scholarly journals Emergence and Control of Fluoroquinolone-Resistant, Toxin A–Negative, Toxin B–PositiveClostridium difficile

2007 ◽  
Vol 28 (8) ◽  
pp. 932-940 ◽  
Author(s):  
Denise Drudy ◽  
Norma Harnedy ◽  
Séamus Fanning ◽  
Margaret Hannan ◽  
Lorraine Kyne

Background.Clostridium difficileis a major cause of infectious diarrhea in hospitalized patients. Between August 2003 and January 2004, we experienced an increase in the incidence ofC. difficile–associated disease. We describe the investigation into and management of the outbreak in this article.Methods.A total of 73 consecutive patients with nosocomialC. difficile–associated diarrhea were identified.C. difficileisolates were characterized using toxin-specific enzyme immunoassays, a tissue-culture fibroblast cytotoxicity assay, polymerase chain reaction (PCR), and antimicrobial susceptibility tests. Rates of recurrence and ofC. difficilecolitis were recorded. Changes in antibiotic use and infection control policies were documented.Results.The incidence ofC. difficile–associated diarrhea peaked at 21 cases per 1,000 patient admissions. Of theC. difficileisolates recovered, 85 (95%) were identical toxin A–negative and toxin B-positive strains, corresponding to toxinotype VIII and PCR ribotype 017. All clonal isolates were resistant to multiple antibiotics, including ofloxacin, ciprofloxacin, levofloxacin, moxifloxacin, and gatifloxacin (minimum inhibitory concentrations [MICs] of greater than 32μg/mL) and erythromycin, clarithromycin, and clindamycin (MICs of greater than 256μg/mL). RecurrentC. difficile–associated disease occurred in 26 (36%) of the patients. At least 10 (14%) of the patients developedC. difficilecolitis. Additional infection control measures introduced included the use of ward memos, a hand-hygiene awareness campaign, increased environmental cleaning, attention to prescribing practices for antibiotics, increased awareness of diarrheal illness, and early isolation of affected patients. Total use of fluoroquinolones did not change throughout the study period. Despite persistence of this toxin-variant strain, the incidence ofC. difficile–associated disease in our institution decreased to fewer than 5 cases per 1,000 admissions.Conclusions.We report on the emergence of a fluoroquinolone- and clindamycin-resistant, toxin A–negative, and toxin B–positive strain ofC. difficileassociated with an outbreak ofC. difficile–associated disease in our institution during a 6-month period. We found that careful attention to improvement of infection control interventions was the most important means of controlling this nosocomial pathogen.

Author(s):  
Majid M. Alshamrani ◽  
Aiman El-Saed ◽  
Azzam Mohammed ◽  
Majed F. Alghoribi ◽  
Sameera M. Al Johani ◽  
...  

Abstract Objective: To describe local experience in managing an outbreak of Candida auris in a tertiary-care setting. Methods: In response to emerging Candida auris, an outbreak investigation was conducted at our hospital between March 2018 and June 2019. Once a patient was confirmed to have Candida auris, screening of exposed patients and healthcare workers (HCWs) was conducted. Postexposure screening included those who had had direct contact with or shared the same unit or ward with a laboratory-confirmed case. In response to the increasing number of cases, new infection control measures were implemented. Results: In total, 23 primary patients were detected over 15 months. Postexposure screening identified 11 more cases, and all were patients. Furthermore, ~28.6% of patients probably caught infection in another hospital or in the community. Infection control measures were strictly implemented including hand hygiene, personal protective equipment, patient hygiene, environmental cleaning, cohorting of patients and HCWs, and avoiding the sharing of equipment. The wave reached a peak in April 2019, followed by a sharp decrease in May 2019 and complete clearance in June 2019. The case patients were equally distributed between intensive care units (51.4%) and wards (48.6%). More infections (62.9%) occurred than colonizations (37.1%). Urinary tract infection (42.9%) and candidemia (17.1%) were the main infections. In total, 7 patients (20.0%) died during hospitalization; among them, 6 (17.1%) died within 30 days of diagnosis. Conclusions: Active screening of exposed patients followed by strict infection control measures, including environmental cleaning, was successful in ending the outbreak. Preventing future outbreaks is challenging due to outside sources of infection and environmental resistance.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jennifer A. Unger ◽  
Estella Whimbey ◽  
Michael G. Gravett ◽  
David A. Eschenbach

