Epidemiological study of an outbreak due to multidrug-resistant Enterobacter aerogenes in a medical intensive care unit.

In 1993, 63 isolates of Enterobacter aerogenes were collected from 41 patients in a medical intensive care unit (ICU). During the same period, only 46 isolates from 32 patients were collected in the rest of the hospital. All isolates were analyzed by antibiotic resistance phenotype, and 77 representative isolates were differentiated by plasmid restriction analysis, ribotyping, and arbitrarily primed (AP)-PCR. The extended-spectrum beta-lactamases produced by 22 strains were characterized by determination of their isoelectric points and by hybridization of plasmid DNA with specific probes. The isolates were divided into 25 antibiotic resistance phenotypes, either susceptible (group I) or resistant (group II) to aminoglycosides, and exhibited three phenotypes of resistance to beta-lactams: chromosomally derepressed cephalosporinase alone or associated with either extended-spectrum beta-lactamases (mainly of the SHV-4 type) or imipenem resistance. The results of the tests divided the 77 representative isolates (group I, n = 21; group II, n = 56) into 15 plasmid profiles, 14 ribotypes, and 15 AP-PCR patterns. Although the resistant isolates (group II) exhibited different plasmid profiles, ribotyping and AP-PCR analysis demonstrated an identical chromosomal pattern, indicating an epidemiological relatedness. They were mainly found in the medical ICU and occasionally in other units. The susceptible strains (group I) had various and distinct markers and were mainly isolated in units other than the medical ICU. In conclusion, the presence of a nosocomial outbreak in an ICU and the spread of a multidrug-resistant epidemic strain throughout the hospital was confirmed. Ribotyping and AP-PCR represent discriminatory tools for the investigation of nosocomial outbreaks caused by E. aerogenes.     

Arbitrarily primed PCR, ribotyping, and plasmid pattern analysis applied to investigation of a nosocomial outbreak due to Enterobacter cloacae in a neonatal intensive care unit.

In December 1992, Enterobacter cloacae was isolated from the oropharynx and respiratory tract of six ventilated neonates hospitalized in the intensive care unit (ICU) of our hospital. To establish the spread of the outbreak, 41 strains of E. cloacae were analyzed for genotypic markers by three methods: plasmid profile analysis, ribotyping with EcoRI or PvuII endonuclease, and arbitrarily primed (AP) PCR. The tested strains included 12 isolates from the 6 epidemic cases, 4 isolates from the respiratory tract of 4 children hospitalized in other wards during the same period, 13 isolates from 12 children hospitalized in pediatric units before or after the outbreak, and 12 epidemiologically unrelated isolates. Ribotyping and AP PCR demonstrated that each of the last 12 strains exhibited distinct genomic patterns, as did each of the strains isolated from neonates hospitalized before or after the epidemic peak. Conversely, two clones of strains were found among the isolates recovered in December, with concordant results being obtained by the three typing methods: the first clone included seven strains from five ventilated children in the ICU and two children from another ward; another clone was shared by one neonate in the ICU and an infant from another ward. These results indicate that ribotyping and AP PCR-the latter applied, to our knowledge, for the first time to the genotypic analysis of E. cloacae--represent very discriminatory tools for the investigation of nosocomial outbreaks caused by this species.     

Nosocomial outbreak of acute gastroenteritis in a neonatal intensive care unit in tunisia caused by multiply drug resistantSalmonella wien producing SHV-2 beta-lactamase

In a Tunisian hospital 27 babies, including 12 who were premature, in a single intensive care unit suffered acute gastroenteritis in the period from January to May 1988. The mean age at the onset of gastroenteritis was 8.4 days; nine babies died.Salmonella wien was isolated from stools (all babies) and blood (4 babies). It was also isolated from the stools of one nurse and from a mattress. Twelve of the babies had received cefotaxime, which was successfully replaced by oral colimycin. The outbreak was stopped by the implementation of infection control measures. All isolates ofSalmonella wien were of the same biotype, and had the same antibiotic resistance pattern (third generation cephalosporins, monobactams, aminoglycosides, chloramphenicol, trimethoprim and sulphonamides) and plasmid DNA restriction pattern. The isolates were all susceptible to a combination of cefotaxime and clavulanic acid (a -lactamase inhibitor), which displayed synergy, suggesting the presence of a -lactamase (geometric mean MICs 11.24 µg/ml for cefotaxime alone and 0.24 µg/ml in combination with 0.1 µg/ml potassium clavulanate). All isolates produced TEM-1 and SHV-2 -lactamase which was not transferable toEscherichia coli by conjugation. The presence of the SHV-2 enzyme inSalmonella wien may allow it to adapt to newer -lactams which is a cause for concern in this hospital.     

