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|Proventricular Dilatation Disease (PDD)|
|Tweet Topic Started: Feb 18 2009, 11:30 AM (1,945 Views)|
|BUUZBEE||Feb 18 2009, 11:30 AM Post #1|
Proventricular Dilatation Disease (PDD)
by Hannis L. Stoddard, III, DVM
PDD was first recognized in macaws by Dr. H. L. Stoddard III in 1978. The condition was initially called "macaw wasting syndrome" and is also known as "psittacine wasting syndrome " or "neuropathic gastric dilation". Proventricular dilatation disease can occur in any psittacine but the most common birds affected are macaws, cockatoos and conures.
PDD is caused by a virus that progressively destroys the nerve supply to the proventriculus (forestomach), ventriculus (gizzard), and portions of the small intestines. As a result of the damage, birds are unable to digest their food properly. As food stays in the digestive tract bacteria accumulates and increases the chances of infection with other organisms. In some birds with PDD, the severely dilated thin wall of the proventriculus may rupture, resulting in the movement of the food into the abdominal cavity causing severe infection which many times leads to death.
Clinical Signs and Diagnosis
Signs suggestive of PDD include weight loss over a period of weeks to months despite a good appetite, passage of undigested food, vomiting, neurological signs, abdominal distention and impaction of the crop. All of these signs may or may not be present. Although PDD is considered to be a fatal illness, this disease can persist for months. Diagnosis of PDD is done by taking a biopsy of the proventriculus. Unfortunately these biopsies are done many times after the bird dies . In some rare cases biopsy of the crop can be done to diagnose PDD. Radiographs can reveal enlarged proventriculus in adult birds which can be highly suggestive of PDD. A contrast study can determine the time it takes for food to pass from the crop through the rest the digestive tract. Many times in birds with PDD, the contrast material is delayed and hours later the ingesta is still retained in the crop.
Incubation and Transmission
At the present time the mode of transmission has not been established. It has been thought that the incubation may be as long as eight years but there has been cases of acute outbreaks which suggest that there is a shorter incubation period. In some cases several birds in an aviary may show clinical signs while in other cases a single bird in a breeding pair may die, with no subsequent losses in the aviary even four or five years later. It is common for many birds exposed directly or indirectly to an affected bird to remain asymptomatic. PDD has been detected in birds as young as ten weeks of age.
Treatment and Control
There is no treatment for PDD at this time. Control and prevention of PDD will require confirmation of the cause of the disease. Exposed birds should be isolated and preferably housed in single bird families.
|BUUZBEE||Feb 18 2009, 11:30 AM Post #2|
Proventricular Dilatation Disease
(Macaw Wasting Syndrome)
Published in Bird Breeder Magazine, Breeder Q & A, October 1996
� 1996 Howard Voren
The contents of this web page, including all text and photographs are copyrighted material. No part of this page may be reproduced, in whole or part, without the express permission of the author, PO Box 152, Loxahatchee, FL 33470
Q: We have approximately 100 pairs of birds set up for breeding and have had a closed aviary for six years. About four months ago, we brought a 3-year-old greenwinged macaw to our avian vet because it was very fluffed and had lost a lot of weight. The bird was born and handraised at our aviaries. He suggested that we hospitalize the bird at his clinic so that it could receive proper supportive care until a definitive diagnosis could be made. The bird had a bacterial infection. Two weeks later, after the vet finished the antibiotic therapy, the bird was returned with a clean bill of health. The bird did appear to be completely recovered and, within the following month, regained most of its lost body weight. We never put the bird back with our other birds. We kept him in the den where he could get special attention.
One month later, the bird began passing very large droppings and losing weight. We brought it back to the vet, and he again asked that we hospitalize the bird at his clinic. Two weeks later, after many costly tests, the vet told us that the bird had wasting syndrome. It was explained to us that there is no cure for this disease and that the bird should be "put to sleep" so it will not continue to suffer a slow death from wasting away. Although this is hard to handle, we understand that we must face reality. His second demand is that we immediately stop all sales to prevent transmitting the disease to other aviaries or pet shops. We also accept that this is the ethical and moral thing to do.
