cause of his spinal stenosis and resultant weakness in hislegs, although he can walk short distances with a walker.Further evaluation of his urinary problems during his re-centhospitalizationrevealedaneurogenicbladderthoughtto be due to his spinal stenosis; the Foley catheter was re-moved and he has learned to use straight catheters. He hadbeenscheduledforsurgeryforthespinalstenosisbutitwaspostponed when he developed CDI.Mr S’s medications include prednisone, 4 mg daily; cy-closporine, 50 mg daily; and diltiazem, trazodone, ateno-lol, minoxidil, furosemide, long-acting nitrates, finaste-ride,anderythropoietin,alongwiththestandingvancomycinand rifaximin.Mr S is retired and lives with his wife and adult son. Hedoesnotsmokeandhedrinksonly1alcoholicbeveragepermonth.On physical examination, Mr S is thin, weighing 135 lb(61kg),andis69in(175cm)tall(bodymassindex,19.9).His blood pressure is 150/70 mm Hg and his heart rate is68/min. No neurological or spinal examination was per-formedforthediscussion,buthisphysicalexaminationwasotherwiseremarkableonlyforhisleftlowerquadrantrenalallograft, which was tender and without bruits, and for 1
pitting edema in his lower extremities.MrS’slaboratorytestresultsshowabaselinecreatininelevelof 1.8 mg/dL and a serum urea nitrogen level of 68 mg/dL.Hisstoolstudieswerepositivefor
C difficile
toxinAdur-inghisinitialhospitalizationfordiarrhea;subsequentsamplesobtained when symptoms have recurred have been nega-tive. Mr S’s most recent urine culture showed resolution of a previous
Pseudomonas
infection.
MR S: HIS VIEW
Iwouldtaketheregimenofmedicinesprescribedbythedoc-tor. Three or four days after finishing the regimen, I wouldgetbetter.ThenIwouldturnrightaround;I’dgetthechillsandstartshaking,sometimesuncontrollably.I’dhavetoputthe covers on, even in the summertime. I would take [acet-aminophen/paracetamol], and it would bring the tempera-ture down and the medicine would control the
C difficile
.This illness has been very distressing. Sometimes I wouldbe on the toilet and would think I’m done. I get about half-waybacktothebedroom,thenIhavetogobackagain.Some-timesthiswouldhappen3timesina15-minuteperiod.Rightnow, it seems the pills are curing me, and I’m getting better.I’m not going as frequently, but I’m still going 4 or 5 times aday. I might wake up in the evening and go once or twice.My back is giving me a lot of problems. I get a lot of painwhen I try to move. I can’t walk as well, and I have to usemy walker. I’m really slow. I had a procedure done on myneck in November. And I was supposed to have the secondprocedure done on my spine, but we had to cancel that be-cause of the
C difficile
.I’d be kind of frightened if somebody told me I had to goback on antibiotics after this. I wouldn’t wish this illnessonanybody.
Cdifficile
isoneofthemostterriblethingsthatI’ve been dealing with in my whole life, and I’ve dealt witha lot of things since my kidney transplant. I hope that thislatest regimen of pills will cure me—because I’m going outof my mind.
ATTHECROSSROADS:QUESTIONSFORDRKELLY
How common is
C difficile
after an initial episode of anti-biotic treatment and how are rates affected by age or im-munestatus?Howshouldthediagnosisbemadeandisem-pirical treatment an acceptable strategy? How common isrecurrentinfectionandaretheseusuallyrelapseorreinfec-tion? What is the evidence for the most effective treatmentforfirstandrecurrentepisodes?Whatshouldphysiciansdoto prevent
C difficile
in terms of prescribing and infectioncontrol practices? What do you recommend for Mr S?
D
R
K
ELLY
:
Mr S is a 76-year-old retiree with a function-ingrenaltransplant,benignprostatichypertrophy,andspi-nalstenosiswhosecaseillustratesthechallengingproblemofCDI.Hereceivedbothceftriaxoneandciprofloxacindur-ing inpatient treatment for a urinary tract infection, devel-oped diarrhea, and was treated with oral metronidazole forpossible CDI. He subsequently experienced multiple epi-sodes of recurrent CDI leading to hospital admissions andrequiringrepeatedandprolongedtreatmentswithoralvan-comycin.
Disease Pathogenesis
Clostridium difficile
is a gram-positive, spore-forming, an-aerobic bacillus first isolated in 1935 from the stool of ahealthy neonate.
1
The finding that
C difficile
is an opportu-nisticpathogenwasnotmadeuntilthelate1970s,whentheclinical entity of antibiotic-associated,
C difficile
–induceddiarrheaandcolitiswasfirstcharacterized.
Clostridium dif- ficile
infectionisnowbyfarthemostcommonknowncauseofinfectiousdiarrheainhospitalpatientsinNorthAmericaand Europe, where both the incidence and severity of dis-ease have increased alarmingly since 2000.
2
Although
C difficile
is common in the general environ-ment, only 1% to 4% of healthy adults carry this organism.A normal colonic microflora confers “colonization resis-tance” against CDI.
2
Neonates, lacking an established in-testinal microflora, frequently have
C difficile
colonizationbut, interestingly, seldom experience
C difficile
toxin–induceddiarrheaorcolitis,possiblybecauseofalackoftoxinreceptor expression in the immature gut.
1
In adults, loss of colonizationresistancetoCDIismostoftentheresultofan-timicrobial therapy. All antimicrobials are not equal in thisregard, and the risk of CDI associated with different anti-microbials results from a complex combination of their lu-minalconcentrations,theireffectsonthenormalintestinalmicroflora, and their activity against
C difficile
.
2-5
The abil-ityofclindamycintoimpaircolonizationresistanceandin-duceCDIiswellknown.
3
However,incurrentmedicalprac-tice, second- and third-generation cephalosporins and
CLINICAL CROSSROADS
©2009 American Medical Association. All rights reserved.
(Reprinted) JAMA,
March 4, 2009—Vol 301, No. 9
955
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