This page contains a Flash digital edition of a book.
INFECTION CONTROL In a review article from 2006,5


the authors


found for SARS CoV–1 that ‘particles of diameters of 1-3 μm remained suspended almost indefinitely, 10 μm took 17 minutes, 20 μm took four minutes, and 100 μm took 10 seconds to fall to the floor’. This article notes that aerosol transmission is a well- known and important exposure pathway for infectious agents such as influenza and other viruses, including coronaviruses. As discussed in the 2006 article, SARS–CoV–1 viral RNA was found in air samples, and long-range aerosol transport was implicated as the cause of the spread of the disease in several studies.5


The droplets are also capable of penetrating deep into the lungs, offering a potential route of infection.8


Penetration deep into the lungs It has been proven that droplets can contaminate surfaces over a range of over 2 metres.7


Susceptibility


to acquiring an infectious agent is determined by factors such as virulence, dose, and pathogenicity of the microorganism, as well as the host’s immune response.8–10


Humans generate


bio-aerosols by talking, breathing, sneezing, or coughing.6


Based on the


infectious status of a person, the bio- aerosols can contain pathogens including influenza,11,12


Mycobacterium tuberculosis,8


Moreover, bio-aerosols can be generated by devices such as ventilation systems, showers, taps, and toilets. Showers and tap water are also able to spread environmental microbes such as Legionella spp.9,10,14


Staphylococcus aureus, Varicella Zoster Virus, Streptococcus spp. or Aspergillus spp.12


It is now commonly accepted that bio- aerosols containing harmful pathogens are very much a common and serious contributor to healthcare-acquired infections, but are these connections new, and what was known of such threats in the past?


In 1981 Cordes et al found that Legionella pneumophila serogroup 6 was present in 9 of 16 shower heads in a Chicago hospital ward where three patients had contracted Legionnaires’ disease caused by serogroup 6 L. pneumophila. Each patient had showered there 2 to 10 days before the onset of disease symptoms. They also isolated the bacteria in two other hospitals, and found the same serogroups that had been causing Legionnaires’ disease in those hospitals: serogroup 1 in Pittsburgh, and serogroups 1 and 4 in Los Angeles. However, showers from hospital wards where no patients had contracted Legionnaires’ disease also yielded L. pneumophila. Whether aerosols of shower water or other exposures to potable water containing L. pneumophila may cause nosocomial Legionnaires’ disease was not proven, but the study’s authors suggested that the matter definitely deserved further study.16


24 Health Estate Journal September 2020


Water from a tap produces significant aerosol dispersal.


A distinctive strain In 1985 Meenhorst et al conducted an investigation into an outbreak of nosocomial Legionella pneumonia.17


numbers of aerosolised L. pneumophila (3 to 5 CFU/15 ft3


[0.43 m3 of air] were


recovered when the air was sampled above the shower doors with the six-stage sampler. Equal numbers of organisms were recovered in the first and second 15- minute sampling periods. A total of 19 paired water and air samples were obtained from 14 hot water taps, and 17 of the water cultures grew L. pneumophila. Two colonies of L. pneumophila (one on stage 1, one on stage 3) were recovered from air around one of the three taps tested with the six- stage unit. A total of 11 colonies were recovered (6 on stage 1, 5 on stage 2) from 5 of the remaining 13 taps tested with the two-stage unit. All positive air cultures from the two-stage unit were obtained during the period when the tap water was running. None were ever obtained before the tap water was turned on, or after it was turned off. No air cultures were positive more than once among the rooms tested two and three times.18


It


revealed that the potable water of the hospital in question was contaminated with a distinctive strain of Legionella pneumophila (designated the Le-l strain), which was by culture and serology linked with human illness. To examine the possible role of this water in the outbreak, eight healthy guinea pigs were exposed to an aerosol of concentrated potable water. Seven animals developed pneumonia due to the Le-l strain of L. pneumophila. In one of these guinea pigs, the Le-l strain was also isolated from the blood and spleen. These results provided support to the theory that exposure of humans to aerosols of potable water contaminated with L. pneumophila may cause Legionella pneumonia.17


A total of two paired water and air samples were obtained from each of the two shower rooms. All four water cultures grew L. pneumophila. Low


Again in 1985, Garye Bollin et al conducted an air sampling test in showers and sink areas at the Youngstown Hospital in Ohio.8


CPE cases at Brussels hospital More recently, at the University Hospital of Brussels, the incidence of new patients with Carbapenemase-producing Enterobacteriaceae (CPE) rose from one case in 2010, to 35 cases in 2015. Environmental samples suggested that a contaminated washbasin was the source of the outbreak. Besides other strains, Citrobacter freundii type OXA-48 was frequently isolated from patients and washbasins. To investigate the relationship between those strains, pulsed-field gel electrophoresis was performed. The strains isolated from patients and the washbasin in the implicated room were highly related, and pointed to sink-to- patient transmission. In total, 7 of 8 sinks in the isolation rooms of the ICU were found to be CPE contaminated. To control the outbreak, the washbasins and their traps and pipework were replaced with new ones. They were then flushed every morning with a glucoprotamin solution, and routines regarding sink practices were improved, which led to discontinuation of the outbreak.19


Risks from toilet flushing


Showers, taps, and washbasins are not the only means of transmission via aerosol. Toilet flushing is another large risk area. Bio-aerosol production during toilet flushing was first reported in the 1950s by Jessen,15


who ‘seeded’ several types of


A toilet without a seat lid, still often found in clinical areas, despite the risk of aerosol transmission.


toilet with Serratia marcescens (then termed Bacillus prodigiosus), and measured bio-aerosols produced by flushing. Agar-filled ‘settle plates’ caught bio-aerosols that fell out of the air because of gravity, and a Bourdillon slit impactor collected air samples. Cistern-fed, gravity- flow toilets and a mains-fed pressure-valve toilet were examined. In addition to


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80  |  Page 81  |  Page 82  |  Page 83  |  Page 84  |  Page 85  |  Page 86  |  Page 87  |  Page 88  |  Page 89  |  Page 90  |  Page 91  |  Page 92