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ORIGINAL ARTICLE Table of Contents  
Ahead of print publication
Comparative study of bacteriological profile in infective exacerbation of chronic obstructive pulmonary disease and community-acquired pneumonia


 Department of General Medicine, Bangalore Medical College and Research Institute, Bengaluru, Karnataka, India

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Date of Submission28-Apr-2022
Date of Decision20-May-2022
Date of Acceptance22-May-2022
Date of Web Publication21-Sep-2022
 

  Abstract 

Background: Community-acquired pneumonia is a differential diagnosis of acute exacerbation of chronic obstructive pulmonary disease (COPD); further both have similar pathogenic spectra. Both the American Thoracic Society and the European Respiratory Society follow similar empirical antibiotic choices for the two conditions. However, there are some differences in the bacterial spectra between the two conditions, particularly when the severity of the disease differs. In the present study, we want to study the differences in the clinical features, bacteriological spectra, and antibiotic susceptibilities in patients with community-acquired pneumonia versus patients with COPD exacerbation and provide a scientific basis for antibiotic selection. Aims: 1. To analyze the differences in the pathogenic spectra and antibiotic sensitivity profile between COPD exacerbation and community acquired pneumonia. 2. To study the differences in the clinical features and outcomes of the two conditions. Subjects and Methods: The study was a prospective observational study conducted from November 2019 to May 2020 in Bangalore Medical College and Research Institute on 30 patients diagnosed with acute exacerbation of COPD and 30 patients diagnosed with community acquired pneumonia. Detailed history, physical examination, and standard laboratory tests were taken on admission. The presence of new consolidation on chest radiograph was recorded. Sputum specimens collected by expectoration and tracheal suctioning or bronchoalveolar lavage were analyzed by Gram staining and microscopy and also by culture. The isolates were also tested for antibiotic sensitivity. The severity of Chronic obstructive pulmonary disease (COPD) exacerbation was assessed by the DECAF score and the severity of the CAP group was assessed by the Pneumonia Severity Index. The differences between the two groups were analyzed. The progression of the disease and the outcomes were observed. Results: Out of 30 (100%) participants in each group, both pneumonia and COPD participants had higher percentage of male participants; 24 (80%) and 26 (86.7%) participants, respectively. The COPD-exacerbation group was significantly older than the community-acquired pneumonia group (63.20 ± 11.82 vs. 43.73 ± 16.58). Klebsiella pneumoniae, Pseudomonas, Streptococcus pneumoniae, and Escherichia Coli were the most commonly isolated species in COPD subjects, whereas S. pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and other organisms were more commonly isolated from pneumonia participants. The drug-resistance rates of S. pneumoniae to penicillin, macrolide and quinolone antibiotics commonly used empirically to treat community acquired pneumonia was 52.6%, 79% and 79% respectively. The sensitivity of Pseudomonas to Carbapenems was 50% and to fluoroquinolones was 16.7% while all the strains were found to be resistant to Aminoglycosides, Penicillin, Cephalosporins, and Macrolides. Conclusions: In our study, we found that K. pneumoniae was the most common pathogen in patients with an exacerbation of COPD while S. pneumoniae was the most common pathogen in patients with community acquired pneumonia. In our study the organisms responsible for community acquired pneumonia were largely resistant to penicillins, macrolides, and tetracyclines, which are the antibiotics of choice for empirical treatment. Similarly, in patients with exacerbation of COPD, the organisms isolated had a far greater degree of resistance to the above-mentioned antibiotics than that seen in our patients with pneumonia. We conclude that antibiotic regimens should be culture driven rather than empirical to be effective while also countering drug resistance.

Keywords: Chronic obstructive pulmonary disease, culture, exacerbation, pneumonia


How to cite this URL:
Menon A, Nagaraja B S, Chandrashekar AP. Comparative study of bacteriological profile in infective exacerbation of chronic obstructive pulmonary disease and community-acquired pneumonia. APIK J Int Med [Epub ahead of print] [cited 2022 Sep 25]. Available from: https://www.ajim.in/preprintarticle.asp?id=356508



  Introduction Top


According to the Global Burden of Disease (GBD) 2018, COPD is currently the third-leading cause of death worldwide. The India GBD Collaborators in October 2018 showed that COPD and asthma make the second largest contribution to the total mortality burden of India at 10.9%.[1]

