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1、State of the Science ReviewNew and emerging infectious diseases (Ebola, Middle Eastern respiratorysyndrome coronavirus, carbapenem-resistant Enterobacteriaceae,Candida auris): Focus on environmental survival and germicidesusceptibilityDavid J. Weber MD, MPHa,b,*, Emily E. Sickbert-Bennett MS, PhDa,b
2、, Hajime Kanamori MD, PhD, MPHc,William A. Rutala PhD, MPHbaDepartment of Hospital Epidemiology, University of North Carolina Hospitals, Chapel Hill, NC, USAbDivision of Infectious Diseases, University of North Carolina School of Medicine, Chapel Hill, NC, USAcInfection Control and Laboratory Diagno
3、stics, Tohoku University, Sendai, JapanKey Words:SurfaceEnvironmentDisinfectionIn the recent past, we have witnessed the emergence of manynew infectious diseases, some of which are major public healththreats. The public health threats posed by emerging diseaseshave been well described in 2 reports f
4、rom the Institute of Medi-cine, 1 in 1992 and 1 in 2001.1,2Since the outbreak of Legionellain 19763,4and AIDS in 19815,6later demonstrated to be due toHIV in 1983,7many emerging infectious diseases have had impor-tant infection control implications. This review will focus on sev-eral of the most imp
5、ortant current infection prevention threatsincludingEbolavirus,MiddleEasternrespiratorysyndrome(MERS) coronavirus (CoV), carbapenem-resistant Enterobacteria-ceae (CRE), and Candida auris with a focus on mechanisms oftransmission, environmental contamination and stability, and ger-micide susceptibili
6、ty. Germicides that will be discussed includechemical sterilants used to process critical equipment and devices(eg, surgical instruments, implants), high-level disinfectants thatare used to disinfect semicritical equipment and devices (ie, med-ical equipment or devices that come into contact with no
7、nintactskin or mucous membranes), low-level disinfectants used for dis-infection of surfaces or shared equipment that come into contactwith intact skin (eg, blood pressure cuffs, room surfaces), andantiseptics (ie, germicides used on skin or mucous membranes toreduce the microbial flora).8,9This rev
8、iew updates a previous arti-cle that reviewed Ebola and MERS and also reviews CRE andC auris.10DEFINITIONSThe World Health Organization (WHO) states, “an emerging dis-ease is one that has appeared in a population for the first time, or thatmay have existed previously but is rapidly increasing in inc
9、idence orgeographic range.”11The Centers for Disease Control and Prevention(CDC) provides the following definition of emerging infections as“infectious diseases whose incidence in humans has increased in thepast 2 decades or threatens to increase in the near future have beendefined as emerging.” The
10、se diseases, which respect no nationalboundaries, include: (1) new infections resulting from changes orevolution of existing organisms; (2) known infections spreading tonew geographic areas or populations; (3) previously unrecognizedinfections appearing in areas undergoing ecologic transformation,an
11、d (4) old infections reemerging as a result of antimicrobial resis-tance in known agents or breakdowns in public health measures.12FACTORS IN THE EMERGENCE OF INFECTIOUS DISEASESAND PREPAREDNESSThe factors leading to the emergence of infectious diseases havebeen described.13-17Importantly, all these
12、 authors noted that we willcontinue to see new and emerging infectious diseases for the foresee-able future. Recent articles have provided recommendations for pre-paredness at the health care facility, local and national levels.10,18-20KEY CONSIDERATIONS IN ASSESSING AND MANAGING THE THREATOF EMERGI
13、NG INFECTIOUS DISEASES IN HEALTH CARE FACILITIESAssessing and managing the threat of an emerging infectious dis-ease requires an understanding of the biology of the pathogen, its epi-demiology, the clinical manifestations of infection, the methods of* Address correspondence to David J. Weber, MD, MP
14、H, University of North CarolinaHospitals, 2163 Bioinformatics, CB #7030, Chapel Hill, NC, 27599-7030.E-mail address: dweberunch.unc.edu (D.J. Weber).Conflicts of interest: None to report.https:/doi.org/10.1016/j.ajic.2019.03.0040196-6553/ 2019 Association for Professionals in Infection Control and E
15、pidemiology, Inc. Published by Elsevier Inc. All rights reserved.American Journal of Infection Control 47 (2019) A29A38Contents lists available at ScienceDirectAmerican Journal of Infection Controljournal homepage: www.ajicjournal.orgdiagnosis, and therapies (if available).10All health care faciliti
16、esshould have a highly communicable disease plan for agents that aretransmitted by droplet or aerosols (eg, severe acute respiratory syn-drome SARS, MERS) or are transmitted by contact (eg, Ebola,Lassa).10Detailed information is best found, especially early in an epi-demic, on the web pages of local
17、 and state health department, theCDC, and the WHO. For highly communicable diseases, there are 2major areas that place a health care facility and the personnel at sub-stantial risk for disease acquisition and transmission.10First, inade-quate screening procedures when patients enter a health care fa
18、cilitycan potentially allow transmission from an ill patient to health carepersonnel, other patients, or visitors. Second, inadequate supplies ofpersonal protective equipment (PPE) and/or training of health carepersonnel (HCP) in proper donning and doffing procedures canincrease the risk of exposure
