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CDC - EID Journal - Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus Infection in Poultry Farm Workers, Washington, USA, 2024 (December 2025)

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  • CDC - EID Journal - Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus Infection in Poultry Farm Workers, Washington, USA, 2024 (December 2025)


    ISSN: 1080-6059
    Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.

    Volume 31, Number 12—December 2025

    Dispatch

    Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus Infection in Poultry Farm Workers, Washington, USA, 2024

    Yasuko Hatta1, Juan A. De La Cruz1, Theresa Murray, Brian Hiatt, Yunho Jang, Julia C. Frederick, Kristine A. Lacek, Juliana C. DaSilva, Dan Cui, Paul Carney, Jimma Liddell, Kay W. Radford, Natasha Burnett, Sabrina Schatzman, Pauline Trinh, Anna Unutzer, Elizabeth A. Pusch, Monique Johnson, Ha T. Nguyen, Benjamin L. Rambo-Martin, Larisa Gubareva, James Stevens, C. Todd Davis, Marie K. Kirby, Allison Black, and Han DiComments to Author
    Author affiliation: Centers for Disease Control and Prevention, Atlanta, Georgia, USA (Y. Hatta, J.A. De La Cruz, Y. Jang, J.C. Frederick, K.A. Lacek, J.C. DaSilva, D. Cui, P. Carney, J. Liddell, K.W. Radford, N. Burnett, S. Schatzman, E.A. Pusch, M. Johnson, H.T. Nguyen, B.L. Rambo-Martin, L. Gubareva, J. Stevens, C.T. Davis, M.K. Kirby, H. Di); Washington State Department of Health, Shoreline, Washington, USA (T. Murray, B. Hiatt, P. Trinh, A. Unutzer, A. Black)

    Suggested citation for this article

    Abstract


    Poultry workers in Washington, USA, were infected with highly pathogenic avian influenza A(H5N1) virus and recovered. The viruses were clade 2.3.4.4b genotype D1.1, closely related to viruses causing poultry outbreaks. Continued surveillance and testing for influenza A(H5) clade 2.3.4.4b viruses remain essential for risk assessment and pandemic preparedness of zoonotic influenza viruses.

    The global spread of A/goose/Guangdong/96-lineage highly pathogenic avian influenza (HPAI) virus of the A(H5) subtype has resulted in numerous clades, subclades, and genotypes because of continuous genetic drift and reassortment. HPAI H5N1 clade 2.3.4.4b virus is the most widespread globally; since December 2021, that clade has circulated in wild birds in the United States, affecting millions of poultry, mammalian wildlife, domestic livestock, and companion animals (1,2). In 2024, two distinct genotypes were responsible for ongoing outbreaks in the United States, B3.13 mainly in dairy cattle and D1.1 mainly in poultry, but outbreaks of both genotypes were reported in cattle and poultry (3,4).

    Sporadic human infections with clade 2.3.4.4b viruses have also been reported in the United States. During April 1, 2024–June 30, 2025, a total of 70 human cases were reported, including 41 cases after dairy cattle exposure, 24 after exposure to commercial poultry flocks, 2 after exposure to backyard flocks, and 3 with an unknown exposure source (5,6). In response to reported human infections with clade 2.3.4.4b viruses in the United States and other countries, several 2.3.4.4b A(H5) prepandemic candidate vaccine viruses (CVVs) have been made available for pandemic influenza preparedness (7).

    In late 2024, the Washington State Public Health Laboratory detected influenza A(H5) virus by real-time reverse transcription PCR among specimens from poultry workers experiencing influenza symptoms. We investigated isolates from human cases in Washington to determine virus transmissibility to humans and susceptibility to existing CVVs.


    The Study


    During October 23–November 5, 2024, the Centers for Disease Control and Prevention (CDC; Atlanta, GA, USA) received multiple presumptive influenza A(H5)–positive human clinical specimens from the Washington State Public Health Laboratory. Testing at CDC confirmed HPAI A(H5) virus in 8 poultry farm workers. All 8 cases occurred in adults exposed to H5N1 virus–infected poultry during depopulation efforts to control an outbreak among poultry in Washington. Each affected person reported conjunctivitis, and some also reported respiratory symptoms (6). The mean cycle threshold (Ct) value to detect influenza A matrix gene from the H5-positive specimens was 33 (range 25–36.9).

