The Incidence and Treatment Outcomes of Macrorhabdus ornithogaster Infection in Budgerigars (Melopsittacus undulatus) in a Veterinary Clinic.
Key words: Macrorhabdus ornithogaster, yeast, undigested seeds, melena, avian, budgerigars, Melopsittacus undulatus
One of the most common causes of gastrointestinal disease in budgerigars (Melopsittacus undulatus) is Macrorhabdus ornithogaster, also called avian gastric yeast. This microorganism can be detected in clinically healthy budgerigars as well (1-4); therefore, onset of the disease is assumed a multifactorial event. (2,5,6) Stressors, such as breeding, molting, poor hygiene, and change of ownership can contribute to the onset of the disease. (5,7,8) Initially, M ornithogaster was assigned to the domain of bacteria. According to recent findings, however, the pathogen belongs to the Saccharomycetes, an anamorphic, ascomycetous yeast that is the only presently known member of its genus. (9)
Macrorhabdus ornithogaster has been detected in many bird species. (5,10-15) In certain studies, male budgerigars were particularly affected by the disease. For that reason, a sex predisposition for males is suspected. (1,6,16) An age predilection has not been determined. (6)
If the disease manifests, the common clinical signs are vomiting, diarrhea (sometimes with undigested seeds), and chronic weight loss. Other nonspecific clinical signs are lethargy and either polyphagia or anorexia. A dilated proventriculus can be seen on radiographs. (14)
At necropsy, emaciation and a catarrhal or hemorrhagic, ulcerative proventriculitis can be found. The changes are often limited to the mucosa; only in very severe cases is the muscle of the proventriculus affected as well. Furthermore, ulcerations and necrosis can be recognized. (8) The distal proventriculus and the isthmus between the ventriculus and proventriculus are dilated in most cases, and the wall of the proventriculus is thin. Opaque mucus layers on the mucosa of the proventriculus and isthmus can also be seen. (14,17)
Macrorhabdus ornithogaster can be found microscopically on the surface of the isthmus glands. The organisms cover the connection to the koilin layer. By penetrating the isthmus glands, the koilin layer is disrupted, leading to atrophy and necrosis of the glands. Therefore, food cannot be digested, leading to the clinical signs of emaciation and undigested seeds in feces. Other histologic findings include moderate epithelial hyperplasia of the superficial glands. The major part of the inflammatory reaction of the lamina propria consists of lymphocytes, plasma cells, and fibroblasts. (17,18)
The disease is diagnosed by microscopic examination of fresh feces. In dead birds, the microorganism can be detected directly by an impression preparation of the isthmus. (13) The yeast is clearly recognized by its length of 20 to 80 [micro]m. (14) The cell walls are found to be weakly gram positive, (5) but with hematoxylin and eosin stain, they present as crystalline. (11,14) With a Giemsa stain, the microorganisms are a reddish-violet color. (12) A demarcation similar to bacteria can be detected by calcofluor white M2R stain with a fluorescent microscope. (14) With that stain, chitin and cellulose are colored, and the typical cell wall can be observed. (14) Because the pathogen is easily identified by microscopic examination of fresh feces, fungal culture is not a routine diagnostic test. This organism cannot be isolated by standard microbiologic isolation techniques. Culture is possible in liquid medium with minimum essential medium or basal medium Eagle and fetal bovine serum with added sucrose or glucose. Furthermore, information differs on the best pH range for growing M ornithogaster. (12,19) Additional diagnostic tests include flotation techniques (20,21) and polymerase chain reaction testing. (20)
Treatment of disease caused by M ornithogaster is difficult. If no clinical signs are present that indicate infection, treatment is not recommended. (20) This appears reasonable because stress is thought to cause disease outbreak. (2,5,6) If clinical signs of gastrointestinal disease caused by M ornithogaster are present, long-term treatment must be administered. (2) Budgerigars can be medicated with amphotericin B at 100 mg/kg PO ql2h for >30 days. (2) Although another treatment option is nystatin (20 000 U orally twice daily for 10 days), efficacy must be monitored by testing fecal samples because drug resistance to nystatin has been reported. (22) Sodium or potassium benzoate have also been used as treatment regimens. (20,23) Prognosis is guarded because recurrence is common. (24)
The aim of this retrospective study was to provide an overview of the occurrence, clinical signs, and treatment success in budgerigars that presented to a veterinary clinic with disease caused by M ornithogaster.
