Understanding Avian Ganglioneuritis (PDD)

Cockatoo KrissyUnderstanding Avian Ganglioneuritis (Proventricular Dilatation Disease - PDD) 2017

Jeannine Miesle M.A., M. Ed.

Academic researcher in the field of avian medicine. Member of the Association of Avian Veterinarians (AAV)

The author is indebted to Robert Dahlhausen D.V.M., M.S. for his assistance and advice and for his review and approval of this document.


Much has been written about the Avian Bornavirus (ABV) and Proventricular Dilatation Disease (PDD) in the past, and a significant amount of it is now out-of-date. In an attempt to clarify the nature of this disease and distinguish it from other viruses which can cause the same symptoms, Drs. R. Dahlhausen and S. Orosz have chosen to refer to PDD as Avian Bornaviral Ganglioneuritis (ABG), which better describes the disease and shifts the emphasis on the proventriculus to all the affected organs and systems.4 In this paper, the term, Avian Bornaviral Ganglioneuritis (ABG)  will be used to denote the disease which causes the specific gastrointestinal and neurological symptoms brought on by Avian Bornaviral infection. 

This is complex disease.  ABV has been shown to be one of the causes of PDD. But most birds that test positive for the virus are clinically normal. Also, there are birds with PDD disease that test negative for the virus. The disease involves an immune response that targets the nerve ganglia. It is theorized that other agents, such as viruses and bacteria, can sensitize the immune system, and through molecular mimicry, cause the host’s immune system to react with self- (nerve ganglia) producing disease that is indistinguishable from PDD.  PDD is not an appropriate term for the disease as there are forms that only show disease in the central nervous system; i.e., there is no proventricular dilatation present. Avian ganglioneuritis is a more appropriate term.”

Robert Dahlhausen

Worldwide Distribution and Impact of ABG (PDD)

The disease originally known as “Macaw Wasting Disease” was initially reported in the late 1970’s in the U.S. and Europe. 4 The term, “Proventricular Dilatation Disease” was given to the disease in a 1983 report describing “impaction, dilatation, and degeneration of the proventriculus.”4 Originally thought to affect only macaws, as of 2009, verified cases had been reported in as many as 80 psittacine and non-psittacine species, both captive and wild.4 Since then, the Avian Borna Virus has been proven as the virus responsible for ABG (PDD), and it has been detected in birds around the world.  This disease “now presents a serious threat to both captive propagation and conservation efforts for endangered psittacines such as the Spix macaw.”4 

Defining Avian Ganglioneuritis (PDD)

The Avian Bornavirus (ABV) is an enveloped, negative-stranded, RNA-virus genome. Avian l Ganglioneuritis (PDD) is a fatal, inflammatory wasting disease affecting mostly birds in the psittacine family (Order Psittaciformes). 1 It is a disorder in which "inflammation of the central, peripheral, and autonomic nervous systems is associated with gastrointestinal (GI) dysfunction and neurologic signs." 2 In clinical terms, Avian Bornaviral Ganglioneuritis is "a lymphocytic-plasmacytic gangioneuritis of the nerve plexi of the crop, proventriculus, ventriculus, and duodenum. " 23,2


Macaw suffering from PDD

Figure 1: A macaw suffering from the effects of the Avian Bornaviral Ganglioneuritis (P). Note the poor condition of the beak and feathers and depressed stance. (Courtesy R. Dahlhausen) Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

Etiology and Pathogenesis of ABG/PDD

In the 1970’s, when the huge influx of captive birds from other countries began showing clinical signs of ABG (PDD), researchers suspected a viral cause.2  In 2008, “inclusion bodies and enveloped particles similar to viruses in the myenteric plexus and celiac ganglion of infected birds” were discovered. 20 Dr. Amy Kistler et al. and Dr. Kirsi.S Honkavuori et al., independent researchers, provided confirmation that the cause of ABG is found in the Bornavirus. They are credited with discovering a novel, enveloped, negative-stranded, RNA virus genome and designating it the “Avian Bornavirus.”1,20  The isolated Borna Disease Virus (BDV) genome revealed a high degree of sequence divergence from all prior Bornavirus isolates.”2   With this, Kistler’s group conclusively establishing the connection between the BDV and ABG/PDD through use of Polymerase Chain Reaction (PCR).2

ABG (PDD) had previously been regarded as carrying a high-mortality but low-infection risk. As of a few years ago, it has been shown to occur much more frequently but involve a “low incidence of clinical disease and a much lower incidence of severe disease.” 15 Although the number of ABV-positive, clinically ill birds is growing, new treatment protocols have moved this disease to a more chronic state and one which often responds to treatment. Nevertheless, an infected bird will ever eliminate the viral infection.2

Avian Bornavirus / BeautyOfBirds

Figure 2: The Avian Bornavirus (courtesy R. Dahlhausen) Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

The Parent Disease: Borna Disease Virus

The Borna Disease Virus (BDV) was originally discovered in cavalry horses in Borna,  Germany in 1885. It has since that time become known as a “neurological disease a wide range of animal species and even in humans.” 2, 4

Most viruses spread by cell-to-cell contact, first invading and destroying the host cell, then moving on to infect more cells.20 The Borna Disease Virus, however, uses the nuclear compartment of the host cells, in which infectious BDV ribonucleoprotiens are present, for transcription and replication.“ 20 The Bornavirus does not destroy the cell; therefore, the infected cells suffer very little damage.3 Because the cell is not destroyed, the virus is able to avoid being recognized by the host’s immune system.2,3    This detection-evasion strategy has led to the conclusion that this is an immune-mediated disease. To accomplish this, the virus must suppress apoptosis. The result is continual and lifelong infection. ABG is now known to be an immune-mediated disease.

