Proventricular Dilation Disease Review: Literature and Research Review, Species Differences, Diagnostics, Prognosis, and Treatment
Presenting Author: James Boutette,DVM and Michael Taylor, DVM
University of Guelph, Ontario Veterinary College, ON, Canada, University of Pennsylvania, PA
Interpretive Review and comments by Dr. Nemetz:
Dr. Boutette and Dr. Taylor first presented an overview of this devastating disease then followed with a more detailed literature review, presentation of the disease, diagnostic tests, and prognosis. Generally, Proventricular Dilation Disease (PDD) or otherwise known as "macaw wasting disease" or more properly histologically described as lymphocytic plasmocytic ganglioneuritis is strongly suspected to be an infectious disease. It was first reported in imported macaws in the 1970s. Now it has been diagnosed in most species of Psittacine birds and generally is a progressive, fatal disease. Early detection is very difficult but crop biopsies of a nerve complex have been very rewarding as an earlier diagnostic procedure. Only supportive care has been available until the last few years when newer non-steroidal anti-inflammatory agents have shown some promise.
Even thought PDD was first reported in the 1970s, not much information became available until the early 1980's. Only 20 years ago it was reported in macaws, an African grey parrot, a conure and cockatoos. Primary symptoms included sudden onset of severe depression, anorexia, weight loss, vomiting/regurgitation, and abnormal droppings. Increased urination and loose stools with decreased quantity was also seen in the presentation. Most of these first cases were imported and recently purchased indicating stress has a factor in the onset of symptoms.
By the late 1980's, a viral cause was being more strongly suggested based upon the finding of inclusion bodies in some sections of affected nerves. In 1986, german researchers reported "viral-like" particles similar to paramyxovirus (see conclusion) in nerve cells of the myenteric plexus of cockatoos diagnosed with PDD.
Statistics started to be performed in the early 1990's. One paper of 127 cases demonstrated 43% were macaws, 21% were cockatoos, 12% were conures, 18% were African Grey Parrots, and the rest represented other mixed species of parrots. By now classic and atypical cases were being described along with acute and chronic presentations.
In 1994, crop biopsy for the diagnosis of PDD showed a 68% correlation but Dr. Nemetz believes today it is higher due to better surgical techniques at nerve recovery.
In 1997 a similar presentation arose in Florida and was confirmed to be a togavirus but determined NOT to be the causative agent of PDD but could cause similar histological findings in young psittacines.
In 2002, the use of NSAIDs (non-steroidal anti-inflammatory drugs) such as Celebrex (celecoxib) and more recently Metacam (Meloxicam) have shown variable success in the treatment of PDD.
Recent work in 2004 was able to experimentally infect birds from tissue homogenates prepared from a bird with naturally acquired PDD. 80-nm, enveloped viral particles were recovered from the tissues and feces of both naturally and experimentally infected birds. This study again demonstrated the variability of the incubation and clinical presentation and its viral origin. The characterization of the virus appears promising, but as of yet has not been identified or its direct causative relationship to PDD.
Peripheral nerve inflammation has been shown in some cases as the only presenting signs. The sciatic nerve of the legs and the brachial nerves of the wing were shown to be affected.
The presentation of this disease is viable and sporadic dependent on the area of the nervous system affected, the species of bird, the age at infection, and the level of stress the bird is exposed to in its environment.
The diagnostic challenge in this disease presentation is first ruling out other disease processes that mimic many of the symptoms presented with PDD cases. Complete blood panels, radiographs (plain and contrast), when possible contrast fluoroscopy, rule out fungal or bacterial enteropathies, heavy metal toxicosis, cancer, and other causes of physical obstruction. After other disease processes are ruled out, crop biopsy is the best first attempt to identify the disease process without invading the abdominal cavity.
Before earlier detection techniques and better recognition of this serious disease, prognosis was very poor. Today with proper COX-2 specific NSAID therapy, many birds seem to be responding favorably; however elimination of the disease in treated birds has not been proven. The author's experience indicates long-term, possibly life-long NSAID therapy may be indicated.
Prevention of new cases remains the key to preventing the spread of this disease. Chronically infected birds must be identified and removed from aviaries and effective hygiene protocols implemented. Techniques to prevent the spread of fresh fecal material have been effective in reducing the spread of PDD. Even though some treated birds may recover, there is no well documented evidence to suggest that they do not continue to serve as a source for new infections.
Dosage of Celebrex has been reported at 10mg/kg PO q12-24hr. Metacam has been used at 0.3 -0.8 mg/kg PO q 12hr.
It is not uncommon to see relapses during the treatment process.
Dr. Boutette and Dr. Taylor did an excellent job explaining the history, clinical signs, diagnosis, possible treatment, and the implication to our psittacine population in regards to PDD.
Dr. Nemetz agrees with these authors and has his own thoughts regarding PDD:
1. A viral cause will eventually be identified and typed. Dr. Nemetz believes it will be in the paramyxovirus family, perhaps type III.
2. Infected birds are permanently infected and treatments only prolong the disease process.
3. Infected birds are a source of viral infection for other birds in the home and should be isolated.
4. If a paramyxovirus is identified as the definitive agent, a vaccine to protect non-infected birds will be possible.