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Commodes: a health hazard
Journal of Hospital Infection (2000) 44: 318–321
Letters to the Editor doi:10.1053/jhin.1999.0714, available online at http://www.idealibrary.com on
The potential risk of transmitting vCJD through surgery Sir, The agents that cause transmissible degenerative encephalopathies (TDEs) such as CreutzfeldtJakob disease (CJD) in humans, and bovine spongiform encephalopathy (BSE) are relatively resistant to inactivation, and can survive autoclaving regimes used to sterilize surgical instruments.1 The UK Department of Health currently recommends disposal of surgical instruments used in ophthalmological surgery or neurosurgery on a) known or suspected cases of CJD, b) recipients of pituitary hormones or dura mater graft material derived from human cadavers, and c) blood-relatives of CJD cases. The precautionary principle has proved to be appropriate, especially because recent data show that some TDE agents are even more thermostable than had been previously demonstrated.2 Disposal has not incurred excessive cost because CJD-like diseases affect less than one in a million of the human population each year. However, this might change because of the emergence of variant (v) CJD that has probably resulted from dietary exposure to the BSE agent. There is no way of knowing whether the 52 cases identified so far herald the onset of a serious epidemic but, if so, the cost of disposing of high-risk neurological or ophthalmological instruments will escalate. Concern could also extend to instruments used in more general surgery because, in contrast to sporadic or iatrogenic CJD, the lymphoreticular tissues of vCJD cases appear to be consistently infected.3 In sheep and experimental rodents infected with BSE or scrapie, infectivity can be detected in lymphoreticular tissues long before the onset of clinical neurological disease. Consequently, instruments used invasively on lymphoreticular tissue in patients without symptoms of vCJD could become suspect.
0195–6701/00/040318+04 $35.00
It is evident from many studies on rodentpassaged scrapie agent that a) establishing infection by a peripheral route such as intraperitoneal challenge is several hundred-fold less effective than intra-cerebral injection, and b) the infectivity titre in lymphoreticular tissue is several hundred-fold lower than in brain-tissue. It has been tempting to use these data to conclude that surgery involving the invasion of lymphoreticular tissue is likely to be much less risky than neurosurgery. This does not necessarily follow, because lymphoreticular tissues were not actually traumatized in these experiments, and infectivity was taken up by these tissues after intraperitoneal injection. The single, lesser known, set of data that is directly relevant shows that the efficiency of establishing scrapie infection in mice by direct inoculation into the spleen is significantly greater than intraperitoneal injection.4 The efficiency of intrasplenic challenge was comparable to that for the intravenous route, which is only around ten-fold less efficient than intracerebral injection. It is these data, and not those derived from intra-peritonal challenge, that need to be considered in calculating the degree of vCJD-related risk related to surgery involving lymphoreticular tissue. The amount of tissue adhering to scalpel blades after cutting through brain-tissue has been shown to be around 5mg,5 and is likely to be greater on instruments that have serrated surfaces. The level of infectivity as expressed by the number of human intracerebral ID50 per gram of CJD-infected human brain is unknown, but is likely to fall within the range of values (108–1010 ID50/g) calculated from the within-species transmission of BSE and scrapie agents. From the animal studies discussed above, it can be calculated that vCJDinfected lymphoreticular tissue could contain 106–108 intracerebral ID50/g, which is equivalent to 105–107 intrasplenic ID50/g. Thus, if an instrument was contaminated with 5mg of vCJD-infected lymphoreticular tissue, this could contain more than 104 intrasplenic ID50. Studies are in progress to
© 2000 The Hospital Infection Society
Molecular typing of S. maltophilia
determine how much infectivity might remain on instruments after washing and autoclaving. D. M. Taylor, J. R. Fraser
Neuropathogenesis Unit, Institute for Animal Health, West Mains Road, Edinburgh EH9 3JF, UK
References 1. Taylor DM, Fraser H, McConnell I et al. Decontamination studies with the agents of bovine spongiform encephalopathy and scrapie. Arch Virol 1994; 139: 313–26. 2. Taylor DM. Inactivation of prions by physical and chemical means. J Hosp Infect 1999; 43(Supplement): S69–S76. 3. Hill AF, Butterworth RJ, Joiner S et al. Investigation of variant Creutzfeldt-Jakob disease and other human prion diseases with tonsil biopsies. Lancet 1999; 353: 83–89. 4. Fraser JR. Infectivity in extraneural tissues following intraocular scrapie infection. J Gen Virol 1996; 77: 2663–2668. 5. Chen SG, Antloga KM, Zou W, Wang W, Gambetti P, Malchesky PS. Effect of consecutive treatments of STERIS™ on protease-resistant prion protein contaminated devices in vitro. (Poster). Abstracts of the 3rd NMHCC Conference on Transmissible Spongiform Encephalopathies. San Diego, 16–17 March 1998.