The effects of Bornaviral Disease and Avian Bornaviral Ganglioneuritis are many. “Manifestations range from fatal meningoencephalitis to subtle behavioral alterations.”2 The animal may even be infected over a long period of time and never exhibit any signs.3 “The virus can remain in the brain, blood, and other body cells for an indeterminate amount of time,” possibly for the lifetime of the individual. The Avian Bornavirus does not grow in mammalian cell lines. Therefore, it does not infect humans or animals. 2

Increasing Infection Rates

Practitioners have been reporting high numbers of birds testing positive for ABV. Even single pet birds housed in the same environment for many years have been diagnosed with the disease.2

Lierz' study revealed an “overall detection rate of 34.3%  for ABV-specific RNA” in the samples taken.3 In a later study of birds living in a stressful shelter situation,  52% tested positive for ABV-specific RNA. 3 And in a screening of birds in another stressful shelter situation in 2012, 71% of the birds tested positive.3

While the number of birds testing positive for ABV is growing, birds seen with clinical signs is much lower. Most birds do not exhibit signs, and those that do show only mild signs. The severe form of the disease resulting in death is a result of on-going, untreated disease. 

The Avian Bornavirus and its Genotypes

A genotype, or subgroup,  refers to the genetic constitution of an individual or a group or class of organisms having the same genetic constitution. As of 2017, the Avian Bornavirus contains a diverse viral group of 15 different genotypes. The number after ABV [e.g., ABV-4, ABV-6], is the number relegated to the individual genotype in order of discovery.6   Viral shedding is intermittent; a sample taken when the virus is not being shed will test negative for the virus.   If the bird is not tested for each specific genotype, the test can result in a false negative. Genotypes 2 and 4 are the ones mostly commonly found in psittacines and therefore are the ones for which most veterinarians test, although sometimes the clinician must expand the testing to other genotypes if his tests results are negative yet he still suspects ABV. (Dahlhausen, personal communication)

Recognition of the virus is dependent upon matching the tests to the specific genogroups, and each genogroup is dominated by a single, distinct protein. A virus can have many sub-groups, depending on the proteins to which they are attached.  Since each genotype is dependent on a particular protein, if the sample were tested for a specific protein and none other, it is possible that the bird could be ABV-positive even if the test results came back negative. 2,4

Detection of Avian Bornaviral Ganglioneuritis (PDD)

Despite the high incidence of viral infection in psittacines, only a small percentage actually exhibit clinical signs and serious disease. Clinical signs vary—all the way from infrequent episodes of mild signs to sudden and severe illness.12 A bird may experience just some of the symptoms, not necessarily all. Some birds become symptomatic years or decades after becoming ABV-infected, and some never show signs at all but may continue to shed the virus and thus infect other birds.4 Healthy birds can experience viremia due to ABV without becoming clinically ill. 2 In fact, most of the ABV-positive birds never display clinical disease.15

Clinicians encounter some challenges when testing for Avian Bornaviral infections. Reasons for this are:

  • Lymphoplasmacytic ganglioneuritis, pathological lesions, or a similar disease state may be caused by another infectious agent. 1,2 Two other viruses have been proven to cause the same ganglioneuritis symptoms as ABV. “Some reported primer sequences used in ABV RT-PCR testing have been shown to also detect paramyxovirus-1, a related virus.” 2  
  • Some psittacine species are more vulnerable to specific genotypes than others.4  
  • The various ABV genotypes may each produce distinctive and specific clinical symptoms.
  • “New mutations may occur in the viral genome that could affect the assay, making it difficult to detect all subtypes.”
  • A bird may be ABV-infected and display signs, but if the results do not match any known genotype, the test results can be negative.
  • “While the virus can be detected in cloacal swabs from both clinically and non-clinically infected birds, cloacal swab samples are not consistently positive in affected birds, possibly due to the high level of RNA enzymes in fecal material that can destroy viral RNA” and inconsistent shedding of the virus.
  • Other destructive factors may be present, like bacteria, enzymes and other contaminants found in the droppings. 4 This results in a high number of false negatives.

(Any relationship between genotype and species infected and/or clinical disease observed remains to be elucidated.  [Dahlhausen, personal communication]).

The bird’s Own System Can Offer Conflicting Test Results:

  • The bird may not be shedding the virus at the time of testing; cloacal swabs are less sensitive because of the intermittent shedding of the virus in some birds.
  • The bird might not be shedding the virus at all because its intestinal tract has not been affected, or the infection might be transient. The result is an inflammatory process that has become latent; this points to ABG as an autoimmune disease.1
  • If a crop biopsy is performed, there is a chance that the sample will not contain the infected ganglions; therefore, it will come back as negative when the bird is actually positive.