    After multiple genetic sequencing attempts at CDC, we obtained complete hemagglutinin (HA) gene sequences from 5 confirmed cases and partial or complete neuraminidase (NA) gene sequences from 4 confirmed cases. On the basis of the available HA and NA sequences, the viruses in the specimens belonged to HPAI H5N1 clade 2.3.4.4b. Sequences of the internal gene segments were only available from 4 human cases at various levels of completion. We observed minimal genetic variation among human cases; we submitted all available gene sequences to GISAID (https://www.gisaid.orgExternal Link) and GenBank (Appendix Table 1).

    We attempted virus isolation by inoculating the positive specimens in 10–11-day-old embryonated chicken eggs, MDCK cells, or both. We isolated A/Washington/239/2024 from a conjunctival specimen in MDCK cells and isolated A/Washington/254/2024 and A/Washington/255/2024 from the conjunctival specimens in eggs. We also isolated A/Washington/240/2024 in eggs from both conjunctival and nasopharyngeal specimens (Table).

    Figure 1. Neighbor-joining phylogenetic trees of highly pathogenic avian influenza A(H5N1) clade 2.3.4.4b viruses isolated from poultry farm workers, Washington, USA, 2024. A) Hemagglutinin gene segment; B) neuraminidase gene segment. Green font...

    Since late 2021, at least 6 distinct introductions of clade 2.3.4.4b A(H5) viruses from Europe and Asia (genotypes A1–A6) have occurred in the United States. Each introduction was followed by reassortment events that generated many different genotypes (8,9). Phylogenetic analysis of the 8 gene segments from H5N1 viruses in the specimens of the Washington human cases determined that they belonged to genotype D1.1. That genotype derived from the Eurasian genotype A3 and acquired North American wild bird lineage polymerase basic (PB) 2 (am24 group), polymerase acidic (am4 group), nucleoprotein (am13 group), and NA (am4N1 group) gene segments (Figure 1; Appendix Figures 1–6). Genotype D1.1 is different from genotype B3.13, which derived from the Eurasian genotype A1 after acquiring North American wild bird lineage PB2 (am2.2 group), PB1 (am4 group), nucleoprotein (am8 group), and nonstructural (am1.1 group) gene segments after reassortment.

    Phylogenetically, HA sequences from the Washington human cases belonged to the Eurasian ea3 group and were closely related to viruses detected from the Washington poultry outbreak. Those HA sequences also resembled sequences from wild birds detected in British Columbia, Canada, during 2024 (Figure 1, panel A). The HA sequences from the Washington D1.1 human cases did not contain mutations known to be associated with increased infectivity or transmissibility among humans (FluSurver, https://flusurver.bii.a-star.edu.sgExternal Link). The NA gene segments of H5N1 clade 2.3.4.4b viruses circulating in the United States have been predominantly Eurasian lineage since their introduction (8). However, the D1.1 viruses detected in the Washington cases all contained North American lineage N1 NA genes closely related to those of H5N1 viruses detected in poultry and wild birds in British Columbia in 2024 and H1N1 viruses detected in wild birds in the United States and Canada in 2023 (Figure 1, panel B). The available NA and internal gene sequences from the Washington D1.1 human cases lacked changes associated with reduced antiviral susceptibility or mammalian adaptation. They also lacked PB2-M631L mutation that was detected in most B3.13 viral sequences (1012).

    Figure 2. Glycan microarray analysis of highly pathogenic avian influenza A(H5N1) clade 2.3.4.4b virus isolated from poultry farm workers, Washington, USA, 2024. Clade 2.3.4.4b genotype D1.1 H5N1 virus A/Washington/240/2024 was isolated from...

