A Chryseobacterium meningosepticum outbreak in a neonatal ward.

OBJECTIVE: To report epidemiologic, bacteriologic, and clinical features of a Chryseobacterium meningosepticum outbreak. DESIGN: Outbreak investigation. SETTING: A neonatal intensive care unit (NICU) of a referral teaching hospital. METHODS: During 2 weeks in September 2001, four neonates in the NICU developed sepsis and underwent laboratory investigation. Multiple samples were obtained for cultures from endotracheal tubes, mechanical ventilators and humidifier boxes, infant incubators, parenteral and antiseptic solutions, feeding bottles, sinks, faucets, doors, and healthcare workers. RESULTS: C. meningosepticum was isolated from the blood cultures of four patients. The first isolate was identified 5 days after the death of the index case. Although all isolates were ciprofloxacin susceptible in vitro, the remaining three patients did not respond to ciprofloxacin therapy given for 6 or 7 days. Therapy was switched to vancomycin and rifainpin and all three patients survived, with one having a complication (hydrocephalus). Environmental surveillance revealed C. meningosepticum in the stock lipid solution as the source of the epidemic. The outbreak was controlled after discontinuation of intravenous lipid solution, restriction of further neonatal admissions, and thorough disinfection of the unit and its equipment. CONCLUSION: Early identification of an epidemic and its source is important in avoiding morbidity and mortality. A contaminated lipid stock bottle was the source of this outbreak associated with multiple cases and one death.     

Outbreak of methicillin-resistant Staphylococcus aureus colonization and infection in a neonatal intensive care unit epidemiologically linked to a healthcare worker with chronic otitis.

OBJECTIVE: To describe the investigation and interventions necessary to contain an outbreak of methicillin-resistant Staphylococcus aureus (MRSA) colonization and infection in a neonatal intensive care unit (NICU). DESIGN: Retrospective case finding that involved prospective performance of surveillance cultures for detection of MRSA and molecular typing of MRSA by repetitive-sequence polymerase chain reaction (rep-PCR). SETTING: Level III NICU in a tertiary care center. PARTICIPANTS: Three neonates in a NICU were identified with MRSA bloodstream infection on April 16, 2004. A point prevalence survey identified 6 additional colonized neonates (attack rate, 75% [9 of 12 neonates]). The outbreak strain was phenotypically unusual. INTERVENTIONS: Cohorting and mupirocin therapy were initiated for neonates who had acquired MRSA during the outbreak. Contact precautions were introduced in the NICU, and healthcare workers (HCWs) were retrained in cleaning and disinfection procedures and hand hygiene. Noncolonized neonates and newly admitted patients had surveillance cultures performed 3 times per week. RESULTS: Two new colonized neonates were identified 1 month later. HCW X, who had worked in the NICU since June 2003, was identified as having chronic otitis. MRSA was isolated from cultures of swab specimens from HCW X's ear canal and nares. HCW X was epidemiologically linked to the outbreak. Molecular typing (by rep-PCR) confirmed that the isolates from HCW X and from the neonates were more than 90% similar. Retrospective review of NICU isolates revealed that the outbreak strain was initially cultured from a neonate 2 months after HCW X began working on the unit. The epidemic strain was eradicated after removing HCW X from patient care in the NICU. CONCLUSION: An outbreak of MRSA colonization and infection in a NICU was epidemiologically linked to a HCW with chronic otitis externa and nasal colonization with MRSA. Eradication was not achieved until removal of HCW X from the NICU. Routine surveillance for MRSA may have allowed earlier recognition of the outbreak and is now standard practice in our NICU.     

