Catherine Nathan

Epidemiology of colonisation of patients and environment with vancomycin-resistant enterococci

BACKGROUND Vancomycin-resistant enterococci (VRE) have emerged as nosocomial pathogens during the past 5 years, but little is known about the epidemiology of VRE. We investigated colonisation of patients and environmental contamination with VRE in an endemic setting to assess the importance of different sources of colonisation. METHODS Between April 12, and May 29, 1995, cultures from body sites (rectum, groin, arm, oropharynx, trachea, and stomach) and from environmental surfaces (bedrails, drawsheet, blood-pressure cuff, urine containers, and enteral feed) were obtained daily from all newly admitted ventilated patients in our medical intensive-care unit (MICU). Rectal cultures were obtained from all non-ventilated patients in the MICU. Strain types of VRE were determined by pulsed-field gel electrophoresis. FINDINGS There were 97 admissions of 92 patients, of whom 38 required mechanical ventilation. Colonisation with VRE on admission was more common in ventilated than in non-ventilated patients (nine [24%] vs three [6%], p < 0.05). Of the nine ventilated patients colonised with VRE on admission, one acquired a new strain of VRE in the MICU. Of the 29 ventilated patients who were not colonised with VRE on admission, 12 (41%) acquired VRE in the MICU. The median time to acquisition of VRE was 5 days (interquartile range 3-8). Of the 13 ventilated patients who acquired VRE, 11 (85%) were colonised with VRE by cross-colonisation. VRE were isolated from 157 (12%) of 1294 environmental cultures. The rooms of 13 patients were contaminated with VRE, but only three (23%) of these patients subsequently acquired colonisation with VRE. Pulsed-field gel electrophoresis of 262 isolates showed 20 unique strain types of VRE. INTERPRETATION Frequent colonisation with VRE on MICU admission and subsequent cross-colonisation are important factors in the endemic spread of VRE. Persistent VRE colonisation in the gastrointestinal tract and on the skin, the presence of multiple-strain types of VRE, and environmental contamination may all contribute to the spread of VRE.

Pseudomonas in the sinks in an intensive care unit: relation to patients.

Sink drains in a medical-surgical intensive care unit (ICU) were cultured during six consecutive weeks as part of a seven month prospective study of acquisition of Pseudomonas aeruginosa by ICU patients. Isolates were typed serologically and by aminoglycoside and chlorhexidine susceptibility patterns. All 11 sinks contained multiple strains of P aeruginosa; some strains persisted for weeks while others were isolated once. Of the sink isolates 56% had high level resistance to gentamicin and tobramycin whereas none of the strains found in patients. In sink isolates chlorhexidine resistance correlated with aminoglycoside resistance and with the presence of a chlorhexidine dispenser at a sink. The sequence of recovery of phenotypically similar isolates suggested that sinks were the source of at most two acquisitions of P aeruginosa by patients during the six weeks. Our study confirms that sinks may be reservoirs for large numbers of highly resistant P aeruginosa but are rarely the source of organisms colonising patients in our ICU.

The effect of glucagon-like peptide 2 on intestinal permeability and bacterial translocation in acute necrotizing pancreatitis

BACKGROUND Acute pancreatitis (AP) initiates a generalized inflammatory response that increases intestinal permeability and promotes bacterial translocation (BT). Impairment of the intestinal epithelial barrier is known to promote BT. Glucagon-like peptide 2 (GLP-2), a 33 residue peptide hormone, is a key regulator of the intestinal mucosa by stimulating epithelial growth. The purpose of this study was to determine whether GLP-2 decreases intestinal permeability and BT in AP. METHODS To examine whether GLP-2 can decrease intestinal permeability and thereby decrease BT in acute necrotizing pancreatitis, 34 male Sprague-Dawley rats (200 to 300 g) were studied. AP was induced in group I and group II by pressure injection of 3% taurocholate and trypsin into the common biliopancreatic duct (1 mg/kg of body weight). The potent analog to GLP-2 called ALX-0600 was utilized. Group I rats received GLP-2 analog (0.1 mg/kg, SQ, BID) and group II rats received a similar volume of normal saline as a placebo postoperatively for 3 days. Group III and group IV received GLP-2 analog and placebo, respectively. At 72 hours postoperatively, blood was drawn for culture of gram-negative organisms. Specimens from mesenteric lymph nodes (MLN), pancreas and peritoneum were harvested for culture of gram-negative bacteria. Intestinal resistance as defined by Ohms law was determined using a modified Ussing chamber to measure transepithelial current at a fixed voltage. A point scoring system for five histologic features that include intestinal edema, inflammatory cellular infiltration, fat necrosis, parenchymal necrosis, and hemorrhage was used to evaluate the severity of pancreatitis. Specimens from MLN, pancreas, jejunum, and ileum were taken for pathology. RESULTS All group I and group II rats had AP. The average transepithelial resistance in group I was 82.8 Omega/cm(2) compared with 55.9 Omega/cm(2) in group II (P <0.01). Gram-negative BT to MLN, pancreas, and peritoneum was 80%, 0%, and 0%, respectively in group I compared with 100%, 30%, and 20% translocation in group II. CONCLUSION GLP-2 treatment significantly decreases intestinal permeability in acute pancreatitis.

