Aeromicrobiological study of indoor air quality in hospitals - characterisation of bioaerosols and their association with nosocomial infections

Abstract

Healthcare facilities are a unique environment, where patients including those with chronic illness requiring longer durations of hospital stay or those with altered immune status are admitted. ometimes patients may acquire a healthcare associated infection after hospitalisation. The environment may occasionally contribute to such infections inadvertently. This study was undertaken to generate baseline data on airborne microorganisms, characterize aerobic bacteria and fungi in different locations of the hospital environment, determine whether temporal variation exists in airborne microbial concentrations of a hospital location, determine the most common isolate across hospitals, study the relationship between environmental and clinical isolates in a select area using molecular typing methods such as Polymerase Chain Reaction (PCR) and Pulsed Field Gel Electrophoresis (PFGE), and determine if endotoxin can be airborne. Methods: Institutional Ethics Committee approval was sought prior to start of the study. Indoor air samples (in duplicates) were collected simultaneously using exposed plate (for 30 minutes), impingement (BioSampler at 12.5 L/min for 20 min) and filtration (personal sampling filter cassette loaded with gelatin filter at 3.5 L/min for 15 min) methods in different locations of different hospitals to characterise airborne microflora. Sampling was also conducted over different periods of the year in the same location of one hospital to determine temporal variation. A walk-through was conducted to assess the extent of activity prior to sampling. Temperature and relative humidity were recorded during sampling. Bacterial plates were incubated at 37°C and observe d for growth after 48 h; fungal plates were incubated at 25°C and 37°C and o bserved upto 7 days. Microorganisms were identified using standard microbiological procedures. PCR targeting Pseudomonas specific 16s rDNA was performed to obtain 618 bp amplicons. Representative strains were sequenced and compared with established sequences of pathogenic Ps