Species Affected by ABV Disease


Psittacines appear to be the most affected by the Avian Bornavirus; therefore, almost all of the studies have concentrated on the captive psittacine population. Most psittacine species have been tested, and the species with the highest number of positive results were:  cockatoos, Amazons, eclectus, African greys, and macaws. Quakers and Lovebirds have been minimally represented.4   Those with the lowest number were cockatiels, budgerigars, pionus and conures. 3

Free-ranging Psittacine Species

In research performed by Dirk Enderlein et al. in 2011, more than 80 free-ranging, clinically healthy psittacines were used in the ABV tests. The birds were located in Brazil and belonged to seven different species.7

ABV RNA was discovered using RT-PCR and qPCR. 7 A fourth test, immunofluorescence assay, was involved in the discovery of ABV-specific antibodies. The results revealed that:

  • 33% of the birds tested demonstrated ABV infection by positive qPCR results. ABV genotype-4 was confirmed by the sequencing of PCR products of the positive samples.
  • More than 50% of the birds presented specific anti-ABV antibodies but tested negative when they were subjected to PCR testing.7

The possibility exists that ABV genotypes other than ABV-2 and 4, or as-yet-unknown genotypes were involved. 7

Non-psittacine Species Affected

Avian species other than psittacines are vulnerable to ABV, specifically waterfowl. In 2011, Payne, et al, using the rt-PCR assay tested Mute Swans, Snow Geese, Ross’ Geese, and Greater White-fronted Geese. The ABV was detected in all but the White-fronted Geese. Of the ducks tested, 11% tested positive for the ABV, and 13% of gulls tested positive. The virus also caused neurological symptoms of ABG/PDD in the form of acute encephalitis in geese and swans. A novel ABV genotype was discovered in a Bald Eagle (Haliaeetus leucocephalus) as well, suggesting that raptors could be vulnerable to ABV through predation. 13, 16

Canaries have been found to host ABV. The canaries in Dr. Monica Rinder’s studies contracted ABV by natural means. One canary showed signs of apathy just three days before it succumbed to the virus.13 Death was caused by both encephalitis and non-suppurative ganglioneuritis of the proventriculus. The lesions found in it were similar to the lesions found in the psittacine birds with ABV. 6

A second canary’s illness was chronic and “included prolonged depression, CNS symptoms, and visual impairment with chorioretinitis (ocular inflammation).” 15 Cortical blindness has been observed; however, the bird may regain vision with treatment.15

Other species affected are the greenfinch, long-wattled umbrella bird, the bearded barbet, toucans, honey creepers, reseate spoonbill, and a peregrine falcon. “The disease presents a serious threat to captive propagation and conservation efforts for endangered psittacines such as the Spix macaw.”4

Periods of Vulnerability

Birds may be more vulnerable to viral attack during some periods in their life cycles than others.  Nestlings and immune-compromised birds are particularly susceptible to infection.

Smith and Kistler et al., studying various species of recently hatched psittacines during a sudden surge of ABG (PDD) in the captive flock, tested an Umbrella Cockatoo (Cacatua alba), a Moluccan Cockatoo (Cacatua molaccensis), a Scarlet Macaw (Ara macao), and several Jenday conures (Aratinga jandaya). They determined that ‘unweaned birds were more vulnerable to the ABV-2 infections than the adults. The estimated incubation period was between two and four weeks.” 6

The breeding season often gives rise to new cases and relapses. Avian Bornaviral Ganglioneuritis  cycles from active to dormant states, and the stresses of increased hormonal state depress the immune system, allowing  symptoms to flare up. Clinicians frequently see upsurges in new cases and relapses in ABV and ABG/PDD patients during this time.2 One clinician has treated a patient who had experienced severe relapses of gastrointestinal symptoms during four consecutive breeding seasons.2

Incubation Periods, Triggers, and Relapses

The Avian Bornavirus’ ordinarily long incubation period is shorter for the immune-compromised or very young.16 It can range from several weeks to many years. 2 In a recent, acute outbreak of ABG (PDD) in an avian nursery which houses and hand-feeds multiple species of psittacines, researchers, using controlled infectivity, noted that symptoms appeared in as few as 20 to 31 days.2

In some naturally occurring flocks, ABG (PDD) is described as a “sporadic disease;” the bird may experience bouts with the symptoms for months, even years, after diagnosis. 2 Even single, pet birds, housed in the same environment for many years, have been diagnosed with the disease.

The clinician should not automatically assume a bird is afflicted with ABG (PDD) simply because it tests positive for antibodies against ABV. It might take years before an ABV-positive bird develops signs of ABG/PDD, and some never become symptomatic. It is not known if or when the bird will become symptomatic or what will trigger the onset of symptoms; however, stress is a major factor.6

R. Dahlhausen attributes the development of clinical disease to the following predisposing factors:

  • Genetics, age, the host species involved, and the developmental competency or compromised condition of the host’s immune system.2
  • Stress due to malnutrition, concurrent disease, reproductive activity, and improper husbandry.  Stress is generally accepted as the primary trigger in the activation or recurrence of ABG/PDD, and it will accelerate the spread of the virus.2

Each of the above factors will change the way the bird reacts to the virus, and these signs differ from case to case. Clinical signs vary and are dependent upon the “host species involved, severity of disease, distribution of lesions and affected organ systems involved.” 4

