David N. Phalen, D.V.M., Ph.D., Diplomat ABVP (Avian)
Assistant Professor, Zoological Medicine Section
Department of Large Animal Medicine and Surgery
Texas A&M University
College Station, Texas 77843
Written December 12, 1997
(Reprinted with permission from: Veterinary Quarterly Review, October-December 2001, Texas A&M University.)
Megabacteriosis is a condition affecting many psittacine and non-psittacine birds. First described in a flock of exhibition budgerigars nearly 25 years ago, the organism has now been detected in wild birds as well as pet and aviary birds around the world.
Megabacteria-associated disease has also been described frequently in lovebirds, cockatiels, parrotlets, canaries, ostrich, domestic chickens, and several species of finch. However, megabacteria have also been detected in birds that show no signs of illness. It is this inconsistency in clinical signs of disease, the lack of a consistently effective therapy and means of prevention in naive birds that contribute to the frustration of the veterinarian and the aviculturist in dealing with affected birds or flocks.
Megabacteria are organisms or a group of organisms whose classification has historically been unclear. They are large (typically 2 to 4 µm x 20 to 70 µm) rod-shaped to filamentous, and Gram-positive. Though more than five times larger than the largest bacillus, this organism was initially believed to be a bacterium and colloquially given the name "megabacteria."
To date, the organism has only been cultured using techniques used to grow yeasts and even then culture is difficult at best. Recently, research at the Texas A&M Schubot Exotic Bird Health Center has shown that the so-called megabacteria are actually a previously undescribed yeast. Because of these findings, it has been proposed that this organism be more descriptively and appropriately known as "avian gastric yeast" (AGY).
AGY colonizes the narrow band between the glandular proventriculus and the muscular, koilin-lined ventriculus, the isthmus. Although the organisms are often present in dense populations, pathologic changes are uncommon in the majority of affected birds.
Commonly reported signs in birds affected with this condition include chronic weight loss, dysphagia, vomiting/regurgitation, diarrhea and death. A "classic" sign in the exhibition budgerigar, the group of birds in which AGY was first noted, was the observation of birds apparently eating seed, but on closer inspection the seed was being finely ground in the beak, without ingestion. This finding is not universal, however, nor is it pathognomonic for avian gastric mycosis. Hematemesis and melena have also been noted in a small number of affected birds.
AGY are also often detected in clinically normal, thriving birds. Therefore, simply noting the presence of the organism does not necessarily imply the existence of disease. This is an important distinction to be made in the decision of whether to treat the AGY-positive bird or flock.
There is no serologic assay to diagnose avian gastric mycosis. Further, routine laboratory diagnostic tests (complete blood count, serum biochemistry, radiographs) have not yielded consistent results in affected birds. Avian gastric mycosis is most commonly diagnosed antemortem by demonstration of the organism in the feces, either by use of a quick stain or Gram stain of fecal smears, or wet-mount analysis of fresh droppings. The most sensitive of these assays is the fecal wet mount viewed at 100X and 400X.
Because infected birds do not shed AGY in every dropping, it is recommended that when screening for the organism, samples be collected and examined over a 5-day period. Postmortem diagnosis of avian gastric mycosis is readily made by examination of mucosal scrapings or histologic examination of the proventricular-ventricular junction.
Attempts at treating birds affected by AGY have met with limited success. Traditional antibacterial drugs have no effect on AGY. Amphotericin B, a polyene macrolide antifungal drug, when administered orally (100 mg/kg twice daily) was found to be effective at ameliorating fecal shedding of AGY organisms in affected budgerigars. It is considered the standard for treating birds diagnosed with avian gastric mycosis.
However, in a follow-up study, several treated birds were observed to return to fecal shedding, suggesting either that reinfection occurred or that therapy was incomplete. Treatment with amphotericin B is also complicated by the need for long-term administration, the cost of the drug and the difficulty of obtaining an oral formulation. Resistance of AGY to amphotericin B has been reported in a flock of budgerigars in Australia.
Oral nystatin and oral lactobacillus are treatments reportedly showing some degree of success; other studies, however, have found these therapies ineffective.
Drug trials using novel antimicrobial agents are under way at Texas A&M University. One drug, fluconazole, has shown promise against AGY. Recently, chickens infected with AGY were administered fluconazole orally twice daily at a dosage of 100 mg/kg in a 4-week study. At the conclusion of this study, fluconazole demonstrated greater efficacy than amphotericin B at resolving AGY infection.
However, neither drug attained 100 percent efficacy in its respective group. One possibility being explored is that drug therapy may need to continue for longer than 4 weeks.
In the author's opinion, not all birds diagnosed with avian gastric mycosis require drug treatment. Given the uncertainty surrounding the gastrointestinal disease reportedly associated with colonization by AGY, it may not be productive or in the bird's (or the client's) best interest to subject the bird to prolonged therapy. Just as not all microorganisms detected on a fecal smear indicate the presence of disease, AGY may prove to be of little concern in an otherwise healthy bird.
In the absence of clinical signs of ill health, consider forgoing drug therapy in favor of monitoring the patient for potential development of any of the clinical signs previously described, and repeat testing for the continued presence of AGY in the droppings.
In light of difficulties of treating birds with AGY, the best way to deal with this organism is to prevent its introduction into the aviary. This requires repeated examination of fecal wet-mounts as previously described. If the organism is already there, then breaking the infection cycle is an alternate approach.
We have shown hat cleaned, incubator-hatched eggs from AGY-positive adult budgerigars produce AGY-free offspring, if the birds are raised in isolation. This may prove a valuable way to interrupt the infection cycle in some aviaries.
However, aviculturalists should be aware that we do not know whether environmental exposure of the organism can result in infection, and there is strong evidence for bird-to-bird transmission. Therefore, if the clean birds are not maintained in isolation, it is possible that they could be re-infected.