Candida profile in VAP at Solapur.Mangala Ghatole. M.Rai, M. Ware, V. Kashetty, P. Nakate.

Ashwini Rural Medical College, Hospital & Research centre.Kumbhari, Solapur.

Dr. V.M. Govt. Medical College, Solapur.

Ventilator associated pneumonia (VAP) is defined as pneumonia developing more than 48 hours after endotracheal intubation and initiation of mechanical ventilation (MV) including pneumonia developing after extubation.

The incidence of VAP varies between 7-70% among patients intubated for more than 48 hours.

Introduction :

• Mechanical ventilation is the support system for critically ill patients. • But this may predispose to development pneumonia.• Ventilator associated pneumonia (VAP) complicates the course

of 8-28% of patients receiving the mechanical ventilation (MV).• It may be of early onset (within 96 hours of MV) late onset (after 96 hours of MV)

• Mortality rate for VAP ranges from 24-50%, can reach up to 76%.• Late onset is associated with higher morbidity & mortality.

Early onset - ˂ 5 days of intubation. - Susceptible to antimicrobials. - Micro-aspiration from oropharynx. - Prognosis is good.

Late onset - > 5 days of intubation. - Drug resistant bacteria. - Aspiration of pathologically colonised. - microorganisms from pharynx and stomach. - Increased morbidity and mortality.

Factors associated with development of VAP :• Host factors –• Types of bacteria colonizing the pharynx, • The recent use of antibiotics may also alter pharyngeal colonization. • Trauma,• Underlying disease., nutritional status, muscular paralysis, duration of hospital stay.• The use of antacids or histamine type 2 (H2) blockers has been associated with an

increased risk of VAP.• The response of the host's humoral, and cellular defence to the invasion.• Micro-organism factors - • The number and virulence of organisms entering the lower airway.• Local trauma and inflammation caused by an endotracheal tube and possible leakage

of contaminated secretions around the cuff.• microorganisms aggregated in biofilm on the surface of the endotracheal tube.• Increased lower airway colonization and the risk of trachea-bronchitis and VAP

Aetiological agents -

Enterobacteriaceae -Klebsiella spps, E.coli, Proteus mirabilis, serratia, Enterobacter, providencia, Citrobacter etcNFGN - Pseudomonas aeruginosa, Acinetobacter spps. etc MRSA.Recently candida spps are also incriminated. They are reported from 9-40% of cases.

Pathogenesis of VAP : 1) Bacterial colonization of the aero-digestive tract. 2) Aspiration of contaminated secretions into respiratory tract.

Diagnosis of VAP - Clinical. Radiological. Microbiological.

The MDR organisms along with complicating risk factors contribute to –

- Prolonged hospital stay.-Escalated health care cost.-Increased morbidity & mortality.

Early & appropriate antimicrobial therapy is important to prevent poor clinical outcome.

So prompt identification of the aetiological agent along with its susceptibility pattern is important in VAP management.

As organisms colonising the oral cavity are source of VAP.Candida spps are part of oral flora.Most of VAP studies have reported mainly MDR GNB or GPC.Recently strong association between pseudomonas aeruginosa and candida spps in the pathogenesis of VAP is reported.With this background the present study was planned to study the candida association in VAP patients.

Aims & objectives :

• To study the association of candida spps in VAP cases.• Speciation the candida isolates.• To study the antifungal profile of these isolates.• To study the association of pseudomonas aeruginosa and

candida in these VAP cases.

Materials & Methods :• Total of 152 cases with clinical and radiological evidence of

VAP showing quantitative culture of > 105 cfu /ml. were included.• Endotracheal aspirate was subjected to -• Gram stain,• Quantitative culture – 5% SBA, MacConkey agar, • Bacteria isolated were identified, AST performed.• Samples showing budding yeast cells with pseudohyphae were

inoculated on Sabouraud dextrose agar (SDA), SDA with cycloheximide and chloramphenicol. • Inoculated media were incubated at room temperature for 48-72

hours.

Yeasts were further identified – colony morphology, Germ tube, Dalmau plate technique, sugar fermentation & assimilation tests.Antifungal susceptibility testing performed as per CLSI M 27-A2, C. albicans ATCC 90028, Candida tropicalis ATCC750 were used as standard strains. This study was limited to only candida spps. Interpretation for fluconazole : <8μg/ml – susceptibility, 8-64 μg/ml- dose dependant susceptibility, > 64 μg/ml- resistant.For Amphotericin : <0.1 μg/ml is susceptible, > 1 μg/ml is resistant.