    The HA sequences from the Washington D1.1 viruses also lacked changes previously associated with increased binding to mammalian-like α2,6 sialic acid receptors. Glycan microarray analysis of the representative virus isolate A/Washington/240/2024 suggested that the Washington D1.1 H5N1 virus retained preferential binding to avian-like α2,3 sialic acid receptors (Figure 2). Three A(H5) clade 2.3.4.4b prepandemic CVVs are available: IDCDC‐RG78A (A/American wigeon/South Carolina/22-000345-001/2021), NIID-002 (A/Ezo red fox/Hokkaido/1/2022), and IDCDC-RG71A (A/Astrakhan/3212/2020). Compared with the most closely related CVV, NIID-002 (HA group ea3), the HA sequences from Washington H5N1 D1.1 viruses (also HA group ea3) all carried 2 amino acid differences at T36A and N476D (mature H5 numbering); neither substitution was located within putative antigenic sites. The HA from Washington H5N1 D1.1 viruses also had 3 amino acid differences relative to IDCDC-RG71A (HA group ea3) and 6 relative to IDCDC‐RG78A (HA group ea1), and 1 difference in the putative antigenic site D (Appendix Table 3). Hemagglutination inhibition (HI) assays indicated that all available Washington H5N1 D1.1 virus isolates cross-reacted well with ferret antisera raised against each of the 3 clade 2.3.4.4b CVVs. Ferret antiserum raised to NIID-002 and IDCDC‐RG78A cross-reacted with the D1.1 viruses at heterologous HI titers equal to or within 2-fold of the homologous HI titer (Table). Ferret antisera raised against IDCDC-RG71A cross-reacted with the D1.1 viruses at heterologous HI titers 2- to 4-fold lower than the homologous HI titer. Ferret antiserum raised against A/Texas/37/2024, the virus isolated from an H5N1 human case in 2024 associated with a dairy cattle outbreak (genotype B3.13), also cross-reacted well with the Washington D1.1 H5N1 virus isolates at heterologous HI titers <2-fold of the homologous HI titer (Table).

    Top

    Conclusions


    We detected human cases of HPAI H5N1 clade 2.3.4.4b genotype D1.1 in poultry farm workers in Washington. Additional human cases of H5N1 D1.1 virus infection have been subsequently reported, including a fatal human case detected in Louisiana, USA (13), and 2 severe human cases, 1 detected in British Columbia, Canada (14), and 1 in Wyoming, USA (15). Among the virus genomes detected in the Washington cases, we noted no changes that are known to be associated with mammalian adaptation, increased infectivity, or transmissibility among humans. Washington H5N1 D1.1 virus retained avian-like α2,3 sialic acid receptor binding preference and cross-reacted well with ferret antiserum raised against A(H5) clade 2.3.4.4b prepandemic CVVs available to vaccine manufacturers. Nonetheless, continued surveillance and testing of clade 2.3.4.4b A(H5) viruses remain essential for influenza pandemic preparedness.

    Top

    Dr. Hatta is a senior service fellow in the Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. Her research interests focus on improving influenza vaccine effectiveness by developing new vaccine platforms and performing antigenic characterizations.


  • #2
    CDC MMWR Weekly / May 7, 2026 / 75(17);221–225​
    Fatal Human Case of Highly Pathogenic Avian Influenza A(H5N5) in a Backyard Flock Owner — Washington, November 2025

    Lynae Kibiger, MPH1; Hanna N. Oltean, PhD1,2; Lisa Leitz3; Emma Krause3; Debra Barrett3; Anna Halloran, MHPA1; Kyle Yomogida, PhD1; Beth Lipton, DVM1; Keely Paris, MPH1; Jared Keirn, MS1; Minden Buswell, DVM1; Allison Black, PhD1; Pauline Trinh, PhD1; Theresa Murray, MT1; Roberto Bonaccorso1; Leticia Banuelos1; Ethan Dieringer1; Jennifer Lenahan, MPH4; Emily Spence Davizon, MPH4; Ellyn P. Marder, DrPH2,4; Jocelyn Mullins, DVM, PhD4; Meagan Kay, DVM2,4; Eric J. Chow, MD2,4,5,6; Sandra J. Valenciano, MD4; John Lynch, MD5,7; Vanessa Makarewicz, MN7; Chloe Bryson-Cahn, MD5,7; Jennifer Hernandez7; Kyla Haggith7; Valicia Linn7; Alex L. Greninger, MD, PhD8; Stephanie Goya, PhD8; Sierra Gulla9; Jennifer Young, MPH9; Sierra Kerns-Funk, MPH10; Brianna da Silva Bhatia, MD10; Hollianne Bruce, MPH11; Krista Kniss, MPH12; Katie Reinhart, PhD12; Rachel Ohlstein13; Shannon Johnson13; Christina Schofield, MD14; Patrick Smith, DO14; Amber Itle, VMD15; Maura Gibson, DVM16; Brandi Torrevillas17; Azeza Falghoush, PhD17; Thomas B. Waltzek, DVM, PhD17; Kevin Snekvik, DVM, PhD17; Mia Torchetti, DVM, PhD16; Timothy M. Uyeki, MD12; Scott Lindquist, MD1 (VIEW AUTHOR AFFILIATIONS)​
    Summary


    What is already known about this topic?

