Pathology in Practice

Clare C. Brown Department of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Starkville, MS

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A. Troy Mulder II Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA

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Elizabeth W. Howerth Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA

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Uriel Blas-Machado Athens Veterinary Diagnostic Laboratory, College of Veterinary Medicine, University of Georgia, Athens, GA

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History

A 1-year-old male Narragansett turkey developed growth-like lesions on the face. This turkey was part of a backyard flock that also included chickens, ducks, and another turkey. The other turkey in the flock simultaneously developed similar cutaneous lesions on the neck.

Clinical and Gross Findings

Two days after the lesions were first noticed, both turkeys were brought to the referring veterinarian for evaluation and were prescribed oxytetracycline (200 mg, PO, q 24 h). Over the next 5 days, the growths progressed to cover much of the left side of the face. Both affected turkeys became lethargic and inappetent, and one was presented for referral examination, after which the owner elected euthanasia for the turkey.

At necropsy, the turkey weighed 9 kg and was in good body condition. On external examination, there were multifocal to coalescing pale pink to tan nodules ranging from 2 to 8 mm in diameter and covering 50% of the head, especially on the palpebra, forehead, and snood (Figure 1). Many of these nodules were covered in tan to yellow friable material or dark brown crusts. Within the oral cavity, multifocal yellow to tan caseous nodules were present on the surfaces of the buccal mucosa and hard palate. No additional gross lesions were evident.

Figure 1
Figure 1

Necropsy photographs of the head (A) and oral cavity (B) of a 1-year-old male Narragansett turkey. A—The head is covered in multifocal nodules of variable size. Focal areas of dark brown crusting are present, especially on the palpebral and rostral skin. B—The oral mucous membranes are covered in multifocal yellow to tan caseous plaques.

Citation: Journal of the American Veterinary Medical Association 260, 5; 10.2460/javma.20.08.0453

Histopathologic Findings

Samples of skin from the head and oral mucosa were fixed in neutral-buffered 10% formalin and prepared for histologic evaluation. Microscopically, sections of the skin and oral mucosa had multifocal to coalescing areas of marked thickening by epithelial hyperplasia (Figure 2). Marked amounts of serocellular crust, containing myriad bacillary and coccoid bacteria, covered the surface of the affected areas. Within the affected areas, keratinocytes had markedly swollen and pale cytoplasm (ballooning degeneration). Many also contained multiple eosinophilic intracytoplasmic inclusion bodies (Bollinger bodies), characteristic for poxviral infection. The underlying dermis or lamina propria was infiltrated by moderate to marked numbers of heterophils and lymphocytes.

Figure 2
Figure 2

Photomicrographs of tissue sections of oral mucosa from the turkey in Figure 1. A—The epithelial layer is markedly hyperplastic, accompanied by a marked amount of serocellular crust on the surface. H&E stain; bar = 1 mm. B—Most of the epithelial cells are moderately to markedly swollen (ballooning degeneration) and contain 1 or more 15- to 30-µm poxviral inclusions (Bollinger bodies; arrows). H&E stain; bar = 20 µm. C—The underlying submucosa is markedly infiltrated by heterophils, with fewer lymphocytes. H&E stain; bar = 50 µm.

Citation: Journal of the American Veterinary Medical Association 260, 5; 10.2460/javma.20.08.0453

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: chronic multifocal proliferative dermatitis and stomatitis with eosinophilic intracytoplasmic inclusion bodies, ballooning degeneration, serocellular crusting, and a mixed population of bacteria consistent with turkeypox and secondary bacterial infection.

Case summary: turkeypox in a Narragansett turkey.

Comments

Turkeypox is a viral disease caused by an enveloped DNA virus within the Avipoxvirus genus of the Poxviridae family.13 Avian pox viruses (eg, turkeypox and fowlpox) are prevalent worldwide and affect wild and domestic poultry, with chickens being the most susceptible.2 There are 2 distinct clinical manifestations of turkeypox. The cutaneous form, known as dry pox, is characterized by epithelial hyperplasia of the unfeathered skin, which results in multifocal proliferative pox lesions.13 The diphtheritic form of the virus, or wet pox, is characterized by caseous necrotic lesions of the mucous membranes of the oral cavity and upper respiratory tract.13 It may also be associated with mild to severe respiratory signs. Wet pox is less common than dry pox but is associated with a higher mortality rate.2 The turkey presented in this report had gross lesions of both cutaneous and diphtheritic forms.

The virus is unable to penetrate intact skin, so transmission of turkeypox virus occurs through exposure of damaged skin or mucous membranes.13 Transmission most commonly occurs via bloodsucking insects, especially mosquitoes, acting as mechanical vectors.13 Humans may also serve as fomites.1,3 The turkey in this report might have been at higher risk, as males are more likely to have open wounds from fighting.2 Outdoor access during late spring in the southern US, when this turkey presented, could also have contributed to increased risk due to greater exposure to mosquitoes. Turkeypox is often prevalent year round, especially in tropical regions, but outbreaks in commercial flocks in temperate climates tend to be more common during winter months because mosquitoes overwinter in poultry houses.2,4 The virus may persist in the environment for months to even years and is resistant to desiccation and most disinfectants, although it is sensitive to heat.1,3

In addition to the classic pock lesions, other clinical signs of turkeypox may include lethargy and anorexia, as were seen in this turkey, as well as poor growth, decreased production, conjunctivitis, dysphagia, and dyspnea.1,3 Death can occur via secondary bacterial and fungal infections or asphyxiation, and the mortality rate tends to be higher with wet pox in comparison with dry pox.2 Decreased egg production and production loss from decreased weight gain are of far greater economic impact than is the mortality rate.1