doi:10.1053/jhin.1999.0713, available online at http://www.idealibrary.com on
Value of surveillance specimens in predicting and classifying ICU infections Sir, Patients in the intensive care unit (ICU) are at a high risk of hospital acquired infection (HAI), with reported incidences ranging from 13 to 42%.1,2,3 Rates of infection in ICU may be 300 to 400% higher than in rest of the hospital2,3,4 and in the region of 50–70% of all HAI, are ICU infections.1 Recently the European Prevalence of Infection in Intensive Care (EPIC) one day prevalence study was carried out.5,6 All patients admitted into our ICU over a 3month period were prospectively studied for infection which was classified according to EPIC criteria as well as by the novel classification proposed by Van Saene et al..7
319
Surveillance samples (throat swabs, gastric aspirates and rectal swabs) were collected from all patients on admission and every Monday and Wednesday thereafter throughout the patient’s stay in the ICU. Additional specimens which included tracheal aspirate, urine, blood culture, wound swabs, pus, CVP line tip etc. were obtained in the event of clinically apparent infection. Both surveillance and clinical specimens were inoculated into appropriate media and organisms identified by standard methods. Clinical information was collected from the case notes and during routine ICU rounds. A total of 53 patients (31 male and 22 female) were studied during the 3-month period, ranging in age from 15 to 85 years. More than 50% of patients staying in the ICU over 5 days developed infection, and the rate increased to 90% after 10 days. Fifteen patients developed 22 episodes of infection. Six patients suffered more than one episode of infecion. Infectious episodes were categorized as community acquired (9%), hospital acquired (18%) or ICUacquired (73%) in line with EPIC study classification (4, 5). The overall rate of infection in this study was 28.3%, the ICU-acquired infection rate being 20.75%. This is comparable to the results from other studies including EPIC study.4,5,7 Chest infections (68%) were commonest. When only ICU-acquired infections were examined, chest infections (56.25%) were followed by blood-stream infections (18.75%), urinary tract infections (12.5%), intra-abdominal sepsis and gastrointestinal tract infection (6.25% each). The surveillance specimen results were used to determine ‘carrier’ and ‘super carrier’ state as proposed by Van Saene et al..7 The ‘carrier state’ refers to the carriage of potentially pathogenic microorganisms by the patient at the time of admission to ICU, whether from the Community or from the wards of the same or a different hospital. Any clinically apparent infection caused by the former group of organisms was considered ‘primary endogenous infection’ regardless of the time for the development of infection. On the other hand ‘carrier state’ may be superseded by other groups of organisms by natural process or as replacement flora following antimicrobial therapy; this then constitutes ‘super carriage’. Sequential sampling of the patient allowed the transition to be recorded. Any clinical episode of infection caused by this group of organism was regarded as ‘secondary endogenous infection’. Analysis of the results obtained from surveillance samples and the clinical samples facilitated
320
Letters to the Editor
Table I
Comparison of EPIC and new classification New Classification
All episodes of infection
ICU Acquired (EPIC criteria)
Secondary Endogenous
Primary Endogenous
Exogenous
22
16 (73%)
10 (45%)
6 (24%)
0
differentiation of infection into three groups, primary endogenous, secondary endogenous and exogenous infections. Secondary endogenous and exogenous infections were considered as true ICU infections. Using this revised criteria the ICU acquired infection was shown to be 45.4% of all infection episodes compared to an original figure of 73%, based on EPIC definition (Table I). In conclusion, we believe the routine surveillance specimens turned out to be a useful tool for following colonization and infection patterns in ICU. Results of surveillance specimens also helped identify probable pathogens in clinical infections. Therefore, antimicrobial therapy could be tailored to the individual clinical situation.
