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Annual report WHO Western Pacific Region Gonococcal Surveillance, 2004 multi-resistant due to the aggregation of different resistance mechanisms. 9 These strains have now spread beyond the WHO WPR. 10,11 Over-reliance on antibiotic treatment as a principal mechanism of gonococcal disease control in the absence of other important measures to decrease disease rates has undoubtedly contributed to the problem of antimicrobial resistance in N. gonorrhoeae. 12 The combination of high gonococcal disease rates and general problems of antibiotic resistance in the WHO WPR will continue without concerted efforts that simultaneously address the linked, but separate, issues of control of sexually transmitted diseases and containment of antimicrobial resistance. 8,12 Surveillance of antimicrobial resistance is an essential component of local, regional and international efforts for control of gonorrhoeae. Acknowledgements Members of the WHO Western Pacific Gonococcal Antimicrobial Surveillance Programme in 2004 are: JW Tapsall and EA Limnios, Australia; Haji Mahani Haj Abu Bakar, Brunei Darussalam; Yin Yue Ping and Su Xiaohong, China; EM Buadromo and S Singh, Fiji: KM Kam and J Lo, Hong Kong; Yuko Watanabe and Masatoshi Tanaka, Japan; K Lee and Y Chong, South Korea; T Phouthavane, Lao PDR; R Goursaud, New Caledonia; M Brokenshire, New Zealand; C Manesikia, Papua New Guinea; CC Carlos, Philippines; Cecilia Ngan, Singapore, M Fakahau, Tonga, Le Thi Phuong, Hanoi, Viet Nam. References 1. World Health Organization Western Pacifi c Region Gonococcal Surveillance Programme. Surveillance of antibiotic susceptibility of Neisseria gonorrhoeae in the WHO Western Pacifi c Region 1992–4. Genitourin Med 1997;73:355–361. 2. WHO Western Pacifi c Gonococcal Antimicrobial Sur veillance Programme. Surveillance of antibiotic resist ance in Neisseria gonorrhoeae in the WHO West ern Pacifi c Region, 2003. Commun Dis Intell 2005;29:62–64. 3. Boslego JW, Tramont EC, Takafuji ET, Diniega BM, Mitchell BS, Small JW, et al. Effect of spectinomycin use on the prevalence of spectinomycin-resistant and of penicillinase-producing Neisseria gonorrhoeae. N Eng J Med 1987;317:272–278. 4. Ito M, Deguchi T, Mizutani KS, Yasuda M, Yokoi S, Ito S, et al. Emergence and spread of Neisseria gonorrhoeae clinical isolates harbouring mosaic-like structure of penicillin-binding protein 2 in Japan. Antimicrob Agent Chemother 2005;49:137–143. 5. Tapsall JW. Antimicrobial resistance in Neisseria gonorrhoeae. WHO/CDS/CSR/DRS/2001.3. World Health Organization, Geneva, Switzerland, 2001. Available from: http://www.who.int/entity/drugresistance/ Antimicrobial_resistance_in_Neisseria_gonorrhoeae.pdf 6. Management of sexually transmitted diseases. World Health Organization 1997; Document WHO/GPA/ TEM94.1 Rev.1 p 37. 7. Shultz TR, Tapsall JW, White PA. Correlation of in vitro susceptibilities to newer quinolones of naturally occurring quinolone-resistant Neisseria gonorrhoeae strains with changes in GyrA and ParC. Antimicrob Agent Chemother 2001;45:734–738. 8. Simonsen GS, Tapsall JW, Allegranzi B, Talbot EA, Lazzari S. The ARCS Approach – A Public Health Tool for antimicrobial resistance containment and surveillance. Bull World Health Org 2004;82:928–934 9. Tanaka M, Nakayama H, Huruya K, Konomi I, Irie S, Kanayama A, et al. Analysis of mutations within mul tiple genes associated with resistance in a clinical isolate of Neisseria gonorrhoeae with reduced ceftriaxone that shows a multidrug-resistant phenotype. Int J Antimicrob Agent 2006;27:20–26. 10. Wang SA, Lee MAC, O’Connor N, Iverson CJ, Ohye RG, Whiticar PM, et al. Multi-Resistant Neisseria gonorrhoeae with decreased susceptibility to cefixime— Hawaii, 2001. Clin Infect Dis 2003;37:849–852. 11. Hoffmann SH, Lambertsen L, Berthelsen L, Cowan S. Neisseria gonorrhoeae with increasing cetriaxon MIC in Denmark in 2004: serotyping, bi-locus sequence typing and sexual preference. In: Proceedings of the 16 th Biennial Meeting of the International Society for STD Research, Amsterdam, 2005: Abstract WP-035. 12. Tapsall JW. What management is there for gonorrhea in the post-quinolone era? Sex Transm Dis 2006;33:8–10. 132 CDI Vol 30 No 1 2006
