Marcescens Infection Research Articles

Cutaneous Serratia marcescens Infection in an Immunocompetent Patient after Filler Injection

®, a permanent filler containing polymethylmethacrylate (PMMA), into the glabellar area, administered by an unlicensed practitioner. Approximately 3 months prior to presentation she visited the same practitioner again and underwent an unknown procedure (explained as removal of collagen materials) along with injections of Juvederm ® , a hyaluronic acid (HA) filler, into the glabella and forehead. Thereafter, her face gradually became swollen, and an inflamed nodular lesion developed on the glabellar area. The lesions had been treated with topical antibiotics (fusidic acid and mupirocin), systemic antibiotics (amoxicillin-clavulanate and ceftezole) and several attempts at incisional drainage, but continued to wax and wane. No accompanying other skin lesions, enlarged lymph nodes, or signs of systemic involvement were detected. Laboratory data revealed normal biochemical and haematological study results. The results of skin tests with tuberculin, radiographic chest studies and atypical mycobacterial cultures were all normal. Histopathological findings showed a non-specific inflammatory reaction. Tissue and pus cultures were positive for S. marcescens and were sensitive to parenteral aminoglyco sides, oral trimethoprim-sulphamethoxazole (TMP-SMX) and ciprofloxacin. Treatment with oral TMP-SMX (160–800 mg twice daily for 3 weeks) and 2 attempts at incisional drainage of abscess were performed, which resulted in resolution of the lesion and negative culture findings (Fig. 1B). No recurrence was observed one year after the completion of therapy. DISCUSSION The use of dermal filler for cosmetic dermatological indications is increasing rapidly. Infection or contamination can occur with the use of soft-tissue augmentation agents, even after the injection of licensed products by experienced aesthetic physicians (1). In our case, the unlicensed practitioner injected HA filler into the patient’s skin in an area that was previously filled with PMMA filler. PMMA filler is a permanent synthetic filler, and such permanent fillers can induce long-lived, low-grade bacterial infections surrounding the implants (2, 3). S. marcescens usually causes infections of the lower respiratory tract, urinary tract, and surgical wounds and otitis, endocarditis, and septicaemia (4, 5). S. marcescens infections are predominantly observed in immunocompromised patients (6). In the reported case, we suppose that the patient’s skin was prone to infection due to the presence of PMMA filler, and that the additional HA filler injection allowed the entry of S. marcescens. Although we cannot specify the exact cause of contamination, it is likely that a lack of proper procedural hygiene played a crucial role in this infec tion. S. marcescens was possibly carried by humans in this case. To our knowledge, this is the first reported case of S. marcescens facial infection after filler injection in an im munocompetent patient. The possibility of pathogenicity of S. marcescens should be considered when treating infections caused by filler injection. To help minimize the risk of infection, clean preparation of the skin is recommended in the area of treatment prior to filler placement, and physicians should consider that skin previously treated with permanent filler may be vulnerable to infection even by minor additional procedures. This

Serratia Marcescens - A Rare Opportunis - tic Nosocomial Pathogen and Measures to Limit its Spread in Hospitalized Patients

In November 2011, 6 patients who were in the ICU of the Sri Guru Ram Dass Institute of Medical Sciences and Research acquired an infection which was caused by Serratia marcescens. We investigated the cause of the increase in frequency of the isolation of Serratia marcesens from hospitalized patients. Various samples from patients and environmental sources, which were collected from the ICU of Sri Guru Ram Das Institute of Medical Sciences and Research during the 6 month period from November 2011 to April 2011, were included in the study. The isolates from the patients and the surrounding environmental sources were examined by using standard techniques. Further, the isolates of Serratia marcescens were identified, depending upon their biochemical and morphological characteristics. Seven isolates of Serratia marcescens were identified (six from the patients in the ICU and one from the soap dispenser in the ICU) among a total of 327 isolates from the clinical samples and 84 isolates were identified from the environmental sources in the ICU. An outbreak of the Serratia marcescens infection in the ICU was traced to the extrinsic contamination of the soap dispenser in the ICU, as after the removal of the dispenser, no further case occurred.

