Coombs

Geoffrey W. Coombs

Gillet

Huijsdens

James O. Robinson

Julie C. Pearson

Keryn J. Christiansen

L’Heriteau

Miller

Moran

O’Brien

Pearman

Ronan J. Murray

Sabrina A. Pozzi Langhi

Urth

Emerging Infectious Diseases

English

PubMed

Directory of Open Access Journals

Intrafamilial Transmission of Methicillin-Resistant Staphylococcus aureus

Crossref

Intrafamilial Transmission of Methicillin-Resistant
                    Staphylococcus aureus

Pozzi Langhi, S.A.

Robinson, J.O.

Pearson, J.C.

Christiansen, K.J.

Coombs, G.W.

Murray, R.J.

Research Repository

LETTERSDuring a pandemic, when supplies are unavailable, the balance of benefit to harm would favor using the expired product. The 1918 influenza pandemic is estimated to have killed 50 million persons worldwide (10), many in de-veloping countries. By better safe-guarding available drug stockpiles, more drugs could be made available to poorer countries that have few drugs stockpiled. Alain Li Wan Po, Peter Farndon, and Nick PalmerAuthor affiliations: National Genetics Educa-tion and Development Centre, Birmingham, UK (A. Li Wan Po, P. Farndon); and House of Parliament, London, UK (N. Palmer).DOI: 10.3201/eid1510.090844References  1.  Jack A. Roche steps up production of Tamiflu. The Times; 2009 May 12 [cited 2009 May 29]. Available from http://www.ft.com/cms/s/0/f7ca6e42-3f1d-11-de-ae4f-00144feabdc0.html  2.  Department of Health UK. Pandemic flu drug stockpiles are set to double [cited 2009 Jul 29]. Available from http://www.medicalnewstoday.com/articles/137256.php  3.  Mroso PV, Li Wan Po A, Irwin WJ. Sol-id-state stability of aspirin in the pres-ence of excipients: kinetic interpreta-tion, modeling, and prediction. J Pharm Sci. 1982;71:1096–101. DOI: 10.1002/jps.2600711004  4.  Li Wan Po A. Too much, too little, or none at all: dealing with substandard and fake drugs. Lancet. 2001;357:1904. DOI: 10.1016/S0140-6736(00)05092-3   5.  European Medicines Agency. European Medicines Agency recommendations on extension of shelf life for Tamiflu. 2009 May 8 [cited 2009 Jul 29]. Available from http://www.emea.europa.eu/humandocs/PDFs/EPAR/tamiflu/28497109en.pdf  6.  Li W, Escarpe PA, Eisenberg EJ, Cundy KC, Sweet C, Jakeman KJ, et al. Iden-tification of GS 4104 as an orally bio-available prodrug of the influenza virus neuraminidase inhibitor GS 4071. Antimi-crob Agents Chemother. 1998;42:647–53.  7.  He G, Massarella J, Ward P. Clinical phar-macokinetics of the prodrug oseltamivir and its active metabolite Ro 64-0802. Clin Pharmacokinet. 1999;37:471–84. DOI: 10.2165/00003088-199937060-00003   8.  Brewster M, Smith JR, Dutkowski R, Robson R. Active metabolite from Tami-flu solution is bioequivalent to that from capsule delivery in healthy volunteers: a cross-over, randomised, open-label study. Vaccine. 2006;24:6660–3. DOI: 10.1016/j.vaccine.2006.05.080   9.  Radonovich LJ, Magalian PD, Hol-lingsworth MK, Baracco G. Stockpil-ing supplies for the next influenza pan-demic. Emerg Infect Dis [serial on the internet]. 2009 Jun [cited 2009 Jul 29]. Available from http://www.cdc.gov/EID/content/15/6/e1.htm10.  Taubenberger JK, Morens DM. 1918 influ-enza: the mother of all pandemics. Emerg Infect Dis. 2006;12:15–22.Address for correspondence: Alain Li Wan Po, National Genetics Education and Development Centre – Pharmacogenetics, Morris House, Birmingham Women’s Hospital, Birmingham B15 2TG, UK; email: a.liwanpo@talk21.comIntrafamilial  Transmission of  Methicillin-Resistant Staphylococcus  aureus1To the Editor: Community-ac-quired methicillin-resistant Staphylo-coccus aureus (CA-MRSA) infection was first described in our region over 15 years ago (1). More recently, CA-MRSA has become a global concern and is now a common cause of skin and soft tissue infections in the Unit-ed States (2). An association between severe CA-MRSA infection (e.g., necrotizing fasciitis and pneumonia) and the synergohymenotrophic exo-toxin Panton-Valentine leukocidin (PVL) has been made (3,4). Reports have documented CA-MRSA trans-mission among household members; however, most cases have been mild or moderate infections or asymptom-atic colonization (5–7). We describe intrafamilial transmission of a PVL-containing CA-MRSA clone com-mon in Australia (ST30-MRSA-IV) between a nurse who experienced recurrent abscesses and her husband, who died of severe pneumonia.  