COPD is a common disease. Over the prolonged, Pneumonic vs Nonpneumonic Acute Exacerbations of COPD*

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1 vs Acute Exacerbations of COPD* David Lieberman, MD; Devora Lieberman, MD; Yevgenia Gelfer, MD; Raiesa Varshavsky, MD; Bella Dvoskin, MD, PhD; Maija Leinonen, PhD; and Maureen G. Friedman, PhD Study objective: To describe and comare the background, clinical manifestations, disease course, and infectious etiologies of neumonic acute exacerbations (PNAE) vs nonneumonic acute exacerbations (NPAE) of COPD. Design: A rosective, observational study. Setting: A tertiary university medical center in southern Israel. Patients: Twenty-three hositalizations for PNAE and 217 hositalizations for NPAE were included in the study. Paired sera were obtained for each of the hositalizations and were tested serologically for 12 athogens. Only a significant change in antibody titers or levels was considered diagnostic. Results: No significant differences were found between the two grous for any of the arameters related to COPD or comorbidity. The clinical tye of the exacerbation was not significantly different between the grous. Comared to NPAE, atients with PNAE had lower PO 2 values at hosital admission ( 0.004) but higher rates of abrut onset ( 0.005), ICU admissions ( 0.006), invasive mechanical ventilation ( 0.01), mortality ( 0.007), and longer hosital stay ( 0.001). In 22 PNAE hositalizations (96%) and in 153 NPAE hositalizations (71%), at least one infectious etiology was identified ( 0.001). Mixed infection was found in 13 atients with PNAE (59%) and in 59 atients with NPAE (39%; not significant [NS]). Viral etiology was identified in 18 atients with PNAE (78%) comared with 99 atients with NPAE (46%; 0.003). Pneumococcal etiology was found in 10 atients with PNAE (43%) and in 38 atients with NPAE (18%; 0.006). An atyical etiology was identified in 8 atients with PNAE (35%) and 64 atients with NPAE (30%; NS). Conclusions: Community-acquired neumonia is common among atients hositalized for an acute exacerbation of COPD and is generally manifested by more severe clinical and laboratory arameters. In PNAE, comared to NPAE, viral and neumococcal etiologies are more common, but the rate of atyical athogens is similar. The theraeutic significance of these findings should be investigated further. (CHEST 2002; 122: ) Key words: COPD; exacerbation; neumonia, community-acquired Abbreviations: acute exacerbation of COPD; CAP community-acquired neumonia; NPAE nonneumonic acute exacerbations; NS not significant; PNAE neumonic acute exacerbations *From the Pulmonary Unit (Dr. Lieberman), and Division of Internal Medicine (Drs. Lieberman, Gelfer, and Varshavsky), Soroka University Medical Center, the Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel; The National Public Health Institute (Dr. Leinonen), Oulu, Finland; and the Deartment of Virology (Drs. Dvoskin and Friedman), the Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Manuscrit received October 12, 2001; revision acceted May 21, Corresondence to: David Lieberman, MD, Pulmonary Unit, Soroka Medical Center, Beer-Sheva, Israel 84101; Lieberma@bgumail.bgu.ac.il COPD is a common disease. Over the rolonged, chronic course of the disease, eisodes of acute exacerbation often occur. These eisodes have a deleterious effect on the atient s quality of life and necessitate utilization of health-care services, including hositalization some of the time. Although the definition of an acute exacerbation of COPD (AE- COPD) is roblematic, 1 it is generally diagnosed and categorized on the basis of clinical criteria of increasing shortness of breath, and/or an increase in the For editorial comment see age 1118 amount or urulence of sutum. 2 Communityacquired neumonia (CAP) is an infectious disease with a broad sectrum of severity. Among CAP atients with the highest severity of disease who require hositalization, COPD is the most common comorbidity. 3 5 These two diagnoses, CAP and, come together when COPD atients acquire 1264 Clinical Investigations

2 caused by CAP. The clinical manifestations of these eisodes meet the acceted criteria for the diagnosis of, and CAP is determined only in those cases in which a chest radiograh is obtained and a ulmonary infiltrate is found. The number of ublished articles on CAP in atients with COPD is very small. In a rosective, multicenter Sanish study, 124 hositalizations for CAP among atients with COPD were investigated. 6 Desite the imortance of this study, the acute eisodes were investigated from the viewoint of CAP and not, so there was no comarison between these cases and cases of without CAP. In the context of a large study on infectious etiologies in atients hositalized with, a database was created for 240 hositalizations and a broad range of infectious etiologies, which were diagnosed serologically in these hositalizations. The frequency distribution of all infectious etiologies found in that study have been resented and discussed in a revious ublication. 