A hospital outbreak of extended-spectrum β-lactamase-producing Klebsiella pneumoniae investigated by RAPD typing and analysis of the genetics and mechanisms of resistance

Between July and September 1997 a ceftazidime- and aminoglycoside-resistant strain of Klebsiella pneumoniae infected or colonized seven patients on three paediatric wards at Guy's Hospital in London. The patients were mostly neonates or infants recovering from cardiac surgery for congenital defects. The organism was probably introduced by an asymptomatic patient from Greece and the subsequent outbreak could largely be explained by person-to-person spread on individual wards and frequent transfers of patients between wards. The outbreak was controlled by patient isolation and attention to handwashing, and there were no fatalities. The organisms were non-typeable by serology but had a characteristic RAPD profile. They produced the extended-spectrum β-lactamase SHV-5 and the aminoglycoside-modifying enzymes AAC(6′) + probably AAC(3)II, encoded on a conjugative plasmid of approximately 160 kb. Two other patients had multi-resistant klebsiellas, one of them an SHV-5 producer and one a TEM-5 producer, but these could be distinguished from each other and from the outbreak strain by serological and RAPD typing and by the genetics and mechanisms of their resistances. Three other multi-resistant enterobacteria were isolated during the outbreak: an Escherichia coli that had acquired the 160 kb resistance plasmid from the epidemic klebsiella, a Citrobacter isolated from one of the patients with the klebsiella but which did not produce SHV-5, and a TEM-5-producing Enterobacter. This outbreak illustrates the importance of screening patients from high-risk areas for multiply-resistant organisms on admission, and the value of bacterial typing and analysis of resistance mechanisms to define the epidemiology of hospital infection.     

Control of a cluster of community-associated, methicillin-resistant Staphylococcus aureus in neonatology

To control an outbreak of community-associated MRSA (CA-MRSA) in a neonatology unit, an investigation was conducted that involved screening neonates and parents, molecular analysis of MRSA isolates and long-term follow-up of cases. During a two-month period in the summer of 2000, Panton-Valentine leukocidin (PVL)-producing CA-MRSA (strain ST5-MRSA-IV) was detected in five neonates. The mother of the index caseshowed signs of mastitis and wound infection and consequently tested positive for CA-MRSA. A small cluster of endemic, PVL-negative MRSA strains (ST228-MRSA-I) occurred in parallel. Enhanced hygiene measures, barrier precautions, topical decolonization of carriers, and cohorting of new admissions terminated the outbreak. Four months after the outbreak, the mother of another neonate developed furunculosis with the epidemic CA-MRSA strain. One infant had persistent CA-MRSA carriage resulting in skin infection in a sibling four years after the outbreak. In conclusion, an epidemic CA-MRSA strain was introduced by the mother of the index case. This spread among neonates and was subsequently transmitted to another mother and a sibling. This is the first report of a successfully controlled neonatology outbreak of genetically distinct PVL-producing CA-MRSA in Europe.     

A simultaneous outbreak on a neonatal unit of two strains of multiply antibiotic resistant Klebsiella pneumoniae controllable only by ward closure.

Two aminoglycoside-resistant strains of Klebsiella pneumoniae caused an outbreak on the neonatal unit at St Thomas' Hospital. One, which affected 18 patients, was capsular type K18 and resistant to newer cephalosporins by the production of the extended-spectrum beta-lactamase SHV-2; the other, which colonized four patients, was capsular non-typeable and did not produce extended-spectrum beta-lactamase. Both strains were probably brought into the unit by carrier patients; the probable carrier of the non-typeable strain was transferred from another hospital but was negative on a single admission screen; the probable carrier of the K18 strain was not screened on admission because he had been born at St Thomas', but his mother had been transferred from another hospital. Despite intensive efforts to control the outbreak by standard methods of hand washing, screening, patient isolation and environmental cleaning, a total of 22 neonates on the unit eventually became colonized or infected. One of three patients with bacteraemia died. A small proportion of samples of expressed breast milk, electronic thermometers and oxygen saturation probes were contaminated by the K18 strain and may have contributed to some of the cross-infection, but this did not explain the extent of the outbreak. The outbreak was controlled only by opening a temporary ward for colonized neonates and another for newly born babies, which allowed the closure and cleaning of the main neonatal unit. Multiply antibiotic resistant klebsiellas may be highly epidemic and cause serious, difficult-to-control outbreaks on neonatal units. All patients, regardless of their admission history, should be screened on admission for carriage of multiply resistant enterobacteria by a sensitive method, and units should have plans for temporary ward closure should outbreaks occur.     

