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Control of methicillin-resistant Staphylococcus aureus
Letters
73
to the Editor
Sir, Control
of methicillin-resistant
Stufihylococcus
aureus
Cox et al.’ give a worrying account of the magnitude of problems likely to afflict hospitals and communities resulting from the new strain of methicillin-resistant Staphylococcus UUYUN (EMRSA-16). At this hospital we have had a similar outbreak, though thankfully of shorter duration, and many other hospitals are currently experiencing outbreaks. I would like to comment on some of the conclusions drawn by Cox, and some of the methods used to control this outbreak. Firstly, they have fallen into the trap of comparing MRSA with methicillinsensitive S. UUY~US(MSSA), stating that they are equally pathogenic: a frequently repeated misconception.’ This ignores the simple truth that there are dozens of strains of MRSA, and hundreds of strains of MSSA, each with their own capabilities, properties and potentials to spread and/or cause serious infection. The method they use, comparing numbers of isolates in blood and from other sources, has several pitfalls. Blood culture growths can be contaminants; screening swabs, if plated on selective medium (using methicillin), may fail to grow MSSA. MSSA if detected might not be reported (e.g. from nasal swabs), as it is of no relevance. They have attempted to exclude ‘screening’ swabs, but it is not always possible to be sure why a sample was taken. During outbreaks surgeons and nursing staff are more likely to take samples from any patient, whether or not they are thought to be infected. The method also fails to recognize that the samples being compared are coming from different populations of patients. I think there is little doubt that EMRSA-16 is a relatively virulent strain of MRSA, but this cannot be extrapolated to all MRSA, or all S. aUreUS. In the last vear we have seen two presumptive cases of endocarditis (persistent bacteraemia with no other septic focus), one spinal osteomyelitis, and one meningitis caused by EMRSA-16. However, in all of these cases, and in all other serious sepsis with MRSA I have ever seen, the patient acquired the organism in hospital at a time when immunosuppressed by illness or chemotherapy, and their defences were bypassed by surgical wound, vascular catheter or endotracheal tube. ‘Ordinary’ S. aUreUScan present with community-acquired infections such as pneumonia, septicaemia, septic arthritis, primary osteomyelitis, toxic-shock syndrome, or food-poisoning, but I have yet to see any of these with MRSA. Secondly, I am bemused by the emphasis placed on screening of staff in this report. The number of staff carriers identified was very small (approximately 0.5’%), and the contribution made by staff carriers during a major outbreak is dubious.” The reservoir of the organism is colonized patients, in particular those with surgical wounds or chronic lesions: staff do not have these. Many centres have stopped screening staff because of the low yield and minimal contribution to control of outbreak (T. W. J. Kelly personal communication,
74
Letters
to the Editor
and G. Calver personal communication). There are three dangers in mass screening of staff. Firstly, this fails to recognize that staff usually acquire the organism from patients, not the other way around. Staff identified as carriers suffer unnecessary treatment (because on rescreening they are often found to have been transient carriers only),4 and can also suffer psychological stress from being unfairly labelled as the cause of the outbreak. If staff are laid off whilst being treated, this creates shortages on the wards (probably exacerbating infection control problems), adds greatly to the costs of an outbreak, and adds the complication of reporting to the Health and Safety Executive.’ Secondly, screening does not identify those staff who act as vectors without ever becoming colonized themselves. These staff members can become falsely reassured about their standards of practice. Thirdly, taking of swabs and completing the necessary paperwork is time-consuming: microbiologists recognize the extra work entailed in the laboratory, but often ignore the extra work on the ward. If this effort replaces a positive contribution to patient care (e.g. adequate handwashing) then it is counterproductive. I believe that staff screening should be limited to staff with eczema, to specialist units with no background endemic problem, or to outbreaks where the epidemiology points to theatre-acquired infection. In the current situation where substantial numbers of long-stay patients are colonized, and increasing numbers of people in the community are carriers, we have to learn to ‘live with MRSA’.6 Total eradication from general hospitals is an unrealistic ambition, and most probably impossible. It has been suggested that MRSA should be ignored.’ I believe the two extremes of over-reaction and inactivity are equally inappropriate. It is important that the infection control cure is not perceived to be worse than the infection, or microbiologists will lose the support of their clinical colleagues,3 and all credibility. I think the conclusion reached by Cox that a secondary outbreak was ‘caused’ by a staff member is unproven and in fact unlikely. Given that they have shown a significant reservoir in their community (and this can be refractory carriage)’ it seems more likely that an unidentified carrier was admitted, and the staff member concerned acquired the organism from this patient, Staff are more often the victims of outbreaks rather then the culprits. My third concern is the apparent semi-routine use of rifampicin and fusidic acid for eradication of carriage. These are both toxic drugs, as shown by the 30% incidence of side-effects reported in this study. I do not think it appropriate that they should be used in this way. Rifampicin in particular can lead to many problems: hepatic necrosis is rare but recognized, drug interaction common. If used for nursing staff, unexpected pregnancy may be an unwanted side-effect. The possibility of generating resistance to these agents should not be ignored by microbiologists, who use this argument frequently to justify controlling use of antibiotics by others. I strongly believe that this therapy should only be used to treat infection (e.g. outpatient treatment for orthopaedic sepsis). To justify use for asymptomatic carriage, a clear benefit for the patient must be identified, otherwise this
Letters
to the Editor
75
use becomes indefensible should adverse effects occur. The only times I have considered this are when patients are unable to be transferred for specialist care (e.g. rehabilitation at Stoke Mandeville) until carriage has been eliminated, and antiseptic/mupirocin therapy has failed. For staff, the only justification would be a surgeon or theatre nurse, shown to be a disseminator, and in whom topical therapy had repeatedly failed. Finally, I find the logic of the proposed surveillance somewhat perverse. Clearly it is simple to screen patients on discharge, but by the very fact of discharge it is likely that any wounds are healed (therefore less likely to be colonized), and having left hospital such patients are no longer a reservoir for hospital cross-infection. The method I am trying to introduce locally is to screen weekly any patients who have been on the ward for longer than two weeks, and those who are predicted to stay for two weeks or more. The first group have been exposed in the hospital longer, and are therefore more likely to be carriers. The second group will remain as a potential source for longer (and are perhaps more likely to have unhealed lesions). In both cases, identifying these patients as carriers so they can be treated will contribute to control or prevention of spread. For patients being discharged ‘isolation’ is already arranged, and treatment will not contribute to control of hospital infection. M. J. Sheppard
All Saints’ Hospital, Magpie Hall Road, Chatham, Kent ME4 SNG, UK References
1. Cox RA, Conquest C, Mallaghan C, Marples RR. A major outbreak of MRSA caused by a new phage-type (EMRSA-16) J Hosp Infect 1995; 29: 87-106. 2. Talon D, Rouget C, Cailleaux V et al. Nasal carriage of Staphylococcus UUY~US and crosscontamination in a surgical intensive care unit: efficacy of mupirocin ointment. J Hasp Infect 1995; 30: 39-50. 3. Barrett SP, Teale EL, Sage R. MRSA in three adjacent Health Districts of South-East England 1986-91. 1993; 24: 313-325. 4. Cookson B, Peters B, Webster M et al. Staff carriage of EMRSA. J Clin Microbial 1989; 27: 1471-1476. 5. Hill S. Intranasal mupirocin (letter). J Hosp Infect 1994; 28: 235. 6. Barrett SP, Mellor JA. Living with EMRSA-1 (letter). J Hosp Infect 1990; 15: 103-104. 7. Lacey RW. MRSA-a suitable case for inactivity? J Hasp Infect 1987; 9: 103-105. 8. Masterton RG, Coia JE, Notman AW et al. MRSA carriage associated with contamination of the home environment. J Hosp Infect 1995; 29: 318-319.
