Proventricular Dilatation Disease

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Proventricular Dilatation Disease is a disease affecting psittacines (Parrots). It was first recognized and described in 1978 by Dr. Hannis L. Stoddard. Since the first reported cases were involving species of Macaw, the condition was termed Macaw Wasting Syndrome.


The clinical presentation of this disease varies with the individual as well as in severity of those symptoms. Often the symptoms include a gastrointestinal component, but many times birds suffering from this disease will present with neurologic signs as well, or in lieu of digestive anomalies.

Gastrointestinal signs may include: Regurgitation, crop impaction, poor appetite, weight loss, or passage of undigested food in the feces.[1] Neurologic symptoms may include: Weakness, ataxia, paresis, proprioceptive deficiets, head tremors, and rarely seizures.[1] Muscle wasting and a generalized poor body condition is usually found as well. The virus can also affect the Purkinje cells of the heart, the adrenal medulla, the brain, and the spinal cord.

On necropsy the affected organs appear dilated and may include the crop, proventriculus, ventriculus, and small intestine. On histopathological examination the tissues will contain a lymphoplasmacytic infiltration in the peripheral and central nervous tissue. The causative virus is believed to commonly affect the myenteric plexuses which will also lead to the presentation of atrophied smooth muscle within the affected gastrointestinal organs.[1] It is this atrophy and loss of tone in the organs that causes the dilation and subsequent gastrointestinal symptoms which are commonly the first sign of disease for the owners.


In July 2008, a team of researchers at the University of California, San Francisco was able to identify the virus that may cause PDD, which they have named Avian Bornavirus (ABV).[2] A member of the bornavirus family, Avian Bornavirus was isolated in 71 percent of samples from infected birds, but in none of the healthy birds. The researchers were able to clone a full-length genome of the virus from avian tissue, and analysis of that tissue revealed that there are at least 5 distinct varieties of the avian virus - not all of them cause PDD. This virus was also identified by Honkavuori et al.[3] in multiple cases of PDD. Gancz et al. succeeded in inducing PDD in cockatiels by inoculation of brain tissue from ABV positive birds [4] while Gray et al. caused PDD in Patagonian conures by inoculation of a tissue-culture derived isolate of Avian Bornavirus.[5] Interestingly despite many reports Avian Bornavirus should not be stated as the cause of PDD.

Avian Bornaviruses (ABV), a group of related viruses, have recently been reported, yet not proven, as the cause of Proventricular Dilatation Disease, PDD, a disease of pet parrots. The use of a 'positive' brain cell culture containing ABV to inoculate another psittacine (parrot) bird resulted in the inoculated bird's death and subsequent histopathological diagnosis of PDD (mononuclear infiltrative ganglioneuritis. Interestingly earlier research with purified inoculant of ABV(while did result in the death of parrots) did not reproduce histopathological changes associated with PDD.

Sadly, there have been several parrots tested positive for ABV without clinical signs of PDD that were prematurely euthanized and revealed no such histopathological tissue changes. Additionally some parrots with clinical signs of PDD have been tested negative for ABV and have later died within weeks of testing. These parrots that had clinical signs of PDD, that tested negative for ABV, were then subsequently diagnosed with PDD on histopathology. In summary Avian Bornavirus should not be referred to the cause of Proventricultar Dilation Disease in psittacines, it is of questionable value to test any psittacine bird for ABV, and the only definitive diagnosis of a live parrot for PDD is a crop biopsy with histopathology. Of great importance is that any parrot tested positive for ABV should be retested 90 days later, and persistently ABV positive parrots should be considered as immunocompromised. PDD is one yet not the only such disease possibly associated with an immunocompromised state.

Thankfully, many parrots with signs of PDD have made apparently full recovery with the veterinary use of non-steroidal anti-inflammatory drugs (NSAID's), yet should be considered a potential infective source of PDD for other parrots.


Traditional diagnosis included radiographs. The vet may ask for a follow up radiograph with a barium marker to collect more data on digestion to aid in confirmation of PDD. A tissue sample is a more reliable method as well but invasive yet the only definitive diagnosis with live parrots.

The presence of Avian Bornavirus may be detected in two ways. Testing fecal samples, choanal swabs and blood for the presence of the virus or examining the bird's blood for ABV-specific antibodies by western blot or ELISA. All tests give a percentage of false positives and false negatives at this time so detection of ABV or antibody against it does not mean that PDD will follow. The disease does not follow a clear path of development or transmission.


  1. ^ a b c Harrison, and Lightfoot. 2006 Clinical Avian Medicine. Spix Publishing, Palm Beach, Florida.
  2. ^ Kristen Bole (2008-07-29). "UCSF researchers identify virus behind mysterious parrot disease". UCSF News Office. Retrieved 2008-07-31. 
  3. ^ Honkavuori, K.S., Shivaprasad, H.L., Williams, B.L., Quan, P.L., Hornig, M., Street, C., Palacios, G., Hutchison, S.K., Franca, M., Egholm, M., Briese, T. and Lipkin, W.I. (2008) Novel borna virus in psittacine birds with proventricular dilatation disease. Emerging infectious diseases 14(12), 1883-6.e
  4. ^ Gancz, A.Y., Kistler, A.L., Greninger, A.L., Farnoushi, Y., Mechani, S., Perl, S., Berkowitz, A., Perez, N., Clubb, S., DeRisi, J.L., Ganem, D. and Lublin, A. (2009) Experimental induction of proventricular dilatation disease in cockatiels (Nymphicus hollandicus) inoculated with brain homogenates containing avian bornavirus 4. Virology journal 6, 100.e
  5. ^ Gray et al. Emerging Infectious Diseases, March 2010

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