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A u g us t 16 -‐ 1 7 th , 2014 AGA F r e st o n Confe rence Chi cag o , IL. D ISCLOS U RES. Y o u r n ame: Elain e O. Petr o f Th e n ame o f th e c o mmerc ial in tere st(s) : N ubi y o ta
Correct Response:2. Vancomycin 125mgpo qid x 14 days
Tes-ng point: determinecorrecttreatment in a paOentwithC. diﬃcileinfecOon based on lab criteria and clinical presentaOon (severity of illness)
Based on levels of clinical evidence and on the IDSAguidelines, “Treatment of the ﬁrstrecurrence of CDI is usuallywith thesameregimen as for the iniOal episode(A-‐II)but should be straOﬁed by disease severity (mild-‐to-‐moderate, severe, orseverecomplicated)”. Based on guidelines, her lab criteria (WBC>12,000,creaOnine) would classify her as severe, but she is not hypotensive and does not have toxicmegacolon so shewould not beconsidered to be severecomplicated CDI. Therefore,correctresponsewould be (2). Theguidelines state “use ofvancomycin is recommended for the ﬁrstrecurrencein paOents with a white blood cell count of 15,000cells/μL or higher (or a rising serumcreaOnine level), since theyareathigherrisk of developingcomplicaOons.” The dosage forvancomycin in severe CDI is 125mg orally4Omes per day for10–14 days (B-‐I)
(1) is incorrect as this paOentwould not beclassiﬁed as a mild CDI, (5) is incorrect for the samereason (and in addiOon one would givemetronidazole po, iv is less eﬀecOve)
Since thisisher ﬁrstrecurrence,FMT would only beconsidered a^er a second recurrence had failed avancomycin taper orpulseregimen according to currentguidelines, therefore (4) is incorrect. (Note:Metronidazole should not be used beyond the ﬁrstrecurrence of CDI or for long-‐termchronic therapy because of potenOal forcumulaOve neurotoxicity(B-‐II).
Treatment of the second or laterrecurrence of CDIwithvancomycin therapy using a tapered and/or pulseregimen is the
preferred next strategy(B-‐III).)
This paOent does not have hypotension or ileus,would not beclassiﬁed as severecomplicated and would notrequire vancomycin dosing above125mg po q6h, therefore (3) is incorrect. For severe,complicated CDI,vancomycin administered orally (and perrectum, if ileus is present) with orwithout intravenously administered metronidazole is theregimen ofchoice. In addiOon, thevancomycin dosage is 500mg orally4Omes per day and 500mg in approximately100mL normal saline perrectumevery6 hours as a retenOon enema, and themetronidazole dosage is 500mg intravenouslyevery8 hours(C-‐III).
REFERENCE:Clinicalprac-ceguidelines for Clostridiumdiﬃcileinfec-oninadults:2010updatebythesocietyforhealthcareepidemiologyof America(SHEA)andthe infec-ousdiseasessocietyof America(IDSA).Cohen SH,GerdingDN,JohnsonS,KellyCP, Loo VG,McDonald LC,Pepin J,Wilcox MH; Society forHealthcare Epidemiology of America; InfecOous Diseases Society ofAmerica. Infect ControlHosp Epidemiol. 2010May;31(5):431-‐55.
Correct Response:5. AtorvastaOn
Tes-ng point:recognizewhich factors are likelyNOT to be potenOal risk factors for the development ofClostridiumdiﬃcile
Of all of the factors listed here, atorvastaOn (opOon 5) is the only one that hasnot been associated with an increased risk of CDI and itmayeven be protecOve (seereferences below).
The singlemost importantmodiﬁablerisk factor for the development of CDI is exposure to anOmicrobial agents. Even verylimited exposure (e.g., single-‐dose surgical anObioOc prophylaxis), increases a paOent’s risk of developing CDI, therefore (1) is incorrect.
DuraOon of hospitalizaOon is a risk factor for CDI; therefore (2) is incorrect. In fact, the daily increase in therisk ofC. diﬃcileacquisiOon during hospitalizaOon suggests that duraOon of hospitalizaOon is a proxy for the duraOon, if not the degree, ofexposure to the organism from other paOents with CDI.
Several studies have suggested an epidemiologic associaOon between use of stomach acid–suppressingmedicaOons,primarily proton pump inhibitors, and CDI, therefore (3) is incorrect.
Previous appendectomy has been associated with development of recurrent CDI, therefore (4) is incorrect.
Sta-nuse andthe riskof Clostridium diﬃcile inacademic medicalcentres. Motzkus-‐Feagans CA,Pakyz A,PolkR,GambassiG,LapaneKL. Gut. 2012Nov;61(11):1538-‐42.
Dosta-nsprotect againstthe developmentof Clostridium diﬃcile-‐associateddiarrhoea? NseirW,Bishara J,Mograbi J,Mahamid M,Khalaila W, Taha M, Farah R. JAn9microb Chemother. 2013Aug;68(8):1889-‐93.
The eﬀects ofsta-nsonthe clinicaloutcomes ofClostridiumdiﬃcileinfec-oninhospitalisedpa-ents.Park SW, Choi AR,LeeHJ, ChungH,ParkJC, Shin SK, Lee SK, Lee YC,KimJE, Lee H.AlimentPharmacol Ther. 2013 Sep;38(6):619-‐27.
TheappendixmayprotectagainstClostridiumdiﬃcilerecurrence.ImGY,Modayil RJ, Lin CT,GeierSJ,Katz DS, FeuermanM,GrendellJH. Clin GastroenterolHepatol. 2011Dec;9(12):1072-‐7.
Clinicalprac-ceguidelines for Clostridiumdiﬃcileinfec-oninadults:2010updatebythesocietyforhealthcareepidemiologyof America(SHEA)andthe infec-ousdiseasessocietyof America(IDSA).Cohen SH,GerdingDN,JohnsonS,Kelly CP, Loo VG,McDonald LC,Pepin J,Wilcox MH; Society forHealthcare Epidemiology of America; InfecOous Diseases Society of America. Infect ControlHosp Epidemiol. 2010May;31(5):431-‐55.
RestoraOon of thecolonizaOon resistance through fecalmicrobiotatransplantaOon (FMT)
Change inbacterialcomposi-onof fecalsample from the same donor
REF:Braceet al.,J CrohnsColi9s(2014)[Epub ahead of print]
A possible alternaOve?
Infuseinto patientvia rectum
Coprococcus comes:resistant to mulOpleanObioOcs tested
E.coli:chose to include more suscepOble strain
“Synthe-c”stoolinfusionpreventsaddi-onal CDI episodes inpa-entswith recurrent
PaOentmicrobiotaremodels overOme to acompositeof RP and paOentmicrobiota
RP = RePOOPulate (syntheOc stool)M6 = Month 6
PT = Pre-‐transplant
Dr. Emma Allen-‐Vercoe & lab
Dr. GregGloor Dr. GregorReid