In July 2006, a 61-year-old pre-viously healthy nurse (Mrs A) sought treatment for an infected seborrheic cyst of the scalp. Culture of pus yield-ed MRSA that was susceptible to clin-damycin. She was treated with oral clindamycin. After resolution of the infection, topical MRSA decoloniza-tion therapy with 3% hexachlorophane body wash (daily), 20% cetrimide shampoo (3×/wk), and 2% mupirocin nasal ointment (3×/d) was adminis-tered for 10 days, as per our institu-tional protocol for MRSA-colonized healthcare workers. Subsequently, MRSA surveillance swabs from the nose, throat, and scalp obtained week-ly for 10 weeks and cultured on selec-tive MRSA chromogenic agar and in selective broth enrichment media were negative. Household members were not screened for MRSA colonization.Six months later, in January 2007, the patient’s husband (Mr A), a 60-year-old smoker who was her only household contact, was admitted with a 1-day history of dyspnea, pleuritic chest pain, cough with sputum, fever, vomiting, and diarrhea. On admission, he was unwell, with tachycardia (pulse rate 132 bpm), hypotension (95/60 mm Hg), tachypnea (40 breaths/min), and hypoxia (oxygen saturation 93% on 15 L O2/min). A chest radiograph showed bilateral infiltrates and a right pleural effusion. He was diagnosed with community-acquired pneumonia and treated with intravenous ceftri-axone and azithromycin as per local protocol. However, within 12 hours, his condition deteriorated, necessitat-ing admission to the intensive care unit for ventilation and inotropic support.  Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 15, No. 10, October 2009 1687 1Results presented in part at the Australasian Society for Infectious Diseases Annual Scientific Meeting, Sunshine Coast, Queensland, Australia, 2008 April 2–5. LETTERSBroncho-alveolar lavage (BAL) fluid demonstrated gram-positive cocci in tetrads, and intravenous vancomycin and dicloxacillin were added to thera-py. Despite aggressive supportive mea-sures, Mr A’s condition continued to deteriorate, and he died 28 hours after admission. MRSA was subsequently cultured from blood, sputum, and BAL fluid; an autopsy was not performed. In June 2007, Mrs A sought treat-ment for an abscess with cellulitis on the left thigh. The abscess was sur-gically drained, and cultures again yielded MRSA. She was treated with intravenous and oral clindamycin for 10 days and subsequently underwent repeat MRSA decolonization therapy; again, swabs taken 1×/wk for 10 weeks postdecolonization were negative. Molecular typing of the MRSA isolates obtained from Mrs A at the time of her initial skin infection, Mr A’s blood culture, and Mrs A’s second skin infection was performed by using contour-clamped homogenous electric field electrophoresis (CHEF) accord-ing to a previously described method (8) (Figure). The CHEF patterns were indistinguishable and were identical to the known CHEF pattern for ST30-MRSA-IV (9). All 3 isolates contained the lukF-PV/lukS-PV genes that en-code PVL and had the same antibio-gram (i.e., isolates were resistant only to β-lactam antimicrobial agents). We describe intrafamilial MRSA transmission (defined as >2 family members who live at the same postal address and who are colonized or in-fected with a MRSA strain having the same CHEF pattern) that resulted in a fatal outcome. The MRSA strain re-sponsible (ST30-MRSA-IV, or West-ern Samoan phage pattern/Oceania strain MRSA) is a common cause of CA-MRSA infection in Australia. Recurrent MRSA infection de-veloped in Mrs A several months after completion of apparently successful MRSA decolonization therapy. We could not determine whether this re-currence was because of persistent MRSA colonization not detected by surveillance (e.g., perineal or gastroin-testinal colonization) or whether Mrs A was successfully decolonized but Mr A’s colonization/infection resulted in recolonization and subsequent in-fection. Whatever the explanation, this case highlights a potential weak-ness in MRSA surveillance programs that rely on short-term, limited-site surveillance.  