Clinical Signs of ABV Infections

Avian Bornaviral Ganglioneuritis signs are classified as gastrointestinal (GI) or Central Nervous System (CNS) in character.”4 Birds may exhibit only the GI or the CNS signs, but some experience both, and the virus affects both, even if they are not initially obvious. The GI signs indicate pathology of the terminal ganglia of the vagus nerve (Cranial Nerve X), also referred to as the pneumogastric nerve.4

A survey of birds affected by Avian Bornavirus and displaying clinical signs of Avian Bornaviral Ganglioneuritis (PDD) revealed that 66% of birds exhibited CNS signs, 22% experienced GI tract signs, 9% displayed feather picking and mutilation, and 9% suffered acute death.4

The Gastrointestinal Signs of Avian Bornaviral Disease

When the virus attacks the gastrointestinal system’s nerves, inflammation results. 18 It is “an immunologic attack of infiltrating immune cells on the autonomous (involuntary) nervous system of the upper digestive tract.”18 Affected birds are unable to digest and absorb their dietary nutrients properly.

When the GI system's nerve ganglions are invaded by lymphocytes and plasmacytes, the result is symptomatic, persistent infections that result in intestinal colic and ganglioneuritis.2, 23 GI symptoms develop from the “disruption of innervation to one of the cranial nerves of the brainstem—the vagus nerve.” 15 The vagus nerve innervates the upper GI tract—from the crop, proventriculus and ventriculus to the duodenum and the heart. Vagus nerve malfunction disrupts the normal GI motility and results in a thinning of the wall of the GI tract.” 15 This can result in the rupture of the proventriculus and immediate, painful death. Finding the infected nerve ganglions confirms that the individual is positive for ABV disease.15 Other signs include varying degrees of abdominal enlargement, muscular and neurogenic atrophy, weakness, crop stasis, impaired GI tract transit, and polyuria.

The most frequently seen clinical GI signs include depression, anorexia and weight loss (due to poor motility), loss of body condition, regurgitation, passage of undigested food in the feces, poor absorption, polyphagia,  and poor appetite. Crop biopsy and radiographs revealed dilation of the proventriculus.2  Unless treated, this gangioneuritis is always fatal.

In addition, clinicians frequently observe secondary bacterial and fungal infections of the GI tract which must be addressed immediately.21 The vagus nerve also controls the “inflammatory reflex, a neural reflex that controls immune responses and inflammation during GI-tract pathogen invasion and tissue injury.”4 When this reflex is impaired, natural resistance to bacterial overgrowth takes place; this leads to alterations in the intestinal microbiome and overgrowth of pathogenic organisms such as Clostridium perfringens and fungal organisms. 4 Many of the affected birds develop C. perfringens and enteritis due to sluggish GI transit and should be treated appropriately if that sign is present. (Dahlhausen, personal communication)

Undigested Seeds in the Stomach of a PDD Victim (Necropsy)

Figure 3: Necropsy photo of a crop containing undigested foods. Whole seeds can be seen in this picture. (Courtesy R. Dahlhausen)

Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

Enlarged Proventriculus

Figure 4: Necropsy photo of an enlarged proventriculus (top arrow) and ventriculus.

(Courtesy R. Dahlhausen) Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

Enlarged Proventriculus (Avian)

Figures 5 and 6: Necropsy photos showing the displacement of organs caused by dilated proventriculus and ventriculus. The large, pale, center organ (the proventriculus) and the smaller yellowish extension of it (the ventriculus) are displacing the lungs, kidneys, heart, and liver. The second picture is the proventriculus and ventriculus from the same necropsy. (Courtesy R. Dahlhausen)Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

Parrot Wasting Disease

Figure 7: A necropsy photo displaying the wasting effect of the disease in a cockatoo. (Courtesy R. Dahlhausen) Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

The Neurological Signs of Avian Bornaviral Ganglioneuritis (PDD)

Some individuals only display neurological signs of ABV (PDD). However, when ABV assaults the Central Nervous System, it assaults all the nerves, so the bird will still eventually experience damage to the GI tract. These signs simply might not be obvious early in the disease process. 

With neurological signs, inflammation leads to encephalomyelitis.23 As a neurotropic virus, ABV preferentially infects nerve cells, causing inflammation of the nerve ganglions and exposing ganglioside proteins.4 The immune response to these causes nerve dystrophy which leads to clinical disease (Dahlhausen, personal communication).

The neurological symptoms are controlled by the area of the brain which was affected by the invasion of the lymphocytes. Since the lymphocytes determine whether or not the tissue contains the virus, finding lymphocytic ganglioneuritis confirms that the individual is positive for the Avian Bornavirus. 15

CNS lesions are usually found in the cerebrum or cerebellum. Disruptions of the cell layers within the cerebellum produce disorders in fine-muscle movement and equilibrium. The affected bird displays “lack of coordination, ataxia, intention tremors, progressive paresis, paralysis, head tremors, seizures, and motor and proprioceptive deficits (inability to know where it is in space.) 4 Neurological signs also include feather plucking and self-mutilation, difficulty balancing, moaning or crying due to digestive discomfort, aggressive behavior, reduced cognitive ability, dysarthria (vocalization abnormalities) and intermittent head-shaking. 4, 2  The bird may be over reactive to sensory input and to pain. He may also feel pain during touch that ordinarily would not cause pain. 4 The nervous system signs are more difficult to control and more rapidly fatal than GI signs. (Dahlhausen, personal communication)

