Patients' safety and hospital acquired infections: the size of the problem of biofilms on the health care surfaces
thesisposted on 28.03.2022, 10:29 by Ahmad Almatroudi
There is incontrovertible evidence that nosocomial pathogens contaminate inanimate items in the hospital environment, such as surfaces and medical equipment. Transmission of infectious agents from contaminated fomites to patients is a known infectious route, although the contribution to overall hospital acquired infections (HAI) is unknown. However, the risk of developing HAI, has been shown to be increased 73% if the patient previously occupying the room had a multi-antibiotic resistant organism (MRO). Acinetobacter baumannii, vancomycin-resistant enterococci and methicillin-resistant Staphylococcus aureus are the main non-sporing infectious agents that have been clearly demonstrated to survive in environmental reservoirs. Bacteria readily adhere to surfaces. Once adhered they secrete a slimy matrix principally composed of protein, carbohydrate and DNA which surrounds them protecting them from the external environment. Bacterial reproduction and recruitment, leads to the development of a mature biofilm. The environmental conditions associated with hospital surfaces, especially in Intensive Care Units (ICU), are conducive to development of biofilm, which could have adverse consequences in these seriously ill patients. Up to 20% of intensive care patients become colonised by MROs increasing their risk of developing a HAI. Dry surfaces biofilms development increases the MDRO persistence rate in the hospital environment, and thereby likely increases the risk of hospital acquired infections and outbreaks. Hence, one cannot emphasise enough the importance of thoroughly cleaning and disinfecting hospital surfaces. The ultimate aim of this project was to determine if persistence of antibiotic resistant human pathogens in the hospital environment was due to MRO being incorporated into biofilms contaminating dry hospital surfaces. If incorporated into biofilms it was hypothetised that they would be protected from environmental desiccation, cleaning and disinfectants agents. The findings of this study revealed that bacteria encased in biofilms, including those causing serious infections, such as S. aureus, were present on over 90% of ICU surfaces. We determined that the majority of clinical biofilms incorporated Staphylococcus species and therefore developed an in vitro model representative of clinical dry-surface biofilms. The thickness of the biofilms and the number of cells in the biofilms in this model was reproducible between repetitions of the experiments, at least for one strain of S. aureus. We then employed this model to assess how effective the commonly used hospital disinfectant 1000 Parts Per Million (PPM) sodium hypochlorite and traditional heat treatment (Autoclaving-121°C for 20 minute, 30 minute, 1 hour and 2 hours) were against dry biofilm. We found that high concentrations of sodium hypochlorite (20,000 ppm) or standard sterilisation (Autoclaving – 121°C for 20 min) did not destroy the S. aureus cells in the biofilms. Through such findings, this study makes a valid contribution to existing understanding of hospital surface biofilms. In conclusion, it can be seen from this study that the consequences of biofilm in health care surfaces is underestimated in the existence infection control practices. The efficacy of hospital infection prevention and control policies and decontamination strategies require re-assessment.