Value of microbiology study in congenital nasolacrimal duct obstruction

PurposeEvaluation of the effect of different microorganisms on congenital nasolacrimal duct obstruction (CNLDO) tightness and whether probing or silastic intubation is likely to fail in a particular microorganism infection. MethodsThe culture and sensitivity results of lacrimal drainage system (LDS) discharge samples from patients with CNLDO were reviewed. Different microorganisms were correlated with the severity of nasolacrimal duct (NLD) obstruction observed during surgical intervention. The success rates of probing and silastic intubation as a primary procedure for each identifiable microorganism were documented. Statistical analysis was conducted to correlate the type of microorganism with the tightness of CNLDO and treatment failure. ResultsOut of 181 specimens, 22 had no growth (12.1%). LDS with positive culture had 76.6% successful probing (n=49) and 82.1% successful silastic intubation (n=78). Gram-positive and Gram-negative species were almost equally detected. The most prevalent organisms were Streptococcus pneumoniae and Hemophilus influenzae (48.1% and 39.2%, respectively). Tight CNLDO was more prevalent in Serratia marcescens (n=2; 100%) and Staphylococcus aureus (n=4; 33.3%) infections with a 7.75 Odds ratio [95% confidence interval (CI), 1.67–34.63]. Staphylococcus aureus had 37.5% successful probing; however, success was achieved in all cases with silastic intubation. Serratia marcescens infections had 100% successful silastic intubation. ConclusionMicrobiology study can predict tight CNLDO and helps in choosing the most successful treatment option. CNLDO with Staphylococcus infection and Serratia marcescens were likely to have tight NLD obstruction and silastic intubation had better outcomes.

Acquired Aplastic Anemia After Nosocomial Serratia marcescens Bone Marrow Infection in an Elderly Patient

Summary A 76-year-old female patient with a multiple medical history developed refractory pancytopenia during treatment for peptic ulcer, bacteremia, pneumonia, and respiratory failure. Bone marrow biopsy revealed hypocellularity with few hematopoietic cells, which was indicative of aplastic anemia. Common causes including viral infection, mycobacterial infection, environmental exposure, congenital bone marrow disorder, and hematologic malignancy were primarily excluded. Identical Serratia marcescens cultures were isolated from the central venous catheter tip and bone marrow, and the pancytopenia improved gradually with proper antibiotics treatment. This case indicates that nosocomial S. marcescens infection may cause potentially fatal acquired aplastic anemia. Crucial issues in avoiding aplastic anemia include confronting increasing mortality and morbidity caused by nosocomial infection, improving environmental hygiene, early diagnosis of proper etiology, and adequate antibiotics treatment.

Outbreak of bloodstream infections because of Serratia marcescens in a pediatric department

Serratia marcescens can cause health care-associated infections. We herewith report the investigation and control of an outbreak of S marcescens bloodstream infections (BSI) in a general pediatric department. From April to May 2009, temporally related cases of S marcescens BSI occurred in a 40-bed general pediatric department of a tertiary care hospital. An outbreak investigation including case identification, review of medical records, environmental cultures, patients' surveillance cultures, personnel hand cultures, pulsed-field gel electrophoresis, and a case-control study were conducted. Controls were patients without S marcescens BSI but hospitalized in the department for at least 48 hours during the outbreak. Enhanced infection control measures were immediately implemented by the Infection Control Committee. During the study period, 4 patients developed BSI because of a S marcescens strain demonstrating the same antimicrobial susceptibility pattern as well as the same molecular profile. Patients' surveillance cultures and personnel hand cultures were negative. In 1 case-patient, S marcescens grew from cultures of intravenous infusion systems. In the case-control study performed, there were no differences in demographics, intravenously administered medications, or place of hospital stay. Case patients had changes in vascular access significantly more frequently than controls. No S marcescens infections occurred in the department during the 18 months following implementation of the enhanced infection control measures. Prompt recognition and strict adherence to infection control measures are of paramount importance in combating an outbreak of S marcescens bloodstream infection.

