Avian Pox in Lories (Neopsittacus sp. ): A Case Report
Helga Gerlach, Antonio J. Ramis, Frank Enders, Miguel Casares, and Uwe Truyen
Grosshesseloher Str. 23, 81479 München Germany (Gerlach); Department of Pathology, School of Veterinary Medicine, Universitat Autònoma de Barcelona, 08193-Bellaterra, Barcelona, Spain (Ramis); Loro Parque, 38400 Puerto de la Cruz, Tenerife, Spain (Enders, Casares); Institut für Medizinische Mikrobiologie, Infektions- und Seuchenmedizin, Veterinärstr. 13, 80539 München, Germany (Truyen)
Abstract. This manuscript describes an outbreak of septicemic avian pox virus infection in lories during quarantine.
Key Words: Avian pox, Lorikeet, Neopsittacus sp. , Septicemia, Virus
Introduction
The genus Avipoxvirus seems to be restricted to birds, but can cause diseases in a variety of avian species. Taxonomically, only 10 poxvirus species are recognized and two are considered tentative species. 1 Evidence of avian poxvirus infection is recognized in 57 different species of birds. 2 From the more recent literature, 36 taxons of the Avipoxvirus are listed with their presumed host spectrum. 3 Most of these taxons have a narrow host spectrum (species- or genus-specific); however, Fowlpox-, Pigeonpox-, Turkeypox-, Waterfowlpox-, Falconpox-, and Psittacinepoxvirus are known to have a wider host spectrum. Disease caused by Avipoxvirus is easily recognized histologically and is characterized by the intracytoplasmic, eosinophilic inclusions called Bollinger bodies. The presence of Bollinger bodies is considered pathognomonic for poxvirus infection. Because a disease diagnosis can be made without isolating the viral strain in question. In the accessible literature, there are no reports of avian poxvirus infections in Lorikeets (loriinae). Therefore, a short description of the disease is given in this case report.
Description of the Disease
Birds and medical histories: Three birds became sick and died in quarantine within 2 to 14 days after arrival at the station (arrival date, 19 December 1997):
Bird #1: Emerald Lorikeet (Neopsittacus pullicauda), 0.1 (female). The bird appeared emaciated on arrival and weighed 31 g. Conjunctivitis of the left eye was present. Moderate numbers of non-haemolysing staphylococci were isolated by microbiological culture. A Chlamydia psittaci-antigen test (Clearviewa ) was negative. Therapy included enrofloxacin,b given locally and intramuscularly. The bird died on 21 December 1997.
Bird #2: Musschenbroek´s Lorikeet (Neopsittacus musschenbroekii), 1.0 (male), juvenile. At arrival, the body weight was 53 g. Determination of chlamydial IgG was negative. The white blood count (WBC) was 8,200 cells /µl. Therapy from 20 December to 23 December included enrofloxacin (given locally and by intramuscular injection) and nystatin c (given orally). Body weight had decreased to 43 g on 27 December. Conjunctivitis was observed in the right eye and the bird appeared listless. Drug therapy was changed to Chibroxin and vibramycin. d The Clearview chlamydia test was negative. The bird died on 28 December 1997.
Bird #3: Emerald Lorikeet (Neopsittacus pullicauda) 1.0 (male). Body weight upon arrival was 37g. Drug therapy administered from 20.December to 23 December included enrofloxacin (locally and intramuscularly) and nystatin (orally). The chlamydia IgG test was negative for antibody. The WBC was 8,600 cells /µl. The bird died on 2 January 1998.
Necropsy findings: The postmortem examination of bird #1 did not reveal many lesions. Conjunctivitis and dark, edematous lungs were observed. The presumptive diagnosis was possible pneumonia. Contact birds #2 and #3 also were necropsied. These birds also had conjunctivitis and similar macroscopic lesions in the lung.
Histologic findings: The histopathology of bird #1 showed hyperplasia and ballooning degeneration of epithelial cells. Bollinger bodies, as usually described in pox infections, were observed in epithelial cells of the bronchi (Figs. 1 & 2), eyelid (Fig. 3) and, surprisingly, the pancreatic duc (Figs. 4 & 5). Lymphocellular depletion was observed in the spleen.
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| Fig. 1. Lorikeet, lung, poxvirus infection, H&E stain, x 33. The bronchus is partially obstructed by epithelial cell hyperplasia. |
Fig. 2. Lorikeet, lung, poxvirus infection, H&E stain, x 100. Higher magnification of Fig.1 showing hyperplastic epithelial cells with ballooning degeneration and Bollinger bodies. |
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| Fig. 3. Lorikeet, eyelid, poxvirus infection, H&E stain, x 100. Hypertrophy and hyperplasia of epidermal prickle cells. Numerous eosinophilic
inclusions (Bollinger bodies) distend the cytoplasm of the affected cells. |
Fig. 4. Lorikeet, pancreas, poxvirus infection, H&E stain, x 25. Massive proliferation and ballooning degeneration of pancreatic duct epithelial cells. |
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| Fig. 5. Lorikeet, pancreatic duct, poxvirus infection, H&E stain, x 100. Ductular epithelial cells contain large, cytoplasmatic, eosinophilic inclusions (Bollinger bodies). |
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| Fig. 6. Musschenbroek´s Lorikeet; lung extract, poxvirus infection, electron micrograph. Typical virion of Avipoxvirus measures approximately 300 nm in length. |
Bird #2 had ballooning degeneration of the epithelial cells of the palpebral conjunctiva. Bollinger bodies were observed within the cytoplasm of some epithelial cells. The tissue also contained multiple bacterial colonies and heavy infiltrate of heterophils in the subcutis. Severe hyperemia and edema were present in the lung; however, cellular infiltrates (suggesting inflammation) were absent. Marked lymphocellular depletion was observed in sections of spleen. Other microscopic lesions included tubulonephrosis and moderate hepatic hemosiderosis. To confirm the presence of poxvirus, lung tissue was prepared for examination by negative staining electron microscopy. Briefly, tissues were ground using sea sand and the resulting 1:10 homogenate was clarified by centrifugation at 14.000 rpm in a microfuge. The supernatant was applied to Formvar-coated copper grids, stained with 5 % phosphotungstic acid, and examined. Many brick-shaped virus particles were observed. The virions measured approximately 300 nm and had a surface pattern and morphology characteristic of avipoxviruses (Fig. 6).