The 2018 GBD Study demonstrated that the lower respiratory tract infections (LRTIs), including pneumonia, are the fourth most common cause of mortality globally and the second most frequent reason for years of life lost. Change in pathogens and increase in the antibiotic resistance rate have caused many problems in the treatment of community acquired pneumonia.[1]

Thus far, the exact pathogenesis of COPD exacerbation has not been determined but most scholars believe LRTIs play a major role. Exacerbations pose a considerable economic burden but more importantly repeated exacerbations of COPD lead to deteriorating health-related quality of life and when associated with ventilatory failure, to premature death.[2]

COPD exacerbation often coexists with community-acquired pneumonia; further both have similar pathogenic spectra. Both the American Thoracic Society and the European Respiratory Society follow similar empirical antibiotic choices for the two conditions.

However, there are some differences in the bacterial spectra between the two conditions particularly when the severity of the disease differs.

In the present study, we want to study the differences in the clinical features, bacteriological spectra and antibiotic susceptibilities in patients with community-acquired pneumonia versus patients with COPD exacerbation and provide a scientific basis for antibiotic selection.

Bronchoscopic sampling of the distal airways of the lung has demonstrated the presence of pathogenic bacteria in 50% of COPD exacerbations. Acquisition of new strains of bacterial pathogens has been associated with a more than two-fold increase in the risk of exacerbation.[3] Bacterial exacerbations are associated with increased numbers of activated neutrophils in sputum and increased frequency of exacerbations[4] that decline with use of antibiotics. Because of chronic colonization, it is difficult to incriminate one of these organisms as a specific cause of an acute infection. However, predominant growth of one organism, its correlation with gram staining, its association with a change or worsening of symptoms in a previously stable COPD patients and the acute elevation of inflammatory markers can resolve this dispute.

In 2015, Sobhy et al. in Cairo[5] found that the most prevalent organism in their study of 110 patients with an exacerbation of COPD was Klebsiella pneumoniae, followed by Acinetobacter spp., Pseudomonas aeruginosa, Enterobacter spp. and Escherichia coli. The most prevalent organisms in both the intensive care unit (ICU) and the ward were K. pneumoniae and Acinetobacter spp. There was a higher incidence of Acinetobacter spp., Pseudomonas spp., and Enterobacter spp. in severe to very severe COPD compared with mild-to-moderate COPD. Acinetobacter spp was found to have a higher incidence in acidotic pH than in patients without acidosis. Klebsiella spp., Acinetobacter spp., Pseudomonas spp., Enterobacter spp. had a higher incidence in ex-smokers. A higher incidence of Proteus spp. and Streptococci spp. was found in smokers.[5]

Shimizu et al. in 2015 in Tokyo found that the most common organisms in COPD exacerbation were Streptococcus pneumoniae, Haemophilus influenza and Enteric or non-fermenting Gram-negative bacilli.[6]

Neutrophil elastase is a major driver of lung injury and is elevated in bacterial exacerbations contributing to the loss of lung function seen in COPD.[7]

In 2011, Li et al. in a study conducted in China found that the most common pathogens in the community-acquired-pneumonia patients were Streptococcus pneumoniae, Haemophilus influenzae, K. pneumoniae, S. aureus, and E. coli. Pseudomonas aeruginosa is especially common in the patients with serious or extremely serious COPD.[8]

In 2010, Gutierrez et al. found that sputum from CAP patients induced the M1 phenotype which promotes inflammation and bactericidal activity and that from AECOPD patients induced an M2-like phenotype which promotes inhibition of inflammation.[9]

The differences in the microenvironment seen in these two diseases and the pattern of inflammation could explain the differences in their pathogenic profile.


  Subjects and Methods Top


  1. Study design: Prospective observational study
  2. Study period: November 2019 to May 2020
  3. Place of study: Bangalore Medical College and Research Institute and hospitals attached to it.
  4. Sample Size: 60 patients.


According to the data obtained from previous studies and considering the local current rates of admission with acute exacerbation of COPD and community acquired pneumonia.

Sample size estimation

  • P1 Probability of variable in sample-1 (Value <1.0) 0.47*
  • P2 Probability of variable in sample-2 (Value <1.0) 0.53*
  • P Arithmetic average of P1 and P2 0.5.


