Membrane interlocking domains in the lens.

"Ball and socket"-like membrane processes interlock fiber cells in the sheep lens cortex, but appear reduced deeper in the lens. Wheat germ agglutinin (WGA) binds preferentially to these ball and socket structures, and more weakly to other membrane regions. On protein blots, 125I WGA binds to glycoproteins with 140,000 and 32,000 apparent molecular weight, the smaller protein also binding 125I fibronectin. In two animal cataract models, the intense WGA labeling of globular bodies replaces the spotty WGA staining pattern associated with the ball and sockets in the normal lens.

The pathology of an inherited cataract of sheep.

Cataracts, inherited in an autosomal dominant manner in New Zealand Romney sheep were first detected at 1 - 2 months of age as focal anterior and posterior cortical opacities. Within a short time these coalesced to form spoke-like patterns which gradually became more diffuse. Total lens opacity developed by 10 - 11 months of age. Congenital mature cataracts occurred in two lambs believed to be homozygous for the mutant gene and in these animals lens resorption later occurred. Histology showed that new lens fibres formed normally at the equator but then underwent progressive degenerative swelling and lysis. Cytoplasmic vacuolation of anterior epithelial cells was a notable feature and occurred apparently in response to adjacent cortical degeneration. Ultrastructurally these vacuoles were interpreted as dilations of endoplasmic reticulum but there were also a number of smaller vacuoles not lined by membrane. Anterior epithelial cells also underwent metaplasia, hyperplasia, and migration beneath the posterior capsule. Analyses of lenses reflecting different stages of cataractogenesis showed a progressive increase in water, sodium and calcium ions with cataract development and a concomitant decrease in potassium and magnesium ions.

Suspected foreign body peritonitis in fitch (Mustela putorius furo).

A severe, fatal, exudative peritonitis was investigated in a flock of 100 breeding fitch Mustela putorius furo. The presence of enteric flora within the lesions and steel spicules within the stomach contents suggested that this disease may have been caused by steel fragments perforating the intestine. Scoring and pitting of a steel mincer plate used for food preparation consistent with the size and shape of the steel particles found in the stomach, further supported this hypothesis. There were no further cases when the feed source was changed.

An epidemiological study of the spread of rabbit haemorrhagic disease virus amongst previously non-exposed rabbit populations in the North Island of New Zealand.

AIM: To monitor the initial releases of rabbit haemorrhagic disease virus (RHDV) into previously unexposed rabbit populations in the North Island of New Zealand. METHODS: The study programme consisted of pre-release spotlight counts of rabbits on the study farms, pre-release serological samples to check for prior exposure to RHDV, a farmer-completed questionnaire and post-release spotlight counts to measure any change in rabbit numbers following the release of RHDV. In total, 23 sites within the lower North Island where RHDV was released during the period November 1997 to June 1998, were monitored. The most common release method involved the spreading of chopped carrot bait laced with a solution of virus-infected material obtained from dead rabbits. RESULTS: Eighty percent of farmers thought that the disease had spread away from the release sites to areas where virus had not been liberated, although only 27% reported finding dead rabbits more than 300 m away from release locations. Seventy-three percent of farmers were satisfied with the overall effectiveness of rabbit haemorrhagic disease (RHD) as a means of reducing rabbit numbers, but 56% indicated they would modify the way they released the virus in the future. Average pre-release night spotlight counts per property ranged from 2.2 rabbits/km to 36.9 rabbits/km, the median being 12.8 rabbits/km. The time interval from initial release to when the first dead rabbit was seen which the farmer believed to have died from RHD varied from 3 to 21 days, the mean being 7.4 days and the median 7 days. The median change in night spotlight counts per site at 3 weeks after release, expressed as a percentage relative to pre-release counts, was -15.5% (range +18.9% to -76.9%) and at 6 weeks was -49.7% (range 0% to -76.9%). The time of the estimated peak of the disease epidemic ranged from 1 to 7 weeks after release of RHDV, the mean being 3.1 and the median 3 weeks. CONCLUSION: Rabbit haemorrhagic disease reduced rabbit numbers on the majority of farms where the virus was released, and appears to be an effective measure for controlling rabbit populations in New Zealand.

Fitch diets in New Zealand: an analytical survey.