7 The aim of the resent study was to use the same database to evaluate eisodes of CAP in atients with COPD from the asect of, by describing and comaring the background, clinical manifestations, diseases course, and infectious etiologies of these eisodes in atients with neumonic acute exacerbations (PNAE) and nonneumonic acute exacerbations (NPAE) of COPD. Study Protocol All atients with were hositalized by decision of the emergency deartment hysicians, without intervention on the art of the investigators. Every 24 to 48 h, a research assistant visited each of the internal medicine and intensive care wards and identified atients hositalized in the interim who met the inclusion criteria for the study. After the atient agreed to articiate in the study, he or she was interviewed concerning their resiratory disease and the regular treatment they received for it, smoking habits, and comlaints and symtoms of their current acute eisode. During the first meeting, a blood samle of 5 ml was drawn for serologic testing. The blood samle was centrifuged shortly after being drawn, and the serum was frozen at a temerature of 20 C until serologic tests were conducted. Additional relevant medical and administrative data were collected from the medical records. On discharge from hositalization, the atient was invited to a follow-u aointment at the ulmonary clinic of the Soroka Medical Center 3 to 5 weeks after admission to the hosital. At that clinic, follow-u data were collected on the course of the convalescence and abnormal events that may have occurred following discharge from the hosital. At this meeting, an arterial blood samle was obtained at ambient ressure and sirometry was erformed. Each of the atients had a second (convalescencehase) serum samle obtained at this meeting for serologic testing. This samle was handled in exactly the same manner as the revious acute-hase samle. Patients whose hositalization eriod extended for 3 weeks, or who were rehositalized at the time of scheduled follow-u aointments, had the serum samle drawn during the hositalization. Patients who were not considered to be in stable condition at the first follow-u aointment (3 to 5 weeks after hositalization) were invited to an additional follow-u aointment including sirometry and arterial blood gas testing a month later. Patients Materials and Methods All atients hositalized for during the eriod between November 1, 1997, and March 15, 1999, in the internal medicine and intensive care wards of the Soroka Medical Center in Beer-Sheva, Israel, who met the inclusion criteria, and gave consent to articiate, were included in the study. All first hositalizations in the study eriod were included as well as reeat hositalizations for of atients in the study oulation, if the hositalization took lace at least 6 months after the initial one for which the atient was recruited into the study. No more than one reeat hositalization was included in the study data for any articular atient. The study was aroved by the Helsinki Committee for research on human beings of the Soroka Medical Center, and all articiants gave informed consent to articiate. Inclusion criteria for the study grou were the fulfillment of all the following five conditions: (1) age 40 years; (2) chronic airway obstruction as determined by sirometry (6 months rior to hositalization or within 1 to 2 months following hositalization) with an FEV 1 value 70% of exected and an FEV 1 /FVC ratio 0.7; (3) smoking history of at least 20 ack-years; (4) increased shortness of breath, a significant increase in sutum roduction, or a new exectoration of urulent sutum or increased sutum urulence in the week rior to hositalization; and (5) no hositalizations during the 3-week eriod rior to the resent hositalization. Sirometry and Arterial Blood Gases In order to analyze the results of the sirometric measurements with the atients in stable resiratory condition as well as to diagnose ermanent obstructive disturbances by sirometry as an inclusion criterion, the definitive sirometry was conducted for these uroses, in the vast majority of atients, at the clinic follow-u aointment 3 to 5 weeks after hositalization. When the test could not be erformed at this occasion, or when the atient was not in stable condition, the criteria for ermanent airway obstruction was assessed on the basis of revious sirometry erformed on the atient, in stable condition, within 6 months rior to hositalization, or at a further follow-u 1 month later. Patients in whom sirometry at the follow-u did not demonstrate a sufficient degree of airway obstruction were withdrawn from the study. In atients who underwent more than one sirometric test during the eriod beginning 6 months before hositalization and ending 2 months after discharge, the best result was used. All sirometric tests were conducted by an exerienced technician using the Vitalograh Comact instrument (Vitalograh, Buckingham, UK), which was calibrated at the beginning of each work day. Predicted values of FEV 1 were calculated in accordance with acceted Euroean values. 