We have a major problem with his third demand. He claims that the disease is so contagious that any birds that breathe the same air as the infected bird are suspect, and once the disease is in an aviary, it will move slowly through the entire flock. He believes that we should kill all the rest of the birds in our aviary, clean and disinfect everything and start over. Do you know of any other alternative? How could our baby have gotten this disease in an aviary that has been closed for six years?
A:Unfortunately, there is still much to be learned about wasting syndrome (proventricular dilatation disease [PDD]). Current information seems to lead one to believe that an exposed bird can break down weeks after exposure or can harbor the disease for several years. Consulting with vets who are very knowledgeable on the subject leads me to believe that six years is more than enough time for the disease to have surfaced if it was present. The question as to where your bird picked up this disease if it was not in your aviaries is difficult to answer. You could have carried it on your hands, in your hair or on your clothes when you were near other birds. From the scenario that you have outlined, it seems highly possible to me that your bird may have picked it up in the vet's clinic while being hospitalized for the bacterial infection. I strongly agree with your vet that you should not sell any of your birds, either babies or breeders. I strongly disagree with the vet that you should kill all of your birds because they might have been exposed to a disease that at this time appears to be airborne. I would wait one full year, and if there are no further breakdowns, forget about it.
If, as you say, the green wing was kept away from your other birds after it came back from its first trip to the vet's clinic, your other birds may not have been exposed. That's a lot more than can be said for all of the other birds that were hospitalized in the vet's clinic at the time your green wing was hospitalized there, waiting for the fateful diagnosis.
|BUUZBEE||Feb 18 2009, 11:31 AM Post #3|
Resolution of Clinical Proventricular Dilatation Disease by Cycloogenase 2 Inhibition
Bob Dahlhausen D.V.M., M.S.
5989 Meijer Dr., Suite 2,
Milford, Ohio 45150
Steve Aldred, MD, FCAP, Ernest Colaizzi
Research Associates Laboratory
14556 Midway Road
Dallas TX 75244
This report highlights important research advancements into the cause and nature of Proventricular Dilatation Disease (Myenteric Ganglioneuritis, or Macaw Wasting Disease) in pet birds. The discovery of a suitable pharmacotherapy that allows for the reversal and resolution of clinical signs is significant and warrants its early dissemination. We have confirmed the effectiveness of this treatment in eight well-documented cases and have seen improvement in numerous other ongoing cases under therapy. It is the author's intent that applied clinical use will further define the guidelines for this approach and immediately benefit those veterinarians managing clinically affected patients.
Proventricular Dilatation Disease (PDD) is a fatal disease of birds characterized by a lymphocytic, plasmacytic inflammatory infiltrate of central (CNS) and peripheral nervous tissues. Nerve ganglia supplying the musculature of the digestive tract are frequently affected, causing atrophy of the smooth muscles of the crop, proventriculus, ventriculus, and/or small intestine resulting in motility disorders and various degrees of dilatation.. Progressive weight loss, regurgitation, crop impaction, passage of undigested food, and secondary enteric bacterial and fungal infections are commonly observed. Lack of coordination, ataxia, motor and proprioceptive deficits are often seen with CNS involvement. While supportive care may help prolong the lives of affected birds, there is no current treatment for this disease. Long-term prognosis is grave, with the majority of birds succumbing after a period of progressive debilitation and wasting.
PDD is a disease of suspected viral etiology with a potentially long incubation period of months to possibly years. Because the lesions of PDD are inflammatory in nature, we speculated that diminishing this reaction might lead to clinical improvement and resolution of clinical signs in affected birds. Anti-inflammatory agents with significant activity in the CNS, peripheral nervous system, and gastrointestinal tract that were safe for use in pet birds were identified. Of these, the non-steroidal anti-inflammatory drugs (NSAIDs) appeared most useful.
NSAIDs, through inhibition of the cycloogenase (COX) enzyme, are effective for relief of inflammatory processes. COX exists in at least two isoenzyme forms: COX-1 and COX-2. COX-1 synthesizes prostaglandins that are involved in the regulation of normal homeostatic cell activity including gastrointestinal tract cytoprotection. COX-2 is an inducible form that causes enhanced formation of prostaglandins involved in acute and chronic inflammation. Conventional NSAIDs inhibit both COX-1 and COX-2. Their use is tempered by the development of side effects from COX-1 inhibition, which primarily involve platelet function, renal function, and the gastrointestinal tract.