An outbreak of extended spectrum beta-lactamase producing Klebsiella pneumoniae in a neonatal intensive care unit

Klebsiella pneumoniae has long been a prominent cause of nosocomial infections and outbreaks have been observed in the intensive care units and in high risk groups. We present here a brief report on an outbreak of Klebsiella pneumoniae which occurred in a neonatal intensive care unit in our teaching hospital. As neonates are at highest risk for acquisition of Klebsiella pneumoniae producing extended spectrum beta-lactamase, infection control policies and procedures should be strictly followed to prevent such outbreaks.     

心胸外科ICU教学的体会

近年来,心胸外科术后转归的不断改善,部分归因于对术后患者监护的重视,而这得益于心胸外科重症监护病房(ICU)的建立和运行。ICU是一个与心内科、呼吸科、麻醉科紧密联系的单位,学生在实习的时候,有别于其它科室,如何带教好ICU的实习,我们进行了有益的探索,获得了一些体会,供同行参考。1心胸外科ICU的特点及特殊要求以监护为中心的心胸外科ICU,其病房特点是监护设备多,医生要求高,综合性极强。为此,对在本科室实习的学生,首先要经过心内科、呼吸科的专科实习,并掌握或了解了ICU常用技能的操作或配合方法。其次,要求学生熟悉环境。专…     

Streptococcus faecium outbreak in a neonatal intensive care unit

An outbreak of bacteremia and meningitis in a neonatal intensive care unit is described. Seven cases occurred in premature infants with severe underlying diseases. An epidemiological investigation failed to document the reservoir of the epidemic strain but suggested that its transmission among the infants was via the hands of hospital personnel. All patients had nasogastric tubes and multiple intravascular devices, and the portal of entry may have been either the gastrointestinal tract or the sites of the intravascular devices. Conventional biotyping of isolates failed to differentiate between isolates from infected patients and isolates recovered from prevalence surveys and from the environment. However, rapid identification systems (API-20S [Analytab Products, Plainview, N.Y.] and the AutoMicrobic system [Vitek Systems, Inc., Hazelwood, Mo.]) were able to distinguish isolates recovered from infected patients and hands of hospital personnel from isolates recovered during prevalence and environmental surveys and 29 isolates from widespread geographical areas. This is the first known report of a nosocomial neonatal outbreak of bacteremia and meningitis due to Streptococcus faecium; it underscores the importance of identifying streptococci to species level.     

Case control study of extended-spectrum betalactamase producing Serratia marcescens outbreak in a paediatric intensive care unit

OBJECTIVES: To identify patient-related risk factors of infection and ways of transmission of extended-spectrum betalactamase (ESBL) producing Serratia marcescens in the paediatric intensive care unit (PICU) of Amiens university hospital (France) between June and July 2002. METHODS: Five cases (four pulmonary infected and one stool contaminated symptom-free neonates) and 35 controls, admitted in the PICU, are included. S. marcescens ESBL analysed are isolated from respiratory tract and faecal samples for cases and urine and pus samples from two non-paediatric other patients. Univariate and multivariate analysis are performed on EPI INFO 6.04 dFr and SPSS 11.0.1. RESULTS: S. marcescens ESBL infections or colonisations rate is 12.5% [4.7-27.6]. The incidence is 8.8 [6.7-11.6] per 1000 hospital-stay days. By univariate analysis, cases and controls don't differ with respect of age, sex, and weight at admission or preterm delivery. Cases don't have more often invasive nursing care than controls. But, they were intubated (P <0.03) and hospitalised (P <0.03) for a longer time than controls. Linear regression analysis showed that duration of intubation was independent predictor of acquisition of S. marcescens ESBL (P <0.008). S. marcescens ESBL strains implicated in pulmonary infections, showed the same pattern of multidrug resistant and ERIC-PCR profile. This clone differs from others isolated from stool or other samples from other hospital wards. CONCLUSION: As S. marcescens cross-colonization appears to be due to lake of hand hygiene and asepsis during invasive nursing care, reinforcing hygiene measures permit to contain the outbreak.     

