- Email: [email protected]
Ointments as a source of meticillin-resistant Staphylococcus aureus spread
Letters to the Editor
195
who are not familiar with gastrointestinal infectious diseases in Japan. The mechanism of the worsening of CDAD by loperamide is considered to be that it causes bowel stasis, which may allow the proliferation of C. difficile and increase the absorption of clostridial toxins from the gut mucosa.8 It is also considered that the slowing of the faecal transit time results in extended toxin-associated damage. Based on these mechanisms, it is considered that loperamide would worsen the clinical course of CDAD. Restrictive antibiotics policies and infection control measures are known to prevent CDAD among hospitalised patients. However, once CDAD occurs, antimicrobials should be discontinued and appropriate treatment should be started. Although the sample size was small, this study suggested that the inappropriate and thoughtless use of loperamide worsens the clinical course of CDAD. Clinicians should recognise that its administration must be avoided in CDAD.
M. Nakamuraa A. Nakamurab R. Uedab a Department of Gastroenterology, Toyokawa City Hospital, Toyokawa, Japan b Department of Internal Oncology and Immunology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan c Department of Bacterial Pathogenesis and Infection Control, National Institute of Infectious Diseases, Tokyo, Japan E-mail address: [email protected] Available online 9 August 2008 * Corresponding author. Address: Department of Gastroenterology, Toyokawa City Hospital, Kohmei-cho 1-19, Toyokawa 4428561, Japan. Tel.: þ0533 86 1111; fax: þ0533 84 1327. ª 2008 The Hospital Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2008.06.010
Conflict of interest statement None declared.
Ointments as a source of meticillin-resistant Staphylococcus aureus spread
Funding sources None.
Madam,
References 1. Bartlett JG. Narrative review: the new epidemic of Clostridium difficile-associated enteric disease. Ann Intern Med 2006;145:758e764. 2. Kelly CP, Pothoulakis C, LaMont JT. Clostridium difficile colitis. N Engl J Med 1994;330:257e262. 3. Burke GW, Wilson ME, Mehrez IO. Absence of diarrhea in toxic megacolon complicating Clostridium difficile pseudomembranous colitis. Am J Gastroenterol 1988;83:304e307. 4. Reese RE, Betts RF. A practical approach to infectious diseases, 4th ed. Boston: Little, Brown & Co. p. 1087e89. 5. Fekety R. Guidelines for the diagnosis and management of Clostridium difficile-associated diarrhea and colitis. American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol 1997;92:739e750. 6. D’Agata EM. Methodologic issues of caseecontrol studies: a review of established and newly recognized limitations. Infect Control Hosp Epidemiol 2005;26:338e341. 7. Brown JW. Toxic megacolon associated with loperamide therapy. J Am Med Soc 1979;241:501e502. 8. Church JM, Fazio VW. A role for colonic stasis in the pathogenesis of disease related to Clostridium difficile. Dis Colon Rectum 1986;29:804e809.
