How much of a problem is Acinetobacter air contamination?

Nosopharm_Acinetobacter_baumanniiWe have known for a while that Acinetobacter baumannii can cause widespread contamination of surfaces and air. But it’s difficult to know how much of a transmission risk this causes. Is contamination of surfaces a cause or effect of transmission? And is contamination of the air an intermediate step between the patient and the surface, or a problem in its own right? A recent US study does not answer these questions, but does offer some useful data on the scale of surface and air contamination emanating from infected and colonised patients.

Extensive air and surface sampling was performed around 25 carbapenem-resistant A. baumannii patients in the ICU. The key finding is that contamination of the air and surfaces was significantly greater around patient who were rectally colonised (38% for air and 16% for surfaces) compared with patients who had colonisation of the respiratory tract (13% for air and 10% for surfaces). This seems a little backwards – you may expect a patient colonised in the respiratory tract to release more resistant bacteria into the air, but on the basis of this study, this does not seem to be the case. This apparent discrepancy may be explained by the presence of closed-circuit ventilation for many patients who had respiratory colonisation. 

This study again highlights the risk of environmental contamination surrounding patients with A. baumannii and underlines the need to address contaminated surfaces and probably air too when formulating strategies for preventing the spread of A. baumannii.


Are UV and Hydrogen Peroxide automated room decon devices clinically effective?

A useful review by Weber et al. explores data from studies with a clinical outcome evaluating UV and hydrogen peroxide automated room (ARD) decon devices. There are now quite a few studies showing that admission to a room previously occupied by a patient with a pathogen associated with HCAI (including C. difficile, MRSA, VRE and others) increases the chances of acquiring these pathogens due to surface contamination that is not dealt with by standard cleaning and disinfection approaches. There is also a sound evidence base showing that both UV and hydrogen peroxide ARD systems do a better job of reducing microbial loads on surfaces than standard cleaning and disinfection. However, evidence from studies linking these environmental reductions to clinical outcomes are rarer, but increasing.
The focuses on some key studies evaluating the clinical impact of ARD systems. There are some convincing studies for HPV (including the impressive Passaretti and McCord studies), and for UVC systems, which put out a continuous dose of germicidal UV (including Napolitano and the much-anticipated BETR-D study). Whilst there are quite a few studies which, on the face of it, suggest that PX-UV, which puts out a pulsed dose of broad spectrum UV, also reduces HCAI, many of these studies have important confounding factors, making it difficult to attribute the reduction specifically to the UV device. For example, in the study by Fornwalt, PX-UV was introduced as a part of a quality improvement programme, and in the study by Simmons, PX-UV was part of a multi-faceted bundle.
The review concludes that ‘A growing number of clinical studies have demonstrated that ultraviolet devices and Hydrogen Peroxide systems when used for terminal disinfection can reduce colonization or health care-associated infections in patients admitted to these hospital rooms.’



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