C-diff update

[CrunchRN, ADN, RN]

if you can't read it all please note the recommendations for hospital precautions! this is from www.medscape.com

http://www.medscape.com/viewarticle/515360_2

it is from the latest idsa meeting.

those dang mods (just kidding siri) made me edit ot for brevity so go to medscape if you want to read it in it's entirety.

clostridium difficile

several sessions of the idsa meeting and a satellite symposium supported by an unrestricted educational grant from viropharma were devoted to the "new" strain of clostridium difficile, which appears to be a new epidemic strain with substantial clinical consequences.[10-16] the following is a summation of the presentations.

epidemiology

l. clifford mcdonald, md,[10] cdc, reported that the rate of reported cases of c difficile-associated diarrhea (cdad) by icd-9 coding in us hospitals has increased from 3.7/10,000 patient-days in 1987 to 5.7/10,000 patient-days in 2001. reports of severe disease attributed to c difficile in 8 facilities in the united states and quebec, ontario. canada, beginning in 2001 are a source of concern. strain typing in these cases showed that these outbreaks were caused by the bi/nap-1 strain, which has unusual virulence factors (described below). the most comprehensive clinical and epidemiologic data were reported by pepin and coworkers[11,13,14] based on the experience at sherbrooke university hospital in quebec. the epidemic began in 2002-2003, when it was noted that there was a substantial increase in cdad cases and patients were severely ill. a review of 1771 cases for 1991-2003 showed a 10-fold increase in the population-based incidence among persons > 6.5 years of age and 4-fold increase in the rate of this complication in quebec hospitals. updated data for 2003-2004 compared with the prior 12 years are shown in table 6 .

the disease. the most important observation about cdad is that this epidemic strain seems to cause serious disease, is less responsive to therapy, and more relapses occur after apparently successful therapy. the quebec experience on these points was particularly impressive. the sequential clinical experience in sherbrooke university hospital for 1991-2003 is summarized in table 7 [13] for 30-day mortality and complicated disease defined as toxic megacolon, requiring colectomy; shock; or death.[13] the most recent analysis of 161 patients showed an attributable mortality of 17%.[14]

a similar experience with severe disease was reported for pittsburgh, pennsylvania, where there was a sudden increase in colectomies for cdad from 5 per year in the 1990s to 44 in 2000.[15,16]

a unique strain? the clinical and epidemiologic experience summarized previously indicates geographically localized outbreaks of serious c difficile-associated disease that are refractory to standard therapy, suggesting a unique strain. analysis of isolates from these outbreaks show that there is a new strain that has unusual toxigenic potential. dr. mcdonald[10] reported results of strain typing by toxinotyping restriction enzyme analysis pulsed-field gel electrophoresis and polymerase chain reaction (pcr) ribotyping. the epidemic strain is type bi, toxinotype iii, north american pulsed-field gel electrophoresis (pfge) type 1, and pcr ribotype 027. it produces toxins a and b, as most strains of c difficile do, but it also has a 18-bp deletion in the tcdc gene in the pathogenicity locus (paloc), which is a negative regulator of toxin a and b production. this may account for the recent observation that this epidemic strain produces 20 times as much toxin a and toxin b in vitro as other c difficile strains.[10,17] this strain also produces a "binary toxin" that is similar to iota toxin of clostridium perfringens, but the role of this toxin in c difficile-associated disease is uncertain. experience showed that toxinotype iii accounted for only 2% to 3% of nonepidemic cases of c difficile-associated disease; it was implicated in 96 of 187 (57%) of cases in the 8 us epidemics investigated by the cdc, and is the strain implicated in quebec.[17]

hospital infection control. methods to deal with outbreaks of c difficile-associated disease were reviewed by dr. muto based on her experience in pittsburgh.[15] c difficile is carried in 1.5% to 3% of healthy adults but increases to 20% to 40% in hospitalized patients. standard infection control practices are appropriate but generally ineffective because of poor compliance. recommendations were:

• handwashing with soap and water (alcohol sanitizers do not eradicate c difficile)
  
• barrier precautions with gowns and gloves
  
• room cleaning with 1:10 dilution of household bleach (a 1:100 dilution did not work)
  
• isolation entire length of stay
  
• permit nurses to order c difficile toxin assays (because they know when patients have diarrhea 1-2 days before doctors do)
  
• identification of high-risk patients by email to physicians
  • high risk was defined as: (1) prior c difficile-associated disease, (2) extended antibiotic use, and (3) leukocytosis or bandemia

  [*]control use of implicated antibiotics: clindamycin, ceftriaxone, and levofloxacin (use decreased 75%, 30%, and 50%, respectively).

these strategies appeared to work: the epidemic curve showed that rates of c difficile-associated disease increased from 2.7 to 7.2 cases per 1000 discharges in 1999 and decreased to 4 per 1000 discharges in 2004.