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Year : 2015  |  Volume : 18  |  Issue : 2  |  Page : 57-60

Ventilator-associated pneumonia: Its incidence, the risk factor and drug resistance pattern in a tertiary care hospital

1 Department of Microbiology, KPC Medical College, Jadavpur, Kolkata, West Bengal, India
2 Department of Microbiology, Calcutta National Medical College, Kolkata, West Bengal, India
3 Department of Microbiology, IPGMER, Kolkata, West Bengal, India

Date of Web Publication14-Jul-2015

Correspondence Address:
Dr. Rajdeep Saha
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DOI: 10.4103/1118-8561.160797

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Background: Ventilator-associated pneumonia (VAP) is an infection of the lung that develops 48 h or longer after mechanical ventilation. Objectives: The present study was aimed to find out the bacteriological profile of VAP along with the resistance pattern of bacteriological isolates. Materials and Methods: A prospective observational study was conducted from January 2013 to May 2014 among 791 patients admitted in critical care units of our tertiary care hospital. After selection by applying inclusion and exclusion criteria endotracheal aspirates were collected from ventilated patients. Samples were subjected to further processing by Gram-staining, culture, biochemical testing and antibiogram. Results : Out of 791 patients admitted in intensive care unit in this tertiary care hospital with VAP 540 (68.2%) patients were culture positive. Pseudomonas aeruginosa was most commonly isolated pathogen of both early onset and late onset VAP. In early VAP Acinetobacter baumannii showed 62.5% metallo-beta-lactamase (MBL) positivity. P. aeruginosa showed 27.5% MBL positivity, whereas in late onset VAP, 71.4% A. baumannii isolates and 75.8% P. aeruginosa isolates showed MBL positivity, respectively. Conclusion : Simple prevention of aspiration, sterilization of equipments, hand washing of personnel can reduce VAP in hospital care setting.

Keywords: Metallo-beta-lactamase, Pseudomonas aeruginosa, ventilator associated pneumonia

How to cite this article:
Mitra S, Saha R, Datta P, Sarkar M. Ventilator-associated pneumonia: Its incidence, the risk factor and drug resistance pattern in a tertiary care hospital. Sahel Med J 2015;18:57-60

How to cite this URL:
Mitra S, Saha R, Datta P, Sarkar M. Ventilator-associated pneumonia: Its incidence, the risk factor and drug resistance pattern in a tertiary care hospital. Sahel Med J [serial online] 2015 [cited 2021 Sep 27];18:57-60. Available from: https://www.smjonline.org/text.asp?2015/18/2/57/160797

  Introduction Top

Ventilator-associated pneumonia (VAP) is an infection of lung parenchyma occurring 48-72 h or more after intubation due to organisms incubating at the time mechanical ventilation (MV) was commenced. [1] It is the most common nosocomial infection encountered in the intensive care unit (ICU), with 9-28% of all intubated patients developing VAP. [2],[3] Intubation independently increases the risk of developing nosocomial pneumonia at least seven-fold, with a peak in incidence occurring around day 5 of ventilation. [4] VAP may be early - onset, when it occurs during the first 4 days of MV, less severe, better prognosis, but late onset VAP, when it develops 5 or more days after initiation of MV, which is caused by multi-drug resistant pathogens and associated with increased morbidity and mortality. Most cases seem to result from aspiration of pathogenic microorganisms that commonly colonizes the oropharyngeal airway of the critically ill patient. Risk factor of VAP includes: (i) Increase the risk of colonization by potential pathogens (e.g. prior antibiotic therapy, contaminated ventilator circuits, decreased gastric acidity), (ii) increased possibility of aspiration of oropharyngeal contents into the lower respiratory tract (e.g. intubation, decrease level of consciousness, presence of nasogastric tube) and (iii) reduced host defense mechanism in the lung and permit overgrowth of aspirated pathogen (e.g. chronic obstructive pulmonary disease, old age, upper abdominal surgery) . Aspiration of oropharyngeal secretions into the bronchial tree is a major factor in the development of VAP. [5]

Common pathogens include aerobic Gram-negative bacilli, such as Pseudomonas aeruginosa,  Escherichia More Details coli, Klebsiella pneumoniae and Acinetobacter spps. Among Gram-positive cocci, Staphylococcus aureus is more common. Simple measures to decrease the incidence of aspiration like minimal use of proton pump inhibitor, H2 antagonist or reduce the burden of colonization of the oropharynx may aid in the prevention of VAP. A favorable outcome seems to be more likely if appropriate antibiotics are given in a timely manner. This study was conducted to detect bacteriological profile of VAP and to determine the antibiotic sensitivity pattern of bacteriological isolates along with their resistance pattern.

