Clinical features and epidemiology of acinetobacter baumannii colonization and infection in spanish hospitals

Society for Healthcare Epidemiology of America and Cambridge University Press are collaborating with JSTOR to digitize, preserve and extend access to Infection Control and Hospital Epidemiology. http://www.jstor.org Clinical Features and Epidemiology of Colonization and Infection in Acinetobacter baumannii Spanish Hospitals Author(s): Jesús Rodríguez‐Baño , MD, PhD, Jose M. Cisneros , MD, PhD, Felipe Fernández‐Cuenca , MD, PhD, Anna Ribera , MD, Jordi Vila , MD, PhD, Alvaro Pascual , MD, PhD , Luis Martínez‐Martínez , MD, PhD, Germán Bou , MD, PhD, Jerónimo Pachón , MD, PhD and Grupo de Estudio de Infección Hospitalaria (GEIH) Source: Infection Control and Hospital Epidemiology, Vol. 25, No. 10 (October 2004), pp. 819-824 Published by: on behalf of Cambridge University Press Society for Healthcare Epidemiology of America Stable URL: http://www.jstor.org/stable/10.1086/502302 Accessed: 29-01-2016 17:58 UTC Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at http://www.jstor.org/page/ info/about/policies/terms.jsp JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact [email protected]. This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions Vol. 25 No. 10 INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY 819 CLINICAL FEATURES AND EPIDEMIOLOGY OF ACINETOBACTER BAUMANNII COLONIZATION AND INFECTION IN SPANISH HOSPITALS Jesús Rodríguez-Baño, MD, PhD; Jose M. Cisneros, MD, PhD; Felipe Fernández-Cuenca, MD, PhD; Anna Ribera, MD; Jordi Vila, MD, PhD; Alvaro Pascual, MD, PhD; Luis Martínez-Martínez, MD, PhD; Germán Bou, MD, PhD; Jerónimo Pachón, MD, PhD; the Grupo de Estudio de Infección Hospitalaria (GEIH)* Multidrug-resistant Acinetobacter baumannii has become an important cause of nosocomial infection worldwide.1This gram-negative organism mainly affects predisposed patients, particularly those in intensive care units (ICUs), thus behaving as a nosocomial opportunistic pathogen.2One of its main features is its ability to develop resistance to multiple antimicrobial agents. During recent years, dissemination of carbapenem- Dr. Rodríguez-Baño is from the Sección de Enfermedades Infecciosas and Drs. Fernández-Cuenca, Pascual, and Martínez-Martínez are from the Servicio de Microbiología, Hospital Universitario Virgen Macarena, Sevilla, Spain. Drs. Cisneros and Pachón are from the Servicio de Enfermedades Infecciosas, Hospitales Universitarios Virgen del Rocío, Sevilla, Spain. Drs. Ribera and Vila are from the Servicio de Microbiología, Hospital Clinic, Barcelona, Spain. Dr. Bou is from the Servicio de Microbiología, Hospital Juan Canalejo, La Coruña, Spain. *Members of the Hospital Infection Study Group (GEIH) from the Spanish Society on Infectious Diseases and Clinical Microbiology included Javier Ariza, Mª Angeles Domínguez, Miquel Pujol, and Fe Tubau (Ciutat Sanitaria i Universitaria de Bellvitge, Barcelona); Juan Pablo Horcajada, Anna Ribera, and Jordi Vila (Hospital Clinic i Provincial, Barcelona); Jordi Cuquet, Carmina Martí, and Dolors Navarro (Hospital General de Granollers, Barcelona); Francisco Alvarez Lerma and Margarita Salvadó (Hospital del Mar, Barcelona); Irene Planells and Oscar del Valle-Ortiz Maestu (Hospital de la Vall d´Hebron, Barcelona); Fernando Chaves and Antonio Sánchez Porto (Hospital del SAS de la Línea de la Concepción, Cádiz); Fernando Rodríguez López and Elisa Vidal (Hospital Universitario Reina Sofía, Córdoba); Alejandro Beceiro and Germán Bou (Hospital Juan Canalejo, A Coruña); Manuel de la Rosa (Hospital Universitario Virgen de las Nieves, Granada); Fernando Chaves and Manuel Lisazoain (Hospital Doce de Octubre, Madrid); Paloma García Hierro and Josefa Gómez Castillo (Hospital Universitario de Getafe, Madrid); Belen Padilla (Hospital Universitario Gregorio Marañón, Madrid); Jesús Martínez Beltrán (Hospital Ramón y Cajal, Madrid); Manuel López Brea and Lucía Pérez (Hospital Universitario de la Princesa, Madrid); Manuel Causse and Pedro Manchado (Complejo Hospitalario Carlos Haya, Málaga); Inés Dorronsoro and José Javier García Irure (Hospital de Navarra, Pamplona); Almudena Tinajas (Hospital Santo Cristo de Piñor, Orense); Gloria Esteban and Begoña Fernández (Hospital Santa María Nai, Orense); Nuria Borrell and Antonio Ramírez (Hospital Universitario Son Dureta, Palma de Mallorca); Isabel Alamo and Diana García Bardeci (Hospital de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria); José Angel García Rodríguez (Hospital Universitario de Salamanca); Carmen Fariñas and Carlos Fernández Mazarrasa (Hospital Universitario Marqués de Valdecilla, Santander); Eduardo Varela and Mercedes Treviño (Hospital Universitario de Santiago de Compostela, Santiago de Compostela); Luis Martínez, Alvaro Pascual, and Jesús Rodríguez-Baño (Hospital Universitario Virgen Macarena, Sevilla); Ana Barrero, Jose Miguel Cisneros, Jerónimo Pachón, and Trinidad Prados (Hospitales Universitarios Virgen del Rocío, Sevilla); Frederic Ballester (Hospital Universitari Sant Joan de Reus, Tarragona); María Eugenia García Leoni and Ana Leturia (Hospital Nacional de Parapléjicos, Toledo); Susana Brea and Enriqueta Muñoz (Hospital Virgen de la Salud, Toledo); and Joaquina Sevillano and Irene Rodríguez Conde (Policlínico de Vigo SA, Vigo). Address reprint requests to Jesús Rodríguez-Baño, Sección de Enfermedades Infecciosas, Hospital Universitario Virgen Macarena, Avda Dr Fedriani, 3, 41071 Sevilla, Spain. Supported in part by a research grant from Merck Sharp & Dohme, Spain, and by the Red Española de Investigación en Patología Infecciosa (Instituto de Salud Carlos III, C03/14). The authors thank the Grupo para el Estudio de la Infección Hospitalaria (GEIH), from the Sociedad Española de Enfermedades Infecciosas y Microbiología Clínica (SEIMC), for supporting the study. Presented in part at the 42nd International Conference on Antimicrobial Agents and Chemotherapy; September 27-30, 2002; San Diego, CA. OBJECTIVE: To investigate the clinical features and the epidemiology of Acinetobacter baumannii in Spanish hospitals. DESIGN: Prospective multicenter cohort study. SETTING: Twenty-seven general hospitals and one paraplegic center in Spain. METHODS: All cases of A. baumannii colonization or infection detected by clinical samples during November 2000 were included. Isolates were identified using phenotypic and genotypic methods. The molecular relatedness of the isolates was assessed by pulsed-field gel electrophoresis. RESULTS: Twenty-five (89%) of the hospitals had 221 cases (pooled rate in general hospitals, 0.39 case per 1,000 patient-days; range, 0 to 1.17). The rate was highest in intensive care units (ICUs). Only 3 cases were pediatric. The mean age of the patients in the general hospitals was 63 years; 69% had a chronic underlying disease and 80% had previously received antimicrobial treatment. Fifty-three percent of the patients had an infection (respiratory tract, 51%; surgical site, 16%; and urinary tract, 11%). Crude mortality was higher in infected than in colonized patients (27% vs 10%; relative risk, 1.56; 95% confidence interval, 1.2 to 2.0; P= .003). Molecular analysis disclosed 79 different clones. In most hospitals, a predominant epidemic clone coexisted with other sporadic clones. Imipenem resistance was present in 39% of the hospitals. CONCLUSIONS: A. baumannii was present in most participating Spanish hospitals (particularly in ICUs) with different rates among them. The organisms mainly affected predisposed patients; half of them were only colonized. Epidemic and sporadic clones coexisted in many centers (Infect Control Hosp Epidemiol 2004;25:819-824). ABSTRACT This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions 820 INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY October 2004 resistant strains has been described in many countries.3,4 Many outbreaks caused by this organism have been described in the literature. Although in some centers a single clone predominates, in others the epidemiologic situation is more complex, with coexistence of epidemic and sporadic strains.5Although most studies on the epidemiology of A. baumannii have been performed in single hospitals, some of the scarce multicenter studies performed to date have shown interinstitutional spread of resistant strains,6-9 thus raising the possible need for control of interhospital transmission.8,9 The objective of this study was to describe the clinical and molecular epidemiology of A. baumannii