Fitch diets from 30 farms were surveyed and analysed for moisture, protein, carbohydrate, fibre, ash, fat and individual fatty acids, fat peroxide value, and infinity-tocopherol. The dietary raw materials most often used were mutton, fish, poultry, beef and cereals. Eight of the 30 breeders added no vitamin or other supplements. Analytical mean (range) values on a wet matter basis were: moisture, 66.3 (49.6-76.8)%; protein, 16.5 (12.4-21.2)%; carbohydrate, 2.5 (<0.1-8.7)%; fibre, 0.4 (0.1-1.0)%; ash, 3.7 (1.2-8.3)%; fat, 10.6 (1.4-26.1)%; peroxide value, 5.7 (0.3-110) m.equiv x /kg fat; infinity-tocopherol, 13 (0.6-103) mg/kg; calculated gross energy value, 7.2 (3.7-13.7) MJ/kg. Protein contributed 42 (20-79)% of the gross energy value; fat, 49 (15-74) %, and carbohydrate, 6 (0-20) %. Polyunsaturated fatty acids (PUFA's) comprised 10 (3.6-39) % of the total fatty acids. The ratio of infinity-tocopherol to PUFA was 2.1(0.1-10.5) mg/g. Results of the survey are discussed in the light of nutrient requirements for the fitch.

Observations on an outbreak of nutritional steatitis (yellow fat disease) in fitch (Mustella putorius furo).

An outbreak of nutritional steatitis in farmed fitch (Mustella putorius furo) caused by feeding high levels of dietary polyunsaturated fat was investigated. The disease affected mainly 13 to 15 week rapidly growing kits; 793 kits were affected and 183 died. The outbreak was quickly controlled by lowering the level of polyunsaturated fat in the diet and administering high doses of vitamin E. Affected animals had severe generalised steatitis characterised grossly by yellow brown granular fat, which histologically consisted of diffusely necrotic adipose tissue heavily infiltrated with macrophages and neutrophils. There were extensive deposits of PAS-positive, fluorescent lipopigment within macrophages and extracellularly throughout the inflamed fat. Affected fitch had normochromic microcytic anaemia, lowered liver iron levels, increased thrombocytes and acute inflammatory leucograms. Skeletal or cardiac myopathy was not observed grossly or histologically in any of the animals examined. The diet contained high levels of polyunsaturated fat (7.7%DM), a high proportion being docosahexaenoic and eicosapentaenoic acids which were derived from the squid component (40%) of the ration. The livers from affected fitch contained correspondingly high levels of polyunsaturated fatty acids. The diet provided 13 mg Vitamin E per fitch daily, which was clearly inadequate considering the high levels of polyunsaturated fat being fed. Liver selenium levels were extremely high as a result of the high selenium levels in the squid portion of the diet.

Phosphorus deficiency in a dairy herd.

Phosphorus deficiency was diagnosed in a 90 cow seasonal supply dairy herd which showed low milk production, ill-thrift, infertility and osteophagia. Serum inorganic phosphorus and pasture phosphorus levels were low, pasture Ca:P ratios high and soil phosphorus levels very low; the soil phosphate retention value was 96%. The deficiency, which had probably existed for several years, was considered to be due to inadequate annual phosphate fertiliser applications on a high phosphate retaining soil. Phosphorus deficiency may have been exacerbated by the application of lime without phosphate several months before the onset of severe clinical disease. The finding of low sodium levels in pasture samples suggested that sodium deficiency may have co-existed and contributed to the clinical picture. Treatment, comprising bone flour dusting of pasture, water trough supplementation and phosphorus-containing injections, appeared to induce ovarian activity in anoestrous cows and suppress osteophagia, though controlled treatment trials were not performed. No improvement was noted in milk production or cow condition. Increased annual super-phosphate and reduced potassium applications were recommended, together with the monitoring of pasture and soil macro elements and serum phosphorus levels. A decision on whether to supplement with sodium would be based on the results of pasture monitoring, since a direct animal test is not currently available. It is suggested that phosphorus deficiency may not be uncommon in dairy herds in some North Island districts; based on the present case, the decline in New Zealand superphosphate quality in the 1970's and recently published data which has shown a high proportion of pasture phosphorus deficient sites in some North Island areas.

An inherited cataract in New Zealand Romney sheep.

A bilateral cataract was noted to occur in sheep on a New Zealand Romney stud. Extensive breeding trials showed that this defect was inherited as an autosomal dominant. As such this form of cataract is of minimal importance to the sheep industry as control is merely by culling affected individuals.