It is generally accepted that the dissemination of microbes between humans and the inanimate environment can occur through direct contact with surfaces or through airborne
release. This last mechanism is very poorly understood.
The investigative team used 16S rRNA gene sequencing to characterize the airborne bacterial
contribution of a single persons sitting in a sanitized custom experimental
climate chamber. This was compared to air sampled in an adjacent, identical,
unoccupied chamber (control room) as well as supply and exhaust air sources.
Next, and this is where things really get clever, the microbial burden in settled particles surrounding each occupant was assessed and characterized.
The results suggests that we shed particles and bacteria in our own distinct and unique way, almost like a bacterial fingerprint. Basically, an occupied space is different microbiologically from an unoccupied space and each participant had their own, distinct microbial cloud.
To me this underscores the dynamic yet still poorly understood mechanism in which we interact with the inanimate environment. Although the bacteria isolated were largely not pathogenic, we certainly cannot exclude that patients colonized or infected with a pathogen will not emit their own 'pathogenic' microbial cloud. The extent to which microbial clouds drive hospital acquired infections is largely unknown.
Until we know better, it may still come down to acknowledging that the inanimate environment is a potential reservoir of hospital pathogens and to employing common sense infection prevention mechanisms to minimize bioburden, such as washing our hands, chlorhexidine bathing patients and performing robust daily and terminal disinfection of hospital rooms.
Next, and this is where things really get clever, the microbial burden in settled particles surrounding each occupant was assessed and characterized.
The results suggests that we shed particles and bacteria in our own distinct and unique way, almost like a bacterial fingerprint. Basically, an occupied space is different microbiologically from an unoccupied space and each participant had their own, distinct microbial cloud.
To me this underscores the dynamic yet still poorly understood mechanism in which we interact with the inanimate environment. Although the bacteria isolated were largely not pathogenic, we certainly cannot exclude that patients colonized or infected with a pathogen will not emit their own 'pathogenic' microbial cloud. The extent to which microbial clouds drive hospital acquired infections is largely unknown.
Until we know better, it may still come down to acknowledging that the inanimate environment is a potential reservoir of hospital pathogens and to employing common sense infection prevention mechanisms to minimize bioburden, such as washing our hands, chlorhexidine bathing patients and performing robust daily and terminal disinfection of hospital rooms.
