Description of the First Case of Psittacine Beak and Feather Disease in Brazil

Karin Werther, Edison L. Durigon, Tania de Freitas Raso, Kenneth S. Latimer, and Raymond P. Campagnoli

Department of Microbiology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil (Durigon), Rua Quintino Bocaiuva 271, 14870-000 Jaboticabal/SP, Brazil (Werther, de Freitas Raso), and The University of Georgia, Athens, Georgia 30605 USA (Latimer, Campagnoli)

Abstract: Beak and Feather Disease was diagnosed in a domestically raised White Cockatoo (Cacatua alba) with symmetrical feather dystrophy and loss. This bird was the progeny of parents that had been imported from Australia 10 years previously. H&E-stained sections of skin contained nuclear inclusions in feather epithelial cells and cytoplasmic inclusions in macrophages. The presence of psittacine beak and feather disease (PBFD) viral nucleic acid was confirmed by DNA in situ hybridization. Eventually the bird died. Studies of tissues and organs obtained at necropsy revealed widespread viral infection involving the skin, feathers, spleen, liver, intestine, thyroid gland, parathyroid gland, adrenal gland, heart, great vessels, lungs, kidney, and ovary. An incidental finding included trematodes within the pancreatic duct.

Key words: Brazil, Circovirus, White Cockatoo, Cacatua alba, Psittacine beak and feather disease, Systemic viral infection, Virus

Introduction

Psittacine beak and feather disease (PBFD) is caused by 14 to 16 nm diameter, nonenveloped virus with an icosahedral capsid containing a 1.7 to 2.0 kb, single-stranded, circular, DNA genome. ¹ The virus has a broad host range and will infect birds of the Cacatuidae, Psittacidae, and Loridae families. ² Classical PBFD is associated with symmetrical feather dystrophy and loss that is progressive with ensuing molts. The disease process may also cause abnormalities in the beak and claws as well. ² The purpose of this report is to describe the first documented case of PBFD in a cockatoo that was domestically raised in Brazil.

Case Report

A 3-year-old White Cockatoo (Cacatua alba) weighing 335g was presented for examination because of progressive feather dystrophy and loss. Feather loss was first noticed in February 1997. The bird had been hatched and raised at a commercial breeding center in Brazil. The breeding center had a total area of 20,000 qm with approximately 120 cages. The breeding flock consisted of 32 cockatoos and other avian species. The facility was attended by a single worker, who had contact with all birds in the breeding center. The hatchling was fed by its parents and reared to maturity in the breeding facility. It was housed in a 100 qm area with its male sibling. Neither the sibling nor the parents had signs of feather dystrophy or loss. Both parents had been imported from Australia 10 years previously and had produced offspring yearly, none of which exhibited feather abnormalities.

In November 1997, the bird was transferred to the University of São Paulo – UNESP, City of Jabotical, State of São Paulo, Brazil to determine the cause of the feather abnormalities. On initial examination, the bird had abnormal feathers over the entire body and beak deformation (Fig. 1). The bird’s behavior, appetite, and feces appeared normal. Two days later, the bird was anesthetized with isoflurane (Forane-Abbott) for a detailed clinical examination, survey radiographs, complete blood cell count (CBC), and skin and feather follicle biopsy.

Fig. 1. White Cockatoo, PBFD. Feather loss is apparent over most of the body.

Symmetrical feather loss and dystrophy involved most of the body. Feather abnormalities included retained feather sheaths, clubbed and deformed feather, circumferential constrictions, and blood within feather shafts. Partial loss of crest and tail feathers also was observed. The upper portion of the beak was elongated with necrosis of the hard palate. The lower beak also appeared abnormal.

The survey radiographs revealed mild renomegaly, a slightly dilated proventriculus, and abundant grit within the ventriculus. The caudal thoracoabdominal air sacs were distended.

The patient’s laboratory data are presented in Table 1. Mild nonregenerative anemia was present, presumably related to chronic disease. Mild monocytosis, which may be observed in both acute and chronic diseases, was a nonspecific finding. Platelet numbers appeared adequate on the stained blood smear and hemoparasites were not observed.

H&E-stained sections of feathers often contained a necrotic pulp with an intense infiltrate of heterophils. Portions of viable feather epithelium exhibited necrosis of basal epithelial cells. Some of these cells also contained glassy, basophilic nuclear inclusions. In addition, macrophages within the basal layers of the feather epithelium contained multiple, globular, basophilic, cytoplasmic inclusions (Fig. 2). Histologically, the feather lesions and inclusions were typical of PBFD. The presence of PBFD viral nucleic acid subsequently was confirmed by DNA in situ hybridization (Fig. 3).