AH Alternate hypothesis ONE sided (1), or TWO sided? (2) 1

  • 1-α Set level of confidence (value <1.0). Usual values 0.95;0.99 0.9
  • 1-β Set level of power of test (value <1.0). Usual values 0.8; 0.9 0.8
  • Z1 Z value associated with set level of alpha (One sided) 1.28
  • Z2 Z value associated with set level of beta 0.84
  • D Absolute precision 0.15
  • n Minimum sample size 30
  • Substituting the values in the above formula, sample size obtained is 30 per group
  • Since there are two groups, total sample size is 30 × 2 = 60.


Inclusion criteria

  1. Patients who are above 18 years of age
  2. Patient or the legally authorized relatives giving informed consent (Annexure-1)
  3. For the patients in COPD exacerbation- Patients were diagnosed by the clinician concerned depending upon the presence of two of the following symptoms in patients with primary diagnosis COPD supported by spirometric evidence of airflow obstruction (FEV1/FVC <0.70) when clinically [Table 1]. Increased cough 2. Increased purulence and/or volume of expectorations 3. Increased severity of dyspnea For those patients not having a baseline spirometry report, on discharge, spirometric evidence of airflow obstruction (FEV1/FVC <0.70)
  4. For community acquired pneumonia group, patients with a new infiltrate in chest radiograph and at least two compatible clinical symptoms (fever, cough, expectoration, and pleuritic chest pain) diagnosed outside the hospital in ambulatory patients or within 48 h of admission into the hospital
  5. Patients with positive sputum microbiology report.
Table 1: Comparison of age between the groups using independent sample t-test

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Exclusion criteria

  1. Patient or the legally authorised relatives not willing to give informed consent
  2. Patient with age <18 years
  3. For patients in the COPD exacerbation group-Patients diagnosed with bronchiectasis or apparent consolidation on chest radiograph
  4. For the patients in the community acquired pneumonia group Patients diagnosed with COPD, patients who have developed signs and symptoms of pneumonia at 48 h or longer after admission
  5. Patients with sputum microbiology showing growth of only normal commensals of the respiratory tract.


Methodology

The prospective observational study will be undertaken from November 2018 to May 2020 in General Medicine Department of Bangalore Medical College and Research Institute and hospitals attached to it. After obtaining approval and clearance from the institutional ethics committee, the patients fulfilling the inclusion criteria will be enrolled for the study after obtaining informed consent.

Patients with primary diagnosis of COPD supported by spirometric evidence of airflow obstruction (FEV1/FVC <0.70) when clinically stable and who had presented with an exacerbation which was diagnosed depending upon the presence of two of the following symptoms: (1) Increased cough (2) Increased purulence and/or volume of expectorations (3) Increased severity of dyspnoea were chosen as one group of the study population. For those patients not having a baseline spirometry report, on discharge, spirometry will be done in order to establish the diagnosis of COPD.

Patients diagnosed with community acquired pneumonia were chosen as the second group of the study population, which was defined as presence of a new infiltrate in chest radiograph and at least two compatible clinical symptoms (fever, cough, expectoration, pleuritic chest pain) diagnosed outside the hospital in ambulatory patients or within 48 h of admission into the hospital.

Details about the patient such as age, sex, smoking history, antibiotic and glucocorticoid use, comorbidities, admission leukocyte count, arterial blood gas analysis, biochemistry panel were collected. The presence of new consolidation on chest radiograph was recorded. Sputum specimens collected by expectoration, tracheal suctioning, or bronchoalveolar lavage were analyzed by Gram staining and microscopy and also by culture. The isolates were also tested for antibiotic sensitivity. The severity of COPD exacerbation was assessed by the DECAF score[10] which includes the following parameters: Extended MRC Dyspnea Scale (eMRCD), Eosinopenia (<0.05 × 109/L), Consolidation on X-ray, Acidemia, and atrial fibrillation.

The severity of the CAP group was assessed by the Pneumonia Severity Index.[11] This system uses 20 clinical parameters in categories of age, presence of comorbidities, vital sign abnormalities, and laboratory and radiologic findings. Based on a point system, five prognostic groups (I–V) were defined. The lowest scores (Group I) are associated with low mortality, and the highest scores (Group V) are associated with the highest mortality. The differences between the two groups were analyzed. The progression of the disease and the outcomes were observed.