A comprehensive MRSA search-and-destroy policy in place for over 25 years has prevented MRSA from becoming endemic in our institution (10). However, the rapidly changing epidemiology of MRSA in becoming a predominantly community pathogen represents a significant challenge to the ongoing success of this policy. In response to this challenge, the West-ern Australian Department of Health has implemented a community-based MRSA search-and-destroy program for patients with MRSA infection caused by exotic PVL-positive clones (e.g., ST30-MRSA-IV, ST93-MRSA-IV, ST80-MRSA-IV, and ST8-MRSA-IV/USA300). This program includes treatment/decolonization therapy for the index case, screening of household members for MRSA infection/coloni-zation, and simultaneous treatment/de-colonization if MRSA is identified. Al-though a similar approach has proved successful in Denmark (6), whether this success can be sustainable on a larger scale remains to be seen.  Acknowledgment We thank our patient for allowing us to discuss her case in this report. This research was supported by the Department of Microbiology and Infec-tious Diseases, Royal Perth Hospital, Perth, Western Australia, Australia. Sabrina A. Pozzi Langhi, James O. Robinson,  Julie C. Pearson,  Keryn J. Christiansen,  Geoffrey W. Coombs,  and Ronan J. Murray 1688 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 15, No. 10, October 20091 2 3 4 5 6 7 8 9Figure. Contour-clamped homogenous electric field electrophoresis of Staphylococcus aureus isolates. Lanes 2, 3, and 4 (Sma1 restriction): methicillin-resistant S. aureus (MRSA) isolated from Mrs A’s first infection, Mr A’s blood culture, and Mrs A’s second infection, respectively. Lanes 6, 7, and 8 (Apa1 restriction): MRSA isolated from Mrs A’s first infection, Mr A’s blood culture, and Mrs A’s second infection, respectively. Lanes 1, 5, and 9: S. aureus NCTC8325. LETTERSAuthor affiliations: Royal Perth Hospital, Perth, Western Australia, Australia (L.S. Pozzi, J.O. Robinson, J.C. Pearson, K.J. Christiansen, G.W. Coombs, R.J. Murray); and Curtin University of Technology, Perth (K.J. Christiansen, G.W. Coombs). DOI: 10.3201/eid1510.081532References   1.  Udo EE, Pearman JW, Grubb WB. Ge-netic analysis of community isolates of methicillin-resistant Staphylococcus au-reus in Western Australia. J Hosp Infect. 1993;25:97–108. DOI: 10.1016/0195-6701(93)90100-E  2.  Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, et al. EMERGEncy ID Net Study Group. Methicillin-resistant S. aureus infections among patients in the emergency depart-ment. N Engl J Med. 2006;355:666–74. DOI: 10.1056/NEJMoa055356  3.  Gillet Y, Issartel B, Vanhems P, Fournet JC, Lina G, Bes M, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leu-kocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet. 2002;359:753–9. DOI: 10.1016/S0140-6736(02)07877-7  4.  Miller LG, Perdreau-Remington F, Rieg G, Mehdi S, Perlroth J, Bayer AS, et al. Necrotizing fasciitis caused by communi-ty-associated methicillin-resistant Staphy-lococcus aureus in Los Angeles. N Engl J Med. 2005;352:1445–53. DOI: 10.1056/NEJMoa042683  5.  L’Heriteau F, Lucet JC, Scanvic A, Bouvet E. Community-acquired methicillin-resis-tant Staphylococcus aureus and familial transmission. JAMA. 1999;282:1038–9. DOI: 10.1001/jama.282.11.1038  6.  Urth T, Juul G, Skov R, Schonheyder HC. Spread of a methicillin-resistant Staphylo-coccus aureus ST80-IV clone in a Danish community. Infect Control Hosp Epidemi-ol. 2005;26:144–9. DOI: 10.1086/502518  7.  Huijsdens XW, van Santen-Verheuvel MG, Spalburg E, Heck ME, Pluister GN, Eijkelkamp BA, et al. Multiple cases of fa-milial transmission of community-acquired methicillin-resistant Staphylococcus au-reus. J Clin Microbiol. 2006;44:2994–6. DOI: 10.1128/JCM.00846-06  8.  O’Brien FG, Udo EE, Grubb WB. Con-tour-clamped homogeneous electric field electrophoresis of Staphylococcus aureus. Nat Protocols. 2006;1:3028–33. DOI: 10.1038/nprot.2006.382  9.  Coombs GW, Pearson JC, O’Brien FG, Murray RJ, Grubb WB, Christiansen KJ. Methicillin-resistant Staphylococcus au-reus clones, Western Australia. Emerg In-fect Dis. 2006;12:241–7.10.  