During the period July 1983 through December 1984, aminoglycoside-resistant Acinetobacter calcoaceticus var anitratus (ACA) were isolated from 98 patients in a university hospital. Eighty-seven percent of patients (85/98) acquired aminoglycoside-resistant ACA in the intensive care unit (ICU) and 92% (90198) of all initial isolates were from sputum. ICU patients with respiratory colonization/infection with aminoglycoside-resistant ACA were compared with matched ICU controls with other gram-negative rods in sputum. Compared with controls, the duration of ICU stay prior to colonization/infection with aminoglycoside-resistant ACA was significantly longer for cases (14.7 days υ 5.9 days, P = 0.002). Although exposures to devices and procedures were not significantly different for the two groups, cases received respiratory therapy significantly longer than did controls (14.7 days υ 6.6 days, P = 0.006). Prior to isolation of aminoglycoside-resistant ACA in sputum, cases received more cephalosporins than did controls (1.9 υ 1.2, P = 0.018); aminoglycoside usage in the two groups was comparable but cases tended to have received aminoglycoside for longer durations before colonization/infection than had controls (9.0 days υ 6.1 days, P = 0.08). Following sputum isolation of ACA, 6 of 22 cases developed ACA bacteremia compared with bacteremia in 2 of 22 controls. We conclude that factors predisposing to colonization/infection with aminoglycoside-resistant ACA were extended ICU care, prolonged respiratory therapy, and prior therapy with cephalosporins and aminoglycoside. In addition, ACA may be a more common cause of secondary bacteremia than previously appreciated.

During the period July 1983 through December 1984, aminoglycoside-resistant Acinetobacter calcoaceticus var anitratus (ACA) were isolated from 98 patients in a university hospital. Eighty-seven percent of patients (85/98) acquired aminoglycoside-resistant ACA in the intensive care unit (ICU) and 92% (90198) of all initial isolates were from sputum. ICU patients with respiratory colonization/infection with aminoglycoside-resistant ACA were compared with matched ICU controls with other gram-negative rods in sputum. Compared with controls, the duration of ICU stay prior to colonization/infection with aminoglycoside-resistant ACA was significantly longer for cases (14.7 days υ 5.9 days, P = 0.002). Although exposures to devices and procedures were not significantly different for the two groups, cases received respiratory therapy significantly longer than did controls (14.7 days υ 6.6 days, P = 0.006). Prior to isolation of aminoglycoside-resistant ACA in sputum, cases received more cephalosporins than did controls (1.9 υ 1.2, P = 0.018); aminoglycoside usage in the two groups was comparable but cases tended to have received aminoglycoside for longer durations before colonization/infection than had controls (9.0 days υ 6.1 days, P = 0.08). Following sputum isolation of ACA, 6 of 22 cases developed ACA bacteremia compared with bacteremia in 2 of 22 controls. We conclude that factors predisposing to colonization/infection with aminoglycoside-resistant ACA were extended ICU care, prolonged respiratory therapy, and prior therapy with cephalosporins and aminoglycoside. In addition, ACA may be a more common cause of secondary bacteremia than previously appreciated.

Hospitals, insurance companies, and federal and state governments are increasingly concerned about reducing patient cost expenditures while maintaining high quality patient care. One method of reducing expenditures has been to tie hospital reimbursement with a prospective payment system based on diagnosis-related groups (DRGs). However, reimbursement under the DRG system is not acceptable for all patients in all hospitals because it is neither an accurate predictor of costs nor of clinical outcome. This deficiency poses significant problems for hospitals because DRGs are used nationwide as the prospective payment system for inpatients covered by Medicare. Several case-mix adjusters have been proposed to modify DRGs to improve their accuracy in predicting costs and outcome. We reviewed five of the most widely available indices: Acute Physiologic and Chronic Health Evaluation (APACHE II), Coded Disease Staging, Computerized Severity Index (CSI), Medical Illness Severity Group System (MEDISGROUPS), and Patient Management Categories (PMC). Recommendations for the use of a single case-mix adjuster cannot be made at this time because all indices have not been compared in sufficiently diverse settings and because some are better predictors of costs while others are better predictors of clinical outcome. Hospital epidemiologists and other infection control practitioners should be informed about these indices and their potential applications as they expand their role beyond infection control problems to issues concerning cost containment, quality assurance, and reimbursement.

Hospitals, insurance companies, and federal and state governments are increasingly concerned about reducing patient cost expenditures while maintaining high quality patient care. One method of reducing expenditures has been to tie hospital reimbursement with a prospective payment system based on diagnosis-related groups (DRGs). However, reimbursement under the DRG system is not acceptable for all patients in all hospitals because it is neither an accurate predictor of costs nor of clinical outcome. This deficiency poses significant problems for hospitals because DRGs are used nationwide as the prospective payment system for inpatients covered by Medicare. Several case-mix adjusters have been proposed to modify DRGs to improve their accuracy in predicting costs and outcome. We reviewed five of the most widely available indices: Acute Physiologic and Chronic Health Evaluation (APACHE II), Coded Disease Staging, Computerized Severity Index (CSI), Medical Illness Severity Group System (MEDISGROUPS), and Patient Management Categories (PMC). Recommendations for the use of a single case-mix adjuster cannot be made at this time because all indices have not been compared in sufficiently diverse settings and because some are better predictors of costs while others are better predictors of clinical outcome. Hospital epidemiologists and other infection control practitioners should be informed about these indices and their potential applications as they expand their role beyond infection control problems to issues concerning cost containment, quality assurance, and reimbursement.