H. Katoa,b,* H. Katoc Y. Iwashimab
The main reservoirs of meticillin-resistant Staphylococcus aureus (MRSA) are colonised and infected patients.1 However, contaminated surfaces may also play an important role.2,3 Transmission mostly occurs via the transiently contaminated hands of healthcare workers.1 The aim of our study was to investigate whether ointments used for MRSA-positive patients are a source of nosocomial MRSA spread in the University Hospital of Innsbruck. A total of 101 ointments from 19 MRSA-positive patients hospitalised at the University Hospital Innsbruck, Austria were collected in the period from July to December 2005 and screened for MRSA contamination. The 101 ointments were used for skin care and other medical indications (Table I). Each patient had his own set of ointments during hospitalisation. All ointments were stored in collapsible tubes and were applied with a single-use spatula according to our hospital guidelines. For MRSA screening, one swab of each ointment was taken from the interior of the screw cap and the same swab was used for the surface of the ointment. All swabs were plated on blood agar and investigated for MRSA and other pathogens according to standard procedures. Presence of the mecA
196 Table I
Letters to the Editor Ointments and their contaminations
Ointments
No. of ointments investigated
Bepanthen cream (dexpanthenol) Bactroban nasal ointment (mupirocin) Bactroban cream (mupirocin) Lasepton cream (protective cream without active substances) Oleovit eye ointment (dexpanthenol, retinolpalmitat) Spoendlin’sche nasal ointment (Bergamot oil, camphor, menthol) Ultrasicc/Ultrabas cream (for skin care without active substances) Scottopect gel (turpentine oil, eucalyptus oil, menthol, camphor) Candio-Hermal soft paste (nystatin) Vidisic eye gel (carbomer) Betaisadona wound gel (povidone-iodine) Vetren gel (heparin-sodium) Diclobene gel (diclofenac-sodium) Dynexan cream (tetracaine hydrochloride, chamomile, sage, arnica, aluminium formiate) Vaseline (white soft paraffin)
18 12 6 10
Microbial contamination
MRSA (N ¼ 3), Enterococcus sp. (N ¼ 1) MRSA (N ¼ 1), MRSE (N ¼ 3) Candida sp. (N ¼ 1)
9
MRSE (N ¼ 2), S. aureus (N ¼ 1)
9
MRSA (N ¼ 1), MRSE (N ¼ 2), Serratia sp. (N ¼ 1), Proteus sp. þ Enterococcus sp. (N ¼ 1)
7 7 6 5 4 4 2 1
MRSA (N ¼ 1), MRSE (N ¼ 2)
Bacillus sp. (N ¼ 1)
1
MRSA, meticillin-resistant Staphylococcus aureus; MRSE, meticillin-resistant Staphylococcus epidermidis.
gene and lukS/lukF gene (encoding for Panton-Valentine Leukocidin) were determined by polymerase chain reaction according to the manufacturer’s instructions (GenoType, Hain, Nehren, Germany). Determination of SCC-mec cassette and agr type was done as described previously.4,5 MRSA strains collected from patients and ointments were typed by automated ribotyping under the conditions recommended by the manufacturer of the Riboprinter microbial characterisation system (Qualicon Europe Ltd, Warwick, UK) using EcoRI as restriction enzyme. Of the 101 ointment specimens, collected from 19 MRSA-positive patients, 80 were culture negative, 21 (20.8%) were contaminated with various bacteria or Candida spp. (Table I). Six (5.9%) ointment specimens were found positive for MRSA: Bepanthen cream (N ¼ 3), Candio-Hermal soft paste (N ¼ 1), Spoendlin’sche nasal ointment (N ¼ 1) and even mupirocin cream (N ¼ 1) (Table I). The unopened ointments which were used as negative control for the MRSA screening were culture negative. The MRSA-positive ointment specimens were those from three patients (A, B and C); all were infected with MRSA before treated with ointments. In patient A, MRSA was isolated from the nasal cavity, the respiratory tract, the skin and decubitus ulcers; in patient B from the nasal cavity, the
respiratory tract, the percutaneous endoscopic gastrostomy (PEG) tube, decubitus ulcers and urine; and in patient C from the nasal cavity and an ulcer. Patient A had nine ointments in use, two of them contaminated with MRSA. One of the 10 ointments used by patient B was contaminated with MRSA, one with meticillin-resistant Staphylococcus epidermidis (MRSE), one with Serratia marcescens and one with Bacillus spp. Three of the six ointments used by patient C were contaminated with MRSA. MRSA from both patients’ body sites and the respective ointments showed the same resistance patterns: all were susceptible to tetracycline, trimethoprim, cotrimoxazole, vancomycin, rifampicin, fusidic acid and mupirocin. All MRSA harboured the mecA gene and lacked the lukS/lukF gene. All MRSA except for one patient isolate carried SCC-mec cassette IVa and agr type 1 (patient A; with SCC-mec cassette I and agr type 2). Molecular typing by automated ribotyping revealed four different ribotypes (RT 2, 3, 6, 12) in the patients and two (RT 2, 6) in ointment specimens. Ribotypes of MRSA from the ointments were identical to those from MRSA collected from the patients (patients A and B yielded RT 6; patient C, RT 2). The fact that 5.9% of ointments were contaminated with MRSA suggests that ointments could
