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Year : 2018  |  Volume : 61  |  Issue : 3  |  Page : 375-379
Bacteriological profile of ventilator-associated pneumonia in a tertiary care hospital

1 Department of Microbiology, S.C.B. Medical College, Cuttack, Odisha, India
2 Department of Microbiology, AIIMS, Raipur, Chhattisgarh, India
3 Department of Microbiology, AIIMS, Bhubaneswar, Odisha, India

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Date of Web Publication13-Jul-2018


Background: Ventilator-associated pneumonia (VAP) is the most frequent intensive care unit (ICU)-acquired infection. The etiology of VAP and their antimicrobial susceptibility pattern varies with different patient populations and types of ICUs. Materials and Methods: An observational cross-sectional study was performed over a period of 2 years in a tertiary care hospital to determine the various etiological agents causing VAP and to detect the presence of multidrug-resistant (MDR) pathogens in these VAP patients. Combination disk method, Modified Hodge test, ethylenediaminetetraacetic acid disk synergy test, and AmpC disk test were performed for the detection of extended-spectrum beta-lactamase (ESBL), carbapenemases, metallo-beta-lactamases (MBL), and AmpC beta-lactamases, respectively. Results: The prevalence of VAP was 35%. Enterobacteriaceae (66.66%) and Staphylococcus aureus (20%) were common in early-onset VAP, while nonfermenters (50%) and Enterobacteriaceae (40.61%) were predominant from late-onset VAP. Nearly 60.87% of the bacterial pathogens were MDR. ESBL was produced by 21.74% of Enterobacteriaceae. AmpC β-lactamase was positive in 35.29% nonfermenters and 26.08% Enterobacteriaceae. MBL was positive in 17.64% nonfermenters and 17.39% Enterobacteriaceae. Among the S. aureus isolates, 75% were cefoxitin resistant. Prior antibiotic therapy (P = 0.001) and hospitalization of 5 days or more (P = 0.001) were independent risk factors for VAP by MDR pathogens. polymyxin B, tigecycline, and vancomycin were the most sensitive drugs for Gram-negative and positive isolates respectively from VAP. Statistical Analysis: SPSS for Windows Version SPSS 17.0 (SPSS Inc., Chicago, IL, USA) and Chi-square with Yates correction. Conclusion: Late-onset VAP is increasingly associated with MDR pathogens. Treatment with polymyxin B, tigecycline, and vancomycin should be kept as last-line reserve drugs against most of the MDR pathogens.

Keywords: Multidrug resistant, risk factors, ventilator-associated pneumonia

How to cite this article:
Patro S, Sarangi G, Das P, Mahapatra A, Mohapatra D, Paty BP, Chayani N. Bacteriological profile of ventilator-associated pneumonia in a tertiary care hospital. Indian J Pathol Microbiol 2018;61:375-9

How to cite this URL:
Patro S, Sarangi G, Das P, Mahapatra A, Mohapatra D, Paty BP, Chayani N. Bacteriological profile of ventilator-associated pneumonia in a tertiary care hospital. Indian J Pathol Microbiol [serial online] 2018 [cited 2021 Jul 24];61:375-9. Available from: https://www.ijpmonline.org/text.asp?2018/61/3/375/236614

   Introduction Top

Ventilator-associated pneumonia (VAP) is the most common nosocomial infection in people receiving mechanical ventilation. VAP is defined as pneumonia occurring more than 48 h after endotracheal intubation/initiation of mechanical ventilation or pneumonia developing even after extubation.[1] VAP developed during the first 4 days of mechanical ventilation is early-onset, usually less severe, mostly caused by antibiotic-sensitive bacteria and with a better prognosis, whereas late-onset VAP develops five or more days after the initiation of mechanical ventilation and is due to multidrug-resistant (MDR) pathogens and is usually associated with increased morbidity and mortality.[2] VAP may be caused by a wide spectrum of bacterial pathogens, which may be polymicrobial and are rarely due to viral or fungal pathogens in immunocompetent hosts.[1] Common etiologic agents are Gram-negative bacilli such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter spp. and Staphylococcus aureus among Gram-positive cocci.[3] Due to the increased incidence of MDR organisms in Intensive Care Units (ICUs), early and correct diagnosis of VAP is mandatory for optimal antibiotic therapy.[2] The frequency of specific MDR pathogens causing VAP varies in hospitals, patient populations, prior use of antibiotics and type of ICUs emphasizing the need for routine surveillance.[4] The objectives of this study were to detect the etiological agents of VAP, determine their antibiotic susceptibility pattern, to screen for the presence of β-lactamases such as extended-spectrum beta-lactamases (ESBLs), AmpC β-lactamases, carbapenemases, and metallo-beta-lactamases (MBL) and to determine the risk factors of MDR pathogens among the VAP patients.