Materials and Methods
This study period was 2.5 years; during which, 580 budgerigars with different disease problems were presented to the Clinic for Birds and Reptiles at the University of Leipzig (Leipzig, Germany). Almost 25% (137 budgerigars) demonstrated gastrointestinal clinical signs, including vomiting, regurgitation, polyphagia, anorexia, emaciation, lethargy, or changes in the feces, such as melena, undigested seeds, and diarrhea.
The 137 birds underwent clinical examination, and fresh fecal samples were examined by microscopic evaluation. If fecal results were negative in a bird suspected of positive results, 2 additional fecal samples were analyzed to screen for M ornithogaster.
The 137 cases were divided into 3 groups: sick budgerigars, in which M ornithogaster was detected; budgerigars with suspected M ornithogaster infection based on gastrointestinal clinical signs, absence of other diseases, and positive treatment success; and budgerigars with gastrointestinal clinical signs from other causes of disease. During hospitalization, all birds were housed in separate cages to prevent disease transmission among birds.
In addition to symptomatic treatment, both sick budgerigars with confirmed positive results for M ornithogaster and budgerigars with suspected M ornithogaster infection were treated with amphotericin B (100 mg/kg PO ql2h) for 28 days. Birds that vomited were also treated with metoclopramide (0.5 mg/kg IM) as needed. Birds with significant weight loss or anorexia were gavage fed (20 mL/kg; Harrison's Recovery Formula, Harrison's Bird Foods, Brentwood, TN, USA) directly into the crop. Treatment was considered successful if clinical signs resolved. Budgerigars with other causes of disease were treated according to the cause.
Sixty-six budgerigars with gastrointestinal signs (48% of budgerigars with gastrointestinal signs and 11% of all budgerigars) had positive results for M ornithogaster on examination of fresh fecal smears (Fig 1). Of those birds, 62% were male (n = 41), 30% (n = 20) were female, and in 8% of birds (n = 5), sex was not recorded.
Of the 66 birds with detected M ornithogaster, 9% (n - 6) were <1 year old, 6% (n = 4) were 1 year old, 14% (n = 9) were 2 years old, 20% (n = 13) were 3 years old, 15% (n = 10) were 4 years old, 6% (n = 4) were 5 years old, and 9% (n = 6) were older than 7 years. In 15% (n = 10) of the birds, the age was unknown.
In 8 of 66 budgerigars (12%), other pathogens, including Trichomonas species, or abnormal bacteria were found. In those cases, diseases were treated accordingly. In 2 patients (3%), other yeasts of Candida species were identified (Table 1).
Of those birds with detected M ornithogaster, 59% (n = 39) presented with lethargy, 55% (n = 36) with vomiting and/or regurgitation, 38% (n = 25) with emaciation, 32% (n = 21) with changes in the feces, 15% (n = 10) with polyphagia, and 11% (n = 7) with anorexia. Of the 21 budgerigars (32%) with changes in the stool, 7 (33%) showed undigested seeds in the feces, 12 (57%) showed diarrhea, and 3 (14%) showed melena.
Radiographs were performed in 21 patients (32%). The proventriculus appeared large in 11 of those 21 birds (52%; Fig 2). Three of those 21 budgerigars (14%) showed a small amount of grit in the ventriculus, whereas 5 birds (24%) had no grit. In 11 birds (52%), the gastrointestinal system was prominent, and in 1 budgerigar (5%), there was grit in the intestines. Additionally, 3 patients (14%) had a full crop. One budgerigar (5%) showed diffuse soft tissue opacity. The characteristic hourglass appearance of the heart, liver, and proventriculus was not apparent in 13 birds (62%; Fig 2b).
Forty-seven of the 66 birds (71%) were monitored and treated in the hospital. The remaining birds were treated by their owners. Altogether, 65 of 66 budgerigars (98%) with positive results were treated with amphotericin B. One budgerigar (2%) was not treated. The owners of this bird elected to observe the bird because, after some initial clinical signs, its health status stabilized, and its body condition was good. There was no follow-up.
Twenty-four animals (36%) recovered, and their clinical condition stabilized within 7 days. In 11 birds (17%), although improvement was noted during treatment, the clinical signs recurred. Thirteen birds (20%) died during treatment without showing improvement; 1 budgerigar died on day 1 of treatment, 1 on day 2, 2 on day 3,4 on day 4, 2 on day 5, 1 on day 7, 1 on day 11, and 1 on day 19. Two birds responded to the treatment in the first 5 days but died subsequently. Six budgerigars (9%) were euthanatized because of the severity of clinical signs.