Letters to the Editor constitute an additional and, until now, neglected reservoir for MRSA in the hospital. To our knowledge there are no other reports in the literature about the prevalence of MRSA in ointments. Interestingly, RT 6 is very rare in our RT database (0.8%) that consists of 366 MRSA specimens from our hospital and suggests that transmission occurred between patients and their ointments and not from the hospital environment. The ointments may contribute to recolonisation or reinfection of patients, suggesting that MRSA is transferred from the patient to the ointment and potentially vice versa. This hypothesis was previously set up by Gilani and coworkers for meticillin-susceptible S. aureus in the same matrix.6 The reason for our finding of MRSA-positive ointments is not yet clear. We can speculate that ointments were either not applied aseptically by the nurses or that patients applied the ointments by themselves and thus contaminated them. Ointments which are in repeated use on different patients could be a source of MRSA transmission between patients. Thus, there is a need for correct storage and aseptic portioning with single-use spatulae to reduce the risk of MRSA spread via ointments in hospital facilities.
Acknowledgments
197 element in methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother 2002;46:2155e2166. 6. Gilani SJK, Gonzalez M, Hussain I, Finlay AY, Patel GK. Staphylococcus aureus re-colonization in atopic dermatitis: beyond the skin. Clin Exp Dermatol 2005;30:10e13.
K. Grifa D. Ortha,* A. Mayra M.P. Diericha R. Wu ¨rznera C. Lass-Flo ¨rla E. Nogler-Semenitzb a Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University, Austria b Hospital Pharmacy, Innsbruck Medical University, Austria E-mail address: [email protected] Available online 23 August 2008 * Corresponding author. Address: Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University and Austrian Reference Laboratory for Enterohemorrhagic Escherichia coli, Scho ¨pfstr. 41, A-6020 Innsbruck, Austria. Tel.: þ43 512 9003 70772; fax: þ43 512 9003 73750.
ª 2008 The Hospital Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2008.06.011
We thank Pharmacia and Pfizer for their generous support of our MRSA studies. Needle protective devices; where are we now? Conflict of interest statement None declared. Funding sources None.
References 1. Martin MA. Methicillin-resistant Staphylococcus aureus: the persistent resistant nosocomial pathogen. Curr Clin Top Infect Dis 1994;14:170e191. 2. Huang R, Mehta S, Weed D, Price CS. Methicillin-resistant Staphylococcus aureus survival on hospital fomites. Infect Control Hosp Epidemiol 2006;27:1267e1269. 3. Kramer A, Schwebke I, Kampf G. How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infect Dis 2006;6:130. 4. Lina G, Boutite F, Tristan A, Bes M, Etienne J, Vandenesch F. Bacterial competition for human nasal cavity colonization role of Staphylococcal agr alleles. Appl Environ Microbiol 2003;69:18e23. 5. Oliveira DC, deLencastre H. Multiplex PCR strategy for rapid identification of structural types and variants of the mec
Dear Madam, It is now seven years since the USA signed into law the Needle Stick Safety and Prevention Act which requires all healthcare facilities to purchase and provide needle protective devices (NPDs) in order to reduce the risk of needlestick injury (NSI). By comparison, both the UK and the rest of Europe have yet to adopt prescriptive legislation on NPDs. Although the UK’s Health Act requires that there must be the provision of medical devices that incorporate sharps protection, there is no associated guidance and therefore the Act is open to wide interpretation.1 Similarly the overall European perspective shows scant advance in securing a requirement for the introduction of NPDs. During 2006, a revision of the European Directive 2000/54/EC on the protection of workers from risks related to exposure to biological agents at work was requested.