Nosocomial nasal myiasis in an intensive care unit

A 73-year-old Chinese man was admitted to the Accident and Emergency Premorbid Ward of a local hospital in Malaysia. The patient complained of shortness of breath with cough and was in a semi-conscious state. He was later admitted to an intensive care unit (ICU) of the hospital. Six days after admission 5-6 maggots were recoverd from the nasal cavity. The maggots were identified as the third-instar larvae of Lucilia cuprina Wiedmann (Diptera: Calliphoridae) based on the morphological characteristics. This patient was classified as having nosocomial myiasis. The presence of the third instar larvae indicated that the infestation was not more than three to four days. An adult sarcophagid identified as Parasarcophaga ruficornis (Fabricius) caught in the ICU where the patient was warded provided further evidence of the potential for the nosocomial infestation.     

Nosocomial pneumonia in medico-surgical intensive care unit.

Cases of hospital acquired pneumonia occurring during the 1st 12 months of Medico-Surgical ICU (Intensive care unit, MSICU) in operation were evaluated retrospectively to determine its incidence, common causative pathogens, outcome and radiological patterns with the new hospital setting providing a unique relatively aseptic environment. Among the 920 admitted patients, 73 episodes of nosocomial pneumonia on 63 patients were identified and the incidence rate was 7%. The most common pathogens were Pseudomonas. Staphylococcus, Serratia, and Enterobacter in the order of frequency of occurrence, and the gram-negative pathogens comprised 70%. Nosocomial pneumonia was more common after use of antibiotics due to such pathogens as Enterobacter, Acinetobacter, and Candida which caused poor outcome. Enterobacter had the greatest tendency to be related with poor outcome and Serratia the least. Overall mortality was 25%. Bronchopneumonia was the most common type of pneumonia caused by any pathogen except Acinetobacter which caused a mixed type of nosocomial pneumonia.     

Nosocomial outbreak of methicillin- and linezolid-resistant Staphylococcus epidermidis associated with catheter-related infections in intensive care unit patients

A total of 128 isolates associated with catheter-related infections was recovered from 101 intensive care unit patients in a Spanish hospital during March 2008 to August 2009, and 27 of these isolates (from 21 patients) were typed as methicillin- and linezolid-resistant Staphylococcus epidermidis. Thirteen of these 21 patients (62%) had received linezolid during the 3 months preceding S. epidermidis recovery. Two closely related pulsotypes (P1a and P1b) were identified among the 27 studied isolates that belonged to the sequence type ST2 and harboured the mecA gene and the SCCmecIII type. The strains recovered from patients 1-4 (pulsotype P1a) showed the nucleotide mutation G2474T inside the amplified fragment of the 23S rRNA region and carried the aac(6')-Ie-aph(2″)-Ia, ant(4'), and catA genes, whereas the strains from patients 5-21 (pulsotype P1b) showed the mutation G2603T and carried the aac(6')-Ie-aph(2″)-Ia gene. None of the strains amplified the cfr gene. The ica gene and the IS256 element were detected in all strains. The emergence of 2 closely related methicillin- and linezolid-resistant S. epidermidis strains with 2 different mutations in the 23S rRNA region (G2474T and G2603T) is reported in this study as a cause of a nosocomial outbreak. The presence of G2474T or G2603T point mutations suggests that there are multiple potential sites within domain V of the 23S rRNA region at which mutations could confer resistance to linezolid in the clinical isolates. To our knowledge, this is the first report in which the G2474T mutation has been detected in domain V of the 23S rRNA gene of clinical S. epidermidis.     

Nosocomial respiratory infection due to an imipenem-resistant Pseudomonas aeruginosa O: 12 strain in a Tunis's neonatal intensive care unit

OBJECTIVE: Investigation of an outbreak caused by an imipenem-resistant Pseudomonas aeruginosa strain and research of its hospital reservoir. PATIENTS AND METHODS: Nine strains isolated from protected tracheal specimens during 14 weeks (October 2004 to January 2005) from 8 infants, and one strain from vacuum interrupter were studied. Epidemiological study was investigated by determination of antibiotics susceptibility, serotyping and Pulsed-field gel electrophoresis (PFGE). RESULTS: Strains were of O:12 serotype, they have the same antibiotype characterised by imipenem resistance. Strains were indistinguishable or closely related as determined by PFGE. The common source of P. aeruginosa O:12 strains was not determined, however eradication of the epidemic strain was obtained by amelioration of hygiene conditions and the change of disinfectors. CONCLUSION: Outbreak of respiratory infections due to an imipenem-resistant P. aeruginosa O:12. The common source of the epidemic strain was not determined.     