H. Panigrahi V. Verghese
Department of Microbiology, North Manchester General Hospital, Delaunays Road, Crumpsall, Manchester M8 5RB
References 1. Bihari DJ. Nosocomial Infections in the Intensive Care Unit. Hospital Update 1992; 18: 266–276. 2. Dashner F, Frey P, Wolff G, Baumann PC, Suter P. Nosocomial infections in Intensive Care wards: a multicentre prospective study. Int Care Med 1982; 8: 5–9. 3. Donowitz F, Wenzel RP, Hoyt JW. High Risk of Hospital Acquired Infection in the ICU Patient. Crit Care Med 1982; 18: 355–357. 4. Wenzel RP, Thompson RL, Landry SM et al. Hospital-acquired infections in intensive care unit patients: an overview with emphasis on epidemics. Infect Control 1983; 4: 371–375. 5. Vincent J-L, Bihari DJ, Suter PM et al. for the EPIC International Advisory Committee. The Prevalence of Nosocomial Infection in Intensive Care Units in Europe. Results of the European Prevalence of Infection in Intensive Care (EPIC) Study. JAMA 1995; 274: 639–644. 6. Rennie MJ. EPIC: Infection in intensive care in Europe. Br J Int Care 1993; 3: 27–36. 7. van Saene HKF, Damjanovic V, Murray AE, de la Cal MA (1996). How to classify infections in intensive care units – the carrier state, a criterion whose times has come? J Hosp Infect 1996; 33: 1–12.
doi:10.1053/jhin.1999.0698, available online at http://www.idealibrary.com on
Commodes: a health hazard Sir, The hospital environment can represent an important source of nosocomial pathogens for vulnerable patients.1 While commodes have not been clearly demonstrated to have a definite role in nosocomial infection, their potential in this respect has been widely acknowledged. Various studies have demonstrated the persistence of nosocomial pathogens on commodes, including spores of Clostridium difficile2, small round structured viruses3, glycopeptideresistant Enterococcus faecium4 and Methicillinresistant Staphylococcus aureus.5 In a study of commodes used in the community it was found that most carers regard the cleaning of commodes very negatively.6 Patients with diarrhoea may soil commodes which then act as vehicles for transmission if cleaning is inadequate. On a recent ward audit it was noticed that a ‘clean’ commode was visibly stained with faeces underneath the seat. This prompted an audit of all existing commodes in the hospital. Forty-two wards were visited. Of these only seven (16.7%) did not use commodes. 102 commodes were studied on 35 (83.3%) wards. The average number of commodes per ward was 2.4 (range of one to nine). Nine (25.7%) of the wards with commodes felt that they had insufficient numbers to cope with patient needs especially when barrier nursing the maximum number of patients in side rooms. Eighty-two (80.4%) commodes were stored in the sluice room. Sixteen (15.7%) were in use in side rooms with barrier-nursed patients. These commodes were used exclusively by the patient in the room and stored there. The remaining four (4%) were kept either in a storeroom or a toilet. When examined, 88 (86.3%) of the commodes were visibly stained with faeces. Of these 73 (83%) were stained on the reverse and 15 (17.0%) on the top of the commode. The faecal staining on the top
Molecular typing of S. maltophilia
was minimal. Forty-one (56.5%) of the commodes stained on the reverse were heavily contaminated with faeces. Ninety-eight (96.1%) commodes had a vinyl cushion. Four cushions were made up of solid rubber. Forty-eight (47.1%) of the vinyl cushions were torn to varying degrees with exposure of the foam underneath. All the rubber cushions were intact. Cleaning was usually the healthcare assistant’s responsibility. Only four (11.4%) wards followed the hospital infection control policy, which recommends use of detergent and water (or a hypochlorite if visible faecal staining) after each patient use. The