195
who are not familiar with gastrointestinal infectious diseases in Japan. The mechanism of the worsening of CDAD by loperamide is considered to be that it causes bowel stasis, which may allow the proliferation of C. difficile and increase the absorption of clostridial toxins from the gut mucosa.8 It is also considered that the slowing of the faecal transit time results in extended toxin-associated damage. Based on these mechanisms, it is considered that loperamide would worsen the clinical course of CDAD. Restrictive antibiotics policies and infection control measures are known to prevent CDAD among hospitalised patients. However, once CDAD occurs, antimicrobials should be discontinued and appropriate treatment should be started. Although the sample size was small, this study suggested that the inappropriate and thoughtless use of loperamide worsens the clinical course of CDAD. Clinicians should recognise that its administration must be avoided in CDAD.
M. Nakamuraa A. Nakamurab R. Uedab a Department of Gastroenterology, Toyokawa City Hospital, Toyokawa, Japan b Department of Internal Oncology and Immunology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan c Department of Bacterial Pathogenesis and Infection Control, National Institute of Infectious Diseases, Tokyo, Japan E-mail address: [email protected] Available online 9 August 2008 * Corresponding author. Address: Department of Gastroenterology, Toyokawa City Hospital, Kohmei-cho 1-19, Toyokawa 4428561, Japan. Tel.: þ0533 86 1111; fax: þ0533 84 1327. ª 2008 The Hospital Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2008.06.010
Conflict of interest statement None declared.
Ointments as a source of meticillin-resistant Staphylococcus aureus spread
Funding sources None.
Madam,
References 1. Bartlett JG. Narrative review: the new epidemic of Clostridium difficile-associated enteric disease. Ann Intern Med 2006;145:758e764. 2. Kelly CP, Pothoulakis C, LaMont JT. Clostridium difficile colitis. N Engl J Med 1994;330:257e262. 3. Burke GW, Wilson ME, Mehrez IO. Absence of diarrhea in toxic megacolon complicating Clostridium difficile pseudomembranous colitis. Am J Gastroenterol 1988;83:304e307. 4. Reese RE, Betts RF. A practical approach to infectious diseases, 4th ed. Boston: Little, Brown & Co. p. 1087e89. 5. Fekety R. Guidelines for the diagnosis and management of Clostridium difficile-associated diarrhea and colitis. American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol 1997;92:739e750. 6. D’Agata EM. Methodologic issues of caseecontrol studies: a review of established and newly recognized limitations. Infect Control Hosp Epidemiol 2005;26:338e341. 7. Brown JW. Toxic megacolon associated with loperamide therapy. J Am Med Soc 1979;241:501e502. 8. Church JM, Fazio VW. A role for colonic stasis in the pathogenesis of disease related to Clostridium difficile. Dis Colon Rectum 1986;29:804e809.