An outbreak due to echovirus type 30 in a neonatal unit in France in 1997: usefulness of PCR diagnosis.

Between February and August 1997, 53 patients with enterovirus meningitis were hospitalized in Clermont-Ferrand, France. All but one were children. Echovirus type 30 was involved in 70% of cases with identified serotype. The outbreak ceased on August 8. Two months later, a neonate was admitted to the neonatal unit with an echovirus type 30 meningitis thought to be acquired at delivery. Twenty days later a nosocomial outbreak of echovirus type 30 involving five neonates occurred. Two of them presented with meningitis and two with febrile seizure; One was asymptomatic. The retrospective examination of the maternal sera in a neutralization test, using the index case strain as a source of antigen, showed that none of the neonates was passively immunized before hospitalization. The use of genome detection in cerebrospinal fluid allowed rapid diagnosis and infection was contained by re-inforcing hygiene measures. Prospective examination of stools in the neonatal and paediatric units showed no further occurrences of the disease. No sporadic case was observed in the general population. Hence, nosocomial infections can occur a long time after an outbreak in the general population; rapid diagnosis with molecular tools is useful both for a definite diagnosis in patients already hospitalized, and to act as a rapid alert, even in intervals between seasonal outbreaks.     

Analysis of plasmid pattern in paediatric intensive care unit outbreaks of nosocomial infection due to Enterobacter cloacae.

Sequential outbreaks of nosocomial infection due to multiply-resistant Enterobacter cloacae occurred in September 1987, and between December 1988 and January 1989, in a paediatric intensive care unit. A total of eight neonates were affected and most had received ventilatory support. Initially, we were unable to determine whether the two outbreaks were caused by the same strain of E. cloacae. After applying plasmid profile analysis to identify epidemic strains, we established that the strain from the first outbreak was different from the second outbreak strain, as each had its own plasmid pattern. During the second outbreak, an environmental bacteriological survey was carried out. We found that the distilled water containers were contaminated with E. cloacae which had the same plasmid profile. After changing the distilled water containers and by reinforcement of aseptic techniques, the nosocomial outbreak was terminated.     

Enterobacter cloacae epidemic on a neonatal intensive care unit due to the use of contaminated thermometers

From December 1999 to March 2000 a nosocomial outbreak of multiresistant Enterobacter cloacae occurred in the neonatal intensive care unit (NICU) at the VU Medical Center, Amsterdam, the Netherlands. Twenty-six patients were infected or colonized with this strain resistant to third generation cephalosporins and with decreased sensitivity for aminoglycosides. Three neonates experienced sepsis with E. cloacae with serious clinical symptoms and two of them died. Comparison of the Enterobacter isolates by amplified-fragment length polymorphism indicated that this outbreak was caused by the spread of a single strain. Infection control precautions were initiated in order to stop further spread; barrier precautions, enforcement of hand disinfection and cohorting of colonized patients. A multidisciplinary crisis team coordinated these infection control precautions and informed all persons involved. Analysis of antibiotic usage in 1999 showed an increase in the use of third generation cephalosporins from November onwards. Due to the resistance pattern of the epidemic strain the use of third generation cephalosporins was discontinued in February 2000. At the end of February the NICU was temporarily closed. The epidemic strain of E. cloacae was isolated from one digital rectal thermometer. Patient use of thermometers and disposable coverings for rectal thermometers were introduced to eliminate this possible means of spread. No spread of multiresistant E. cloacae was found following the introduction of these interventions. Once all the neonates had been transferred, the NICU was disinfected and reopened in March.     