A prospective study of 147 intermediate care ward (ICW) patients for acquisition of gentamicin-resistant Enterobacteriaceae (GRE) was carried out. Fifty (34%) were colonized or infected with one or more strains of GRE. Fifteen of these patients and one nurse were colonized with 22 strains (including ten species) of GRE bearing identical 60 kb plasmids encoding a novel β-lactamase determinant, OHIO-l and ANT (2“). Analysis of the time course of colonized patients on the ICW revealed one probable episode of cross-transmission. Five colonized patients had been residing in the ICW from one to four months prior to study initiation. Eight patients were admitted to the ICW from other hospital areas already colonized and one additional patient acquired colonization on the ICW from an unknown source. Thus, eight of ten patients admitted to the ICW during the prospective study were already colonized on admission to the ICW. To control this level of colonization it would therefore be necessary to direct efforts at limiting admission of colonized patients or attempting to eliminate the strain from persistently colonized patients, rather than trying to limit transmission within the ward.

A prospective study of 147 intermediate care ward (ICW) patients for acquisition of gentamicin-resistant Enterobacteriaceae (GRE) was carried out. Fifty (34%) were colonized or infected with one or more strains of GRE. Fifteen of these patients and one nurse were colonized with 22 strains (including ten species) of GRE bearing identical 60 kb plasmids encoding a novel β-lactamase determinant, OHIO-l and ANT (2“). Analysis of the time course of colonized patients on the ICW revealed one probable episode of cross-transmission. Five colonized patients had been residing in the ICW from one to four months prior to study initiation. Eight patients were admitted to the ICW from other hospital areas already colonized and one additional patient acquired colonization on the ICW from an unknown source. Thus, eight of ten patients admitted to the ICW during the prospective study were already colonized on admission to the ICW. To control this level of colonization it would therefore be necessary to direct efforts at limiting admission of colonized patients or attempting to eliminate the strain from persistently colonized patients, rather than trying to limit transmission within the ward.

Surveillance methods vary in different hospitals, but are mainly based on laboratory reports, as in Sweden. These reports are supplemented by ward visits by the infection control nurse and by the usual epidemiologic methods in the investigation of outbreaks.

An increasing interest in surveillance of hospital infection occurred in the 1950s when outbreaks of staphylococcal infection were causing problems throughout the world. The appointment of an MD as infection control officer in every hospital was suggested in 1955 by Colebrook in the Birmingham Accident Hospital, but no full-time officer has so far been appointed in the United Kingdom (UK). The task was taken on by medical microbiologists, who are usually physicians and, currently in England and Wales, make up 82% of infection control officers.”

In the early days, the recording of the incidence of infection was usually confined to surgical wounds, as in the US. The problem of collecting a large amount of data by the microbiologist was recognized by Moore who appointed the first infection control nurse.” He also described the importance of laboratory reports in the early detection of outbreaks.

Surveillance was a major topic for discussion at the international Conference on Nosocomial Infections in 1970, and Moore suggested that incidence rates were of little value for determining changes in a hospital or for comparisons between hospitals. The number of infections in individual hospitals was too small for statistical comparison, particularly if rates were low and infections influenced bv many factors were not corrected for in the overall rates.

Surveillance methods vary in different hospitals, but are mainly based on laboratory reports, as in Sweden. These reports are supplemented by ward visits by the infection control nurse and by the usual epidemiologic methods in the investigation of outbreaks.

An increasing interest in surveillance of hospital infection occurred in the 1950s when outbreaks of staphylococcal infection were causing problems throughout the world. The appointment of an MD as infection control officer in every hospital was suggested in 1955 by Colebrook in the Birmingham Accident Hospital, but no full-time officer has so far been appointed in the United Kingdom (UK). The task was taken on by medical microbiologists, who are usually physicians and, currently in England and Wales, make up 82% of infection control officers.”

In the early days, the recording of the incidence of infection was usually confined to surgical wounds, as in the US. The problem of collecting a large amount of data by the microbiologist was recognized by Moore who appointed the first infection control nurse.” He also described the importance of laboratory reports in the early detection of outbreaks.

Surveillance was a major topic for discussion at the international Conference on Nosocomial Infections in 1970, and Moore suggested that incidence rates were of little value for determining changes in a hospital or for comparisons between hospitals. The number of infections in individual hospitals was too small for statistical comparison, particularly if rates were low and infections influenced bv many factors were not corrected for in the overall rates.