Some like it hot: the effects of climate change on reproduction, immune function and disease resistance in the cricketGryllus texensis

In many parts of the world, climate change is increasing the frequency and severity of heat waves. How do heat waves impact short-lived poikilotherms such as insects? In the cricket, Gryllus texensis, 6 days of elevated temperatures (i.e. 7°C above the average field temperature and 5°C above their preferred temperature) resulted in increased egg laying, faster egg development and greater mass gain. The increased temperature also increased activity of phenoloxidase and lysozyme-like enzymes, two immune-related enzymes, and enhanced resistance to the Gram-negative bacterium Serratia marcescens. When given a sublethal S. marcescens infection, G. texensis maintained increased reproductive output at the elevated temperature (33°C). These data suggest that heat waves could result in more numerous, disease resistant, crickets. However, resistance to the Gram-positive bacterium, Bacillus cereus was lower at temperatures above or below the average field temperature (26°C). A sublethal infection with B. cereus reduced egg laying at all temperatures and suppressed the increase in egg laying induced by higher temperatures. These results suggest that for some species-pathogen interactions, increased temperatures can induce trade-offs between reproduction and disease resistance. This result may partly explain why G. texensis prefers temperatures lower than those that produce maximal reproductive output and enhanced immune function.

Entomopathogenicity of endophytic Serratia marcescens strain SRM against larvae of Helicoverpa armigera (Noctuidae: Lepidoptera)

An endophytic Serratia marcescens strain SRM (MTCC 8708) isolated from the flowers of summer squash was found to be entomopathogenic against the larvae of Helicoverpa armigera. Natural epizootic of this bacterial strain on the larvae collected from summer squash flowers ranged from 19.9 to 72.3%. Under laboratory conditions, a dose of 6 × 1010 c.f.u./ml diet induced 66.3% mortality of first instar H. armigera larvae. Similarly all other growth and development parameters of the insect were severely retarded in a dose-dependent manner. The bacterium invaded the entire alimentary canal and haemolymph with successful replacement of all other gut-associated microflora. There was a great reduction in midgut proteinase activity due to inhibition of five major proteinase isozymes by S. marcescens infection. Further, a synergistic interaction between chitinases isolated from this strain and Bacillus thuringiensis Cry1Ac toxin was observed. The present findings suggest that this plant-associated S. marcescens strain SRM could be suitably exploited for the management of H. armigera.

Fatal Aortic Endocarditis Associated with Community-Acquired Serratia marcescens Infection in a Dog

A 12 yr old Dalmatian was referred for evaluation of acute lethargy, fever, neurologic signs, and a recently ausculted heart murmur. Echocardiography in combination with blood cultures resulted in a diagnosis of nonhospital-acquired Serratia marcescens bacteremia and aortic valve endocarditis. Despite early diagnosis and aggressive therapy, the dog failed to respond to antimicrobials and died within 6 hr after admission. Necropsy findings included aortic valve endocarditis, septicemia, and diffuse thromboembolic disease. There was no history of pre-existing underlying disease or immunosuppressive therapy, and the dog had not been hospitalized before referral.

Investigation of an outbreak of Serratia marcescens in a neonatal intensive care unit

Serratia marcescens is a well-known but relatively uncommon cause of nosocomial infections, particularly in neonatal intensive care unit (NICU) patients. We investigated an outbreak of S marcescens in the NICU at the Farabi Hospital of Karadeniz Technical University in Trabzon, Turkey. Between March 21 and May 27, 2006, nine of the neonates were identified with cultures of S marcescens, and there were three deaths because of septicemia. For the purpose of identifying the source of infection, 85 environmental samples, two breast milk samples from two babies' mothers, and 38 hand-washing samples from the health care workers (HCWs) were collected for the detection of S marcescens. All the S marcescens isolates were genotyped by pulsed-field gel electrophoresis with endonuclease SpeI restriction enzyme. Serratia marcescens was identified from one hand-washing sample and two breast milk samples. None of the environmental samples yielded S marcescens. Of the 13 isolates analyzed, four belonged to one major genotype, whereas eight (6 from neonates and 2 from breast milk) were indistinguishable; two isolates (2 from neonates) were closely related; and three isolates (2 other neonates and 1 from HCW's hand) were different. Our intensive efforts failed to determine the source of the outbreak despite the finding that S marcescens strain was isolated from a HCW's hand. Present investigation suggested that an outbreak of S marcescens infection was caused by a major clone in our NICU, possibly transmitted through the hands of HCWs, emphasizing that strict hand washing before and after contact with patients must be the rule of the thumb.

