Bacteria's in the air, everywhere we look around

30 July 2008

Dr Anna Snelling and Professors Clive Beggs and Kevin Kerr, from the Bradford Infection Group, look at research into the factors that could affect the spread of C. difficile.

There was a time not so long ago when, if media reports were to be believed, there was only one hospital 'superbug'. MRSA, it seemed, was king. In recent years, however, despite various other pretenders to the throne, such as ESBLs, Pseudomonas and Acinetobacter, Clostridium difficile has been catapulted from relative obscurity into the full glare of the media spotlight to challenge MRSA for the superbug crown. High profile outbreaks of C. difficile associated disease (CDAD) at Stoke Mandeville hospital in 2004 and 2005, and, more recently, at the Maidstone and Tunbridge Wells NHS Trust – where 90 patients are thought to have died in two separate outbreaks – have helped to cement the reputation of C. difficile among the media, patients and public as a very new and dangerous adversary. Data from the Health Protection Agency's voluntary reporting scheme had, in fact, shown a steady increase in the number of cases since the early 1990s. Indeed, the total number of cases for England, Wales and Northern Ireland increased from 22,066 in 2001 to 55,213 in 2006.¹

As healthcare associated pathogens, C. difficile and MRSA are often considered together, yet they are notably different in a number of respects. MRSA is a bacterium that can be carried without symptoms at a number of body sites (most often the nose) and is associated with a very wide range of infections, including bacteraemia. C. difficile colonises only the large bowel and CDAD is confined to the gut, with patients presenting with severe diarrhoea. CDAD patients have nearly always just had treatment with antimicrobials, especially so-called 'broad spectrum' agents that wipe-out most of the bacteria that normally inhabit the gut. Given the sites of colonisation of MRSA, decontamination with nasal antibacterials and antiseptic body washes is possible, whereas eradication of C. difficile from the large bowel is not straight-forward. Unlike MRSA, C. difficile produces spores that are resistant to many physical and chemical agents (including many disinfectants and alcohol hand rubs) and that allow the bacterium to persist for long periods in the environment. Given the differences in the microbiological features of the bacteria, their sites of colonisation and the natural history of infections associated with them, it is not unreasonable to think that the infection control measures intended to prevent acquisition and spread of these two pathogens might vary accordingly. Yet, until recently, this was not the case and infection prevention and control strategies have focused primarily on good hand hygiene and isolation nursing of colonised or infected patients. By comparison, relatively little attention was paid to the cleanliness of the clinical environment – possibly because of the fact that the contribution of environmental contamination to the spread of nosocomial pathogens such as MRSA remains ill characterised. However, there is accumulating evidence to suggest that the environment may play a more important role than hitherto acknowledged – not only for MRSA but also for CDAD and infections associated with other bacteria such as Acinetobacter baumannii.^2-7 Patient and public concern over the potential role that the hospital environment might play in the epidemiology of healthcare associated infection was recognised with the announcement of the programme of deep cleaning of hospitals, which was due to be completed by March of this year. Although this initiative has generated much debate as to its likely effectiveness⁸, it appears to represent a shift in approach to the containment of healthcare associated infection, with a tacit recognition that environmental contamination can contribute, at least in part, to the spread and persistence of some pathogens.

So how strong is the evidence that environmental contamination with C. difficile is of importance in the epidemiology of CDAD? Results from several studies suggest that environmental contamination, particularly of beds and furniture, may, indeed, play an important role in the spread of C. difficile infection.4-6 If consideration is given to the events, which might occur in relation to a case of CDAD, it is not difficult to see why this might be so. Patients with symptomatic C. difficile infection are usually elderly and have diarrhoea, which may be complicated by incontinence with associated faecal soiling of bedclothes and the immediate environment. When staff attend such a patient they will remove and dispose of soiled material, which may result in contamination of the surrounding area. Once in the environment, bacteria may sporulate – a process that may actually be enhanced by exposure to some disinfectants used by cleaning staff⁹ – and the spores can then persist for extended periods. Spores can also be excreted in the faeces. Ingestion of persisting spores may result in re-infection of the original patient or a new infection in another individual. This is supported by the observation that nosocomial outbreaks of CDAD frequently occur in spatial clusters¹⁰, suggesting that physical proximity to infected patients is an important risk factor for acquisition of C. difficile¹¹.

Activities such as bed making have been shown to liberate large numbers of bacteria carrying particles into the air¹², and we at the Bradford Infection Group (BIG), together with colleagues at the University of Leeds, are conducting an ongoing programme of research, funded amongst others by the Department of Health, into the behaviour of healthcare associated pathogens in the air as well as the survival of these bacteria in the general hospital environment. Environmental surveillance for C. difficile on an elderly care ward at a district general hospital was extended to investigate whether or not aerial dissemination of C. difficile bacteria or their spores could be occurring. The findings of this study, which we recently published¹³, revealed that C. difficile was isolated from ward air (with average counts of 53-426 colony forming units/m3 of air) on 23 occasions. Molecular typing (genetic fingerprinting) identified 22 of the 23 isolates as belonging to a single type – ribotype 001 – suggesting a common source for the bacteria recovered from the air. This is the first report of C. difficile in hospital air and could have important implications for our understanding of the transmission of the bacterium in healthcare settings – beyond being spread by contaminated hands. Clearly, more studies are necessary to quantify the frequency and degree of airborne dispersal of C. difficile, especially in the setting of wards with one or more patients with symptomatic CDAD. These studies could provide valuable data that would not only contribute to our understanding of the transmission of C. difficile in healthcare facilities but could also be used to improve ward ventilation and develop novel strategies to interrupt and reduce such transmission.

1 Health Protection Agency voluntary surveillance of Clostridium difficile in England, Wales and Northern Ireland, 2006. Available from www.hpa.org.uk/web/HPAwebFile/HPAweb_C/1194947320939 (last accessed 12/05/08)
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6 Fawley W N, Wilcox M H: Molecular epidemiology of endemic Clostridium difficile infection. Epidemiol Infect 2001, 126(3):343-350
7 Beggs C B, Kerr K G, Snelling A M, Sleigh P A: Acinetobacter spp. and the clinical environment. Indoor and Built Environment 2006, 15(1):19-24
8 Vere-Jones E: Will the deep clean solve the HCAI problem? Nursing Times 2007 103(40):8-9
9 Fawley W N, Underwood S, Freeman J, Baines S D, Saxton K, Stephenson K, Owens R C Jr, Wilcox M H: Efficacy of hospital cleaning agents and germicides against epidemic Clostridium difficile strains. Infect Control Hosp Epidemiol 2007 28(8):920-5
10 Foulke G E, Silva J, Jr: Clostridium difficile in the intensive care unit: management problems and prevention issues. Crit Care Med 1989, 17(8):822-826
11 Chang V T, Nelson K: The role of physical proximity in nosocomial diarrhoea. Clin Infect Dis 2000, 31(3):717-722
12 Roberts K, Hathway A, Fletcher L A, Beggs C B, Elliott M W, Sleigh P A: Bioaerosol production on a respiratory ward. Indoor and Built Environment 2006, 15(1):35-40
13 Roberts K, Smith C F, Snelling A M, Kerr K G, Banfield K, Sleigh P A, Beggs C B: Aerial dissemination of Clostridium difficile spores. BMC Infect Dis. 2008 24;8:7