19、 for HCP.A key focus of this article is to review the transmission routes ofnew and emerging infectious agents. Preventing disease acquisitionvia person-to-person transmission or contact with the contami-nated environment depends on rapid and appropriate institution ofisolation precautions, appropri
20、ate hand hygiene, and appropriatedisinfection of medical equipment, devices, and the surface envi-ronment. Importantly, once the nature of the emerging disease isknown (ie, enveloped virus, bacteria, fungi, nonenveloped virus,mycobacteria), it is possible to determine the proper antiseptics anddisin
21、fectants, even in the absence of studies of the exact infectiousagent.21For example, an enveloped virus (eg, Ebola, MERS-CoV) orvegetative bacterium (eg, CRE) would be inactivated by any agentactive against nonenveloped viruses or mycobacteria. It is impor-tant to remember that alcohol has reduced a
22、ctivity against nonen-veloped viruses (eg, norovirus) and no activity against spores (eg,Clostridioides difficile).EBOLAHistory and microbiologyThe first recognized outbreak of Ebola occurred in West Africa in1976. In the 40 years since the initial outbreaks in Zaire and Sudan,20 outbreaks have occu
23、rred.22The largest outbreak occurred inWest Africa (Guinea, Sierra Leone, and Liberia) from 2014-2016, andresulted in 28,600 cases and 11,325 deaths.23Importantly, in the2014-2016 outbreak 850 HCP developed confirmed or probableEbola virus disease (EVD).24The percentage of exposed HCP whodeveloped E
24、VD has ranged from 12.5%-76%.24The mortality of HCPwho developed Ebola has frequently exceeded 50%.24Key concernsfor HCP include the low inoculating dose required for transmission;high frequency of HCP infections, especially in resource poor coun-tries; and high mortality. As of 2019, an EVD outbrea
25、k is continuingwith moderate intensity in the Democratic Republic of the Congo.Overall, 11 people were treated for Ebola in the United States dur-ing the 2014-2016 epidemic.23Two out of 149 HCP who cared for apatient with EVD in the United States developed EVD; bothrecovered.24The microbiology, epid
26、emiology, diagnosis, clinical features, andtreatment of Ebola have been reviewed.22,25-30Ebola is caused by anonsegmented, single-stranded negative RNA virus of the family Filo-viridae. There are 5 identified Ebola virus species, 4 of which areknown to cause disease in humans: Zaire, Sudan, Tai Fore
27、st (formerlyCote dIvoire), and Bundibugyo. The fifth, Reston virus, has caused dis-ease in nonhuman primates, but not in humans. The natural reservoirhost of Ebola virus remains unknown. However, the detection of anti-bodies against Ebola and Ebola virus fragments in fruit- and insecti-vore bats are
28、 highly suggestive that these animals serve as areservoir.EVD is characterized by the sudden onset of fever, headache,myalgias, arthralgias of the large joints, and back pain. Typically, 2-3 days after the initial symptoms gastrointestinal symptoms occurincluding abdominal pain, nausea, vomiting, an
29、d diarrhea. A macularor maculopapular skin rash may appear on days 5-7 of the disease.Hemorrhage is less common, occurring in only 15%-20% of patients.Terminal cases develop disseminated intravascular coagulation, sep-tic shock, and multiorgan system failure. Mortality ranges from 40%-90% and depend
30、s, in part, on the infecting strain.Epidemiology and transmissionEbola is transmitted person-to-person most commonly throughdirect contact (ie, nonintact skin or via mucous membrane contact)with blood, body fluids (eg, urine, saliva, sweat, feces, vomit, breastmilk, and semen) of an ill person, or i
31、ndirectly via objects such as nee-dles and syringes that have been contaminated with body fluids froman ill person (Table 1).31Less common mechanisms include acquisi-tion from infected fruit bats or nonhuman primates. Sexual transmis-sion has also been described. Ebola is not transmitted via the air
32、 or bywater. However, in Africa it has been acquired by handling bushmeat. The incubation period of Ebola is generally 8-10 days (range, 2-21 days). Person-to-person transmission has only occurred from per-sons with signs or symptoms of EVD. Diagnostic testing is achievedwith the use of real time (R
33、T) polymerase chain reaction (PCR) onblood.32Viral RNA is usually detectable by PCR between 3 and10 days after the onset of symptoms.Patients with EVD should be provided appropriate critical careincluding fluid and electrolyte replacement; oxygen therapy to main-tain oxygen status; medications to su
34、pport blood pressure, reducingvomiting and diarrhea, and to manage fever and pain; oral or paren-teral nutrition; and treating coexisting infections (eg, malaria), ifpresent.33-34Althoughtherearecurrentlynoantiviraldrugsapproved by the US Food and Drug Administration (FDA), a numberof therapies are
35、under investigation including antibody-based thera-pies (eg, convalescent blood products, monoclonal antibodies), anddrugs and small molecules (eg, Ebola virus gene expression inhibitors,and Ebola virus entry and inhibitors).33-35A number of preventivevaccines are currently in clinical trials.33-35E
36、nvironmental contamination and survivalEbola virus has been isolated by cell culture from multiple bodyfluids of infected or convalescent patients including blood, saliva,stool, vaginal fluid, sweat, and urine for days or months after illness.36Given the high volume of diarrhea and vomiting and the