  Materials and Methods Top

This prospective observational study was conducted from January 2013 to May 2014 in patients admitted in critical care units of our tertiary care hospital who were on MV and showed clinical suspicion of VAP. Any patient with modified clinical pulmonary infection score >6 [6],[7] and quantitative culture of endotracheal aspirate with growth thresholds ≥10 5 CFU/ml was taken as a case of VAP.

After selection of patients, aspirates were obtained with a sterile precaution using a 22 inch, no 14 Fr suction catheter and were transported immediately to the microbiological laboratory for processing. The samples were inoculated on Sheep Blood agar, Chocolate agar, and MacConkey agar. All the plates were incubated overnight aerobically at 37° C. Bacterial isolates were identified by standard identification protocol.

For a definitive diagnosis of VAP in this study, the quantitative culture threshold was considered as >10 5 CFU/ml. [8],[9]

Antimicrobial susceptibility testing was performed for all the isolates with positive quantitative cultures according to Kirby-Bauer's disk diffusion method.

  Results Top

The present study was carried out with 791 patients admitted in ICU in this tertiary care hospital with VAP. Of 791 patients, 322 developed VAP within 4 days of admission and hence were considered as early onset VAP and 236 (73.3%) patients among them showed culture positivity [Table 1]. Rest of them (469) were taken as late onset VAP cases, and 304 (64.8%) ou 97 (17.9%), Citrobacter freundii 18 (3.3%), E. coli 40 (7.4%), Pneumococcus 23 (4.3%) Proteus mirabilis 12 (2.2%) Proteus vulgaris 9 (1.7%) and Staphylococcus aureus 66 (12.3%) [Pie chart 1]. Early VAP and late VAP showed considerable differences regarding causative agents and their antibiotic sensitivity pattern.
Table 1: Distribution of cases of VAP according to culture positivity

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In comparison to early onset VAP, organisms responsible for late onset VAP showed multi drug resistance [Table 2], [Table 4], [Table 6].
Table 2: Distribution of pathogen according to onset of VAP

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In early VAP A. baumannii showed 62.5% metallo-beta-lactamase (MBL) positivity. P. aeruginosa showed 27.5% MBL positivity. C. freundii showed 45.5% extended spectrum beta lactamase positivity, whereas in late onset VAP, 71.4% A. baumannii isolates and 75.8% P. aeruginosa isolates showed MBL positivity, respectively [Table 3] and [Table 5].
Table 3: Antibiotic resistance pattern of clinically isolated Gram-negative bacilli causing early onset VAP

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Table 4: Antibiotic resistance pattern of clinically isolated Gram-positive cocci causing early onset VAP

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Table 5: Antibiotic resistance pattern of clinically isolated gram-negative bacilli causing late onset VAP

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Table 6: Antibiotic resistance pattern of clinically isolated Gram-positive cocci causing late onset VAP

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All Streptococcus pneumoniae strains isolated from early onset VAP were penicillin sensitive.

Out of 9 S. pneumoniae isolates 6 isolates were resistant to penicillin (minimal inhibitory concentration ≥2 μg/ml).

  Discussion Top

Ventilator-associated pneumonia is defined as nosocomial pneumonia occurring in a patient after 48 h of MV via a tracheal or tracheostomy tube including pneumonia developing even after extubation. [10]

Ventilator-associated pneumonia occurs in 1-4 patient/1000 ventilator-days is responsible for a mean of 10 extra hospital days and extra cost per episode.

The study was carried out in the department of microbiology of Calcutta National Medical College and Hospital on patients admitted in the various critical care units of the institution coronary care unit, intensive coronary care unit and trauma stabilization unit over a period of 1 year 5 months commencing from January 2013 to May 2014. A total of 791 patients were selected who fulfilled the clinical, radiological and laboratory criteria of VAP. Samples were collected from them and their etiological bacterial agents were determined. Of 791 samples, 540 samples showed bacterial growth. The nonbacterial causes like fungus, e.g. VAP caused by Candida sp. were not taken into consideration. The antibiotic sensitivity and the resistance pattern noted for the bacterial isolates.

It has been shown in the present study that 540 patients came out as culture positive out of 791 samples comprising 68.2% positivity. P. aeruginosa was most commonly isolated organism. Most of these findings are nearly similar to the observation made by Sharma et al. [11] where they have shown out of the 50 cases 20 (40%) were early onset VAP whereas 30 (60%) were late onset VAP and P. aeruginosa as the predominant pathogen with maximum sensitivity to imipenem. In the present study, primary causative organism has been P. aeruginosa both in early VAP (29.3%) and late VAP (39.5%). Acinetobacter along with P. aeruginosa were the predominant pathogen in late VAP. This is different from the observation made by Joseph et al., at (JIPMER) Pondicherry, [12] India where the causative organism of early and late VAP are different. The difference in the observation by the different study might be due to the variation in the resident bacterial flora at the place of study, its sensitivity pattern and other factors like duration of hospitalization prior to ventilation, prior use of antibiotics, type of invasive procedure the patient has undergone and presence of any co-morbidity influences the final outcome.