Thirty-five birds (53%) were treated successfully. Eleven birds (17%) presented with a new M ornithogaster infection within 2.5 years. Two of the 66 birds (3%) died during the repeat manifestation of clinical signs.
Melena appeared to be associated with a poor prognosis. Budgerigars with melena died or showed only minimal improvement with treatment.
Budgerigars with suspected M ornithogaster infection
In 24 birds (36%) with suspected M ornithogaster infection, results of fecal examination were negative. All 24 birds were treated exclusively with antifungal agents. There were no significant differences in the distribution of age or sex compared with the group with positive results.
Of those 24 birds, 20 (83%) presented with lethargy, 8 (33%) with vomiting or regurgitation, 7 (29%) with emaciation, 6 (25%) with anorexia, 6 (25%) with changes in the feces, and 4 (17%) with polyphagia. Of the 6 birds with fecal changes, 3 budgerigars (50%) had undigested seeds in the feces, 2 (33%) had diarrhea, and 1 (17%) had melena. In 14 of the 24 patients (58%), radiographs were performed. In 4 of the 14 birds (29%), the proventriculus appeared large. Six (43%) showed a small amount of grit in the ventriculus, whereas 4 (29%) had no grit. In 11 of the 14 birds (79%), the gastrointestinal system appeared enlarged. Two budgerigars (14%) had diffuse soft tissue shadowing. In 1 bird (7%), the crop appeared dilated.
Of the 24 birds with suspected M ornithogaster infection, 18 (75%) were monitored and treated in the hospital. In 7 birds (29%), clinical signs resolved within 7 days of treatment. In 7 birds (29%), recovery was slow with persistent or intermittent clinical signs. In 4 birds (17%), treatment with amphotericin B was successful, but the birds did not gain weight during hospitalization (7-9 days of amphotericin B treatment). Six of the 24 birds (25%) were treated at home and were lost to follow-up. Nine birds (38%) presented again with recurrence of clinical signs but again had negative results for M ornithogaster on fecal examination.
Budgerigars with gastrointestinal clinical signs from other causes of disease
Forty-six birds with clinical signs of gastrointestinal disease had negative results for M ornithogaster but had evidence of other disease processes.
Older birds were more common in this group. The sex ratio was relatively balanced: 52% (n = 24) of the birds were male, 41% (n = 19) female, and in 7% (n = 3), sex was not recorded. The distribution of the clinical signs did not deviate significantly from the other groups.
A primary diagnosis was possible in only 18 of the 46 birds (39%). Of those, 3 birds (17%) each had candidiasis, trichomoniasis, Escherichia coli infection, or neoplasia. In 2 birds (11%), Klebsiella species was diagnosed on bacterial culture. One bird each (6%) had a distended crop, infection with Capillaria and Ascciris species, had ingluvitis, or had an abdominal hernia as the cause of the clinical signs. In the remaining 28 patients (61%), a final diagnosis was not possible because the bird died without necropsy or the financial constraints of the owner limited diagnostic testing.
Although M ornithogaster can be found in the feces of healthy birds, this yeast was one of the most common causes for gastrointestinal diseases in budgerigars in the past 2.5 years in our clinic. In cases with positive results, the yeast is easily visualized microscopically because of its size (Fig 1). Nevertheless, infection can be missed because the microorganism is intermittently present on microscopic examination. Results of this study highlight the importance of this yeast as a cause of clinical signs of gastrointestinal disease in budgerigars, including vomiting, diarrhea (often containing undigested seeds), and chronic weight loss, whereas food consumption remains unchanged.
Other causes for gastrointestinal clinical signs are infection with other yeasts, with Trichomonas species, or with bacterial pathogens, such as E coli, Pseudomonas species, or Klebsiella species. However, those pathogens appear less important clinically. Noninfectious causes, such as distended crop or hernias, were insignificant as causes for the described clinical signs.
Because of the retrospective evaluation, this study depended on case documentation. Therefore, age and sex could not be determined in cases in which those data were not recorded. The available data showed that more male budgerigars than females were affected with gastrointestinal signs. This compares with the results reported by Filippich and Hendrikz (6) and Lanzarot et al. (1) However, whether the sex distribution of clinical signs is correlated with social and feeding behavior (male birds regurgitate food to feed the females) is unknown. In our study, age of the bird did not appear associated with the confirmed or suspected presence of M ornithogaster infection. Furthermore, we found no correlation between confirmed or suspected M ornithogaster and severity of clinical signs and treatment success. However, the time of presentation may have been a factor because signs of clinical disease in birds often are not recognized immediately, and birds may be brought in for examination in an advanced disease state. Therefore, we could not evaluate the time of disease onset at presentation to the clinic.
