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Amazon Tracheitis in Australian Parakeets: A Case Report
Helga Gerlach, Frank Enders, Miguel Casares, and Uwe Truyen
Grosshesseloher Strasse 23, 81479 München, Germany (Gerlach); Loro Parque, 38400 Puerto de la Cruz, Tenerife, Spain (Enders, Casares); and Institut für Medizinische Mikrobiologie, Infektions- und Seuchenmedizin, Veterinärstr. 13, 80539 München, Germany (Truyen)
Abstract. An outbreak of Amazon tracheitis, a Herpesvirus induced, mainly respiratory disease is described. Several new species are added to the host spectrum.
Key Words: Amazon tracheitis, Herpesvirus, host spectrum, clinical disease, pathology, histopathology, electron microscopy.
Introduction
Amazon tracheitis (AT) in psittaciform birds is caused by an a-herpesvirus that shows serologic relationship to the infectious laryngotracheitis (ILT) virus of chickens, but not to the so-called Pacheco´s disease virus. 1 Amazon tracheitis is a rare viral disease in birds kept in captivity, and not much is known about the host spectrum. In addition to the genus Amazona, a herpesviral disease pathologically similar to AT also has been reported in the Bourke´s Parrot (Neopsephotus bourkii). 2,3 However, the virus in question has not been isolated so comparisons between the virus strains are not possible. A full description of the clinical signs and the pathological lesions of AT (including experimental reproduction) has been published previously. 2-5 Recent deaths in a quarantine station, involving several species of the platycercidae family, were observed and attributed to an outbreak of AT. A description of the findings in these birds is presented in this manuscript .
Medical Histories and Description of Disease
The affected birds in the AT outbreak and their clinical histories are presented below. All of the birds arrived at the quarantine station on 19 December 1997.
Bird #1: Yellow Rosella (Platycercus flaveolus), 0.1 (female). The bird escaped from its cage on 24 December 1997 and had marked dyspnea after being caught. It died one hour later. Clinical signs of disease were not present before escape.
Bird #2: Bourke´s Parrot (Neopsephotus bourkii), 1.0 (male). A Chlamydia psittaci antigen test (Clearviewa ) was positive upon arrival in quarantine. The bird was treated with vibramycin given by intramuscular injection. The bird died unexpectedly on 26 December 1997.
Bird #3: Red-capped Parrot (Purpureicephalus spurius), 1.0 (male). The bird had good body condition on arrival (body weight = 102 g on 24 December 1997) and a negative chlamydial antigen test (Clearviewa ). Cloacal culture revealed moderate numbers of E. coli colonies. Respiratory distress was noticed prior to death on 10 January 1998.
Bird #4: Scarlet-chested Parrot (Neophema splendida), 0.1 (female). Good body condition was noted on 25 December 1997. Dyspnea was observed prior to death on 2 February 1998.
Bird #5: Scarlet-chested Parrot (Neophema splendida), 0.1 (female). Good body condition on 25 December 1997. Central nervous system signs were observed prior to death on 3 February 1998.
Birds #6,7,8, & 9: Four Whiskered Lorikeets (Oreopsittacus arfaki), 2.2 (2 males and 2 females). Body weight ranged from 15 to 18 g on 22 December 1997. Breast muscle palpation revealed good body condition only in the two heavier (18 gm) birds. Chlamydial antigen tests (Clearviewa ) were negative. Cloacal culture of all birds revealed moderate to high numbers of E. coli colonies and moderate to high numbers of C. albicans colonies. All of the birds were treated with Cefotaximb (100 mg/kg BM sc BID) and Ketoconazolc (30 mg/kg BM oral SID) on 24 and 25 December 1997. All 4 birds died during the night of 26 December 1997.
The necropsy examination of all birds showed severe hyperemia, edema, and a dark red lungs indicating either hemorrhage or pneumonia. In addition, the airsacs of the Yellow Rosella (Platycercus flaveolus, bird #1), were thickened and covered with yellow material, presumably fibrin. The other lesions were more or less non-specific, including hyperemia of the internal organs. The liver and kidney were swollen probably due to secondary E. coli infection. Brownish-blackish material was observed in the intestinal tract. Bacterial cultures of liver and heart of the dead birds disclosed a variable degree of E. coli infection.