37、potential forfomite transmission, the frequency of environmental contaminationand survival of Ebola virus is of high concern. Several studies haveassessed the frequency of contamination within the health careTable 1Modes of transmission of Ebola virusCommon? Person-to-person via direct contact via b
38、ody fluids (ie, urine, saliva, sweat, feces,vomit, breast milk, and semen)? Person-to-person via indirect contact due to environmental contamination(eg, needles, syringes)Less Common? Infected fruits bats? Nonhuman primates (eg, apes, monkeys)? Sexual transmission via semen from a man who recovered
39、from Ebola virusdisease (via oral, vaginal, or anal sex)?Ingestion of bush meat? Exposure in a laboratoryA30D.J. Weber et al. / American Journal of Infection Control 47 (2019) A29A38environment of a patient with EVD by culture37,39or RT-PCR.37-42Although the frequency of environmental contamination
40、was vari-able, all studies reported some environmental samples were positiveby RT-PCR. Contamination was most often demonstrated for bloodstained items,37,42and toilet/latrine,39,40,42or objects in close proxim-ity to the patient (eg, mattress, bed rails).37,42Samples from PPE (eg,gloves) have teste
41、d positive by RT-PCR for Ebola virus.37,42Viablevirus was not isolated in either of the 2 studies that cultured environ-mental samples.The environmental survival of Ebola virus has been studied usingculture-based techniques under a variety of environmental condi-tions (eg, temperature, humidity), in
42、 various liquids, aerosols, andsurfaces.43-49These studies may be summarized as follows. First, via-ble Ebola can survive in liquids (eg, liquid media, tissue culture media,water, liquid blood, plasma) for days to weeks. Second, viable Ebolavirus can also survive dried on a variety of surfaces (eg,
43、plastic, glass,stainless steel, polypropylene, nitrile, bank notes) for days to weeks.Third, Ebola survives in liquids and on surfaces for a longer durationof time at lower temperatures (eg, 4C vs 21C). Fourth, althoughaerosol transmission has not been observed, Ebola virus has beendemonstrated to s
44、urvive in an aerosol for 3 hours. Fifth, survival ofEbola on porous surfaces, such as cotton, is substantially less than onsteel and plastic surfaces.Using macaques, viable Ebola virus was demonstrated to survivein corpses for at least 3 days and RNA could be detected for tissues forthe entire 10-we
45、ek study period.50Ebola virus was detected by RT-PCR in a deceased patients house 14 days after a patient was bur-ied.41Consistent use of appropriate PPE with strict adherence to don-ning and doffing protocols is crucial to preventing acquisition of EVDduring patient care.28,51,52A key component of
46、reducing HCP risk isproper training in PPE donning and doffing with ongoing training tomaintain competency.Susceptibility to germicidesEbola virus is not inactivated by detergents.53Using RT-PCR, Cooket al54demonstrated that Ebola virus outbreak variants dried with anorganic soil load on a stainless
47、 steel carrier were inert after 5 minutesexposure to sodium hypochlorite (0.5%) and after 2.5 minutes expo-sure to 70% ethanol. Smither et al55confirmed the activity of sodiumhypochlorite; 104Ebola viruses as measured by PCR were inactivatedby 0.75% sodium hypochlorite with 10 minutes contact time.
48、In a laterstudy, Smither et al56reported that multiple disinfectants (ie, 0.5%hypochlorite, 10% hypochlorite, 5% peracetic acid, 70% ethanol) wereeffective against dried cell culture medium containing Ebola virus.However, only 5% peracetic acid consistently reduced Ebola virustiters in dried blood t
49、o undetectable levels. Based on the hierarchy ofmicrobial susceptibility to germicides and studies of germicide effi-cacy, the CDC states that any US Environmental Protection Agency-(EPA) registered hospital disinfectant with a label claim for a nonen-veloped virus (eg, norovirus, rotavirus, adenovi
50、rus) can be used todisinfect environmental surfaces in rooms of patients with known orsuspected EVD.57In a systematic review, Kampf58reported that 80% ethanol washighly effective against all 21 tested, enveloped viruses within 30 sec-onds. A 4-log10reduction of an Ebola strain was achieved in 15 sec
51、-onds using the following povidone-iodine solutions: 4%, 7.5%, 10%,and 3.2% iodine with 78% alcohol.59Therefore, data suggests thathand antisepsis for skin contamination with Ebola virus can beobtained with either povidone-iodine or 70%-80% alcohol (althoughproper PPE should always be worn).An ultra
52、violet-light (UV-C) booth was demonstrated to inactivate3-log10bacteriophage MS2 (a nonenveloped virus) and could beuseful for disinfection of contaminated PPE.60MERSHistory and microbiologyThe history of MERS has been reviewed.61-63MERS, a new viralrespiratory disease of humans, was first described
53、 in 2012 and laterdiscovered to be caused by a novel coronavirus, MERS-CoV (lineage2C b CoV). The WHO has reported that between 2012 and December2018, there were 2,279 laboratory-confirmed cases of MERS, includ-ing 806 associated deaths (case-fatality rate=35.3%), reported glob-ally.64Although cases
54、 have been reported from 27 countries, themajority of cases (ie, 1,901) have been reported from Saudi Arabia.64Two cases of MERS have been reported in the United States, both ofwhom were health care providers who acquired infection in SaudiArabia.65No transmission has been reported in the United Sta
