Biomedical subjects

S M Markowitz

Publications and source records attributed to S M Markowitz.

At least 37 records · Page 2Linked to original sources

PubMed1997

Adenosine-sensitive ventricular tachycardia: right ventricular abnormalities delineated by magnetic resonance imaging.

BACKGROUND: Adenosine-sensitive ventricular tachycardia (VT) is thought to be due to cAMP-mediated triggered activity. It typically originates from the RVOT and occurs in patients with apparently normal hearts. Using magnetic resonance imaging (MRI), we tested the hypothesis that adenosine-sensitive VT occurs in patients without structural heart disease. METHODS AND RESULTS: Fourteen patients (9 women; age, 47+/-19 years) presented with sustained VT (n=3), repetitive monomorphic VT (n=7), or both (n=4). VT terminated with adenosine in each patient and was sensitive to vagal maneuvers in 9 of 11 and verapamil in 10 of 12. VT originated from the right ventricular outflow tract in 10 patients, the right ventricular apex in 1, and the left ventricular septum in 3. Conventional studies included normal signal-averaged ECGs in 9 of 9, normal right ventricular echocardiography in 10 of 10, and normal left ventriculography and coronary angiography in 6 of 7. In contrast, MRI scans were abnormal in 10 of 14 patients. These abnormalities included focal thinning (6), fatty infiltration (4), and wall motion abnormalities (4) of the right ventricle. The most common site of MRI abnormalities was the right ventricular free wall, but there was a poor correlation between the site of MRI abnormalities and the origin of VT. Among 18 control patients without clinical heart disease, thinning of the right ventricular wall was noted in only 1 patient (patients versus control subjects, P=.0001). CONCLUSIONS: Patients with idiopathic adenosine-sensitive VT comprise a heterogeneous group as assessed by MRI, with 70% demonstrating mild structural abnormalities. However, it is unlikely that these findings are causally related to tachycardia, and the functional significance of these anatomic abnormalities is uncertain.

Adenosine↗

PubMed1997

Comparison of the in-vitro and in-vivo efficacy of FK037, vancomycin, imipenem and nafcillin against staphylococcal species.

The activity of methicillin, oxacillin, vancomycin, imipenem and FK037 against 106 isolates of staphylococci was assessed using a microbroth dilution method with low (10(5) cfu/mL) and high (10(7) cfu/mL) inoculum sizes. Overall, FK037, an oxime-type cephem antibiotic, was as active as imipenem, but less active than vancomycin (MIC90s 25, 25 and 6.25 mg/L, respectively) at the lower inoculum. Efficiency of plating experiments were also performed to characterize phenotypic expression of resistance to FK037, imipenem and methicillin. Five of 24 isolates and 18 of 24 isolates contained subpopulations resistant to FK037 and imipenem, respectively. In a rabbit model of endocarditis, FK037 was equally effective as other antibiotics tested in the treatment of methicillin-sensitive Staphylococcus aureus infection. In the treatment of endocarditis due to a homotypic methicillin-resistant S. aureus, FK037 and vancomycin were the most active antibiotics. The presence of subpopulations resistant to imipenem and FK037, as demonstrated by efficiency of plating and high inoculum MIC testing, did not correlate with antibiotic effectiveness in the rabbit model of endocarditis. Cultures of vegetation material following treatment with imipenem and FK037 demonstrated a lower frequency of organisms resistant to FK037 when compared with imipenem. Thus FK037 shows in-vitro and in-vivo activity against some methicillin-resistant staphylococcal species.

Animals↗

PubMed1997

Response of neurocardiac syncope to beta-blocker therapy: interaction between age and parasympathetic tone.

Beta-blockers are a first line therapy for neurocardiac syncope, but are not always effective. The purpose of this study was to determine whether differential autonomic responses to orthostasis predict the response of patients with neurocardiac syncope to beta-adrenergic blockade. We computed the RMS successive difference of the RR intervals (RMSSD: a measure of cardiac parasympathetic tone) during supine and upright phases of the initial tilt test in 28 patients with syncope and positive tilt tests who were treated with atenolol. Follow-up tilt testing was performed to assess the efficacy of the drug in preventing tilt induced neurocardiac syncope. RMSSD did not differ at baseline (supine) between those who did (n = 20) and did not (n = 8) respond to beta-blockade. However, withdrawal of parasympathetic tone in response to tilt varied inversely with age (r = -0.69; P < 0.01). Reduced age adjusted parasympathetic withdrawal during orthostasis was associated with a 47% versus 8% risk of beta-blockade failure (odds ratio = 11; P = 0.01). Patients with diminished age adjusted parasympathetic withdrawal during orthostatic stress are less likely to respond to beta-blocker therapy of neurocardiac syncope than their counterparts. This may reflect a correspondingly greater sympathetic response to orthostasis in these patients, but the mechanism for this interaction is undetermined.