remaining 31 (88.6%) wards just wiped the top surface of commodes with a Cliniwipe (0.1% quaternary ammonium compound in 70% ethanol, Adams health care) with a thorough wash with detergent and water at weekends. Our findings show that although the top of the commode was usually clean the reverse was frequently heavily stained with faecal matter. This lack of cleanliness could be attributed mainly to inadequate cleaning procedures but also to faulty design of the commodes, which did not allow access for thorough cleaning underneath the metal supporting framework. Healthcare workers handling inadequately cleaned commodes may contaminate their hands. This occurred on two occasions during the audit when one of the author’s hands was contaminated with faeces while handling the framework of two of the commodes. The hospital policy with regards to cleaning of commodes was not being followed by majority of the wards. The vinyl cushion on the top is easily torn. This allows faecal matter to seep through the foam and contaminate and infect subsequent handlers and users. And vinyl covering should be intact to allow adequate cleaning. The rubber cushions observed on some wards were in better condition. These were not torn or cracked, appeared impervious to fluids and body waste and easy to clean. This simple yet revealing study about the state of commodes in the hospital leads to various conclusions. We should actively search for alternative designs of commodes that allow more effective cleaning. Commodes with a plastic moulded base and rubber cushion would be easier to clean and maintain than commodes with vinyl cushions and uncovered steel framework. Adequate numbers of
321
commodes must be provided. Healthcare assistants responsible for the cleaning need to be reminded of the importance of following hospital guidelines. The underside of the commode appears to be a neglected area for cleaning. Healthcare workers need to be made aware that the splattering of faecal matter underneath the seat is common in patients with diarrhoea and that cleaning efforts should be focused in this area. Commodes are a potential reservoir of hospital infection. Gross faecal contamination is not aesthetically acceptable, and may contribute to spread of infection and the resulting expenditure of scarce resources. Following this audit, infection control link nurses were asked to remind staff of proper cleaning procedures and posters were circulated to all wards. Infection control teams are advised to undertake similar audits in order to ensure that staff are following cleaning policy. M. S. Vardhan, K. D. Allen, G. DeRuiter
Departments of Microbiology & Infection Control, Whiston Hospital, Dragon Lane, Prescot, Merseyside L35 5DR
References 1. Pannuti CS. Hospital environment for high-risk patients In: Wenzel RF Ed Prevention and control of nosocomial infections, 3rd edn. Williams & Wilkins, 1997: 463–489. 2. Department of Health and Public Health Laboratory Service Joint Working Group. Clostridium difficile infection. Prevention and mangement. London, 1994. 3. Green J, Wright PA, Gallimore CI, Mitchell O, Morgan-Capner PM & Brown DWG. The role of environmental contamination with small round structured viruses in a hospital outbreak investigated by reverse-transcriptase polymerase chain reaction assay. J Hosp Infect 1998; 39: 39–45. 4. Chadwick PR, Oppenheim BA, Fox A, Woodford N, Morgenstern GR & Scarffe JH. Epidemiology of an outbreak due to glycopeptide-resistant Enterrococcus faecium on a leukaemia unit. J Hosp Infect 1996; 34: 171–182. 5. Blythe D, Keenlyside D, Dawson SJ, Galloway A. Environmental contamination due to methicillinresistant Staphylococcus aureus (MRSA). J Hosp Infect 1998; 38: 67–70. 6. Naylor JR, Mulley GP. Commodes: Inconvenient inconveniences. BMJ 1993; 307: 1258–1260.