55、tes.The microbiology, epidemiology, and clinical manifestations ofMERS have been reviewed.66-72MERS-CoV, a betacoronavirus, is asingle-stranded, positive-sense enveloped RNA virus that can causean acute respiratory illness in humans. MERS-CoV is a zoonotic dis-ease that is transmitted from animals-t
56、o-humans. Dromedary camels,hosts for MERS-CoV, have been implicated in direct and indirecttransmission to humans, although the exact mode of transmission isunknown.63,67,71Bats are likely the main mammalian reservoir.71The clinical spectrum of MERS infection ranges from asymptom-atic or mild respira
57、tory symptoms to severe acute respiratory diseaseand death. Typical symptoms of MERS include fever, cough, andshortness of breath. Pneumonia is common but not always present.Gastrointestinal symptoms (vomiting, diarrhea) frequently occur.Risk factors for more severe disease include older age, comorb
58、idities(eg, chronic lung diseases, diabetes), and immunosuppression. Thediagnosis is confirmed by a positive RT-PCR assay targeting at least 2different genomic regions. Currently, there are no specific therapiesor vaccines available.Epidemiology and transmissionMERS may be transmitted from person-to
59、-person via direct con-tact likely due to droplet transmission (Table 2). This occurs mostcommonly when there is close contact such as providing unprotectedcare to an infected patient. Thus far, no sustained community trans-mission has been documented. Studies of family clusters and HCPcontacts of p
60、atients have reported low frequencies of transmission(ie, 1%-3%). However, increased transmission has occurred in healthcare settings with limited infection control procedures. Importantly,MERS may be transmitted from an asymptomatic source.73However,super spreaders have also been reported.74The epi
61、demiology and prevention of MERS in health care settingshas been reviewed.10,75-77Infection prevention strategies have beeninformed by the multiple reports of outbreaks of MERS involvinghealth care facilities,78-81and by the large outbreak in South Korea.82Importantly, during these outbreaks 20% of
62、cases may have occurredin health care providers. Factors contributing to intrahospital trans-mission include: (1) the initial symptoms of MERS are nonspecificTable 2Modes of transmission of Middle Eastern respiratory syndrome coronavirusTransmission Well Established?Human-to-human transmission via d
63、irect contact due to droplet spread(source may be asymptomatic)? Animal-to-human transmission (dromedary camels to humans)Transmission Unclear? Human-to-human transmission via direct contact due to airborne transmission? Human-to-human transmission via indirect contact (ie, fomites, contaminatedsurf
64、aces)D.J. Weber et al. / American Journal of Infection Control 47 (2019) A29A38A31leading to a failure to isolate the patient; (2) inadequate compliancewith infection control practices; (3) inadequate health care facilities(eg, overcrowding, close proximity of patients to cases); (4) use ofaerosol g
65、enerating procedures; and (5) prolonged viral shedding.83Environmental contamination and survivalExtensive environmental contamination has been documented byboth culture and RT-PCR in clinical areas housing MERS patients.84,85Positive sites have included patient room surfaces (eg, bed sheets,bedrail
66、s, intravenous fluid hangers), anteroom surfaces, medical devi-ces (eg, portable x-ray machines, thermometers), and air-ventilatingequipment. Touchable surfaces have been found to be contaminatedthroughrespiratorysecretionsfromclinicallyfullyrecoveredpatients.84MERS-CoV has also been detected in air
67、 samples in thevicinity of patients.85However, 1 large outbreak evaluation failed todemonstrate any transmission via the potentially contaminated envi-ronment without direct contact with the index case.86MERS-CoV has been shown to be recoverable after 48 hours onsteel or plastic washers (20C and 40%
68、 relative humidity).87Further,no decrease in stability was observed during aerosolization experi-ments. Multiple studies on CoVs other than MERS-CoV have demon-strated that these viruses can remain viable for days to weeks onenvironmental surfaces.88,89Survival is enhanced at low tempera-tures (ie,
69、4C vs 20C).89Susceptibility to germicidesAs MERS-CoV is an enveloped virus, it is likely susceptible to EPA-registered hospital disinfectants and FDA-approved antiseptics. Stud-ies on inactivation of surrogates for SARS-CoV (mouse hepatitis virusand transmissible gastroenteritis virus) demonstrated
70、the followinginactivation after 1-minute contact time: (1) for transmissible gastro-enteritis virus, there was a log10reduction factor of 3.2 for 70% etha-nol, 2.0 for phenolic, 2.3 for ortho-phthalaldehyde, 0.35 for 1:100hypochlorite, 4.0 for 62% ethanol, and 3.5 for 71% ethanol; and (2) formouse h
71、epatitis virus, log10reduction factors were 3.9 for 70% etha-nol, 1.3 for phenolic, 1.7 for ortho-phthalaldehyde, 0.62 for 1:100hypochlorite, 2.7 for 62% ethanol, and 2.0 for 71% ethanol.90Guidance from the CDC for managing patients with MERS states,“HCP should perform hand hygiene before and after
72、all patient con-tact, contact with potentially infectious material, and before puttingon and upon removal of PPE, including gloves. Hand hygiene inhealthcare settings can be performed by washing with soap andwater or using alcohol-based hand rubs. If hands are visibly soiled,use soap and water, not
