Evaluation of Parent to Offspring Transmission of PDD in Companion Birds
Presenting Author: Branson Ritchie, DVM, PhD, Dipl ABVP, Dipl ECAMS
Emerging Diseases Research Group, University of Georgia , College of Veterinary Medicine , Athens , GA
Interpretive Review and comments by Dr. Nemetz:
Proventricular dilatation disease (PDD), now termed Lymphoplasmacytic Ganglioneuritis, used to describe an inflammatory response characterized by the accumulation of lymphocytes and plasma cells in the central and peripheral nervous systems, especially the nerves that supply the muscles of the digestive organs (GI). We presently know that he disease is really segmental and may present with only gastrointestinal signs, central nervous system signs, peripheral nervous signs, or any combination.
PDD was first discussed in the late 1970's in birds imported to the United States and Germany . Many etiologies have been proposed, but to date none have been proven. Most of the evidence suggests a viral etiology with a paramyxovirus having the most support. Diagnosis is still difficult as signs can be very subtle. A presumptive diagnosis is based on historical information, clinical signs, and radiographic evidence of GI dilatation or dysfunction. However, the presence of characteristic histologic lesions (lymphoplasmacytic ganglioneuritits) in nervous tissues is necessary for a definitive diagnosis. For a diagnosis when the bird is still alive (antemortem), crop biopsies are the easiest diagnostic procedure for a qualified veterinarian to perform and in two studies had a 68-76% sensitivity in diagnosing PDD. Thus a positive diagnostic crop biopsy that includes at least one large blood vessel and its associated ganglia is suggestive of disease, but a negative crop biopsy does not rule out PDD.
Dr. Ritchie studied some breeding pairs of cockatiels where at least one individual was histologically positive for PDD. Results confirmed that some birds can be in direct contact with PDD-positive birds for prolonged periods (years) without developing disease, diseased adults can produce clinically normal offspring, chicks produced by positive parents are susceptible to disease, any immunity passed from the hen to her chicks is only transient, and the period from exposure to the suspected PDD agent to the development of overt clinical signs can be more than a year.
Individuals without clinical symptoms but diagnosed microscopically with PDD lesions should be considered at extra risk of developing disease, be isolated, but not euthanized. Birds with clinical signs that are to be treated should be placed in strict isolation.
Conclusion:
Proventricular Dilatation Disease (PDD) or Lymphoplasmacytic ganglioneuritits continues to perplex researchers, but helpful information continues to be brought to the avian veterinary community from researchers such as Dr. Ritchie. With this new information added to what we have learned in the past, I have the following predictions, comments, and recommendations:
1. Eventually a paramyxovirus, probably PMV-3, will be proven as the etiologic agent.
2. Because of its variable clinical course and pathogenicity, despite excellent hygiene, valid quarantine procedures, and the absence of new additions to the flock, PDD will continue to be a risk to all avian species until an etiologic agent is confirmed, an antemortem serologic diagnostic test developed, and a vaccine produced.
3. Avian patients presented with GI dysfunction, dilatation shown on radiographs, or peripheral neuropathies that are non-responsive to medical therapy justify a diagnostic crop biopsy.
4. PDD can be a devastating disease for the patient as well as the owner. The diagnostic work up can be frustrating and expensive, but have some comfort that many researchers are working to identify and classify the true etiologic agent. There are new medications to help afflicted patients have a better quality of life. However, I presently DO NOT believe we are curing the disease process, but only mitigating the clinical symptoms and possibly creating asymptomatic carriers. 2008: Presented at the AAV conference there is new support for a Bornavirus as the cause of this disease. It fits many of the characteristics of this disease but as of yet has not been proven convincely to be the true etiologic virus. Several papers will be presented at the August 2009 annual conference on further research.