- Email: [email protected]
Investigation of a severe nosocomial outbreak of hepatitis A among healthcare workers and adult patients
70
Letters to the Editor / Journal of Hospital Infection 78 (2011) 65–78
this set showed clinically non-significant differences including the presence of an enterococcus (a single set) or a heavier growth of CoNS (three sets) on the wet swabs. Growth on the dry swabs compared to that on the wet swabs demonstrated no significant difference (c2-test: P ¼ 0.76). We conclude that the ‘wet’ swab technique improved the growth of skin flora but there was no significant difference in the detection rate of significant pathogens. The dry swab technique provides an adequate sampling method for skin pathogens. Conflict of interest statement None declared. Funding sources None. References 1. Weatherhead SC, Lawrence CM. Antibiotics for skin surgery. Pre-operative integrity of skin surface predicts infection risk. BMJ 2009;338:b516. 2. Noble WC, Somerville D. Microbiology of human skin. 2nd ed., vol. 2. London: Lloyd-Luke; 1981. p. 407.
A. Foulkesa,* M. Narayananb C.M. Lawrencea a Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, UK b
*
Department of Microbiology, Freeman Hospital, Newcastle upon Tyne, UK Corresponding author. Address: Department of Dermatology, First Floor, Doctors’ Residence, Royal Victoria Infirmary, Newcastle upon Tyne, NE3 1EF, UK. Tel.: þ44 1912829125; fax: þ44 1912824569. E-mail address: [email protected] (A. Foulkes) Accepted by S.J. Dancer Available online 28 January 2011
Ó 2011 The Healthcare Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2010.11.007
Investigation of a severe nosocomial outbreak of hepatitis A among healthcare workers and adult patients Madam, Hepatitis A virus (HAV) is a major cause of acute hepatitis worldwide. Infection is easily spread via the faecal–oral route, either
through person-to-person contact or by ingestion of contaminated food or water.1 Nosocomial HAV infection is uncommon. Several risk factors were reported to be associated with nosocomial HAV infection, including taking care of the index patient, poor hygiene practice and contact precautions, and exposure to faeces during periods of viral shedding.2 We report an outbreak of six cases of hepatitis A which occurred from January to March 2008 in a 26-bed neurology department of a 415-bed acute care hospital. We were informed that one nurse, two nurse assistants and one patient discharged from the neurology department were hospitalised for a symptomatic HAV infection. The medical staff was immediately warned about the importance of strictly conforming with basic hygienic principles, e.g. careful handling of stools and rigorous hand hygiene. The four cases had the following clinical symptoms: asthenia, anorexia, fever, but neither diarrhoea nor faecal incontinence. Their serum alanine aminotransferase was elevated at more than 100 times the normal value at the time of admission. The prothrombin time was <65% for all patients. The diagnosis of HAV infection was based on detection of IgM anti-HAV in serum. On 2 February, a new case of HAV infection was diagnosed in a hospital laundry worker. On 3 March, another HAV infection was diagnosed in a laboratory technician from the same hospital. The almost simultaneous occurrence of the first four cases, around 20 January, suggested that they had been infected at the same time and led us to search for a common exposure which was deemed to have occurred between 1 December and 5 January. No common food exposure was identified. We reviewed all records from patients hospitalised in the neurology department between 1 December and 5 January and investigated their liver enzymes to find the index case. Among these 87 patients, only one had increased serum aminotransferase: a 42-year-old homeless male patient, who had been admitted to the intensive care unit on 24 November for attempted suicide by drowning in the local river. On admission he had no symptoms of hepatitis and his liver enzymes were normal. He was transferred to the neurology department on 12 December. The patient had neither jaundice, diarrhoea nor vomiting but an increase of serum aminotransferase from 23 to 610 IU/L with a peak on 11 January. The hepatitis B and C tests ordered on 7 February were negative. The serum was stored at 20 C according to the local routine procedure. Serum samples obtained from the six outbreak cases were positive for HAV RNA detection. A single genotype IA strain was identified by phylogenetic analysis in all cases (Table I). For the suspected index case, HAV RNA amplification was negative in the sample collected on 24 November 2007 but positive on 7 February 2008. A genotype IA strain was identified that was 100% homologous to the outbreak strain. Avidity indices in all the samples obtained from the six acutely infected cases were <50%, suggesting a contamination having occurred less than one month before the testing, as we have previously reported.3 By contrast, the suspected index patient had an avidity index of 81% on 7 February, suggesting a contamination more than two months before, i.e. before 7 December.