Objective. An outbreak of 20 peripartumClostridium difficileinfections (CDI) occurred on the obstetrical service at the University of Washington Medical Center (UWMC) between April 2006 and June 2007. In this report, we characterize the clinical manifestations, describe interventions that appeared to reduce CDI, and determine potential risk factors for peripartum CDI.Methods. An investigation was initiated after the first three peripartum CDI cases. Based on the findings, enhanced infection control measures and a modified antibiotic regimen were implemented. We conducted a case-control study of peripartum cases and unmatched controls.Results. During the outbreak, there was an overall incidence of 7.5 CDI cases per 1000 deliveries. Peripartum CDI infection compared to controls was significantly associated with cesarean delivery (70% versus 34%;P=0.03), antibiotic use (95% versus 56%;P=0.001), chorioamnionitis (35% versus 5%;P=0.001), and the use of the combination of ampicillin, gentamicin, and clindamycin (50% versus 3%;P<0.001). Use of combination antibiotics remained a significant independent risk factor for CDI in the multivariate analysis.Conclusions. The outbreak was reduced after the implementation of multiple infection control measures and modification of antibiotic use. However, sporadic CDI continued for 8 months after these measures slowed the outbreak. Peripartum women appear to be another population susceptible to CDI.


2012 ◽  
Vol 140 (7) ◽  
pp. 1151-1160 ◽  
Author(s):  
J. D. GREIG ◽  
M. B. LEE

SUMMARYThe purpose of this study was to review documented outbreaks of enteric illness associated with nosocomial norovirus infections and to identify modes of transmission, morbidity and mortality patterns, and recommendations for control. Searches of electronic databases, public health publications, and federal, state/provincial public health websites were completed for 1 January 2000 to 31 December 2010. Computer-aided searches of literature databases and systematic searches of government websites identified 54 relevant outbreak reports. Transmission routes included person-to-person (18·5%), foodborne (3·7%) and in the majority (77·8%) the route was unknown. Actions taken during the outbreak to control infection included restricting the movements of patients and staff (22·5%), enhanced environmental cleaning (13·6%) and hand hygiene (10·3%). Rapid identification of norovirus outbreaks in hospitals is vital for the immediate implementation of infection control measures and isolation of infected individuals in this mainly immunocompromised population. Studies that statistically evaluate infection control measures are needed.


2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S75-S75
Author(s):  
Sarah Rehou ◽  
Sydney Rotman ◽  
Melisa Avaness ◽  
Marc G Jeschke ◽  
Shahriar Shahrokhi

Abstract Introduction Antimicrobial resistance is an increasing problem in hospitals worldwide, though the prevalence of carbapenemase-producing Enterobacteriaceae (CPE) in our region is low. Burn patients are among the most vulnerable to infection because of the loss of the protective skin barrier. Because of this, burn centres prioritize infection prevention and control with measures like additional precautions, enhanced environmental cleaning, dedicated facilities, and mandatory use of personal protective equipment (PPE). Methods This report describes a CPE outbreak in a regional burn centre. We hypothesized that contamination of in-room hand hygiene sinks with CPE was a potential source of transmission. In a period of 2.5 months, four nosocomial cases of CPE were identified, three containing the KPC gene and one VIM gene. There was more than one month between the first and second KPC case, with no overlap in patient stay or rooms. Results The first two cases were identified while there was no CPE patient source on the unit. CPE KPC gene was isolated in sink drains of three different rooms. In addition to the rigorous infection control practices already in place due to the unique patient population, additional outbreak control measures were implemented. The burn centre restricted admissions to complex burns or burns &gt;10% total body surface area, in consultation with the attending surgeon. No elective admissions were permitted. To avoid CPE exposure to new patients, initial admissions were rerouted to the emergency department and, if possible, the patient was admitted to another unit. Patient cohorting was implemented through nursing team separation for CPE positive and negative patients and geographical separation of CPE positive cases to one side of the unit. Conclusions Despite aggressive infection control measures already in place at our burn centre, there was hospital acquired CPE colonization/infection. Given there was CPE acquisition when there was no positive patients on the unit and CPE contaminated sinks of the same enzyme were identified, it suggests that hospital sink drains can become a potential source of CPE.