The histopathologic changes in the respiratory tract varied because of the disease and because different samples were taken from the respiratory tract of the various birds. In the Yellow Rosella, a fibrinous bronchopneumonia was diagnosed. Smaller bronchi were obliterated by mucus, detritus, and extravasated erythrocytes. Foci of necrosis and development of sequestra also were observed. Bronchial and airsac epithelial cells were degenerate and had syncytia (multinucleated cellular masses produced by merging of cells). Closer inspection revealed eosinophilic inclusion bodies within nuclei (Fig. 1 ). Airsac thickening was caused by fibroplasia and neovascularization, indicating that the infection was not acute. The bird died from asphyxiation, but also had myocardial degeneration. The spleen had some lymphoid follicles and many individual lymphocytes.
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| Fig. 1. Yellow Rosella; airsac, epithelium with syncytia and inclusion bodies; H&E stain, x 400. |
In addition to Chlamydia psittaci infection, the Bourke´s Parrot (Neopsephotus bourkii, bird #2), also had polyserositis with severe hyperemia and hemorrhages of the lung. The bronchial submucosae also contained activated lymphoid follicles and edema. Both the bronchial and serosal epithelia showed degeneration, necrosis, scattered syncytia, and a few eosinophilic intranuclear inclusions. The spleen was largely depleted of lymphocytes. The liver and kidney had hemosiderosis and tubular nephrosis, respectively.
The Red-capped Parrot (Purpureicephalus spurius, bird #3) had microscopic lesions indicating a more prolonged course of disease. The lung was characterized by hyperemia and edema. Airways contained mucus, detritus, and extravasated erythrocytes and were lined by a markedly hyperplastic columnar epithelium. The goblet cells were extremely dilated and some of them apparently lacked mucous granules. Because the diseased and desquamated epithelium had regenerated, nuclear inclusions were no longer observed. However, the submucosa contained mononuclear cell infiltrates that were also disseminated throughout the pulmonary interstitium. The myocardial fibers appeared vacuolated. Hemosiderosis was observed within the liver and kidney. Adequate lymphocytes and lymphoid follicles were present within the spleen.
The lung of bird #4 (Scarlet-chested Parrot, Neophema splendida) had diffuse hyperemia, edema, and hemorrhage. The parabronchial and bronchial lumina were obliterated, suggesting that the bird died of asphyxiation. The bronchial lining had masses of degenerate epithelial cell syncytia and lightly eosinophilic nuclear inclusions (Fig. 2). Myocardial degeneration also was observed.
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| Fig. 2. Scarlet-chested Parrot; bronchial tissue proliferation and epithelial syncytia with inclusion bodies; H&E stain, x 250. |
The lung of the second Scarlet-chested Parrot (Neophema splendida, bird #5) had hyperemia, edema, and hemorrhages. The lumina of parabronchi and bronchi were filled with edematous fluid, mucus, and extravasated erythrocytes. The epithelial cells of the bronchi showed degeneration, syncytia, and nuclear inclusions that were not as distinct as in the other birds. The brain had moderate hyperemia with severe dilatation of Virchow-Robin´s spaces. The nuclei of ependymal cells had inclusions reminiscent of avian polyomavirus infection (In adult, non-budgerigar, psittaciform birds the morphology of these inclusions is not as characteristic as in budgerigars. Therefore, molecular techniques, such as the polymerase chain reaction or DNA probes are required for definitive diagnosis). Lastly, this bird also had myocardial degeneration.