and the clinical features of A. baumannii infections in a wide sample of Spanish hospitals. METHODS Setting The members of the Hospital Infection Study Group (GEIH) from the Spanish Society on Infectious Diseases and Clinical Microbiology were asked to participate in the GEIH-Ab 2000 project, promoted by the GEIH with the objective of investigating the epidemiology, mechanisms of resistance, and clinical implications of A. baumannii in Spanish hospitals. Members from 28 hospitals agreed to participate. The 28 participating hospitals serve a population of 11 million inhabitants (approximately 25% of the Spanish population). Twenty-seven are general hospitals and one is a specialized reference center for paraplegic patients. Twenty-six (92.8%) are public hospitals, 14 (50%) are university hospitals, and 19 (67.8%) have active transplant programs. Eleven hospitals (39.3%) have 500 to 999 beds, 10 (35.7%) have more than 1,000 beds, and 7 (25%) have fewer than 500 beds (Table 1). Patients Every new case of colonization or infection due to A. baumannii detected from clinical samples during November 2000 in the participating hospitals was included in the study. Cases detected only from surveillance samples were excluded as surveillance policies differ from hospital to hospital. All of the isolates presumptively identified as A. baumannii in each participating hospital were sent to a reference laboratory (Hospital Clinic, Barcelona), where identification was performed following phenotypic and genotypic methods. For each case, only one isolate (the first) was studied. Only those cases in which the organism was finally identified as A. baumannii were included. For each case, the following variables were recorded: hospital ward (ICU, medical, surgical, and pediatric), gender, age, type of sample, type and severity of underlying disease (according to McCabe classification),10 invasive procedures, and previous antimicrobial treatment. A. baumannii was considered to have been nosocomially acquired if the sample had been obtained more than 2 days after the patient’s admission. Patients colonized or infected during the first 2 days of admission and who had been directly moved from another center were considered to be imported cases. The clinical significance (colonization or infection) of the A. baumannii isolation and type of infection in each case were assessed according to Centers for Disease Control and Prevention criteria.11,12 Sepsis, severe sepsis, septic shock, and multi-organ failure were defined according to standard criteria.13 Patients were observed until discharge or death, or until 30 days after the sample had been obtained if the patient was still hospitalized. Microbiological Studies Identification of A. baumannii was performed by traditional phenotypic methods and amplified ribosomal DNA restriction analysis.14 Genotyping of isolated organisms was performed by pulsed-field gel electrophoresis TABLE 1 CHARACTERISTICS OF THE 28 SPANISH HOSPITALS PARTICIPATING IN THE STUDY No. of Cases Hospital No. of Type of No. of per 1,000 No. of No. Beds Hospital Cases Patient-Days Clones 1 220 R 27 5.19 15 2 200 G 1 0.31 1 3 240 G 3 0.50 3 4 266 G, U, P 0 0 - 5 308 G, P 1 0.14 1 6 343 G, P 0 0 - 7 424 G, T 1 0.08 1 8 517 G, T 10 0.71 1 9 500 G, T 1 0.7 1 10 540 G, U 3 0.23 3 11 540 U, T 12 0.67 1 12 601 G 7 0.44 3 13 650 G, T 9 0.56 3 14 727 G, U, T 1 0.05 1 15 873 G, U, T 5 0.22 4 16 931 G, U 5 0.19 1 17 940 G, U, T 0 0 - 18 960 G, U, T 37 1.17 9 19 1,054 G, U, T 1 0.07 1 20 1,075 G, T 1 0.04 1 21 1,085 G, U, T 15 0.54 1 22 1,126 G, U, T 12 0.50 2 23 1,176 G, T 7 0.23 4 24 1,300 G, T 4 0.13 1 25 1,300 G, T 3 0.09 3 26 1,442 G, U, T 12 0.32 3 27 1,550 G, U, T 2 0.05 2 28 1,606 G, U, T 42 1.04 14 R = paraplegic reference center; G = general hospital; U = university hospital; P = private hospital; T = active transplantation program. This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions Vol. 25 No. 10 ACINETOBACTER BAUMANNII IN SPANISH HOSPITALS 821 (PFGE) analysis. Genomic DNA was prepared in agarose plugs, as described elsewhere.15 DNA inserts were restricted with SmaI, according to the manufacturer’s instructions (New England BioLabs, Beverly, MA). Isolates were assigned to clonal groups, according to the