Celecoxib (Celebrex, Pfizer), part of a new family of NSAIDs, is a potent and selective inhibitor of the COX-2 isoenzyme. The specific inhibition of COX-2 has been shown to effectively reduce many parameters of inflammation, including edema, white blood cell infiltration, and activation. At therapeutic levels, it does not inhibit COX-1 and has been shown to be well tolerated and safe. The incidence of adverse events is similar to placebos in most instances. In addition to its use in osteoarthritis, celecoxib has potent anti-inflammatory and anti-neoplastic activity in the gastrointestinal tract and has also been shown to inhibit certain CNS viruses in vivo and in vitro.
We have used celecoxib at 10 mg/kg orally once daily for the treatment of birds with clinical PDD. Diagnosis was based on history, clinical exam, characteristic radiographic changes, and crop biopsy pathology. Treatment duration was for a period of 6 to 12 weeks with the decision to cease medication based upon the return to normal body weight, condition, and diet. Contrast radiography was also used to monitor the progression of clinical improvement. Premature cessation of treatment can result in the recrudescence of clinical signs. In these instances, clinical improvement resumed with additional medical therapy. Supportive care to improve gastrointestinal transit (fluids, apple pectin), nutritional support with easily digested hand-feeding formulas, and appropriate therapy to eliminate bacterial (Clostridial) and fungal enteric infections were utilized as needed. Improvement in clinical condition is generally observed within the first week of treatment with a gradual resolution of clinical signs and a return to normal diet over the course of therapy. Periodic monitoring of clinical hematology and serum chemistry profiles have not demonstrated any adverse side effects related to this extended therapy. No adverse effects were observed clinically either during or after cessation of treatment. The majority of birds treated demonstrated marked clinical improvement including those in advanced stages of the disease. Most treated birds maintained their improved clinical status after treatment cessation. The longest we have observed is a Blue & Gold Macaw that finished therapy over 1.5 years ago.
We are currently accumulating additional clinical data to further evaluate the safety and efficacy of celecoxib use in pet birds. Our experience has shown that it significantly improves the functional status of PDD-affected birds, and appears to be safe and well tolerated in these species. Until such time when a particular agent that causes PDD is identified and a suitable diagnostic assay developed to identify infected individuals, the infectious status of treated/recovered individuals remains unknown. A detailed report with clinical case summaries has been submitted for presentation at the next AAV convention.
The author acknowledges that support from the Midwest Avian Research Expo, Miami Valley Bird Club, Central Indiana Caged Bird Club, and Kentuckiana Bird Club made this research possible.
|BUUZBEE||Feb 18 2009, 11:32 AM Post #4|
Progress in Understanding
Proventricular Dilatation Disease
Christopher R. Gregory, DVM, PhD; Branson W. Ritchie, DVM, PhD; Kenneth S. Latimer, DVM, PhD;
W. L. Steffens, PhD, Denise Pesti, MS; Raymond Campagnoli, MS; Phil D. Lukert, DVM, PhD
Psittacine Disease Research Group
College of Veterinary Medicine
University of Georgia
Athens, GA 30602
From the Proceedings of the International Aviculturists Society, March 4 - 8, 1998, Orlando, Florida
Proventricular Dilatation Disease
Proventricular dilatation disease (PDD) is used to describe an inflammatory response characterized by the accumulation of lymphocytes and plasma cells in the nervous system, especially the nerves that supply the muscles in the proventriculus and other digestive organs including crop, ventriculus and small intestine. 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. 1,2 Central nervous system signs associated with PDD, which may occur in addition to, or independent of, gastrointestinal signs, may include ataxia, abnormal head movements, seizures and proprioceptive or motor deficits. 1,2
This disease was first discussed in the late 1970's in birds imported into the United States and Germany. 3-6 Subsequently, an epornitic of this disease has been occurring in psittacine birds in North America and Europe, probably as a result of the widespread importation and shipment of birds to satisfy the demands of the pet trade. 3-5,7-10 In the order Psittaciformes, PDD has been reported in more than 50 species. Suggestive lesions also have been reported in toucans, honey-creepers, canaries, weaver finches, two free-ranging Canada Geese, and captive and free-ranging roseate spoonbills. 2,11 (Dr. Robert Schmidt, personal communication) The description of PDD in multiple families of birds would suggest that its cause is not restricted to a particular host. It is expected that additional non-psittacine birds will be diagnosed with this disease as improved diagnostic test are used to accurately detect affected individuals. There is no reference to spontaneous disease in free-ranging psittacine birds; however, there is every reason to assume that these birds would be susceptible. Given the severe nature of PDD and its apparent ability to affect a wide range of bird species, the importation of psittacine birds, or their eggs, into any region with indigenous Psittaciformes must be considered extremely risky.
