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January 8, 2024

One Cooper’s hawk (Accipiter cooperii) was found down during a larger die-off of multiple corvid and raptor species.

It presented unable to fly, was emaciated, depressed, dehydrated, and was easily captured. There was no evidence of trauma. On examination the hawk demonstrated multiple clinical signs including knuckling, pelvic weakness, and mild anisocoria. The hawk died overnight after receiving fluids. Several other birds (jays, crows, and other raptors) were found dead or with neurological signs within the same area.

Gross Findings: On external examination the keel was prominent. The oral cavity (to include the tongue) and larynx contained multiple raised white nodules. There were multiple abrasions on the dorsal and lateral aspects of the carpi and multiple hyperemic foci throughout the legs. Internally there was minimal subcutaneous, visceral, and epicardial fat. Air sacs were thickened and opaque with multiple, irregular, yellow to green nodules (Figure 1A). Lungs were light pink and aerated with multiple yellow to green plaques on the surface, the largest of which was 2 x 2 mm. The liver had multifocal slightly raised white to tan nodules throughout that were 1 mm in diameter as well as innumerable miliary foci (Figure 1B). Spleen and kidneys had similar nodules as those in the liver.

Gross photographs from a Cooper’s hawk showing Air sac overlying the lung and liver with yellow to green, irregular nodules.
Figure 1. Gross photographs from a Cooper’s hawk (Accipiter cooperii). (A) Air sac overlying the lung and liver have multiple yellow to green, irregular nodules (arrows). (B) Liver (asterisk) has multiple 1 mm, round to irregular, tan nodules in addition to innumerable miliary foci.

Histopathological Findings: Affecting over 50% of all lung sections, there are multifocal to coalescing, random nodules that obliterate tissue architecture and compress surrounding, more normal parenchyma. Nodules are centered on eosinophilic, necrotic debris surrounded by abundant epithelioid macrophages and few lymphocytes and plasma cells (Figure 2B). The cytoplasm of macrophages is greatly expanded by innumerable, poorly staining to amphophilic bacilli bacteria (H&E Figure 2B). With Ziehl-Neelsen stain, intrahistiocytic and extracellular 1 x 2 µm acid-fast bacteria are brightly magenta (Figure 2B insert). Within the submucosa of the soft palate, similar granulomas are present with the addition of many multi-nucleated giant cells surrounding the necrotic core, further surrounded by epithelioid macrophages (Figure 2A) and contained acid-fast bacteria (figure 2B insert). Similar granulomas were found in the air sacs, liver, esophagus, kidney, proventriculus, and ventriculus. The liver was severely affected with over 90% of the normal parenchyma replaced by granulomas. Additional ancillary findings include cross-sections of aphasmid nematodes within the tongue and spirurid nematodes in the proventricular glands.

Photomicrographs showing lesions in Cooper’s hawk soft palate and lung.
Figure 2. (A) Soft palate of a Cooper’s hawk (Accipiter cooperii). The submucosa is expanded by a myriad of epithelioid macrophages (arrow) surrounding multinucleated giant cells centered on a necrotic center (asterisk). H&E stain. Insert: Intrahistiocytic and extracellular acid-fast bacilli. Multinucleated giant cells are prominent between extracellular bacteria within necrotic center and epithelioid macrophages. Ziehl-Neelson stain. (B) Lung from a Cooper’s hawk. Granulomas (asterisk) efface normal architecture and compress surrounding parenchyma. H&E stain. Insert: Intrahistiocytic, acid-fast bacilli. Ziehl-Neelson stain.

Morphologic Diagnosis/es: Soft palate, esophagus, air sacs, lungs, liver, spleen, kidneys, proventriculus, ventriculus: granulomas, multifocal to coalescing, severe, with innumerable intrahistiocytic and extracellular acid-fast bacteria consistent with Mycobacterium avium in a Cooper’s hawk (Accipiter cooperii).

Disease: Mycobacteriosis, avian tuberculosis.

Etiology: Mycobacterium avium.

Distribution: Found ubiquitously throughout most of the world although specific types can be associated with certain areas. Occurrence in wild birds is more common in species that interact frequently with domestic stock animals or in areas of high avian density.

Seasonality: There is no true seasonality associated with this disease although occurrence may vary with migration and other factors.

Host range: Both avian and mammalian species can be affected by Mycobacterium avium to varying degrees. Birds, pigs, mink, and rabbits are the most likely to be susceptible. Domestic chickens, quail, and partridge are the most frequently affected birds.

Transmission: This organism can persist in the environment for many months allowing transmission through multiple routes. Common modes include direct contact, inhalation, consumption, or contaminated wounds.

Clinical signs: Clinical signs vary depending on the form of the disease and what body systems develop granulomas, making it difficult to diagnose from clinical signs alone. The most consistent findings include emaciation, weakness, lethargy, and wasting which occur due to the chronicity of disease.

Pathology: In avian species, the most commonly affected organs are the liver and spleen, but lesions can be found in all organ systems, even within joints and spinal cord. This is different than mammalian species which are more likely to have lesions in lungs and lymph nodes. The primarily lesions are granulomas that measure 1 to several millimeters in diameter, are tan to yellow, and occasionally friable. Most birds exhibit emaciation and atrophy of the pectoral muscles.

Diagnosis: Diagnosis is most accurate during post-mortem examination. Acid-fast staining of histologic sections can provide a diagnosis of Mycobacterium sp. Isolation and identification through PCR is required for diagnosing the species.

Public health concerns: Humans are considered fairly resistant to avian tuberculosis, but cases have been reported. Affected individuals generally have a comorbidity or are immunosuppressed allowing for easier infection.

Wildlife population impacts: In wildlife, mycobacteriosis is more commonly causes the death of single animals rather than die-off events. Contamination of water or soil from a domestic outbreak has the potential to cause disease in exposed wildlife species.

Management: Tuberculosis is difficult to detect in living animals and treatment is often ineffective; because of these factors, if feasible, flock depopulation is the best response to prevent further spread in wild populations. Due to the persistence of Mycobacterium sp. in the environment, effective decontamination of the environment surrounding outbreaks (domestic and wild) is a vital step to prevent wildlife exposure. Birds should be prevented from entering the area of an outbreak until decontamination can occur.

References:

  • Tell LA, Ferrel ST, Gibbons PM, 2004, Avian Mycobacteriosis in Free-Living Raptors in California: 6 cases (1997-2001). J. of Avian Med. Surg. 18(1):30-40.
  • United States Geological Survey. 1999. Field manual of wildlife diseases: general field procedures and diseases of birds, https://pubs.er.usgs.gov/publication/itr19990001. Accessed December 2023.
  • Wunschmann A, Armien AG, Hofle U, Kinne J, Lowenstine LJ, Shivaprasad HL. 2018. Birds of Prey. In: Pathology of Wildlife and Zoo Animals. Terio KA, McAloose D, St. Leger J, editors. Academic Press, Elsevier. San Diego. 729-30. https://doi.org/10.1016/B978-0-12-805306-5.00030-4

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