Cerebral Abscesses and Septic Pulmonary Emboli due to Serratia marcescens Infection Arising from a Portacath

Percutaneous intravenous devices are an essential component of modern health care. Although they are generally associated with a low incidence of vascular access device-related sepsis, the events following a vascular catheter-related sepsis can be clinically significant and difficult to treat. Here we report a case of Portacath-related sepsis with Serratia marcescens resulting in cerebral and pulmonary emboli, which in our knowledge, has not been reported before. Definitive identification and prolonged antimicrobial treatment according to culture sensitivities can lead to resolution of septic and pulmonary emboli.

Serratia marcescens bullous cellulitis after iguana bites

To the Editor: Iguana iguana, a natural inhabitant of Southern Mexico and Brazil, is becoming increasingly popular as a US household pet, and there are an estimated 700,000 of these creatures within the United States.1Rosen T. Jablon J. Infectious threats from exotic pets: dermatological implications.Dermatol Clin. 2003; 21: 229-236Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar We report herein two cases of Serratia marcescens bullous cellulitis after the bite of I iguana and discuss empiric antibiotic therapy. An otherwise healthy 54-year-old man presented 2 days after being bitten by his Mexican pet iguana (I iguana) on the posterior midcalf. He developed a circumferential area of indurated and tender erythema with small vesicles spread throughout the site (Fig 1). A nonbacteriostatic saline aspirate of the cellulitis grew S marcescens. The only oral agent to which the isolate was sensitive was trimethoprim-sulfamethoxazole (TMP-SMX). The patient was placed on TMP-SMX 160 to 800 mg twice daily; the eruption resolved uneventfully within 2 weeks. A similar case presented in a healthy 25-year-old man who was bitten on the medial aspect of the left ankle by his pet Mexican iguana (I iguana). The following day, a blister appeared at the site. Within 48 hours, the blister evolved into a hemorrhagic bulla (Fig 2). Fluid obtained by sterile aspiration of the bulla yielded solitary growth of S marcescens, which was sensitive to parenteral aminoglycoside antibiotics and oral TMP-SMX. He was subsequently treated in the same manner as the first case, with a resolution of the signs and symptoms in 10 days. There is a paucity of data regarding the expected oral flora of I iguana, so it is not clear if S marcescens is a normal constituent for this reptile. In our cases, S marcescens was the only organism identified in bacterial culture of lesional aspirates. Both cases are unique in that there has been only one reported case of S marcescens nonbullous cellulitis after an iguana bite2Hsieh S. Babl F.E. Serratia marcescens cellulitis following an iguana bite.Clin Infect Dis. 1999; 28: 1181-1182Crossref PubMed Scopus (43) Google Scholar and only one report of bullous cellulitis that was determined to be solely caused by S marcescens.3Cooper C.L. Wiseman M. Brunham R. Bullous cellulitis caused by Serratia marcescens.Int J Infect Dis. 1998; 3: 36-38Abstract Full Text PDF PubMed Scopus (19) Google Scholar The latter case occurred within the setting of chlorhexadine solution contaminated by S marcescens.3Cooper C.L. Wiseman M. Brunham R. Bullous cellulitis caused by Serratia marcescens.Int J Infect Dis. 1998; 3: 36-38Abstract Full Text PDF PubMed Scopus (19) Google Scholar Antibiotics used to treat S marcescens infection include third-generation cephalosporins, aminoglycosides, carbapenems, fluoroquinolones, and TMP-SMX.3Cooper C.L. Wiseman M. Brunham R. Bullous cellulitis caused by Serratia marcescens.Int J Infect Dis. 1998; 3: 36-38Abstract Full Text PDF PubMed Scopus (19) Google Scholar Other than parenteral aminoglycoside antibiotics, S marcescens isolates from our patients were sensitive to TMP-SMX. However, the current recommendations for the prophylactic treatment of reptile bite wounds is amoxicillin-clavulanate, presumably for coverage of enteric Gram-negative bacteria and anaerobes.4American Academy of Pediatrics Committee on Infectious DiseasesPickering L.K. Baker C.J. Long S.S. McMillian J.A. Red book: 2006 report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics, Elk Grove, IL2006: 191Google Scholar The findings in our two cases—and in those of a previous report of an infected iguana bite2Hsieh S. Babl F.E. Serratia marcescens cellulitis following an iguana bite.Clin Infect Dis. 1999; 28: 1181-1182Crossref PubMed Scopus (43) Google Scholar—are particularly important because the current recommendations for prophylactic treatment of reptile bites would not routinely cover for S marcescens as an infecting microbe. In a recent study examining the susceptibility of various microbial pathogens, only 1.2% to 2.7% of S marcescens isolates were susceptible to amoxicillin-clavulanate, while 96% to 96.8% were resistant.5Dowzicky M.J. Park C.H. Update on antimicrobial susceptibility rates among gram-negative and gram-positive organisms in the United States: results from the Tigecycline Evaluation and Surveillance Trial (TEST) 2005 to 2007.Clin Ther. 2008; 30: 2040-2050Abstract Full Text PDF PubMed Scopus (55) Google Scholar In the setting of I iguana bites with clinical evidence of infection, empiric therapy with TMP-SMX or a fluoroquinolone antibiotic is advisable until culture results and sensitivities are available. Both patients were placed on TMP-SMX according to isolate sensitivities, and symptoms resolved within 2 weeks.