criteria of Tenover et al.16 Antimicrobial susceptibility was studied by microdilution following the recommendations of the National Committee for Clinical Laboratory Standards.17 Statistical Analysis Rates were estimated by dividing the number of new cases by the number of patient-days in the study period. Categorical and continuous variables were compared using chi-square and the Mann-Whitney Utest, respectively. For continuous dependent variables, correlations with independent variables were assessed by analysis of variance. For dichotomous dependent variables, relative risk (RR) or odds ratio (OR) and 95% confidence interval (CI95) were calculated. RESULTS During the study period, 240 isolates presumptively identified as A. baumannii by the local laboratories were sent to the reference laboratory. Nineteen cases were excluded: 1 was not an Acinetobacter species, 15 were identified as Acinetobacter genospecies 3, and 3 were another Acinetobacter species. Thus, 221 isolates and cases of A. baumannii colonization or infection were included. Twenty-five of the 28 participating hospitals (89.2%) had cases of A. baumannii colonization or infection (range per hospital, 0 to 42 cases) during the study period (Table 1). The 221 cases were distributed as follows: 104 (47%) were in ICUs, 57 (26%) were in medical wards, 54 (24%) were in surgical wards, and 3 (1%) were in pediatric wards (only 1 case in a neonatal unit). These data were not available for 3 (1.3%) of the patients. In the 27 general hospitals, the pooled rate of A. baumannii colonization or infection was 0.39 case per 1,000 patient-days (range, 0 to 1.17 cases) or 0.30 case per 100 admissions (range, 0 to 1.48 cases). The median rate was 0.22 case per 1,000 patients-days, and the 75th percentile was 0.50. ICUs had higher rates than did medical or surgical wards (Table 2). The frequency distribution of tertiary-care hospitals according to the incidence is shown in the figure. There were no geographic trends in the distribution of the incidence and no relation between the rates and the size of the hospitals (number of beds) (r2= 0.04; P= .2) or other hospital features (data not shown). The rate in the paraplegic center was 5.19 cases per 1,000 patient-days. A. baumannii was isolated from respiratory samples in 87 (39.3%) of the patients, exudates or abscesses in 52 (23.5%), urine cultures in 51 (23%), vascular catheter tips in 8 (3.6%), blood cultures in 7 (3.1%), cerebrospinal fluid in 4 (1.8%), and other samples in 3 (1.3%). Data were unavailable in 9 (4%) of the cases. Overall, 206 (93.2%) of the cases were nosocomially acquired and 8 (3.6%) were community acquired; 7 nosocomially acquired cases were considered to be imported from other centers. These data were unavailable in 7 (3.2%) of the cases. Predisposing conditions of the colonized or infected patients were available for 206 (93.2%) of the cases and are summarized in Table 3; no significant differences in the frequency of these conditions were found among hospitals in different areas (data not shown). There were 203 adult and 3 pediatric patients. Among these 206 patients, 109 (52.9%) had an infection due to A. baumannii and the rest were only colonized. The types of infections among the 102 infected patients in general hospitals were as follows: respiratory tract infections, 52 (pneumonia, 36); incisional surgicalsite infections, 16; urinary tract infections, 11; nonsurgical skin and soft tissue infections, 9; phlebitis, 5; meningitis, 4, primary bacteremia, 3; and intra-abdominal infections, 2. Among the 7 infected patients in the paraplegic center, 6 had a urinary tract infection and 1 had a non-surgical skin and soft tissue infection. Regarding systemic response, 51 (46.8%) of the patients with infection presented with sepsis, 12 (11%) with severe sepsis, 9 TABLE 2 RATES OF ACINETOBACTER BAUMANNII COLONIZATION OR INFECTION IN 27 TERTIARY-CARE SPANISH HOSPITALS DURING THE 1-MONTH STUDY PERIOD* Pooled Rate Median (Range) Global 0.39 0.22 (0–1.17) Medical wards†0.14 0 (0–0.73) Surgical wards†0.22 0 (0–0.94) Intensive care units†4.55 1.96 (0–13.2) *New cases per 1,000 patient-days. †The 3 pediatric cases are not included. FIGURE. Distribution of rates of Acinetobacter baumannii colonization and