|
Proventricular Dilatation Disease
Susan Clubb, D.V.M.
Proventricular dilatation disease (Often referred to as PDD) has been reported since the late 1970's. Initially, the disease seemed to be limited to macaws and was referred to as Macaw wasting syndrome. The disease has now been found in a wide variety of species and is now commonly referred to as Proventricular dilatation disease or psittacine proventricular dilatation syndrome.
PDD is characterized by inflammation in both central and peripheral nervous tissues, and migration of lymphocytes and plasma cells into the ganglia of nerves of the proventriculus and other digestive organs including crop, ventriculus and small intestine. The central nervous system (CNS) can also be involved without changes in the nerves of the ventriculus or proventriculus.
PDD has been reported in more than 50 species of parrots, (see attached list). Suggestive lesions also have been reported in Canada Geese, Spoonbills, Toucans and Weavers.
Adults are affected more frequently than juveniles (3:1, adults: juveniles) and both sexes are affected. PDD has been diagnosed in birds as young as 10 weeks to more than 45 years old. We have seen strong evidence implicating egg transmission in chicks that were incubator hatched and hand raised from the egg.
Clinical features
The most common clinical signs of PDD include depression, weight loss (with or without decreased appetite), constant or intermittent regurgitation, and/or passage of undigested seeds in the feces indicating a malabsorptive or maldigestive disorder. Proventricular impaction, muscle atrophy, abdominal enlargement, lethargy, weakness, polyuria, diarrhea, scant feces and hypo tension have also been reported in affected birds.
Neurological signs may include ataxia, abnormal head movements, seizures, and motor deficits. Birds can have lesions in the brain and/or spinal cord and not have lesions in the digestive tract.
Clinical laboratory findings in PDD-affected birds are inconsistent. Hypoproteinemia (low blood protein) hypoglycemia, (low blood sugar) heterophilia (elevated heterophil count) and anemia, have been reported. Fungal or bacterial secondary infections are common in affected birds. An elevation of the enzyme creatninephosphokinase (CPK) is also suggestive of PDD. This enzyme can be elevated as a result of muscle trauma, or heart problems, but is also as an indication of nerve tissue damage.
Etiology (What causes PDD)
The exact agent causing PDD is not known but it is widely believed to be caused by a virus and to be infectious. Disease does not develop in all exposed birds, which suggests that some birds have an innate resistance, develop a protective immune response, lack factors that are required for inducing the disease, possess factors which prevent development of the disease, or develop a carrier state. The disease apparently has sub acute, acute and chronic stages; however, the majority of diseased birds die within several months to a year after developing clinical signs. Histopathologic lesions are most consistent with an inflammatory response to viral infection. It is possible, but still unknown, that the virus may come, start an abnormal immune response and not be required for long-term disease. Viral isolation and characterization has been difficult. Development of an accurate blood test has been on going but so far not successful. There is still much to learn about PDD.
The suspect virus appears to be sensitive to environmental factors and is not long lived. Housing birds outdoors and spread out so they have fresh-air and sunshine will reduce transmission.
Diagnosis
A presumptive diagnosis of PDD often is based on history, clinical signs, and radiographic evidence of proventricular dilatation or dysfunction. PDD should be suspected in any bird which is thin, has repeated non-specific illnesses and especially intestinal infections and any signs of poor digestive function.
Radiographs are useful diagnostic techniques. Distension of the proventriculus, ventriculus, and/or intestines, is common. For better differentiation of abdominal organs we often give barium and repeat the radiographs at various times as the barium passes through the intestinal tract. Barium is radiopaque (white on the radiograph) and outlines the digestive organs so we can see the true extent of these organs. Increased transit time of barium is another common finding. Endoscopic examination may show dilatation of the proventriculus.
On necropsy examination emaciation, pectoral muscle atrophy, and dilatation of the esophagus, proventriculus, ventriculus, or small intestine are observed commonly. The proventriculus may appear thin-walled and easily torn, and it is usually distended with food. But none of the physical, laboratory, radiographic or gross changes are can confirm PDD. Bacterial, fungal or tuberculosis infections, parasites, gastrointestinal obstructions, tumors, trauma, maldigestion disorders, toxin ingestion or malnutrition may cause similar changes and also must be considered.