In bird #3, only the tip of the tongue had the typical lesions of Avipoxvirus infection. Sections of lung contained hemorrhages into the atria and parabronchi. Also, there was some desquamation of pneumocytes forming detritus within the parabronchi. The spleen was totally depleted of lymphocytes. Liver, heart, lung, and skeletal muscles had multifocal necrosis containing fungal hyphae, possibly Candida sp. pseudohyphae.
Discussion
From the clinical and histopathological points of view, these birds had both the septicemic and mucosal forms of avipoxvirus infection. The presence of avipoxvirus infection was confirmed by electron microscopy. Severe diseases by Avipoxvirus occur only if the infection takes a two-cycle course. In the mucosal form of the disease, the virus targets the mucosa of the beak cavity, pharynx, larynx, and, rarely, lower respiratory epithelia. Clinical signs usually appear during generalization of the disease process following the second episode of viremia. The septicemic form of avian poxvirus infection is characterized by death of the birds during the second viremia. By this phase of the disease, cutaneous or mucosal lesions are absent or scarcely developed.
The occurrence of Bollinger bodies in the ductal epithelium of the exocrine pancreas is additional evidence for the septicemic form of poxvirus infection. With the septicemic form of disease, most birds die within 3 days after developing clinical signs. Although bird #3 never exhibited clinical signs of disease, the pulmonary hemorrhages observed at necropsy and in tissue sections are typical of the septicemic form of avian poxvirus infection. In all three birds, severe immunosuppression was obvious and probably inhibited the usual focal pneumonia. Although Avipoxvirus is known to induce mild to moderate immunosuppression, the marked lymphocellular depletion of the spleen might have an additional etiology. Whether or not transport and change of environment are sufficient explanations for this additional etiology remains doubtful. Because of the immunosuppression present in these birds, the question of the virulence of the Avipoxvirus strain cannot be answered.
Although the septicemic form of disease has a short incubation period (a minimum of 4 days for canaries),4 the source of infection must have been the original flock. Avipoxvirus infection can remain latent for years. 5,6 Non-specific stressors are associated with viral reactivation, which might be in this case in these birds. Avipoxvirus cannot penetrate the intact epithelium; however, very small lesions such as slight abrasions during transport or minor trauma from new cages might allow entrance of the virus into the body.
The Avipoxvirus called Psittacinepoxvirus (a recognized species1) has a wide host spectrum, including South and Middle American parrots and parakeets. The genus Neopsittacus, which includes the birds of this report, originate in the mountains of New Guinea. Therefore, the virus infecting these birds is probably not Psittacinepoxvirus and may represent a new taxon. Ultimately, characterization of the poxvirus infecting Lorikeets will be necessary to refute or confirm any similarity to Psittacinepoxvirus or other known members of the Avipoxvirus family.
Sources and Manufacturers
a. Clearview, Abbott Unipath, Bedford, UK
b. Enrofloxacin as Baytril™, Bayer, Germany
c. Nystatin, Squibb
d. Vibramycin™ (corresponds to doxycyclin for injection), Pfizer, Germany
References
1. Esposito JJ, et al: Genus Avipoxvirus. In: Virus taxonomy - 6th report of the International Committee on Taxonomy in Viruses. Springer-Verlag, Wien, New York, 1995, p. 85.
2. Potel K: Geflügelpocken Variola avium. In: Röhrer, H. : Handbuch der Virusinfektionen bei Tieren. Gustav Fischer Verlag, Jena .Vol. II, pp. 603-613.
3. Gerlach H: Avipoxvirus. In: Ritchie BW, Harrison G J & Harrison L R (eds): Avian Medicine: Principles and Application. Wingers Publishing, Inc. , Lake Worth, FL, 1994, pp. 865-874.
4. Mayr A: Vogelpocken. In: Heider-Monreal (eds. ): Krankheiten des Wirtschaftsgeflügels. Gustav Fischer Verlag Jena, Stuttgart, 1992, pp. 486-491.
5. Hanson LE, Tripathy DN: Fowlpox and latency. Proc 24th Western Poultry Dis Conf, pp. 43-45.
6. Kirmse P: Host specificity and pathogenicity of pox viruses from wild birds. Bull Wildlife Dis Assoc 5:376-386, 1969.
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