An outbreak of multiply resistant Pseudomonas aeruginosa in a neonatal unit: plasmid pattern analysis

An outbreak of infection due to multiply resistant Pseudomonas aeruginosa occurred from March to April 1986 in a neonatal unit. Affected neonates were receiving ventilation support and the mortality rate was high. Plasmid analysis and antibiograms indicated that the outbreak was due to a single strain. A survey of bacteria isolated from respirators, potable water and hands of personnel working in the unit failed to recover the outbreak strain. Lack of sterilization of respirators and overcrowding were considered to be the causes of the outbreak and reinforcement of the importance of aseptic techniques helped in its termination.     

Investigation of a pyoderma outbreak caused by methicillin-susceptible Staphylococcus aureus in a nursery for newborns

An outbreak of pyoderma caused by methicillin-susceptible Staphylococcus aureus occurred in a nursery for newborns over 26 days. During this period, six neonates were involved. The mother of the first case had trunk pyoderma before delivery, which was regarded as the source of the outbreak. Contamination of the environment and equipment were implicated as the reservoirs of further pathogen spread, as supported by pulsed-field gel electrophoresis (PFGE) results, which showed that some screening isolates were indistinguishable from the epidemic strain. Termination of the outbreak was achieved by the reinforcement of infection control practices and disinfection of environmental surfaces.     

Molecular epidemiology of Serratia marcescens outbreaks in two neonatal intensive care units.

OBJECTIVE: Serratia marcescens can cause serious infections in patients in neonatal intensive care units (NICUs), including sepsis, pneumonia, urinary tract infection, and conjunctivitis. We report the utility of genetic fingerprinting to identify, investigate, and control two distinct outbreaks of S. marcescens. DESIGN: An epidemiologic investigation was performed to control two clusters of S. marcescens infections and to determine possible routes of transmission. Molecular typing by pulsed-field gel electrophoresis determined the relatedness of S. marcescens strains recovered from neonates, the environment, and the hands of healthcare workers (HCWs). SETTING: Two geographically distinct level III-IV NICUs (NICU A and NICU B) in two university-affiliated teaching hospitals in New York City. RESULTS: In NICU A, one major clone, "F," was detected among isolates recovered from four neonates and the hands of one HCW. A second predominant clone, "A," was recovered from four sink drains and one rectal surveillance culture from an asymptomatic neonate. In NICU B, four neonates were infected with clone "D," and three sink drains harbored clone "H." The attributable mortality rate from bloodstream infections was 60% (3 of 5 infants). The antimicrobial susceptibilities of clone F strains varied for amikacin, cefepime, and piperacillin/tazobactam. CONCLUSIONS: S. marcescens causes significant morbidity and mortality in preterm neonates. Cross-transmission via transient hand carriage of a HCW appeared to be the probable route of transmission in NICU A. Sinks did not harbor the outbreak strains. Antimicrobial susceptibility patterns did not prove to be an accurate predictor of strain relatedness for S. marcescens.     

Investigation of an outbreak of infection with Acinetobacter calcoaceticus in a special care baby unit

During a period of 6 months, an 'epidemic strain' of Acinetobacter calcoaceticus was isolated from 10 pre-term neonates in a special care baby unit (scbu). Of these, nine had pulmonary infections. The tenth was found to have conjunctival colonization only. The 'epidemic strain' was characterized by serotyping, biotyping, bacteriocin typing and antibiograms. An identical strain was isolated from an 'Ambu' resuscitation device but not from other environmental samples or from staff on the unit. The outbreak ceased after the colonized resuscitator was removed and an appropriate disinfection policy implemented for the replacement resuscitators.     

Analysis of three outbreaks due to Klebsiella species in a neonatal intensive care unit.

