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International Journal of Research in Medical Sciences

Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245


www.msjonline.org pISSN 2320-6071 | eISSN 2320-6012

DOI: 10.5455/2320-6012.ijrms20140246
Research Article

Clinical and microbiological facets of ventilator associated pneumonia


in the main stream with a practical contact
Shaik Mohammed Usman*, Pratibha Malini James, Rashmi M

Department of Clinical Microbiology, Kempegowda Institute of Medical Sciences and Research Centre, Bangalore,
Karnataka, India

Received: 9 November 2013


Accepted: 2 December 2013

*Correspondence:
Dr. Shaik Mohammed Usman,
E-mail: [email protected]

© 2014 Usman SM et al. This is an open-access article distributed under the terms of the Creative Commons
Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction
in any medium, provided the original work is properly cited.

ABSTRACT

Background: Ventilator-associated pneumonia (VAP), the most apparent infection in ICUs; life threatening,
symbolizes an additional healthcare burden. Clinical traits and etiological agents vary. Early diagnosis is captious &
apt tactic of quantitative culture is advocated. Regular surveillance is imperative to define strategies. The objective
was to conceptualize VAP; put forth our experience of its occurrence, causative bacteria, clinical silhouette and
associated variables; and to pattern antimicrobial resistance in ICUs; contributing this data to devise more pertinent
approach.
Methods: A prospective survey, executed at a tertiary care set up (multidisciplinary ICUs) analysed clinical and
microbiological aspects of 120 patients (>48 hours-mechanical ventilation) in congruence with a clinical criteria of
pneumonia by standard microbiological means. Cases were keenly observed to assess mortality.
Results: Occurrence of VAP was 42.5% with dominance of males (65%) and age group of 41-60 years (Mean ± SD:
42.26 ± 19.53). Late onset type (60.8%) predominated. Principal symptom/sign was fever (82.5%)/crepitation
(67.5%). Cases of OP poisoning (21.7%), associated diabetes mellitus (31.7%) were pre-eminent. Gram negative
Bacteria (GNB) formed the major etiology (78.6%), cardinal being Acinetobacter baumannii (32.1%) and
Pseudomonas aeruginosa (25%). Multi-drug resistant (MDR)-Acinetobacter baumannii, MDR-Pseudomonas
aeruginosa, imipenem resistant Klebsiella pneumoniae and Methicillin resistant Staphylococcus aureus (MRSA) were
noticed in 66.7%, 35%, 25% and 42.8% of respective isolates. Mortality record was 21.6%.
Conclusions: Reliable mode of isolation (quantitative culture), less invasive sampling (ETA) and antibiotic recycling
will augment VAP management. Regular intuition into contemporary trends of antimicrobial profile of etiological
agents is crucial to avert undesirable consequences.

Keywords: Acinetobacter baumannii, Gram negative bacteria, Intensive care units, Pseudomonas aeruginosa,
Ventilator associated pneumonia

INTRODUCTION pneumonia (NP). Patients who are intubated and


mechanically ventilated have 6 to 20 fold risk of
It is indeed a paradox that the use of advanced medicine pneumonia.1 The incidence of NP in all intubated
has brought in its wake the dangerous and too frequent mechanically ventilated patients ranges between 9–27%.1
botheration of nosocomial infections. The widespread use Ventilator-associated pneumonia (VAP) is defined as
of tracheal intubation and mechanical ventilation to pneumonia that develops more than 48 hours after
support critically ill has defined an expanding group of initiation of mechanical ventilation or conceptually, as an
patients, at particularly high risk of nosocomial inflammation of the lung parenchyma caused by

International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 239
Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245