Etiology of PDD
Since its initial description in the late 1970's, multiple etiologies have been proposed for the lymphoplasmacytic ganglioneuritis described as PDD. Adenovirus-like particles were demonstrated within intranuclear inclusion bodies in the cells lining the kidneys of one affected bird.12 Paramyxovirus-like viral particles were demonstrated within inclusion bodies located in the neural cells of the spinal cord and in visceral nerve ganglia of another.4,13,14 Similar inclusion bodies have been described in the nerves of pigeons with paramyxovirus infections.3 Birds with PDD have been shown to lack detectable levels of antibodies to paramyxovirus (serotypes 1, 2, 3, 4, 6 and 7), Pacheco's disease virus (an avian herpesvirus), avian polyomavirus and avian encephalitis virus.5,10 Because an infectious agent had not been recovered from affected birds, it was suggested that the observed changes in the nerves may be a result of an autoimmune process.4 However, most autoimmune diseases that affect nerves cause demyelination which is uncommon in birds with PDD.
An eastern equine encephalomyelitis (EEE) virus was recovered from neonates with abdominal distention from an aviary with a history of PDD. The disease in these neonates was termed avian viral serositis. This finding was used to suggest that PDD may be caused by EEE virus,15 even though EEE virus occurs primarily in the eastern portion of the United States, and PDD has been shown to occur throughout the United States, Canada and Europe.
PDD and EEE Virus
Over 30 alphaviruses have been described. Each occurs in a fairly restricted geographic region that is governed by the natural range of specific insects that transmit the particular virus. Eastern equine encephalitis virus, western equine encephalitis (WEE) virus and Highlands J (HJ) viruses are the most common alphaviruses in North America.
The natural susceptibility of various species of birds to alphaviruses varies widely; however, all avian species are considered susceptible to experimental infections.16 While the response to infection varies with the species of bird and the route of inoculation, these viruses typically cause subclinical infections in free-ranging birds native to an area where the virus naturally occurs. In some non-native bird species, these viruses have been associated with encephalitis or enteritis. Some indigenous species of birds infected with these viruses can develop clinical signs of disease following experimental infection, particularly when they are exposed by unnatural routes. While alphavirus infections generally do not cause easily recognizable clinical changes or death, they may cause as-yet-undefined subtle effects on free-ranging birds, including reduced ability to gather food or increased susceptibility to predation.16
When they occur, clinical changes associated with EEE are most common in young birds and may include depression, anorexia, weakness, profuse diarrhea and signs of central nervous system abnormalities (incoordination, tremors, head tilt, paralysis). A partial or complete paralysis of one or both legs may be the only sign noted, while others may show circling movements with partial paralysis involving one or both wings.17-19 Clinical changes in Lady Gouldian finches suspected to be infected with EEE virus included partial paralysis and difficulty in breathing.20 In some species (chukars and turkeys), EEE virus infections have been associated with reproductive problems and decreased egg production.
It has been suggested that most birds are susceptible to alphaviruses, and that the prevalence of infection in a bird population is a function of behavioral and ecological factors and is not controlled by host susceptibility.16,21 Generally, alphaviruses have geographically localized natural ranges. Cyclic outbreaks are dependent on specific regional insects that serve as biologic vectors and on vertebrate hosts that serve as reservoirs.
