Abstract
Summary
For many years, in clinical avian practice, the authors have noted what appears to be a syndrome in conure species (Aratinga and the related Cyanoliseus patagonus). The clinical history and/or physical examination may elucidate or suggest episodes of bleeding; hence we have coined the name "Hemorrhagic Conure Syndrome.'' The purpose of this report is to alert practitioners to our findings and to stimulate research on this perplexing problem.
Case I.
In December of 1983, a young bluecrowned conure (Aratinga acuticaudata) was rushed to our hospital for diagnosis and treatment. The bird had been purchased from a local pet store seven months previously. The patient was exhibiting apparent ataxia or profound weakness and polyuria on the day of presentation and had a history of intermittent polyuria and diarrhea. On the day of presentation, bloody fluid was noticed exuding from the nostrils. The bird died in transit to the hospital and was necropsied. Histopathologic examination of the submitted tissues revealed a large number of immature neoplasticappearing RBCs within the hepatic sinusoids with a similar cluster also present in the pancreas. The diagnosis was Erythremic Myelosis (L.A. County Pathology Laboratory case record #111013).
Case II.
In early January of 1981, a mature golden-crowned conure (Aratinga aurea) was presented for diagnosis and treatment. The previous history included epistaxis, considered by the client to be a simple "nosebleed." On the day of presentation the bird was comatose and dyspneic and died shortly after being hospitalized. Histopathology examination of the submitted tissues revealed a considerable amount of hemosiderin within the lungs, suggestive of past hemorrhage. There was massive hemorrhage within the pectoral muscle, with central pseudocyst formation due to the presence of blood. Peripheral muscle fibers were degenerating secondarily. The liver sinusoids had diffuse influx of malignant hematopoietic blast cells. Moderate non-suppurative inflammation was seen in the pericardium. Focal incidental endocardial cartilage metaplasia was also seen. The bone marrow was hypercellular and populated by blasts with little evidence of significant maturation. The following diagnoses were rendered by Dr. James 0. Britt, Jr., of the Los Angeles County Veterinary Pathology Laboratory (Case record #90912).
1. Erythroleukemia
2. Pericarditis, mild
3. Consolidating, multifocal pneumonia
4. Acute hemorrhage, muscle
Dr. Britt made the comment that spontaneous atrial rupture does occur in chickens and in caged birds and that it would be interesting to speculate that it and the hemorrhagic syndrome are associated with the myeloproliferative disease.
Case III.
In February of 1981, a mature halfmoon conure (Aratinga canicularis) was presented for weakness and dyspnea. The history included previous episodes of dyspnea with nasal bleeding. The bird expired shortly after presentation and was necropsied. Lesions included hemosiderin-ladened macrophages within the lungs (around the vessels and bronchioles) and clusters of "hemosiderophages" beneath the air sacs. The hemosiderin accumulation was apparently due to previous hemorrhage into the respiratory system. The bone marrow (femoral) was populated by blasts, with early erythrocytic differentiation and leukemic blast cells seen in the hepatic sinusoids. The spleen was packed with masses of monomorphic hematopoietic cells. The diagnosis (Case record #91414) was Erythroblastosis (Erythremic Myelosis).
Case IV.
On June 23, 1983, a mature halfmoon conure (Aratinga canicularis) was presented for diagnosis and treatment. This solo pet had been purchased at a local pet store five years previously and had been perfectly healthy. No recent exposure to other birds had occurred.
The bird was extremely weak, and exhibited an unusual trance-like posture on its perch. (The authors have often observed that conures weak from blood loss-Hemorrhagic Syndrome, injury, other causes-seem to prefer to remain perched in unusual positions, rather than lie on the cage bottom as other avian species prefer.) It was extremely thin (58.3 g) and the owner noted that bleeding episodes had occurred the previous week. The owner had assumed the bird had been injured and had suffered a "nosebleed." To facilitate diagnosis, a blood sample was collected (no appreciable stress occurred) via the nail clip technique and a gram stain was performed on the bird's feces. Tentative diagnoses included: 1) Hemorrhagic Conure Syndrome, 2) Gram Negative Septicemia, 3) Psittacosis, 4) Internal Injury, 5) Trauma, 6) other rarer conditions,
7) combinations of the above.
The laboratory work-up showed many abnormalities: the bird's PCV was 26%, there was a marked leukocytosis (27,500/mm) with a heterophilia (84%), heavy polychromasia and anisocytosis were evident, the total protein was markedly low, there was a borderline hypoglycemia and a marked hypocalcemia, and both the SGOT (SAST) and creatinine values were elevated. Many young red blood cells were seen in the peripheral blood suggestive of a response to recent blood loss. The fecal gram stain showed positive cocci and light gram negative rods.
Initial treatment consisted of i.m. injections of 5 mg of cefotaxime (Claforan - Hoechst-Roussel), .2 mg of dexamethasone, .20 cc Calphosan (Carlton), .05 cc Winstrol-V (Winthrop), and .05 cc B-complex. The bird was gently force-fed 3 cc of feeding mix three times daily with 5 mg of doxycycline (Vibramycin® - Pfizer) added to two of the feedings because of the possibility of psittacosis. Surprisingly, the bird tolerated the handling without struggling or exhibiting undue stress.
The bird showed signs of increased strength and was more alert but still critically weak two days later. It died in the late evening of June 25, 1983, and was necropsied.
Gross pathologic findings included a hemorrhagic left lung and a slightly pale liver and heart. No other abnormalities were noted. Tissues were sent to Dr. James 0. Britt, Jr. at the Los Angeles County Veterinary Pathology Laboratory for histopathology.
Dr. Britt reported that the liver had a relatively heavy influx of immature hyperchromatic cells throughout the sinusoids, most compatible with neoplastic, immature RBCs. The lung had an area of recent hemorrhage with many hemosiderin-laden macrophages. Other tissues were normal. No bone marrow, unfortunately, was submitted. The diagnosis was Erythremic Myelosis (Case# 106888).