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Read-Only Case Details Reviewed: Oct 2010
AFIP SYSTEMIC PATHOLOGY

JPC SYSTEMIC PATHOLOGY

INTEGUMENTARY SYSTEM

November 2019

I-V03

 

 

Signalment (JPC# 1851279): 10‑day‑old budgerigar (Melopsittacus undulatus)

 

HISTORY: This bird was from a flock with increased mortality in birds under 15 days of age.

 

SLIDE A:

HISTOPATHOLOGIC DESCRIPTION: Feathered skin: Multifocally, individual and clusters of keratinocytes within the epidermis and feather follicle epithelium are swollen and contain abundant, microvacuolated, pale eosinophilic cytoplasm (hydropic degeneration). Nuclei of these cells are enlarged and often contain variably shaped, up to 20 um diameter, indistinct, pale amphophilic or clear to glassy intranuclear viral inclusion bodies that marginate the chromatin. Diffusely there is moderate orthokeratotic hyperkeratosis.

 

MORPHOLOGIC DIAGNOSIS: Feathered skin, epidermal and follicular epithelium: Hydropic degeneration, multifocal, moderate, with moderate orthokeratotic hyperkeratosis and amphophilic intranuclear viral inclusion bodies, budgerigar, avian.

 

ETIOLOGIC DIAGNOSIS: Polyomaviral dermatitis

 

SLIDE B:

HISTOPATHOLOGIC DESCRIPTION: Kidney: The interstitium is multifocally infiltrated by moderate numbers of lymphocytes, plasma cells, and macrophages admixed with hemorrhage. Multifocally, tubular epithelial cells and glomerular mesangial cells are enlarged with enlarged nuclei that contain round to oval, up to 20 um diameter, indistinct, pale eosinophilic to amphophilic to clear, glassy intranuclear viral inclusion bodies that marginate the chromatin. Multifocally, moderate numbers of tubular epithelial cells are swollen with vacuolated cytoplasm (degenerate) or less frequently are shrunken with hypereosinophilic cytoplasm and pyknotic or karyorrhectic nuclei (necrotic). Tubules occasionally contain sloughed cellular and karyorrhectic debris (cellular or granular cast).

 

MORPHOLOGIC DIAGNOSIS: Kidney: Nephritis, interstitial, lymphohistiocytic, multifocal, mild, chronic, with tubular degeneration and necrosis, and tubular and mesangial cell intranuclear viral inclusion bodies, budgerigar, avian.

 

ETIOLOGIC DIAGNOSIS: Polyomaviral nephritis

 

ETIOLOGY: Avian polyomavirus (APV)

 

CONDITION: Budgerigar fledgling disease (BFD)

 

GENERAL DISCUSSION:

·      Budgerigar fledgling disease virus (BFDV-1) is a non-enveloped, double stranded DNA virus in the family Polyomaviridae

·      In general, polyomaviruses cause latent infections that become apparent following a stressful event

·      APV is highly infectious and causes high mortality especially in budgerigars less than 15 days old, also affects other psittacine birds (the most susceptible psittacines are macaws, conures, eclectus, ring-necked parakeets, lovebirds, and budgerigars), and may infect non-psittacines (finches)

·      Polyomaviruses are antigenically and morphologically similar but show marked differences in clinical presentation, lesion distribution, and epidemiologic effects among susceptible species

 

PATHOGENESIS:

·      Transmission may occur by vertical and horizontal routes

·      Virus replicates at the portal of entrance > viremia > virus distributed throughout the body > May destroy or inhibit development of normal lymphoid tissue

·      Cell mediated immunity, not antibody, is necessary to clear viremia

·      In some species, polyomaviruses are potentially oncogenic

·      Large T-antigen is involved in initiation of viral replication and cellular transformation; cell transformation correlates with binding of large T-antigen to Rb

·      Small T-antigen binds cellular transcription factors

·      Middle T-antigen becomes associated with src proto-oncogene protein product of the plasma membrane, enhancing its tyrosine kinase activity

 

TYPICAL CLINICAL FINDINGS:

Neonatal budgerigars:

·      +/- abdominal distention, subcutaneous hemorrhage, head/neck tremors, ataxia, reduced formation of down and contour feathers; widespread bleeding is often evident terminally

·      Hatchlings that survive infection often have dystrophic feathers (French moult)

Non-budgerigar psittacines:

·      Disease often occurs in outbreaks, often at weaning

·      Depression, anorexia, weight loss, delayed crop emptying, regurgitation, dehydration, subcutaneous hemorrhages, dyspnea, polyuria; death follows in 12 to 48 hours

·      Survivors are considered asymptomatic carriers; virus shedding from cloaca may continue for up to 4.5 months

·      Feather abnormalities are less common in the larger psittacines

·      Occurs in both hand-raised and parent-raised birds

·      Disease in adult psittacines is rare and often associated with PBFD

·      Chronic disease – Birds recover and appear normal, some birds have been found to die later on from renal failure

 

TYPICAL GROSS FINDINGS:

·      Excellent overall condition; full crops and gastrointestinal tracts, indicating acute death

·      Skin lesions: Feather growth and formation abnormalities

·      Other lesions: Pallor and hemorrhages in multiple organs; splenomegaly; hepatomegaly with multifocal necrosis (white pinpoint foci); cardiomegaly and hydropericardium; congested and swollen kidneys

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

·      Karyomegaly, hydropic degenerative changes

·      Intranuclear inclusion bodies that are large, glassy, clear to opaque to mildly basophilic and marginate chromatin

·      Inclusions may be present in the spleen, liver, lung, kidney, heart, brain, skin, feather follicle, intestine, trachea, crop, bursa of Fabricius, and proventriculus

·      Skin: Ballooning degeneration, karyomegaly in epithelium, follicular and epidermal hyperplasia, inclusions (epithelial cells)

·      Kidney: Membranous glomerulopathy; inclusions (mesangial, endothelial and tubular epithelial cells); vacuolar degeneration

·      Spleen: Lymphoid depletion, histiocytosis with inclusions, necrosis

·      Liver: Necrosis, histiocytosis, inclusions (hepatocytes, Kupffer cells), hemorrhage, vacuolar degeneration;

·      Non-budgerigar psittacines frequently have massive hepatocellular necrosis with karyomegalic inclusions

·      Heart: Myocardial degeneration and necrosis, hemorrhage, inclusions (interstitial macrophages, myocytes)

·      GI tract: Hemorrhage, necrosis, inclusions

·      Brain: Inclusions most prominent in cerebellar neuronal and glial cells

 

ULTRASTRUCTURAL FINDINGS:

·      Virions: intranuclear, icosahedral, 40 to 50 nm, arranged in paracrystalline arrays

 

ADDITIONAL DIAGNOSTIC TESTS:

·      PCR – swab of cut surface of spleen, liver, kidney are best samples; cloacal swab

·      Immunohistochemistry with viral specific antibodies

 

DIFFERENTIAL DIAGNOSIS:

Gross

·      Acute death in young birds: Herpesvirus (Pacheco’s disease, D-V13, H-V03), chlamydiosis (Chlamydophila psittaci, D-B12), salmonellosis or other bacterial septicemias

·      Feather lesions in older birds: Psittacine beak and feather disease (PBFD, avian circovirus, I-V04)

 

Microscopic

·      Intranuclear inclusions: Herpesviruses and PBFD may produce amphophilic to basophilic intranuclear inclusions; avian adenoviruses may produce karyomegaly and intranuclear inclusions

·      Hepatic necrosis and splenomegaly: Herpes virus (Pacheco’s disease), chlamydiosis (Chlamydophila psittaci), salmonellosis or other bacterial septicemias

 

COMPARATIVE PATHOLOGY:

Avian polyomaviruses in non-psittacine birds: Lesions suggestive of polyomavirus have been seen in nonpsittacine birds

·      Finches: Acute mortality; affects fledglings, young adults, and mature birds; poor feather development and long, tubular, misshapen beaks

·      Geese: Goose hemorrhagic polyomavirus is the causative agent of hemorrhagic nephritis enteritis of geese, a fatal disease of European geese (Garmyn Avian Diseases 2017)