Ventilator-associated pneumonia is a common and serious nosocomial infection. A clinical suspicion of VAP should prompt collection of lower respiratory tract secretions for microbiological analysis and the rapid administration of appropriate empirical antibiotics. Antibiotic therapy should be routinely evaluated according to clinical response and microbiological results.

The study has provided very important information regarding prevalent microbiological flora in the hospital and choice of antibiotic in this particular hospital setting. Though carbapenems belong to high-end category drug but early initiation of treatment (based on presumptive diagnosis) can cut down cost of treatment by lowering hospital stay, preventing invasive diagnostic and therapeutic interventions and thus reduce morbidity and mortality.

As for any nosocomial infection simple measures like hand washing, use of personal protective equipments such as gloves, face mask, and shoe cover can prevent infection thereby avoiding unnecessary use of antibiotics and will lead to cost curtailment.

Further, it will be prudent enough if a proper antibiotic protocol is developed (keeping in consideration the prevalent microorganism and their sensitivity pattern) and followed rigidly. It will prevent the emergence of resistant strains, and many commonly used drugs can be prevented from falling into the resistant category. The clinicians and the microbiologist should work in tandem to bring about the necessary changes.

  Acknowledgment Top

To all laboratory technician and staffs of all the medical colleges. Without their help, these study would not be completed.

  References Top

Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J Respir Crit Care Med 2002;165:867-903.  Back to cited text no. 1
Craven DE. Epidemiology of ventilator-associated pneumonia. Chest 2000;117:186S-7.  Back to cited text no. 2
Cook DJ, Walter SD, Cook RJ, Griffith LE, Guyatt GH, Leasa D, et al. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med 1998;129:433-40.  Back to cited text no. 3
Heyland DK, Cook DJ, Griffith L, Keenan SP, Brun-Buisson C. The attributable morbidity and mortality of ventilator-associated pneumonia in the critically ill patient. The Canadian Critical Trials Group. Am J Respir Crit Care Med 1999;159:1249-56.  Back to cited text no. 4
Safdar N, Crnich CJ, Maki DG. The pathogenesis of ventilator-associated pneumonia: Its relevance to developing effective strategies for prevention. Respir Care 2005;50:725-39.  Back to cited text no. 5
Koenig SM, Truwit JD. Ventilator-associated pneumonia: Diagnosis, treatment, and prevention. Clin Microbiol Rev 2006;19:637-57.  Back to cited text no. 6
Fartoukh M, Maitre B, Honoré S, Cerf C, Zahar JR, Brun-Buisson C. Diagnosing pneumonia during mechanical ventilation: The clinical pulmonary infection score revisited. Am J Respir Crit Care Med 2003;168:173-9.  Back to cited text no. 7
Valencia Arango M, Torres Martí A, Insausti Ordeñana J, Alvarez Lerma F, Carrasco Joaquinet N, Herranz Casado M, et al. Diagnostic value of quantitative cultures of endotracheal aspirate in ventilator-associated pneumonia: A multicenter study. Arch Bronconeumol 2003;39:394-9.  Back to cited text no. 8
Marquette CH, Georges H, Wallet F, Ramon P, Saulnier F, Neviere R, et al. Diagnostic efficiency of endotracheal aspirates with quantitative bacterial cultures in intubated patients with suspected pneumonia. Comparison with the protected specimen brush. Am Rev Respir Dis 1993;148:138-44.  Back to cited text no. 9
Niederman MS, Craven DE. Guidelines for the management of adults with hospital - Acquired and ventilator associated and Health care associated pneumonia. Am J Respir Crit Care Med 2005;171:388-416.  Back to cited text no. 10
Sharma PC, Raut SS, More SR, Rathod VS, Gujar VM. The microbiological profile of ventilator associated pneumonia. J Evol Med Dent Sci 2012; 1:192.  Back to cited text no. 11
Joseph NM, Sistla S, Dutta TK, Badhe AS, Rasitha D, Parija SC. Ventilator-associated pneumonia in a tertiary care hospital in India: Role of multi-drug resistant pathogens. J Infect Dev Ctries 2010;4:218-25.  Back to cited text no. 12


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


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