Letters to the Editor doi:10.1053/jhin.1999.0714, available online at http://www.idealibrary.com on
The potential risk of transmitting vCJD through surgery Sir, The agents that cause transmissible degenerative encephalopathies (TDEs) such as CreutzfeldtJakob disease (CJD) in humans, and bovine spongiform encephalopathy (BSE) are relatively resistant to inactivation, and can survive autoclaving regimes used to sterilize surgical instruments.1 The UK Department of Health currently recommends disposal of surgical instruments used in ophthalmological surgery or neurosurgery on a) known or suspected cases of CJD, b) recipients of pituitary hormones or dura mater graft material derived from human cadavers, and c) blood-relatives of CJD cases. The precautionary principle has proved to be appropriate, especially because recent data show that some TDE agents are even more thermostable than had been previously demonstrated.2 Disposal has not incurred excessive cost because CJD-like diseases affect less than one in a million of the human population each year. However, this might change because of the emergence of variant (v) CJD that has probably resulted from dietary exposure to the BSE agent. There is no way of knowing whether the 52 cases identified so far herald the onset of a serious epidemic but, if so, the cost of disposing of high-risk neurological or ophthalmological instruments will escalate. Concern could also extend to instruments used in more general surgery because, in contrast to sporadic or iatrogenic CJD, the lymphoreticular tissues of vCJD cases appear to be consistently infected.3 In sheep and experimental rodents infected with BSE or scrapie, infectivity can be detected in lymphoreticular tissues long before the onset of clinical neurological disease. Consequently, instruments used invasively on lymphoreticular tissue in patients without symptoms of vCJD could become suspect.
0195–6701/00/040318+04 $35.00
It is evident from many studies on rodentpassaged scrapie agent that a) establishing infection by a peripheral route such as intraperitoneal challenge is several hundred-fold less effective than intra-cerebral injection, and b) the infectivity titre in lymphoreticular tissue is several hundred-fold lower than in brain-tissue. It has been tempting to use these data to conclude that surgery involving the invasion of lymphoreticular tissue is likely to be much less risky than neurosurgery. This does not necessarily follow, because lymphoreticular tissues were not actually traumatized in these experiments, and infectivity was taken up by these tissues after intraperitoneal injection. The single, lesser known, set of data that is directly relevant shows that the efficiency of establishing scrapie infection in mice by direct inoculation into the spleen is significantly greater than intraperitoneal injection.4 The efficiency of intrasplenic challenge was comparable to that for the intravenous route, which is only around ten-fold less efficient than intracerebral injection. It is these data, and not those derived from intra-peritonal challenge, that need to be considered in calculating the degree of vCJD-related risk related to surgery involving lymphoreticular tissue. The amount of tissue adhering to scalpel blades after cutting through brain-tissue has been shown to be around 5mg,5 and is likely to be greater on instruments that have serrated surfaces. The level of infectivity as expressed by the number of human intracerebral ID50 per gram of CJD-infected human brain is unknown, but is likely to fall within the range of values (108–1010 ID50/g) calculated from the within-species transmission of BSE and scrapie agents. From the animal studies discussed above, it can be calculated that vCJDinfected lymphoreticular tissue could contain 106–108 intracerebral ID50/g, which is equivalent to 105–107 intrasplenic ID50/g. Thus, if an instrument was contaminated with 5mg of vCJD-infected lymphoreticular tissue, this could contain more than 104 intrasplenic ID50. Studies are in progress to
© 2000 The Hospital Infection Society
Molecular typing of S. maltophilia
determine how much infectivity might remain on instruments after washing and autoclaving. D. M. Taylor, J. R. Fraser
Neuropathogenesis Unit, Institute for Animal Health, West Mains Road, Edinburgh EH9 3JF, UK
References 1. Taylor DM, Fraser H, McConnell I et al. Decontamination studies with the agents of bovine spongiform encephalopathy and scrapie. Arch Virol 1994; 139: 313–26. 2. Taylor DM. Inactivation of prions by physical and chemical means. J Hosp Infect 1999; 43(Supplement): S69–S76. 3. Hill AF, Butterworth RJ, Joiner S et al. Investigation of variant Creutzfeldt-Jakob disease and other human prion diseases with tonsil biopsies. Lancet 1999; 353: 83–89. 4. Fraser JR. Infectivity in extraneural tissues following intraocular scrapie infection. J Gen Virol 1996; 77: 2663–2668. 5. Chen SG, Antloga KM, Zou W, Wang W, Gambetti P, Malchesky PS. Effect of consecutive treatments of STERIS™ on protease-resistant prion protein contaminated devices in vitro. (Poster). Abstracts of the 3rd NMHCC Conference on Transmissible Spongiform Encephalopathies. San Diego, 16–17 March 1998.