Australian Rotavirus Surveillance Program, 2004-05 Annual report National Rotavirus Surveillance Program annual report, 2004-05 Carl D Kirkwood, 1 Nada Bogdanovic-Sakran, 2 David Cannan, 3 Ruth F Bishop, 4 Graeme L Barnes 5 Abstract The National Rotavirus Reference Centre together with collaborating laboratories Australia-wide has conducted rotavirus surveillance since June 1999. This report describes the serotypes of rotavirus strains responsible for the hospitalisation of children with acute gastroenteritis during the period 1 July 2004 to 30 June 2005. Six hundred and twelve faecal samples from across Australia were examined using monoclonal antibody immunoassays, reverse transcription-polymerase chain reaction and polyacrylamide gel analysis. Serotype G1 was the dominant serotype nationally, representing 48.3 per cent of all strains, followed by serotype G3 (36.7%) and serotype G9 (6.9%). As in previous years, there was substantial geographic variation in the prevalence of rotavirus serotypes. Commun Dis Intell 2006;30:133–136. Keywords: rotavirus, annual report, disease surveillance Introduction Group A rotaviruses are the single most important cause of severe gastroenteritis in young children worldwide. An estimated 500,000 children die annually of severe diarrhoea, however, few of these deaths occur in developed countries. 1 Rotavirus induced disease accounts for up to 50 per cent of childhood hospitalisations for diarrhoea, with 10,000 Australian children hospitalised each year, 2 costing an estimated $26 million in direct costs. There is wide acceptance of the need for a vaccine to prevent rotavirus disease in children under 5 years of age throughout the world, as a component of the United Nations Millennium Development Goal 4 (‘Reduce childhood mortality’). The fi rst oral rotavirus vaccine was shown to be highly effi cacious for the prevention of severe diarrhoea and hospitalisation due to rotavirus infection. A major setback was an apparent association with intussusception, a form of bowel obstruction in infants, which forced a withdrawal of the vaccine 9 months after introduction. 3 Two new rotavirus vaccines (Rotarix®, GlaxoSmithKline; and Rotateq®, Merck) have been developed, and are nearing licensure in many countries. National rotavirus surveillance is an important component in decisions about rotavirus vaccine implementation. The previous rotavirus surveillance report from the National Rotavirus Surveillance Program, covering the period 1 July 2003 to 30 June 2004, documented the re-emergence of serotype G1 as the major serotype in Australia. 4 Prior to this, serotype G9 had been dominant in 2002/03, representing 74.7 per cent of samples nationally at that time. 5 The surveillance and characterisation of rotavirus strains causing annual epidemics of severe diarrhoea in young children in Australia continues to be undertaken by the National Rotavirus Reference Centre in Melbourne, together with eight collaborating centres. In this report we describe the results for the period 1 July 2004 to 30 June 2005, and identify the geographic distribution of the predominant rotavirus serotypes. Methods Rotavirus positive specimens detected by enzyme immunoassay (EIA) or latex agglutination in collaborating laboratories were collected, stored frozen and forwarded to Melbourne, together with relevant age and sex details of patients. Specimens were then serotyped using an in-house monoclonal antibody (MAb) based serotyping EIA. The EIA employed a 1. Senior Research Fellow, Murdoch Children’s Research Institute, Parkville, Victoria 2. Research Assistant, Murdoch Children’s Research Institute, Parkville, Victoria 3. Research Assistant, Murdoch Children’s Research Institute, Parkville, Victoria 4. Senior Principal Research Fellow, Murdoch Children’s Research Institute, Parkville, Victoria 5. Senior Principal Research Fellow, Murdoch Children’s Research Institute, Parkville, Victoria Corresponding author: Dr Carl Kirkwood, Enteric Virus Research Group, Murdoch Childrens Research Institute, Royal Children’s Hospital, Flemington Road, Parkville, VIC 3052. Telephone: +61 3 9345 5970. Facsimile: +61 3 9345 6240. Email: carl.kirkwood@mcri.edu.au CDI Vol 30 No 1 2006 133
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