This letter was shown to Dr Cox and her colleagues and their reply follows: Sir, Dr Sheppard makes a number of points which reflect the current debate on the management of outbreaks caused by epidemic methicillin-resistant
73
to the Editor
Sir, Control
of methicillin-resistant
Stufihylococcus
aureus
Cox et al.’ give a worrying account of the magnitude of problems likely to afflict hospitals and communities resulting from the new strain of methicillin-resistant Staphylococcus UUYUN (EMRSA-16). At this hospital we have had a similar outbreak, though thankfully of shorter duration, and many other hospitals are currently experiencing outbreaks. I would like to comment on some of the conclusions drawn by Cox, and some of the methods used to control this outbreak. Firstly, they have fallen into the trap of comparing MRSA with methicillinsensitive S. UUY~US(MSSA), stating that they are equally pathogenic: a frequently repeated misconception.’ This ignores the simple truth that there are dozens of strains of MRSA, and hundreds of strains of MSSA, each with their own capabilities, properties and potentials to spread and/or cause serious infection. The method they use, comparing numbers of isolates in blood and from other sources, has several pitfalls. Blood culture growths can be contaminants; screening swabs, if plated on selective medium (using methicillin), may fail to grow MSSA. MSSA if detected might not be reported (e.g. from nasal swabs), as it is of no relevance. They have attempted to exclude ‘screening’ swabs, but it is not always possible to be sure why a sample was taken. During outbreaks surgeons and nursing staff are more likely to take samples from any patient, whether or not they are thought to be infected. The method also fails to recognize that the samples being compared are coming from different populations of patients. I think there is little doubt that EMRSA-16 is a relatively virulent strain of MRSA, but this cannot be extrapolated to all MRSA, or all S. aUreUS. In the last vear we have seen two presumptive cases of endocarditis (persistent bacteraemia with no other septic focus), one spinal osteomyelitis, and one meningitis caused by EMRSA-16. However, in all of these cases, and in all other serious sepsis with MRSA I have ever seen, the patient acquired the organism in hospital at a time when immunosuppressed by illness or chemotherapy, and their defences were bypassed by surgical wound, vascular catheter or endotracheal tube. ‘Ordinary’ S. aUreUScan present with community-acquired infections such as pneumonia, septicaemia, septic arthritis, primary osteomyelitis, toxic-shock syndrome, or food-poisoning, but I have yet to see any of these with MRSA. Secondly, I am bemused by the emphasis placed on screening of staff in this report. The number of staff carriers identified was very small (approximately 0.5’%), and the contribution made by staff carriers during a major outbreak is dubious.” The reservoir of the organism is colonized patients, in particular those with surgical wounds or chronic lesions: staff do not have these. Many centres have stopped screening staff because of the low yield and minimal contribution to control of outbreak (T. W. J. Kelly personal communication,
74
Letters
to the Editor
and G. Calver personal communication). There are three dangers in mass screening of staff. Firstly, this fails to recognize that staff usually acquire the organism from patients, not the other way around. Staff identified as carriers suffer unnecessary treatment (because on rescreening they are often found to have been transient carriers only),4 and can also suffer psychological stress from being unfairly labelled as the cause of the outbreak. If staff are laid off whilst being treated, this creates shortages on the wards (probably exacerbating infection control problems), adds greatly to the costs of an outbreak, and adds the complication of reporting to the Health and Safety Executive.’ Secondly, screening does not identify those staff who act as vectors without ever becoming colonized themselves. These staff members can become falsely reassured about their standards of practice. Thirdly, taking of swabs and completing the necessary paperwork is time-consuming: microbiologists recognize the extra work entailed in the laboratory, but often ignore the extra work on the ward. If this effort replaces a positive contribution to patient care (e.g. adequate handwashing) then it is counterproductive. I believe that staff screening should be limited to staff with eczema, to specialist units with no background endemic problem, or to outbreaks where the epidemiology points to theatre-acquired infection. In the current situation where substantial numbers of long-stay patients are colonized, and increasing numbers of people in the community are carriers, we have to learn to ‘live with MRSA’.6 Total eradication from general hospitals is an unrealistic ambition, and most probably impossible. It has been suggested that MRSA should be ignored.’ I believe the two extremes of over-reaction and inactivity are equally inappropriate. It is important that the infection control cure is not perceived to be worse than the infection, or microbiologists will lose the support of their clinical colleagues,3 and all credibility. I think the conclusion reached by Cox that a secondary outbreak was ‘caused’ by a staff member is unproven and in fact unlikely. Given that they have shown a significant reservoir in their community (and this can be refractory carriage)’ it seems more likely that an unidentified carrier was admitted, and the staff member concerned acquired the organism from this patient, Staff are more often the victims of outbreaks rather then the culprits. My third concern is the apparent semi-routine use of rifampicin and fusidic acid for eradication of carriage. These are both toxic drugs, as shown by the 30% incidence of side-effects reported in this study. I do not think it appropriate that they should be used in this way. Rifampicin in particular can lead to many problems: hepatic necrosis is rare but recognized, drug interaction common. If used for nursing staff, unexpected pregnancy may be an unwanted side-effect. The possibility of generating resistance to these agents should not be ignored by microbiologists, who use this argument frequently to justify controlling use of antibiotics by others. I strongly believe that this therapy should only be used to treat infection (e.g. outpatient treatment for orthopaedic sepsis). To justify use for asymptomatic carriage, a clear benefit for the patient must be identified, otherwise this
Letters
to the Editor
75
use becomes indefensible should adverse effects occur. The only times I have considered this are when patients are unable to be transferred for specialist care (e.g. rehabilitation at Stoke Mandeville) until carriage has been eliminated, and antiseptic/mupirocin therapy has failed. For staff, the only justification would be a surgeon or theatre nurse, shown to be a disseminator, and in whom topical therapy had repeatedly failed. Finally, I find the logic of the proposed surveillance somewhat perverse. Clearly it is simple to screen patients on discharge, but by the very fact of discharge it is likely that any wounds are healed (therefore less likely to be colonized), and having left hospital such patients are no longer a reservoir for hospital cross-infection. The method I am trying to introduce locally is to screen weekly any patients who have been on the ward for longer than two weeks, and those who are predicted to stay for two weeks or more. The first group have been exposed in the hospital longer, and are therefore more likely to be carriers. The second group will remain as a potential source for longer (and are perhaps more likely to have unhealed lesions). In both cases, identifying these patients as carriers so they can be treated will contribute to control or prevention of spread. For patients being discharged ‘isolation’ is already arranged, and treatment will not contribute to control of hospital infection. M. J. Sheppard
All Saints’ Hospital, Magpie Hall Road, Chatham, Kent ME4 SNG, UK References
1. Cox RA, Conquest C, Mallaghan C, Marples RR. A major outbreak of MRSA caused by a new phage-type (EMRSA-16) J Hosp Infect 1995; 29: 87-106. 2. Talon D, Rouget C, Cailleaux V et al. Nasal carriage of Staphylococcus UUY~US and crosscontamination in a surgical intensive care unit: efficacy of mupirocin ointment. J Hasp Infect 1995; 30: 39-50. 3. Barrett SP, Teale EL, Sage R. MRSA in three adjacent Health Districts of South-East England 1986-91. 1993; 24: 313-325. 4. Cookson B, Peters B, Webster M et al. Staff carriage of EMRSA. J Clin Microbial 1989; 27: 1471-1476. 5. Hill S. Intranasal mupirocin (letter). J Hosp Infect 1994; 28: 235. 6. Barrett SP, Mellor JA. Living with EMRSA-1 (letter). J Hosp Infect 1990; 15: 103-104. 7. Lacey RW. MRSA-a suitable case for inactivity? J Hasp Infect 1987; 9: 103-105. 8. Masterton RG, Coia JE, Notman AW et al. MRSA carriage associated with contamination of the home environment. J Hosp Infect 1995; 29: 318-319.
This letter was shown to Dr Cox and her colleagues and their reply follows: Sir, Dr Sheppard makes a number of points which reflect the current debate on the management of outbreaks caused by epidemic methicillin-resistant