Comparison of the human and canine Schiotz tonometry conversion tables in clinically normal dogs.

Intraocular pressure (IOP) was measured in 114 eyes of 57 clinically normal dogs with 2 applanation tonometers (Tono-Pen and Mackay-Marg) and the Schiotz indentation tonometer, using the 5.5- and 7.5-g weights. Significant differences were not detected between measurements obtained with the Tono-Pen and Mackay-Marg tonometers the Mackay-Marg and Schiotz tonometers using either weight and conversion with the human calibration table, or the Tono-Pen and Schiotz tonometers using the 7.5-g weight and the human calibration table. Values obtained by use of the Tono-Pen tonometer were significantly less (P less than 0.005) than values obtained with the Schiotz tonometer when a 5.5-g weight and the human calibration table were used, but the amount was clinically unimportant. Estimates of IOP using the Schiotz tonometer and the canine calibration table, and either the 5.5- or 7.5-g weight were clinically and significantly much higher (P less than 0.0001) than estimates obtained with the Tono-Pen, Mackay-Marg, or Schiotz tonometers, using the human calibration table and either weight. Sixty to 70% of clinically normal dogs had an IOP greater than or equal to 30 mm of Hg when Schiotz scale measurements were converted with the canine conversion table. For clinically normal dogs, the human calibration table was the most clinically useful table for converting Schiotz tonometer measurements to mm of Hg. Normal mean (+/- SD) canine readings with the Schiotz tonometer and the 5.5-g weight was 4.9 +/- 1.5 tonometer scale units (range, 2 to 11; 95% confidence interval, 1.9 to 7.9).(ABSTRACT TRUNCATED AT 250 WORDS)     

Summaries of lectures presented at a binational UK—Israel conference agriculture in a cleaner environment — new technologies from Britain and Israel

Extended summaries and abstracts of the lectures on pest and disease control, and on reduction of pesticidal pollution in the environment, presented within the framework of a conference which was organized by the Biotechnology & Biological Sciences Research Council (BBSRC), Swindon, UK, and the Agricultural Research Organization (ARO), The Volcani Center, Bet Dagan, Israel.     

Ophthalmic examination findings in a colony of Screech owls (Megascops asio)

Objective To report ophthalmic findings in the Screech owl (Megascops asio). Sample population Twenty‐three, apparently healthy adult captive Screech owls in Maryland. Procedures OU of all owls underwent complete ophthalmic examination. One randomly assigned eye of each bird was measured by phenol red thread tear test (PRT), and the other eye by Schirmer tear test (STT). TonoVet^® rebound tonometry and TonoPen‐XL^® applanation tonometry were performed in each eye to measure IOP. Conjunctival swabs were cultured from one eye of 10 birds, corneal diameter was measured in OU of eight birds, and streak retinoscopy was performed on OU of seven birds. Ten birds were anesthetized, and A‐scan ultrasonography using a 15‐MHz probe was performed to obtain axial intraocular measurements. Results Ophthalmic abnormalities were noted in 24/46 (52%) of eyes. Median STT result was ≤ 2 mm/min, ranging ≤ 2–6 mm/min, and mean ± SD PRT was 15 ± 4.3 mm/15 s. Mean ± SD IOP were 9 ± 1.8 mmHg TonoVet^®‐P, 14 ± 2.4 mmHg TonoVet^®‐D, and 11 ± 1.9 mmHg TonoPen‐XL^®. Coagulase negative staphylococcal organisms were cultured from all conjunctival swabs. Mean ± SD corneal dimensions were 14.5 ± 0.5 mm vertically and 15.25 ± 0.5 mm horizontally. All refracted birds were within one diopter of emmetropia. Mean ± SD axial distance from the cornea to the anterior lens capsule was 4.03 ± 0.3 mm, from cornea to the posterior lens capsule was 10.8 ± 0.5 mm, and from cornea to sclera was 20.33 ± 0.6 mm. Conclusions This study reports ophthalmic examination findings in Screech owls, and provide means and ranges for various ocular measurements. This is the first report of rebound tonometry and PRT in owls.     

