Avian Orthobornavirus Study Guide

Overview and Clinical Importance

Avian orthobornaviruses are neurotropic RNA viruses belonging to the family Bornaviridae within the order Mononegavirales. These viruses are the causative agents of Proventricular Dilatation Disease (PDD), also known as macaw wasting disease, avian ganglioneuritis, or neuropathic gastric dilatation. PDD is a chronic, progressive, and often fatal neurological disease that primarily affects psittacine birds (parrots) worldwide.

First recognized in the late 1970s in imported macaws in the United States and Germany, the causative agent remained unknown for three decades until 2008, when two independent research groups identified avian bornavirus through advanced molecular techniques. PDD has since been reported in more than 80 species of psittacine birds across all continents, representing a significant threat to captive breeding programs, zoological collections, and endangered species conservation efforts.

Etiology and Taxonomy

Viral Classification

Avian bornaviruses are enveloped, non-segmented, single-stranded negative-sense RNA viruses. Following taxonomic revisions, the original term "avian bornavirus" has been replaced by specific virus names classified into distinct viral species within the genus Orthobornavirus.

Parrot Bornavirus Genotypes and Classification

Epidemiology

Species Susceptibility

PDD has been reported in more than 80 species of psittacine birds. The disease occurs worldwide in captive populations and represents a significant threat to endangered species conservation programs. The following species are most commonly affected:

• Macaws (Ara spp.) - Originally most affected; includes Blue-and-gold, Scarlet, Green-winged, and Military macaws
• African Grey Parrots (Psittacus erithacus) - Highly susceptible; commonly affected
• Cockatoos (Cacatua spp.) - Including Umbrella, Moluccan, and Sulphur-crested
• Amazon Parrots (Amazona spp.) - Various species affected
• Conures (Aratinga, Pyrrhura spp.) - Sun conures, Green-cheeked conures commonly affected
• Cockatiels (Nymphicus hollandicus) - Commonly used in experimental studies
• Lovebirds (Agapornis spp.) - Susceptible but less commonly reported

Transmission

The exact mode of transmission remains incompletely understood. Current evidence suggests:

• Fecal-oral route: Most likely primary route; virus shed intermittently in feces and urine
• Vertical transmission: Documented through infected eggs; viral RNA detected in embryos
• Respiratory secretions: Possible aerosol transmission
• Direct contact: Inefficient in immunocompetent adult birds

Pathophysiology

PDD is fundamentally a neurological disease despite its gastrointestinal manifestations. The pathogenesis involves:

• Viral entry and neurotropism: Bornavirus replicates in the nucleus of infected cells, establishing persistent, non-cytolytic infection primarily targeting neurons
• Immune-mediated damage: Lymphoplasmacytic infiltration of ganglia and nerves; T-lymphocytes and macrophages predominate in lesions
• Ganglioneuritis: Inflammation of autonomic ganglia, particularly the myenteric plexus of the GI tract
• GI dysfunction: Loss of intestinal motility leads to proventricular dilatation, crop stasis, and maldigestion
• CNS involvement: Non-suppurative encephalomyelitis with perivascular cuffing, particularly in thalamus and hindbrain

Clinical Signs

Clinical presentation is highly variable and can be categorized into gastrointestinal and neurological forms, though overlap is common. The average age at presentation is approximately 3-4 years, though birds of any age can be affected.

Exam Focus: The classic clinical triad for PDD includes: (1) Passage of undigested seeds in feces, (2) Progressive weight loss despite normal or increased appetite, and (3) Regurgitation. However, remember that neurological signs may occur WITHOUT gastrointestinal involvement, and sudden death from cardiac ganglioneuritis can occur.

Diagnosis

Antemortem Diagnostic Approaches

Diagnostic Imaging

Radiography: Survey and contrast radiographs are valuable initial screening tools.

• Moderately to markedly dilated proventriculus containing ingesta and gas
• Proventriculus extends beyond the liver edge
• Proventricular diameter-to-keel height ratio greater than 0.52 suggests dilatation
• Barium contrast studies may show delayed GI transit time (normal: 90 min to 3 hours to cloaca)

Laboratory Diagnostics

Postmortem Diagnosis

Gross Pathology

• Dilated, thin-walled proventriculus (present in approximately 70% of cases) - often translucent with visible seeds through wall
• Emaciation and pectoral muscle atrophy
• Possible crop, ventriculus, and intestinal dilatation
• Proventricular rupture with peritonitis (severe cases)
• Enlarged adrenal glands
• Cardiomegaly (cardiac cases)

Histopathology

Pathognomonic lesion: Lymphoplasmacytic infiltration of ganglia and nerves throughout the peripheral and central nervous system.

• PNS lesions: Myenteric ganglia of crop, proventriculus, ventriculus, intestine; epicardial ganglia; celiac ganglion; adrenal gland
• CNS lesions: Non-suppurative encephalomyelitis with perivascular cuffing (primarily lymphocytes, plasma cells, macrophages); thalamus and hindbrain most commonly affected
• Immunohistochemistry: Intranuclear (and intracytoplasmic) staining of neurons with anti-PaBV antibodies confirms diagnosis

Differential Diagnoses

Treatment and Management

There is no curative treatment for PDD. Once clinical signs develop, the disease is generally fatal. Treatment is palliative and supportive, aimed at managing clinical signs and maintaining quality of life.

Prognosis

• Guarded to grave once clinical signs develop
• Disease is progressive and generally fatal
• Some birds survive months to years with supportive care
• Positive ABV test is NOT a death sentence: Many infected birds never develop clinical disease
• One report documented spontaneous apparent resolution in a flock of cockatiels

Prevention and Control

• Quarantine: All new birds should be isolated and tested (RT-PCR and serology) before introduction; minimum 90 days recommended
• Serial testing: Due to intermittent shedding, test at least 3 times at monthly intervals
• Biosecurity: Strict hygiene; separate housing for positive birds; avoid overcrowding
• Isolation: PDD-positive birds should be separated for life to prevent transmission
• Necropsy: Perform diagnostic necropsy on all birds dying of unknown causes
• No vaccine available: Experimental MVA-based vaccines show promise but are not commercially available

PDD = 'Parrots Dining Desperately'

• Proventriculus dilated with undigested seeds
• Diagnosis requires histopathology (lymphoplasmacytic ganglioneuritis)
• Deadly once clinical signs develop (no cure)

ABV Testing: 'Test THREE Times to Be FREE'

Due to intermittent shedding, three negative RT-PCR tests at monthly intervals are needed to declare a bird negative.

Species Most Affected: 'MAC-CAGE'

• Macaws
• African Grey parrots
• Cockatoos and Cockatiels
• Amazon parrots
• Green-cheeked conures
• Eclectus parrots