   Materials and Methods Top

Study design

Study design involves observational cross-sectional study.

Study site

Study site includes the Department of Microbiology, S.C.B. Medical College and Hospital, Cuttack.

Study period

Study period includes October 2011–September 2013.

Study subject

Study subject includes

endotracheal tube aspirate (ETA) obtained from patients admitted to the ICU of medicine (MICU) and central ICU (CICU) with clinical suspicion of VAP.

Inclusion criteria

  1. Patients admitted to the CICU/MICU developing pneumonia after 48 h of endotracheal intubation/initiation of MV/even after extubation
  2. Those who are intubated or on MV having a Modified Clinical Pulmonary Infection Score (CPIS) >6.[5]

Exclusion criteria

Exclusion criteria include those developed pneumonia within 48 h of mechanical ventilation.

Confirmation of ventilator-associated pneumonia diagnosis

Confirmation of VAP diagnosis involves observing >105 colony-forming unit (CFU)/ml by quantitative culture of endotracheal tube aspirate (ETA).[6]

Demographic information collection

Data such as age, gender, date of admission into ICU, duration of hospitalization, duration of mechanical ventilation, details of antibiotic therapy, history of surgery, underlying diseases, use of steroids, presence of neurological disorders, and impairment of consciousness were recorded from the medical records and bedside charts.

Specimen collection (endotracheal tube aspirates)

ETA were obtained with sterile precaution using a 22 inch, No. 14 Fr suction catheter and collected in a sterile container. A length of approximately 24 cm of the catheter was passed through the endotracheal tube, and secretions were aspirated without instilling saline. After the catheter was withdrawn, 10-fold serial dilution of ETA was done with 0.9% normal saline and then plated for quantitative culture and Gram stain.

Microbiological processing

ETA were mechanically homogenized using sterile glass beads and were centrifuged for 1 min. The samples were then serially diluted in 0.9% sterile saline solution with final dilutions of 10−2, 10−3, and 10−4 and plated on sheep blood agar, chocolate agar, MacConkey agar and two Saboraud's dextrose agar (SDA) by using 2 mm nichrome wire loop (Hi-media, Mumbai, India), which holds 0.005 ml of solution. All plates were incubated overnight aerobically at 37°C except one SDA plate which was kept at room temperature. The plates for bacterial culture were incubated up to 48 h and SDA plates up to 1 week. For definitive diagnosis of VAP, quantitative culture threshold of >105 CFU/ml was considered significant. And growth of any organism below 105 CFU/ml was assumed to be due to colonization or contamination.[6] Any significant growth was identified based on standard microbiological techniques.[7] Antimicrobial susceptibility was performed for all the isolates with positive quantitative cultures according to Kirby Bauer's disk diffusion method.[8] For Gram-positive bacteria, vancomycin (30 μg), linezolid (30 μg), ciprofloxacin (1 μg), azithromycin (30 μg), gentamicin (5 μg), cefoxitin (30 μg), and tigecycline (15 μg) were selected. For Gram-negative bacteria, piperacillin + tazobactam (100 μg/10 μg), amikacin (5 μg), ciprofloxacin (1 μg), cefotaxime (30 μg), ceftazidime (30 μg), meropenem (10 μg), polymyxin B (300 μg), and tigecycline (15 μg) were selected. Suspected ESBL-producing organisms were confirmed by combination disk test using ceftazidime (30 μgm) and ceftazidime + clavulanic acid (30 μg/10 μg) disks.[9] Isolates that yielded a cefoxitin zone diameter of <18 mm and resistant to third-generation cephalosporins were tested for AmpC enzyme production, by the popular AmpC disk test.[10] Modified Hodge Test was carried out for the detection of carbapenemase.[11] Isolates showing resistance to carbapenems were selected for the detection of MBL enzymes by imipenem–ethylenediaminetetraacetic acid disk synergy test.[11] The Gram-negative isolates from VAP expressing ESBL, AmpC β-lactamases or MBL and Methicillin-resistant S. aureus (MRSA) among the Gram-positive isolates were considered as MDR pathogens.[2],[12]

Statistical analysis

Data entry and analysis were done using SPSS for Windows Version SPSS 17.0 (SPSS Inc., Chicago, IL, USA). Statistical analysis was done by Chi-square with Yates correction.

