Pathology Case of the Month - Wild Turkey

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Case History: In September 2015, a landowner in Minnesota, USA reported a wild turkey (Meleagris gallopavo) that was acting abnormally (did not run away when approached). Upon investigation the next day, the turkey was found dead with no visible signs of injury.  This turkey was submitted for necropsy examination and diagnostic testing.

Gross Findings: Completely covering the eyelids, head, and neck were numerous multifocal to coalescing, yellow, papillary proliferations with a region of ulceration and necrosis around the beak (Fig. 1A). Extending from the commissures into the oral cavity, around the larynx, and throughout the mucosa of the esophagus, there were slightly elevated irregular areas of mucosal necrosis (plaques) (Fig. 1B). The pectoral muscles were severely atrophied, and there were no fat stores throughout the body. The proventriculus and ventriculus were empty and contained only a small amount of grit. The intestines contained minimal amounts of pale fluid. The kidneys had a diffuse lobular pale pattern. The remaining major organs were unremarkable.

Photographs from a wild turkey showing yellow lesions covering the eyelids, head, and neck

Figure 1. Photographs from a wild turkey (Meleagris gallopavo) found dead in Minnesota, USA.  (A) There are numerous multifocal to coalescing yellow proliferative lesions covering the eyelids, head, and neck with a region of ulceration and necrosis (*).  (B) Yellow irregular plaques (arrow heads) multifocally cover the oral cavity. (Credit: Jaimie Miller, USGS National Wildlife Health Center. Public domain.)

Histopathological Findings: Microscopic findings for the skin and both oral and esophageal mucosa were similar. There was multifocal, severe expansion of the epidermis/mucosal epithelium by irregular hyperplasia of the stratum spinosum (Fig. 2A). The hyperplastic cells had mild to moderate cytoplasmic swelling (vacuolar degeneration) (Fig. 2B), that occasionally became severe with peripheral nuclei (ballooning degeneration). Multifocally epithelial cells contained intracytoplasmic, brightly eosinophilic viral inclusion bodies (Bollinger bodies) (Fig. 2C). There was superficial to full thickness loss of the epidermis/mucosal epithelium (erosions and ulcerations) and replacement by eosinophilic, amorphous, karyorrhectic debris (necrosis) admixed with partially dehydrated serum (serocellular crusts) and numerous clusters of bacteria.

Pink and purple photomicrographs showing lesions in epithelium.

Figure 2. Photomicrographs from a wild turkey (Meleagris gallopavo) found dead in Minnesota, USA.  (A) The normal epithelium becomes markedly thickened due to hyperplasia of the stratum spinosum (left to right) with regions of ulceration and crusting (arrow). H&E stain.  (B) Epithelial cells in hyperplastic regions are multifocally swollen (vacuolar degeneration) (arrows), and there is serocellular crusting over the surface (*). H&E stain. (C) Some epithelial cells contain eosinophilic intracytoplasmic inclusion bodies (Bollinger bodies) (arrowheads). H&E stain. (Credit: Jaimie Miller, National Wildlife Health Center. Public domain.)

 

Morphologic Diagnosis/es:

  1. Multifocal to coalescing, severe, chronic, hyperplastic, necrotizing, and ulcerative dermatitis, stomatitis, and esophagitis, with intracytoplasmic eosinophilic inclusion bodies and coccobacilli

Disease: Fowl pox

Etiology: Avian poxvirus, an enveloped double stranded DNA virus

Distribution: Worldwide

Seasonality: Wild birds can be infected year-round, however, disease outbreaks have been associated with environmental conditions (affecting virus survival outside of the bird host), emergence of vector populations (i.e. mosquito season), and the habits of the species affected (i.e. congregation during migration, at bird feeders, etc.).

Host range: Within the Avipoxvirus genus, there are numerous species that can infect a wide range of wild, captive, and domestic birds. If adequately exposed, most avian species are susceptible to one or more of the avian poxvirus strains or species.

Transmission: Transmission most commonly occurs via direct contact with infected birds, biting insect vectors (primarily mosquito), and fomites (i.e. bird feeders). Transmission of some strains can also occur by inhalation or infection through open skin wounds.

Clinical signs: Avian pox should be suspected in birds with wart-like nodules on one or more of the featherless areas of the body, including the feet, legs, base of the beak, and eye margin. If extensive enough to interfere with their feeding or air passages, the birds may appear weak and emaciated or may show signs of labored breathing. Although the course of this disease can be prolonged, birds with extensive lesions have been known to completely recover if they are able to feed.

Pathology: There are two forms of this disease. One or both manifestations may be present in an affected bird.

  • Cutaneous form (dry pox) (most common): Warty nodules develop on the featherless parts of the bird, including the head, neck, vent, legs, and feet. These nodules can become enlarged and clustered leading to sight and breathing impairment and feeding difficulty.  Secondary bacterial and other infections are common with this form of the disease, and these infections can contribute to bird mortality. This form of the disease is usually self-limiting; the lesions regress and leave minor scars.
  • Diphtheritic form (wet pox): The diphtheritic form has moist, necrotic lesions on the mucus membranes of the mouth and upper digestive and respiratory tracts. It is primarily a problem of young chickens and turkeys, though this form probably occurs more frequently in wild birds than is reported because it is less observable than the cutaneous form. Also, the more severe consequences of wet pox undoubtedly cause greater morbidity and mortality, thereby leading to removal of infected birds by predators and scavengers.

Regardless of the form, both dry and wet pox have similar microscopic findings. The affected epithelium is hyperplastic, often with ballooning (hydropic) degeneration. Eosinophilic intracytoplasmic inclusion bodies (Bollinger bodies) within the epithelial cells are pathognomonic. Secondary changes such as erosions, ulcerations, or bacterial infection can also be seen.

Diagnosis: While a presumptive diagnosis of avian pox can be made from the gross appearance of the wart-like growths on the featherless parts of the bird, a definitive diagnosis requires microscopic examination for characteristic intracytoplasmic viral inclusion bodies. Avian pox can also be confirmed by virus isolation and serological identification.

Public health concerns: Avian poxvirus is part of a larger family of poxviruses that include human diseases such as variola (smallpox). However, there is no evidence that avian poxviruses can infect humans.

Wildlife population impacts: Most avian pox infections reported in individual wild birds are mild and self-limiting. However, increased mortality has been reported in naïve populations (such as native birds on an island) or in captive situations.

Management: Vector control (primarily mosquitoes) and decontamination of fomites (i.e. bird feeders) can help control this disease. Removing heavily infected animals from an area can diminish the source of the virus for vector populations and reduce transmission to noninfected birds. The poultry industry uses modified live vaccines to prevent avian pox, but their safety and efficacy in wild birds have not been determined.

References:

Van Riper III C and Forrester DJ. 2007. Avian Pox.  In: Infectious diseases of wild birds. Thomas NJ, Hunter DB, Atkinson CT, editors. Blackwell Publishing, Iowa, pp. 131-176.

Trupkiewicz J, Garner MM, and Juan-Sallés C. 2018. Passeriformes, Caprimulgiformes, Coraciiformes, Piciformes, Bucerotiformes, and Apodiformes. In: Pathology of Wildlife and Zoo Animals. Terio KA, McAloose D, St. Leger J, editors. Elsevier, San Diego, CA, pp. 805-807.

U.S. Geological Survey. 1999. Field manual of wildlife diseases: general field procedures and diseases of birds, https://pubs.er.usgs.gov/publication/itr19990001. Accessed April 2021.

 

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