Fig. 2. White Cockatoo, feather section, H&E stain. Necrosis of basal epithelial cells is present (top). Scattered epithelial cells contain nuclear inclusions while macrophages contain globular, basophilic, cytoplasmic inclusions.	Fig. 3. White Cockatoo, feather section, DNA in situ hybridization for PBFD nucleic acid. Abundant PBFD viral nucleic acid is present (dark blue staining).

The bird died 14 days later and was necropsied. Sections of various tissues and organs were collected, preserved in 10% neutral-buffered formalin, processed, embedded in paraffin wax, sectioned at 3 µm, and subjected to DNA in situ hybridization to determine the distribution of PBFDV nucleic acid. ³ PBFDV nucleic acid was detected within the skin, feathers, spleen, liver, intestine, thyroid gland, parathyroid gland, adrenal gland, heart, great vessels, lungs, kidney, and ovary (Figs. 4 & 5). These observations confirmed systemic distribution of the virus. An incidental finding included the presence of trematodes within the pancreatic duct.

Fig. 4. White Cockatoo, liver, DNA in situ hybridization for PBFD nucleic acid. Abundant PBFD viral nucleic acid is present within Kupffer cells (dark blue staining).	Fig. 5. White Cockatoo, myocardium, DNA in situ hybridization for PBFD nucleic acid. PBFD viral nucleic acid is present within myocytes and capillary endothelial cells (dark blue staining).

Discussion

This case report represents the first documented case of PBFD in Brazil. This White Cockatoo developed the disease as a young adult. It had been hatched and reared in a commercial breeding center and had led a relatively isolated life. The source of the infection was undetermined, but probably originated from birds that had been imported from Australia previously and were used to establish the breeding stock in the aviary. PBFD has been shown to be endemic in wild flocks of psittacine birds in Australia, varying from an incidence of 10% - 20% in histopathologic surveys to an incidence of 41% to 94% in seroprevalence surveys. ^4,5 In the latter survey, the highest incidence of infection was observed in Sulphur-crested Cockatoos. ⁵ Transmission of PBFD is usually via aerosol exposure to PBFDV contaminated feather dander or feces. Because other birds in the breeding center did not exhibit signs of PBFD, the possibility of latent viral infection must be considered. ²

The hematologic changes in PBFD are highly variable, depending on the length and severity of disease and presence or absence of secondary infections. The anemia and mild monocytosis probably are a reflection of chronic viral infection. The incidental finding of pancreatic trematodiasis is unusual in captive birds. However, biliary trematodiasis is observed occasionally in wild caught cockatoos. ^6,7 Perhaps immunosuppression related to PBFD predisposed this bird to development of trematodiasis.

References

1. Ritchie BW, Niagro FD, Lukert PD, Steffens WL, Latimer KS: Characterization of a new virus from cockatoos with psittacine beak and feather disease. Virology 171:83-88, 1989.

2. Ritchie BW: Avian Viruses: Function and Control. Wingers Publishing, Inc. , Lake Worth, FL, 1995, pp. 223-252.

3. Latimer KS, Niagro FD, Campagnoli RP, Ritchie BW, Pesti DA, Steffens WL: Diagnosis of concurrent avian polyomavirus and psittacine beak and feather disease virus infections using DNA probes. J Assoc Avian Vet 7:141-146, 1993.

4. McOrist S, Black DG, Pass DA, Scott PC, Marshall D: Beak and feather dystrophy in wild sulphur-crested cockatoos (Cacatua galerita). J wildlife Dis 20:120-124, 1984.

5. Raidal SR, McElnea CL, Cross GM: Seroprevalence of psittacine beak and feather disease in wild psittacine birds in New South Wales. Aust Vet 70:137-139, 1993.

6. Greiner EC, Ritchie BW: Parasites. In: Ritchie BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Principles and Application. Wingers Publishing Inc. , Lake Worth, FL, 1994, p. 1021.

7. Minsky L, Petrak ML: Diseases of the digestive system. In: Petrak ML (ed): Diseases of Cage and Aviary Birds, 2^nd ed. Philadelphia, Lea & Febiger, 1982, pp. 432-443

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