Performance Improvement in Pharmacy Education

As our college has struggled to develop perspective about the monumental task of assessing our curriculum, a familiar mantra from my days as a hospital pharmacist emerged above the clatter: high risk, high cost, high volume. This adage reminded the hospital performance improvement team to focus its efforts on the aspects of health care that are high risk or high cost for the patient and institution, and those that are performed frequently. To apply this principle to the knowledge, skills, and values we impart to our graduates through pharmacy education, there would be no more high risk (or high cost) skill than compounding. That our graduates can do serious harm by compounding poorly is well documented in the literature. A migraine patient developed atropine toxicity and remained comatose for 48 hours after administration of a compounded atropine sulfate 0.25 mg suppository that actually contained 25 mg of atropine sulfate.1 In 2006, Civen et al described 11 cases of Serratia marcescens infection associated with improperly compounded betamethasone injection.2 Morbidity and Mortality Weekly Reports describes several other outbreaks of infection resulting from poor compounding practices, and there have been numerous reports of the hazards of calcium phosphate precipitate in parenteral nutrition solutions.3-5 What is the evidence that pharmacy educators have trained our graduates well? In 2005, Kadi et al evaluated the compounding skills of pharmacy students by quantifying the concentrations of potassium permanganate and caffeine citrate compounded solutions. They found that approximately 54% of the P2 pharmacy students were able to prepare the 2 solutions within ± 10% of the target concentrations on the first try.6 In a study of the retention of compounding skills, Eley and Birnie found that only 17% of pharmacy students demonstrated a competency level of 80% when asked to prepare metoprolol capsules a second time a year after learning the skill.7 A survey of compounded drug products by the FDA's Center for Drug Evaluation and Research revealed that 9 out of 29 samples collected failed the assay for potency (all were subpotent) and a tenth sample failed the assay for endotoxin.8 If we acknowledge then that we could improve our compounding educational process, how should this be done? Again, drawing from the performance improvement literature, we need to identify best practices, standardize our processes, and check the results. Standards of practice have become increasingly clear; USP 797, which set the standards for compounding sterile products, details the validation of sterile compounding skills at 3 levels: high risk, medium risk, and low risk. All graduates of an accredited school of pharmacy should have successfully validated their skills at the level of low risk sterile compounding. USP 795 and the Pharmacy Compounding Accreditation Board have articulated standards and compliance indicators for non-sterile compounding practice. All graduates should be familiar not only with these standards but be able to demonstrate that they can properly prepare selected compounded products within a specified standard. While we can identify best practices in pharmacy practice, what are the academy's best practices? Which of these compounding skills should a new graduate possess, and what are the best ways to teach for a student to learn to compound and to retain an understanding of the significant principles of formulation, equipment selection and product preparation, and assessment to ensure patient safety? Should we count the number of lecture hours on parenteral products offered by each school of pharmacy, or ensure that the outcomes of the pharmaceutics courses include the ability to weigh and measure within the standard ± 5% error? I would submit to you that there is no substitute for quality laboratory education. The evidence we have so far suggests that we need to model the best practices identified by our practitioners in the laboratory, provide opportunities for students to practice their skills — practice, practice, practice — and finally require students to demonstrate competency in those key aspects of compounding that could put their future patients at risk.9-13 These are the obligations of pharmacy educators, and as we all strive to improve the quality of our educational programs, we have the opportunity to identify our own best practices and share them with the academy.