The seroprevalence of alphaviruses in birds varies from 0% to 100% depending on the species of birds being tested and their geographic location.21,22 The majority of seropositive birds are detected in the expected geographic range for each virus. For example, WEE virus activity is rare on the east coast of the United States, and consequentially, the number of birds on the east coast with antibodies to the virus is correspondingly low. By comparison, EEE virus activity is common on the east coast of the United States, and antibodies to the virus can be detected in over 75% of the birds in some flocks, indicating previous infections. In free-ranging birds and domestic poultry, the prevalence of EEE virus antibodies is generally higher in areas near fresh-water swamps.23
If companion birds are as susceptible to alphavirus infections as free-ranging species of birds, then psittacines in outdoor aviaries with natural exposure to mosquitoes should have a prevalence of antibodies that is at least as high as those demonstrated for birds that are permanent residents of the same geographic area. In a group of captive Psittaciformes from the eastern United States (Florida and Tennessee), up to 10% of the tested birds had EEE virus-neutralizing antibodies while none of the birds had WEE virus-neutralizing antibodies.24 This finding indicates that psittacine birds are susceptible to EEE virus infections. Another seroprevelance study was performed on a subpopulation of eclectus parrots from Florida that had been experiencing high neonatal mortality. Sixty percent of the unaffected eclectus parrots from this flock were found to have EEE virus antibodies. This seroprevalence was higher than that described for other psittacine birds in the same collection and from other psittacine birds in Tennessee.
Avian Viral Serositis, A Strain of EEE virus in Psittacines
An enveloped 55-to 62-nm viral particle, which was shown to be a strain of EEE virus was recovered from a group of young macaws and a ring-necked parakeet (ages ranged from 63 to 107 days) that died acutely over a 2-week period. The disease was characterized by ascites. Based on the gross and microscopic changes, it was termed avian viral serositis. Gross changes varied with each bird, but collectively included distention of the abdomen with fluid, an enlarged, yellowish liver and congested edematous lungs. The most consistent microscopic changes were lymphocytic proventriculitis, hepatic necrosis and serositis. The lymphoid organs, heart muscle and nervous tissue appeared to be the primary target organs for this virus.15
The EEE virus recovered from these affected psittacine birds induced AVS-like clinical and gross changes in experimentally infected young chickens.25 Antibodies to the virus were detected in the chickens that recovered from experimental infections but not in the originally affected macaws, ring-necked parakeet or other psittacine birds that died from proventricular dilatation syndrome.26
Two nestling budgerigars died following oral inoculation with a psittacine isolate of EEE while 3 budgerigars that were in contact with the affected birds, and fed with the same feeding utensils, remained clinically normal.25 In another experimental trial, EEE virus caused a transient diarrhea, polyuria and passage of undigested food in a cockatoo, an eclectus parrot and a macaw infected by intramuscular inoculation.24 These infected birds seroconverted, recovered completely and remained clinically normal for more than 12 months after infection. An eclectus parrot and a macaw inoculated orally with the same preparation of EEE virus remained clinically normal and did not seroconvert suggesting that they had not been infected when exposed to EEE virus by this route.24
The outbreak of avian viral serositis described initially occurred in a group of birds that had been experiencing intermittent problems with PDD. Many of the young psittacine birds that were exposed to the affected macaws developed PDD and died 4 to 18 months after the avian viral serositis outbreak. Additionally, many of the microscopic lesions in birds with naturally or experimentally induced avian viral serositis were similar to those described with PDD. These findings led to speculation that the EEE virus that causes avian viral serositis may also cause PDD.15 However, EEE virus antibodies were not detected in a group of psittacine birds that died from PDD.26 Moreover, seroprevalence studies have indicated that there is no significant difference in EEE virus-neutralizing antibodies in birds that died from PDD when compared to the population as a whole.24 Also, as previously discussed, psittacine birds experimentally infected with EEE virus developed transient diarrhea, seroconverted and remained clinically normal; they did not develop the progressive clinical changes suggestive of PDD.24 Additionally, in a group of psittacine birds diagnosed with PDD, only 1 of 17 of the birds had antibodies to EEE, WEE and VEE viruses; another had antibodies to EEE and WEE viruses.27 Further, serologic surveys indicate EEE antibodies are detected with a similar prevalence in birds with and without PDD.24 Collectively, these findings alone suggest that the EEE virus that causes avian viral serositis does not cause PDD.
