Heya
Been away for a while writing my thesis but thought I'd post some snippets from a recent article on Bornavirus. It's scientific so admittedly can be a bit boring and long winded, I've only pasted the bird relevant info as I'm sure not many of you are interested in sheep and cow bornavirus
Before I go on, my condolenses again to OG's parents as well as little Earlyn parents...
Here goes...going to be a long post but hopefully a few of you will find the info interesting...
Avian Bornavirus Associated with Fatal Disease in Psittacine Birds
Peter Staeheli,1* Monika Rinder,2 and Bernd Kaspers3
Proventricular dilatation disease (PDD) is a fatal disease of mainly psittacine birds which was initially reported as a unique disease entity in macaws in the late 1970s (51) but subsequently also described as occurring in a growing number of other parrots (31). Even though the disease is now commonly referred to as PDD, several synonyms have been used in the literature, including macaw wasting syndrome, proventricular dilatation syndrome, neuropathic gastric dilatation of psittaciforms, myenteric ganglioneuritis, and others (13, 31). Birds presenting with PDD frequently show weight loss associated with reduced appetite or polyphagia and various degrees of gastrointestinal dysfunction (51). Regurgitation, undigested seeds in the feces, impactation of the proventriculus, and diarrhea are commonly reported clinical features. Affected birds may also show abdominal enlargement, muscle atrophy, weakness, and polyuria to different degrees. Central nervous system symptoms, such as seizure, ataxia, abnormal head movement, reduced proprioceptive skills, and motor deficit, can be observed with some but not all cases of PDD (31).
Clinical laboratory parameters are generally inconclusive in PDD and may simply reflect the gastrointestinal dysfunction (hypoproteinemia, hypoglycemia) or the presence of opportunistic infections (heterophilia) which are frequently associated with the disease (77). Consequently, ante mortem diagnostics rely on contrast radiographic procedures and the histopathological examination of biopsy specimens. Contrast radiography is routinely applied to diagnose the dilatation of the proventriculus, as well as duodenum descendens and extended transit times of ingesta (61). In rare cases, even spontaneous ruptures of the dilated proventriculus with ingesta filling the caudal air sac group may be observed. As expected, the typical findings in postmortem examination are dilatation of the esophagus, proventriculus, ventriculus, or small intestine and atrophy of the proventricular muscle (Fig. 1A) and pectoral muscles, which is a consequence of malnutrition (42). A highly characteristic feature of PDD is the presence of lymphoplasmacytic infiltrates in the enteric nerve plexuses of the proventriculus and ventriculus and, less frequently, of the esophagus, crop, and duodenum (64). However, lymphocytic infiltrates are not restricted to the neural tissue of the gastrointestinal tract and may also be seen in conduction fibers of the heart, the adrenal gland, the brain (Fig. 1B), and the spinal cord. The pons, medulla, and midbrain are most frequently affected, showing perivascular cuffing, lymphoplasmacytic encephalitis, and myelitis (21, 31). Several independent studies have shown that lymphoplasmacytic infiltrates in the ventriculus and proventriculus are highly characteristic of PDD (42) and may therefore be used to confirm a presumptive diagnosis of PDD by histopathological examination of biopsy samples (14, 30).
Initially, PDD was reported only for captive parrots in North America and Europe, but since then, the disease has been diagnosed for psittacines worldwide (13). It is assumed that intensive trading has contributed to spreading in the pet bird population (28). PDD has been reported for more than 50 species of Psittaciformes (8, 51, 81). African gray parrots, blue and gold macaws, cockatoos, and Amazon parrots seem to be most frequently affected (69) but, as Gregory and colleagues pointed out, this may reflect a population bias rather than a species predisposition (31). Interestingly, PDD does not seem to be restricted to psittacine birds. Proventricular dilatation associated with a nonsuppurative encephalitis and ganglioneuritis in wild Canada geese (Branta canadensis) was reported (9), and cases of PDD-like clinical and pathological findings have been described for a canary (Serinus canaria), a greenfinch (Carduelis chloris), a long-wattled umbrella bird (Cephalopterus penduliger), a bearded barbet (Lybius dubius) (56), and a falcon (Falco peregrinus) (73). Suggestive lesions in toucans, honeycreepers, weaver finches, and roseate spoonbills have also been reported (29).
Prognosis of PDD-affected birds is poor, and a specific treatment is not available to date. Birds can survive for months to years if treated symptomatically by being fed liquid or semisolid diets and by having antimicrobials applied to control secondary infections (22, 28, 77). Even though the etiology of PDD was unclear until recently, isolation of affected birds was recommended (31, 64). This suggestion was originally based on the observation of PDD outbreaks in aviaries (57), the demonstration that PDD can be transmitted experimentally (28), and the identification of viral particles in tissues and feces of birds affected by PDD.
