Some observations on reproductive performance in selected commercial beef herds

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Although the opinion has been expressed (Andrews, 1971 Andrews, E. D. 1971. Cobalt deficiency in sheep and cattle. N.Z. Dept. Agric. Bull., : 180–180.  [Google Scholar]) that cobalt deficiency among cattle has virtually disappeared in New Zealand and that specimens for laboratory examination are rarely required, 15 to 20% of the liver samples submitted by veterinarians to the Animal Health Reference Laboratory for vitamin B₁₂ assay are from cattle. Diagnostic criteria for cobalt (vitamin B₁₂) deficiency cy have long been established for sheep but not for cattle In view of the continuing requests for vitamin B₁₂ analyses on bovine livers, it was desirable to establish normal values for clinically normal cattle so that results of routine diagnostic analyses could be more readily interpreted.     

Acute enteritis and deaths in sheep from Salmonella hindmarsh associated with oral dosing with zinc oxide

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Madam:– The administration of zinc salts to sheep at the time they are exposed to spores of Pithomyces chartarum will reduce the amount of liver damage from the mycotoxin contained in these spores.(7 Smith, B.L., Embling, P.P., Towers, N.R., Wright, D.E. and Payne, E. 1977. The protective effect of zinc sulphate in experimental sporidesmin poisoning of sheep. N.Z. vet. J., 25: 124–127. [Taylor &; Francis Online], [Web of Science ®] , [Google Scholar])(10 Towers, N.R., Smith, B.L., Wright, D.E. and Sinclair, D.P. 1975. Preventing facial eczema by using zinc. Proc. Ruakura Farmers Conference 1975, : 57–61.  [Google Scholar])(11 Towers, N.R., Wright, D.E., Aitken, W.M., Smith, B.L., Sim, A.L. and Sinclair, D.P. 1976. Zinc and facial eczema. Proc. Ruakura Farmers Conference 1976, : 65–68.  [Google Scholar]) It is a recommended practice in facial eczema susceptible areas of New Zealand.(9 Towers, N.R. and Smith, B.L. 1983. Facial eczema. Zinc dosing for prevention. Revised recommendations 1984, AgLink FPP 496 end revise [Google Scholar]) We wish to report a suspected outbreak of salmonellosis that occurred only in a ZnO-dosed group of trial animals and suggest that there may be an association between ZnO administration and salmonellosis.     

Diffuse mesangioproliferative glomerulonephritis in a horse

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Spontaneous glomerulonephritis has been considered an uncommon and ill-defined disease in domestic animals (Jubb and Kennedy, 1970 Jubb, K. V. F. and Kennedy, P. C. 1970. Pathology of Domestic Animals, 2nd ed., Vol. 2, 296–298. New York: Academic Press.  [Google Scholar]). In a survey of 236 cases of nephritis in horses, cattle, sheep, pigs and dogs, Langham and Hallman (1941 Langham, R. F. and Hallman, E. I. 1941. The incidence of glomerulonephritis in domesticated animals. J. Am. vet. Med. Ass., 99: 471–475.  [Google Scholar]) detected primary glomerular abnormalities in only 7. However, recent studies incorporating electron microscopic, or immunofluorescence examination, or both, of renal tissue suggest that glomerulonephritis is not uncommon. During the past 5 years it has been reported in sheep (Angus et al., 1973 Angus, K. W., Gardiner, A. C., Sykes, A. R. and Davison, A. M. 1973. A rapidly progressing mesangio-capillary glomerulonephritis in Finnish Landrace lambs. Vet. Rec., 92: 337–338.  [Google Scholar]), dogs (Krohn et al., 1973 Krohn, K., Jokelainen, P. I. and Sandholm, M. 1973. Light and electron microscopic observations on glomerular changes in canine interstitial nephritis. Acta path., microbiol. scand. Section A, 81: 461–473.  [Google Scholar]) and cats (Slauson et al., 1971 Slauson, D. O., Russell, S. W. and Schechter, R. D. 1971. Naturally occurring immune-complex glomerulonephritis in the cat. J. Path., 103: 131–133.  [Google Scholar]; Farrow and Huxtable, 1971 Farrow, B. R. H. and Huxtable, C. R. R. 1971. Membranous nephropathy and the nephrotic syndrome in the cat. J. comp. Path., 81: 463–467.  [Google Scholar]), and in 6 of 45 horses examined at a commercial slaughterhouse in the U.S.A. (Banks and Henson, 1972 Banks, K. L. and Henson, J. B. 1972. Immunologically mediated glomerulonephritis of horses. II. Antiglomerular basement membrane antibody and other mechanisms in spontaneous disease. Lab. Invest., 26: 708–715.  [Google Scholar]).     