73、alcohol-based handrubs.”91The CDC furtherstates “Standard cleaning and disinfection procedures (eg, usingcleaners and water to pre-clean surfaces prior to applying an EPA-registered disinfectant to frequently touched surfaces or objects forappropriate contact times as indicated on the products label
74、) areappropriate for MERS-CoV in healthcare settings, including thosepatient-care areas in which aerosol-generating procedures are per-formed. If there are no available EPA-registered products that have alabel claim for MERS-CoV, products with label claims against humancoronaviruses should be used a
75、ccording to label instructions.”91CREDefinition and microbiologyThe CDC defines CRE for surveillance purposes as Enterobacteria-ceae that are “resistant to imipenem, meropenem, doripenem, orertapenem OR documentation that the isolate possess a carbapene-mase.”92The CDC further elaborates that CRE is
76、 “a phenotypic defini-tion (ie, based on the antibiotic susceptibility pattern of theorganism) and it includes bacteria that are not susceptible to carbape-nems via more than one type of mechanism.” The CDC specifies thatcarbapenem resistance mechanisms include the following: (1) theproduction of ca
77、rbapenemases (called carbapenemase-producing-CRE), enzymes that break down carbapenems and related antimicro-bials making them ineffective. This includes enzymes like Klebsiellapneumoniae carbapenemase; and (2) the combination of mechanismsother than carbapenemase production (called non-carbapenemas
78、e-producing-CRE), most commonly the production of b-lactamases (eg,AmpC) in combination with alterations in the bacterias cell mem-brane (eg, porin mutations). The CDC has reported the following typesof CRE in the United States: NDM, OXA48, VIM, IMP, and Klebsiellapneumoniae carbapenemase.93Epidemio
79、logy and transmissionThe biology, epidemiology, and management of CRE have beenreviewed.94-97Recent articles have reviewed newer antibiotic thera-pies for CRE.98,99Follow-up of hospitalized CRE colonized patientsdemonstrated that the mean duration of colonic carriage was 1year.100However, HCP are ra
80、rely, if ever, colonized. A study of fecalcarriage among HCP in a hospital endemic for CRE revealed none of177 evaluated health care providers were colonized with CRE.101The main reservoir leading to human CRE infections is the humangut. Person-to-person transmission via direct and indirect contact
81、arethe most common mechanisms of transmission (Table 3). Multiplehospital outbreaks have resulted from contaminated endoscopes,especially duodenoscopes.102-104These outbreaks have occurreddespite all steps in cleaning and high-level disinfection of endoscopescompliant with current guidelines. Strate
82、gies to provide pathogen-free endoscopes have been reviewed.104Water sources in the hospital(eg, faucets, wash basins, showers, toilets), especially sinks have beendemonstrated to be a reservoir of CRE.105-107Strategies and successrates of interventions to eliminate CRE from water reservoirs havebee
83、n reviewed.105,106Companion animals have been demonstratedto occasionally be colonized with CRE.108This is of relevance to healthcare facilities considering that US health care facilities must permitpersons with “service” animals in the facility and many hospitals per-mit animal-assisted therapy.Str
84、ategies to manage CRE colonized/infected patients and to con-trol outbreaks in health care facilities have been reviewed.109-111Both the WHO112and the CDC113provide detailed guidance on meth-ods to control CRE. The use of bundles to control horizontal transmis-sion of CRE in health care facilities h
85、ave been reviewed.114Environmental contamination and survivalCRE has been isolated from the environment in the vicinity of hos-pitalized colonized/infected patients including pillows, infusionpumps, bedside tables, and toilet areas.115-117The frequency ofrecovery has varied among studies, but object
86、s closer to the patientare more likely contaminated with 5%-15% of samples from bedrailsand over bed tables yielding CRE.115,116Fecal continence is anTable 3Modes of transmission and reservoirs of carbapenem-resistant Enterobacteriaceae? Patient-to-patient via direct contact? Patient-to-patient via
87、indirect contactTransient hand carriage by health care personnelContaminated shared medical devicesContaminated endoscopes (especially duodenoscopes)? Health care facility reservoir to patientContaminated sinksContaminated endoscopes (especially duodenoscopes)A32D.J. Weber et al. / American Journal
88、of Infection Control 47 (2019) A29A38independent predictor of being a nonspreader of CRE.117CRE has alsobeen isolated in the environment of long-term care facilities.118Havill et al119reported survival of CRE on stainless steel discs for10 days. However, Weber et al120reported that 3 species of CRE(
89、Klebsiella, Enterobacter, and Escherichia coli) survived poorly (85%die-off in 24 hours). Likely this difference was owing to the fact thatHavill et al119used a high inoculum (ie, 5-7-log10) whereas Weberused a low inoculum (ie, 2-log10), which is similar to the actualamount of CRE found on surfaces
90、 in the vicinity of patients colonized/infected with CRE.Susceptibility to germicidesWith rare possible exceptions, antibiotic-resistant bacteria includ-ing multidrug-resistant organisms do not have reduced susceptibilityto EPA-registered germicides.121Even when reduced susceptibility toa germicide