Experimental Induction of PDD
The lymphoplasmacytic ganglioneuritis that characterizes PDD can be experimentally induced by exposing susceptible adult psittacine birds to a tissue homogenate, derived from affected birds, which contains an enveloped virus approximately 80 nm in diameter. 28 A virus with similar ultrastructural characteristics was recovered from the excrement of a macaw in Europe using macaw embryos to produce a primary cell culture.29
Clinical changes in experimentally infected birds varied from acute onset of a combination of central nervous system and gastrointestinal signs, followed by death within 11 days of inoculation, to induction of only gastrointestinal signs that were first noted 3 months after inoculation.28 Virus particles, ultrastructurally similar to those of the virus in the experimental inoculum, were recovered from the tissues and/or excrement of the experimentally infected birds. None of the contact controls used in this study developed clinical signs of PDD, suggesting that the suspect PDD virus is not readily transmissible or requires a specific route of inoculation that was not favored by the experimental conditions. Alternatively, it could be speculated that the unaffected contact controls were already immune to infection. However, all birds, both those that received the virus containing inoculum and the birds which received the control inoculum were derived from the same initial group of research birds. All of the experimentally infected birds were susceptible and none of the contact control birds developed disease. These findings suggest that a lack of successful transfer of the virus from an infected to an uninfected bird was more likely than some specific immunity in all of the contact control birds.
Clinical laboratory findings in PDD-affected birds are inconsistent. 1,2 Survey and contrast radiographs are useful for demonstrating gastric dysfunction in suspect birds. Distention of the proventriculus and increased transit time of barium are common findings in chronically affected birds. The proventriculus of neonates is normally dilated, a condition which should not be misinterpreted as PDD. Ultrasonic examination may be used to demonstrate dilatation and impaction of the proventriculus. Endoscopic examination may show impaction, ulceration and dilatation of the proventriculus. 1,2,7,30,31 Fluoroscopy has been used to demonstrate reduced gastric motility which can be an indication of PDD.32
A presumptive diagnosis of PDD often is based on historical information, clinical signs, and radiographic evidence of proventricular dilatation or dysfunction. However, the presence of characteristic histologic lesions in nervous tissues is necessary for a definitive diagnosis. 1-3,7,30,31 In most cases, a post-mortem diagnosis is rendered when a complete set of tissues (including proventriculus, ventriculus and brain) are examined microscopically. In some suspect patients, it is possible to obtain a diagnosis before death by submitting a biopsy of the crop. In one study, histologic evaluation of a crop biopsy correctly diagnosed PDD in (68%) of positive birds33 and in another study the sensitivity of crop biopsy was 76%. 34 Thus, a positive crop biopsy in a bird with suggestive clinical changes is of diagnostic value, but a negative crop biopsy in a bird with suggestive clinical changes does not rule out PDD. To increase the likelihood of histologic detection of PDD-associated lesions, practitioners should obtain full-thickness crop biopsies containing at least one large blood vessel and its associated ganglia. Evaluating step sections of the biopsy sample may also increase the likelihood of detecting segmental lesions.
Because the suspect PDD virus could be demonstrated in the excrement of naturally and experimentally infected birds, it was anticipated that electron microscopic examination of excrement might provide a reliable method for detecting birds that were passing the virus. During a 3 year period, the suspect PDD virus was consistently identified by electron microscopy in the fresh excrement of experimentally (n = 2) and naturally (n = 34) infected birds that were either maintained in a research setting or presented to the Teaching Hospital for evaluation. During this study period, more than 200 excrement samples from affected birds were evaluated. While the quantity of detectable virus (estimated concentration between 106 and 109 virus particles per ml) varied among individual birds and among the same bird evaluated at differing times, the virus was consistently detectable, except in 3 naturally infected birds. The suspect virus was not detected in the excrement of these 3 positive birds (confirmed by histologic evaluation of a crop biopsy) when the excrement was examined within several days after the birds were shipped to our research group. However, the suspect virus was detected in the excrement when evaluated several weeks after the birds' arrival. The suspect virus was not detected in excrement samples (n = 76) of any birds that did not have microscopic changes of PDD.