2017 ◽  
Vol 2 ◽  
pp. 16 ◽  
Author(s):  
Esther van Kleef ◽  
Nantasit Luangasanatip ◽  
Marc J Bonten ◽  
Ben S. Cooper

Background: Large reductions in the incidence of antibiotic-resistant strains of Staphylococcus aureus and Clostridium difficile have been observed in response to multifaceted hospital-based interventions. Reductions in antibiotic-sensitive strains have been smaller or non-existent. It has been argued that since infection control measures, such as hand hygiene, should affect resistant and sensitive strains equally, observed changes must have largely resulted from other factors, including changes in antibiotic use. We used a mathematical model to test the validity of this reasoning. Methods: We developed a mechanistic model of resistant and sensitive strains in a hospital and its catchment area. We assumed the resistant strain had a competitive advantage in the hospital and the sensitive strain an advantage in the community. We simulated a hospital hand hygiene intervention that directly affected resistant and sensitive strains equally. The annual incidence rate ratio (IRR) associated with the intervention was calculated for hospital- and community-acquired infections of both strains. Results: For the resistant strain, there were large reductions in hospital-acquired infections (0.1 ≤ IRR ≤ 0.6) and smaller reductions in community-acquired infections (0.2 ≤ IRR ≤  0.9). These reductions increased in line with increasing importance of nosocomial transmission of the strain. For the sensitive strain, reductions in hospital acquisitions were much smaller (0.6 ≤ IRR ≤ 0.9), while communityacquisitions could increase or decrease (0.9 ≤ IRR ≤ 1.2). The greater the importance of the community environment for the transmission of the sensitive strain, the smaller the reductions. Conclusions: Counter-intuitively, infection control interventions, including hand hygiene, can have strikingly discordant effects on resistant and sensitive strains even though they target them equally, following differences in their adaptation to hospital and community-based transmission. Observed lack of effectiveness of control measures for sensitive strains does not provide evidence that infection control interventions have been ineffective in reducing resistant strains.


2012 ◽  
Vol 17 (7) ◽  
Author(s):  
A Zagorianou ◽  
E Sianou ◽  
E Iosifidis ◽  
V Dimou ◽  
E Protonotariou ◽  
...  

We report 570 carbapenemase-producing Klebsiella pneumoniae (CPKP) clinical isolates in a 1,040-bed Greek tertiary hospital during 2004 to 2010. The first CPKP (VIM-producing) was isolated in September 2004. Despite initial containment, VIM producers have become endemic since 2006. KPC-producing K. pneumoniae was first isolated in August 2007 from a patient who came from Israel, spread rapidly, and outcompeted VIM. Overall, 267 (47%) VIM-producing and 301 (53%) KPC-producing strains were isolated, including 141 (24.7%) from patients with bacteraemia. Two isolates carrying both VIM and KPC were isolated in two consecutive months in 2009, but not since. The prevalence of CPKP increased from 0% in 2003 to 38.3% in 2010 (p<0.0001). All genotyped KPC producers harboured blaKPC-2 and belonged to two clones, among which the hyperepidemic Greek clone, related to those from the United States and Israel, predominated. Most metallo-beta-lactamase (MBL) producers carried the blaVIM-1 gene and belonged to several clones, whereas all but one isolate with blaVIM-12 were clustered within a five-month period, arising from one clone. Resistance to non-beta-lactam antibiotics was also increased among CPKP. They were almost invariably resistant to ciprofloxacin and trimethoprim-sulfamethoxazole. Resistance to colistin increased from 3.5% (4/115) in 2008 to 20.8% (25/120) in 2010, and resistance to tigecycline also increased. Following reinforcement of infection control measures, prevalence of CPKP (mainly KPC) has been reduced since mid-2009 (from 46% in 2009 to 38.3% in 2010). In view of the exhaustion of available therapies, investment in infection control resources and optimal antibiotic use is urgently required.