Nosocomial infection of malnourished patients in an intensive care unit

Malnutrition is one of the most important factors for the development of nosocomial infection (NI). We performed a study of the correlation between abnormal nutritional factors and NI risk by investigating the patients who stayed longer than 3 days in the intensive care unit (ICU) of our university hospital. The patients were classified into three groups based on serum albumin levels and total lymphocyte counts (TLC). The criteria of Group I (well nourished group) were serum albumin level of 3.5 g/dl or higher and TLC of 1,400/mm3 or higher. The criteria of Group III (severely malnourished group) were serum albumin of less than 2.8 g/dl and TLC of less than 1,000/mm3. The other patients were classified as Group II (moderately malnourished group). The occurrences of NI were monitored during the study period and the APACHE III Score was calculated. The probability of first NI infection in Group III was 2.4 times higher than that in Groups I and II. The mortality rate of 20.5% was more significantly correlated with APACHE III Score than nutritional status. Nineteen (53%) of the total 36 NI patients were infected within 10 days after ICU admission and they all belonged to Group III. When we compared the gap period between infections, the time to first infection was significant.     

Detection of resistance due to inducible beta-lactamase in Enterobacter aerogenes and Enterobacter cloacae.

Thirty-six of 36 strains of Enterobacter cloacae and E. aerogenes with inducible beta-lactamase developed resistance when cefoxitin (inducer) was added to cefuroxime disks. Constitutive beta-lactamase producers (n = 23) were all resistant to cefuroxime. Cefuroxime resistance correlated with the amount of induced or constitutive beta-lactamase. Cefuroxime was a better indicator of induced resistance than cefamandole, cefazolin, cephalothin, ceftriaxone, cefotaxime, ticarcillin with or without clavulanic acid, or cefotetan. Induction by addition of cefoxitin to disks occasionally reduced zone sizes but not enough to change interpretations for ceftazidime, ceftizoxime, aztreonam, cefoperazone with or without sulbactam, and piperacillin with or without tazobactam. Most enterobacters were resistant to cefmetazole. The cefoxitin inducer-cefuroxime indicator method can be used in routine clinical laboratories to detect latent resistance due to chromosomally mediated inducible beta-lactamase in enterobacters.     

Subtractive Hybridization Yields a Silver Resistance Determinant Unique to Nosocomial Pathogens in the Enterobacter cloacae Complex

The heterogeneity and the increasing clinical importance of the Enterobacter cloacae complex have often been discussed. However, little is known about molecular factors causing pathogenicity within this nomenspecies. Here, we analyzed the genetic differences between an avirulent plant isolate and a pathogenic strain causing an outbreak with septicemia in three patients. We identified an IncHI-2 plasmid as a major difference between these two strains. Besides resistance to several antibiotics, this plasmid encoded a silver resistance determinant. We further showed that this sil determinant was present not only in the analyzed outbreak strain but also in the vast majority of clinical isolates of the E. cloacae complex, predominantly in (sub)species that frequently cause nosocomial infections. The identified sil determinant was highly conserved within the E. cloacae complex and mediated resistance to up to 600 μM silver nitrate. As silver is often used as a disinfectant and treatment for burn wounds, we present here an important fitness factor within the clinically most prevalent subspecies of the E. cloacae complex. This provides a possible explanation for their unequal involvement in nosocomial and especially burn wound infections.     

Nosocomial infections due to adenovirus in a paediatric unit

OBJECTIVE: We carried out a retrospective analysis of an outbreak of adenovirus (AdV) infections in a paediatric unit. The aim of the study was to analyse cases, determine the route of transmission and to evaluate the efficacy of the prevention measures. PATIENTS AND METHODS: The study was performed by recollection of AdV infection cases during a period of 1 year and the results were compared with the list of clinical cases recorded during the epidemic. The clinical files of children with a positive specimen were retrospectively analysed. During that period, five members of the medical staff showed clinical signs and symptoms of AdV infection. A throat swab was collected from a subset of the staff. RESULTS: Among nine patients with positive AdV detection, six were infected with an Adv type 2. Six were nosocomially-acquired, the other two were only probable nosocomial infections. The index case was a child presenting a febrile diarrhoea 48 h prior to being admitted to the hospital. Nosocomial transmission was associated with the prolonged shedding of the virus with faeces of the infected cases. The specimens collected from the staff remained negative. The outcome was favourable for all children. CONCLUSIONS: Prevention measures, implemented when the epidemic was characterised, allowed the control of the nosocomial outbreak.     

