Ocular and encephalic toxoplasmosis in canaries

In this report we describe the lesions produced by the protozoal organism, Toxoplasma gondii, in the eyes and brain of the common yellow canary (Serinus canaria). Nine of 15 birds in a flock were affected with blindness, which developed over a 3-mo span, and two birds developed torticollis. Microscopic alterations within the eye consisted of a nonsuppurative chorioretinitis with large numbers of macrophages that contained the tachyzoite form of T. gondii in the subretinal space, and aggregates of tachyzoites were found in the nerve fiber layer of the retina with and without necrosis. Tissue cysts with bradyzoites were scattered throughout the meninges and neuropil of the cerebrum and cerebellum. Both forms were confirmed by transmission electron microscopy in the eye and brain. Frozen brain samples reacted with T. gondii-specific cat sera in indirect fluorescent antibody tests. The source of infection was hypothesized to be from a stray cat the owner kept that had access to some of the bird feed. Treatment (trimethoprim 0.08 g/ml H2O and sulfadiazine 0.04 g/ml in water for 2 wk) was instituted by the referring veterinarian on the remaining birds. A second treatment regime was given for 3 wk. The owner of the canaries did not return for further treatment.     

Blindness associated with toxoplasmosis in canaries.

Seven of 30 canaries in an aviary in New Zealand developed ophthalmic problems. Clinically, 5 birds had unilateral and 2 birds had bilateral lesions characterized by conjunctivitis, crusty exudates on eyelids, and collapse of the eyeball. Microscopic lesions in 12 of 14 eyes examined included inflammation of the choroid and retina, with osseous replacement of the globe in some. Numerous Toxoplasma gondii tachyzoites were seen in the detached retina and vitreous humor of acutely affected birds. The diagnosis of toxoplasmosis was confirmed by immunohistochemical staining with T gondii antiserum. Affected birds had encephalitis, and T gondii was localized in the brains of these by immunohistochemical examination and by use of bioassays in mice. Toxoplasmosis should be considered in differential diagnosis of ophthalmitis in canaries.     

Spontaneous cataracts in laboratory rabbits

Objective To document the occurrence and incidence of spontaneously occurring cataracts in older New Zealand White (NZW) and New Zealand White × New Zealand Red (NZW × NZR – F1) rabbits during prescreening examinations at Alcon Laboratories. Procedures A retrospective study was conducted on prescreening examination records of NZW and NZW × NZR (F1) rabbits at Alcon Laboratories between April 1999 and May 2001. Results A total of 946 rabbits (670 NZW and 276 NZW × NZR) ranging in age from 77 to 288 days were examined. Of the NZW rabbits, 333 were males and 337 were females. Of the NZW × NZR (F1) rabbits, 139 were males and 137 were females. Thirty‐eight NZW rabbits (23 males and 15 females) exhibited immature cataracts in one or both eyes, and three NZW × NZR (F1) rabbits (one male and two females) exhibited cataracts in one or both eyes. The overall incidence of cataracts was 4.3% of all rabbits. Males and females were equally affected, but a significant difference in the incidence of cataracts existed between the NZW and NZW × NZR (F1) rabbits with 5.7% of the NZW rabbits affected and 1.1% of the NZW × NZR (F1) rabbits affected. Conclusion Spontaneous juvenile cataracts occur in rabbits and may develop as incidental lesions during toxicologic studies. The incidence of cataracts noted in our studies is consistent with an autosomal recessive mode of inheritance, but further studies are needed to confirm the mode or modes of inheritance. Hybrid pigmented rabbits (F1 or NZW × NZR) exhibited a significantly lower incidence of cataracts.     

Increasing incidence of megabacteriosis in canaries (Serinus canarius domesticus)

A total of 312 post-mortem examinations of 178 canaries (Serinus canarius domesticus), 40 parakeets (Melopsittacus undulatus, Nymphicus hollandicus) and 94 parrots (Amazona aestiva, Psitaccus erithacus) were conducted at the Birds and Rabbits Service of the University of Liège, Belgium. After a detailed gross examination, tissue samples were collected for virological and/or bacteriological and/or parasitological examination to complete the diagnosis. In all cases, a microscopic examination of the proventricular mucus layer was undertaken for the detection of the anamorphic ascomycetous yeast Macrorhabdus ornithogaster, which causes the non-zoonotic but important disease in cage birds known as megabacteriosis. At the time of death, megabacteriosis was diagnosed respectively in 28% of canaries and 22.5% of budgerigars (P value for Fisher's exact test=0.5576), but was not diagnosed in parrots (P value for Fisher's exact test <0.0001). The incidence of megabacteriosis significantly increases along the years (P value for chi2 test <0.0001, Cramer's coefficient=0.3405). The most common gross lesions seen at necropsy of the 59 megabacteriosis cases was proventricular dilatation (86.1%). All the birds diagnosed as typical megabacteriosis cases were free of Salmonella spp. infections and of any parasitic infections. Four megabacteriosis cases (three canaries, one parakeet) were not included in statistical analysis as salmonellosis, pseudotuberculosis, coccidiosis and chlamydophilosis were diagnosed concomitantly in these birds. With the exception of megabacteriosis, the most frequent causes of death were protozoan (coccidiosis, lankesterellosis) infections (18.4%) and salmonellosis (17.1%) in canaries, and psittacosis (31.5%) and viral hepatitis (26.3%) in parakeets. In parrots, the most common causes of death were psittacosis (28.6%) and aspergillosis (28.5%).     