Table I Origins of isolates collected during the hepatitis A virus (HAV) outbreak Successive case Nurse assistant Nurse Patient Nurse assistant 2 Laundry worker Technician Suspected index patient
Sex/age (years) F/31 F/39 F/55 F/38 F/37 F/52 M/41
Date of serum sampling 22 24 25 23 2 3 24 7
Jan 2008 Jan 2008 Jan 2008 Jan 2008 Feb 2008 Mar 2008 Nov 2007 Feb 2008
RT–PCR, reverse transcription–polymerase chain reaction; ND, not done.
HAV IgM
RT–PCR
Genotype
Avidity index
þ þ þ þ þ þ þ
þ þ þ þ þ þ ND þ
IA IA IA IA IA IA ND IA
47% 10% 43% 34% 25% 21% ND 81%
Onset of symptoms 16 16 16 20 1 23 12
Jan 2008 Jan 2008 Jan 2008 Jan 2008 Feb 2008 Feb 2008 Dec 2007
Letters to the Editor / Journal of Hospital Infection 78 (2011) 65–78
This outbreak of hepatitis A is a typical hospital outbreak: the index case was probably incubating upon admission, required high dependency care, and had an underlying condition that prevented the recognition of the infection.4,5 We suggest that the mechanism of transmission in the neurology department was a contact transmission, either direct or indirect, through contact with environment soiled by stools, followed by poor hand hygiene. Moreover, the infected discharged patient was the only patient of the neurology department who was able to get out of his bedroom, and was helped for feeding (i.e. to peel his fruit). Mbithi et al. established that HAV virus can persist on hands and inert environmental surfaces for several hours or weeks.6 The laundry worker and the laboratory technician are unlikely to have acquired hepatitis A from the index patient. They probably represent indirect transmission of hepatitis A. The laundry worker may have been contaminated through contact with contaminated linen without wearing gloves and without sufficient hand hygiene, as suggested by the literature.7 The laboratory technician may have been infected by handling blood samples of viraemic cases in contravention of standard precautions. In conclusion, phylogenetic analysis combined with avidity measurement contributed to the identification of an asymptomatic patient as the index case. In addition, this outbreak underlines the importance of standard hygiene precautions.
Acknowledgements Service de Médecine du Travail, et Service de Neurologie, Hopital d’Evreux. J.H.B. van de Bovenkamp, PhD, Clinical Molecular Biologist, Laboratory of Medical Microbiology, Stichting PAMM, Veldhoven, The Netherlands, for critical reading of the manuscript. Conflict of interest statement None declared. Funding sources None.
References 1. Ciocca M. Clinical course and consequences of hepatitis A infection. Vaccine 2000;18:S71–S74. 2. Park JY, Lee JB, Jeong SY, Lee SH, Lee MA, Choi HJ. Molecular characterization of an acute hepatitis A outbreak among healthcare workers at a Korean hospital. J Hosp Infect 2007;67:175–181. 3. Roque-Afonso AM, Grangeot-Keros Liliane, Roquebert B, et al. Diagnostic relevance of immunoglobulin G avidity for hepatitis A virus. J Clin Microbiol 2004; 42:5121–5124. 4. Centers for Disease Control. Outbreak of viral hepatitis in the staff of a pediatric ward – California. Morb Mortal Wkly Rep 1977;26:77–78. 5. Hanna J. Hospital acquired hepatitis A. Commun Dis Intell 1994;18:312–313. 6. Mbithi JN, Springthorpe VS, Boulet JR, Sattar SA. Survival of hepatitis A virus on human hands and its transfer on contact with animate and inanimate surfaces. J Clin Microbiol 1992;30:757–763. 7. Borg MA, Portelli A. Hospital laundry workers – an at-risk group for hepatitis A? Occup Med (Lond) 1999;49:448–450.