The first evidence for a viral etiology of PDD came from transmission electron microscopy studies more than 20 years ago, demonstrating inclusion bodies and enveloped virus-like particles 30 to 250 nm in size in the myenteric plexus and celiac ganglion of affected birds (51). This study and subsequent work (32, 33) proposed the idea that a paramyxovirus might be the causative agent of PDD. However, this assumption was not supported by serological studies, which failed to demonstrate paramyxovirus-specific antibodies in diseased birds (10, 28). Other viruses proposed as causative agents of PDD included coronavirus (23), equine encephalitis virus (20), and avian herpesvirus. Polyomavirus, adeno-like viruses, enteroviruses, reoviruses, and avian encephalitis virus (63) have likewise been discussed as possible etiological agents of PDD. Enveloped virus-like particles of 80 to 140 nm were identified in organs (23) and fresh feces (24) from PDD cases. Evidence for the transmissibility of PDD came from experiments in which organ extracts from diseased birds containing the described viral particles were injected into healthy birds. All birds receiving the tissue homogenates developed clinical symptoms and showed histopathological lesions consistent with PDD (28). Since attempts to isolate the potential viral agent were unsuccessful at the time, it was proposed that PDD might represent an autoimmune disease triggered by virus infection (25) or gangliosides (65).
The discovery of ABV as causative agent of PDD represents a first important step toward a rational approach to fight this devastating disease of parrots. Several problems deserve our special attention in the near future.
First, ABV infections are currently monitored by analyzing biopsy or postmortem tissue samples for viral nucleic acids using reverse transcription-PCR (RT-PCR). However, presently used primer sets can probably not detect all circulating ABV strains. It is further unclear if the PCR assay has sufficient sensitivity to detect ABV infections before clinical symptoms have developed. Serological assays might be superior. It should be noted that serological assays do not work very well for diagnosing BDV infections of mammals, as antibody titers of infected horses and sheep are notoriously low (reviewed in reference 1). However, since ABV shows a less restricted organ tropism than BDV (Fig. 1), and since ABV antigen is abundantly present in many organs of infected birds (18, 62, 81, 82), it remains possible that the immune response to ABV is more robust than the immune response to BDV. Finally, as antisera recognizing conserved epitopes of ABV are now becoming available (55, 78), highly sensitive intra vitam or postmortem detection of ABV antigen in tissue samples should soon be feasible.
Second, currently available epidemiological data suggest that ABV may be found in psittacine birds from most parts of the world. However, we do not yet have a good sense of the true extent of the virus distribution and of the medical problems the virus may cause globally. The recent detection of ABV in a diseased canary (82) demonstrates that the host range of ABV is not restricted to psittacine birds. In this context, it is of interest that a paralytic syndrome in young ostriches from Israel has been reported (80); based on serological testing, this syndrome was suggested to be the consequence of infection with BDV (2). The syndrome could be transferred to naïve birds by intramuscular injection or oral application of brain homogenates derived from diseased animals. From today's point of view, it seems that ABV rather than BDV might have caused the disease in the ostriches.
Third, it is of great interest to know whether symptomless persisting infections of parrots and other birds occur frequently and whether such persistently infected birds serve as a virus reservoir. Recent reports (11, 45) suggest that this is a likely scenario. Further, the routes of virus transmission must be studied. It should be noted that viral nucleic acid was found in feces of diseased birds (62), but it remains unknown whether the virus in feces remained infectious. It is of interest that PCR analysis of fecal samples from wild birds in Sweden suggested the presence of BDV in a wide range of apparently healthy avian species (4). This observation requires reassessment with PCR primers that can clearly distinguish between genetic material from ABV and that from BDV.
Fourth, as PDD has now been recognized as representing a virus-triggered disease, it might be possible to develop a protective vaccine. From previous vaccine studies aimed at preventing BDV-induced disease in rats and mice (17, 36, 38, 47, 54), we would predict that an effective vaccine might need to induce a robust antiviral CD8 T-cell response rather than neutralizing antibodies. To evaluate any candidate vaccines, simple and affordable animal models that mimic the hallmarks of the ABV-induced disease in parrots are required. Animal models will also play a critical role for the evaluation of therapeutic approaches with antiviral substances. It was reported that BDV shows a high degree of sensitivity to ribavirin (43, 46, 52) and AraC (3), which are used to treat viral infections and cancer in humans. These drugs might be used to treat diseased birds or to block virus transmission in affected breeding colonies.
by el-parrot » Sat Oct 23, 2010 7:15 pm 
Bobbin
OG flies in birdie heaven