   Results Top

Totally 486 patients were admitted in the MICU and CICU from October 2011 to September 2013, and 100 among them were enrolled for the study according to the inclusion criteria. Out of 100 clinically diagnosed VAP cases, 35 (35%) were confirmed by quantitative culture, of which 10 (10%) were categorized under early-onset and 25 (25%) under late-onset VAP. The infection rates were found to be more common in males than in females, and the predominant age group involved were 41–60 years, in both males and females. Majority of patients involved in VAP were road traffic accidents 9 (25.71%), renal failure 8 (22.86%), and chronic obstructive pulmonary disease 5 (14.29%). Out of 35 culture positive cases, 23 (65.71%) showed monomicrobial and 12 (34.29%) polymicrobial growth. A total of 47 pathogens were isolated including 15 (31.91%) from early-onset and 32 (68.09%) from late-onset VAP. Gram-negative and Gram-positive bacteria isolated were 40 (85.10%) and 6 (12.77%), respectively, from both types of VAP. The pathogens isolated from early-onset VAP were Enterobacteriaceae 10 (66.66%), P. aeruginosa 1 (6.67%), S. aureus 3 (20%), and Coagulase-negative staphylococci (CONS)1 (6.67%). Pathogens isolated from late-onset VAP were nonfermenters 16 (50%) including Pseudomonas spp. 5 (15.62%), Burkholderia spp. 1 (3.13%), Acinetobacter spp. 10 (31.25%), Enterobacteriaceae 13 (40.61%), S. aureus 1 (3.13%), Enterococcus spp. 1 (3.13%), and Candida spp. 1 (3.13%). The etiological agents and their antibiotic resistance patterns were summarized in [Table 1] and [Table 2]. Acinetobacter spp. showed 100% resistance to ceftazidime, amikacin and ciprofloxacin and 75% of the S. aureus isolates were MRSA. Nonfermenters 9 (69.23%) were isolated mostly from CICU whereas members of Enterobacteriaceae 20 (58.81%), nonfermenters 8 (23.52%), Gram-positive bacteria 5 (14.71%) and Candida spp. 1 (2.94%) were isolated from the MICU. Twenty-eight (60.87%) of the 46 bacterial isolates were MDR. MDR pathogens found among late-onset and early-onset VAP were 19 (67.85%) and 9 (32.15%), respectively [Table 3]. AmpC β-lactamase was detected in 6 (35.29%) and 6 (26.08%) of nonfermenters and members of Enterobacteriaceae, respectively. Nearly 21.74% (5/23) of Enterobacteriaceae were positive for ESBL. MBL were detected in both nonfermenters 3 (17.64%) and Enterobacteriaceae 4 (17.39%) [Table 3]. However, ESBL production among nonfermenters was nil in our study. About 75% (3/4) of MRSA and one methicillin-resistant CONS spp. were isolated from early-onset VAP [Table 4]. Prior antibiotic therapy (P = 0.000) and current hospitalization of 5 days or more (P = 0.001) were independent risk factors for VAP caused by MDR pathogens [Table 5].
Table 1: Antibiotic resistance pattern of isolates from early-onset ventilator-associated pneumonia (n=15)

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Table 2: Antibiotic resistance pattern of isolates from late-onset ventilator-associated pneumonia (n=32)

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Table 3: Mechanisms of drug resistance in different bacterial isolates

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Table 4: Prevalence of multidrug-resistant pathogens in early- and late-onset ventilator-associated pneumonia (n=46)

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Table 5: Risk factors associated with ventilator-associated pneumonia pathogens

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   Discussion Top

VAP is an important nosocomial infection among ICU patients receiving mechanical ventilation. The risk of VAP is approximately 3%/day during the first 5 days of ventilation, gradually decreasing to 2% during 5–10 days of ventilation and approximately 1%/day thereafter, thus highest during the early course of hospital stay.[13]

The principal factor for the pathogenesis of VAP is reported to be due to aspiration of oropharyngeal pathogens and the leakage of secretions containing bacteria around the endotracheal tube.[14]

The bacteriological approach for the management of VAP avoids the problem of over treatment by separating colonizers from infecting pathogens.[15] Quantitative cultures of endotracheal aspirate or broncho-alveolar lavage is recommended by the American Thoracic Society for confirmation of VAP.[16] Endotracheal tube aspirate is comparatively less expensive compared to BAL and hence is widely preferable in most of the hospital settings. Investigators have also reported quantitative cultures of ETA to be of equal diagnostic accuracy to other invasive techniques.[17] VAP was confirmed by correlating positive quantitative culture results with the clinical outcome of patients. In the present study, a total of 100 clinically diagnosed VAP cases were evaluated, of which 35% were diagnosed as VAP by quantitative cultures. Age group of 41–60 years were more prone to get VAP in both males and females. Out of 35 culture positive cases, 65.71% had monomicrobial and 34.29% had polymicrobial growth. Several studies have shown up to 40% of VAP to be polymicrobial.[18]