    Since 2022, highly pathogenic avian influenza (HPAI) A(H5) viruses have circulated among wild birds in the United States. Seventy human cases of influenza A(H5), most with mild illness, have been reported in the United States since 2024; 14 human influenza A(H5N1) cases were previously identified in Washington.

    What is added by this report?

    In November 2025, Washington reported the first human case of HPAI A(H5N5) infection worldwide. A positive laboratory result was obtained from a lower respiratory sample after multiple negative upper respiratory sample results; the patient experienced respiratory failure and died 28 days after symptom onset. The public health investigation identified approximately 135 exposed persons.

    What are the implications for public health practice?

    Symptom management and testing of exposed persons are critical to monitoring for human-to-human transmission of novel influenza infection. Environmental and animal investigations, including genomic analysis, can identify epidemiologic risk factors.

    Abstract

    Clade 2.3.4.4b influenza A(H5N1) viruses have circulated across migratory bird flyways in the United States since 2022, including in Washington, where backyard flock detections have been reported annually. In November 2025, a Washington resident died from acute respiratory failure after receiving a positive influenza A(H5) test result at a hospital laboratory. Washington Public Health Laboratories confirmed influenza A(H5), and genomic sequencing identified influenza A(H5N5) virus (A6 genotype). Polymerase chain reaction testing detected highly pathogenic avian influenza A(H5) virus clade 2.3.4.4b from an apparently healthy backyard flock of ducks and sediment from a watering basin on the patient’s property. Six of eight gene segments from the environmental sample and one duck sample (partial neuraminidase segment) were highly genetically similar to the patient’s virus sequence. Although existing wild bird surveillance had not detected influenza A(H5N5) virus (A6) in the U.S. Pacific Flyway, introduction via wild birds into the environment of the backyard flock was likely the source of the patient’s exposure. The public health investigation identified approximately 135 exposed persons; symptom monitoring and influenza testing detected no additional cases. The overall risk for avian influenza A remains low among the general U.S. population; however, novel avian influenza A virus infection should be considered in persons with symptoms of influenza and potential exposures.

    Investigation and Results

    Illness Onset, Hospital Course, and Laboratory Testing

    Symptom onset. In late October 2025, a Grays Harbor County, Washington, resident aged ≥65 years with a history of non-Hodgkin lymphoma developed fever, diarrhea, nausea, and cough (day 0) (Figure). The next day (day 1), the patient was evaluated in hospital A’s emergency department and discharged without a diagnosis. Nucleic acid testing (NAT) of a nares swab specimen was negative for influenza A virus, the first of multiple negative upper respiratory specimen influenza test results during the first 14 days of illness, which resulted in inconsistent implementation of isolation precautions.

    First hospitalization (hospital A) and pneumonia. On day 10, the patient was admitted to hospital A with confusion, an inability to walk, lower back pain, and a sore throat. A chest radiograph revealed right-sided pneumonia. A nares swab specimen tested negative for influenza by NAT.

    Clinical deterioration and intensive care (hospital B). On day 12, because of worsening respiratory status, the patient was transferred to an intensive care unit (ICU) at hospital B and received endotracheal intubation, with invasive mechanical ventilation using a high efficiency particulate air (HEPA) filter. A nasal swab specimen tested with a respiratory viral polymerase chain reaction (PCR) panel was negative (day 14).

    First positive influenza A results (hospital C). On day 15, the patient was transferred to hospital C’s ICU for an extracorporeal membrane oxygenation consultation. Bronchoalveolar lavage (BAL) and nasal swab specimens both tested positive for influenza A virus by reverse transcription–polymerase chain reaction (RT-PCR), and oseltamivir treatment was initiated (day 16). An infectious disease consult raised concern for avian influenza virus given the patient’s history of contact with a backyard flock. On day 17, aerosol contact precautions with eye protection were implemented (e.g., National Institute for Occupational Safety and Health–approved respirator, gown, gloves, and eye protection) (1,2).