Comparison of Routine Glove Use and Contact-Isolation Precautions to Prevent Transmission of Multidrug-Resistant Bacteria in a Long-Term Care Facility

Objectives: To compare routine glove use by healthcare workers for all residents, without use of contact‐isolation precautions, with contact‐isolation precautions for the care of residents who had vancomycin‐resistant enterococci or methicillin‐resistant Staphylococcus aureus isolated from a clinical culture

Structural and phenotypic varieties of gentamicin resistance plasmids in hospital strains of Staphylococcus aureus and coagulase-negative staphylococci.

We previously described a neonatal nursery epidemic of infections caused by a single strain of Staphylococcus aureus bearing a gentamicin resistance plasmid (Vogel et al., Antimicrob. Agents Chemother. 13:466-472, 1978). The same plasmid was present in two isolates of Staphylococcus epidermidis from the patients in this nursery and was transferable interspecifically from either S. aureus or S. epidermidis. During the ensuing 3 years, in the absence of further epidemics, we collected 162 gentamicin-resistant strains of S. aureus and coagulase-negative staphylococci from patients distributed throughout our hospital. Gentamicin resistance plasmids obtained from 41 representative S. aureus and coagulase-negative staphylococcal strains differed as determined by phenotypic and molecular analyses from the plasmid in the neonatal nursery epidemic. Nevertheless, these plasmids were structurally related to each other and to the plasmid of the original epidemic. Our results suggest an evolutionary relationship among these plasmids and support the hypothesis of a genetic reservoir of gentamicin resistance in coagulase-negative staphylococci transferable to S. aureus. Images

External sources of vancomycin-resistant enterococci for intensive care units

OBJECTIVE The incidence of colonization and infection with vancomycin-resistant enterococci (VRE) has increased dramatically in the last 5 yrs, especially in intensive care units (ICUs). We studied VRE-colonization in patients on admission to a medical ICU (MICU) where VRE colonization is endemic. DESIGN Prospective, descriptive analysis. SETTING An MICU of a public hospital. PATIENTS Three hundred and one consecutively admitted patients. MEASUREMENTS AND MAIN RESULTS Rectal swabs were obtained on admission from all patients. VRE isolates from all colonized patients were genetically fingerprinted by pulsed-field gel-electrophoresis (PFGE). Forty-three (14%) of 301 patients were colonized with VRE on MICU admission. Three (7%) of these 43 patients were admitted directly from the community without prior hospital contact. Risk of colonization on admission was related to the length of stay in the hospital before MICU-admission (odds ratio 4.65 for patients with a stay of at least 3 days) and previous in-hospital use of antibiotics. Of 22 VRE PFGE strain types recognized in the MICU during the study period, four (18%) were introduced by patients admitted directly from the community and ten (45%) were introduced by patients admitted from other hospital wards. CONCLUSIONS These results show that although ICUs are considered epicenters for antibiotic resistance, sources extraneous to our MICU (e.g., other wards) contributed the majority of VRE strain types in the unit.

Gram-negative bacilli in human milk feedings: Quantitation and clinical consequences for premature infants

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In Vitro Comparison of Netilmicin, a Semisynthetic Derivative of Sisomicin, and Four Other Aminoglycoside Antibiotics

One hundred isolates of Pseudomonas and Enterobacteriaceae, of which 85 were chosen because of their resistance to gentamicin or amikacin, were tested for susceptibility to netilmicin (SCH 20569), a new semisynthetic derivative of sisomicin, and to four other aminoglycosides. Tests were performed in Mueller-Hinton agar and, with 43 of these isolates, also in Mueller-Hinton broth. Most isolates of Escherichia coli, Klebsiella, Enterobacter, Citrobacter, and Serratia that were gentamicin resistant proved to be susceptible to netilmicin and amikacin. Tests of representative isolates of this group showed that they owed their resistance to the production of aminoglycoside-adenylylating enzymes. Four isolates of Serratia, detected by their resistance to amikacin, were also highly resistant to netilmicin but were susceptible to gentamicin. These isolates produced aminoglycoside-acetylating enzymes. Gentamicin-resistant Proteus and Providencia were, in general, highly resistant to netilmicin but were susceptible to amikacin. These isolates also produced aminoglycoside-acetylating enzymes. Most gentamicin-resistant strains of Pseudomonas were resistant to netilmicin, either by enzymatic aminoglycoside modification or by other undefined mechanisms. Thus, like amikacin, netilmicin extends the aminoglycoside susceptibility pattern of Enterobacteriaceae to include gentamicin-resistant isolates that produce aminoglycoside-adenylylating enzymes. It is ineffective against strains, some of them susceptible to amikacin, gentamicin, or tobramycin, that produce aminoglycoside-acetylating enzymes. Images