8 Arterial blood gas determinations resented in the Results were also conducted with the atient in stable condition and were obtained at the same time the definitive sirometry test was done. Arterial blood was obtained by uncturing the brachial or radial artery, and it was tested immediately with the Blood Gas System 520 (Radiometer; Coenhagen, Denmark). CHEST / 122 / 4/ OCTOBER,

3 Radiograhic Diagnosis of Pneumonia In each hositalization, a chest radiograh was obtained while the atient was still in the emergency deartment. For study uroses, each week all radiograhs were analyzed searately by a senior ulmonologist and a senior radiologist. All radiograhs that were interreted by at least one of the exerts as neumonia were classified, at this stage, as susected neumonia, and only those atients underwent reeat radiograhs at the clinic follow-u 3 to 5 weeks after hositalization. The aired radiograhs of these atients (acute hase and convalescence hase) were again interreted searately by the same exerts. Pneumonia was diagnosed only if both exerts indeendently reorted a ulmonary infiltrate in the acute-hase radiograh that disaeared or retreated significantly in the follow-u radiograh. Those cases in which the two exerts did not agree were not considered neumonia for the urose of the study. In atients who died in the hosital, neumonia was diagnosed by the resence of a tyical infiltrate on the admission chest radiograh that was not resent in a revious radiograh. Etiologic Tests The etiologic worku in this study was based exclusively on serologic testing. Serologic tests were conducted to identify 12 athogens known to be infectious agents in the uer and lower resiratory tract that can be diagnosed by serologic methods. The aired sera for each atient were tested in the same run in all cases. Serologic tests for seven resiratory tract viruses, Mycolasma neumoniae, Stretococcus neumoniae, Haemohilus influenzae, and Moraxella catarrhalis were conducted using the enzyme immunoassay method. Microimmunofluorescence serology was used for identification of Legionella s. Only a significant change in the antibody level or titer for a secific athogen between the acute-hase and convalescence-hase serum samles was considered diagnostic for infection with that athogen. In light of this requirement, only atients for whom aired sera were obtained were included in the final data analyses. The methods, kits, and criteria used for serologic diagnoses were described in detail in our revious ublication. 7 Data Analysis The results were analyzed using statistical software (Ei Info, Eidemiology Program Office, Centers for Disease Control and Prevention, Atlanta, GA). The 2 test or its equivalent served to comare roortions between grous, and analysis of variance was done to comare continuous variables among two or more grous. Statistical significance was set at Results The study consisted of 250 hositalizations for among 219 different COPD atients during the 16.5-month eriod. In 241 cases (96.4%), a convalescence-hase serum samle was obtained at a mean SD interval of days (range, 17 to 53 days) after the first samle was obtained at the beginning of the hositalization. Since the etiologic diagnoses in this study were based on changes in antibody level/titer between the acute-hase and convalescence-hase sera, we did not include in the final analyses of the study the nine hositalizations for which no convalescence-hase serum was obtained. One other hositalization was not included because we found a olyclonal resonse to all of the athogens tested. In all, 240 hositalizations of 213 atients were included in the final analyzed study oulation. In all 240 hositalizations, the atients were treated during the course of their hositalization with systemic corticosteroids. In 37 hositalizations (15%), chest radiograhs were classified by acute-hase imaging as susected neumonia, but only 28 of these radiograhs (12%) were classified as neumonia by one of the exerts on the basis of the aired radiograhs (acute hase and convalescence hase). In 23 hositalizations (10%), aired chest radiograhs were classified by the two examiners as neumonia and were considered such for study uroses. These 23 hositalizations were for 23 different atients, who were designated as the PNAE grou of the study. In 13 atients, the neumonia was right sided; in 8 atients, it was