tetano
Editor, Senior Moderator
Vet Pathol
. 2026 Jul 3:3009858261457964.
doi: 10.1177/03009858261457964. Online ahead of print.
An outbreak of H5N1 clade 2.3.4.4b highly pathogenic avian influenza in California condors (Gymnogyps californianus)
Rebecca Kagan[SUP] 1 [/SUP], Tabitha C Viner[SUP] 1 [/SUP], Nicole M Nemeth[SUP] 2 [/SUP], John Buchweitz[SUP] 3 [/SUP], Birgit Puschner[SUP] 3 [/SUP], Rachel Sheffler[SUP] 3 [/SUP]
Affiliations
In March and April of 2023, an outbreak of highly pathogenic avian influenza virus, H5N1 strain Eurasian lineage goose/Guangdong H5 clade 2.3.4.4b, resulted in at least 17 mortalities of free-ranging California condors (Gymnogyps californianus) in Arizona. Condors presented dead or with neurologic signs and lethargy. Infection resulted in multisystemic inflammation and necrosis that most consistently and severely affected the brain, spleen, and adrenal glands. Immunohistochemistry performed on tissues from a subset of condors labeled cells in multiple organ systems for influenza A virus, most abundantly in neurons, epithelial cells, and mononuclear inflammatory cells and often colocalized with areas of inflammation. Acute blunt force trauma, presumably from ground collision after falling from a height, was a common finding and indicated a rapidly debilitating disease course and neurologic impairment. Hepatic lead concentrations were relatively low with no concurrent incidences of acute lead toxicosis, an otherwise common cause of death in free-ranging California condors. Bone lead reflected long-term lead accumulation in several condors. Assessment of ingesta in 8 condors via morphologic hair identification showed a mix of consumed taxa, most commonly Bovidae. In summary, California condors, like other New World vultures (family Cathartidae), are highly susceptible to this strain of H5N1, and this should be taken into consideration when planning release, feeding, and morbidity and mortality responses.
Keywords: California condor; H5N1 avian influenza virus; adrenal necrosis; encephalitis; lead toxicity; splenic necrosis.
. 2026 Jul 3:3009858261457964.
doi: 10.1177/03009858261457964. Online ahead of print.
An outbreak of H5N1 clade 2.3.4.4b highly pathogenic avian influenza in California condors (Gymnogyps californianus)
Rebecca Kagan[SUP] 1 [/SUP], Tabitha C Viner[SUP] 1 [/SUP], Nicole M Nemeth[SUP] 2 [/SUP], John Buchweitz[SUP] 3 [/SUP], Birgit Puschner[SUP] 3 [/SUP], Rachel Sheffler[SUP] 3 [/SUP]
Affiliations
- PMID: 42399721
- DOI: 10.1177/03009858261457964
In March and April of 2023, an outbreak of highly pathogenic avian influenza virus, H5N1 strain Eurasian lineage goose/Guangdong H5 clade 2.3.4.4b, resulted in at least 17 mortalities of free-ranging California condors (Gymnogyps californianus) in Arizona. Condors presented dead or with neurologic signs and lethargy. Infection resulted in multisystemic inflammation and necrosis that most consistently and severely affected the brain, spleen, and adrenal glands. Immunohistochemistry performed on tissues from a subset of condors labeled cells in multiple organ systems for influenza A virus, most abundantly in neurons, epithelial cells, and mononuclear inflammatory cells and often colocalized with areas of inflammation. Acute blunt force trauma, presumably from ground collision after falling from a height, was a common finding and indicated a rapidly debilitating disease course and neurologic impairment. Hepatic lead concentrations were relatively low with no concurrent incidences of acute lead toxicosis, an otherwise common cause of death in free-ranging California condors. Bone lead reflected long-term lead accumulation in several condors. Assessment of ingesta in 8 condors via morphologic hair identification showed a mix of consumed taxa, most commonly Bovidae. In summary, California condors, like other New World vultures (family Cathartidae), are highly susceptible to this strain of H5N1, and this should be taken into consideration when planning release, feeding, and morbidity and mortality responses.
Keywords: California condor; H5N1 avian influenza virus; adrenal necrosis; encephalitis; lead toxicity; splenic necrosis.