Pearman JW, Christiansen KJ, Annear DI, Goodwin CS, Metcalf C, Donovan FP, et al. Control of methicillin-resistant Staphy-lococcus aureus (MRSA) in an Australian metropolitan teaching hospital complex. Med J Aust. 1985;142:103–8.Address for correspondence: James O. Robinson, Department of Microbiology and Infectious Diseases, PathWest Laboratory Medicine, Royal Perth Hospital, Wellington Street, Perth 6000, Western Australia, Australia; email: owen.robinson@health.wa.gov.au Rhombencephalitis and Coxsackievirus A16 To the Editor: Hand, foot, and mouth disease (HFMD) is a com-mon illness in children and is mainly caused by coxsackievirus A16 (CA16) and enterovirus 71 (EV71). Although its clinical course is usually unevent-ful and most patients experience a full recovery, serious neurologic compli-cations, including encephalitis, can occur secondarily to HFMD caused by EV71. Such neurological compli-cations occurred during an epidemic in Taiwan in 1998 (1). Encephalitis caused by EV71 is characterized by rhombencephalitis, which is a com-bination of brainstem encephalitis and cerebellitis. Signs and symptoms of rhombencephalitis are irritability, myoclonus, ataxia, and cranial nerve involvement (1). In contrast to EV71, HFMD caused by CA16 is associated with few neurologic complications with the exception of infrequent asep-tic meningitis (2). We report a case of rhombencephalitis that developed in an infant as a complication of HFMD caused by CA16.HFMD was diagnosed in a 23-month-old girl on the basis of high fever (>40°C, 3 d duration), stomati-tis, and multiple papules on her palms, soles, and buttocks. Her illness oc-curred in the summer of 2007, when sentinel surveillance in the region in-dicated an epidemic of HFMD caused by both CA16 and EV71. She was admitted to our hospital in Fukoka, Ja-pan, on day 4 of illness because of ab-normal eye movement, irritability, and inability to stand. She had intermittent to-and-fro, horizontal oscillations of the eyes (ocular flutter). She also had truncal and limb ataxia and myoclonus in her head and limbs. Brain magnetic resonance imaging (MRI) showed T1-low and T2-high bulbopontine and cerebellar lesions around the fourth ventricle (Figure). Peripheral blood showed a mild leukocytosis (13.13 × 109/L) and a C-reactive protein level within reference range (0.9 mg/L). Blood chemistry results were unre-markable. Cerebrospinal fluid (CSF) examination showed mononuclear pleocytosis (74/µL) with normal pro-tein and glucose levels. CA16 was isolated from her stool specimen on day 4 of illness. Based on reverse transcription–PCR, CSF was negative for enterovirus RNA. Without specific treatment, our patient’s fever resolved on day 5 of illness. The myoclonus, ocular flutter, and irritability subsided by day 16, when MRI findings returned to nor-mal. Ataxia disappeared gradually ≈1 month after onset, and no neurologic sequelae occurred. Neutralizing anti-body titers against CA16 and EV71 on day 21 of illness were 32 and <8, respectively. Based on the sequence analysis of the partial VP1 region (876 bp), we classified the patient’s CA16 strain phylogenetically as ge-netic lineage C (3). This lineage was identical to lineage 2 (4), which be-came the dominant circulating strain in Asia, including Japan, after the late 1990s (98.2% identical to the 1018T/VNM/05 strain isolated in Vietnam  Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 15, No. 10, October 2009 1689 

Intrafamilial transmission of methicillin-resistant Staphylococcus aureus

Pozzi Langhi, S.

Robinson, James

Pearson, J.

Christiansen, K.

Coombs, Geoffrey

Murray, R.

espace@Curtin

Address for correspondence: James O.

aureus infections among patients in the emergency department.

Genetic analysis of community isolates of methicillin-resistant Staphylococcus aureus in Western Australia.

Methicillin-resistant Staphylococcus aureus clones, Western Australia. Emerg Infect Dis.

Spread of a methicillin-resistant Staphylococcus aureus ST80-IV clone in a Danish community. Infect Control Hosp Epidemiol.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2866382

Intrafamilial Transmission of Methicillin-Resistant Staphylococcus aureus1

Intrafamilial Transmission of Methicillin-Resistant Staphylococcus aureus1

Abstract

Similar works

Full text

Available Versions

Directory of Open Access Journals

Crossref

Research Repository

espace@Curtin