left sided; and in 2 atients, it was bilateral. In 13 atients, the neumonic infiltrate was homogeneous; in 10 atients, it was nonhomogenous; and in 3 atients, more than one lobe was involved in the neumonic rocess. The other 217 hositalizations were among 190 different atients with COPD, who were designated as the NPAE grou of the study. Table 1 resents a comarison of data between the 23 atients with PNAE and the 190 atients with Table 1 Comarison of Data Between the and Grous* Variables (n 190) Male gender 18 (78) 161 (85) NS Mean age, yr NS Baseline FEV 1,%of NS exected Baseline Po 2,mmHg NS Baseline Pco 2,mmHg NS Home oxygen 10 (43) 72 (38) NS Chronic oral steroid theray 3 (13) 59 (31) NS Comlications of COPD 17 (74) 116 (61) NS Influenza vaccination 6 (26) 80 (42) NS Pneumococcal vaccination 4 (17) 25 (13) NS Diabetes mellitus 8 (36) 55 (29) NS Ischemic heart disease 2 (9) 38 (20) NS Left-sided heart failure 1 (4) 17 (9) NS *Data are resented as No. (%) or mean SD. Baseline FEV 1,Po 2, and Pco 2 values were determined 6 months rior to hositalization, or within 1 to 2 months osthositalization, at room air with the atient in stable condition. Documentation of at least one of the following: chronic hyoxemia (Po 2 60 mm Hg), hyercanea (Pco 2 50 mm Hg), olycythemia (hematocrit 50%), ulmonary hyertension ( 40 mm Hg) Clinical Investigations

4 NPAE. These include demograhic data, baseline sirometry, and arterial blood gas test results in atients in stable condition, rate of chronic steroid theray, rate of COPD comlications, rates of influenza and neumococcal vaccination, and rates of chronic comorbidity. No significant difference was observed for any of these variables between the two grous. Table 2 resents a comarison of clinical exressions of the exacerbation and arterial Po 2 and Pco 2 levels at admission between the two study grous. Comared to the NPAE grou, the PNAE grou had significantly higher rates of abrut onset of acute exacerbation, fever during the acute exacerbation, creitations on lung auscultation, and severe hyoxemia. There was no significant difference in the distribution of the exacerbations according to the classification of Anthonisen et al 2 between the two grous, but there was a clear trend to a higher rate of tye 1 exacerbation in then PNAE grou. Table 3 resents a comarison of the rates of invasive mechanical ventilation, admission to intensive care, duration of hositalization, mortality, and the course of recovery following discharge from the hosital between the two grous. In all of the first four arameters, which are markers of severity of the acute exacerbation, the PNAE grou had significantly more severe results. In contrast, no significant difference was found between the two grous in the Table 2 Comarison of Clinical Exressions of the Exacerbation and Arterial PO 2,PCO 2, and H Between the and Grous* Variables (n 217) Clinical tye of 1 16 (70) 110 (51) NS 2 1 (4) 37 (17) NS 3 6 (26) 70 (32) NS Abrut onset of 11 (48) 47 (22) exacerbation Mental status change 3 (13) 12 (6) NS Feeling of shaking chills 12 (52) 72 (33) NS Fever during exacerbation 21 (91) 148 (68) 0.02 Creitations on lung 15 (65) 47 (22) auscultation Po 2 at hosital admission 50.3 [10.3] 56.9 [10.2] (room air) Pco 2 at hosital admission 46.5 [15.2] 46.8 [13.9] NS (room air) PH at hosital admission 7.39 [0.08] 7.39 [0.07] NS *Data are resented as No. (%) or No. [SD]. In accordance with the classification of Anthonisen et al. 2 Develoment of all symtoms of exacerbation within 12 h. Table 3 Comarison of Hosital Factors Between and Grous* Variables two arameters that relate to the course of recovery from the acute exacerbation following discharge from the hosital. In 22 of the PNAE hositalizations (965) and in 153 of the NPAE hositalizations (71%), at least one infectious etiology for the AE was identified by serologic testing. There was a significantly higher rate of viral etiologies in the PNAE grou, esecially in relation to arainfluenza virus tye 2 and adenovirus. The PNAE grou also had a significantly higher rate of bacterial etiologies, articularly neumococcal. There was no difference between the grous in the rate of atyical bacterial etiologies. Comared to the NPAE grou, a vary small and significantly lower ercentage of atients in the PNAE grou had no infectious etiology identified by serologic tests. More than one etiologic agent (mixed etiology) was found in 13 atients with PNAE atients and in 59 atients with NPAE, who reresent 59% and 39%, resectively, of the atients in whom at least one etiologic agent was identified ( not significant [NS]). In two hositalizations, blood culture findings were ositive at admission. One atient with PNAE had a blood culture finding ositive for S neumoniae and also had a ositive serology for that athogen. This atient also had