Feather-picking and self-mutilation have been associated with peripheral neuritis.  The correlation between ABV infections and feather-picking has been established. In one study, 54.4% of feather-plucking birds and 68.4% of neurologically diseased birds tested positive for Avian Bornavirus. 7,8

Self-mutilation and Feather Destruction

Feather Plucking associated with PDD

Figure 8: Neurological signs of self-mutilation. (Courtesy R. Dahlhausen)

 Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

PDD parrot with signs of self-mutilation

Figure 9: Signs of self-mutilation in an African Grey (Courtesy R. Dahlhausen)

Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

Figures 10-18

Cockatoo suffering from PDDCockatoo / PDDCockatoo with PDDCockatoo PDDAfrican Grey / PDDAfrican Grey with PDDCockatiel with PDDMini Macaw with PDDMini Macaw with PDD

These video clips demonstrate cockatoos, an African Grey, cockatiel and macaw experiencing nervous system signs: tremors, ataxia, and agitation.  (Courtesy R. Dahlhausen) Copyright © February, 2016. All rights reserved. Images and videos may not be reproduced or used without the express written consent of the owner.

Other organs affected

The ABV attacks a wide variety of tissues in the body, not only the GI tract and nervous system. The viral RNA has been discovered in the liver, kidney, adrenal glands, heart, and lungs.

Cardiac Impairment (Autonomic Nervous System)

Myocarditis has been reported as a component of ABG (PDD). 2 ABV is known to attack the myocardium (the heart muscle), and clinicians have discovered lesions in heart muscle fibers.23

The right side of the heart contains a high density of nerve tissue, and lesions are more severe on that side. 4 These lesions often result in acute death of seemingly normal birds. 4 Also, the heart is innervated and controlled by the vagus nerve, and the right ventricle is enlarged in affected birds. 4 Arrhythmias and alterations in blood pressure and heart rate have been noted in these birds also. Cardiac lesions are known to result in acute death in birds that appear clinically normal. 4

Ocular Damage

The Avian Bornavirus is also responsible for disorders of the eyes, leading to optic lobe lesions and blindness.4 In studies, birds which were naturally infected with ABV, and were clinically ill with ABG (PDD), experienced lesions within the retina of the eye and decreased visual acuity. 11 Cortical blindness is also found in ABV birds. In this case, the eye is functioning properly, but the nerves between the eye and brain have become infected. In most cases of cortical blindness, the eyes respond to correct treatment.2, 4

Avian Bornaviral Disease as an Auto-immune Disease

The pathogenesis of ABV is the result of an auto-immune reaction.6, 17 The immune system’s failure to recognize and destroy an infectious agent results in fatal disease.” 17 Auto-immune disease is a result of the breakdown of “self-tolerance of the immune system.”17 Different phases of an individual’s life alter the immune system. 17

The leakage of ganglioside proteins from the damaged nerves causes an auto-immune reaction, and the resulting inflammation produces the symptoms of the disease.15 These are regarded as the definitive indicators of the presence of ABV. 6 The virus is triggered by an infection which leads to the production of specific antibodies. These antibodies bind to gangliosides; this leads to immune-mediated damage to peripheral nerves and results in clinical symptoms. 17  The white blood cells are turning on the body, attacking the body’s own nerves. It is this reaction and the inflammation due to the immune system’s attack that leads to the onset of clinical symptoms of ABG (PDD).12


Horizontal Transmission

The Avian Bornavirus is transmitted by the fecal, oral, and nasal routes. 6 Although some clinicians consider the virus to be highly contagious at all times, others believe it is more likely to spread in homes and aviaries in which good hygiene is not practiced. This is now considered a chronic disease; "asymptomatic, long-term survival does not mean that the bird has been cured. The bird will continue to carry and shed the virus even after symptoms cease, and the virus can be detected many weeks after infection.” 2

Since the affected bird is a potential source of transmission to other birds, some clinicians believe it is essential that the affected bird be isolated from others in the flock.2, 21  Others believe that isolation is necessary in a shelter or breeding situation, but in a home, careful hygiene and distance are usually sufficient to prevent infection. For the most part, horizontal transmission is thought to “require long-term, close contact among birds.”4 While other RNA viruses are more stable in the environment, The Avian Bornavirus enzymes degrade rapidly.4 It is now known that the virus only lives 8 hours outside the host. (Dahlhausen, personal communication.) Cleaning with soap and dilute bleach is generally sufficient to disinfect enclosures, bowls, toys, surfaces,  and any items that come in contact with the ABV-positive individual. 4

Vertical transmission, from the hen to the egg, is now considered to be the primary means of ABV transmission.

Vertical transmission

It has been proven that the Avian Bornavirus is passed from hen to egg through vertical transmission. It is now considered to the primary cause of Avian Bornaviral transmission in birds. According to Helga Gerlach, the virus is passed through the vitaline membrane. (Dahlhausen, personal communication.)