H. Katoa,b,* H. Katoc Y. Iwashimab
The main reservoirs of meticillin-resistant Staphylococcus aureus (MRSA) are colonised and infected patients.1 However, contaminated surfaces may also play an important role.2,3 Transmission mostly occurs via the transiently contaminated hands of healthcare workers.1 The aim of our study was to investigate whether ointments used for MRSA-positive patients are a source of nosocomial MRSA spread in the University Hospital of Innsbruck. A total of 101 ointments from 19 MRSA-positive patients hospitalised at the University Hospital Innsbruck, Austria were collected in the period from July to December 2005 and screened for MRSA contamination. The 101 ointments were used for skin care and other medical indications (Table I). Each patient had his own set of ointments during hospitalisation. All ointments were stored in collapsible tubes and were applied with a single-use spatula according to our hospital guidelines. For MRSA screening, one swab of each ointment was taken from the interior of the screw cap and the same swab was used for the surface of the ointment. All swabs were plated on blood agar and investigated for MRSA and other pathogens according to standard procedures. Presence of the mecA
196 Table I
Letters to the Editor Ointments and their contaminations
Ointments
No. of ointments investigated
Bepanthen cream (dexpanthenol) Bactroban nasal ointment (mupirocin) Bactroban cream (mupirocin) Lasepton cream (protective cream without active substances) Oleovit eye ointment (dexpanthenol, retinolpalmitat) Spoendlin’sche nasal ointment (Bergamot oil, camphor, menthol) Ultrasicc/Ultrabas cream (for skin care without active substances) Scottopect gel (turpentine oil, eucalyptus oil, menthol, camphor) Candio-Hermal soft paste (nystatin) Vidisic eye gel (carbomer) Betaisadona wound gel (povidone-iodine) Vetren gel (heparin-sodium) Diclobene gel (diclofenac-sodium) Dynexan cream (tetracaine hydrochloride, chamomile, sage, arnica, aluminium formiate) Vaseline (white soft paraffin)
18 12 6 10
Microbial contamination
MRSA (N ¼ 3), Enterococcus sp. (N ¼ 1) MRSA (N ¼ 1), MRSE (N ¼ 3) Candida sp. (N ¼ 1)
9
MRSE (N ¼ 2), S. aureus (N ¼ 1)
9
MRSA (N ¼ 1), MRSE (N ¼ 2), Serratia sp. (N ¼ 1), Proteus sp. þ Enterococcus sp. (N ¼ 1)
7 7 6 5 4 4 2 1
MRSA (N ¼ 1), MRSE (N ¼ 2)
Bacillus sp. (N ¼ 1)
1
MRSA, meticillin-resistant Staphylococcus aureus; MRSE, meticillin-resistant Staphylococcus epidermidis.
gene and lukS/lukF gene (encoding for Panton-Valentine Leukocidin) were determined by polymerase chain reaction according to the manufacturer’s instructions (GenoType, Hain, Nehren, Germany). Determination of SCC-mec cassette and agr type was done as described previously.4,5 MRSA strains collected from patients and ointments were typed by automated ribotyping under the conditions recommended by the manufacturer of the Riboprinter microbial characterisation system (Qualicon Europe Ltd, Warwick, UK) using EcoRI as restriction enzyme. Of the 101 ointment specimens, collected from 19 MRSA-positive patients, 80 were culture negative, 21 (20.8%) were contaminated with various bacteria or Candida spp. (Table I). Six (5.9%) ointment specimens were found positive for MRSA: Bepanthen cream (N ¼ 3), Candio-Hermal soft paste (N ¼ 1), Spoendlin’sche nasal ointment (N ¼ 1) and even mupirocin cream (N ¼ 1) (Table I). The unopened ointments which were used as negative control for the MRSA screening were culture negative. The MRSA-positive ointment specimens were those from three patients (A, B and C); all were infected with MRSA before treated with ointments. In patient A, MRSA was isolated from the nasal cavity, the respiratory tract, the skin and decubitus ulcers; in patient B from the nasal cavity, the
respiratory tract, the percutaneous endoscopic gastrostomy (PEG) tube, decubitus ulcers and urine; and in patient C from the nasal cavity and an ulcer. Patient A had nine ointments in use, two of them contaminated with MRSA. One of the 10 ointments used by patient B was contaminated with MRSA, one with meticillin-resistant Staphylococcus epidermidis (MRSE), one with Serratia marcescens and one with Bacillus spp. Three of the six ointments used by patient C were contaminated with MRSA. MRSA from both patients’ body sites and the respective ointments showed the same resistance patterns: all were susceptible to tetracycline, trimethoprim, cotrimoxazole, vancomycin, rifampicin, fusidic acid and mupirocin. All MRSA harboured the mecA gene and lacked the lukS/lukF gene. All MRSA except for one patient isolate carried SCC-mec cassette IVa and agr type 1 (patient A; with SCC-mec cassette I and agr type 2). Molecular typing by automated ribotyping revealed four different ribotypes (RT 2, 3, 6, 12) in the patients and two (RT 2, 6) in ointment specimens. Ribotypes of MRSA from the ointments were identical to those from MRSA collected from the patients (patients A and B yielded RT 6; patient C, RT 2). The fact that 5.9% of ointments were contaminated with MRSA suggests that ointments could