Outcome measures

Efficacy parameters (clinical outcome parameters).

  1. Mortality rates out of the patients studied the percentage of deaths during the period of hospitalization
  2. Ventilator requirements percentage of patients that developed respiratory failure necessitating ventilator requirement
  3. Number of days of hospital stay.


Statistical analysis

SPSS (Statistical Package for the Social Sciences) software version 20. (IBM SPSS statistics [IBM corp. Armonk, NY, USA released 2011]) was used to perform the statistical analysis.

The data collected were analyzed systematically using the descriptive statistics, namely mean, standard deviation, percentage wherever applicable.

Appropriate parametric and nonparametric tests were used. Inferential statistics such as Chi-square test and Fischer's exact test were used.

P < 0.05 was considered to be statistically significant.

Statistical power for the intragroup comparison in the study was 80%.


  Results Top


Out of the 60 patients studied, 30 patients were cases of acute exacerbation of COPD and 30 patients were cases of community acquired pneumonia.

In our study, the mean age of the COPD patients was higher than that of the pneumonia group (63.20 ± 11.82 years vs. 43.73 ± 16.58 years) [Table 1]. Most pneumonia participants belonged to the age range of 46–60 years, whereas COPD participants belonged to the age group of 61–75 years [Figure 1]. Chi-square test was applied to associate the age with groups. Chi-square test showed statistically significant association between age and groups (χ2 = 20.81, P = 0.00).
Figure 1: Comparison of age between the groups

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Both pneumonia and COPD participants were predominantly males (24 [80%] and 26 [86.7%] subjects respectively). Chi-square test showed no statistically significant association between gender and groups (χ2 = 0.48, P = 0.48). 53.3% of the COPD patients were smokers while 46.7% who were nonsmokers were all exposed to biomass fuel.

Diabetes mellitus was present in 11 out of 30 (36.7%) pneumonia subjects and 14 out of 30 (46.7%) COPD subjects. HTN was seen in 10 out 30 (3%) subjects each in pneumonia and COPD subjects. Chi-square test showed no statistically significant association between any of the co-morbidities and groups [Table 2].
Table 2: Distribution of habits and co-morbidities

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Mean total leukocyte count was higher in pneumonia subjects as compared to COPD subjects (14,851.67 ± 6571.12 vs. 13,632.93 ± 4362.06). However, independent sample t-test showed no statistically significant difference between groups with respect to the total leukocyte count (P = 0.40). The mean neutrophil count (%) was slightly higher in COPD subjects as compared to pneumonia subjects (80.73 ± 9.97 vs. 80.53 ± 9.77) however by the independent sample t-test this was not found to be statistically significant (P = 0.93). Among the patients with pneumonia, 16.7% (5/30) patients belonged to PSI Class I, 36.7% (11/30) to Class II, 30% (9/30) to Class III, 6.7% (2/30) to Class IV and 10% (3/30) to Class V. Patients with acute exacerbation of COPD were classified based on their DECAF score. 13.3% (4/30) patients had a DECAF score of 2, 36.7% (11/30) had a DECAF score of 3, 30% (9/30) had a DECAF score of 4 and 20% (6/30) had a DECAF score of 5.

Gram positive cocci in pairs and short chains were more commonly isolated in pneumonia subjects (19 out of 30 patients [63.3%]). Gram positive cocci in clusters and Gram-negative cocci were seen more commonly in pneumonia subjects (8 out of 30 [26.7%] and 4 out of 30 [13.3%] subjects, respectively). Gram-negative bacilli were isolated more commonly from the COPD subjects (21 out of 30 patients [70%]) [Table 3].
Table 3: Distribution of microorganisms among the groups

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K. pneumoniae, Pseudomonas, S. pneumoniae, and E. Coli were the most commonly isolated species in COPD subjects whereas S. pneumoniae, Staphylococcus aureus (methicillin sensitive), H. influenzae and other organisms were more commonly isolated from pneumonia subjects. Chi-square test showed statistically significant association with respect to the isolation of S. pneumoniae, K. pneumoniae, Pseudomonas, and H. influenzae from the sputum of patients of each group [Table 3].