    Identification of influenza A(H5N5), whole genome sequencing of BAL specimen, and death of patient.On day 18, the University of Washington laboratory identified influenza A(H5) virus by PCR from the influenza A–positive BAL and nasal swab specimens. The patient was moved to an airborne infection isolation room, and the local health jurisdiction was notified. Washington Public Health Laboratories (WA PHL) confirmed the BAL influenza A(H5) subtyping result (collected on day 16) with a cycle threshold (Ct) value* of 25.26 (day 20). The University of Washington virology laboratory conducted whole genome sequencing of the BAL specimen and identified influenza A(H5N5) virus (genotype A6) (day 21). On day 24, WA PHL confirmed influenza A(H5) virus in a sputum sample (Ct = 28.00). Despite supportive critical care and aggressive treatment with influenza antiviral therapy (oseltamivir, baloxavir, amantadine, and peramivir), the patient died on day 28. Epidemiologic Investigation


    Illness in two ducks kept by patient. The patient lived on a multiacre, rural property that was frequented by wild birds, including waterfowl. One family member lived in the house with the patient; another lived in a separate residence on the property. Grays Harbor County Public Health obtained exposure details via proxy interviews. The patient was the owner and primary caretaker of a backyard free-range poultry flock of 25 dabbling ducks and approximately 30 chickens, with multiple basins embedded in the ground for the birds’ enrichment and watering. During the week preceding symptom onset, the patient cared for the flock daily, handled eggs, and used a hose to clean and fill watering basins without using personal protective equipment (PPE). The patient owned no other animals, including livestock and had no known exposure to raw dairy products. On day 2 after the patient’s symptom onset, two ducks in the flock appeared ill; a household member removed them from the flock to a cage. These ducks died overnight and were disposed of on the property. The patient did not handle the ill or dead birds; daily care ceased at the time of the patient’s illness.


    Animal health investigation. After notification by the Washington Department of Health (WA DOH), the Washington State Department of Agriculture (WSDA) and U.S. Department of Agriculture conducted an animal health investigation, including diagnostic sampling (day 21). Although the flock appeared healthy, oropharyngeal and cloacal swabs from all ducks on the property and a pooled sample of oropharyngeal swabs from chickens were collected and submitted to the Washington Animal Disease Diagnostic Laboratory (WADDL). The same day, WADDL reported weak Ct detections among all ducks by at least one of the following PCR assays: 1) avian influenza matrix PCR, 2) avian influenza A(H5) PCR, or 3) avian influenza (A[H5], 2.3.4.4) PCR; the pooled chicken swabs tested negative by avian influenza A(H5) PCR. The flock was depopulated on day 22. Positive specimens were forwarded to the National Veterinary Services Laboratories (NVSL), where six of the ducks tested positive for influenza A by PCR, all with Ct values >35; virus isolation and direct sequencing were unsuccessful.

    Environmental evaluation. On day 21, WA DOH conducted an environmental investigation and collected samples at the patient’s property, including swabs from a feather, material suspected to be duck feces in the holding cage, and bottom sediment from one watering basin. The sediment tested nonnegative (presumptive positive result before confirmation)§ for avian influenza A(H5) clade 2.3.4.4b by PCR at WADDL (day 27) and was forwarded to NVSL, which confirmed highly pathogenic avian influenza (HPAI) A(H5), isolated the virus, and characterized the virus as A(H5N5), genotype A6 (partial genome with six of eight genes sequenced) (day 39).

    A partial genome from one duck sample (Ct = 35.07; partial neuraminidase segment) was obtained by WADDL. The viral sequences from the sediment sample and the duck were highly genetically similar to the patient’s viral genome sequence.

    Public Health Response

    A tiered health care personnel (HCP) risk assessment was generated in coordination with CDC, WA DOH, and local health jurisdictions as an option for health care partners in the event of staffing shortage concerns (Box) (3). HCP (124), family contacts (seven known), and state and federal government employees (four) with possible exposure to the patient, flock, or flock’s environment were monitored for influenza symptoms through day 10 after their last exposure. During symptom monitoring, 15 exposed persons developed compatible symptoms; none received positive test results for influenza (Table). Monitoring was primarily conducted using Research Electronic Data Capture (REDCap; version 16.0.18) databases with automated daily text message questionnaires.