infectious agent/s not present or incubating at the time, Risk factors2 can be those which can be patient related
mechanical ventilation was started.1 illnesses, cause colonisation and pneumonia because of
disease associated impairment in host defence function.
For VAP to occur, the equilibrium between host defences These include acute or chronic illnesses, coma,
and microbial propensity for colonization and invasion malnutrition, prolonged hospitalization, CNS
must shift in favour of the ability of the pathogens to dysfunction, COPD, diabetes mellitus, alcoholism,
persist and invade lower respiratory tract. VAP may be azotemia & respiratory failure. Advanced age is a
caused by spectrum of bacterial pathogens which may be predisposing factor due to increased frequency of serious
polymicrobial and rarely due to anaerobic bacteria, comorbidity and associated immune changes. Poor
viruses or fungi. The microbiology of VAP is different infection control related practices can lead to the
from that of the more common community-acquired transmission of hospital acquired pathogens. A number of
pneumonia (CAP). In particular, viruses and fungi are intervention related factors can impair host defence.
uncommon causes in people who are immunocompetent. Endotracheal intubation predisposes by impairing
The clinical characteristics and organisms causing are mucociliary clearance from lower respiratory tract as well
unique to a set up. Frequency of specific bacterial as injuring epithelial surface and thereby increased
pathogens causing VAP may also vary by patient bacterial binding. Prolonged & inappropriate usage of
population, and changes over time, emphasizing the need antibiotics may increase colonisation by antibiotic
for timely local surveillance data. Rapid diagnosis and resistant bacteria.
initiation of appropriate antimicrobial agent is critical, as
this delay parallels rise in mortality. The bacteriologic strategy for diagnosis uses quantitative
cultures of lower respiratory specimens (Endotracheal
The American Thoracic Society (ATS) consensus aspirate-ETA, Broncho-alveolar lavage-BAL or Protected
statement2 suggests the categorization of NP as Early specimen brush-PSB collected with or without a
onset NP-occurring within 4 days after hospital admission bronchoscope) to define both the presence of pneumonia
& Late onset NP-occurring 5 or more days after hospital and the etiologic pathogen. Growth above a threshold
admission. This categorization helps predict the concentration is required to diagnose VAP. Infra-
implicated pathogens and guides us in the initial empiric threshold growth is assumed to be due to colonization or
therapy, which is known as the epidemiological approach. contamination. This has a good diagnostic utility
Early-onset pneumonia commonly results from aspiration especially if clinical suspicion is low or equivocal.1,10 The
of endogenous community acquired pathogens colonizing consensus threshold value of quantitative culture is 10 5 or
the oropharynx. Conversely, late-onset VAP may be 106 cfu/ml for ETA secretions, 104 cfu/ml for BAL
caused by more unusual or MDR pathogens following specimens and 103cfu/ml for PSB material.1,11
aspiration of oropharyngeal and gastric secretions.3
Oropharyngeal or tracheal colonization with Psuedomonas Currently the exact role of VAP in worsening the
aeruginosa or enteric Gram negative bacilli is common in prognosis of ICU patients is difficult to assess, as such
ICU patients, increases with length of hospitalization.4 patients are critically ill and thus their clinical status is
severe enough to potentially cause death.
The incidence of VAP in eight developing countries
(Argentina, Brazil, Colombia, India, Mexico, Morocco, With a keen focus on its microbiology, this work
Peru and Turkey) was shown to vary between 10%- highlights the trend of this clinical condition.
52.7% by Rosenthal et al.5 The incidence was reported to
be around 45% by some south Indian Prospective METHODS
studies.6,7 Bacterial pathogens associated with VAP are
Streptococcus pneumoniae, Haemophilus influenzae, A prospective clinico-microbiological analysis was
Serratia marcescens and more commonly Methicillin undertaken enrolling 120 intubated patients who were
sensitive Staphylococcus aureus in early onset type, mechanically ventilated for more than 48hrs, with a
whereas members of Enterobacteriaceae (Escherichia clinical suspicion of pneumonia11,12 (a
coli, Klebsiella spp., Citrobacter spp., Enterobacter spp., new/progressive/persistent infiltrate on the chest
Proteus spp.), Methicillin resistant Staphylococcus aureus radiograph and at least one of the following: leucocytosis
(MRSA), Pseudomonas aeruginosa and Acinetobacter >12×109/ml, fever >38.3°C, or the presence of purulent
baumannii are implicated in late-onset type.8 Gram tracheobronchial secretions) extending from January
negative bacteria including Pseudomonas aeruginosa, 2011 to June 2012 from the multidisciplinary ICUs of a
Acinetobacter baumannii & Enteric Gram negative rods tertiary care set up (Kempegowda Institute of Medical
are implicated in majority of VAP episodes (41-92%) Sciences and Research Centre, Bangalore). Patients with
with predominance of either Pseudomonas aeruginosa or pre-existing pneumonia were excluded. A questionnaire
Acinetobacter baumannii and Gram positive cocci was prepared and each patient was screened and
particularly Staphylococcus aureus account for 6-58% of monitored accordingly. Data such as name, age, gender,
the isolates.9 date of admission into intensive care unit, chief
complaints, risk factors involved, duration of mechanical
ventilation, clinical signs was obtained. Data related to

International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 240
Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245

general physical examination, a battery of routine


investigations-radiological and haematological
investigations was collected. The VAP group was
classified into two groups, early-onset type (<96 hrs) and
late-onset type (≥96 hrs).