OBJECTIVE: To investigate the clinical, microbiological, and epidemiologic features of three outbreaks caused by Klesiella during 3 years. SETTING: Neonatal intensive care unit of a university hospital. PATIENTS: Thirty affected neonates. METHODS: Data were collected through chart reviews and conversations with physicians. Screening samples were obtained from the staff, the neonates, and the environment. Antibiogram typing and arbitrarily primed polymerase chain reaction-based fingerprinting were used to type the strains. RESULTS: The first outbreak had 13 K. pneumoniae strains isolated. The second outbreak had 10 K. oxytoca strains isolated. The third outbreak had 20 K. pneumoniae strains isolated. More than half of the patients had low birth weights, were premature, and underwent mechanical ventilation and intravenous catheterization. Approximately three-fourths of the patients died. The isolates tested were completely susceptible to meropenem, cefoxitin, and ciprofloxacin and were resistant to cephalothin. More than half of these strains were resistant to many beta-lactam antibiotics, amikacin, and trimethoprim/sulfamethoxazole. Typing procedures yielded 3 antibiotypes and 3 genotypes among the isolates of the first outbreak, 3 antibiotypes with 1 subtype and 2 genotypes with 1 subtype in the second outbreak, and 2 antibiotypes and 2 genotypes in the third outbreak. CONCLUSIONS: Klebsiella outbreaks mainly affected premature neonates with intravenous catheters, mechanical ventilation, or both. The high mortality rate (76.7%) was notable. Resistance to multiple antibiotics, but mainly to broad-spectrum beta-lactam antibiotics, was observed, particularly in K. pneumoniae isolates. Molecular typing indicated that the three outbreaks were not related to one other.     

Investigation of a cluster of cutaneous aspergillosis in a neonatal intensive care unit

Between December 2007 and July 2008, three neonates in a neonatal intensive care unit (NICU) in Salford, UK, were diagnosed with primary cutaneous aspergillosis (PCA) due to Aspergillus fumigatus. The first PCA case, in December 2007, developed multi-organ failure leading to death within a short time frame: the other two cases survived after treatment with intravenous antifungal therapy followed by oral posaconazole. Air, surface, and water samples were collected within the NICU and from the incubators that were occupied by the neonates. All recovered fungal isolates were confirmed as A.?fumigatus by sequencing the beta-tubulin region. Microsatellite strain typing demonstrated genotypically related A.?fumigatus isolates from the neonates and the humidity chambers (HCs) of the neonates' incubators, suggesting that the source of the infection may have been the HCs/incubators used in the NICU. Aspergillus strain typing may be a useful tool in clinical outbreak settings to help understand the source of exposure and to design targeted environmental interventions to prevent future infections.     

Nosocomial outbreak of diarrhoea by enterotoxigenic Escherichia coli among preterm neonates in a tertiary care hospital in India: pitfalls in healthcare

An outbreak of watery diarrhoea accompanied by low-grade fever and weight loss in 16 preterm neonates (age range 2-20 days) admitted to a neonatal intensive care unit (NICU) over four days in August 2000 is reported.Escherichia coli having similar antibiograms were identified on routine bacterial stool cultures in 14 (87.5%) neonates and none of the other known enteropathogens were detected. An investigation was undertaken to trace the source of infection. Surveillance cultures of swabs from the utensils used to prepare milk feed, culture of the formula feed and all items handled by one particular cook yielded growth of E. coli as did culture of his hand swabs and faecal sample. The causative agent was identified as enterotoxigenic E. coli (ETEC) as toxin production could be demonstrated by reverse passive latex agglutination in all the strains of E. coli isolated both from the infected neonates and the source of infection. The outbreak was effectively controlled by appropriate therapy and institution of proper measures of hygiene after identification of the source of infection.     

Methicillin-resistant Staphylococcus aureus in neonatal intensive care unit

A neonatal intensive care unit outbreak was caused by a strain of methicillin-resistant Staphylococcus aureus previously found in the community (ST45-MRSA-IV). Fifteen infected neonates were identified, 2 of whom died. This outbreak illustrates how a rare community pathogen can rapidly spread through nosocomial transmission.     

