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.     

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.     

Neonatal toxoplasmosis in kittens

The occurrence of toxoplasmosis is described in the cat-mother and three kittens. Clinical symptoms were not significant: bristled hair, conjunctivitis, sneezing and hypertrophy of mandibular and popliteal lymph nodes. The titres of antibodies to Toxoplasma gondii were demonstrated in all kittens and also in the cat: Sabin-Feldman reaction titre 4-32, complement-fixing reaction titre 5-40. Microprecipitation in agar gel was positive in all animals. Oocytes of Toxoplasma gondii were eliminated through faeces by the cat and two 16-day-old kittens. An isolation trial on white mice with a negative finding of toxoplasmosis (inoculation of brain, liver and spleen samples) has demonstrated toxoplasmosis in all animals under study. Most probably the kittens were infected transplacentally.     

Chorio-retinitis in porcine toxoplasmosis

Porcine toxoplasmosis generally occurs as a latent disease in adolescent and adult pigs, but now and then also manifests itself as a fatal congenital disease in piglets. It is known to occur in USA (Farrel et al. 1952), Germany (Becker 1954), Denmark (Momberg-Jørgensen 1956), Mexico (Varela et al. 1956), Japan (Sato et al. 1958), England (Harding et al. 1961) and Sweden (Hansen et al. to be published).     

Ovine toxoplasmosis in Sweden

Sera from 155 ewes representing 21 different sheep flocks from the central parts of Sweden were examined for the presence of antibodies to Toxoplasma gondii by the indirect fluorescent-antibody test. Seropositive animals were found in 14 flocks, which corresponded to 55 % of the tested sera. Animals from the same flock were with few exceptions either all positive or all negative. Some ewes with a history of abortion a few months before blood sampling showed high titers indicating causative correlation with toxoplasmosis. These are the first verified cases of ovine toxoplasmal abortions in Sweden.Key words: Toxoplasma gondii, sheep, abortion, fluorescent antibody test     

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.     

Mitochondriopathy with regional encephalic mineralization in a Jack Russell Terrier

A 10-month-old female Parson Jack Russell Terrier was euthanatized because of therapy-resistant ataxia, hypermetria, and deafness that had first been observed at 10 weeks of age. Severe, bilateral, symmetrical neuronal degeneration and mineralization of the brain were found in the cochlear and cerebellar nuclei, dorsal areas of the medulla oblongata, the vestibulocochlear nerve, plexus choroideus, and within the granule cell layer of the ventral cerebellar hemispheres. The mineralized deposits were located free in the parenchyma, around intact or degenerate neurons, in myocytes of small- and medium-sized arteries, and around capillaries. Hepatocytes and cardiac myocytes showed oncocytotic change with increased numbers of enlarged or misshapen mitochondria filled with densely packed cristae and electron-dense inclusions. Skeletal myocytes had only minor increases in the number of mitochondria. The microscopic and ultrastructural lesions were consistent with mitochondrial encephalopathy with similarities to mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes in humans.     

猪弓形体病的诊断与防治

猪弓形体病是人畜共患的疾病，该病近两年来在不少地方是老病新暴发，如何诊断与防治该病具有很大的意义。本文对该病的临床症状，病理变化，及从活体症状、用药、病原学、细菌分离培养、动物接种五个方面对该病的综合诊断和药物治疗、预防方面作了简述。     

Porcine toxoplasmosis in Indiana.

Toxoplasmosis was diagnosed at necropsy in a 4-week-old pig from a litter of 16 born to a clinically normal sow. Multifocal acute necrosis of blood vessels and parenchyma was found in the small intestine, mesenteric lymph nodes, liver, lungs, and brain. Numerous tachyzoites, ultrastructurally indistinguishable from Toxoplasma gondii, were found in lesions. The affected pig and seven other littermates died after diarrhea had developed within 1 to 2 weeks of birth. The most likely source of infection was oocysts from cats on the farm.     

Immunity to toxoplasmosis in hamsters

Protective immunity to Toxoplasma was studied in hamsters. Immunity developed in 2 to 3 weeks after vaccinations were performed. Vaccination with live RH, T-45, and ts-4 strains afforded the best protection against challenge exposure with the most pathogenic RH strain used. Even a killed-toxoplasma vaccine protected all hamsters against the slightly less pathogenic T-1 strain through 24 weeks, but it did not protect hamsters against challenge exposure with the RH strain. Both ts-4, a nonpersistent strain, and killed-toxoplasma vaccine provided protective immunity in hamsters that was not dependent upon premunition. Toxoplasma antibody titers in hamsters given the 2 vaccines were similar. However, there was a difference in the quality of immunity: fever and body weight loss were seen in hamsters vaccinated with the killed-toxoplasma vaccine after they were challenge exposed with T-1 strain, whereas these changes were rarely seen in hamsters given the live-toxoplasma vaccine and then challenge exposed with RH strain. Delayed-type hypersensitivity to Toxoplasma antigen always appeared before protective immunity and was detected in all hamsters by 4 days after vaccination with live-toxoplasma strains. Although the development of delayed-type hypersensitivity preceded protective immunity, it was not indicative that protective immunity was present or would develop.