ETA was collected under aseptic precautions by non-


bronchoscopic method. A sterile 22 inches suction
catheter (Ramsons-12 F) was introduced into respiratory
tract for a distance of 20-25cms and the specimen was
aspirated into a sterile container, transported to the
laboratory immediately. Samples were mechanically
liquefied and homogenized by vortexing for 1 min. The
specimen was subjected to Gram’s stain (Microscopy),
Figure 1: Age and sex distribution.
further diluted using sterile saline (1 in 100) and was then
inoculated for quantitative culture using standard
techniques onto MacConkey agar, Blood agar and
Chocolate agar plates using a 4mm sterile nichrome loop
(0.01 ml), and then incubated at 37°C for up to 48 hrs.
The cfu/ml was calculated, considering the reciprocals of
the dilution factor & volume (ml) of specimen used for
inoculation. Bacterial isolate obtained with 105 or more
cfu/ml was regarded as a pathogen (otherwise as a
contaminant or colonizer), further identified using
appropriate biochemical tests.13

Antimicrobial susceptibility of the obtained isolate was


Figure 2: Clinical distribution of cases.
done by Kirby-Bauer's disc diffusion method using
commercially available disks (Himedia Laboratories, (OP-Poisoning-Organophosporous poisoning; RTA- Road
Mumbai) and interpreted as per Clinical laboratory traffic accident; COPD- Chronic obstructive pulmonary disease;
Standards Institute (CLSI)-guidelines.14 Methicillin CRF- Chronic renal failure; DKA- Diabetic ketoacidosis; IHD-
resistance in Staphylococcus aureus was recognized using Ischemic heart disease)
cefoxitin disc (30μg) by disc diffusion.14

The patients were observed till their stay in the hospital to


record their mortality.

Data collected was analyzed statistically by computing


percentage, mean and standard deviation. Appropriate
tests were employed. Wherever necessary, the results
were depicted in the form of charts.

RESULTS

This review analysing 120 patients clinically assessed the Figure 3: Risk factors associated.
occurrence of VAP and has delineated the profile of
pathogens. The occurrence of VAP in this study was (COPD- Chronic obstructive pulmonary disease; CRF- Chronic
42.5% (51/120). Age group of 41-60 years (34.2%) renal failure)
predominated with Mean ± SD: 42.26 ± 19.53. Male
dominance (65%) was identified. (Figure 1) The pre- 51 patients (42.5%) showed significant growth (above
eminent conditions were OP poisoning (21.7%), and road threshold) while there was insignificant result in 8 cases
traffic accident (17.5%). (Figure 2) The associated factors and no bacteria could be recovered in 61 cases. The
were Diabetes mellitus-31.7%, advancing age (>60 isolates were polymicrobial in 9.8% (5/51) of the samples
years)-20%, COPD-17.5% and head trauma-17.5%. showing significant growth. (Table 1) Gram negative
(Figure 3) Majority (82.5%) had fever, while the major bacteria were the major etiological agents (78.6%).
signs elicited were crepitations, tachycardia and tubular Acinetobacter baumannii (32.1%) was the preponderant
breathing in 67.5%, 55% and 30% of the cases organism isolated followed by Pseudomonas aeruginosa
respectively. Consolidation was predominantly seen in (25%), former being predominant in late onset (5/21
lower lobe of right lung (60%). Majority of the confirmed isolates) variety & the latter in the early type (14/35
VAP episodes were of late onset type (60.8%). isolates) (Figure 4).

International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 241
Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245

Table 1: Aetiological profile of the polymicrobial Table 2: Mean antibiogram of the isolates.
infections.
Mean antibiotic
Organisms Antibiotics
Profile (above Early-onset Late-onset Total resistance (%)
threshold) cases cases isolates Gram Amoxyclav 78.5
(Pseudomonas positive
aeruginosa+ bacteria Cefuroxime 61.4
Klebsiella
1 2 (2×3)=6
pneumoniae) Ampicillin 100
(Acinetobacter Amoxyclav 100
baumannii+
- 1 (2×1)=2 Gram
Pseudomonas Cefuroxime 75.6
aeruginosa) negative
bacteria Cefepime 67.9
(Acinetobacter
- 1 (2×1)=2 Ciprofloxacin 63.4
baumannii+
Escherichia coli)
Cotrimoxazole 63
Amoxyclav 93.9
Cefuroxime 75.6
Both
Cefepime 63.9
Ciprofloxacin 62.8