These experimental findings were sufficiently encouraging to warrant the evaluation of electron microscopy as a method for detecting the suspect PDD virus. However, when clinicians submitted excrement from known histologically positive birds, or mailed both excrement and crop biopsies to our group for evaluation, the suspect PDD virus was detected by electron microscopy in approximately 30% of samples (n = 28). Ongoing research suggests that the suspect PDD virus is unstable when outside of the host. Thus, demonstrating a dramatic difference in the sensitivity of electron microscopy for detecting the virus in fresh versus stored feces is not surprising. In one trial, the suspect PDD virus was detected by electron microscopy in the fresh excrement of 3 known positive birds, but could not be detected in the same excrement sample 3 days later (a typical interval between collection of a excrement sample in the field and its processing and evaluation by electron microscopy).
If submitting fresh excrement to a regional electron microscopy laboratory for evaluation, please be advised that "normal" birds (chickens, turkeys, psittacines, etc) pass, in some cases in large quantities, what has been termed "fringed membrane proteins or fecal fringes", which can appear quite similar in size and morphology to the suspect PDD virus. An electron microscopist who does not routinely evaluate excrement from birds, or screen excrement for virus, may incorrectly identify these fringed membrane proteins as the suspect PDD virus.
Immunoelectron microscopy can be used to demonstrate that birds with histologic lesions characteristic of PDD develop antibodies to the suspect virus being shed in excrement. While effective as a research tool, we consider the inherent high cost and low sensitivity of immunoelectron microscopy to render it of minimal value as a serologic assay for epizootiologic studies.
The suspect PDD virus has been shown to cause cytopathic effects in primary tissue culture.29 However, despite intensive manipulations using high concentrations of relatively pure virus, we have been unable to maintain the virus past 5 passages and the titer of virus produced in cell culture is too low to be of value for research purposes.
The presence of lymphoplasmacytic ganglioneuritis and variable clinical signs (GI only, CNS only or GI and CNS ) have led several researchers to propose that PDD might be caused by more than one etiologic agent. Our experimental transmission studies have demonstrated that the same virus containing inoculum can cause varying clinical changes even within birds of the same species. Additionally, a morphologically similar virus has been recovered from the tissues or excrement of birds that were diagnosed by crop biopsy with PDD, even though some of these naturally affected birds had predominately CNS signs, some had gastrointestinal signs and some had both.
It should be cautioned that PDD should not be diagnosed based on clinical changes or gross lesions, particularly in birds with predominately neurological signs. Paramyxovirus-3 has been isolated from several birds with neurologic signs suspected to be associated with PDD, and serologya was effective in documenting these infections. (Dr Judy St Leger, personal communication) We suggest that tissues (including the pancreas when paramyxovirus is suspected) from birds that die following a progressive neurologic disease be submitted for virus isolation (available through many state diagnostic laboratories or the Infectious Diseases Laboratory at the UGA College of Veterinary Medicine). In addition to the suspect PDD virus, virus particles with morphologic characteristics of paramyxovirus and reovirus have been detected in the excrement of some PDD positive birds.
Proventricular dilatation disease can occur in any aviary despite excellent hygiene, valid quarantine procedures and the absence of new additions to the flock. In some aviaries, numerous cases of PDD will occur simultaneously. In others, several affected birds may die, and the problem seemingly resolves, only to reappear 1 to 2 years later. 15,30 In other cases, a single bird in a breeding pair may die, with no subsequent losses in the aviary even 4 to 5 years later. It is common for many birds exposed directly or indirectly to an affected bird to remain asymptomatic.
Mates, offspring or siblings of birds that are diagnosed microscopically with PDD should be considered at extra risk of developing the disease; however, they should not be euthanized. Many of the birds that are directly exposed to those with PDD never develop the disease. Until appropriate preventative measures can be developed, it would be prudent to place exposed birds in isolation.
Provided with an easily digested high energy diet, a stress-free environment and treatment for secondary bacterial or fungal infections, affected companion birds can survive for months or years. Any bird with the disease that is being treated should be placed in strict isolation with no direct or indirect contact with other birds. Some birds with clinical changes suggestive of PDD have been reported to recover when provided supportive care. However, a positive diagnosis of this disease requires the demonstration of microscopic lesions in the nerves and none of the reported recoveries have been in birds confirmed to have PDD.