Sulbactam/ampicillin was recently marketed for use in several infections caused by beta-lactamase-producing organisms. Sulbactam is the second beta-lactamase inhibitor to become available in the United States. Interest in inhibition of beta-lactamases arose in the late 1960s when a combination consisting of an antibacterial agent and an enzyme inhibitor was found effective in the treatment of certain resistant gram-negative infections. It is now well accepted that the addition of a beta-lactamase inhibitor to a beta-lactam antibiotic may expand its usefulness in a variety of infections.

The penicillin derivatives, known as beta-lactam antibiotics, possess a four-membered ring (beta-lactam ring) fused to a second ring (Figure). It is the beta-lactam ring that is essential for the inhibition of bacterial cell wall synthesis and subsequent bactericidal activity of these agents. The development of resistance to beta-lactam antibiotics may occur by a number of mechanisms, although the most important is bacterial production of enzymes (beta-lactamases) that are capable of beta-lactam ring hydrolysis and inactivation.

Sulbactam resembles the penicillin derivatives in structure (Figure) and is able to preserve their activity by its ability to inhibit the action of beta-lactamases, particularly those of the Richmond classes II-V (gram-negative) and the group A beta-lactamases (gram-positive). Sulbactam is referred to as a “suicide inhibitor” because while forming an irreversible complex with the enzyme, it is destroyed in the process. By virtue of its ability to render the beta-lactamases inactive, sulbactam has been combined with ampicillin in an effort to restore its activity against a number of pathogens that have developed resistance by this mechanism.

Sulbactam/ampicillin was recently marketed for use in several infections caused by beta-lactamase-producing organisms. Sulbactam is the second beta-lactamase inhibitor to become available in the United States. Interest in inhibition of beta-lactamases arose in the late 1960s when a combination consisting of an antibacterial agent and an enzyme inhibitor was found effective in the treatment of certain resistant gram-negative infections. It is now well accepted that the addition of a beta-lactamase inhibitor to a beta-lactam antibiotic may expand its usefulness in a variety of infections.

The penicillin derivatives, known as beta-lactam antibiotics, possess a four-membered ring (beta-lactam ring) fused to a second ring (Figure). It is the beta-lactam ring that is essential for the inhibition of bacterial cell wall synthesis and subsequent bactericidal activity of these agents. The development of resistance to beta-lactam antibiotics may occur by a number of mechanisms, although the most important is bacterial production of enzymes (beta-lactamases) that are capable of beta-lactam ring hydrolysis and inactivation.

Sulbactam resembles the penicillin derivatives in structure (Figure) and is able to preserve their activity by its ability to inhibit the action of beta-lactamases, particularly those of the Richmond classes II-V (gram-negative) and the group A beta-lactamases (gram-positive). Sulbactam is referred to as a “suicide inhibitor” because while forming an irreversible complex with the enzyme, it is destroyed in the process. By virtue of its ability to render the beta-lactamases inactive, sulbactam has been combined with ampicillin in an effort to restore its activity against a number of pathogens that have developed resistance by this mechanism.

As the consumers and regulators of health care have become more concerned with quality of delivered services, interest has focused on hospital- and physician-specific mortality rates as an index of quality. Mortality rates have several characteristics that promote their use as a performance indicator. The numerator, death, is generally (but perhaps incorrectly) accepted as an adverse outcome of health care. Death is thought to be easily measured, and is recorded in several locations, including the medical record abstract and death certificates, where the information is accessible without provider consent. The denominator, persons or patients, is also available from several public sources. The desirability of mortality data is further enhanced by the wide variety of statistical methods to manipulate and compare rates and proportions. The conceptual validity of mortality rates as reflecting quality is supported by a long tradition of using mortality rates at the “macro” level to compare the quality of national health care delivery systems (eg, infant mortality rates) and at the “micro” level to compare the outcome of different therapies (eg, thrombolytics for acute myocardial infarction). However, despite face validity, ease of measurement, and widespread acceptance in other areas, hospital-specific mortality rates, as calculated from current data sources, have a variety of potential problems.This article will explore the clinical, administrative, and information-based difficulties in using mortality rates as an indicator of the quality of medical care delivered by specific hospitals or physicians.

As the consumers and regulators of health care have become more concerned with quality of delivered services, interest has focused on hospital- and physician-specific mortality rates as an index of quality. Mortality rates have several characteristics that promote their use as a performance indicator. The numerator, death, is generally (but perhaps incorrectly) accepted as an adverse outcome of health care. Death is thought to be easily measured, and is recorded in several locations, including the medical record abstract and death certificates, where the information is accessible without provider consent. The denominator, persons or patients, is also available from several public sources. The desirability of mortality data is further enhanced by the wide variety of statistical methods to manipulate and compare rates and proportions. The conceptual validity of mortality rates as reflecting quality is supported by a long tradition of using mortality rates at the “macro” level to compare the quality of national health care delivery systems (eg, infant mortality rates) and at the “micro” level to compare the outcome of different therapies (eg, thrombolytics for acute myocardial infarction). However, despite face validity, ease of measurement, and widespread acceptance in other areas, hospital-specific mortality rates, as calculated from current data sources, have a variety of potential problems.This article will explore the clinical, administrative, and information-based difficulties in using mortality rates as an indicator of the quality of medical care delivered by specific hospitals or physicians.