L. Gueta,* D. Desboisb A.M. Roque-Afonsoc J.M. Germainc V. Merled a CHI Eure Seine, Evreux, France b Centre National de Référence pour les Virus des Hépatites à Transmission Entérique, AP-HP, Hôpital Paul Brousse, Laboratoire de Virologie, Villejuif, France
c
71
Regional Coordinating Center for Nosocomial Infections Control, CCLIN Paris-Nord, France
d
Department of Epidemiology and Public Health, Rouen University Hospital, Rouen, France * Corresponding author. Address: CHI Eure Seine, rue Léon Schwartzenberg, 27015 Evreux CEDEX, France. Tel.: þ33 232338366; fax: þ33 232338213. E-mail address: [email protected] (L. Guet) Accepted by S.J. Dancer Available online 31 January 2011
Ó 2010 The Healthcare Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2010.11.010
Complicated infections with meticillin-resistant Staphylococcus aureus in Hong Kong Madam, The prevalence of meticillin-resistant Staphylococcus aureus (MRSA) in Hong Kong has increased to >50% in 2006, higher than that in the USA, UK, Australia and most of the European region (10–50%), and the mortality rate from MRSA bacteraemia has been found to be almost one-third.1,2 Complicated MRSA infections, including bacteraemia, endocarditis, osteomyelitis, meningitis and pneumonia, are associated with high mortality and treatment cost. The objective of this study was to evaluate the clinical and economic outcomes of complicated MRSA infections and to identify predictors of treatment failure and cost. A retrospective cohort study was conducted among adult patients hospitalised with complicated MRSA infections in a 1350-bed teaching hospital in Hong Kong, identified from microbiology reports and patient medical charts between January 2000 and December 2008. Complicated MRSA infections were defined as bacteraemia, endocarditis, osteomyelitis, meningitis and pneumonia caused by MRSA.3 Patients with culture labelled ‘contaminated’ in the culture report, who did not receive any antibiotic treatment or died <72 h after initiation of MRSA treatment were excluded from the analysis.4,5 Clinical ethics approval was obtained from The Chinese University of Hong Kong–New Territories East Cluster Clinical Ethics Committee. Patient demographics and clinical data were collected from the patient medical records. Outcome assessment included clinical response, mortality rate and total direct medical cost per patient. Treatment failure was defined as persistence or progression of MRSA infection, addition to or change of primary anti-MRSA treatment, surgical drainage of abscess, debridement, or infection-related death after 72 h of MRSA therapy. Death was defined as infectionrelated (IR) if the patient died with active infection at the time of death without other apparent alternative causes and/or MRSA infection was indicated as a cause of death on the death certificate.6 IR hospital cost was estimated from antimicrobial usage, hospitalisation, laboratory and diagnostic tests during the IR length of hospital stay (LOS). IR LOS was defined as the length of hospitalisation [including general medical wards and intensive care unit (ICU)] between time of first positive MRSA isolation in sterile-body site and end of infection-related antimicrobial therapy, discharge or death, whichever occurred first. The data were analysed by SPSS 16.0 (SPSS Inc., Chicago, IL, USA). All statistical tests were two-tailed and P < 0.05 was considered
Letters to the Editor / Journal of Hospital Infection 78 (2011) 65–78
this set showed clinically non-significant differences including the presence of an enterococcus (a single set) or a heavier growth of CoNS (three sets) on the wet swabs. Growth on the dry swabs compared to that on the wet swabs demonstrated no significant difference (c2-test: P ¼ 0.76). We conclude that the ‘wet’ swab technique improved the growth of skin flora but there was no significant difference in the detection rate of significant pathogens. The dry swab technique provides an adequate sampling method for skin pathogens. Conflict of interest statement None declared. Funding sources None. References 1. Weatherhead SC, Lawrence CM. Antibiotics for skin surgery. Pre-operative integrity of skin surface predicts infection risk. BMJ 2009;338:b516. 2. Noble WC, Somerville D. Microbiology of human skin. 2nd ed., vol. 2. London: Lloyd-Luke; 1981. p. 407.
