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Characterisation of Hospital Ward–Based Transmission Using Extensive Epidemiological Data and Molecular Typing


Background:
Clostridium difficile infection (CDI) is a leading cause of antibiotic-associated diarrhoea and is endemic in hospitals, hindering the identification of sources and routes of transmission based on shared time and space alone. This may compromise rational control despite costly prevention strategies. This study aimed to investigate ward-based transmission of C. difficile, by subdividing outbreaks into distinct lineages defined by multi-locus sequence typing (MLST).

Methods and Findings:
All C. difficile toxin enzyme-immunoassay-positive and culture-positive samples over 2.5 y from a geographically defined population of ∼600,000 persons underwent MLST. Sequence types (STs) were combined with admission and ward movement data from an integrated comprehensive healthcare system incorporating three hospitals (1,700 beds) providing all acute care for the defined geographical population. Networks of cases and potential transmission events were constructed for each ST. Potential infection sources for each case and transmission timescales were defined by prior ward-based contact with other cases sharing the same ST. From 1 September 2007 to 31 March 2010, there were means of 102 tests and 9.4 CDIs per 10,000 overnight stays in inpatients, and 238 tests and 15.7 CDIs per month in outpatients/primary care. In total, 1,276 C. difficile isolates of 69 STs were studied. From MLST, no more than 25% of cases could be linked to a potential ward-based inpatient source, ranging from 37% in renal/transplant, 29% in haematology/oncology, and 28% in acute/elderly medicine to 6% in specialist surgery. Most of the putative transmissions identified occurred shortly (≤1 wk) after the onset of symptoms (141/218, 65%), with few >8 wk (21/218, 10%). Most incubation periods were ≤4 wk (132/218, 61%), with few >12 wk (28/218, 13%). Allowing for persistent ward contamination following ward discharge of a CDI case did not increase the proportion of linked cases after allowing for random meeting of matched controls.

Conclusions:
In an endemic setting with well-implemented infection control measures, ward-based contact with symptomatic enzyme-immunoassay-positive patients cannot account for most new CDI cases.

: Please see later in the article for the Editors' Summary


Vyšlo v časopise: Characterisation of Hospital Ward–Based Transmission Using Extensive Epidemiological Data and Molecular Typing. PLoS Med 9(2): e32767. doi:10.1371/journal.pmed.1001172
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pmed.1001172

Souhrn

Background:
Clostridium difficile infection (CDI) is a leading cause of antibiotic-associated diarrhoea and is endemic in hospitals, hindering the identification of sources and routes of transmission based on shared time and space alone. This may compromise rational control despite costly prevention strategies. This study aimed to investigate ward-based transmission of C. difficile, by subdividing outbreaks into distinct lineages defined by multi-locus sequence typing (MLST).

Methods and Findings:
All C. difficile toxin enzyme-immunoassay-positive and culture-positive samples over 2.5 y from a geographically defined population of ∼600,000 persons underwent MLST. Sequence types (STs) were combined with admission and ward movement data from an integrated comprehensive healthcare system incorporating three hospitals (1,700 beds) providing all acute care for the defined geographical population. Networks of cases and potential transmission events were constructed for each ST. Potential infection sources for each case and transmission timescales were defined by prior ward-based contact with other cases sharing the same ST. From 1 September 2007 to 31 March 2010, there were means of 102 tests and 9.4 CDIs per 10,000 overnight stays in inpatients, and 238 tests and 15.7 CDIs per month in outpatients/primary care. In total, 1,276 C. difficile isolates of 69 STs were studied. From MLST, no more than 25% of cases could be linked to a potential ward-based inpatient source, ranging from 37% in renal/transplant, 29% in haematology/oncology, and 28% in acute/elderly medicine to 6% in specialist surgery. Most of the putative transmissions identified occurred shortly (≤1 wk) after the onset of symptoms (141/218, 65%), with few >8 wk (21/218, 10%). Most incubation periods were ≤4 wk (132/218, 61%), with few >12 wk (28/218, 13%). Allowing for persistent ward contamination following ward discharge of a CDI case did not increase the proportion of linked cases after allowing for random meeting of matched controls.

Conclusions:
In an endemic setting with well-implemented infection control measures, ward-based contact with symptomatic enzyme-immunoassay-positive patients cannot account for most new CDI cases.

: Please see later in the article for the Editors' Summary


Zdroje

1. CohenSHGerdingDNJohnsonSKellyCPLooVG 2010 Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the society for healthcare epidemiology of America (SHEA) and the infectious diseases society of America (IDSA). Infect Control Hosp Epidemiol 31 431 455

2. LooVGPoirierLMillerMAOughtonMLibmanMD 2005 A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality. N Engl J Med 353 2442 2449

3. McDonaldLCKillgoreGEThompsonAOwensRCJrKazakovaSV 2005 An epidemic, toxin gene-variant strain of Clostridium difficile. N Engl J Med 353 2433 2441

4. VonbergRPKuijperEJWilcoxMHBarbutFTullP 2008 Infection control measures to limit the spread of Clostridium difficile. Clin Microbiol Infect 14 Suppl 5 2 20

5. MutoCABlankMKMarshJWVergisENO'LearyMM 2007 Control of an outbreak of infection with the hypervirulent Clostridium difficile BI strain in a university hospital using a comprehensive “bundle” approach. Clin Infect Dis 45 1266 1273

6. ValiquetteLCossetteBGarantMPDiabHPepinJ 2007 Impact of a reduction in the use of high-risk antibiotics on the course of an epidemic of Clostridium difficile-associated disease caused by the hypervirulent NAP1/027 strain. Clin Infect Dis 45 Suppl 2 S112 S121