91、(eg, quaternary ammonium compounds by methicillin-resistant Staphylococcus aureus MRSA) has been demonstrated, thepathogen has not demonstrated resistance to the use concentrationof the germicide.121Kanamori et al122assessed the efficacy of 21 ger-micides against multiple CRE Enterobacteriaceae stra
92、ins at 1-minutecontact time and in the presence of 5% fetal calf serum. Four high-level disinfectants achieved 4-log10kill for all tested strains, but0.55% ortho-phthalaldehyde achieved a 2.4-4.8-log10kill dependingon the CRE strain tested. Eight disinfectants all achieved a 4-log10kill. Among the 9
93、 antiseptics tested (70% ethanol, 10% povidone-iodine, 2% and 4% chlorhexidine gluconate, 70% isopropyl alcohol,and 1% chloroxylenol) achieved 2.9-log10kill against all test CREstrains. Based on this study, EPA-registered disinfectants and FDA-approved antiseptics can be used with assurance for equi
94、pment/instrument high-level disinfection, surface disinfection, and handantisepsis. A UV-C device for room disinfection has been shown toinactivate 5-log10CRE reduction in direct line of sight and 4-log10CRE reduction in indirect line of sight when used at the recom-mended cycle time (ie, 5-10 minut
95、es).123The effectiveness of UV-Cfor room disinfection was confirmed in another study.124C AURISHistory and microbiologyC auris is a novel Candida species that was first reported followingits isolation from the ear canal of a patient in Japan in 2009.125Sincethen, C auris has been reported from multi
96、ple countries throughoutthe world.126-128The CDC reported that as of January 22, 2019, 551cases of C auris had been reported from 12 states, with some states(ie, New York, Illinois, New Jersey) reporting 100 cases.129C auris isan emerging pathogen that presents a serious global health threat forthe
97、following reasons: (1) it causes serious infections with a highmortality; (2) it is often difficult to identify with standard laboratorymethods and can be misidentified in laboratories unless specializedtechnology is used; (3) it is often multidrug resistant (intrinsic or rap-idly inducible antifung
98、al resistance); (4) it is becoming more wide-spreadgeographically;(5)increasingprevalence;(6)biofilmformation; (7) persistence in the environment; and (8) it has causedmultiple outbreaks in health care facilities.128,130,131The microbiology, clinical syndromes, diagnosis, and treatment ofC auris hav
99、e been reviewed.127,132-136Genetic analyses have shown thatC auris is most closely related to C lusitaniae and C haemulonii, althoughit has a striking divergence from some other Candida species.127C aurisis often misidentified in conventional diagnostic laboratories using bio-chemical typing.127C au
100、ris most commonly has been misidentified asC haemulonii, but also as C famata, C sake, Rhodotorula glutinis, R mucila-ginosa,andSaccharomycesboulardii.127,137,138Currently,accurateidentification of C auris can be accomplished by the use of MALDI-TOFor PCR assays specific for C auris. Multiple virule
101、nce factors have beendescribed.133The most common clinical syndromes reported have been blood-stream infections (candidemia), wound infections, and ear infec-tions.129Other clinical syndromes reported have included infectionsof the respiratory tract, central nervous system, urogenital system,intra-a
102、bdominal, skin and soft tissues, and bone.127Patients with Cauris infection have almost always presented with underlying ill-nesses or comorbidities such as diabetes, chronic or acute renal fail-ure, pulmonary disease, immunosuppressive conditions, tumor ormalignancies, liver disease, or solid organ
103、 transplants.137Risk factorsfor infection have usually included care in an intensive care unit, thepresence of indwelling central venous catheters, arterial lines, Foleycatheters, invasive surgical procedures, mechanical ventilation, andprior or continued exposure to broad-spectrum antibiotics and a
104、nti-fungal agents.132,133,136Mortality rates 30% have been reported forpatients with invasive infections.127,132,133At the present time, there are no clinical breakpoints for C auris.High minimum inhibitory concentrations have been reported to flu-conazole and other triazole antifungals such as vori
105、conazole, itraco-nazole, and isavaconazole.127,132Variability in susceptibility ofisolates has also been reported to amphotericin.127Epidemiology and transmissionC auris has been associated with multiple nosocomial outbreaks,especially in the intensive care setting.139-144An evaluation of C aurisin
106、New York City health care facilities demonstrated epidemiologiclinks between cases in multiple hospitals and long-term care facili-ties.138Importantly, colonization with C auris has been detected atmultiple body sites including nares, groin, axilla, and rectum.127Pro-longed colonization has been rep
107、orted with C auris detected 3months after initial isolation and despite multiple negative screensand antifungal therapy.136,138Multiple mechanisms for transmission of C auris are likely basedon outbreak investigations (Table 4). Risk factors for colonization orinfection have been reported to include
108、 contact with patients knownto harbor C auris.138,145Sharing an environment with a C auris patientor sequential bed occupancy that was previously occupied by apatient with C auris has also been described as a risk.145Importantly,patients occupying a room that previously housed a patient withC auris