DISCUSSION

This local survey has addressed the occurrence, clinical


peculiarities and microbiology of VAP. It has used the
more appropriate channel i.e. quantitative culture (to
differentiate pathogens from colonizers/contaminants) of
ETA (obtained by minimally invasive technique) as
advocated by various studies. In different studies, the
incidence of VAP was reported different; depending on
Figure 4: Frequency of the etiological agents isolated. the type of hospital or ICU, the population studied and
the organisms prevalent; and varied from 7% to 70%. 16-18
High mean antibiotic resistance was exhibited to Our study showed occurrence of VAP to be 42.5%,
pencillins - ampicillin (100%), amoxyclav (93.9%); which was in close agreement with many other
cephalosporins - cefuroxime (75.6%), cefepime (63.9%); studies.6,7,19,20
fluoroquinolone - ciprofloxacin (62.8%). MDR15 -
Acinetobacter baumannii & Pseudomonas aeruginosa The higher incidence seen in age group of 41-60 years
were noticed in 66.7% and 35% of the respective isolates. can be attributed to more number of patients getting
Imipenem resistance in Klebsiella pneumoniae isolates admitted in that age and to their associated comorbid
was seen in 25%. Methicillin resistance in conditions. This type of age dominance was documented
Staphylococcus aureus was exhibited in 42.8%. in other studies too.6,7 The male gender predominance
identified here was also observed by other studies.6,21
The drugs which were highly efficient as per our study
were ceftriaxone - tazobactam (100%), tobramycin The predisposing conditions identified cause colonisation
(100%), piperacillin - tazobactam (94.9%), gentamicin and pneumonia because of disease associated impairment
(83.8%), levofloxacin (83.8%) and amikacin (83.5%) for in host defence function2 and were considered as
gram negative bacteria. For gram positive bacteria, important risk factors, as shown by various studies. 6,7,20
efficacious drugs were Linezolid (100%), vancomycin
(90%), clindamycin (90%) and tetracycline (86.9%). The higher percentage of infiltrates in the right lung-
Mean resistance exhibited by Gram-Positive and Gram- lower lobe is due to more common occurrence of
negative bacteria is depicted (Table 2). aspiration there, attributed to anatomical fact of more
deviant left bronchus. Late onset type of VAP was found
Mortality rate in cases showing significant growth was in majority, as seen in other studies.21,22
found to be 21.6% (11/51).

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Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245

The report of high incidence of aerobic gram negative In early onset VAP, the organism found in large number
bacteria is consistent with some prior reports,5,23 which was Pseudomonas aeruginosa accounting for 23.8% of
can be attributed to oropharyngeal colonization of aerobic isolates which was in accordance with a study.30
Gram negative bacteria, to which the critically ill patients Acinetobacter baumannii-40% and Pseudomonas
in ICU are more susceptible.24 The incidence of the aeruginosa-25.7% were the commonly isolated pathogens
polymicrobial isolates was well comparable with other in late onset VAP in our study. The results are concordant
studies (Table 3).7,20,22,25-29 with a study.6

Table 3: Comparison of pathogens isolated from various Indian studies.

No. of isolates (%)


Total
Study Acinetobacter Pseudomonas Klebsiella Staph.
isolates
spp. spp. spp. aureus
86 77 11 2
Singhal et al26 (2005) 192
(44.8) (40.1) (5.7) (1.05)
4 11 7 6
Rakshit et al20 (2005) 34
(11.7) (32) (20) (17.6)
5 4 2 1
Rajashekar et al27 (2006) 16
(31) (25) (1.2) (6.25)
5 37 4 25
Ahmed et al28 (2007) 103
(4.8) (35.9) (3.8) (24.2)
23 12 6 -
Arindam Dey et al7 (2007) 47
(48.9) (25.5) (12.7)
*156 106 93 38
Kumari et al29 (2007) 489
(31.9) (21.5) (19) (7.8)
38 57 22 3
Goel et al25 (2009) 161
(23.6) (35) (13.6) (1.8)
14 10 03 07
Joseph et al22 (2010) 47
(29.8) (21.3) (6.4) (14.9)
18 14 09 07
Present study 56
(32.1) (25) (16.1) (12.5)

(* indicates non-fermenters)