Results :• Male – 101.• Female 51.

• Types of VAP :• < 5 days (early onset) -58(38.2%).

> 5 days (Late onset) -94.(61.8%)

• Total bacterial isolates – 184. candida spps - 32 (21.1%) Only candida – 19(59.4%) candida + bacteria -13.(40.6%)• In this study all the patients had the risk factors –1)prior use of antibiotics.2)use of H2 blockers / antacids.

38%

62%

Early onsetLate onset

Speciation of candida : Candida albicans 17 (53.12%)

Candida krusei 05(15.6%)

Candida tropicalis 04 (12.5%)

Candida dubliensis 03 (9.4%)

Candida glabrata 02(6.3%)

Candida parapsilosis 01(3.12%)

C.albicans

C.kruse

i

C.tropica

lis

C.dubliensis

C.glabrata

C.parapsilosis

0

10

20

30

40

50

60

distribution of candida spps

candida spps

% d

istrib

ution

Distribution of candida with bacteria : Organisms Number

Candida + pseudomonas aeruginosa

09(69.2%)

Candida + Klebsiella aerogenes

01(7.7%)

Candida +E. coli

01 (7.7%)

Candida + MSSA

02 (15.4%)

Candida +pseudo

Candida+kleb

Candida+E.coli

Candida +MRSA0

10203040506070

Candida association with bacteria

Combination of organisms

% d

istrib

ution

organism FluconazoleMIC ≤ 8 μg/ml 8-16 μg/ml 16-32 μg/ml 32-64 μg/ml ≥ 64 μg/ml

C.albicans(17) 15(88.2%) 02(11.6%) --- --- ---

C. krusei (5) 1(20%) 2(40%) ----- ---- 2(40%)

C. tropicalis (4) --- 1(25%) 1(25%) ----- 2(50%)

C. dubliensis (3) 3 (100%) ----- ------ ------ -----

C. glabrata (2) ----- ------ ------ ----- 2(100%)

C. parapsilosis(1) ----- ------ ----- ----- 1(100%)

Organism Amphotericin

MIC ≤ 01 μg/ml ≥ 1.0 μg/ml

C.albicans(17) 16(94.1%) 1(5.9%)

C. krusei (5) 3(60%) 2(40%)

C. tropicalis (4) 03(75%) 1(25%)

C. dubliensis (3) 3 (100%) -----

C. glabrata (2) ----- 2(100%)

C. parapsilosis(1) 1(100%) ------

Discussion :studies Candida

Present study Candida – (21.1%,)C. albicans (53.1% ), C.tropicali (12.5%) C. glabrata (6.3%), C.dubliensis (9.4%)

Heyland DK et al (1999)France

Candida (15%).

Cook D et al (1998)Canada

Candida (3.2%)

Rodrigues PMA et al ((2009)Brazil

Candida (5%)

Abukhabar H et al (2007)Egypt

Candida (3.1%)

Azoulay E et al. (2014) Candida (39.7%),C. albicans(67.7%), C. tropicalis(13%)C. glabrata ( 20%),

Summary & Conclusions:• Candida was isolated from 21.1% of VAP cases.• Candida albicans was the predominant spps.(53.13%).• 88.23% and 94.1% of Candida albicans were susceptible to

fluconazole & amphotericin respectively. • Candida association with Pseudomonas aeruginosa was observed in

69.2% cases. So association of candida may enhance the Pseudomonas aeruginosa VAP.

References :1)Heyland DK, Cook DJ, Griffith L, Keenan SP et al. Am J Respir Critic Care Med (1999);159, 1249-1256.2)Cook D, Guyatti G, Marshall J, Leasa D, Fuller H et alN. Eng J Med (1998);338:791-7973)Rodrigues PMA, Neto EC, Santos LRC, Knibel MF.J. Bras Pneumol (2009);35(11) :1084 -1091.4)Abukhabar H, Atta S, Bedewy K, Youssef A, Moustafa A. Egypt J Broncho (2007);1(1):53-605)Azoulay E, Timsit JF, Tafflet M, Lassence AD, Darmon M et al Respir infn (2014);110-117.6)Nseir S, Jozefowlez E, Cavestri B, et al.Intensive care Med (2007):33:137-142.7) Joseph NM, Sistla S, Dutta TK, Badhe AS, Rasitha D, Parija SC.J infect Dev Ctries 2010; 4(4):218 -225.