2017 ◽  
Vol 2 ◽  
pp. 16 ◽  
Author(s):  
Esther van Kleef ◽  
Nantasit Luangasanatip ◽  
Marc J Bonten ◽  
Ben S. Cooper

Background: Large reductions in the incidence of antibiotic-resistant strains of Staphylococcus aureus and Clostridium difficile have been observed in response to multifaceted hospital-based interventions. Reductions in antibiotic-sensitive strains have been smaller or non-existent. It has been argued that since infection control measures, such as hand hygiene, should affect resistant and sensitive strains equally, observed changes must have largely resulted from other factors, including changes in antibiotic use. We used a mathematical model to test the validity of this reasoning. Methods: We developed a mechanistic model of resistant and sensitive strains in a hospital and its catchment area. We assumed the resistant strain had a competitive advantage in the hospital and the sensitive strain an advantage in the community. We simulated a hospital hand hygiene intervention that directly affected resistant and sensitive strains equally. The annual incidence rate ratio (IRR) associated with the intervention was calculated for hospital- and community-acquired infections of both strains. Results: For the resistant strain, there were large reductions in hospital-acquired infections (0.1 ≤ IRR ≤ 0.6) and smaller reductions in community-acquired infections (0.2 ≤ IRR ≤ 0.9). These reductions increased in line with increasing importance of nosocomial transmission of the strain. For the sensitive strain, reductions in hospital acquisitions were much smaller (0.6 ≤ IRR ≤ 0.9), while community acquisitions could increase or decrease (0.9 ≤ IRR ≤ 1.2). The greater the importance of the community environment for the transmission of the sensitive strain, the smaller the reductions. Conclusions: Counter-intuitively, infection control interventions, including hand hygiene, can have strikingly discordant effects on resistant and sensitive strains even though they target them equally. This follows from differences in their adaptation to hospital- and community-based transmission. Observed lack of effectiveness of control measures for sensitive strains does not provide evidence that infection control interventions have been ineffective in reducing resistant strains.


2020 ◽  
Vol 41 (9) ◽  
pp. 1084-1089
Author(s):  
Thana Khawcharoenporn ◽  
Wipada Laichuthai

AbstractWe demonstrated a 20% rate of subsequent carbapenem-resistant Enterobacteriaceae (CRE)–associated infections among hospitalized CRE carriers. Independent factors associated with the infections were number of colonization sites, central-line insertion, and receiving vancomycin before colonization. These findings underscore the importance of antibiotic stewardship and device-related infection control measures to prevent CRE infections.


1997 ◽  
Vol 18 (09) ◽  
pp. 628-632 ◽  
Author(s):  
Kwan Kew Lai ◽  
Zita S. Melvin ◽  
Mary Jane Menard ◽  
Helen R. Kotilainen ◽  
Stephen Baker

Abstract Objectives: To evaluate the effectiveness of specific infection control measures on the incidence of Clostridium difficile-associated diarrhea (CDAD) and to identify risk factors for its development. Setting: 370-bed, tertiary-care teaching hospital with approximately 12,000 to 15,000 admissions per year. Methods: Several infection control measures were implemented in 1991 and 1992, and the attack rates of CDAD were calculated quarterly. Antibiotic use for 1988 through 1993 was analyzed. A case-control study was conducted from January 1992 to December 1992 to identify risk factors for acquisition of CDAD. Results: From 1989 to 1992, the attack rate of CDAD increased from 0.49% to 2.25%. An increase in antibiotic use preceded the rise in the incidence of CDAD in 1991. Despite implementation of various infection control measures, the attack rate decreased to 1.32% in 1993, but did not return to baseline. Ninety-two cases and 78 controls (patients with diarrhea but with negative toxin assay) were studied. By univariate analysis, history of prior respiratory tract infections (odds ratio [OR], 3.6; 95% confidence interval [CI95], 1.2-10.4), the number of antibiotics, and the duration of exposure to second-generation cephalosporins (OR, 3.55; CI95, 1.47-9.41) and to ciprofloxacin (OR, 7.27; CI95, 1.13-166.0) were related significantly to the development of CDAD. By stepwise logistic regression analysis, only exposure to antibiotics and prior respiratory tract infections (P=.0001 and .0203, respectively) were found to be significant. Conclusion: Antibiotic pressure might have contributed to failure of infection control measures to reduce the incidence of CDAD to baseline.


1999 ◽  
Vol 20 (8) ◽  
pp. 565-567 ◽  
Author(s):  
Marie Eve Dy ◽  
Jill A. Nord ◽  
Vincent J. LaBombardi ◽  
Jay W. Kislak

AbstractA prospective study was undertaken to determine colonization rates, susceptibility profiles, and outcomes in patients with clinical isolates of Acinetobacter baumannii. Fifty percent of patients became colonized with A baumannii, and 29% of these patients had clinical and colonizing isolates with discordant susceptibility profiles, without apparent relation to antibiotic use. Barrier infection control measures are necessary to prevent nosocomial transmission.


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