doi:10.1053/jhin.1999.0713, available online at http://www.idealibrary.com on
Value of surveillance specimens in predicting and classifying ICU infections Sir, Patients in the intensive care unit (ICU) are at a high risk of hospital acquired infection (HAI), with reported incidences ranging from 13 to 42%.1,2,3 Rates of infection in ICU may be 300 to 400% higher than in rest of the hospital2,3,4 and in the region of 50–70% of all HAI, are ICU infections.1 Recently the European Prevalence of Infection in Intensive Care (EPIC) one day prevalence study was carried out.5,6 All patients admitted into our ICU over a 3month period were prospectively studied for infection which was classified according to EPIC criteria as well as by the novel classification proposed by Van Saene et al..7
319
Surveillance samples (throat swabs, gastric aspirates and rectal swabs) were collected from all patients on admission and every Monday and Wednesday thereafter throughout the patient’s stay in the ICU. Additional specimens which included tracheal aspirate, urine, blood culture, wound swabs, pus, CVP line tip etc. were obtained in the event of clinically apparent infection. Both surveillance and clinical specimens were inoculated into appropriate media and organisms identified by standard methods. Clinical information was collected from the case notes and during routine ICU rounds. A total of 53 patients (31 male and 22 female) were studied during the 3-month period, ranging in age from 15 to 85 years. More than 50% of patients staying in the ICU over 5 days developed infection, and the rate increased to 90% after 10 days. Fifteen patients developed 22 episodes of infection. Six patients suffered more than one episode of infecion. Infectious episodes were categorized as community acquired (9%), hospital acquired (18%) or ICUacquired (73%) in line with EPIC study classification (4, 5). The overall rate of infection in this study was 28.3%, the ICU-acquired infection rate being 20.75%. This is comparable to the results from other studies including EPIC study.4,5,7 Chest infections (68%) were commonest. When only ICU-acquired infections were examined, chest infections (56.25%) were followed by blood-stream infections (18.75%), urinary tract infections (12.5%), intra-abdominal sepsis and gastrointestinal tract infection (6.25% each). The surveillance specimen results were used to determine ‘carrier’ and ‘super carrier’ state as proposed by Van Saene et al..7 The ‘carrier state’ refers to the carriage of potentially pathogenic microorganisms by the patient at the time of admission to ICU, whether from the Community or from the wards of the same or a different hospital. Any clinically apparent infection caused by the former group of organisms was considered ‘primary endogenous infection’ regardless of the time for the development of infection. On the other hand ‘carrier state’ may be superseded by other groups of organisms by natural process or as replacement flora following antimicrobial therapy; this then constitutes ‘super carriage’. Sequential sampling of the patient allowed the transition to be recorded. Any clinical episode of infection caused by this group of organism was regarded as ‘secondary endogenous infection’. Analysis of the results obtained from surveillance samples and the clinical samples facilitated
320
Letters to the Editor
Table I
Comparison of EPIC and new classification New Classification
All episodes of infection
ICU Acquired (EPIC criteria)
Secondary Endogenous
Primary Endogenous
Exogenous
22
16 (73%)
10 (45%)
6 (24%)
0
differentiation of infection into three groups, primary endogenous, secondary endogenous and exogenous infections. Secondary endogenous and exogenous infections were considered as true ICU infections. Using this revised criteria the ICU acquired infection was shown to be 45.4% of all infection episodes compared to an original figure of 73%, based on EPIC definition (Table I). In conclusion, we believe the routine surveillance specimens turned out to be a useful tool for following colonization and infection patterns in ICU. Results of surveillance specimens also helped identify probable pathogens in clinical infections. Therefore, antimicrobial therapy could be tailored to the individual clinical situation.