infection in 27 general hospitals in Spain. This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions 822 INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY October 2004 (8.3%) with septic shock, and 8 (7.3%) with multi-organ failure syndrome. Thirty-nine patients died (crude mortality, 18.9%). Mortality was higher among patients with infection than among those with colonization (26.6% vs 10.4%; RR, 1.56; CI95, 1.2 to 2.0; P= .003). The mean duration of hospitalization after A. baumannii isolation in the surviving cases was 21 days (range, 1 to > 30 days), and was significantly longer among patients with infection than among those with colonization (mean, 23.1 vs 19.2 days; P= .02). Molecular analysis disclosed 79 different PFGE types among the 221 isolates of A. baumannii included in the study. A PFGE type could not be obtained in 1 isolate. Fifty-two (65.8%) of the clones were each isolated from a single patient, 18 (22.7%) from 2 to 5 patients, 5 (6.3%) from 6 to 10 patients, and 4 (5%) from more than 10 patients. No clones were present in more than one hospital. The number of clones in an individual hospital ranged from 1 to 4 except in the 3 hospitals with higher rates, where there were 9, 14, and 15 clones, respectively (Table 1). A predominant clone (ie, a clone that caused more than 50% of the cases) was observed in the 14 hospitals with 4 or more cases; in 5 of them, all of the cases were caused by that clone. In 4 of the 8 cases considered to be community acquired, the isolates belonged to clones that were epidemic in the centers where the cases were detected. Similarly, in 5 of the 7 cases considered to be imported from other hospitals, the isolates belonged to epidemic clones in the centers where the cases were detected. Among the 221 isolates, 91 (41.2%) were imipenem resistant and 14 (6.3%) had intermediate susceptibility. Seventy isolates (31.6%) showed high-level imipenem resistance (minimum inhibitory concentration ⭓64 mg/L). Imipenem-resistant strains were detected in 11 hospitals (39.3%). Imipenem resistance was more frequent among university hospitals than among non-university hospitals (57.1% vs 15.4%; OR, 7.3; CI95, 1.1 to 46.2; P= .04). No other hospital features (ie, the number of beds or having a transplantation program) were associated with imipenem resistance. Imipenem-resistant isolates belonged to 28 (35.4%) of the 79 clones; in 11 of these clones there were isolates showing different imipenem susceptibility. Imipenem-resis- tant clones were more frequently epidemic (isolated from more than one patient) than were imipenem-susceptible clones (63% vs 21.2%; OR, 6.3; CI95, 2.2 to 17.6; P< .001). The mean number of isolates (± standard deviation) in each clone was 4.5 (± 5.3) for imipenem-resistant clones and 1.8 (± 2.3) for imipenem-susceptible clones (P = .01). Also, ciprofloxacin-resistant clones were more frequently epidemic than were ciprofloxacin-susceptible clones (88.9% vs 11.1%; OR, 3.8; CI95, 1.02 to 14.7; P= .03). DISCUSSION A. baumannii is an important cause of nosocomial infections in most countries. Many outbreaks have been described in the literature, and the organism has become endemic in many centers.5,8,18-20 Multicenter studies on the epidemiology of A. baumannii colonization and infection are scarce. Our study was performed in a wide sample of Spanish hospitals. Because participation was voluntary, this sample cannot be considered a representative sample of Spanish centers. It is possible that those hospitals with A. baumannii–related problems might have been more prone to participate. Nevertheless, the participating hospitals included small and large university and non-univer- sity centers, were located in small and large towns, provided healthcare to more than 25% of the Spanish population, and had different rates of A. baumannii colonization or infection during the study period. Due to the nature of our objectives (which included the use of appropriate methods for the identification of A. baumannii and the performance of molecular analysis), it was necessary to limit the number of isolates to be investigated and, consequently, the study period was necessarily short. Thus, seasonal variations could not be investigated. However, we believe our data