A tentative diagnosis of turkeypox can usually be made based on clinical signs and gross lesions. Differential diagnoses for proliferative cutaneous lesions in a turkey should include bacterial dermatitis, viral-induced papillomas, and, if lesions affect the limbs, scaly leg mite (Knemidocoptes mutans) infestation.1 Oral lesion differential diagnoses should include Trichomonas gallinae infection and mycotoxicosis due to T-2 fusariotoxin.5 Definitive diagnosis of turkeypox is typically achieved through histopathology, which reveals hyperplasia of the epidermis or oral mucosa with the presence of cytoplasmic inclusions or Bollinger bodies,13 as seen in this case. Diagnosis may also be achieved or confirmed via PCR assay or virus isolation.1,3

Turkeypox poses no known zoonotic risk and has not been proven to be transmissible to non-avian animals.1—,3 There is currently no known treatment for avian pox viruses, so management should instead be aimed at prevention.1,2 A live fowlpox vaccine is available for both chickens and turkeys, and success with in ovo vaccination has also been documented but is more relevant to commercial flocks.1 Small backyard flocks that would not necessarily have access to in ovo vaccinations can be vaccinated as 4-week-old chicks, and pullets can be vaccinated 1 to 2 months prior to egg production via the wing-web method.1 Additional management strategies should be employed to minimize and prevent the spread of fowlpox. Backyard flocks, such as in the case presented here, are at particular risk because of their close contact with mosquitoes and other mechanical vectors and because their environment tends to be more contaminated, compared with that of commercial flocks.2 Efforts should be made to reduce exposure to vectors and improve hygiene. Additionally, proper husbandry will limit the impact of turkeypox cases because a higher mortality rate is associated with flocks affected by poor nutrition or stress.2 In the aforementioned case, it is also important to consider the risk to the chickens and ducks that live on the premises, because other poultry species are susceptible to turkeypox as well.

References

  • 1.

    Tripathy DN, Reed WM. Pox. In: Swayne DE, Hoboken NJ, eds. Diseases of poultry. 13th ed. Wiley-Blackwell; 2013:333346.

  • 2.

    Alehegn E, Chanie M, Mengesha D. A systematic review of serological and clinicopathological features and associated risk factors of avian pox. Br J Poult Sci. 2014;3(3):7887. doi:10.5829/idosi.bjps.2014.3.3.8553

    • Search Google Scholar
    • Export Citation
  • 3.

    Giotis ES, Skinner MA. Spotlight on avian pathology: fowlpox virus. Avian Pathol. 2019;48(2):8790. doi:10.1080/03079457.2018.1554893

  • 4.

    Butcher GD, Jacob JP, Mather FB. Common poultry diseases. University of Florida IFAS Extension. Last modified February 19, 2019. Accessed June 29, 2020. https://www.edis.ifas.ufl.edu/ps044

    • Search Google Scholar
    • Export Citation
  • 5.

    Wyatt RD, Weeks BA, Hamilton PB, Burmeister HR. Severe oral lesions in chickens caused by ingestion of dietary fusariotoxin T-21. Appl Microbiol. 1972;24(2):251257. doi:10.1128/aem.24.2.251-257.1972

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1

    Necropsy photographs of the head (A) and oral cavity (B) of a 1-year-old male Narragansett turkey. A—The head is covered in multifocal nodules of variable size. Focal areas of dark brown crusting are present, especially on the palpebral and rostral skin. B—The oral mucous membranes are covered in multifocal yellow to tan caseous plaques.

  • Figure 2

    Photomicrographs of tissue sections of oral mucosa from the turkey in Figure 1. A—The epithelial layer is markedly hyperplastic, accompanied by a marked amount of serocellular crust on the surface. H&E stain; bar = 1 mm. B—Most of the epithelial cells are moderately to markedly swollen (ballooning degeneration) and contain 1 or more 15- to 30-µm poxviral inclusions (Bollinger bodies; arrows). H&E stain; bar = 20 µm. C—The underlying submucosa is markedly infiltrated by heterophils, with fewer lymphocytes. H&E stain; bar = 50 µm.

  • 1.

    Tripathy DN, Reed WM. Pox. In: Swayne DE, Hoboken NJ, eds. Diseases of poultry. 13th ed. Wiley-Blackwell; 2013:333346.

  • 2.

    Alehegn E, Chanie M, Mengesha D. A systematic review of serological and clinicopathological features and associated risk factors of avian pox. Br J Poult Sci. 2014;3(3):7887. doi:10.5829/idosi.bjps.2014.3.3.8553

    • Search Google Scholar
    • Export Citation
  • 3.

    Giotis ES, Skinner MA. Spotlight on avian pathology: fowlpox virus. Avian Pathol. 2019;48(2):8790. doi:10.1080/03079457.2018.1554893

  • 4.

    Butcher GD, Jacob JP, Mather FB. Common poultry diseases. University of Florida IFAS Extension. Last modified February 19, 2019. Accessed June 29, 2020. https://www.edis.ifas.ufl.edu/ps044

    • Search Google Scholar
    • Export Citation
  • 5.

    Wyatt RD, Weeks BA, Hamilton PB, Burmeister HR. Severe oral lesions in chickens caused by ingestion of dietary fusariotoxin T-21. Appl Microbiol. 1972;24(2):251257. doi:10.1128/aem.24.2.251-257.1972

    • Crossref
    • Search Google Scholar
    • Export Citation

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