Atoxoplasma spp. infection in captive canaries (Serinus canaria)

Clinical signs, histopathological and ultrastructural findings associated with Atoxoplasma spp. natural infection in captive canaries (Serinus canaria) are described. Intracytoplasmic Atoxoplasma-like protozoa were found in the liver and lung. In the liver, protozoa were found in hepatocytes and Kupffer's cells and were associated with granulomatous hepatitis and a marked bile duct hyperplasia. An usual finding was the presence of infected mononuclear cells adhered to the endothelium of the blood vessels in lung. The diagnosis was confirmed by ultrastructural examination of reprocessed paraffin-embedded tissues.     

Clinical evaluation of intranasal benzodiazepines, alpha-agonists and their antagonists in canaries

OBJECTIVE: To evaluate the effects of intranasal benzodiazepines (midazolam and diazepam), alpha(2)-agonists (xylazine and detomidine) and their antagonists (flumazenil and yohimbine) in canaries. STUDY DESIGN: Prospective randomized study. ANIMALS: Twenty-six healthy adult domesticated canaries of both sexes, weighing 18.3 +/- 1.0 g. METHODS: In Study 1 an attempt was made to determine the dose of each drug that allowed treated canaries to be laid in dorsal recumbency for at least 5 minutes, i.e. its effective dose. This involved the evaluation of various doses, during which equal volumes of the tested drug were administered slowly into each nostril. In study 2 the onset of action, duration and quality of sedation induced by each drug at its effective dose were evaluated. The efficacy of flumazenil and yohimbine in antagonizing the effects of the sedative drugs was also studied. RESULTS: In study 1 administration of 25 microL per nostril diazepam (5 mg mL(-1) solution) or midazolam (5 mg mL(-1) solution) to each bird caused adequate sedation within 1-2 minutes; birds did not move when placed in dorsal recumbency. After administration of 12 microL per nostril of either xylazine (20 mg mL(-1)) or detomidine (10 mg mL(-1)), birds seemed heavily sedated and assumed sternal recumbency but could not be placed in dorsal recumbency. Higher doses of xylazine (0.5 mg per nostril) or detomidine (0.25 mg per nostril) prolonged sedation but did not produce dorsal recumbency. In study 2 in all treatment groups, onset of action was rapid. Duration of dorsal recumbency was significantly longer (p < 0.05) with diazepam (38.4 +/- 10.5 minutes) than midazolam (17.1 +/- 2.2 minutes). Intranasal flumazenil (2.5 microg per nostril) significantly reduced recumbency time. Duration of sedation was longer with alpha(2)-agonists compared with benzodiazepines. Detomidine had the longest duration of effect (257.5 +/- 1.5 minutes) and midazolam the shortest (36.9 +/- 2.4 minutes). Nasally administered flumazenil significantly reduced the duration of sedation with diazepam and midazolam while yohimbine (120 microg per nostril) effectively antagonized the effects of xylazine and detomidine. CONCLUSION: Intranasal benzodiazepines produce rapid and effective sedation in canaries. Intranasal alpha(2) agonists produce sedation but not sustained recumbency. Specific antagonists are also effective when used by this route. Clinical relevance Intranasal sedative drug administration is an acceptable alternative method of drug delivery in canaries.     

Evaluation of selected plants for their toxic effects in canaries.

Leaves or fruit from 14 plants considered to be toxic to pet birds were administered by gavage to 15 pairs of canaries (Serinus canaria). Each bird was given 0.12 to 0.70 g of plant material. One pair served as a control and was given distilled water. The plant materials were flash-frozen in liquid nitrogen, pulverized, and resuspended in deionized water for administration. Of the plants tested, 5 (oleander, lupine, foxglove, yew leaves, and dieffenbachia) were considered highly toxic and were associated with acute death of birds. The remaining plant samples caused no, or only transient, clinical illness.