Letters to the Editor constitute an additional and, until now, neglected reservoir for MRSA in the hospital. To our knowledge there are no other reports in the literature about the prevalence of MRSA in ointments. Interestingly, RT 6 is very rare in our RT database (0.8%) that consists of 366 MRSA specimens from our hospital and suggests that transmission occurred between patients and their ointments and not from the hospital environment. The ointments may contribute to recolonisation or reinfection of patients, suggesting that MRSA is transferred from the patient to the ointment and potentially vice versa. This hypothesis was previously set up by Gilani and coworkers for meticillin-susceptible S. aureus in the same matrix.6 The reason for our finding of MRSA-positive ointments is not yet clear. We can speculate that ointments were either not applied aseptically by the nurses or that patients applied the ointments by themselves and thus contaminated them. Ointments which are in repeated use on different patients could be a source of MRSA transmission between patients. Thus, there is a need for correct storage and aseptic portioning with single-use spatulae to reduce the risk of MRSA spread via ointments in hospital facilities.
Acknowledgments
197 element in methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother 2002;46:2155e2166. 6. Gilani SJK, Gonzalez M, Hussain I, Finlay AY, Patel GK. Staphylococcus aureus re-colonization in atopic dermatitis: beyond the skin. Clin Exp Dermatol 2005;30:10e13.
K. Grifa D. Ortha,* A. Mayra M.P. Diericha R. Wu ¨rznera C. Lass-Flo ¨rla E. Nogler-Semenitzb a Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University, Austria b Hospital Pharmacy, Innsbruck Medical University, Austria E-mail address: [email protected] Available online 23 August 2008 * Corresponding author. Address: Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University and Austrian Reference Laboratory for Enterohemorrhagic Escherichia coli, Scho ¨pfstr. 41, A-6020 Innsbruck, Austria. Tel.: þ43 512 9003 70772; fax: þ43 512 9003 73750.
ª 2008 The Hospital Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2008.06.011
We thank Pharmacia and Pfizer for their generous support of our MRSA studies. Needle protective devices; where are we now? Conflict of interest statement None declared. Funding sources None.
References 1. Martin MA. Methicillin-resistant Staphylococcus aureus: the persistent resistant nosocomial pathogen. Curr Clin Top Infect Dis 1994;14:170e191. 2. Huang R, Mehta S, Weed D, Price CS. Methicillin-resistant Staphylococcus aureus survival on hospital fomites. Infect Control Hosp Epidemiol 2006;27:1267e1269. 3. Kramer A, Schwebke I, Kampf G. How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infect Dis 2006;6:130. 4. Lina G, Boutite F, Tristan A, Bes M, Etienne J, Vandenesch F. Bacterial competition for human nasal cavity colonization role of Staphylococcal agr alleles. Appl Environ Microbiol 2003;69:18e23. 5. Oliveira DC, deLencastre H. Multiplex PCR strategy for rapid identification of structural types and variants of the mec
Dear Madam, It is now seven years since the USA signed into law the Needle Stick Safety and Prevention Act which requires all healthcare facilities to purchase and provide needle protective devices (NPDs) in order to reduce the risk of needlestick injury (NSI). By comparison, both the UK and the rest of Europe have yet to adopt prescriptive legislation on NPDs. Although the UK’s Health Act requires that there must be the provision of medical devices that incorporate sharps protection, there is no associated guidance and therefore the Act is open to wide interpretation.1 Similarly the overall European perspective shows scant advance in securing a requirement for the introduction of NPDs. During 2006, a revision of the European Directive 2000/54/EC on the protection of workers from risks related to exposure to biological agents at work was requested.