The Whiskered Lorikeets (Oreopsittacus arfaki, birds #6-9) died from pulmonary hemorrhage. Examination of the bronchial epithelium failed to disclose severe cellular degeneration or nuclear inclusions. Therefore, lung specimens were submitted for electron microscopic evaluation. Lung tissue from two birds was examined using negative staining. Briefly, the lung specimens were ground using sterile sea sand and clarified by centrifugation at 14,000 rpm in a microfuge. The supernatant was collected, applied to Formvar-coated copper grids, stained with 5 % phosphotungstic acid, and examined. Single viral particles were observed that measured approximately 200 nm in diameter for intact virions approximately 100 nm in diameter for viral nucleocapsids. The ultrastructural morphology of the intact virions and nucleocapsids was characteristic for herpesvirus in lung preparations from both birds (Fig. 3 & 4). All four birds had myocardial degeneration. The spleens were either depleted of lymphocytes or exhibited lymphoid hyperplasia.
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| Fig. 3. Whiskered Lorikeet, electron micrograph, herpesvirus from the lung tissue, bar = 100 nm. |
Fig. 4. Whiskered Lorikeet, electron micrograph, herpesvirus with distinct envelope and capsid, bar = 100 nm. |
Discussion
The histologic lesions within the respiratory tract are consistent with published descriptions of AT. 2,3 In contrast to previous studies, we did not observe viral inclusions within renal epithelial cells. Hepatitis and other evidence of inflammation generally were not present; however, small foci of inflammation were observed in the Yellow Rosella with E. coli infection and in the Bourke´s Parrot with chlamydial infection.
Published literature on AT in Amazon Parrots (Amazona sp. ) indicates that the disease is more severe than that observed in the platycercus family. Replicate tissue sections from the Whiskered Lorikeets are being subjected to DNA in situ hybridization to further characterize this viral disease; particularly to prove beyond doubt that the herpesvirus seen by electron microscopy is not Pacheco's virus. An additional problem is that there are no commercially available antisera to type this virus. It is known that there is a double-sided cross reaction between the ILT- and the AT-herpesviruses; however, the successful DNA hybridization will depend upon the construction of the probe. The AT-herpesvirus is considered to be a mutation of the ILT virus. So far, the known host spectrum has included the genus Amazona and Bourke's Parrot (Neopsephotus bourkii). This case report shows that three other members of the platercercidae, apart from the Whiskered Lorikeets (Oreopsittacus arfaki), also are susceptible to infection by the AT-herpesvirus.
The natural incubation period of AT is unknown; however, experimental studies have shown that intramuscular infection of Amazon Parrots will cause death between 3 and 6 days post inoculation. 5 Peracute death is characterized by lack of clinical signs of disease. In our investigation, the Yellow Rosella died 5 days after arrival at the quarantine station. Therefore, this bird probably introduced the AT viral infection to other birds housed at this location. The birds that subsequently died in January and February probably were infected with AT herpesvirus during quarantine. Virus could not be isolated from these birds because only formalin-fixed tissues were submitted for examination. Currently, we are attempting to isolate herpesvirus from living birds that were in contact with these diseased individuals.
Sources and Manufacturers
a. Clearview, Abbott Unipath, Bedford, United Kingdom
b. Cefotaxim as Claforan®, Höchst, Frankfurt, Germany
c. Ketoconazol, Janssen, Germany
References
1. Gerlach H: Amazon tracheitis. In: Ritchie BW, Harrison G J, and Harrison LR (eds): Avian Medicine:
Principles and Application. Wingers Publishing, Inc. , Lake Worth, Florida, 1994, pp. 876-877.
2. Helfer DH, Schmitz JA, Seefeldt SC, et al. : A new viral respiratory infection in Parakeets. Avian Dis 24:781-783, 1980.
3. Lowenstine LJ: Diseases of psittacines differing morphologically from Pacheco’s disease but associated with herpesvirus-like particles. Proc 31st Western Poultry Dis Conf, 1982, pp.141-142.
4. Winteroll G und Gylstorff I: Schwere durch Herpesvirus verursachte Erkrankung des Respirationsapparates bei Amazonen. Berl Münch Tierarztl Wochen 92:277-280, 1979.
5. Kitzing D: Zur Charakterisierung eines mit dem ILT - Virus serologisch verwandten Herpesvirus aus Amazonen. Diss Med Vet, München, 1981.
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