Gram-negative bacteria were isolated in 85.1%, which is well correlated with the study of Rajesh Chawla (87%) in the year 2008.[19] The microbial flora of critically ill patients in hospitals becomes drastically altered within days after admission. The nosocomial Gram-negative pathogens colonize on healthy skin of ICU people, catheters, instruments, and environments that can be even transmitted through the air.[20] Earlier reports showed, among the Gram-negative organisms, P. aeruginosa was the commonest causative agent.[1],[17] However, in the present study, Acinetobacter spp. was found to be the most common isolate (21.27%) followed by K. pneumoniae (19.15%) and Pseudomonas spp. (12.76%). The distribution of etiological agents varies in different ICUs as per patient demographics, methods of diagnosis, duration of hospitalization, ICU stays, and antibiotic policy. In the present study, Enterobacteriaceae (66.66%) were the predominant isolates from early-onset VAP followed by S. aureus (20%). Only single isolate of nonfermenter, i.e., P. aeruginosa (6.67%) was obtained from early-onset VAP. Previous studies by Dey et al. revealed Acinetobacter spp. (48.94%) as the most common isolate from early-onset VAP, in contrast to ours where no Acinetobacter spp. isolated from early-onset cases.[21] But the probable cause for this could not be explained.

Among the Gram-negative isolates, K. pneumoniae showed 100% resistance to ceftazidime, cefotaxime, and ciprofloxacin followed by meropenem (75%). Among the Gram-positive isolates from early-onset VAP, MRSA (66.66%) predominated over methicillin-susceptible S. aureus (MSSA) as reported earlier.[3] Similar to other studies, we also found all the Gram-positive isolates to be 100% sensitive to vancomycin irrespective of MRSA and MSSA.[3],[20] Late-onset VAP was associated with higher rates of infection with MDR pathogens (67.85%) [Table 4]. Acinetobacter spp. (31.25%) was the predominant isolate followed by Pseudomonas spp. (15.62%) and K. pneumoniae (15.625%), which correlated well with other reports.[18] We isolated only one fungus, i.e., non-albicans Candida spp. from an elderly chronic psychiatric patient with septicemia and acute renal failure. The antibiogram of Gram-negative isolates showed highest resistance to ceftazidime (100%) followed by ciprofloxacin (89.65%), amikacin (86.21%), and piperacillin–tazobactam (62.06%). All the Acinetobacter spp. were resistant to ceftazidime, amikacin, and ciprofloxacin. Among the MDR isolates, majority were associated with risk factors such as prior antibiotic therapy (23/28) or current hospitalization for 5 days or more (27/28) [Table 5]. This may be the cause for almost similar pattern of susceptibility in both late- and early-onset VAP. The American Thoracic Society guidelines have also recommended similar treatment options for both early- and late-onset VAP due to MDR pathogens.[2] Present study observed nonfermenters (69.23%) to be the predominant cause of VAP in CICU, while members of Enterobacteriaceae (58.81%) were common in the MICU followed by nonfermenters (23.52%). VAP episodes due to Gram-positive bacteria (7.69%) were relatively less common in the CICU. Knowledge regarding this difference in pathogens causing VAP in different ICU settings will definitely guide for choosing the appropriate empirical antibiotic therapy. AmpC β-lactamases, ESBLs, and MBLs were of much concern in our study. Members of Enterobacteriaceae (21.74%) were positive for ESBL only, but AmpC β-lactamase was produced by most of the nonfermenters as well as Enterobacteriaceae [Table 3]. MBL was produced by most of the Acinetobacter spp. and Klebsiella spp., which differs from other studies.[18],[22],[23] Evaluation of risk factors for VAP revealed that prior antibiotic therapy (P = 0.000) and current hospitalization of 5 days or more (P = 0.001) were independent predictors of VAP caused by MDR pathogens [Table 5]. Hence, the rational use of appropriate antibiotics and unnecessary prolonged hospitalization may reduce patient colonization and subsequent development of VAP with MDR pathogens. Moreover, the increasing occurrence of MDR Gram-negative bacteria is no longer responding to monotherapy and is necessitating the use of combination therapies. However, these findings may not be reflected exactly in other centers. Hence, we suggest further multicentered studies to confirm our findings. Although for the diagnosis of VAP, we did quantitative culture of ETA (>105 CFU/ml) and corroborated our findings with modified CPIS scoring >6, the results are yet to be compared to histology of lung tissue which is considered as the gold standard. So to conclude, quantitative culture of ETA is a practical diagnostic method to confirm clinically suspected VAP and a negative quantitative ETA culture can guide the physicians to focus their attention to extrapulmonary origin of infection.

   Conclusion Top

Knowledge of the susceptibility pattern of the local pathogens can guide the clinicians to choose the appropriate antibiotics according to the likelihood of organisms of early/late-onset VAP. polymyxin B, tigecycline, and vancomycin should be used for successful targeted therapy of MDR pathogens as they showed good in vitro activity. Combined approaches of rational antibiotic therapy might be beneficial to combat high antibiotic resistance in our setup.

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Conflicts of interest

There are no conflicts of interest.

   References Top

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Correspondence Address:
Ashoka Mahapatra
Department of Microbiology, AIIMS, Bhubaneswar, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJPM.IJPM_487_16

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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