are indicative of the incidence of A. TABLE 3 CHARACTERISTICS OF THE 206 PATIENTS COLONIZED OR INFECTED WITH ACINETOBACTER BAUMANNII IN SPANISH HOSPITALS General Paraplegic Characteristic Hospitals Hospital No. of patients 183 23 Median age, y (range) 63 (0–91) 34 (14–67) Male 129 (70.5%) 20 (87%) Chronic underlying disease Nonfatal 85 (46.4%) 21 (91.3%) Ultimately fatal 37 (20.2%) 2 (8.7%) Rapidly fatal 4 (2.2%) 0 Diabetes mellitus 30 (16.4%) 2 (8.7%) Neoplasia 35 (19.1%) 0 Chronic pulmonary disease 27 (14.8%) 1 (4.3%) Chronic renal insufficiency 9 (4.9%) 1 (4.3%) Transplantation 4 (2.2%) 0 Central venous catheter 134 (73.2%) 4 (17.4%) Current or previous ICU stay 142 (77.6%) 14 (60.9%) Bladder catheter 144 (78.7%) 17 (73.9%) Cerebrospinal fluid shunt 13 (7.1%) 0 Parenteral hyperalimentation 52 (28.4%) 0 Mechanical ventilation 103 (56.3%) 11 (47.8%) Surgical procedure 94 (51.4%) 5 (21.7%) Previous antimicrobial treatment 148 (80.9%) 16 (69.6%) Aminopenicillins 39 (21.3%) 6 (26.1%) Piperacillin/tazobactam 26 (14.2%) 5 (21.7%) Carbapenems 30 (16.4%) 3 (13%) Cephalosporins 72 (39.3%) 5 (21.7%) Aminoglycosides 60 (32.8%) 6 (26.1%) Fluoroquinolones 30 (16.4%) 4 (17.4%) ICU = intensive care unit. This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions Vol. 25 No. 10 ACINETOBACTER BAUMANNII IN SPANISH HOSPITALS 823 baumannii colonization and infection in most Spanish hospitals. A. baumannii was present in almost 90% of the hospitals. The rate of colonization and infection in the month studied was different among general hospitals. We did not find any relationship between size, teaching condition, or existence of transplantation programs in the hospitals and the rates. Although clinical practice is probably similar in the participating hospitals, a bias due to different frequency of submission of samples for culture among the hospitals cannot be discarded. However, we do not think that this could explain the differences in the rates. Thus, local epidemiologic circumstances, such as differences in infection control programs and compliance with infection control measures, are probably more important than the general features of the hospitals in the rates of A. baumannii. As expected, the rates were highest in ICUs (median, 1.93 cases). In U.S. hospitals, the median annual rate of Acinetobacter infections in ICUs between 1987 and 1996 was 0.72 case per 1,000 patient-days.21 However, comparison of these data is not possible as we included colonized patients and excluded non-baumannii species of Acinetobacter. It is remarkable that only 3 cases were pediatric and that only 1 occurred in a neonatal unit. Outbreaks of A. baumannii in neonatal units have been described,22-25 but it seems that this organism does not affect these units as frequently as do other multidrugresistant, gram-negative bacilli such as extended-spec- trum beta-lactamase–producing Klebsiella pneumoniae. The rate in the reference center for paraplegic patients was high. This hospital receives patients from other Spanish hospitals, including many of the participating ones. In this center, A. baumannii was mostly isolated from urine samples in catheterized patients, suggesting that urine of catheterized patients was an important reservoir of the organism. Some outbreaks of Acinetobacter infections have been previously described in spinal cord units.26-28 Our data confirm that A. baumannii is still confined to hospitals and only rarely causes community-acquired infections. The fact that some so-called “communityacquired” cases were caused by a clone that was epidemic in the institutions might suggest that those patients could have acquired the organism during a previous admission or, alternatively, that the nosocomial acquisition of A. baumannii occurred during the first 48 hours of admission, which has been reported in colonization studies of ICU patients in the context of an outbreak.29 This also could have occurred in a patient transferred from another center, whose isolate was clonally related to an epidemic clone in the institution that he or she was transferred into. In our study, half of the patients were considered to be only colonized. A similar rate has been described for Stenotrophomonas maltophilia.30 These data underscore the