Patients with an exacerbation of COPD were found to be sensitive to Penicillin, cephalosporins, carbapenems, macrolides, vancomycin, linezolid and daptomycin whereas pneumonia subjects were more sensitive to Quinolones and aminoglycosides. Equal number of subjects in both groups were sensitive to vancomycin. Chi-square test showed statistically significant association with respect to sensitivity to cephalosporin, carbapenems, vancomycin, linezolid and daptomycin among the two groups (P ≤ 0.05) [Table 4].
Table 4: Distribution of antibiotics among the groups

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Mean hospital stay (in days) was longer among the COPD subjects 11.5 ± 5.08 days as compared to pneumonia subjects whose mean hospital stay was 9.2 ± 4.156 days. However, the independent sample t-test showed no statistically significant difference between the groups with respect to mean hospital stay (P = 0.06).

ICU admission was higher in COPD subjects -16 (53.3%) as compared to pneumonia subjects -6 (20%). The Chi-square test showed statistically significant association with respect to admission to the ICU (P = 0.007).

Ventilator requirement was higher in COPD subjects-10 (33.3%) as compared to pneumonia subjects-4 (13.3%). Chi-square test showed no statistically significant association with respect to ventilator requirement (P = 0.067).

Three (10%) participants died in pneumonia group as compared to 6 (20%) participants in COPD group. Chi-square test showed no statistically significant association with respect to death (P = 0.27).

Among the patients in the pneumonia group, 3 patients had a Pneumonia Severity Index of Class V and all 3 had S. pneumoniae and S. aureus (methicillin sensitive) isolated from the sputum while one of the three patients had Escherichia coli additionally. In patients with less severe pneumonia, S. pneumoniae and H. influenzae were the leading organisms isolated [Table 5].
Table 5: Cross tabulation of pneumonia severity index and micro organisms

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Among the patients with exacerbation of COPD those with DECAF score of 5, Pseudomonas was the most common organism isolated from the sputum (3/6 patients with DECAF score 5%–50%), one patient had both S. pneumoniae and S. aureus (methicillin sensitive), one patient had Enterococcus while one had Klebsiella isolated from the sputum [Table 6].
Table 6: Cross tabulation of dyspnoea, eosinopenia, consolidation, acidemia and atrial fibrillation and micro organisms

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Out of the total of 60 patients, 14 patients required ventilator support and out of these 4 were pneumonia patients and 10 were patients with exacerbation of COPD. Pseudomonas (4/14 ventilated patients-28.6%, statistically significant association of isolation of Pseudomonas from sputum with need for mechanical ventilation P = 0.008), Klebsiella (3/14 ventilated patients-21.4%) and S. aureus (methicillin sensitive) (3/14 ventilated patients-21.4%) were the most common organisms isolated from patients with either pneumonia or exacerbation of COPD requiring mechanical ventilation. Enterococcus and Acinetobacter were isolated only from one COPD patient each and both of these patients required mechanical ventilation (statistically significant with P = 0.03) [Table 7] and [Figure 2].
Figure 2: Ventilator requirement and microorganisms

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Table 7: Cross tabulation of ventilator requirement and micro organisms

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Among the three patients who died in the pneumonia group, one patient had both S. pneumoniae and Escherichia coli isolated from the sputum, one had K. pneumoniae while the other had S. aureus (methicillin sensitive).

Out of the 6 patients in the COPD group who died, two patients had Pseudomonas isolated from the sputum, one had MRSA, one each had Acinetobacter and Enterococcus and the last one had both S. pneumoniae and S. aureus (methicillin sensitive). There was no statistically significant association between the organism isolated and mortality [Table 8] and [Figure 3].
Figure 3: Death and micro-organisms

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Table 8: Cross tabulation of death and micro organisms

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The sensitivity of P. aeruginosa to carbapenems was 50% while the sensitivities to all the other tested antibiotics were lower. Three out of the six patients (50%) with Pseudomonas isolated from sputum had pan antibiotic resistant species.

The sensitivity of Klebsiella species to Carbapenems was 50% and Quinolones 25%, while the sensitivity to other antibiotics was much lower.