Serratia marcescens Infections and Outbreaks in Neonatal Intensive Care Units

Serratia marcescensis an important cause of hospital-acquired infections, especially in neonatal intensive care units (NICUs). this review analyzes clinical signs, risk factors, biotyping and sources of infection in newborns exhibited by this bacteria as well as the therapy which is commonly used and management. This review examines the reported cases of outbreaks of S. marcescensin NiCUs published in pubmed over the last 10 years. This report highlights the different prevention and control strategies employed in order to eradicate Serratia out breaks in NICUs, including all healthcare procedures such as hand washing, introduction of alcohol-based antiseptic gel, enhanced cleaning and disinfection of medical equipment and wards, use of single-patient medical instruments, cohorting of colonized and infected infants, periodic screening cultures, earliest discharge of the infants.

Outbreaks of Serratia marcescens in neonatal and pediatric intensive care units: Clinical aspects, risk factors and management

The following recommendations are derived from a systematic analysis of 34 Serratia marcescens outbreaks described in 27 publications from neonatal and pediatric intensive care units (NICU, PICU), in which genotyping methods were used to confirm or exclude clonality. The clinical observation of two or more temporally related cases of nosocomial S. marcescens infection should raise the suspicion of an outbreak, particularly in the NICU or PICU setting. Since colonized or infected patients represent the most important reservoir for cross transmission, hygienic barrier precautions (contact isolation/cohortation, the use of gloves and gowns in addition to strictly performed hand disinfection, enhanced environmental disinfection) should immediately be implemented and staff education given. Well-planned sampling of potential environmental sources should only be performed when these supervised barrier precautions do not result in containment of the outbreak. The current strategy of empiric antibiotic treatment should be reevaluated by a medical microbiologist or an infectious disease specialist. Empiric treatment of colonized children should use combination therapy informed by in vitro susceptibility data; in this context the high propensity of S. marcescens to cause meningitis and intracerebral abscess formation should be considered. In vitro susceptibility patterns do not reliably prove or exclude the clonality of the outbreak isolate. Genotyping of the isolates by pulse-field gel electrophoresis or PCR-based methods should be performed, but any interventions to interrupt further nosocomial spread should be carried out without waiting for the results.

Outbreak of Serratia marcescens in a neonatal intensive care unit: contaminated unmedicated liquid soap and risk factors

This study describes an outbreak of Serratia marcescens and its investigation and control in a neonatal intensive care unit (NICU). During a three-month period, five infants were colonised or infected by a single strain of S. marcescens. A case-control study, culture surveys and pulse-field gel electrophoresis analysis implicated a bottle soap dispenser as a reservoir of S. marcescens (P=0.032). Infants with S. marcescens colonisation or infection were also more likely to have been exposed to a central or percutaneous venous catheter (P=0.05) and had had longer exposure to endotracheal intubation (P=0.05). Soap dispensers are used in many hospitals and may be an unrecognised source of nosocomial infections. This potential source of infection could be reduced by using 'airless' dispensers which have no air intake for the distribution of soap. Prompt intervention and strict adherence to alcoholic hand disinfection were the key factors that led to the successful control of this outbreak.

Morphological and genetic analysis of three bacteriophages ofSerratia marcescensisolated from environmental water

Increases in multidrug-resistant strains of Serratia marcescens are of great concern in pediatrics, especially in neonatal intensive care units. In the search for bacteriophages to control infectious diseases caused by multidrug-resistant S. marcescens, three phages (KSP20, KSP90, and KSP100) were isolated from environmental water and were characterized morphologically and genetically. KSP20 and KSP90 belonged to morphotype A1 of the family Myoviridae, and KSP100 belonged to morphotype C3 of the family Podoviridae. Analysis of the DNA region coding virion proteins, together with their morphological features, indicated that KSP20, KSP90, and KSP100 were related to the P2-like phage (temperate), T4-type phage (virulent), and phiEco32 phage (virulent), respectively. Based on amino acid sequences of the major capsid protein, KSP90 formed a new branch with a Stenotrophomonas maltophilia phage, Smp14, in the T4-type phage phylogeny. Both Smp14 and phiEco32 have been reported as potential therapeutic phages. These results suggest that KSP90 and KSP100 may be candidate therapeutic phages to control S. marcescens infection.

