Case of the Month - July 2026

Signalment and History

Three hatch-year American white pelicans (Pelecanus erythrorhynchos) were found at a rookery in Minnesota. These animals exhibited presumed neurologic signs, including a lack of fear toward humans, an inability to walk straight, and an inability to straighten their necks. The birds were also reported to have insects on their eyes. Concurrently, a large die-off of hatch-year pelicans was reported in the surrounding area. Two of the neurologic birds (Pelican #1 and Pelican #3) were euthanized, and one freshly dead bird (Pelican #2) was recovered from the same location. All three carcasses were submitted to the Minnesota Veterinary Diagnostic Laboratory for postmortem examination.

Gross Findings

A necropsy was performed. Two birds (Pelicans #1 and #3) were in good nutritional condition, while one bird (Pelican #2) was in poor nutritional condition. Numerous lice (likely pouch lice) were present on all three birds. The epicardial surface of the heart of Pelican #1 was covered by fibrin strands.

Histopathology

Brain: Multifocally throughout the tissue, the Virchow-Robin spaces of numerous small-caliber blood vessels are expanded by inflammatory infiltrates composed of 1-3 layers of lymphocytes and plasma cells (perivascular cuffs; figure 1 A). Numerous small, poorly demarcated glial nodules are scattered throughout the section. Additionally, rare, scattered neurons are hypereosinophilic, with nuclear fading or karyorrhexis (neuronal necrosis), and are surrounded by small numbers of inflammatory and/or glial cells (satellitosis; figure 1 B).

Heart: The myocardial interstitium is multifocally infiltrated by moderate numbers of lymphocytes and plasma cells, with fewer histiocytes (figure 2). The inflammatory infiltrates frequently dissect between cardiomyocytes and multifocally form stellate aggregates and linear streams that surround, isolate, and replace individual cardiomyocytes.

Figure 1. West Nile virus infection, brain, pelican #2. (A) Perivascular cuffing and gliosis, H&E. (B) Neuronal necrosis (arrow) and satellitosis, H&E. (C) Strong cytoplasmic immunoreactivity for WNV antigen, IHC-DAB.

Figure 2. West Nile virus infection, heart, pelican #1. Lymphoplasmacytic myocarditis, H&E. Inset: Strong cytoplasmic immunoreactivity for WNV antigen, IHC-DAB.

Ancillary Testing

• Molecular diagnostics: 
  • Combined oropharyngeal/cloacal swabs of all birds were negative for influenza A virus matrix gene and Newcastle disease virus matrix gene by PCR.
  • Brain samples were positive for West Nile virus and negative for Eastern Equine Encephalitis virus by PCR (performed at the Minnesota Department of Health).
• Immunohistochemistry: 
  • Brain (Figure 1C): Strong immunolabeling for WNV antigen was present within the cytoplasm and processes of glial cells and neurons.
  • Heart (Figure 2, inset): Strong immunolabeling for WNV antigen was present within the cytoplasm of cardiomyocytes.

Morphologic Diagnosis

1. Brain, encephalitis, lymphoplasmacytic, widespread, moderate to marked, with glial nodules, neuronal necrosis, and satellitosis.
2. Heart, myocarditis, lymphoplasmacytic, multifocal, moderate.

Etiologic Diagnosis

West Nile virus (Flavivirus).

Discussion

West Nile virus (WNV) is a mosquito-borne, zoonotic arbovirus that first emerged in North America in 1999 in New York. Since its introduction, WNV spread rapidly (within 4 years) across the continent, infecting a broad range of avian species—including the American white pelican (Pelecanus erythrorhynchos). WNV-associated mortality in pelicans was first documented in 2002 across four major breeding colonies in the Northern Plains of North America, including Marsh Lake in Minnesota. These sites are vital to conservation efforts, as they host nearly half of the entire breeding population.

Since 2002, WNV has been a source of unusually high mortality among pelican chicks each year. Prior to the virus's arrival, chick mortality from mid-July to fledging (when chicks are less vulnerable to severe weather and predation) remained below 4%. Following the introduction of WNV to the region, however, mortality rates in these colonies rose dramatically—reaching peaks as high as 44%—and have remained elevated ever since. This sustained loss highlights the high vulnerability of American white pelican chicks to WNV. In contrast, mature pelicans are considered fairly resistant to WNV, given the rare confirmations of fatal WNV infections in adult birds.

In pelicans, clinical presentation of WNV infection includes neurological signs such as head tilts, ataxia, and disorientation. Brain hemorrhage may also be present. The dominant histopathologic lesions in American white pelicans are encephalitis (or meningoencephalitis) and myocardial necrosis and myocarditis, as observed in all three pelicans in this case. However, similar brain and cardiac lesions can also be caused by the infection of white pelicans with highly pathogenic avian influenza virus, which should be considered as a primary differential diagnosis in American white pelicans since they are also highly susceptible to this virus.

References

1. Sovada, M. A., Pietz, P. J., Converse, K. A., King, D. T., Hofmeister, E. K., Scherr, P., & Ip, H. S. (2008). Impact of West Nile virus and other mortality factors on American white pelicans at breeding colonies in the northern plains of North America. Biological Conservation, 141(4), 1021-1031.
2. Hofmeister, E. (2013). West Nile Virus in American White Pelican Chicks: Transmission, Immunity, and Survival. American Journal of Tropical Medicine and Hygiene.
3. Johnson, G., Nemeth, N., Hale, K., Lindsey, N., Panella, N., & Komar, N. (2010). Surveillance for West Nile virus in American white pelicans, Montana, USA, 2006–2007. Emerging infectious diseases, 16(3), 406.
4. Stidworthy, M. F., & Denk, D. (2026). Sphenisciformes, gaviiformes, podicipediformes, procellariiformes, and pelecaniformes. In Pathology of wildlife and zoo animals (pp. 647-669). Academic Press.