ositive serologic test results for arainfluenza virus tye 1, adenovirus, and M neumoniae. One atient in the NAPE grou had a blood culture finding ositive for Stretococcus mitis. In this atient, serologic testing results were also ositive for adenovirus (Table 4). Discussion (n 217) Invasive ventilation 4 (17) 10 (5) 0.01 Admission to intensive 6 (26) 14 (7) care Mortality 3 (13) 2 (1) Hositalization, d 7.9 [8.3] 4.6 [4.1] Readmission 2 (10) 36 (17) NS Recovery within 30 d 16 (80) 166 (77) NS *Data are resented as No. (%) or No. [SD]. The combination of clinical symtoms tyical of that develo because of CAP brings u the question as to whether it is justified to diagnose such an eisode as. The name of this CHEST / 122 / 4/ OCTOBER,

5 Table 4 Comarison of the Frequency Distribution of Infectious Etiologies Between and Grous* Etiology (n 217) Viral agents Influenza virus tye A 0 (0) 23 (11) NS Influenza virus tye B 3 (13) 12 (6) NS Parainfluenza virus tye 1 3 (13) 16 (7) NS Parainfluenza virus tye 2 9 (39) 29 (13) Parainfluenza virus tye 3 1 (4) 6 (3) NS Adenovirus 5 (22) 15 (7) 0.03 Resiratory syncytial virus 2 (9) 14 (7) NS At least one of the above 18 (78) 99 (46) Bacterial agents S neumoniae 10 (43) 38 (18) H influenzae 3 (13) 7 (3) NS M catarrhalis 1 (4) 8 (4) NS At least one of the above 10 (43) 48 (22) 0.02 Atyical bacterial agents Legionella s. 5 (22) 35 (16) NS M neumoniae 3 (13) 31 (14) NS At least one of the above 8 (35) 64 (30) NS Agent not identified 1 (4) 64 (30) *Data are resented as No. (%). article exresses the osition we take on this question, even though the issue is controversial. According to American Thoracic Society standards, CAP is not excluded from the diagnosis of, 1 but according to the British Thoracic Society guidelines, COPD atients with CAP do not receive a diagnosis of. 9 In a recent review of treatment for 10 and in other studies related to, 11,12 neumonia was excluded; in the studies by Anthonisen et al 2 and Connors et al, 13 neumonia was not excluded; and in still another study, 14 only severe neumonia was excluded. Finally, in one study, neumonia was listed as excluded, but the study was conducted on an outatient basis and chest radiograhs were not obtained routinely on every atient with. 15 This semantic controversy has led to a state in which CAP in a atient with COPD with clinical manifestations of will be called neumonic by some and CAP in a atients with COPD by others. Our decision to refer the aroach that does not exclude atients with CAP from the diagnosis of stemmed from the two following rimary considerations: (1) in a atient in whom the clinical exression of the eisode comletely meets the acceted criteria for and only by chest radiograhy does one know that CAP is resent, there is no justification to eliminate the diagnosis of and it is aroriate to note that the atient has a neumonic exacerbation, thereby strengthening the theraeutic significance of this combination of events; (2) most eisodes take lace and are treated in the community framework on an outatient basis. 16 In this framework, chest radiograhs are not routinely obtained and exclusion of CAP is not a ractical alternative. The comarison of demograhic data and clinical background between the PNAE grou and the NPAE grou shows that there is no significant difference between them in arameters that reflect the severity of the baseline airway obstruction and baseline gas exchange, nor is there any significant difference between them in chronic comorbidity. In contrast, a statistically significant difference was found in most of the arameters that reflect the clinical and laboratory severity of the acute eisode. As exected, this difference demonstrated a more severe exacerbation in the PNAE grou. It should be noted that these differences are based on grou means. A atient-by-atient analysis of these same arameters shows that a substantial number of atients in the NPAE grou had more severe values than some of the PNAE atients. The significance of this finding, in our oinion, is that the clinical and laboratory severity of cannot serve as a reliable redictor of CAP in these acute eisodes. Similarly, the clinical tye of the exacerbation cannot redict whether the acute disease was caused by CAP. The imortant finding of this study is the frequency distribution of infectious etiologies in the two grous. The issue of the referred method to determine the infectious etiology in resiratory infections in general and in CAP and in articular is very comlicated, and a detailed discussion would be beyond the scoe of this article. The factors that brought us to choose the serologic method as the diagnostic method in this study have been detailed and discussed in our revious ublication. 