An outbreak of human salmonellosis caused by ampicillin-resistant Salmonella enterica serovar Enteritidis PT13 in the Czech Republic

In summer 2004, an outbreak caused by Salmonella enterica serovar Enteritidis phage type 13 (S. Enteritidis PT13) was recorded in the Czech Republic. As well being a relatively rare phage type the strain was also ampicillin resistant. Outbreak (n=39) and pre-outbreak isolates (n=13) were characterized by pulsed-field gel electrophoresis (PFGE), beta-lactamase gene polymerase chain reaction and plasmid profile. The majority of outbreak isolates (n=37) were identical in XbaI PFGE profile, and two other outbreak isolates each differed from this profile by one or two fragments respectively. The pre-outbreak isolates were uniform in PFGE profile but distinct from the outbreak strain. Ampicillin resistance was confirmed to be encoded by the blaTEM gene located on the TnA transposon. This gene was readily transferable to a S. Enteritidis recipient strain and was associated with the transfer of a 200-kb plasmid. Our results indicate that all S. Enteritidis PT13 tested from 2004 belonged to a single outbreak strain which prior to 2004 had not been recognized in the Czech Republic.     

Outbreak of Serratia marcescens infection in a neonatal intensive care unit.

We report an outbreak of Serratia marcescens infection in the neonatal intensive care unit of a community hospital. The outbreak involved eight neonates, (five infected and three colonized), one of whom died. Pulsed-field gel electrophoresis confirmed that all isolates were identical strains. Cohorting and isolation of the infected neonates helped to control the outbreak. No environmental source of infection was found.     

2004 Lowbury Lecture: the Western Australian experience with vancomycin-resistant enterococci - from disaster to ongoing control

The first hospital outbreak of a vancomycin-resistant enterococcus (VRE) in Western Australia (WA) started in the Royal Perth Hospital in July 2001 and initially involved the Intensive Care Unit (ICU) and the Nephrology and Dialysis Units. The outbreak was caused by vancomycin-resistant Enterococcus faecium (VREF) of the vanB genotype. Pulsed-field gel electrophoresis and plasmid analysis of the isolates demonstrated a single-strain outbreak. Despite the isolation of carriers and implementation of all the additional precautions recommended to control VRE, VREF spread rapidly. Two months after the index patient was detected, the epidemic strain had spread to 22 wards and units and one outpatient unit (Satellite Dialysis). Four patients were infected and 64 were colonized. A Hospital VRE Executive Group, which included the Chief Executive and Directors of Clinical Services and Nursing, was formed to eradicate the outbreak and to prevent the epidemic strain from becoming endemic in the hospital. The WA Department of Health agreed to provide substantial extra funding to enable the hospital to use expensive enhanced infection control practices, as follows. Control was handicapped by the slowness of conventional laboratory methods, which took four to five days to identify VRE and allowed environmental contamination and nosocomial transmission to occur before carriers were detected and isolated. A laboratory procedure to make rapid provisional identification of VRE within 30-48h was developed by performing multiplex polymerase chain reaction (PCR) for vanA and vanB genes directly on 24-h selective enrichment broth cultures. On average, four rectal swabs, each collected on separate days, were needed to detect >90% of carriers. In total, 1977 ward contacts were screened after discharge from hospital and 54 (2.73%) were found to be carrying VREF. The electronic labelling and active follow-up of ward contacts resulted in a significant number of carriers being detected who otherwise posed a risk of initiating further outbreaks in hospital if they were re-admitted. The outbreak was terminated after five months and the cost of the enhanced infection control practices was 2,700 000 Australian dollars (1,000,000 pounds sterlings). Ongoing control has been facilitated by targeted active surveillance cultures: on admission to high-risk units (ICU, Burns, Nephrology, Haematology, Bone Marrow Transplant Unit), on transfer out of the ICU to other hospital units, by monthly screening of patients regularly attending Dialysis Units, and by opportunistic laboratory screening of inpatient faecal specimens submitted for Clostridium difficile culture and toxin. Vigilance needs to be maintained as the epidemic strain of VREF remains in the Perth community. Ward contacts of the first outbreak have caused small outbreaks in two hospitals, and seven to 19 sporadic new carriers have been detected annually since the first outbreak. The key elements of the VRE control programme are as follows: To date, this programme has prevented VRE from becoming established in any WA hospital.