Difference in the incidence of Clostridium difficile among patients infected with human immunodeficiency virus admitted to a public hospital and a private hospital

OBJECTIVE To compare the occurrence of Clostridium difficile among inpatients infected with human immunodeficiency virus (HIV) in two different hospitals. DESIGN Prospective, observational study. SETTING Specialized HIV inpatient units. PATIENTS HIV-infected inpatients at Cook County Hospital (CCH) and Rush Presbyterian St. Lukes Medical Center (RPSLMC). INTERVENTIONS A clinical and epidemiologic assessment of patient risk factors for C. difficile was performed. C. difficile isolates found on stool, rectal, and environmental cultures were typed by pulsed-field gel electrophoresis. RESULTS Twenty-seven percent of patients admitted to CCH versus 4% of patients admitted to RPSLMC had positive cultures for C. difficile (P = .001). At CCH, 14.7% of environmental cultures were positive versus 2.9% at RPSLMC (P = .002). Risk factors for C. difficile acquisition included hospitalization at CCH, more severe HIV, use of acyclovir and H2-blockers, and longer hospital stay. Patients admitted to CCH were taking more antibiotics, had longer hospital stays, and more frequently had a history of C. difficile infection. During the study, two strains (CD1A and CD4) extensively contaminated the CCH environment. However, only CD1A caused an outbreak. CONCLUSIONS The C. difficile acquisition rate at CCH was sevenfold higher than that at RPSLMC, and CCH had a more contaminated environment. Differences in patient acquisition rates likely reflect a greater prevalence of traditional C. difficile risk factors and a concurrent outbreak at CCH. Although two strains heavily contaminated the environment at CCH, only one caused an outbreak, suggesting that factors other than the environment are important in initiating C. difficile outbreaks.

The effect of interleukin-6 on bacterial translocation in acute canine pancreatitis

SummaryBackground. Bacterial translocation from the gut to mesenteric lymph nodes and other extraintestinal sites is an important source of infection in acute pancreatitis. Impaired host immunity is known to promote bacterial translocation. Interleukin-6 (IL-6) is a multifunctional cytokine that regulates the immune response, acute phase reaction, and hematopoiesis. Methods. Twenty-four mongrel dogs (18–29 kg) were studied in four equal groups. In Groups I and II, acute pancreatitis was induced by direct pressure injection of 4% taurocholate and trypsin into the pancreatic duct at laparotomy. Groups III and IV had only laparotomy. Group I and III dogs were given IL-6 (50 µg/kg/d, sq) daily starting 24 h after operation and Group II and IV dogs received an equal volume of saline administered at similar time. All animals had blood drawn for culture, complete blood count (CBC), platelets, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and amylase on d 0, 1, 4, and 7. On d 7, mesenteric lymph nodes (MLN), spleen, liver, pancreas, and cecum were harvested for pathology study and for cultures of aerobic and anaerobic bacteria. Quantitative cecal cultures of aerobic and anaerobic bacteria were obtained. Results. All Group I and Group II dogs had severe pancreatitis. The increase of plasma CRP in Group I was sustained throughout treatment (1.3±0.3 on d 0 vs 3.1±0.3*, 3.0±0.3*, and 2.9±0.3* and d 1,4, and 7, respectively). Plasma CRP was increased in Group II on d 1 and d 4 (1.3±0.3 mg/dL on d 0 vs 3.6±0.3* mg/dL on d 1, and 3.1±0.3* on d 4, *p<0.05). There were no differences in white blood cell (WBC) count, differential, platelets, and ESR between Groups I and II. Bacterial translocation to MLN was lower in Group I (1/6) than in Group II (6/6) (p<0.05). All 6 dogs in Group II had bacterial spread to distant sites compared to 2 of 6 dogs in Group I (p=0.066). Both MLN and other distant organ cultures were negative in Group III and only 1 of 6 MLN cultures was positive in Group IV.Conclusions. IL-6 treatment decreases bacterial translocation to MLN and may be beneficial in reducing septic complications in acute pancreatitis.