H. Panigrahi V. Verghese
Department of Microbiology, North Manchester General Hospital, Delaunays Road, Crumpsall, Manchester M8 5RB
References 1. Bihari DJ. Nosocomial Infections in the Intensive Care Unit. Hospital Update 1992; 18: 266–276. 2. Dashner F, Frey P, Wolff G, Baumann PC, Suter P. Nosocomial infections in Intensive Care wards: a multicentre prospective study. Int Care Med 1982; 8: 5–9. 3. Donowitz F, Wenzel RP, Hoyt JW. High Risk of Hospital Acquired Infection in the ICU Patient. Crit Care Med 1982; 18: 355–357. 4. Wenzel RP, Thompson RL, Landry SM et al. Hospital-acquired infections in intensive care unit patients: an overview with emphasis on epidemics. Infect Control 1983; 4: 371–375. 5. Vincent J-L, Bihari DJ, Suter PM et al. for the EPIC International Advisory Committee. The Prevalence of Nosocomial Infection in Intensive Care Units in Europe. Results of the European Prevalence of Infection in Intensive Care (EPIC) Study. JAMA 1995; 274: 639–644. 6. Rennie MJ. EPIC: Infection in intensive care in Europe. Br J Int Care 1993; 3: 27–36. 7. van Saene HKF, Damjanovic V, Murray AE, de la Cal MA (1996). How to classify infections in intensive care units – the carrier state, a criterion whose times has come? J Hosp Infect 1996; 33: 1–12.
doi:10.1053/jhin.1999.0698, available online at http://www.idealibrary.com on
Commodes: a health hazard Sir, The hospital environment can represent an important source of nosocomial pathogens for vulnerable patients.1 While commodes have not been clearly demonstrated to have a definite role in nosocomial infection, their potential in this respect has been widely acknowledged. Various studies have demonstrated the persistence of nosocomial pathogens on commodes, including spores of Clostridium difficile2, small round structured viruses3, glycopeptideresistant Enterococcus faecium4 and Methicillinresistant Staphylococcus aureus.5 In a study of commodes used in the community it was found that most carers regard the cleaning of commodes very negatively.6 Patients with diarrhoea may soil commodes which then act as vehicles for transmission if cleaning is inadequate. On a recent ward audit it was noticed that a ‘clean’ commode was visibly stained with faeces underneath the seat. This prompted an audit of all existing commodes in the hospital. Forty-two wards were visited. Of these only seven (16.7%) did not use commodes. 102 commodes were studied on 35 (83.3%) wards. The average number of commodes per ward was 2.4 (range of one to nine). Nine (25.7%) of the wards with commodes felt that they had insufficient numbers to cope with patient needs especially when barrier nursing the maximum number of patients in side rooms. Eighty-two (80.4%) commodes were stored in the sluice room. Sixteen (15.7%) were in use in side rooms with barrier-nursed patients. These commodes were used exclusively by the patient in the room and stored there. The remaining four (4%) were kept either in a storeroom or a toilet. When examined, 88 (86.3%) of the commodes were visibly stained with faeces. Of these 73 (83%) were stained on the reverse and 15 (17.0%) on the top of the commode. The faecal staining on the top
Molecular typing of S. maltophilia
was minimal. Forty-one (56.5%) of the commodes stained on the reverse were heavily contaminated with faeces. Ninety-eight (96.1%) commodes had a vinyl cushion. Four cushions were made up of solid rubber. Forty-eight (47.1%) of the vinyl cushions were torn to varying degrees with exposure of the foam underneath. All the rubber cushions were intact. Cleaning was usually the healthcare assistant’s responsibility. Only four (11.4%) wards followed the hospital infection control policy, which recommends use of detergent and water (or a hypochlorite if visible faecal staining) after each patient use. The