Proventricular Dilatation Disease (PDD)

Proventricular Dilatation Disease, or PDD, is a disorder of the central nervous system and a fatal viral disease that currently affects 50 different species of domesticated and wild psittacine parrots as well as 5 other Orders of birds. PDD was previously known as “macaw wasting syndrome” when it was mistakenly thought to infect only macaws. The Spix’s macaw, whose current population is estimated at 100 live birds, is currently one of the most endangered species of birds in the world, with its very existence being threatened by PDD.

Clinically affected parrots may exhibit abnormal behavior, show ataxia (i.e. off balance and wobbly) progressing to paralysis, or will slowly starve to death. The area of the proventriculus (the cranial part of the stomach which secretes gastric juice) is particularly sensitive to damage, causing paralysis. That area of the abdomen becomes visibly bloated. The virus also affects the ventriculus, or gizzard, which is the portion of the digestive tract responsible for grinding their food. Since the bird will be unable to digest and absorb food, infected birds will often regurgitate, pass undigested seeds, and show signs of wasting, such as loss of weight and muscle. These birds become lethargic and weak. Diarrhea, scant feces, polyuria (increase in urination), and hypotension have all been seen clinically. Neurological signs of disease may also include abnormal head movements, seizures, and motor deficits. Secondary infections, either bacterial or fungal, may develop as the bird grows weaker.

The symptoms of PDD are actually caused by inflammation to both central and/or peripheral nerve tissue. The pathology is caused by the migration of inflammatory cells, primarily lymphocytes and plasma cells, into local nerve ganglia of the proventriculus and other portions of the digestive tract. Alternatively the virus may directly invade the central nervous system infecting the brain and spinal cord with or without local involvement.

Any age bird may be infected with PDD. Although adults are more commonly found to be infected by a ratio of 3-to-1, young birds are more severely affected. There is no sexual preference, with both sexes being equally infected.

Not all birds exposed to the virus develop clinical disease. It is proposed that some individuals have an innate resistance, develop a protective immune response, become carriers of the virus or lack certain factors necessary for inducing clinical disease.

Clinical signs of disease typically develop within weeks of exposure. The majority of infected birds will die within several months to a year following the development of clinical signs due to starvation.

Blood chemistry results are often inconsistent but may include the following: hypoproteinemia (low blood protein levels), hypoglycemia (low blood glucose levels), heterophilia (an increase in the heterophil count), and anemia. The enzyme creatinine phosphokinase may also be elevated and is an indication of nerve tissue damage.

Recently, several groups of researchers have independently identified the cause of PDD to be a virus currently named “Avian Bornavirus”, or ABV. This viral family is also responsible for encephalitis found in horses and other livestock species.

The virus is spread through fecal material. By nature, these parrots are social and tend to frequent the same areas; therefore, the virus is highly contagious.

Researchers at Texas A&M University have developed a test for the detection of antibodies to the PDD virus. The test is currently exhibiting a specificity of about 90%. Until the antibody test was developed, PDD could only be confirmed by crop biopsy, which is invasive, can give rise to complications, and only has an accuracy of 60% in confirming a PDD diagnosis. Crop biopsies can also show false positive results, causing the unnecessary euthanasia of these magnificent birds. The test is currently being offered to the public only through Texas A&M University.

Necropsy results seen as a result of PDD include emaciation, atrophy of the pectoral muscles, and dilatation of the esophagus, proventriculus, ventriculus, or small intestinal tract. The proventriculus may also appear thin-walled and is easily torn.

Most birds suffering from PDD are euthanized. Since PDD results in inflammation of nerve tissue, anti-inflammatory drugs have been used to alleviate symptoms.    Affected birds will often respond favorably to drugs such as Celebrex (celocoxib) or Metacam (meloxicam) which are COX-2 inhibitors often used in the treatment of arthritis. Texas A&M is currently researching the efficacy of the antiviral drug Amantadine that is often used for Parkinson’s disease on infected parrots and its effect on the shedding of virus in fecal material. Amantadine has been extremely useful in treating birds that exhibit central nervous system signs such as seizures and ataxia. Affected birds may show signs of recovery with treatment, but the effects of treatment on viral shedding are currently unknown. Infected birds should be housed separately from any other susceptible birds until tests are available to determine recovery and the effect on viral shedding.
 

References:

Clubb, Susan. “Fighting PDD in Birds.” Pet Age. September 2009. Pp. 56-59.

King, A.S., and J. McLelland. Birds their Structure and Function. Bailliere Tindall, Second Edition. 1984. Pp. 95-96.

“Researchers Identify Virus Linked to Fatal Parrot Disease.” Pet Product News International. October, 2008. P. 14.

“Researchers Identify Virus Linked to PDD.” Veterinary Practice News. September, 2008. P. 34.

Subramanian, Roma. “Flashes of Color: Research to save Macaws.” Summer, 2009. DVM Today. Pp. 13-15.

Tizard, Ian. “Researchers Find the Virus that Causes PDD.” Bird Talk Magazine. November, 2008. Pp. 28-29.