ABV-Positive Birds in Collections and the Importance of Screening

Previously considered of little risk in avian collections, the Avian Bornavirus is now considered a major threat to both avicultural and companion birds. As many as 71% of some populations are testing positive for ABV, making management of affected flocks very difficult. 2

Some clinicians believe it is important to rule out other diseases before they screen for ABV infection. However, it is prudent to test for ABV at the same time rather than wait for other test results to come in; this way treatment can begin sooner. Screening allows the clinician to discover the ABV RNA, or serum antibodies, that fight infection by attacking foreign substances, even before the bird demonstrates clinical signs. 6

In the past, screening presented a problem, even in verified ABV cases, due to conflicting test results. But today’s molecular diagnostic tests have removed that difficulty. Screening is vital for "the management of subclinical infections” and for breeding purposes.1 Buyers need to have confidence that their new birds are healthy, and aviary owners need to know that any bird entering or leaving has not tested positive for ABV.


Until just a few years ago, clinicians would base their ABV-ABG (PDD) diagnosis on a "systematic investigation based on serology tests, signs, cytological evidence, and radiography or CT-scan to view the dilated proventriculus.” 2, 6 As a result, clinicians were often unsure of their diagnoses.

Many clinicians wish to explore the differential diagnoses for the ganglioneuritis symptoms the bird is experiencing before diagnosing it as Avian Bornaviral Disease. There are other diseases or conditions which can cause the same gastrointestinal signs as ABV/PDD. These are:

  • Tumors or papillomas of the crop, proventriculus, ventriculus, and intestines. The presence of internal papillomas may lead to a chronic wasting signs similar to ABG (PDD).
  • Ingestion of foreign bodies and Heavy metal poisoning.”4
    Megabacteriosis and Parasitism
  • Inflammatory disease and neoplastic diseases 4

As long as the intestinal tract is distended, the proventriculus and ventriculus will not become fully emptied, and motility will be inhibited. Gastrointestinal stasis will result.4

Other diseases that produce similar CNS signs in birds are:

  • Traumatic injuries, hydrocephalus.4
  • Heavy metal poisoning, neoplasia
  • Viral, bacterial, and fungal infections of the CNS
  • Nutritional deficiencies. 4

ABV (PDD) should be considered as a possible differential diagnosis in any bird with CNS and GI signs. Once a presumptive diagnosis is made based on history, clinical signs and radiographs of the digestive tract, it may be confirmed by the discovery of histopathologic lesions in the bird’s tissues and molecular diagnostic testing.


  • Radiographs and CT-Scans: Radiographs will show the distension of the proventriculus, ventriculus and other GI organs and to determine the time it takes for food to pass through the digestive tract. 
  • Crop Biopsy: Crop biopsies are useful in locating viral infiltrates in the neural tissues. A section of crop and a prominent blood vessel are removed and examined. The presence of lymphoplasmacytic gangioneuritis in the crop tissue is required for a positive result.1 If the sample contains pathological lesions consistent with ABV, the test results will be positive for ABV, even if the bird is asymptomatic. 1 If the biopsy sample does not contain the infected ganglia, the test will be negative, even if the bird is actually positive. False negatives occur at least one-fourth of the time.

One drawback to both radiography and crop biopsy is that they must be performed when the bird is displaying advanced clinical symptoms. In addition, crop biopsy is invasive and can be dangerous; it often results in false negatives and false positives due to inconsistent data. 6

  • ELISA (Enzyme-linked Immunosorbent Assay): This is a serology test which looks for immunological exposure to specific ABV antigens. ELISA is a primary binding test used to detect either antigens (proteins) or antibodies in the blood.  1

New, more accurate testing methods:

  • Molecular Diagnostics: These are genetic DNA tests which will detect shedding of the Avian Bornavirus.1 Direct rt-PCR detects the presence of ABV-specific RNA. 1
  • Anti-ganglioside antibody test. This is a non-invasive serology test which detects the presence and increase of anti-ganglioside antibodies in the blood of parrots. 21

Molecular Diagnostics

With the standard tests, only necropsy findings are definitive, providing proof of nerve destruction in the proventriculus, ventriculus and brain. 2

The field of Molecular Diagnostic Veterinary Pathology specializes in the diagnosis of diseases through examination of molecules within organs, tissues or body fluids. Due to its sensitivity and specificity in detecting nucleic acid targets, PCR is one of the most important tools in molecular diagnostics.2

Identification of the ABV genome has allowed researchers to use PCR genetic analysis in order to identify the virus in tissue samples. This allows practitioners to “detect a broad range of ABV genotypic variants which can be used for a wide spectrum of clinical samples and necropsy materials.”6

The standard tests continue to be performed, but they are now ancillary to the more sophisticated genetic testing. (Dahlhausen, personal communication) Today, identification of ganglioneuritis in the lymphocytes and plasma cells (lymphoplasmacytic ganglioneuritis) provides a definitive diagnosis of ABV.”  2, 4

It is important to note that, while some drugs, including meloxicam, continue to be dispensed to PDD-affected birds, only one, Celebrex, has shown  continual, long-term relief from both gastrointestinal and Central Nervous System signs.