remaining 31 (88.6%) wards just wiped the top surface of commodes with a Cliniwipe (0.1% quaternary ammonium compound in 70% ethanol, Adams health care) with a thorough wash with detergent and water at weekends. Our findings show that although the top of the commode was usually clean the reverse was frequently heavily stained with faecal matter. This lack of cleanliness could be attributed mainly to inadequate cleaning procedures but also to faulty design of the commodes, which did not allow access for thorough cleaning underneath the metal supporting framework. Healthcare workers handling inadequately cleaned commodes may contaminate their hands. This occurred on two occasions during the audit when one of the author’s hands was contaminated with faeces while handling the framework of two of the commodes. The hospital policy with regards to cleaning of commodes was not being followed by majority of the wards. The vinyl cushion on the top is easily torn. This allows faecal matter to seep through the foam and contaminate and infect subsequent handlers and users. And vinyl covering should be intact to allow adequate cleaning. The rubber cushions observed on some wards were in better condition. These were not torn or cracked, appeared impervious to fluids and body waste and easy to clean. This simple yet revealing study about the state of commodes in the hospital leads to various conclusions. We should actively search for alternative designs of commodes that allow more effective cleaning. Commodes with a plastic moulded base and rubber cushion would be easier to clean and maintain than commodes with vinyl cushions and uncovered steel framework. Adequate numbers of
321
commodes must be provided. Healthcare assistants responsible for the cleaning need to be reminded of the importance of following hospital guidelines. The underside of the commode appears to be a neglected area for cleaning. Healthcare workers need to be made aware that the splattering of faecal matter underneath the seat is common in patients with diarrhoea and that cleaning efforts should be focused in this area. Commodes are a potential reservoir of hospital infection. Gross faecal contamination is not aesthetically acceptable, and may contribute to spread of infection and the resulting expenditure of scarce resources. Following this audit, infection control link nurses were asked to remind staff of proper cleaning procedures and posters were circulated to all wards. Infection control teams are advised to undertake similar audits in order to ensure that staff are following cleaning policy. M. S. Vardhan, K. D. Allen, G. DeRuiter
Departments of Microbiology & Infection Control, Whiston Hospital, Dragon Lane, Prescot, Merseyside L35 5DR
References 1. Pannuti CS. Hospital environment for high-risk patients In: Wenzel RF Ed Prevention and control of nosocomial infections, 3rd edn. Williams & Wilkins, 1997: 463–489. 2. Department of Health and Public Health Laboratory Service Joint Working Group. Clostridium difficile infection. Prevention and mangement. London, 1994. 3. Green J, Wright PA, Gallimore CI, Mitchell O, Morgan-Capner PM & Brown DWG. The role of environmental contamination with small round structured viruses in a hospital outbreak investigated by reverse-transcriptase polymerase chain reaction assay. J Hosp Infect 1998; 39: 39–45. 4. Chadwick PR, Oppenheim BA, Fox A, Woodford N, Morgenstern GR & Scarffe JH. Epidemiology of an outbreak due to glycopeptide-resistant Enterrococcus faecium on a leukaemia unit. J Hosp Infect 1996; 34: 171–182. 5. Blythe D, Keenlyside D, Dawson SJ, Galloway A. Environmental contamination due to methicillinresistant Staphylococcus aureus (MRSA). J Hosp Infect 1998; 38: 67–70. 6. Naylor JR, Mulley GP. Commodes: Inconvenient inconveniences. BMJ 1993; 307: 1258–1260.