesized mechanisms

• 1. Alteration in intestinal flora
• 2. Previous infection with c dif prior to therapy
• 3. Increased use of antibiotics
• 4. Increased colonic mucosa damage
• 5. Reduction in repair capabilities of mucosal

epithelium

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Background/Aims: Researchers reviewed PPI use compared to H2RA for stress ulcer prophylaxis

• Proton pump inhibitors (PPIs) reduce the production of acid by blocking

the enzyme in the wall of the stomach that produces acid. Acid is necessary for the formation of most ulcers . Trade name Nexium

• H2 antagonists ( H2RA) competitively inhibits histamine at the H2

receptors and leads to a reduction in secretion of gastric acid. Trade names Zantac, Pepcid etc.

Continued

Methods: Identified 12 studies that reported the hospital-acquired CDI occurrence following H2RA and PPI use for the prevention and treatment of stress gastric ulcers Findings : Results: A total of 74,132 patients from 12 observational studies were

• analyzed. Compared to H2RAs, PPIs increased the risk of CDI by 38.6%

Conclusions: The use of PPIs for both the prevention and treatment of stress ulcers was associated with a 38.6% increased risk of hospital-acquired CDI

• ccurrence compared to H2RA use.

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Test

Useful for epidemiologic studies

• Molecular tests are increasingly used to diagnose C difficile

infection (CDI),

• Many molecular test-positive patients lack toxins that historically

defined disease,

• Sometimes unclear if patients need treatment

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Study

 Prospective observational cohort study  Single academic medical center  1416 hospitalized adults tested for C difficile toxins 72

hours or longer after admission between December 1, 2010, and October 20, 2012

 Test included both toxin and PCR

Conclusion

 Among hospitalized adults with suspected CDI, virtually

all CDI-related complications and deaths occurred in patients with positive toxin immunoassay

 Patients with a positive molecular test result and a

negative toxin immunoassay test result had outcomes that were comparable to patients without C difficile by either method

 Over reliance on molecular tests may result in over

diagnosis, over treatment and increased cost

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Review

C difficile toxin- If tests for C. difficile and C. difficile toxin are positive, it is likely that the person's diarrhea and related symptoms are due to the presence of toxin- producing C. difficile GDH -This test detects an antigen that is produced in high amounts by C. difficile, both toxin and non-toxin producing strains. It is considered to be very sensitive, but it is not very specific for toxin-producing C. difficile. This test indicates if C. difficile is present but the bacteria May not be producing toxins.

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Study Continued

 Twenty-one percent (293 of 1416) of hospitalized

adults tested for C difficile were positive by PCR

 44.7% (131 of 293) had toxins detected by the clinical

toxin test Baseline Tox−/PCR+ patients had lower C difficile bacterial load and less antibiotic exposure, fecal inflammation, and diarrhea than Tox+/PCR+ patients (P < .001 for all

Findings

 Patients with a positive PCR but negative toxin EIA had

a significantly lower 14-day all-cause mortality (11%) than patients with a positive PCR and positive toxin EIA test P = 0.01

 A positive toxin EIA test was a significant independent

predictor of death odds ratio (OR): 4.7 P = 0.01 and prolonged diarrhea (OR: 8.6 P < 0.001), but a positive PCR (given positive GDH EIA) was not.

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Conclusions

 TOXIN- PCR + : Questionable Results  What is the take home message here?  Implications for clinical practice:

Testing Guidelines Do not over test

Future Directions

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Control Transmission

2 Strategies were independently weighted as being independent statistically Significant interventions 1. Hand Hygiene 2. Pre-emptive isolation when patients have diarrhea and suspected C. difficile

Chasing Zero Infections - Connecting the Dots to Reduce Patient Harm: Hot Topics in Infection Prevention and Stewardship Thursday, May 25, 2017 Mission to Care FHA HIIN 16  Compared 3 techniques  Structured vs unstructured

Regular WHO WHO- SR

 Prepared C difficile seeding

solution

Technique and Results

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Guidelines Tier Strategy

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The most common means of C diff transmission is on hands.

Environmental Contamination “Fecal Veneer”

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Supportive Evidence

• Skin contamination and environmental shedding may persist at the

time

• of resolution of diarrhea
• Recurrent shedding is common 1-2 weeks after therapy
• Recurrent shedding may persist 1-6 weeks after therapy

The Environment

• Study demonstrated that gloved hands can be easily

contaminated

• Education, audit and feedback are essential

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Novel Technologies

UV Hydrogen Peroxide Many observational studies No good RCTs Experience demonstrates efficacy