A. Foulkesa,* M. Narayananb C.M. Lawrencea a Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, UK b
*
Department of Microbiology, Freeman Hospital, Newcastle upon Tyne, UK Corresponding author. Address: Department of Dermatology, First Floor, Doctors’ Residence, Royal Victoria Infirmary, Newcastle upon Tyne, NE3 1EF, UK. Tel.: þ44 1912829125; fax: þ44 1912824569. E-mail address: [email protected] (A. Foulkes) Accepted by S.J. Dancer Available online 28 January 2011
Ó 2011 The Healthcare Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2010.11.007
Investigation of a severe nosocomial outbreak of hepatitis A among healthcare workers and adult patients Madam, Hepatitis A virus (HAV) is a major cause of acute hepatitis worldwide. Infection is easily spread via the faecal–oral route, either
through person-to-person contact or by ingestion of contaminated food or water.1 Nosocomial HAV infection is uncommon. Several risk factors were reported to be associated with nosocomial HAV infection, including taking care of the index patient, poor hygiene practice and contact precautions, and exposure to faeces during periods of viral shedding.2 We report an outbreak of six cases of hepatitis A which occurred from January to March 2008 in a 26-bed neurology department of a 415-bed acute care hospital. We were informed that one nurse, two nurse assistants and one patient discharged from the neurology department were hospitalised for a symptomatic HAV infection. The medical staff was immediately warned about the importance of strictly conforming with basic hygienic principles, e.g. careful handling of stools and rigorous hand hygiene. The four cases had the following clinical symptoms: asthenia, anorexia, fever, but neither diarrhoea nor faecal incontinence. Their serum alanine aminotransferase was elevated at more than 100 times the normal value at the time of admission. The prothrombin time was <65% for all patients. The diagnosis of HAV infection was based on detection of IgM anti-HAV in serum. On 2 February, a new case of HAV infection was diagnosed in a hospital laundry worker. On 3 March, another HAV infection was diagnosed in a laboratory technician from the same hospital. The almost simultaneous occurrence of the first four cases, around 20 January, suggested that they had been infected at the same time and led us to search for a common exposure which was deemed to have occurred between 1 December and 5 January. No common food exposure was identified. We reviewed all records from patients hospitalised in the neurology department between 1 December and 5 January and investigated their liver enzymes to find the index case. Among these 87 patients, only one had increased serum aminotransferase: a 42-year-old homeless male patient, who had been admitted to the intensive care unit on 24 November for attempted suicide by drowning in the local river. On admission he had no symptoms of hepatitis and his liver enzymes were normal. He was transferred to the neurology department on 12 December. The patient had neither jaundice, diarrhoea nor vomiting but an increase of serum aminotransferase from 23 to 610 IU/L with a peak on 11 January. The hepatitis B and C tests ordered on 7 February were negative. The serum was stored at 20 C according to the local routine procedure. Serum samples obtained from the six outbreak cases were positive for HAV RNA detection. A single genotype IA strain was identified by phylogenetic analysis in all cases (Table I). For the suspected index case, HAV RNA amplification was negative in the sample collected on 24 November 2007 but positive on 7 February 2008. A genotype IA strain was identified that was 100% homologous to the outbreak strain. Avidity indices in all the samples obtained from the six acutely infected cases were <50%, suggesting a contamination having occurred less than one month before the testing, as we have previously reported.3 By contrast, the suspected index patient had an avidity index of 81% on 7 February, suggesting a contamination more than two months before, i.e. before 7 December.
Table I Origins of isolates collected during the hepatitis A virus (HAV) outbreak Successive case Nurse assistant Nurse Patient Nurse assistant 2 Laundry worker Technician Suspected index patient
Sex/age (years) F/31 F/39 F/55 F/38 F/37 F/52 M/41
Date of serum sampling 22 24 25 23 2 3 24 7
Jan 2008 Jan 2008 Jan 2008 Jan 2008 Feb 2008 Mar 2008 Nov 2007 Feb 2008
RT–PCR, reverse transcription–polymerase chain reaction; ND, not done.
HAV IgM
RT–PCR
Genotype
Avidity index
þ þ þ þ þ þ þ
þ þ þ þ þ þ ND þ
IA IA IA IA IA IA ND IA
47% 10% 43% 34% 25% 21% ND 81%
Onset of symptoms 16 16 16 20 1 23 12
Jan 2008 Jan 2008 Jan 2008 Jan 2008 Feb 2008 Feb 2008 Dec 2007
Letters to the Editor / Journal of Hospital Infection 78 (2011) 65–78
This outbreak of hepatitis A is a typical hospital outbreak: the index case was probably incubating upon admission, required high dependency care, and had an underlying condition that prevented the recognition of the infection.4,5 We suggest that the mechanism of transmission in the neurology department was a contact transmission, either direct or indirect, through contact with environment soiled by stools, followed by poor hand hygiene. Moreover, the infected discharged patient was the only patient of the neurology department who was able to get out of his bedroom, and was helped for feeding (i.e. to peel his fruit). Mbithi et al. established that HAV virus can persist on hands and inert environmental surfaces for several hours or weeks.6 The laundry worker and the laboratory technician are unlikely to have acquired hepatitis A from the index patient. They probably represent indirect transmission of hepatitis A. The laundry worker may have been contaminated through contact with contaminated linen without wearing gloves and without sufficient hand hygiene, as suggested by the literature.7 The laboratory technician may have been infected by handling blood samples of viraemic cases in contravention of standard precautions. In conclusion, phylogenetic analysis combined with avidity measurement contributed to the identification of an asymptomatic patient as the index case. In addition, this outbreak underlines the importance of standard hygiene precautions.
Acknowledgements Service de Médecine du Travail, et Service de Neurologie, Hopital d’Evreux. J.H.B. van de Bovenkamp, PhD, Clinical Molecular Biologist, Laboratory of Medical Microbiology, Stichting PAMM, Veldhoven, The Netherlands, for critical reading of the manuscript. Conflict of interest statement None declared. Funding sources None.