Presumed and confirmed striatocapsular brain infarctions in six dogs

OBJECTIVE: To describe the clinical and diagnostic features of the canine sensorimotor syndrome caused by striatocapsular brain infarctions (SCI). ANIMALS STUDIED: Six dogs with diagnostic imaging or postmortem evidence of SCI. PROCEDURES: Medical records of dogs with SCI were retrospectively reviewed and the signalment, history, clinical signs, antemortem clinicopathologic test results, diagnostic imaging findings, case outcomes, and pathologic findings recorded. RESULTS: All dogs had an acute onset of nonprogressive homonymous visual field deficits and contralateral general proprioceptive (GP) deficits. Contralateral hemiparesis and facial hypalgesia were noted in 5/6 dogs. CT scans were normal in 2/4 dogs, and revealed poorly defined hypoattenuating lesions in the subcortical white matter in two dogs. MRI exams were performed in 5/6 dogs and revealed unilateral, variably sized, striatocapsular lesions consistent with nonhemorrhagic infarctions. Diagnostic imaging (6/6) and postmortem examinations (2/6) suggested that SCI resulted from lesions in the vascular territories of the rostral choriodal (6/6) and lenticulostriate arteries (2/6). Diseases predisposing to infarction were not identified in 5/6 dogs. Improvements in mentation, behavior, proprioceptive deficits, and hemiparesis were seen in surviving dogs, but persistent, symptomatic sensory deficits were noted during the follow-up period. CONCLUSIONS: SCI should be considered as a differential diagnosis for dogs with acute onset, nonprogressive homonymous hemianopia, contralateral GP deficits or hemiparesis, and facial hypalgesia. MRI is the preferred modality for the antemortem imaging diagnosis of SCI. Although partial recovery occurred in all surviving dogs, visual and facial sensory disturbances persisted.     

Epidemic of blindness in kangaroos - evidence of a viral aetiology

OBJECTIVE: To determine the cause of an epidemic of blindness in kangaroos. DESIGN AND PROCEDURES: Laboratory examinations were made of eyes and brains of a large number of kangaroos using serological, virological, histopathological, electron microscopical, immunohistochemical methods, and PCR with cDNA sequencing. In addition, potential insect viral vectors identified during the disease outbreak were examined for specific viral genomic sequences. SAMPLE POPULATION: For histopathological analysis, 55 apparently blind and 18 apparently normal wild kangaroos and wallabies were obtained from New South Wales, Victoria, South Australia, and Western Australia. A total of 437 wild kangaroos and wallabies (including 23 animals with apparent blindness) were examined serologically. RESULTS: Orbiviruses of the Wallal and Warrego serogroups were isolated from kangaroos affected with blindness in a major epidemic in south-eastern Australia in 1994 and 1995 and extending to Western Australia in 1995/96. Histopathological examinations showed severe degeneration and inflammation in the eyes, and mild inflammation in the brains. In affected retinas, Wallal virus antigen was detected by immunohistochemical analysis and orbiviruses were seen in electron microscopy. There was serological variation in the newly isolated Wallal virus from archival Wallal virus that had been isolated in northern Australia. There were also variations of up to 20% in genotype sequence from the reference archival virus. Polymerase chain reactions showed that Wallal virus was present during the epidemic in three species of midges, Culicoides austropalpalis, C dycei and C marksi. Wallal virus nucleic acid was also detected by PCR in a paraffin-embedded retina taken from a blind kangaroo in 1975. CONCLUSION: Wallal virus and perhaps also Warrego virus are the cause of the outbreak of blindness in kangaroos. Other viruses may also be involved, but the evidence in this paper indicates a variant of Wallal virus, an orbivirus transmitted by midges, has the strongest aetiological association, and immunohistochemical analysis implicates it as the most damaging factor in the affected eyes.     

Farmers' knowledge and perceptions of the stunting disease of Napier grass in Western Kenya

Production of Napier grass, Pennisetum purpureum, the most important livestock fodder in Western Kenya, is severely constrained by Napier stunt (Ns) disease. Understanding farmers' knowledge, perceptions and practices is a prerequisite to establishing an effective disease management approach. Using a random sample of 150 farmers drawn from Bungoma, Busia and Teso districts of Western Kenya, this study sought to: (i) assess farmers' perceptions and knowledge of Ns disease, including its effects on the smallholder dairy industry; (ii) record farmers' current practices in managing Ns disease; and (iii) identify Ns disease management challenges and intervention opportunities in order to develop an efficient integrated disease management approach. The majority (86·7%) of the farmers were aware of Ns disease and observed that it was spreading rapidly in the region, which was perfectly predicted by farmers' access to agricultural information (marginal effect = 0·164), indicating a need for extension platforms for knowledge sharing among the industry stakeholders. The disease had affected Napier grass yields so most farmers could not feed their livestock on the amounts they produced, and they were buying Napier grass. Those who relied on income from selling Napier grass received less due to loss in productivity. Milk production had reduced by over 35%. The cause of the disease was unknown to the farmers, with no effective disease management strategy available to them. An integrated disease management approach needs to be developed to fit within the mixed farming systems, supported by simple decision aids.