109、have acquired C auris even though the room had beendecontaminated prior to occupancy.145An outbreak evaluation foundthat use of reusable probes for temperature monitoring was associ-ated with a significantly increased risk of C auris colonization with anodds ratio of 6.80.142Transmission of C auris
110、via transplantation oflung from a patient with respiratory tract colonization or infection tothe lung transplant recipient has been reported.146C auris has occasionally been isolated from health care providers.Biswal et al144reported that C auris was detected on the hands of 4Table 4Modes of transmi
111、ssion of Candida aurisCommon? Patient-to-patient via direct contact?Patient-to-patient via indirect contact due to environmental contamination(ie, sharing same hospital room, admission to a hospital room previouslyoccupied by a patient with C auris)Less Common? Patient-to-patient via indirect contac
112、t: shared equipment due to inadequatedisinfection (eg, thermometer)? Patient-to-patient via direct contact: donor-derived transmission(eg, lung transplantation)?Person-to-person via indirect contact due to transiently colonized healthcare providers handsD.J. Weber et al. / American Journal of Infect
113、ion Control 47 (2019) A29A38A33health care providers (2.8%), although this was likely due to inade-quate hand hygiene rather than long-term colonization. Schelenzet al,139while conducting an outbreak investigation in the UnitedKingdom, screened (nose, axilla, groin, and throat) 250 health careprovid
114、ers for colonization and found only a single person (nurse)transiently colonized with C auris.Environmental contamination and survivalWidespread contamination of the surface environment has beenreported by multiple investigators.138Importantly, contaminatedsites have included sites in the patients r
115、oom such as surfaces, toilets,ventilator/respiratory equipment, and sites outside of the patientsroom such as computer workstations, thermometers, glucometers,housekeeping carts, dialysis equipment, ultrasound equipment, andvital sign machines.138The environmental survival of C auris hasbeen studied
116、.144,147,148In laboratory tests, C auris and other Candidaspp were demonstrated to persist for 7 days on moist or dry (steeldisks) surfaces.147Survival on dry linen for up to 7 days has beendemonstrated.148C auris cells have been demonstrated to remain via-ble on plastic surfaces for at least 4 week
117、s, or 2 weeks after they wereno longer culturable.148Susceptibility to germicidesSeveral reviews have included a discussion of the susceptibility ofC auris to germicides.149The susceptibility of C auris to germicides (ie,antiseptics and disinfectants) has been studied by several investiga-tors.139,1
118、44,150-153Rutala et al153assessed the germicidal activity ofhigh-level disinfectants and/or chemical sterilants and reported thatall agents (ie, 0.20% peracetic acid, 2.4% glutaraldehyde, 0.65% hydro-gen peroxide plus 0.14% peroxyacetic acid, 2% accelerated hydrogenperoxide) achieved a 4.1-log10redu
119、ction of C auris with the excep-tion of 0.55% ortho- phthalaldehyde that achieved only a 2.3-log10inactivation for E coli. Importantly, these in vitro experiments weredone under challenging conditions (ie, 5% fetal calf serum and 1-min-ute exposure time). It is likely that all high-level disinfectan
120、ts that arecurrently approved by the FDA when used appropriately (ie, afterappropriate cleaning and the manufacturers recommended concen-tration and duration) are effective against C. auris.The activity of low-level disinfectants has been evaluated by severalinvestigations.152,153Directcomparisonbet
121、weenthestudiesisimpeded by the use of different test conditions including test method,duration of exposure, and presence or absence of proteins such as fetalcalf serum. The activity of low-level disinfectants has been most com-prehensively investigated using the disc-based quantitative carrier testa
122、nd is summarized in Table 5.152,153Importantly, both investigatorsadded 5% fetal calf serum to assess germicidal efficacy under morestringent conditions (ie, presence of proteins). Importantly, quaternaryammonium disinfectants alone were significantly less effective againstC auris than other product
123、s.152,153Some investigators reported thatconcentrations of sodium hypochlorite 1,000 ppm were effective inkilling 4-log10C auris in 3-5 minutes,150,151whereas others153reported sodium hypochlorite 1,200 ppm at an exposure time of1 minute resulted in only a 1.6-log10reduction in C auris. It is unclea
124、rwhether the longer exposure times and lack of protein load led to thehigh reduction rates reported by Abdolrasouli et al150and Mooreet al.151However, all investigators have reported that a 1:10 dilutionof 5.25% sodium hypochlorite is effective in killing 4-log10C auriseven with short exposure times
125、 (ie, 1 minute) and in the presence ofprotein.152,153Based on current studies, the CDC states “Quaternaryammonium compounds (QACs) that are routinely used for disinfectionmay not be effective against C auris.Until further information isavailable for C auris, CDC recommends use of an Environmental Pr
126、otec-tionAgency(EPA)-registeredhospital-gradedisinfectanteffectiveagainst Clostridium difficile spores (List K)”.154CDC further states thatwhen the use of products on List K is not feasible, published researchhas found that the following products led to a substantial reductionTable 5Susceptibility o