The sensitivity of S. pneumoniae from the community acquired pneumonia patients to Carbapenems was 100%, Cephalosporins 78.9% and Penicillin 47.4%, while the sensitivities to Tetracyclines, Macrolides, and Quinolones were lesser probably due to wide spread use of these antibiotics. The sensitivity of S. pneumoniae from community-acquired pneumonia patients was greater than that from COPD exacerbation patients, which could be because S. pneumoniae is isolated less often from community-acquired-pneumonia patients. In patients with exacerbation of COPD, sensitivity to Carbapenems was 60% while the sensitivity to Penicillin and Cephalosporins was 40% [Table 9] and [Table 10].
Table 9: Antibiotic sensitivities across microbial spectrum in community-acquired pneumonia patients

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Table 10: Antibiotic sensitivities across microbial spectrum in chronic obstructive pulmonary disease exacerbation patients

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  Discussion Top


Both community-acquired pneumonia and COPD exacerbation have high morbidity and mortality and are caused by bacterial infections. At present the same empirical treatment is offered for both conditions, however there are some differences in the bacterial spectra between the two conditions particularly when the severity of the disease differs.

COPD exacerbations may be caused by the acquisition of a new bacterial species or by an increase in the absolute number of the same bacteria or a different strain of the same bacteria that already colonizes the airways.

In our study, out of the 60 patients studied, 30 patients were cases of acute exacerbation of COPD and 30 patients were cases of community acquired pneumonia.

The mean age of the COPD patients was higher than that of the pneumonia group (63.20 ± 11.82 years vs. 43.73 ± 16.58 years). Both pneumonia and COPD subjects were predominantly males (24 (80%) and 26 (86.7%) subjects respectively). The mortality rate was higher among the patients with an exacerbation of COPD as compared to patients with pneumonia (20% vs. 10%) as is the rate of mechanical ventilation (71.4% of patients in COPD group vs. 28.6% of patients in the pneumonia group). These characteristics are in agreement with the clinical features of the two diseases.[8]

Due to differences in disease severity, the bacterial distribution was significantly different between the two groups. S. pneumoniae and H. influenzae were the major bacteria in patients with pneumonia of Class I-III (64% of the cases in this class had S. pneumoniae while 16% had H. influenzae). S. aureus (methicillin sensitive) was the most common bacteria in the patients with level IV or greater community acquired Pneumonia as it was seen in all 5 patients falling in Classes IV-V PSI. These results are in keeping with several studies.[12],[13]

K. pneumoniae (33.3%-5 out of 15 patients with DECAF score of 2 and 3), S. pneumoniae (26.7%–4/15 patients with DECAF score of 2 and 3) and E. Coli (26.7%-4/15 patients with DECAF score of 2 and 3) were the major bacteria in patients with mild COPD exacerbation. In the patients with severe COPD exacerbation, Pseudomonas (40%–6/15 patients with DECAF score 4 and 5), K. pneumoniae (20%–3/15 patients with DECAF score 4 and 5) whereas the percentage of S. pneumoniae was only 6%. Overall, across all severities of exacerbation of COPD, K. pneumoniae was the most common bacterium to be isolated. These results coincide with those of Lin et al.,[14] who found that the most prevalent microorganism in the sputum culture of patients with acute exacerbation of COPD was K. pneumoniae (19.6%), followed by P. aeruginosa (16.8%), H. influenzae (7.5%), and Acinetobacter baumannii (6.9%), of Enterobacter spp. In accordance with these results, Li et al.[15] concluded that K. pneumoniae and P. aeruginosa are the most common sputum pathogens in hospitalized patients with Acute exacerbation of COPD. However, in the study by Chawla et al.,[16] Pseudomonas aeruginosa (25.92%) was the predominant organism in hospitalized patients, whereas K. pneumoniae (33.33%) was the most common pathogen isolated from out-patients. This difference in the predominant organism could be because the study by Chawla et al.[16] included both in-patients and out-patients with in-patients more likely to acquire Pseudomonas from the hospital setup. The non-fermenting bacteria (e.g., P. aeruginosa and A. baumannii) were found only in patients with a high DECAF score. H. influenzae was not isolated in our study and other Asian studies[16] as well, though it is a common pathogen in western countries. This difference may be due to the different environmental conditions and the use of antibiotics.

Hence the etiology varies between patients with an exacerbation of COPD and those with community-acquired-pneumonia and also within each group based on the severity of the disease.