importance of adequately interpreting the clinical significance of these organisms when isolated from clinical samples to avoid unnecessary use of antimicrobials. The relevance of patients’ colonization in the epidemiology of A. baumannii is well known.29 Regarding the molecular epidemiology, a wide heterogeneity was found among the isolates, although surveillance samples were not included. The heterogeneity was more evident in hospitals with higher rates, in most of which sporadic and epidemic clones coexisted, as described by Villers et al.5However, a predominant clone was observed in all centers with 4 cases or more. Imipenem-resistant or quinolone-resistant clones were more frequently epidemic, in accordance with the results of Koeleman et al.31 Our data support the hypothesis that antimicrobial resistance may favor the epidemic behavior of some A. baumannii clones. Interinstitutional spread of A. baumannii clones has been reported in some areas,6,8,9 suggesting that the epidemiology of A. baumannii cannot be viewed as merely a local problem. We could not demonstrate interinstitutional spread of A. baumannii clones, even in hospitals close to one another or in the paraplegic center. Interinstitutional transfer of patients and healthcare workers among hospitals is probably less frequent in Spain than in other countries. However, our study has limitations that need to be considered when interpreting these data: the study period was short and surveillance samples were not included. A longer study including surveillance cultures would be necessary for adequately evaluating interinstitutional spread of A. baumannii in Spain and for having a more profound knowledge of the spread of endemic strains. A. baumannii was present in most of the participating Spanish hospitals, but the rates were different among them; interinstitutional spread of A. baumannii clones was not found, and in many centers, epidemic and sporadic clones coexisted. The organisms mainly affected predisposed patients and mainly caused respiratory tract infections. REFERENCES 1. Gales AC, Jones RN, Forward KR, Liñares J, Sader HS, Verhoef J. Emerging importance of multidrug-resistant Acinetobacter species and Stenotrophomonas maltophilia as pathogens in seriously ill patients: geographic patterns, epidemiological features, and trends in the SENTRY Antimicrobial Surveillance Program (1997-1999). Clin Infect Dis 2001;32(suppl 2):S104-S113. 2. Bergogne-Bérézin E, Towner KJ. Acinetobacter spp. as nosocomial pathogens: microbiological, clinical, and epidemiological features. Clin Microbiol Rev 1996;9:148-165. 3. Afzal-Shah M, Livermore DM. Worldwide emergence of carbapenemresistant Acinetobacter spp. J Antimicrob Chemother 1998;41:576-577. 4. Jones ME, Thornsberry C, Livermore DM, Sahm DF. Prevalence of Acinetobacter spp. isolates with reduced susceptibility to imipenem, as determined by a USA-wide electronic surveillance network. J Antimicrob Chemother 1999;43:429-431. 5. Villers D, Espaze E, Coste-Burel M, et al. Nosocomial Acinetobacter baumannii infections: microbiological and clinical epidemiology. Ann Intern Med 1998;129:182-189. 6. Vahaboglu H, Öztürk R, Aygün G, et al. Widespread detection of PER- 1-type extended-spectrum beta-lactamases among nosocomial Acinetobacter and Pseudomonas aeruginosa isolates in Turkey: a nationwide multicenter study. Antimicrob Agents Chemother 1997;41:2265- 2269. 7. Sader HS, Mendes CF, Pignatari AC, Pfaller MA. Use of macrorestriction analysis to demonstrate interhospital spread of multiresistant Acinetobacter baumannii in Sao Paulo, Brazil. Clin Infect Dis 1996;23:631-634. 8. Manikal VM, Landman D, Saurina G, Oydna E, Lal H, Quale J. This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions 824 INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY October 2004 Endemic carbapenem-resistant Acinetobacter species in Brooklyn, New York: citywide prevalence, interinstitutional spread, and relation to antibiotic usage. Clin Infect Dis 2000;31:101-106. 9. Landman D, Quale JM, Mayorga D, et al. Citywide clonal outbreak of multiresistant Acinetobacter baumannii and Pseudomonas aeruginosa in Brooklyn, NY: the preantibiotic era has returned. Arch Intern Med 2002;162:1515-1520. 