Adrenergic beta-Antagonists↗

PubMed1997

Vasodepressor syncope due to subclinical myocardial ischemia.

INTRODUCTION: Vasodepressor syncope is a common cause of syncope, but the initiating event that triggers the vasodepressor response remains incompletely understood. Although ischemia due to acute right coronary occlusion may precipitate hypotension and bradycardia through the Bezold-Jarisch reflex, an ischemic precipitant for the common vasodepressor faint has not been previously identified. In the present study, we present evidence for a causal relationship between myocardial ischemia and vasodepressor syncope. METHODS AND RESULTS: Two patients referred for evaluation of syncope underwent upright tilt table testing with either ST segment monitoring, sestamibi scintigraphy and echocardiography during the tilt test, or coronary angiography. Both patients had positive tilt table tests during the control study. Patient 1 was documented to have reproducible ischemic ECG changes during atypical chest pressure induced by upright tilt, despite a normal coronary angiogram with ergonovine provocation. Subsequent tilt testing with simultaneous sestamibi perfusion imaging and echocardiography revealed reversible anterolateral hypoperfusion corresponding with anterolateral hypokinesis during upright tilt that preceded syncope. Ischemic ECG changes during incremental rapid atrial pacing further suggested ischemia on the basis of microvascular disease. Follow-up tilt testing on verapamil was negative. Patient 2 developed ischemic ECG changes during the recovery phase of an exercise stress test, which was followed by a vasodepressor response and frank syncope. Coronary angiography revealed a 90% distal right coronary artery stenosis that was successfully dilated, after which follow-up tilt table testing off all other medication was negative. CONCLUSIONS: These two cases illustrate a previously unrecognized causality between myocardial ischemia and clinical vasodepressor syncope, and demonstrate that subtle manifestations of myocardial ischemia, associated with either atypical angina or silent ischemia, can provoke syncope.

Cardiac Pacing, Artificial↗

PubMed1997

Mechanisms of idiopathic left ventricular tachycardia.

Idiopathic left ventricular tachycardia (ILVT) differs from idiopathic right ventricular outflow tract (RVOT) tachycardia with respect to mechanism and pharmacologic sensitivity. ILVT can be categorized into three subgroups. The most prevalent form, verapamil-sensitive intrafascicular tachycardia, originates in the region of left posterior fascicle of the left bundle. This tachycardia is adenosine insensitive, demonstrates entrainment, and is thought to be due to reentry. The tachycardia is most often ablated in the region of the posteroinferior interventricular septum. A second type of ILVT is a form analogous to adenosine-sensitive RVOT tachycardia. This tachycardia appears to originate from deep within the interventricular septum and exits from the left side of the septum. This form of VT also responds to verapamil and is thought to be due to cAMP-mediated triggered activity. A third form of ILVT is propranolol sensitive. It is neither or initiated or terminated by programmed stimulation, does not terminate with verapamil, and is transiently suppressed by adenosine, responses consistent with an automatic mechanism. Recognition of the heterogeneity of ILVT and its unique characteristics should facilitate appropriate diagnosis and therapy in this group of patients.

Humans↗

PubMed1996

Mechanism of ventricular rate control after radiofrequency modification of atrioventricular conduction in patients with atrial fibrillation.

BACKGROUND: Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification. METHODS AND RESULTS: Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 micrograms/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356 +/- 72 versus 371 +/- 78 ms versus 432 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/- 56 ms, P < .0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485 +/- 88 versus 533 +/- 116 ms versus 637 +/- 142 ms for mean RR, P < .0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion. CONCLUSIONS: Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.

Adult↗

PubMed1996

Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia.