S. pneumoniae was the most common organism isolated in patients with community acquired pneumonia with an isolation rate of 63.3% and an isolation rate of 16.7% among patients with an exacerbation of COPD. In our study the drug resistance rates of S. pneumoniae to penicillin, macrolide and quinolone antibiotics commonly used empirically to treat community acquired pneumonia was 52.6%, 79% and 79% respectively. This leaves only Cephalosporins and Carbapenems with acceptable sensitivity patterns. This could be due to widespread use of these oral antibiotics possibly in combinations to treat out patient cases. This was similar to the study by Li et al.,[8] where the drug resistance rates of S. pneumoniae to penicillin and macrolide antibiotics could reach 42% and 90%, respectively.

Methicillin sensitive S. aureus was the next most common organism to be isolated from patients with community acquired pneumonia with an isolation rate of 30% of the total number of cases. In our study none of the patients with pneumonia had MRSA isolated. This differs from the study by Li et al.[8] where the percentage of isolated methicillin-resistant S. aureus was 69%. This could be due to different environmental conditions and inadvertent use of antibiotics.

P. aeruginosa was the common bacteria in severe COPD exacerbation and was especially common in older patients. In our study, Pseudomonas was the causative agent in 20% of patients with exacerbation of COPD, while none of the patients with community acquired pneumonia had Pseudomonas cultured from their sputum. The sensitivity to Carbapenems was 50% and to fluoroquinolones was 16.7% while all the strains were found to be resistant to Aminoglycosides, Penicillin, Cephalosporins and Macrolides. This was in keeping with other studies. Chawla et al.[16] found that about 60% of isolated Pseudomonas aeruginosa was resistant to the commonly used first and second generation cephalosporins. The resistance to aminoglycosides is probably because these drugs have a weak sterilization effect in an acidic and hypoxic environment and are hence readily susceptible to resistance.[17] The percentage of multiple-drug-resistant P. aeruginosa was relatively high in our study, which might be due to the patients' advanced ages, comorbidities and long hospitalization period.

Out of the total of 60 patients, 14 patients required ventilator support and out of these 4 were pneumonia patients and 10 were patients with exacerbation of COPD. Pseudomonas (4/14 ventilated patients-28.6%, statistically significant association of isolation of Pseudomonas from sputum with need for mechanical ventilation P = 0.008), Klebsiella (3/14 ventilated patients-21.4%) and S. aureus (methicillin sensitive) (3/14 ventilated patients-21.4%) were the most common organisms isolated from patients with either pneumonia or exacerbation of COPD requiring mechanical ventilation. Enterococcus and Acinetobacter were isolated only from one COPD patient each and both of these patients required mechanical ventilation (statistically significant with P = 0.03). This could be because these organisms are usually isolated from patients with advanced age, comorbidities and preexisting structural lung damage.

The mortality rates of the COPD exacerbation and community acquired pneumonia groups were 20% and 10% respectively. There was no statistically significant association between the organisms isolated from either pneumonia patients or COPD patients and mortality.

The limitation of our study was that viruses which are a leading cause for both community acquired pneumonia and acute exacerbations of COPD were not researched.


  Conclusions Top


In our study, we found that K. pneumoniae was the most common pathogen in patients with an exacerbation of COPD while S. pneumoniae was the most common pathogen in patients with community-acquired pneumonia. There were significant differences in the bacterial spectra between the two conditions, particularly when the severity of the disease differs. In our study, the organisms responsible for community-acquired pneumonia were largely resistant to penicillins, macrolides, and tetracyclines, which are the antibiotics of choice for empirical treatment. This is probably due to widespread out patient use of these oral antibiotics, which leaves only Cephalosporins, Fluoroquinolones, and Carbapenems with reasonable degree of sensitivity. Similarly, in patients with exacerbation of COPD, the organisms isolated had a far greater degree of resistance to the above mentioned antibiotics than that seen in our patients with pneumonia. This indicates a probability of more recurrent infections in the COPD population and also inadvertent use of antibiotics which is not culture driven. Hence, it is the need of the hour to attempt to obtain and culture respiratory specimens as early as possible in spite of initiation of an empirical treatment regimen to further guide an appropriate antibiotic course.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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Correspondence Address:
Anindita Menon,
001, Ansal Krsna 2, Hosur Road, Adugodi, Bengaluru - 560 030, Karnataka
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_58_22



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    -  Nagaraja B S
    -  Chandrashekar AP


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