127、f Candida auris to low-level disinfectants used for surface disinfection*Highly Effective (3.8-log10Reduction) ET, minutesModerately Effective (2.0-3.8-log10Reduction) ET, minutesLess Effective (2.0-log10Reduction)ET, minutes? 70% isopropyl alcohol 1? 1:10 dilution, 5.25% sodiumhypochlorite (6,100-6
128、,700 ppm) 1? 1:128 dilution, 9.09% o-phenylphenol,7.66% p-tertiary amylphenol 1?1.4% hydrogen peroxide 1?58% ethanol, 0.1% QACy1? 55% isopropyl alcohol, 0.5% QACz1? 28.7% isopropyl alcohol, 27.3% ethylalcohol, 0.61% QACx1? 0.65% sodium hypochlorite 1? 0.39% sodium hypochlorite 1?0.825% sodium hypoch
129、lorite 1?Peracetic acid 1200 ppm, hydrogenperoxide 5% acetic acid (pH 2.0)(white distilled vinegar) 3? 1:50 dilution, 5.25% sodiumhypochlorite(1,245 ppm) 1? 1:256 dilution, 21.7% QACk1? QAC1?QAC#1NOTE. Susceptibility of Candida auris to low-level disinfectants used for surface disinfection.152,153ET
130、, exposure time; ppm, parts per million; QAC, quaternary ammonium compound.*Disc-based quantitative carrier test, 1 minute exposure time unless otherwise noted, 5% fetal calf serum.yQAC: alkyl (C14 50%, C12 40%, C16 10%) dimethyl benzyl ammonium saccharinate 0.1%.zQAC: n-alkyl (C12 68%, C14 32%) dim
131、ethyl ethylbenzyl ammonium chlorides 0.25%; n-alkyl (C14 60%, C16 30%, C12 5%, C18 5%) dimethyl benzyl ammonium chlorides 0.25%.xQAC: didecyl dimethyl ammonium chloride 0.61%.kQAC: octyl decyl dimethyl ammonium chloride 6.51%; dioctyl dimethyl ammonium chloride 2.604%; didecyl dimethyl ammonium chlo
132、ride 3.906%; alkyl (50% C14, 40% C12, 10%C16) dimethyl benzyl ammonium chloride 8.68%.Alkyl dimethyl benzyl ammonium chlorides.#Didecyl dimethyl ammonium chloride, n-alkyl dimethyl benzyl ammonium chloride.A34D.J. Weber et al. / American Journal of Infection Control 47 (2019) A29A38(4-log10) of C au
133、ris in laboratory testing: Oxivir TB (Diversey Inc.,Charlotte, NC), Clorox Healthcare Hydrogen Peroxide Cleaner Disinfec-tant (Clorox, Oakland, CA), Prime Sani-Cloth Wipe (PDI, Inc., Woodcliff,NJ), and Super Sani-Cloth Wipe (PDI, Inc., Woodcliff, NJ).154Room disinfection with a UV-C device has been
134、investigated for itsability to inactivate Candida spp, MRSA, and Clos difficile.155C aurisdemonstrated substantially less susceptibility to UV-C than MRSAand less susceptibility than C albicans or C glabrata at 10 minutesexposure time.155Reductions in C auris and Clos difficile were similarat 10 min
135、utes.155With regard to room disinfection devices, the CDCstates that “data on hands-free disinfection methods, like germicidalUV irradiation, are limited, and these methods may require cycletimes similar to those used to inactivate bacterial spores (eg, Clostrid-ium difficile) when used for C auris.
136、”154We recommend that daily andterminal room cleaning/disinfection be done with an agent demon-strated to be effective against C auris. The use of a UV-C device for ter-minal disinfection should be considered as a supplemental method.The activity of antiseptics against C auris has been studied by se
137、v-eral investigators (Table 6). There is good agreement that 70% alcohol(both isopropyl and ethyl) is effective against C auris at 1 minute.Importantly, the activity of alcohol has not been studied at the timesused by most health care providers when performing hand hygiene(ie, 10-15 seconds). Unfort
138、unately, studies on the activity of otherimportant antiseptics such as chlorhexidine gluconate and povidone-iodine have produced variable results (Table 6). This variability islikely explained by differences in the test conditions including in vitroversus human challenge, duration of exposure, and p
139、resence of a pro-tein load (eg, fetal calf serum). It appears that 10% povidone-iodinewould provide adequate skin antisepsis if applied for 1 minute.Using a panel of C auris clinical isolates, Kean et al,156screened themfor their planktonic and sessile susceptibilities to skin disinfectionchallengeu
140、singpovidone-iodine,chlorhexidinegluconate,andhydrogen peroxide. C auris biofilms displayed increased tolerance toantisepsis compared with planktonic cells. Analysis using a complexbiofilm model demonstrated reduced susceptibility against clinicallyrelevant concentrations of chlorhexidine gluconate
141、(0.05%) andhydrogen peroxide (3%), with eradication achieved only with povi-done-iodine (10%). As noted by Forsberg et al,136whether topicalantiseptics might reduce the burden of C auris on the skin, and there-fore provide a potentially valuable tool for infection prevention,remains unclear. The CDC
142、 states that when caring for patients with Cauris “healthcare personnel should follow standard hand hygienepractices, which include alcohol-based hand sanitizer use or, if handsare visibly soiled, washing with soap and water. Wearing gloves isnot a substitute for hand hygiene.”154References1. Instit
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159、9153CHG0.5%6.0 (NS)Biswal et al, 20171442.0%1.6 (1)zRutala et al, 20191534.0%1.9 (1)zRutala et al, 2019153CHG/alcohol2% CHG/61% ethanol5.06 (2)Moore et al, 20171511% CHG/61% ethanol2.0 (1)zRutala et al, 2019153Povidone-Iodine10%4.56 (2)Moore et al, 201715110%2.5 (1)zRutala et al, 2019153Triclosan0.5
160、%1.4 (1)zRutala et al, 2019153Hydrogen peroxide3.0%1.4 (1)zRutala et al, 2019153Chloroxylenol1%2.8 (1)zRutala et al, 2019153CHG, chlorhexidine gluconate; NS, not stated.*All tests were conducted in vitro unless otherwise noted.yHuman challenge study.zTest conditions included addition of 5% fetal cal
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