Current Treatment Protocols

Clinicians are unable to stop the progression of Avian Bornaviral Ganglioneuritis, so they attempt to halt the action of the gangliosides in order to calm the inflammation. Cox-2 inhibitors (celecoxib) interrupt the cytokine production and reduce the ganglioside sensitivity. These drugs reduce inflammation and thus diminish the symptoms of ABG/PDD; however, these drugs have diminishing ability to control symptoms over long periods of time. 21 Some birds respond to these medications and some do not, depending on the individual’s immune system and its auto-immune reaction.15

Recommended Formulary

  • Celebrex: Cox-2 inhibitor (celecoxib). Treats gangioneuritis in the central, peripheral, and autonomic nervous systems;  inhibits pain, inflammation,  and peripheral neuritis
  • Robenacoxib: Cox-2 inhibitor, injectable NSAID agent used to treat pain and inflammation from ganglioneuritis
  • Metoclopramide: GI prokinetic agent, for nausea and vomiting, easing digestive discomfort
  • Gabapentin: for self-mutilation, seizures, neurological/neurogenic pain
  • Cisipride: GI prokinetic agent for improving transit in birds with GI tract involvement, particularly early in the course of therapy.
  • Leuprolide acetate and Deslorelin implants: for managing hormonal increases which occur with the onset of breeding activity.

(Specific dosages may be obtained from Carpenter's Exotic Animal Formulary.)


Supplements used to improve the quality of life of affected birds:

  • Antibacterial and antifungal therapy is advised to “control overgrowth of intestinal anerobes, yeasts, and Macrorhabdus.4 GI tract disease alters the intestinal microbiome,so probiotics, prebiotic, and prokinetics may aid in restoring the intestinal environment back to normal.4 They are particularly effective early in the course of therapy.
  • Omega fatty acids are helpful in reducing inflammation
  • Semi-elemental diets, such as Lafeber’s Emeraid Omnivore and Carnivore Critical Care Nutrition, “require minimal digestion and provide a readily absorbable source of essential nutrients and Omega fatty acids.”4
  • Herbal supplements like Silymarin (Milk Thistle), Gaia herbs, and ginger are “helpful in reducing inflammation, preserving hepatic function, and improving GI tract transit.”4 The liver is often affected by the bacteria coming from the abnormal intestinal environment.4

Although some dietary supplements have been used to treat Avian Bornaviral Ganglioneuritis (PDD), none has shown consistent, positive results. (Dahlhausen, personal communication) The addition of the supplements has proven useful in alleviating some of the symptoms, but their benefits decrease over time.

Guidelines for Current Diagnosis of Avian Bornaviral Disease

Recently, G. Dorrenstein has advanced the following recommendations. The avian practitioner is encouraged to consult these guidelines when diagnosing ABV/ABG/PDD:

  • A bird is considered negative for ABV if he is healthy, has had repeated negative blood tests, and has had no contact with any other ABV-positive birds.
  • A bird is considered positive for ABV if he is ill with clinical symptoms of Avian Bornaviral Ganglioneuritis (PDD), has had blood tests which are positive for antibodies against ABV, and the results can be confirmed by PCR.
  • A bird that is ill, and is suspected of having ABV, is considered free of ABV if the serology is negative. He has probably not contracted the disease, and the PCR should validate that.
  • A bird that is clinically healthy, but serologically positive, is considered a carrier of ABV. If repeated PCR testing results are negative, he may be considered “clean.” 6

Avian Bornaviral Disease should be considered as one of the differential diagnoses in any bird displaying gastrointestinal or central nervous system signs.”

R. Dahlhausen

Recommendations to Clinicians

  • Prolonged therapy is advised to prevent future attacks.4
  • Wait before euthanizing a bird in order to give treatment protocols a chance to work.
  • Be careful when choosing the lab for ABV PCR testing and test interpretation due to the inability of some tests to detect all genotypes.2 Also, some labs test at temperatures for dogs and cats and results may be incorrect since birds’ temperatures are not the same as mammals'. (Dahlhausen, personal communication)
  • Screen collections to aid in preventing the spread of ABV in existing flocks and averting future outbreaks of the disease. 6
  • Repeat testing in affected flocks. Testing of apparently negative birds is strongly suggested for the highest reliability in diagnosis of ABV infection.22


Long-term survival does not mean that the bird has been cured. It still carries the virus and is a potential source of transmission to other birds. 2 The owner is advised to:

  • Avoid overcrowding.
  • Pay attention to hygiene. This is particularly important for owners who keep multiple birds. Scrupulous, constant attention must be paid to cleanliness.
  • Immediately remove feces and dust and disinfect all inanimate objects with which the bird has come in contact. This is vital in the prevention of the spread of the disease. 22
  • Clean inanimate surfaces, such as toys and food/water dishes, frequently, to avert transmission through fomites.
  • Take proper precautions to clean any exposed skin (particularly the hands and arms) and change clothing after handling the affected bird.
  • Keep the aviary or home adequately ventilated.
  • Provide superior nutrition and clean water.
  • Avoid stressful conditions, particularly in aviary collections and in shelters.
  • Do not smoke around the bird. Second-hand smoke and the use of other tobacco products inhibit the immune system. Smokers should not handle the bird unless they have cleansed their arms and hands thoroughly and changed clothing; the toxins on the skin can cause pododermatitis and lesions on the legs and skin.
  • Isolate or remove any ABG/PDD-exposed, ABV-positive birds from the rest of the population in high-density situations, and separate them in home environments.2
  • Do not wait to euthanize until the bird is nearly dead. The proventriculus can rupture, causing a quick but extremely painful death.


Clinicians, informed breeders, and bird owners are capable of curbing the spread of Avian Bornaviral Ganglioneuritis by closely monitoring their flocks and preventing the reproduction of ABV-positive birds. Through screening and treatment protocols, affected birds may have extended longevity and considerably enhanced quality of life.