Immune status is important in the outbreak and course of disease. The immune system is not as developed in young birds as it is in adults. Additionally, younger birds are often under greater stress because of changes in their environment and ownership. The role of avian bornavirus was not evaluated in this study. Infection with M ornithogaster can be seen as a multifactorial occurrence that places younger birds at higher risk. However, in the present study, a predilection for young birds was not seen.
Clinical signs in birds with M ornithogaster infection were usually nonspecific (lethargy, vomiting, and regurgitation) and were similar to those of birds with gastrointestinal clinical signs from other causes of disease. A more-specific clinical sign was undigested seeds in feces; although only seen in 10 birds in this study, undigested seeds were limited to birds with confirmed or suspect M ornithogaster infection. Melena was associated with poor prognosis. In the present study, all birds with melena died or showed minimal improvement with treatment.
Diagnosis from fresh feces is simple because of the large size of the yeast. However, quantifying the amount of the pathogen in the feces is not useful because the number of excreted microorganisms is not correlated with the infection strength. (6) This supports why M ornithogaster cannot be definitively diagnosed in some patients, but treatment is still successful. Additionally, excretion is intermittent, which makes the diagnosis more difficult with only one fecal screening test. Disease cannot be excluded if the yeast is not observed microscopically. A physiologic occurrence in clinically healthy birds, as described by Baker, (7) cannot be validated based on the results of our study because we found no asymptomatic birds with positive results for M ornithogaster. Nevertheless, a thorough evaluation of the clinical signs, appropriate diagnostic tests, and evaluation of possible differential diagnoses should be performed.
Proventricular dilatation was seldom seen on radiographs of the budgerigars in this study. However, dilatation can be difficult to recognize in these small patients. Nevertheless, radiographic examination can be helpful to rule out differential diagnoses such as heavy metal toxicosis.
Secondary infections that aggravate the clinical disease did not feature in the M ornithogaster findings in the birds in this study. Influence of any potential pathogens on the course of the disease was also not seen.
Treatment results with amphotericin B treatment were unsatisfactory in this study. Only 33% of birds with confirmed M ornithogaster infection were asymptomatic after completion of therapy. Eleven birds presented again after a relapse. The handling and oral dosing of amphotericin B twice daily during an extended treatment period is stressful for the bird. Furthermore, this therapy often does not lead to eradication of the yeast. Therefore, amphotericin B treatment of an asymptomatic bird with detectable M ornithogaster in a stool sample should always be evaluated in a clinical context.
Treatment success may depend on the chronicity of disease before presentation. The duration of the disease typically is unknown by the owner, but body condition can be an indication of disease chronicity. With advanced infection, gastric ulcers can develop that negatively influence the prognosis. Affected birds show melena clinically. In the present study, birds with that clinical sign died or showed only minimal improvement with treatment.
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Ronja Pustow, Med Vet, and Maria-Elisabeth Krautwald-Junghanns, Med Vet. Dipl. ECZM (Avian)
From the Klinik fur Vogel und Reptilien. Universitat Leipzig. An den Tierkliniken 17, 04103 Leipzig, Germany
Caption: Figure 1. Photomicrograph of a direct fecal cytologic examination from a budgerigar with clinical signs of gastrointestinal disease. Macrorhabdus ornithogaster is visible as numerous elongated rod-shaped organisms.
Caption: Figure 2. (a) Lateral radiograph of a budgerigar infected with Macrorhabdus ornithogaster. The crop is distended (black arrow), and the gastrointestinal system is dilated (white arrow), (b) Ventrodorsal radiograph of a budgerigar with Macrorhabdus ornithogaster infection. The lack of an hour-glass shape between the heart and liver (arrow) is due to the enlarged proventriculus.