OBJECTIVES: This study sought to present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may participate in typical AV node reentry. BACKGROUND: Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the preferred therapeutic approach in patients with AV node reentrant tachycardia. Despite the success achieved with this approach, electrophysiologic changes consistent with fast pathway ablation are occasionally observed. One potential explanation is the presence of an aberrant posterior fast pathway. METHODS: The location of fast and slow AV node pathways was determined by atrial activation mapping along the tricuspid valve annulus during tachycardia and was further confirmed by the effect of radiofrequency catheter ablation. RESULTS: Seven patients with AV node reentrant tachycardia had evidence of a posterior fast pathway near the coronary sinus os. Abolition of anterograde and retrograde fast pathway conduction followed radiofrequency ablation in the posteroseptal region in six patients. Consistent with fast pathway ablation, the AH interval increased from 70 +/- 24 to 195 +/- 35 ms (mean +/- SD), and tachycardia was no longer inducible. Selective slow pathway ablation was performed in one other patient with a posterior fast pathway. CONCLUSIONS: Functionally fast AV node pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed. These data delineate the limitation of an anatomically guided slow pathway ablative approach and emphasize the importance of detailed mapping and localization of the retrograde fast pathway exit site before ablation. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV block, complicating posteroseptal ablation in patients with AV node reentry.

Adult↗

PubMed1996

The effect of respirator training on the ability of healthcare workers to pass a qualitative fit test.

OBJECTIVES: To determine the effect of different methods of training on the ability of hospital workers to wear respirators and pass a qualitative fit test, and to compare the direct cost of the training. DESIGN: 179 hospital employees were recruited for study and were stratified into three groups based on the type of training they received in the use of respirators. Employees in Group A received one-on-one training by the hospital's industrial hygienist and were fit tested as part of this training. Employees in Group B received classroom instruction and demonstration by infection control nurses in the proper use of respirators, but were not fit tested as part of training. Employees in Group C received no formal training. Each participant in our study underwent a subsequent qualitative fit test using irritant smoke to check for the employee's ability to adjust correctly the fit and seal of the respirator. The direct cost of each method of training was determined by accounting for the cost of trainers and the cost of employee-hours lost during training. SETTING: 775-bed Veterans' Affairs hospital. RESULTS: 94% of Group A participants (49 of 52) passed the qualitative fit test, compared to 91% of Group B participants (58 of 64) and 79% of Group C participants (50 of 63; P = .036, 2 x 3 chi-square). Group A had a significantly higher pass rate than Group C (P = .043), but Group B did not differ significantly from Group A or Group C. Location or professional status did not affect pass rate, but prior experience wearing respirators did. When the study groups were compared after stratifying for prior experience, we found no difference in pass rates, except when Groups A and B (those with any training) were combined and compared with Group C (107 of 116 versus 50 of 63, P = .05, Mantel-Haenszel chi-square). We estimate that the method of training involving individual instruction followed by fit testing took 20 minutes per employee to complete, compared to 10 minutes per six employee class for the method of classroom demonstration. The difference in direct cost between the two methods, applied to the training of 1,200 employees at our hospital, would be approximately $19,000 per year. CONCLUSION: Our study indicates that training in the proper use of respirators is important, but the method of training may not be, as the two methods we evaluated were nearly equivalent in their pass rates on fit testing (94% versus 91%). Fit testing as part of training may have enhanced the performance of our participants marginally, but was more time consuming and accounted for most of the excess cost.

Chi-Square Distribution↗

PubMed1996

Idiopathic right ventricular outflow tract tachycardia: a clinical approach.

Right ventricular outflow tract (RVOT) tachycardia is the most common form of idiopathic ventricular tachycardia (VT). Phenotypically, RVOT tachycardia segregates into two predominant forms, one characterized by repetitive monomorphic nonsustained VT and the other by paroxysmal exercise induced sustained VT. There is an increasing body of evidence to support the concept that both forms of tachycardia reflect disparate clinical manifestations of an identical cellular mechanism (i.e., cAMP-mediated triggered activity), which is identified clinically by the tachycardia's sensitivity to adenosine. The clinical characteristics, natural history, and approaches to therapy of RVOT tachycardia are delineated herein.

Adenosine↗

PubMed1996

Adenosine-sensitive ventricular tachycardia: a conceptual approach.

Idiopathic ventricular tachycardia (VT) is a term that refers to tachycardia that arises from ventricles devoid of apparent structural abnormalities. This form of VT is now recognized to be related to several distinct entities and includes a reentrant form typically located in the region of the left posterior fascicle, an automatic form that may originate from either ventricle, and a form that originates from the right ventricular outflow tract. This last type can account for up to 80% of cases of idiopathic VT and with few exceptions can be further subdivided into repetitive monomorphic VT and paroxysmal stress-induced VT. Evidence has accumulated suggesting that both forms of VT are related to cAMP-mediated triggered activity. The experimental underpinnings of this conclusion as well as the clinical characteristics of this form of idiopathic VT are elucidated in this review.

