DISPATCHESBecause international travel can contribute to the spreadof multidrug-resistant pathogens, enhanced surveillanceis necessary to control the dissemination of antimicrobialdrug resistance. Improved hygiene, infection control plans,and better education for travelers are also required.This work was supported by a grant from the Korea Centers forDisease Control and Prevention [4847-311-210].Dr Jin Seok Kim is a researcher at Center for Infectious Diseasein the Korea National Institute of Health. His primary researchinterests include antimicrobial drug susceptibility and molecularepidemiology of enteric bacteria.References1. Kotloff KL, Winickoff JP, Ivanoff B, Clemens JD, Swerdlow DL,Sansonetti PJ, et al. Global burden of Shigella infections:implications for vaccine development and implementation ofcontrol strategies. Bull World Health Organ. 1999;77:651–66.2. Boveé L, Whelan J, Sonder GJ, van Dam AP, van den Hoek A.Risk factors for secondary transmission of Shigella infection withinhouseholds: implications for current prevention policy. BMC InfectDis. 2012;12:347. http://dx.doi.org/10.1186/1471-2334-12-3473. Gupta A, Polyak CS, Bishop RD, Sobel J, Mintz ED. Laboratoryconfirmedshigellosis in the United States, 1989–2002:epidemiologic trends and patterns. Clin Infect Dis. 2004;38:1372–7. http://dx.doi.org/10.1086/3863264. Vinh H, Nhu NT, Nga TV, Duy PT, Campbell JI, Hoang NV, et al.A changing picture of shigellosis in southern Vietnam: shiftingspecies dominance, antimicrobial susceptibility and clinicalpresentation. BMC Infect Dis. 2009;9:204. http://dx.doi.org/10.1186/1471-2334-9-2045. Clinical and Laboratory Standards Institute. Performance standardsfor antimicrobial susceptibility testing. 22nd informationalsupplement (M100–S22). Wayne (PA): The Institute; 2012.6. Kim JS, Kim J, Jeon SE, Kim SJ, Kim NO, Hong S, et al.Complete nucleotide sequence of the IncI1 plasmid pSH4469encoding CTX-M-15 extended-spectrum beta-lactamase in aclinical isolate of Shigella sonnei from an outbreak in theRepublic of Korea. Int J Antimicrob Agents. 2014;44:533–7.http://dx.doi.org/10.1016/j.ijantimicag.2014.08.0077. Carattoli A, Bertini A, Villa L, Falbo V, Hopkins KL, Threlfall EJ.Identification of plasmids by PCR-based replicon typing.J Microbiol Methods. 2005;63:219–28. http://dx.doi.org/10.1016/j.mimet.2005.03.0188. García-Fernández A, Chiaretto G, Bertini A, Villa L, Fortini D,Ricci A, et al. Multilocus sequence typing of IncI1 plasmids carryingextended-spectrum beta-lactamases in Escherichia coli andSalmonella of human and animal origin. J Antimicrob Chemother.2008;61:1229–33. http://dx.doi.org/10.1093/jac/dkn1319. Holt KE, Thieu Nga TV, Thanh DP, Vinh H, Kim DW,Vu Tra MP, et al. Tracking the establishment of localendemic populations of an emergent enteric pathogen.Proc Natl Acad Sci U S A. 2013;110:17522–7. http://dx.doi.org/10.1073/pnas.130863211010. Woodford N, Carattoli A, Karisik E, Underwood A, Ellington MJ,Livermore DM. Complete nucleotide sequences of plasmidspEK204, pEK499, and pEK516, encoding CTX-M enzymes inthree major Escherichia coli lineages from the United Kingdom,all belonging to the international O25:H4–ST131 clone. AntimicrobAgents Chemother. 2009;53:4472–82. http://dx.doi.org/10.1128/AAC.00688-0911. Folster JP, Pecic G, Bowen A, Rickert R, Carattoli A, Whichard JM.Decreased susceptibility to ciprofloxacin among Shigella isolatesin the United States, 2006 to 2009. Antimicrob Agents Chemother.2011;55:1758–60. http://dx.doi.org/10.1128/AAC.01463-1012. Ciesielczuk H, Hornsey M, Choi V, Woodford N, Wareham DW.Development and evaluation of a multiplex PCR for eight plasmidmediatedquinolone-resistance determinants. J Med Microbiol.2013;62:1823–7. http://dx.doi.org/10.1099/jmm.0.064428-013. Lartigue MF, Poirel L, Decousser JW, Nordmann P. MultidrugresistantShigella sonnei and Salmonella enterica serotypeTyphimurium isolates producing CTX-M b-lactamases as causesof community-acquired infection in France. Clin Infect Dis.2005;40:1069–70. http://dx.doi.org/10.1086/428667Address for correspondence: Junyoung Kim, Division of EntericDiseases, Center for Infectious Diseases, Korea National Institute ofHealth, Osong-eup, Heungdeok-gu, Cheongju-si, Chungcheongbuk-do,363-709, Republic of Korea; e-mail: jun49@hanmail.net1250 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 21, No. 7, July 2015