7 Among the etiologies tested for, two viruses known to cause infection in atients with COPD are missing. These are coronavirus and rhinovirus (the cause of the common cold). The serologic diagnosis of these two viruses is articularly difficult, so they were not included in this study. However, at least concerning rhinovirus, the rate of atients with COPD with this infection who require hositalization is very low comared to other viruses. 17 Another resiratory athogen that is consicuously missing from the list of etiologies is Chlamydohila (Chlamydia) neumoniae. This athogen is recognized as an imortant etiological agent in CAP 18 and was included in the original list of etiologies tested for in this study. However, in the data-analysis stage, there was no case, in any of the 240 hositalizations, in which the antibody titer for C neumoniae changed signifi Clinical Investigations

6 cantly between the aired sera for any of the antibody tyes tested. We believe that the feasibility of diagnosing an acute infection with this athogen on the basis of a high, unchanging titer is articularly roblematic in atients with COPD who are known to have a high revalence of chronic infection with this athogen, as diagnosed by a high antibody titer. 19 In these circumstances, we referred to exclude this etiology, desite the obvious roblems associated with this solution. It is reasonable to assume that at least some of the atients who were defined in this study as agent not identified were infected by one of these athogens that are missing from the list of etiologies for infections. As exected, neumococcal etiology, identified in 43% of the PNAE grou, was the most common etiology in that grou. It is interesting that this rate of 43% for neumococcal etiology is identical to the rate found in our revious study in which similar methods were used to test 346 hositalized atients with CAP, only a few of whom were atients with COPD. 20 Even more surrising and interesting is the identity between this finding in the resent study and the rate of neumococcal etiology of 43% reorted in the Sanish study that evaluated CAP etiologies in atients with COPD. 6 This identity was found even though that study used a sectrum of diagnostic methods that are totally different from those used in the resent study. In our oinion, this identity in the rates of neumococcal etiology in the two studies lends suort to the robustness of the finding. Furthermore, we see in this identity indirect, but convincing, roof of the reliability of the serologic method for diagnosing neumococcal infections. Comarison of the other findings in our study with the Sanish studies oints to a substantial difference in the viral etiologies that were identified in 78% of atients in our study comared to a miniscule rate in the Sanish study. Atyical bacterial agents were also found at much lower rates in the Sanish study comared to ours. Based on our knowledge of the sensitivity of the various methods that were used in both studies, we assume that the differences relating to viral and atyical bacterial etiologies stem from the high sensitivity of the methods used in our study. In addition, a convalescence serum samle was obtained from all atients in our study, which has great imortance in the serologic diagnosis of viral and atyical bacterial etiologies. Two imortant bacterial etiologies, H influenzae and M catarrhalis, were identified in this study at much lower rates than reviously ublished studies in which the culture methodology was used to identify causative organisms for. In those studies these two bacteria, esecially H influenzae, were identified as the redominant organisms. The exlanation for these results in the resent study is that the immunologic/serologic reaction to these two bacteria is strain secific. 21,22 The serologic assay for the two bacteria utilized antigens derived from nonhomologous strains and therefore underestimated the role of infections with these two bacteria in the exacerbations. This limitation of the serologic method in relation to these two bacteria is articularly imortant from the oint of view of the frequency distribution of all etiologies for found in our study and for any theraeutic conclusions that may be derived from it. From the oint of view of the frequency distribution of etiologies in the PNAE grou comared to the NPAE grou, there is a significant difference in revalence for some of the etiologies, but not to the extent that would justify basing a different theraeutic strategy for on the resence or absence of CAP. The American Thoracic Society guidelines for the management of adults with CAP that were recently ublished 23 were based, among others, on two imortant observations that have been confirmed in a number of studies over the ast decade. One observation is the relatively high revalence of atyical athogens among the causes of CAP, and the other observation is the not-uncommon