7. ZelnerJLKingAAMoeCLEisenbergJN 2010 How infections propagate after point-source outbreaks: an analysis of secondary norovirus transmission. Epidemiology 21 711 718

8. GlynnJRPalmerSR 1992 Incubation period, severity of disease, and infecting dose: evidence from a Salmonella outbreak. Am J Epidemiol 136 1369 1377

9. MedleyGFAndersonRMCoxDRBillardL 1987 Incubation period of AIDS in patients infected via blood transfusion. Nature 328 719 721

10. HornickRBGreismanSEWoodwardTEDuPontHLDawkinsAT 1970 Typhoid fever: pathogenesis and immunologic control. N Engl J Med 283 686 691

11. MagnusonHJThomasEWOlanskySKaplanBIDe MelloL 1956 Inoculation syphilis in human volunteers. Medicine (Baltimore) 35 33 82

12. CookGCZumlaA 2009 Manson's tropical diseases, 22nd edition. Edinburgh Saunders/Elsevier

13. WilcoxMMintonJ 2001 Role of antibody response in outcome of antibiotic-associated diarrhoea. Lancet 357 158 159

14. GriffithsDFawleyWKachrimanidouMBowdenRCrookDW 2010 Multilocus sequence typing of Clostridium difficile. J Clin Microbiol 48 770 778

15. PlancheTWilcoxM 2011 Reference assays for Clostridium difficile infection: one or two gold standards? J Clin Pathol 64 1 5

16. PlancheTAghaizuAHollimanRRileyPPolonieckiJ 2008 Diagnosis of Clostridium difficile infection by toxin detection kits: a systematic review. Lancet Infect Dis 8 777 784

17. BestELFawleyWNParnellPWilcoxMH 2010 The potential for airborne dispersal of Clostridium difficile from symptomatic patients. Clin Infect Dis 50 1450 1457

18. Department of Health 2009 Clostridium difficile infection: how to deal with the problem. London Health Protection Agency 140

19. KyneLWarnyMQamarAKellyCP 2000 Asymptomatic carriage of Clostridium difficile and serum levels of IgG antibody against toxin A. N Engl J Med 342 390 397

20. McFarlandLVMulliganMEKwokRYStammWE 1989 Nosocomial acquisition of Clostridium difficile infection. N Engl J Med 320 204 210

21. SamoreMHDeGirolamiPCTluckoALichtenbergDAMelvinZA 1994 Clostridium difficile colonization and diarrhea at a tertiary care hospital. Clin Infect Dis 18 181 187

22. PalmoreTNSohnSMalakSFEaganJSepkowitzKA 2005 Risk factors for acquisition of Clostridium difficile-associated diarrhea among outpatients at a cancer hospital. Infect Control Hosp Epidemiol 26 680 684

23. GrundmannHBarwolffSTamiABehnkeMSchwabF 2005 How many infections are caused by patient-to-patient transmission in intensive care units? Crit Care Med 33 946 951

24. EastwoodKElsePCharlettAWilcoxM 2009 Comparison of nine commercially available Clostridium difficile toxin detection assays, a real-time PCR assay for C. difficile tcdB, and a glutamate dehydrogenase detection assay to cytotoxin testing and cytotoxigenic culture methods. J Clin Microbiol 47 3211 3217

25. RiggsMMSethiAKZabarskyTFEcksteinECJumpRL 2007 Asymptomatic carriers are a potential source for transmission of epidemic and nonepidemic Clostridium difficile strains among long-term care facility residents. Clin Infect Dis 45 992 998

26. Rodriguez-PalaciosAReid-SmithRJStaempfliHRDaignaultDJaneckoN 2009 Possible seasonality of Clostridium difficile in retail meat, Canada. Emerg Infect Dis 15 802 805

27. GouldLHLimbagoB 2010 Clostridium difficile in food and domestic animals: a new foodborne pathogen? Clin Infect Dis 51 577 582

28. GoldenbergSDFrenchGL 2011 Diagnostic testing for Clostridium difficile: a comprehensive survey of laboratories in England. J Hosp Infect 79 4 7

29. WilcoxMHEastwoodK 2009 Evaluation report: Clostridium difficile toxin detection assays. London NHS Purchasing and Supply Agency

30. BroukhanskiGSimorAPillaiDR 2011 Defining criteria to interpret multilocus variable-number tandem repeat analysis to aid Clostridium difficile outbreak investigation. J Med Microbiol 60 1095 1100

31. TannerHEHardyKJHawkeyPM 2010 Coexistence of multiple multilocus variable-number tandem-repeat analysis subtypes of Clostridium difficile PCR ribotype 027 strains within fecal specimens. J Clin Microbiol 48 985 987

32. van den BergRJAmeenHAFurusawaTClaasECvan der VormER 2005 Coexistence of multiple PCR-ribotype strains of Clostridium difficile in faecal samples limits epidemiological studies. J Med Microbiol 54 173 179

33. WroblewskiDHannettGEBoppDJDumyatiGKHalseTA 2009 Rapid molecular characterization of Clostridium difficile and assessment of populations of C. difficile in stool specimens. J Clin Microbiol 47 2142 2148

34. EyreDWWalkerASGriffithsDWilcoxMHWyllieDH 2012 Clostridium difficile mixed infection and reinfection. J Clin Microbiol 50 142 144

35. ShimJKJohnsonSSamoreMHBlissDZGerdingDN 1998 Primary symptomless colonisation by Clostridium difficile and decreased risk of subsequent diarrhoea. Lancet 351 633 636

36. WilcoxMH 2011 Laboratory diagnosis of Clostridium difficile infection: in a state of transition or confusion or both? J Hosp Infect 79 1 3

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PLOS Medicine


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