Table 1. Distribution by presenting clinical signs and clinical course of 66 budgerigars with detected Macrorhabdus ornithogaster. Range Mean Lethargy Progress Weight (g) Clinical signs Improvement during initial 24 26-57 37 14 treatment, n Body Condition No information 1 45 45 Good 5 39-57 44 3 Moderate 10 28-51 37 4 Poor 8 26-39 31 7 Improvement, with relapse 11 26-54 39 6 in clinical signs, n Body Condition Good 3 26-54 38 1 Moderate 5 32-49 40 3 Poor 3 27-42 36 2 Improvement initially 2 27-29 28 1 then died, n Body condition poor 2 27-29 28 1 Died with no improvement, n 13 27-43 35 8 Body Condtion Moderate 4 31-42 37 4 Poor 9 27-43 34 4 Euthanasia, n 6 30-38 33 S Body Condtion Moderate 1 32 32 1 Poor 5 30-38 33 4 No information regarding 10 31-45 37 5 clinical course, n Body Condition Very good 1 44 44 Good 1 45 45 Moderate 6 31-38 34 4 Poor 2 34-37 36 1 Vomiting/ Regurgitation Anorexia Progress Clinical signs Improvement during initial 24 13 2 treatment, n Body Condition No information 1 Good 5 3 Moderate 10 9 Poor 8 1 2 Improvement, with relapse 11 6 1 in clinical signs, n Body Condition Good 3 1 Moderate 5 4 1 Poor 3 1 Improvement initially 2 2 then died, n Body condition poor 2 2 Died with no improvement, n 13 7 1 Body Condtion Moderate 4 2 Poor 9 5 1 Euthanasia, n 6 4 Body Condtion Moderate 1 1 Poor 5 3 No information regarding 10 4 1 clinical course, n Body Condition Very good 1 1 Good 1 1 Moderate 6 2 1 Poor 2 Undigested Polyphagia seeds in feces Progress Clinical signs Improvement during initial 24 3 treatment, n Body Condition No information 1 Good 5 1 Moderate 10 1 Poor 8 1 Improvement, with relapse 11 3 4 in clinical signs, n Body Condition Good 3 1 1 Moderate 5 1 2 Poor 3 1 1 Improvement initially 2 1 then died, n Body condition poor 2 1 Died with no improvement, n 13 2 1 Body Condtion Moderate 4 Poor 9 2 1 Euthanasia, n 6 2 Body Condtion Moderate 1 1 Poor 5 1 No information regarding 10 1 clinical course, n Body Condition Very good 1 1 Good 1 Moderate 6 Poor 2 Diarrhea Melena Progress Clinical signs Improvement during initial 24 2 treatment, n Body Condition No information 1 Good 5 1 Moderate 10 Poor 8 1 Improvement, with relapse 11 3 in clinical signs, n Body Condition Good 3 Moderate 5 2 Poor 3 1 Improvement initially 2 1 then died, n Body condition poor 2 1 Died with no improvement, n 13 4 Body Condtion Moderate 4 Poor 9 4 Euthanasia, n 6 2 Body Condtion Moderate 1 Poor 5 2 No information regarding 10 2 1 clinical course, n Body Condition Very good 1 Good 1 Moderate 6 2 1 Poor 2 Bacterial Candida spp. infections infection Progress Additional findings Improvement during initial 24 treatment, n Body Condition No information 1 Good 5 Moderate 10 Poor 8 Improvement, with relapse 11 2 in clinical signs, n Body Condition Good 3 1 Moderate 5 Poor 3 1 Improvement initially 2 then died, n Body condition poor 2 Died with no improvement, n 13 1 2 Body Condtion Moderate 4 Poor 9 1 2 Euthanasia, n 6 Body Condtion Moderate 1 Poor 5 No information regarding 10 2 clinical course, n Body Condition Very good 1 Good 1 1 Moderate 6 Poor 2 1 Trichomniasis Progress Additional findings Improvement during initial 24 1 treatment, n Body Condition No information 1 Good 5 Moderate 10 1 Poor 8 Improvement, with relapse 11 in clinical signs, n Body Condition Good 3 Moderate 5 Poor 3 Improvement initially 2 1 then died, n Body condition poor 2 1 Died with no improvement, n 13 Body Condtion Moderate 4 Poor 9 Euthanasia, n 6 Body Condtion Moderate 1 Poor 5 No information regarding 10 clinical course, n Body Condition Very good 1 Good 1 Moderate 6 Poor 2
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|Title Annotation:||Retrospective Study|
|Author:||Pustow, Ronja; Krautwald-Junghanns, Maria-Elisabeth|
|Publication:||Journal of Avian Medicine and Surgery|
|Date:||Dec 1, 2017|
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