10. McCabe WR, Jackson GG. Gram-negative bacteremia: I. Etiology and ecology. Arch Intern Med 1962;110:847-855. 11. Garner JS, Jarvis WR, Emori TG, Horan TC, Hughes JM. CDC definitions for nosocomial infections, 1988. Am J Infect Control 1988;16:128- 140. 12. Horan TC, Gaynes RP, Martone WJ, Jarvis WR, Emori TG. CDC definitions of nosocomial surgical site infections, 1992: a modification of CDC definitions of surgical wound infections. Infect Control Hosp Epidemiol 1992;13:606-608. 13. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 1992;101:1644-1655. 14. Vaneechoutte M, Dijkshoorn L, Tjernberg I, et al. Identification of Acinetobacter genomic species by amplified ribosomal DNA restriction analysis. J Clin Microbiol 1995;33:11-15. 15. Allardet-Servent A, Bouziges N, Carles-Nurit MJ, Bourg G, Gouby A, Ramuz M. Use of low-frequency-cleavage restriction endonucleases for DNA analysis in epidemiological investigations of nosocomial bacterial infections. J Clin Microbiol 1989;27:2057-2061. 16. Tenover FC, Arbeit RD, Goering RV, et al. Interpreting chromosomal DNA restriction patterns produced by pulsed-field gel electrophoresis: criteria for bacterial strain typing. J Clin Microbiol 1995;33:2233-2239. 17. National Committee for Clinical Laboratory Standards. Methods for Dilution Antimicrobial Susceptibility Tests for Bacterial That Grow Aerobically. Wayne, PA: National Committee for Clinical Laboratory Standards; 2000. Approved standard M7-A5. 18. Villari P, Iacuzio L, Vozzella EA, Bosco U. Unusual genetic heterogeneity of Acinetobacter baumannii isolates in a university hospital in Italy. Am J Infect Control 1999;27:247-253. 19. Martínez-Pellús A, Ruiz Gómez J, Jaime Sánchez F, Simarro Córdoba E, Fernández Lozano JA. Incidence of colonization and infection by Acinetobacter baumannii in an endemic setting (ICU): analysis of risk factors by means of a surveillance study [in Spanish]. Enferm Infecc Microbiol Clin 2002;20:194-199. 20. Rodríguez Baño J, Pascual A, Galvez J, et al. Acinetobacter baumannii bacteremia: clinical and prognostic features [in Spanish]. Enferm Infecc Microbiol Clin 2003;21:242-246. 21. McDonald LC, Banerjee SN, Jarvis WR. Seasonal variation of Acinetobacter infections: 1987-1996. Clin Infect Dis 1999;29:1133-1137. 22. Thurm V, Ritter E. Genetic diversity and clonal relationships of Acinetobacter baumannii strains isolated in a neonatal ward: epidemiological investigations by allozyme, whole-cell protein and antibiotic resistance analysis. Epidemiol Infect 1993;111:491-498. 23. Nagels B, Ritter E, Thomas P, Schulte-Wissermann H, Wirsing von Konig CH. Acinetobacter baumannii colonization in ventilated preterm infants. Eur J Clin Microbiol Infect Dis 1998;17:37-40. 24. Huang YC, Su LH, Wu TL, et al. Outbreak of Acinetobacter baumannii bacteremia in a neonatal intensive care unit: clinical implications and genotyping analysis. Pediatr Infect Dis J 2002;21:1105-1109. 25. Melamed R, Greenberg D, Porat N, et al. Successful control of an Acinetobacter baumannii outbreak in a neonatal intensive care unit. J Hosp Infect 2003;53:31-38. 26. Wise Ka, Tosolini FA. Epidemiological surveillance of Acinetobacter species. J Hosp Infect 1990;16:319-329. 27. Pedraza F, Andreu A, Saune M, Moreno A, Ramírez L, García L. A urinary outbreak of Acinetobacter baumannii in a spinal cord injury unit [in Spanish]. An Med Interna 1993;10:55-58. 28. Marcos MA, Abdalla S, Pedraza F, et al. Epidemiological markers of Acinetobacter baumannii clinical isolates from a spinal cord injury unit. J Hosp Infect 1994;28:39-48. 29. Corbella X, Pujol M, Ayats J, et al. Relevance of digestive tract colonization in the epidemiology of nosocomial infections due to multiresistant Acinetobacter baumannii. Clin Infect Dis 1996;23:329-334. 30. del Toro MD, Rodríguez-Baño J, Herrero M, et al. Clinical epidemiology of Stenotrophomonas maltophilia colonization and infection: a multicenter study. Medicine (Baltimore) 2002;81:228-239. 31. Koeleman JG, van der Bijl MW, Stoof J, Vanderbroucke-Grauls CM, Savelkoul PH. Antibiotic resistance is a major risk factor for epidemic behavior of Acinetobacter baumannii. Infect Control Hosp Epidemiol 2001;22:284-288. This content downloaded from 150.214.216.21 on Fri, 29 Jan 2016 17:58:21 UTC All use subject to JSTOR Terms and Conditions