Major sustained contributions that have made this work possible have been provided by the UGARF Avian Health Fund, the International Avian Research Foundation, Veterinary Medical Experiment Station, Dr. Joe and Sue Still, Terry Clyne, Loro Parque Fundacion, Zoo Atlanta, Riverbanks Zoological Park, Dr. Richard and Luanne Porter, Knick Enterprises, Bobbi Brinker, International Aviculturists Society, Midwest Avian Research Expo, National Aviary, Puerto Rican DNR, Ann Arbor Cage Bird Club, Aviary and Cage Bird Club of South Florida, Avicultural Society of Puget Sound, Central Indiana Cage Bird Club, Charlotte Metrolina Cage Bird Society, Cream City Feathered Friends, Dallas Cage Bird Society, Feathered Friends Society, Gateway Parrot Club, Georgia Cage Bird Society, Greater Brandon Avian Society, Hookbill Hobbyists of Southern California, Kenosha Exotic Bird Club, Louisiana Aviculture Society, Northwest Ohio Exotic Bird Club, South Jersey Bird Club, Wasatch Avian Education Society, West Valley Bird Society and Zeigler Brothers Inc. Hundreds of aviculturists, bird clubs and veterinarians have also made important contributions. A special thanks to Dr. Frank Niagro for his years of dedicated service to improving the health of companion birds.
Services or Products Mentioned in the Text
a. Serologic screening for paramyxovirus, California Veterinary Diagnostic Laboratory, San Bernardino, CA, 909-383-4287.
b. Virus isolation, Infectious Disease Laboratory, Athens, Ga, 30602, 706-542-8092.
1. Gregory CR (1995). Proventricular dilatation disease. Avian Viruses: Function and Control Ed. B. W. Ritchie. Lake Worth, Wingers Publishing. 439-448.
2. Gregory CR, Latimer KS, Niagro FD, et al. A review of proventricular dilatation syndrome. J Assoc Avian Vet 1995;8:69-75.
3. Gerlach S. Macaw wasting disease- a 4 year study on clinical case history, epizootiology, analysis of species, diagnosis, microbiological and virological results. Proc Europ Chap Assoc Avian Vet, 273-281, 1991.
4. Graham DL. Infiltrative splanchnic neuropathy, a component of the "wasting macaw" complex. Proc Assoc Avian Vet, 275, 1984.
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|BUUZBEE||Feb 18 2009, 11:33 AM Post #5|
ASK THE VET (Proventricular Dilatation Syndrome, Neuropathic Gastric Dilatation or Macaw Wasting Disease)
by Linda Pesek, DVM
Westbury Animal Hospital
319 Union Avenue
This article first appeared in SQUAWK, the newsletter of the Big Apple Bird Association, and appears here with permission.
Proventricular Dilatation Syndrome, Neuropathic Gastric Dilatation or Macaw Wasting Disease, is a very devastating, fatal disease affecting not only macaws, but many other species as well. This disease was first recognized in 1971 and since then has been seen in many species including cockatoos, conures, grey parrots, cockatiels, Eclectus parrots, thick billed Amazons, Blue fronted Amazons, and budgies, as well as macaws. These birds have been as young as 10 weeks of age and as old as 17 years.
This disease is thought to be caused by a virus. Birds often present with a history of regurgitation, chronic bacterial or fungal crop infections, pendulous crops, history of weight loss, passage of whole intact seeds in droppings, incoordination, or sudden death. These signs, unfortunately, are not specific for this disease. Other conditions such as lead poisoning, bacterial and fungal infections, foreign bodies and obstructions can mimic this disease.
Antemortem diagnosis of Proventricular Dilatation can be difficult. Suspicion of this disease is based upon history and physical examination. A complete workup should be performed which includes a CBC, blood chemistry, bacterial and fungal cultures and sensitivities, and a chlamydia test. Survey and contrast X-rays may demonstrate a dilated proventriculus (glandular stomach) and delayed passage of barium from the gastrointestinal tract. These findings further support a tentative diagnosis but are not conclusive. A definitive diagnosis is based upon a biopsy of the crop, ventriculous (gizzard) or proventriculous, demonstrating characteristic histopathologic changes. The characteristic lesions may not be uniformly distributed throughout the affected organ, so multiple biopsies are necessary.
Proventricular Dilatation Syndrome is a very difficult disease because its transmission, incubation and latency are unknown. Once it occurs in an aviary, it is difficult, if not impossible, to irradicate.
No effective treatment is known. Supportive care may help prolong the lives of affected birds. It is considered to be a fatal disease.
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