    Public health officials identified seven family members with exposure to the patient or the property, including two living on the property grounds. Six family members agreed to passive weekly monitoring by phone. During the patient’s final hospitalization, only family visitation was permitted; the hospital provided PPE, including non–fit-tested respirators. Additional family members were identified through hospital visitation logs but contact information was not provided. Thus, the total number of exposed family members is unknown.

    Discussion

    This detection of influenza A(H5N5) in a Washington resident is the first human influenza A(H5N5) virus detection worldwide. Diagnosis of influenza A(H5N5) clade 2.3.4.4b, genotype A6, in this patient resulted in a multijurisdictional public health response to ascertain exposure sources, identify exposed persons, and monitor for additional cases. WA DOH and WSDA sampling identified influenza A(H5N5) virus in the backyard flock environment and in apparently healthy ducks on the patient’s property. Although existing federal and state-based wildlife surveillance had not detected influenza A(H5N5) virus (genotype A6) in the U.S. Pacific Flyway, introduction of the virus into the environment of the backyard flock via wild waterfowl and the presence of amplifying hosts on the property were the most likely sources of exposure. The overall avian influenza risk to the general U.S. population remains low (3).

    Avian influenza A viruses pose a higher human transmission risk when direct or close and prolonged exposure to infected poultry or other infected animals occurs without recommended PPE use (2). However, three cases of human infection with HPAI A(H5N1) viruses without a clear exposure source have been identified in the United States (4). To assist in early identification, appropriate treatment, and isolation, HCP should routinely inquire about relevant exposures, including contact with ill or dead animals or their environments, consumption or handling of raw animal products, and contact with a confirmed or suspected human case of avian influenza virus infection when evaluating patients with acute respiratory illness (particularly those with severe illness requiring hospitalization) (2,5).

    The diagnosis of influenza A(H5N5) virus infection in the patient described in this report was complicated by early and repeated negative influenza test results from upper respiratory swab specimens. Negative influenza results from initial upper respiratory specimens have been described in three similar patients with lower respiratory tract disease hospitalized with avian influenza A(H5N1) infection (4). Thus, avian influenza virus infection should not be ruled out in hospitalized patients based on negative influenza laboratory test results from upper respiratory tract specimens if the patients have lower respiratory tract disease, relevant exposures, and no confirmed etiology for their disease. If avian influenza virus infection is suspected in a patient with severe respiratory disease, both upper and lower respiratory tract specimens should be collected for influenza testing by RT-PCR at a public health laboratory (6).

    Early negative influenza results delayed initiation of isolation precautions, reporting to public health authorities, and symptom monitoring. Although isolation precautions were not established consistently until the ninth day of inpatient care, no cases among HCP were identified. Likewise, no cases were detected among family members, despite lengthy exposure to both the symptomatic patient and the property. One household member reported direct contact with the ill and dead ducks but remained asymptomatic. Establishing a tiered risk assessment for HCP exposures based on setting and PPE use allowed staff members to continue working while having their symptoms monitored and limited new HCP exposures. The investigation was complicated by its occurrence during viral respiratory season and symptom development among several persons whose symptoms were being monitored. Human-to-human transmission of avian influenza A viruses has only rarely been reported globally and has not been reported in the United States (3,7).

    Timely HPAI risk evaluation is important for persons with influenza symptoms requiring hospitalization to support infection prevention and control, early notification of public health authorities, and robust epidemiologic investigation, including genomic sequencing to identify possible transmission pathways. Ill or dead animals should be reported to animal health authorities for surveillance and potential testing and to reduce human exposure. Public health guidance for evaluating suspected cases of avian influenza should include immediate isolation precautions, prompt initiation of antiviral treatment, repeated influenza testing, and specimen collection from multiple sites (2,6,8). Considering the successive influenza A–negative laboratory results in the Washington patient, sampling from both upper and lower respiratory tracts in hospitalized patients should be considered to increase the likelihood of laboratory detection.

    Acknowledgments

    Tacoma-Pierce County Health Department; Harborview Medical Center; University of Washington; MultiCare Capital Medical Center; Harbor Regional Health; Lauren Sarkissian, Anna Unutzer, Washington State Department of Health.

    This report describes a fatal human case of highly pathogenic avian influenza in Washington.






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