Anyone wishing to obtain and more technical, complete version of this paper, including studies, ganglioside involvement, cytokine storms, viral invasion,  transmission, continuing research, and glossary, may contact the author: Miesle.jeannine@gmail.com.


1 Clubb S, de Kloet S. A Comparison of Crop Biopsy, Serology, and PCR for Diagnosis of Subclinical Proventricular Dilation Disease. Proc Annu Conf Assoc Avian Vet. 2009:3-9.

2 Dahlhausen R. Avian Bornavirus and Proventricular Dilatation Disease. Proc Annu Conf Assoc Avian Vet. 2010

3 Dahlhausen R, Orosz S.  Avian Bornavirus Infection Rates in Domestic Psittacine Birds.  Proc Annu Conf Assoc Avian Vet. 2010: 13-15

4 Dahlhausen R, Orosz S.  Avian Bornaviral Ganglioneuritis in Clinical Practice. Proc Annu Conf Assoc Avian Vet. ExoticsCon, 2015

5 De Kloet AH, Kerski A, de Kloet SR. Diagnosis of Avian Bornavirus Infection in Psittaciformes by Serum Antibody Detection and Reverse Transcription Polymerase Chain Reaction Assay Using Feather Calami.  In: Journal of Veterinary Diagnostic Investigation. 2011 May: 23(3): 421-9. Source: Animal Genetics, Inc.

6 Dorrestein G. Avian Bornavirus, the Most Likely Cause for Inducing Proventricular Dilatation Disease (PDD) in Parrots, A Review.  Diagnostic Pathologic Laboratory, Veldhoven, The Netherlands. Poultry Conference at the Wroclaw University of Environmental and Life Sciences, July 11-22, 2011.

7 Enderline D, et al. Avian Bornavirus Infections in Free-Ranging Psittacines (abstract). In: Proc Int. Conf on Avian, Herpetological and Exotic Mammal Medicine: 349-350 Giessen, Germany. April, 2013.

8 Fluck A, et al. Avian Bornavirus infection in Psittacine Birds with Neurological Signs and Feather Plucking (abstract). In: Proc Int. Conf on Avian, Herpetological and Exotic Mammal Medicine. 2013:388

9 Gray P, Jianhua, G, Shivaprasad B, Tizard I. Use of Antiviral Drugs for Treatment of Avian Bornavirus Infection (abstract).  Proc Annu Conf Assoc Avian Vet. 2010:19

10 Hoppes S, et al. Treatment of Avian Bornavirus-infected Cockatiels with Oral Meloxicam and Cyclosporine (abstract).  Proc Annu Conf Assoc Avian Vet. 2012:27

11 Korbel R, Rinder M. Ocular Findings in Psittacine Birds Infected with Avian Bornavirus (ABV) (abstract). Oberschleissheim, Germany. Proc Annu Conf Assoc Avian Vet. 2012:21

12 Lierz M, et al. Do We Understand Avian Bornavirus in Psittacines? (Abstract) Proc Annu Conf Assoc Avian Vet. 2011:19

13 Lierz M, et al. Vertical Transmission of ABV in Psittacines (letter). Emerg Infectious Diseases (serial on the internet). 2011 Dec, Vol 17, No. 12.

14 Monaco E, Hoppes S, Jianhua, G, Tizard I. Egg Transmission of Avian Bornavirus (abstract). Proc Annu Conf Assoc Avian Vet. 2012:303

15 Orosz S. Unraveling the Puzzle of Avian Bornavirus and PDD. In: Avian Medicine. LafeberCares.com. Posted on Sept. 24, 2012

16 Payne S, et al. Presence and Impact of Avian Bornaviruses in Waterfowl (abstract). Proc Annu Conf Assoc Avian Vet. 2012:323

17 Pendl H, Speer, B. Immune-mediated Disease in Avian Species: Hypersensitivity and Autoimmune Disease. Proc Annu Conf Assoc Avian Vet. 2012:169-179

18 Rinder M, Kronthaler F, Hufen H, Korbel R. Avian Bornavirus Infections in Canaries (Serinus canaria) (abstract). Proc Annu Conf Assoc Avian Vet.  2012:331

19 Smith. J. Unusual Outbreak of PDD in a Psittacine Nursery.  Proc Annu Conf Assoc Avian Vet. 2009:12-13

20 Staeheli, Rinder M, Kaspera B. Avian Bornavirus Associated with Fatal Disease in Psittacine Birds. In: Journal of Virology: 2010 July: 84 (13) 6269-6275. www.ncbi.nlm.nih.gov/pmc/articles/PMC2903261/

21 Waugh D. Innovative Research to Treat Proventricular Dilatation Disease in Parrots. Avian Biotech International, Avian Disease Center. Avianbiotech.com.

22 Waugh D. Occurrence of Avian Bornavirus Infection in Captive Psittacines in Various European Countries and its association with Proventricular Dilatation Disease. Avian Pathol. 40 (4) 419-26, 2011.

23 Weissenbock H, et al, Avian Bornaviruses in Psittacine Birds from Europe and Australia with Proventricular Dilatation Disease. In: Emerging Infectious Diseases (serial on the Internet), Vol. 15, #9, Sept 2009/ Available from http://wwwnc.cdc.gov/eid/article/15/9/09-0353_article.htm

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