Adenosine↗

PubMed1996

Chromosomal DNA restriction endonuclease digestion patterns of beta-lactamase-producing Enterococcus faecalis isolates collected from a single hospital over a 7-year period.

Twenty-three beta-lactamase (beta-lac)-producing, highly gentamicin-resistant Enterococcus faecalis isolates collected over a 7-year period from the same hospital were examined by pulsed-field gel electrophoresis of SmaI-digested genomic DNA. The beta-lac+ isolates appeared to form a single clonal group, which had been previously designated the mid-Atlantic pattern. Eleven variations of the mid-Atlantic clone, differing by one to six bands, were identified; some of the changes were likely due to plasmid bands. However, a number of isolates had indistinguishable patterns, including some recovered over a 4-year period. There was a surprising lack of movement of the beta-lac determinant to other strains, although this trait was transferable in vitro by conjugation. We conclude that a single clone (the mid-Atlantic clone) of beta-lac+ E. faecalis has remained endemic in this hospital for at least 7 years. The reason(s) for the apparent lack of spread to other strains of E. faecalis is unknown.

Anti-Bacterial Agents↗

PubMed1995

Do protective devices prevent needlestick injuries among health care workers?

OBJECTIVES: To determine the effectiveness and direct of two protective devices-a shielded 3 ml safety syringe (Safety-Lok; Becton Dickinson and Co., Becton Dickinson Division, Franklin Lakes, N.J.) and the components of a needleless IV system (InterLink; Baxter Healthcare Corp., Deerfield, Ill.)--in preventing needlestick injuries to health care workers. DESIGN: Twelve-month prospective, controlled, before-and-after trial with a standardized questionnaire to monitor needlestick injury rates. SETTING: Six hospital inpatient units, consisting of three medical units, two surgical units (all of which were similar in patient census, acuity, and frequency of needlesticks), and a surgical-trauma intensive care unit, at a 900-bed urban university medical center. PARTICIPANTS: All nursing personnel, including registered nurses, licensed practical nurses, nursing aides, and students, as well as medical teams consisting of an attending physician, resident physician, interns, and medical students on the study units. INTERVENTION: After a 6-month prospective surveillance period, the protective devices were randomly introduced to four of the chosen study units and to the surgical-trauma intensive care unit. RESULTS: Forty-seven needlesticks were reported throughout the entire study period, 33 in the 6 months before and 14 in the 6 months after the introduction of the protective devices. Nursing staff members who were using hollow-bore needles and manipulating intravenous lines accounted for the greatest number of needlestick injuries in the pre-intervention period. The overall rate of needlestick injury was reduced by 61%, from 0.785 to 0.303 needlestick injuries per 1000 health care worker-days after the introduction of the protective devices (relative risk = 1.958; 95% confidence interval, 1.012 to 3.790; p = 0.046). Needlestick injury rates associated with intravenous line manipulation, procedures with 3 ml syringes, and sharps disposal were reduced by 50%; however, reductions in these subcategories were not statistically significant. No seroconversions to HIV-1 or hepatitis B virus seropositivity occurred among those with needlestick injuries. The direct cost for each needlestick prevented was $789. CONCLUSIONS: Despite an overall reduction in needlestick injury rates, no statistically significant reductions could be directly attributed to the protective devices. These devices are associated with a significant increase in cost compared with conventional devices. Further studies must be concurrently controlled to establish the effectiveness of these devices.

Direct Service Costs↗

PubMed1995

AV nodal-His-Purkinje reentry: a novel form of tachycardia.

INTRODUCTION: Bundle branch reentry (BBR) typically occurs in patients with dilated cardiomyopathy and infra-Hisian conduction system disease. The macroreentrant circuit of BBR is confined to the His-Purkinje system (HPS) and ventricular myocardium. As such, the atrioventricular (AV) node plays no role in the tachycardia circuit. METHODS AND RESULTS: In the present study, we identified a novel form of wide complex tachycardia in a patient with coronary disease and severe aortic regurgitation. The tachycardia morphology was right bundle branch block with a left superior axis. Ventriculoatrial block was present during tachycardia. An unusual feature of this rhythm was two sequential His-bundle deflections (H and H') for each ventricular beat of tachycardia. The H'V interval was identical to the HV interval during supraventricular rhythm. Changes in the ventricular cycle length (VV) preceded changes in the HH interval, consistent with retrograde activation of the first His-bundle deflection. Changes in the H'H' interval preceded changes in the VV interval, consistent with anterograde activation of the second His-bundle deflection. Tachycardia could be terminated with ventricular extrastimuli that did not capture the proximal HPS as well as with ventricular extrastimuli that advanced the His deflection, consistent with block in the HPS and in the AV node, respectively. Reproducible termination of the tachycardia following the first His deflection was demonstrated with adenosine, consistent with an upper pivot in the AV node. CONCLUSIONS: We have identified a new form of reentrant tachycardia in which the AV node, HPS, and ventricular myocardium each obligatorily participates in the tachycardia circuit, with the left posterior fascicle and right bundle functioning as the anterograde and retrograde limbs, respectively. Unlike BBR, however, the His bundle is activated twice as the wavefront pivots in the AV node. This model requires longitudinal dissociation at the levels of the AV node and His bundle.