ossibility that more than one athogen (mixed infection) articiated in the athogenesis of CAP. From the viewoint of these two observations, the findings of the resent study indicate a similar rate of atyical etiologies in both grous and the absence of a significant difference in the rate of mixed infections between the two grous, even though the rate is higher in the PNAE grou. These findings raise the seculative question of whether it does not make sense to recommend the same antibiotic theray for atients with with and without CAP? This imortant question should be tested in further studies designed to secifically address this issue. We conclude that CAP is common among atients hositalized with and usually causes the exacerbation to have more severe clinical and laboratory arameters, but the rate of atyical etiologies is similar in both grous. The theraeutic imlications of these findings should be investigated further. References 1 American Thoracic Society. Standards for the diagnosis and care of atients with chronic obstructive ulmonary disease. Am J Resir Crit Care Med 1995; 152:S77 S120 2 Anthonisen NR, Manfreda J, Warren CPW, et al. Antibiotic theray in exacerbations of chronic obstructive ulmonary disease. Ann Intern Med 1987; 106: Marrie TJ, Durant H, Yates L. Community-acquired neumonia requiring hositalization: 5-year rosective study. Rev Infect Dis 1989; 11: CHEST / 122 / 4/ OCTOBER,

7 4 Pachon J, Prados MD, Caote F, et al. Severe communityacquired neumonia: etiology, rognosis and treatment. Am Rev Resir Dis 1990; 142: Torres A, Serra-Batlles J, Ferrer A, et al. Severe communityacquired neumonia: eidemiology and rognostic factors. Am Rev Resir Dis 1991; 144: Torres A, Dorca J, Zalacain R, et al. Community-acquired neumonia in chronic obstructive ulmonary disease: a Sanish multicenter study. Am J Resir Crit Care Med 1996; 154: Lieberman D, Lieberman D, Ben-Yaakov M, et al. Infectious etiologies in acute exacerbation of COPD. Diagn Microbiol Infect Dis 2001; 40: Quanjer PH, Tammeling GJ, Cotes JE, et al. Lung volumes and forced ventilatory flows: reort of the Working Party for the Standardization of Lung Function Tests, Euroean Community for Steel and Coal; Official Statement of the Euroean Resiratory Society. Eur Resir J Sul 1993; 16: British Thoracic Society. Guidelines for the management of chronic obstructive ulmonary disease: management of acute exacerbations of COPD. Thorax 1997; 52(sul 5):S16 S21 10 Calverley PMA, Rennard S, Agusti AGN, et al. Current and future management of acute exacerbations of chronic obstructive ulmonary disease. Eur Resir Rev 1999; 9: Smith JA, Redman P, Woodhead MA. Antibiotic use in atients admitted with acute exacerbations of chronic obstructive ulmonary disease. Eur Resir J 1999; 13: Soler N, Torres A, Ewig S, et al. Bronchial microbial atterns in severe exacerbations of chronic obstructive ulmonary disease (COPD) requiring mechanical ventilation. Am J Resir Crit Care Med 1998; 157: Connors AF Jr, Dawson NV, Thomas C, et al. Outcomes following acute exacerbation of severe chronic obstructive lung disease: The SUPPORT investigators (Study to Understand Prognosis and Preferences for Outcomes and Risks of Treatments). Am J Resir Crit Care Med 1996; 154: Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive ulmonary disease. N Engl J Med 1995; 333: Dewan NA, Rafique S, Kanwar B, et al. Acute exacerbation of COPD: factors associated with oor treatment outcome. Chest 2000; 117: Snow V, Lascher S, Mottur-Pilson C, et al. Evidence base for management of acute exacerbations of chronic obstructive ulmonary disease. Ann Intern Med 2001; 134: Walsh EE, Falsey AR, Hennessey PA. Resiratory syncytial and other virus infection in ersons with chronic cardioulmonary disease. Am J Resir Crit Care Med 1999; 160: Lieberman D. Atyical athogens in community-acquired neumonia. Clin Chest Med 1999; 20: von Hertzen L, Alakara H, Koskinen R, et al. Chlamydia neumoniae infection in atients with chronic obstructive ulmonary disease. Eidemiol Infect 1997; 118: Lieberman D, Schlaeffer F, Boldur I, et al. Multile athogens in adult atients admitted with community-acquired neumonia: a one year rosective study of 346 consecutive atients. Thorax 1996; 51: Yi K, Sethi S, Murhy TF. Human immune resonse to nontyeable Haemohilus imfluenzae in chronic bronchitis. J Infect Dis 1997; 176: Murhy TF, Kirkham C, DeNardin E, et al. Analysis of antigenic structure and human immune resonse to outer membrane rotein CD of Moraxella catarrhalis. Infect Immun 1999; 67: American Thoracic Society. Guidelines for the management of adults with community-acquired neumonia: diagnosis, assessment of severity, initial antimicrobial theray, and revention. Am J Resir Crit Care Med 2001; 163: Clinical Investigations

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