The frequency of drug resistant pathogens in our series VAP has evolved as a frequent culprit in ICUs. Due to
was comparable in part with other studies;22,25,29 but en concordant risk factors and comorbid conditions,
masse, this frequency was quite low compared to recent intubated individuals with advancing age in ICUs show a
verdicts. soaring tendency to develop VAP. The risk tends to
upsurge with the duration of mechanical ventilation, and
A Medline review concluded that VAP is associated with accordingly late onset VAP is usually predominant.
a crude mortality ranging between 16 to 94 %.9 The Aerobic gram negative bacteria are the isolates frequently
conflicting results could be explained by differences in found, especially Acinetobacter baumannii and
patient characteristics, adequacy of initial antimicrobial Pseudomonas aeruginosa. Antimicrobial resistance varies
treatment, antimicrobial resistance of the organisms in different settings. As per recent reviews and according
responsible, severity of illness, co-morbid factors, and to this series, some drugs tend to possess high efficacy,
host response factors. and hence could be given due consideration.

CONCLUSION More apt tactic of isolating the pathogen (quantitative


culture), less invasive sampling (ETA) & rotational
Nosocomial infections can negate the interest of even the antibiotic usage will augment enhanced and prompt
best of medical care, underscoring the need for regular management of VAP. Regular intuition into
surveillance. Among hospital-acquired infections, VAP contemporary trends of the etiological agents responsible
has been contemplated to be the most detrimental, if not with their drug resistance is of paramount importance for
promptly managed. restricting the use of empiric broad spectrum antibiotics

International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 243
Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245

which predisposes to colonization. Practice of post-mortem lung biopsies. Thorax 1999;54:867-


microbiological surveillance with timely availability of 73.
data and programs to reduce or alter antibiotic prescribing 12. Johanson WG, Pierce Ak, Sandford JP. Nosocomial
practices is vital to avert the terrible impact of respiratory infections with gram-negative bacilli: the
antimicrobial resistance. significance of colonization of the respiratory tract.
Ann Intern Med 1972;77:701-6.
Funding: No funding sources 13. Koneman EW, Allen SD, Janda WM, Schreckberger
Conflict of interest: None declared PC, Winn CW Jr. The Enterobacteriaceae. In:
Ethical approval: The study was approved by the Colour Atlas and textbook of diagnostic
institutional ethics committee Microbiology. 5th ed. PA: Lippincott Williams and
Wilkins Company; 1997: 171-252.
REFERENCES 14. CLSI. Performance Standards for Antimicrobial
Susceptibility Testing: Twenty-Third Infromational
1. Chastre J, Fagon JY. Ventilator-associated Supplement. CLSI Document. Wayne PA: Clinical
pneumonia. Am J Respir Crit Care Med and Laboratory Standards Institute; 2013: M100-
2002;165:867-903. S23.
2. Campbell GD, Niederman MS, Broughton MA, 15. Jones R N, Deshpande L, Fritsche T R, Sader H S.
Craven DE, Fein AM, Fink MP et al. American Determination of epidemic clonality among
Thoracic Society. Hospital-acquired pneumonia in multidrug-resistant strains of Acinetobacter spp. and
adults: diagnosis, assessment of severity, initial Pseudomonas aeruginosa in the MYSTIC
antimicrobial therapy, and preventive strategies. A Programme (USA, 1999–2003). Diagn Microbiol
consensus statement. Am J Respir Crit Care Med Infect Dis 2004;49:211-6.
1995;153:1711-25. 16. Cook DJ, Walter SD, Cook RJ, Griffith LE, Guyatt
3. Ewig S, Bauer T, Torres A. The pulmonary GH, Leasa D et al. Incidence of and risk factors for
physician in critical care: Nosocomial pneumonia. ventilator-associated pneumonia in critically ill
Thorax 2002;57:366-71. patients. Ann Intern Med 1998;129:433-40.
4. Bergmans DC, Bonten MJ, van Tiel FH. Cross- 17. Apostolopoulou E, Bakakos P, Katostaras T,
colonization with Pseudomonas aeruginosa of Gregorakos L. Incidence and risk factors for
patients in an intensive care unit. Thorax ventilator-associated pneumonia in 4
1998;53:1053-8. multidisciplinary intensive care units in Athens,
5. Rosenthal VD, Maki DG, Salomao R, Moreno CA, Greece. Respir Care 2003;48:681-8.
Mehta Y, Higuer F et al. Device-associated 18. Rosenthal VD, Guzman S, Orellano PW.
nosocomial infections in 55 intensive care units of 8 Nosocomial infections in medical-surgical intensive
developing countries. Ann Intern Med care units in Argentina: attributable mortality and
2006;145:582-91. length of stay. Am J Infect Control 2003;31:291-5.
6. Arindam Dey, Indira Bairy. Incidence of multidrug 19. Trivedi TH, Shejale SB, Yeolekar ME. Nosocomial
resistant organisms causing ventilator- associated pneumonia in Medical intensive care unit. JAPI
pneumonia in a tertiary care hospital: A nine months 2000;48:1070-3.
prospective study. Annals of thoracic medicine 20. Panwar Rakshit P, Nagar VS, Deshpande AK.
2007;2:52-7. Incidence, clinical outcome and risk stratification of
7. Girish L. Dandagi. Nosocomial pneumonia in ventilator-associated pneumonia: a prospective
critically ill patients. Lung India 2010;27:149-53. cohort study. Indian J Crit Care Med 2005;9:211-16.
8. Craven DE, Steger KA. Epidemiology of 21. Hina Gadani, Arun Vyas, Akhya Kumar. A study of
nosocomial pneumonia: New perspectives on an old ventilator-associated pneumonia: Incidence,
disease. Chest 1995;108:1S-16S. outcome, risk factors and measures to be taken for
9. Yaseen Arabi, Nehad Al-Shirawi, Ziad Memish, prevention. Indian J Anaesth 2010;54:535-40.
Antonio Anzueto. Ventilator-associated pneumonia 22. Noyal Mariya Joseph, Sujatha Sistla, Tarun Kumar
in adults in developing countries: a systematic Dutta- Ventilator-associated pneumonia in a tertiary
review. International journal of infectious diseases care hospital in India: role of multi-drug resistant
2008;12:505-51. pathogens. J Infect Dev Ctries 2010;4:218-25.
10. Heyland DK, Cook DJ, Marshall J, Heule M, 23. Mukhopadhyay C, Bhargava A, Ayyagari A. Role
Guslits B, Lang J et al. Canadian Critical Care of mechanical ventilation & development of
Trials Group. The clinical utility of invasive multidrug resistant organisms in hospital acquired
diagnostic techniques in the setting of ventilator- pneumonia. Indian J Med Res 2003;118:229-35.
associated pneumonia. Chest 1999;115:1076-84. 24. Bergmans DC, Bonten MJ, van Tiel FH. Cross-
11. Fabregas N, Ewig S, Torres A, El-Ebiary M, colonization with Pseudomonas aeruginosa of
Ramirez J, Puig de la Bellacasa et al. Clinical patients in an intensive care unit. Thorax
diagnosis of ventilator associated pneumonia 1998;53:1053-8.
revisited, comparative validation using immediate 25. Nidhi Goel, Uma Chaudhary, Ritu Aggarwal, Kiran
Bala. Antibiotic sensitivity pattern of gram negative