Aged↗

PubMed1993

Comparison of ampicillin-sulbactam with vancomycin for treatment of experimental endocarditis due to a beta-lactamase-producing, highly gentamicin-resistant isolate of Enterococcus faecalis.

Increasing antibiotic resistance in the enterococci, including the capacity for beta-lactamase production and the development of high-level aminoglycoside resistance, has complicated the treatment of serious enterococcal infections, which often require synergistic antibiotic combinations for cure. We utilized the rabbit model of aortic valve endocarditis to investigate the effects of various antibiotics, alone and in combination, against a multiply antibiotic-resistant isolate of Enterococcus faecalis. Female New Zealand White rabbits were infected with either a beta-lactamase-producing, gentamicin-resistant isolate of E. faecalis or a non-beta-lactamase-producing, aminoglycoside-susceptible isolate, and the mean log10 CFU per gram of vegetation were determined. The most active agents were low-dose ampicillin-sulbactam (200 mg/kg of body weight per day), high-dose ampicillin-sulbactam (400 mg/kg of body weight per day), and vancomycin (150 mg/kg of body weight per day), which reduced the titers of bacteria by 2.27, 2.76, and 2.85 log10 (CFU/g, respectively, compared with controls. While ampicillin-sulbactam and vancomycin were equally efficacious in reducing titers of bacteria in vegetations, no animals were cured (defined as < 2 log10 CFU/g of vegetation) by either agent, whether treatment was continued for 3 or 7 days. The addition of gentamicin was not associated with increased killing in rabbits infected with the aminoglycoside-resistant isolate. Both high-dose ampicillin-sulbactam and vancomycin regimens demonstrated significant, continued reduction in bacterial titers with the longer periods of treatment (P < or = 0.05); 7-day treatment with high-dose ampicillin-sulbactam produced a greater reduction in bacterial titers in vegetation than 7-day treatment with vancomycin (P < or = 0.05). We conclude that ampicillin-sulbactam and vancomycin are equally effective in the treatment of experimental endocarditis due to beta-lactamase-producing, highly gentamicin-resistant E. faecalis. The optimum therapy for such infections in humans is not known.

Ampicillin↗

PubMed1992

Infections due to beta-lactamase-producing, high-level gentamicin-resistant Enterococcus faecalis.

OBJECTIVE: To investigate the risk factors, clinical features, molecular epidemiology, and treatment outcomes associated with an outbreak of infections due to beta-lactamase-producing, high-level gentamicin-resistant Enterococcus faecalis. DESIGN: Case-control and molecular genetics study. SETTING: Tertiary care Veterans Affairs hospital. PATIENTS: Sixty-five patients infected or colonized with beta-lactamase-producing high-level gentamicin-resistant E. faecalis (case patients) were matched and compared with 65 randomly selected patients infected or colonized with beta-lactamase-negative, gentamicin-susceptible E. faecalis. MEASUREMENTS AND MAIN RESULTS: During the 20-month study period, 124 of 1506 isolates (8.2%) of E. faecalis from 70 patients were found to produce beta-lactamase. Univariate analysis showed older age, higher APACHE II score, nosocomial acquisition, recent surgical procedure, total parenteral nutrition, and antibiotic treatment to be significantly associated with the acquisition of beta-lactamase-producing, high-level gentamicin-resistant E. faecalis. A multivariate analysis, done using stepwise multiple logistic regressions, showed that only two variables remained significant: an APACHE II score greater than 6 (odds ratio, 9.5; 95% CI, 4.4 to 20.3) and antibiotic treatment (odds ratio, 10.2; CI, 4.5 to 23.2). The mortality rate for case patients was 7.7% (5 of 65 patients; CI, 1.2% to 14.2%); no control patient died. Of 23 infections occurring in case patients, 13 were treated with "inappropriate" antibiotics (regimens that included a beta-lactamase-unstable antibiotic); 2 patients improved and 11 had complete resolution of disease. "Appropriate" treatments (regimens that included a beta-lactamase-stable antibiotic) were used in 10 patients; 5 of 10 infections were fatal. Restriction enzyme digests of total chromosomal DNA showed nearly identical patterns for selected isolates of beta-lactamase-producing, high-level gentamicin-resistant E. faecalis, suggesting dissemination through the hospital of a single strain of E. faecalis. CONCLUSIONS: Fatal infections were observed despite treatment with beta-lactamase-stable antibiotics. The risk for infection or colonization with beta-lactamase-producing, high-level gentamicin-resistant E. faecalis was strongly associated with severe underlying disease (acute physiology and chronic health evaluation [APACHE] II score, greater than 6) and previous antibiotic treatment. These results may be useful in targeting high-risk patients for infection-control interventions.