Genotypic and phenotypic analysis of Enterobacter sakazakii strains from an outbreak resulting in fatalities in a neonatal intensive care unit in France

In 1994, an outbreak of Enterobacter sakazakii infections occurred in a neonatal intensive care unit in France from 5 May to 11 July. During the outbreak, 13 neonates were infected with E. sakazakii, resulting in 3 deaths. In addition, four symptomless neonates were colonized by E. sakazakii. The strains were subjected to 16S rRNA gene sequence analysis, genotyped using pulsed-field gel electrophoresis, and phenotyped for a range of enzyme activities. E. sakazakii was isolated from various anatomical sites, reconstituted formula, and an unopened can of powdered infant formula. A fourth neonate died from septic shock, attributed to E. sakazakii infection, during this period. However, 16S rRNA gene sequence analysis revealed that the organism was Enterobacter cloacae. There were three pulsotypes of E. sakazakii associated with infected neonates, and three neonates were infected by more than one genotype. One genotype matched isolates from unused prepared formula and unfinished formula. However, no pulsotypes matched the E. sakazakii strain recovered from an unopened can of powdered infant formula. One pulsotype was associated with the three fatal cases, and two of these isolates had extended-spectrum beta-lactamase activity. It is possible that E. sakazakii strains differ in their pathogenicities, as shown by the range of symptoms associated with each pulsotype.     

Successful management of an MRSA outbreak in a neonatal intensive care unit

We report an MRSA outbreak in our 25-bed tertiary neonatal intensive care unit (NICU), which was successfully contained. Methods include a retrospective review of patient files, microbiology records and meeting protocols. During the seven months of outbreak, 27 patients and seven health care workers (HCWs) had positive cultures for MRSA. The outbreak was caused by the epidemic Rhine-Hessen strain; cultured isolates were monoclonal. After a sharp increase of the number of new MRSA-cases the installation of an outbreak management team (OMT) and implementation of comprehensive measures (extensive screening and decolonization strategy including orally applied vancomycin, isolation wards, intensive disinfection regimen) successfully terminated the outbreak within one month. Ten (53%) of 19 patients with completed follow-up and all of the HCWs were decolonized successfully. Gastrointestinal colonization was present in 15 of 27 (56%) neonates, and was associated with poor decolonization success (30% vs. 78% in absence of gastrointestinal colonization). A comprehensive outbreak management can terminate an outbreak in a NICU setting within a short time. Thorough screening of nares, throat and especially stool is necessary for correct cohorting. Gastrointestinal decolonization in neonates seems difficult.     

Nosocomial spread of a Staphylococcus capitis strain with heteroresistance to vancomycin in a neonatal intensive care unit

A premature infant in a neonatal intensive care unit (NICU) developed a bloodstream infection caused by coagulase-negative staphylococci (CoNS) sensitive to vancomycin. The infection persisted for 3 weeks, despite therapy with vancomycin and replacement of all intravenous catheters. The neonate died due to necrotizing enterocolitis which developed during the ongoing sepsis. We screened this strain and 216 other strains of CoNS from cultures of blood obtained from neonates between 1997 and 2000 for heteroresistance to vancomycin. Forty-eight isolates, including the strain that caused ongoing sepsis, proved heteroresistant. All isolates were identified as Staphylococcus capitis and were identical, just as their resistant stable subcolonies were, when they were genetically fingerprinted by amplified-fragment length polymorphism analysis. The heteroresistant phenotype of this endemic strain was confirmed by population analysis. We conclude that heteroresistance to vancomycin occurs in S. capitis and might be the cause of therapeutic failures in NICUs. Moreover, heteroresistant strains can become endemic in such units.     

Nosocomial infection in newborns by Pichia anomala in a Brazilian intensive care unit.

Disseminated candidiasis is the most common nosocomial fungal infection, and Candida albicans has been reported to account for 50% to more than 70% of cases of invasive candidiasis. However, recent reports have also suggested the emergence of infections caused by non-albicans species. In addition, less-common pathogenic yeasts (Malassezia, Trichosporon, Rhodotorula, Debaryomyces and Pichia) have recently been reported, with increased frequency, as causes of nosocomial infections with high mortality. This article describes two cases of fungemia caused by Pichia anomala in newborns that occurred in an intensive care unit (ICU), in November 2004 at the Instituto da Crian?a (Pediatric Institute) of the Hospital das Clínicas of the School of Medicine, S?o Paulo University, Brazil. The principal factors related to virulence (proteinase and phospholipase) and the susceptibility of the isolated strains to antifungal agents were also evaluated, and the biotype of each strain was determined through the use of an epidemiological marker (killer biotype).