·      Gouldian finches and other pet birds: Polyomavirus infection caused a syndrome of apathy, diarrhea, high mortality in nestlings; gross lesions included liver enlargement, pulmonary congestion, and urate accretions in the kidney; microscopic findings included Cowdry type B intranuclear inclusion bodies; PCR detected polyomavirus (Circella J Comp Pathol 2017)

 

Polyomaviruses in other species:

·      Polyomaviruses are typically of little or no significance in domestic species

·      Horses: Recent report of polyomavirus-associated nephritis in 2 horses (Jennings Vet Pathol 2013)

·      Rhesus and cynomolgus macaques: Simian virus 40 (SV40) polyomavirus (U-V09); causes nephritis, pneumonia, and neurologic lesions in immunocompromised monkeys (e.g. those infected with simian immunodeficiency virus)

·      Mice:

·      Murine polyomavirus: Multifocal necrosis and inflammation in nude mice followed by tumor formation in multiple tissues; multisystemic wasting disease with paralysis and demyelination also reported in nude mice

·      K-Virus (murine pneumotropic virus or Kilham polyomavirus): Carried as a latent infection in mice; not primarily pneumotropic; when orally inoculated into neonatal mice, initially replicates in intestinal endothelium > disseminates hematogenously to other organs > replicates in vascular endothelium > 6-15 days post-inoculation > pulmonary vascular edema and hemorrhage > dyspnea > death

·      Hamster: Hamster polyomavirus causes transmissible lymphoma in young hamsters and keratinizing skin tumors of hair follicles (trichoepitheliomas); lymphomas do not have detectable infectious virus while trichoepitheliomas do have viral replication in keratinizing epithelium

·      Rabbit: Rabbit kidney vacuolating virus causes intranuclear inclusions in renal tubular epithelium; no known pathogenic effect

·      Raccoon: A novel polyomavirus (raccoon polyomavirus) was identified and may be associated with olfactory tumors in raccoons (Giannitti Vet Pathol 2014)

 

REFERENCES:

1.    Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents and Rabbits. 4th ed. Ames, IA: John Wiley and Sons, Inc. 2016: 19-21, 122, 176-8, 197, 261.

2.    Branson WR, Harrison GJ, Harrison LR. Avian Medicine Principles and Application. Lakeworth, FL: Wingers Publishing, Inc; 1994:885-894.

3.    Circella E, Caroli A, Marino M, et al. Polyomavirus Infection in Gouldian Finches (Erythrura gouldiae) and Other Pet Birds of the Family Estrildidae. J Comp Pathol. 2017;156:436-439.

4.    Garmyn AAB, Verlinden MA, Bosseler LA, Adriaensen C, Martel AA. Persistent Goose Hemorrhagic Polyomavirus Infection on a Belgian Goose Farm. Avian Diseases. 2017; 61:536–538.

5.    Giannitti F, Higgins RJ, Pesavento PA, et al. Temporal and geographic clustering of polyomavirus-associated olfactory tumors in 10 free-ranging raccoons (Procyon lotor). Vet Pathol. 2014;51(4): 832-45.

6.    Guerin JL. Hemorrhagic nephritis enteritis of geese. In: Glisson JR, McDougald LR, Nolan LK, Suarez DL, Venugopal N., eds. Diseases of Poultry. 13th ed. Ames, IA: Wiley Blackwell; 2013; 440-3.

7.    Jennings SH, Wise AG, Nickeleit V, Maes RK, Cianciolo RE, Del Piero F, Law JM, et al. Polyomavirus-associated nephritis in 2 horses. Vet Pathol. 2013; 50(5):769-74.

8.    Jones TC, Hunt RD, King NW. Veterinary Pathology, 6th ed. Baltimore, MD: Williams and Wilkins; 1997: 104-106, 256-257.

9.    Nemeth NM, Gonzalez-Astudillo V, Oesterle PT, Howerth EW. A 5-year retrospective review of avian diseases diagnosed at the Department of Pathology, University of Georgia. J Comp Pathol. 2016; 155(2-3):105-


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