Case-Control Studies↗

PubMed1992

Isolation of a beta-lactamase-producing, aminoglycoside-resistant strain of Enterococcus faecium.

Beta-Lactamase-producing, aminoglycoside-resistant strains of Enterococcus faecalis have been isolated from different geographic areas and are endemic at our institution. We report the isolation of a beta-lactamase-producing, aminoglycoside-resistant strain of E. faecium. The beta-lactamase was plasmid mediated and transferable with high frequency into a plasmid-free E. faecalis recipient strain. MICs suggested that the E. faecium strain also contained intrinsic (chromosomal) resistance to penicillins.

Aminoglycosides↗

PubMed1992

Molecular typing of ampicillin-resistant, non-beta-lactamase-producing Enterococcus faecium isolates from diverse geographic areas.

Molecular typing methods were compared by using 66 ampicillin-resistant, non-beta-lactamase-producing Enterococcus faecium clinical isolates from diverse geographic areas. Whole-plasmid analysis, restriction enzyme analysis of plasmid DNA with EcoRI and HindIII, and contour-clamped homogeneous electric field electrophoresis with digestion by SmaI and ApaI were performed on all isolates. Whole-plasmid analysis identified 47 different groups. Restriction enzyme analysis of plasmid DNA identified 50 groups when EcoRI was used and 51 groups when HindIII was used. Results with EcoRI and HindIII differed in 9 of 66 isolates. Grouping results with whole-plasmid analysis differed from results of restriction enzyme analysis of plasmid DNA (combining EcoRI and HindIII) in 20 of 66 isolates. Contour-clamped homogeneous electric field electrophoresis identified 46 groups when SmaI was used and 44 groups when ApaI was used. Results with SmaI and ApaI differed in 3 of 66 isolates. Grouping results with contour-clamped homogeneous electric field electrophoresis (combining SmaI and ApaI) differed from results of restriction enzyme analysis of plasmid DNA (combining EcoRI and HindIII) in 17 of 66 isolates. The combined use of whole-plasmid analysis, restriction enzyme analysis of plasmid DNA with two enzymes, and contour-clamped homogeneous electric field electrophoresis with two restriction enzymes should be considered when E. faecium is typed for epidemiologic investigation.

Ampicillin Resistance↗

PubMed1991

Are universal precautions effective in reducing the number of occupational exposures among health care workers? A prospective study of physicians on a medical service.

Using a daily questionnaire, we prospectively studied 277 physicians from two hospital medical services for incidents of exposure to blood and body fluids and barrier use before and after the implementation of universal precautions. We found that implementation significantly increased the frequency of barrier use during exposure incidents from 54% before implementation to 73% after implementation of universal precautions. Implementation led to a decrease in the number of exposure incidents that resulted in direct contact with blood and body fluids (actual exposures), from 5.07 to 2.66 exposures per physician per patient care month, and to an increase in averted exposures in which direct contact was prevented by the use of barrier devices, from 3.41 exposures per patient care month before implementation to 5.90 exposures per patient care month after implementation. Implementation affected neither the types of body fluid or procedures involved nor the overall rate of exposure incidents (8.5 per patient care month) but, through an increase in barrier use, it did prevent direct contact with blood and body fluids and thus converted what would have been an actual exposure into an averted one. We conclude that universal precautions were effective in reducing the risk of occupational exposures among physicians on a medical service.

Body Fluids↗