Rapidly Expanding Range of Highly PathogenicAvian Influenza VirusesJeffrey S. Hall, Robert J. Dusek, Erica SpackmanThe movement of highly pathogenic avian influenza (H5N8)virus across Eurasia and into North America and the virus’propensity to reassort with co-circulating low pathogenicityviruses raise concerns among poultry producers, wildlifebiologists, aviculturists, and public health personnel worldwide.Surveillance, modeling, and experimental researchwill provide the knowledge required for intelligent policy andmanagement decisions.The recent introduction of highly pathogenic avian influenza(HPAI) subtype H5N8 virus into Europe andNorth America poses major risks to poultry industries,zoologic collections, and wildlife populations; thus, thisintroduction warrants continued and heightened vigilance.First discovered in early 2014 in poultry and wild birds inSouth Korea, HPAI H5N8 virus apparently arose in Chinafrom reassortment events between HPAI subtype H5N1 virus(clade 2.3.4.4) and several low pathogenicity viruses(LPAIVs) (1–3). The H5N8 virus was subsequently detectedin waterfowl in Russia in September 2014, and sincethen, H5N8 virus and reassortants have been detected inpoultry and wild birds in Europe (Netherlands, Germany,Italy, the United Kingdom, Hungary, and Sweden), Taiwan,Japan, Canada (British Columbia), and the westernand central United States (Washington, Oregon, California,Idaho, Utah, Minnesota, Missouri, Arkansas, Kansas, Iowa,Wyoming, and Montana).Wild waterfowl are a primary natural host for LPAIVs,and infection rates in these populations peak at autumn migratorystaging locations, where large numbers of immunologicallynaive juvenile birds congregate (4). The HPAIH5N8 virus has apparently adapted to wild waterfowlhosts: few or no clinical signs or adverse effects are apparentin these hosts when infected with the virus. Thus, itseems probable that the virus was disseminated out of Russiainto Europe, East Asia, and North America by migratingwaterfowl during autumn 2014 (5).The HPAI H5N8 virus has encountered, interactedwith, and reassorted with co-circulating LPAIVs in migratoryand overwintering waterfowl populations, creatingAuthor affiliations: US Geological Survey National Wildlife HealthCenter, Madison, Wisconsin, USA (J.S. Hall, R.J. Dusek); USDepartment of Agriculture, Athens, Georgia, USA (E. Spackman)DOI: http://dx.doi.org/10.3201/eid2107.150403new HPAI viruses (HPAIVs). In Taiwan, new Eurasian lineagereassortant HPAIVs (i.e., H5N2 and H5N3 subtypes)and the parental H5N8 subtype virus have been detected inpoultry and wild birds (6). In North America, HPAI H5N8virus continues to circulate among waterfowl and commercialand backyard poultry flocks. In addition, new HPAIVreassortants (i.e., H5N2 and H5N1 subtypes) that are combinationsof HPAI H5N8 virus and genetic elements fromEurasian and North American viruses are also circulatingin these populations (7,8) (Figure).Persistence of the original HPAI H5N8 virus for >1year, the creation of multiple reassortant viruses that havemaintained high pathogenicity in poultry, and adaptation ofthe virus to migrating waterfowl all indicate that these virusescould persist and spread in Northern Hemisphere waterfowlpopulations for an extended period. This dynamicof HPAIVs being transported by wild birds to new populationsraises critical issues and poses a series of questionsthat researchers and modelers should examine in more detail.The risks are significant that these HPAIVs will continueto circulate and that new genetic combinations willarise in concentrations of overwintering waterfowl andthen spill over into poultry operations and aviculture. Thespillover risk is particularly high for operations with rudimentarybiosafety practices (e.g., backyard flocks) andthat trend toward outdoor access for organic poultry. Suchevents have already occurred in commercial poultry operationsin Canada and some US states (California, Minnesota,Missouri, Iowa, and Arkansas), and subsequent culling operationsand trade restrictions have caused substantial localeconomic losses. As wild birds begin their spring migrationsand disperse into their breeding ranges, will they betransporting these viruses to new regions, including the restof North America? Is this an inevitable outcome of HPAIH5N8 transmission in wild bird populations? Can these virusesbe transported from Europe to eastern North Americaby migratory birds via North Atlantic routes (9)? Are thererisks of these viruses reassorting with viruses from otherspecies, such as swine, particularly feral swine whose populationsare rapidly expanding, and will these reassortantviruses present greater risk of zoonotic disease?These HPAIVs do not appear to pose substantial risksto waterfowl populations, but they may have detrimentaleffects on other, perhaps more sensitive, wildlife populations.Birds of prey seem to be particularly susceptible toHPAIV infection (10), including the HPAIV H5N8 virusthat killed captive gyrfalcons (Falco rusticolus) thatEmerging Infectious Diseases • www.cdc.gov/eid • Vol. 21, No. 7, July 2015 1251
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