References 1. Ciocca M. Clinical course and consequences of hepatitis A infection. Vaccine 2000;18:S71–S74. 2. Park JY, Lee JB, Jeong SY, Lee SH, Lee MA, Choi HJ. Molecular characterization of an acute hepatitis A outbreak among healthcare workers at a Korean hospital. J Hosp Infect 2007;67:175–181. 3. Roque-Afonso AM, Grangeot-Keros Liliane, Roquebert B, et al. Diagnostic relevance of immunoglobulin G avidity for hepatitis A virus. J Clin Microbiol 2004; 42:5121–5124. 4. Centers for Disease Control. Outbreak of viral hepatitis in the staff of a pediatric ward – California. Morb Mortal Wkly Rep 1977;26:77–78. 5. Hanna J. Hospital acquired hepatitis A. Commun Dis Intell 1994;18:312–313. 6. Mbithi JN, Springthorpe VS, Boulet JR, Sattar SA. Survival of hepatitis A virus on human hands and its transfer on contact with animate and inanimate surfaces. J Clin Microbiol 1992;30:757–763. 7. Borg MA, Portelli A. Hospital laundry workers – an at-risk group for hepatitis A? Occup Med (Lond) 1999;49:448–450.
L. Gueta,* D. Desboisb A.M. Roque-Afonsoc J.M. Germainc V. Merled a CHI Eure Seine, Evreux, France b Centre National de Référence pour les Virus des Hépatites à Transmission Entérique, AP-HP, Hôpital Paul Brousse, Laboratoire de Virologie, Villejuif, France
c
71
Regional Coordinating Center for Nosocomial Infections Control, CCLIN Paris-Nord, France
d
Department of Epidemiology and Public Health, Rouen University Hospital, Rouen, France * Corresponding author. Address: CHI Eure Seine, rue Léon Schwartzenberg, 27015 Evreux CEDEX, France. Tel.: þ33 232338366; fax: þ33 232338213. E-mail address: [email protected] (L. Guet) Accepted by S.J. Dancer Available online 31 January 2011
Ó 2010 The Healthcare Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jhin.2010.11.010
Complicated infections with meticillin-resistant Staphylococcus aureus in Hong Kong Madam, The prevalence of meticillin-resistant Staphylococcus aureus (MRSA) in Hong Kong has increased to >50% in 2006, higher than that in the USA, UK, Australia and most of the European region (10–50%), and the mortality rate from MRSA bacteraemia has been found to be almost one-third.1,2 Complicated MRSA infections, including bacteraemia, endocarditis, osteomyelitis, meningitis and pneumonia, are associated with high mortality and treatment cost. The objective of this study was to evaluate the clinical and economic outcomes of complicated MRSA infections and to identify predictors of treatment failure and cost. A retrospective cohort study was conducted among adult patients hospitalised with complicated MRSA infections in a 1350-bed teaching hospital in Hong Kong, identified from microbiology reports and patient medical charts between January 2000 and December 2008. Complicated MRSA infections were defined as bacteraemia, endocarditis, osteomyelitis, meningitis and pneumonia caused by MRSA.3 Patients with culture labelled ‘contaminated’ in the culture report, who did not receive any antibiotic treatment or died <72 h after initiation of MRSA treatment were excluded from the analysis.4,5 Clinical ethics approval was obtained from The Chinese University of Hong Kong–New Territories East Cluster Clinical Ethics Committee. Patient demographics and clinical data were collected from the patient medical records. Outcome assessment included clinical response, mortality rate and total direct medical cost per patient. Treatment failure was defined as persistence or progression of MRSA infection, addition to or change of primary anti-MRSA treatment, surgical drainage of abscess, debridement, or infection-related death after 72 h of MRSA therapy. Death was defined as infectionrelated (IR) if the patient died with active infection at the time of death without other apparent alternative causes and/or MRSA infection was indicated as a cause of death on the death certificate.6 IR hospital cost was estimated from antimicrobial usage, hospitalisation, laboratory and diagnostic tests during the IR length of hospital stay (LOS). IR LOS was defined as the length of hospitalisation [including general medical wards and intensive care unit (ICU)] between time of first positive MRSA isolation in sterile-body site and end of infection-related antimicrobial therapy, discharge or death, whichever occurred first. The data were analysed by SPSS 16.0 (SPSS Inc., Chicago, IL, USA). All statistical tests were two-tailed and P < 0.05 was considered