International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 244
Usman SM et al. Int J Res Med Sci. 2014 Feb;2(1):239-245

bacilli isolated from the lower respiratory tract of Prospective study. Indian J Crit care Med
ventilated patients in the intensive care unit. Indian J 2007;11:117-21.
Crit Care Med 2009;13:148-51. 29. Kumari HB, Nagarathna S, Chandramuki A.
26. Singhal R, Mohanty S, Sood S, Das B, Kapil A. Antimicrobial resistance pattern among aerobic
Profile of bacterial isolates from patients with gram-negative bacilli of lower respiratory tract
ventilator associated pneumonias in a tertiary care specimens of intensive care unit patients in a
hospital in India. Indian J Med Res 2005;121:63-4. neurocentre. Indian J Chest Dis Allied Sci
27. Rajasekhar T, Anuradha K, Suhasini T, Lakshmi V. 2007;49:19-22.
The role of quantitative cultures of non- 30. Ibrahim EH, Ward S, Sherman RN, Kollef MH. A
bronchoscopic samples in ventilator associated comparative analysis of patient with early-onset vs.
pneumonia. Indian J Med Microbiol 2006;24:107- late-onset nosocomial pneumonia in the ICU setting.
13. Chest 2000;117:1434-42.
28. Ahmed SM, Choudhary J, Ahmed M, Arora V, Ali
PS. Treatment of Ventilator Associated Pneumonia DOI: 10.5455/2320-6012.ijrms20140246
with Piperacillin/Tazobactum and amikacin vs Cite this article as: Usman SM, James PM, Rashmi
Cefpime and Levofloxacin: a randomized M. Clinical and microbiological facets of ventilator
associated pneumonia in the main stream with a
practical contact. Int J Res Med Sci 2014;2:239-45.

International Journal of Research in Medical Sciences | January-March 2014 | Vol 2 | Issue 1 Page 245

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