Hand washing soap as a source of neonatal Serratia marcescens outbreak

To describe an outbreak of Serratia marcescens infections in a neonatal intensive care unit (NICU) and to report investigations and interventions having led to the cessation of the outbreak. Observational study of microbiological and epidemiological investigations realised during a S. marcescens outbreak between March and October 2006. Nine cases were observed in a 5 months period. A Serratia outbreak was therefore identified, and all the strains were compared by pulsed-field gel electrophoresis (PFGE). Data from medical notes were gathered retrospectively. Environmental samples were gathered prospectively. Four infants were colonized and five infants were infected by S. marcescens. PFGE revealed that three different strains were present. Seven of the nine babies were infected by only one of these strains. This same strain was found in a nonantimicrobial soap bottle (NAS) that could be the source of contamination. It is the first time that S. marcescens is found in a NAS during a neonatal nosocomial outbreak. Molecular analysis is a method of choice to compare different strains. Identification and elimination of the nosocomial source and adherence to the infection control policies are essential to succeed in the containment of a nosocomial epidemic.

Outbreak of Serratia marcescens Bloodstream and Central Nervous System Infections After Interventional Pain Management Procedures

To determine the cause of an outbreak of Serratia marcescens infections in patients after interventional pain management procedures at an outpatient pain clinic. We conducted a case-control study and collected clinical and environmental samples. We identified 5 culture-confirmed case-patients and 2 presumptive case-patients who had no bacteria recovered from cultures. The 7 case-patients were compared with 28 controls who underwent procedures at the same clinic but did not develop symptoms of infection. All confirmed case-patients had S. marcescens bloodstream infections; 2 had concurrent S. marcescens central nervous system infections. Case-patients were more likely than controls to have procedures that used contrast solution or entered the epidural or intervertebral disc space (P< or =0.01 for each). All S. marcescens clinical isolates were indistinguishable by pulsed-field gel electrophoresis. We did not isolate S. marcescens from medications or environmental samples; however, S. marcescens was shown to survive and grow in contrast solution that was experimentally contaminated for up to 30 days. Single-dose vials of medication, including contrast solution, were used for multiple procedures; multiple medications were accessed with a common needle and syringe. The findings of this investigation suggest contamination of a common medication, likely contrast solution, as the source of the outbreak. Practices, such as reusing single-dose medication vials and using a common needle and syringe to access multiple medications, could have led to contamination and propagation of S. marcescens and should be avoided in interventional pain management procedures.

Outbreak of Multidrug-Resistant Serratia marcescens Infection in a Neonatal Intensive Care Unit

Serratia marcescens causes healthcare-associated infections and significant morbidity and mortality in neonatal intensive care units (NICUs). We report the investigation and control of an outbreak of multidrug-resistant (MDR) S. marcescens infection at an NICU. An outbreak investigation and a case-control study were undertaken at a 36-bed NICU in a tertiary care hospital in Baltimore, Maryland, for the period from October 2004 through February 2005. The outbreak investigation included case identification, review of medical records, environmental cultures, patient surveillance cultures, personnel hand cultures, and pulsed-field gel electrophoresis (PFGE). The case-control study included case identification and review of medical records. Infection control measures were implemented. Eighteen NICU neonates had cultures that grew MDR S. marcescens during the study period. The case-control study included 16 patients with the outbreak strain or an unidentified strain of MDR S. marcescens and 32 control patients not infected and/or colonized with MDR S. marcescens, treated in the NICU for at least 48 hours during the study period. PFGE analysis identified a single strain of MDR S. marcescens that infected or colonized 15 patients. Two patients had unique strains, and 1 patient's isolate could not be subtyped. An unrelated MDR S. marcescens isolate was recovered from a sink drain. Exposure to inhalational therapy was an independent risk factor for MDR S. marcescens acquisition after adjusting for birth weight. Extensive investigation failed to reveal a point source for the outbreak. A single epidemic strain of MDR S. marcescens spread rapidly and threatened to become endemic in this NICU. Transient carriage on the hands of healthcare personnel or on respiratory care equipment was the likely mode of transmission. Cohorting patients and staff, at the cost of bed closures and additional personnel, interrupted transmission and halted the outbreak.

Hand Hygiene

Hand Hygiene