The most accurate and safe means for diagnosis at this time is the crop biopsy. While surgery and anesthesia always presents some risk, this procedure is minimally invasive. The bird is anesthetized and a small incision is made in the skin over the crop. A small piece of crop tissue is removed and the crop is sutured closed followed by closure of the skin. An antibiotic injection is given to prevent infection. The sutures are absorbable but can be removed after 10 days. Side effects of the procedure are uncommon. The entire procedure takes about 15 minutes and the bird can go home immediately after recovery. Some vomiting may occur postoperatively and the bird may be lethargic for a day. Pathology results are usually complete in about 2 weeks.
The pathologist will examine tissues collected either by crop biopsy or necropsy (autopsy) and look for characteristic histopathological (microscopic) lesions in nervous tissue of the gastro-intestinal tract. The characteristic lesions are described as lymphoplasmacytic ganglioneuritis – an invasion of inflammatory cells (plasma cells and lymphocytes) into the ganglia (body) of nerve cells. If the pathologist sees these characteristic lesions he will report it as positive. A positive crop biopsy is a definitive positive.
A negative crop biopsy does not eliminate the possibility of PDD. Lesions of PDD can occur in many areas of the Gastro-intestinal tract as well as the Central nervous system and peripheral nerves. Lesions may not occur in all parts of the intestinal tract. As stated before some birds only have lesions in the brain. Small biopsy samples may not contain any or enough nerve ganglia to make a diagnosis. Our pathologist likes to see at least 3 ganglia before making a diagnosis. If the pathologist does not see at least 3 normal ganglia he will report it as ISF (Insufficient ganglia). If the pathologist does see at least 3 ganglia and does not see affected gangliaor inflammatory response around the ganglia they report it as Not-detected, not as negative, because you cannot prove that they are negative. A recent study published by University of Georgia researchers, surmised that probably 70% of birds with PDD would have lesions found on crop biopsy.
Sometimes we receive a report of suspicious. In these cases the pathologist sees abnormal levels of inflammatory cells in the crop tissues, often surrounding the ganglia but not invading it. We don’t know if these are pre-PDD cases or some other abnormal inflammatory response. At this time we are isolating these bird and either treating, re-examining them, or preferably both.
Therapy and prevention
Currently, there is no specific therapy for PDD; however, many affected birds respond favorably to anti-inflammatory drugs that inhibit the Cox 2 enzymatic system. Celebrex (celecoxib) an anti-inflammatory commonly used for treating arthritis in humans has been used most extensively. The dosage we use is 20 mg/kg given orally once daily, or 40 mg/kg if given in food. Other Cox 2 inhibitors (human and veterinary drugs) are available and the dosage on those drugs may not be the same as the concentration of the drugs may not be the same. The duration of treatment needed is not really known and may require more than a year of treatment. Progress should be monitored by repeated crop biopsies at 6 to 12 month intervals. Side effects may include gastro-intestinal bleeding, development of ulcers, and possible allergic reactions. If very dark or black stools develop, indicating bleeding into the GI tract, the drug should be discontinued immediately.
While affected birds improve in condition and may look normal with treatment, it is unknown if they can continue to be infectious. Birds under treatment should be housed separately from any susceptible birds. Until the virus causing this syndrome can be characterized, preventative measures cannot be well defined. Quarantine of new birds should include screening crop biopsy of any suspicious birds or birds of questionable origin. Positive or suspicious birds must be isolated with avoidance of direct or indirect contact between isolated groups. Caretakers should exercise caution with clothing, utensils, etc which may spread the virus. Pressure cleaners that aerosolize fecal particles may also spread the virus. It is believed that the virus is not long lived outside the body. Fresh air and sunshine will help to dilute and kill the virus. Keeping infected birds closely confined indoors helps to concentrate the virus and may enhance spread. Treatment should not be considered curative at this time.
On-going research into PDD is being conducted at numerous Universities including University of Georgia, Texas A & M University and several leading Universities of Europe.
Special thanks should go to the Psittacine Disease Research Group led by Dr. Branson Ritchie- for long term-ongoing interest and exhaustive research efforts to understand and control PDD.
|