Importance of the ewe as a source of trichostrongyle infection for lambs: Control of the spring-rise phenomenon by a single postlambing anthelmintic treatment

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There are two principal sources of initial infection for the young lamb, the ewe grazing with it and the residual pasture infection resulting from any previous grazing. Several workers (Hawkins et al., 1944 Hawkins, P. A., Cole, C. L., Kline, E. E. and Drudge, J. H. 1944. Studies of sheep parasites. I. The course of untreated nematode infections. Vet. Med., 39: 154–161.  [Google Scholar]; Leiper, 1951 Leiper, J. W. G. 1951. Anew approach to phenothiazine therapy in sheep. Vet. Rec., 63: 885–889.  [Google Scholar]; Spedding and Brown, 1956 Spedding, C. R. W. and Brown, T. H. 1956. The “spring rise” in the nematode egg-count of sheep. J. Helminth., 29: 171–178. [Crossref] , [Google Scholar]; Spedding, 1962 Spedding, C. R. W. 1962. Modern trends in animal health and husbandry. The agricultural ecology of sheep grazing. Brit. vet. J., 118: 461–481.  [Google Scholar]; Crofton, 1958 Crofton, H. D. 1958. Nematode parasite populations in sheep on lowland farms. V. Further observations on the post-parturient rise and a discussion of its significance. Parasitology, 48: 243–250.  [Google Scholar]; Soulsby, 1962 Soulsby, E. J. L. 1962. “Immunity to helminths and its effect on helminth infections”. In Animal Health and Production, 165–183. London: Butterworths.  [Google Scholar]) believe that the former is generally the more important.     

The diagnosis and treatment of vitamin B12 deficiency in young lambs

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In the course of some earlier experiments, it was observed that vitamin B₁₂ deficiency in 2 hoggets was corrected by injection of hydroxocobalamin (vitamin B_12b) (E. D. Andrews, pers. comm., 1972). Since this form of therapy offered a convenient and effective means of treating young lambs suffering from vitamin B₁₂ deficiency, more detailed investigations were desirable. It has been known for some time that lambs on the cobalt-deficient area at the Ministry of Agriculture and Fisheries Kaitoke Farm lose condition after weaning. Abnormal amounts of methylmalonic acid (MMA) had been found in the urine of some of these lambs, indicating a state of vitamin B12 deficiency Andrews et al, (1970 Andrews, E. D., Hogan, K. G., Stephenson, B. J., White, D. A. and Elliott, D. C. 1970. Cobalt and thiabendazole live-weight responses in grazing sheep, and their relation to the urinary excretion of methylmalonic acid. N.Z. Jl agric. Res., 13: 950–965. [Taylor &; Francis Online], [Web of Science ®] , [Google Scholar]).     

Cutaneous antigen-antibody reactions in the sheep

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It is clear that the early permeability response in the sheep that follows chemical and thermal injury, is mediated by histamine (Lancaster and Vegad, 1967 Lancaster, M. C. and Vegad, J. L. 1967. Suppression of the early inflammatory response in the sheep by strophanthin G. Nature, Lond., 213: 840–841.  [Google Scholar]; Vegad, 1971a Vegad, J. L. 1971a. Effect of thermal injury on vascular permeability in the sheep. Indian J. exp. Biol., 9: 111–112.  [Google Scholar], b Vegad, J. L. 1971b. Leucocyte emigration following intradermal injection of histamine, 5-hydroxytrypta-mine and bradykinin in the sheep. Indian J. exp Biol., 9: 113–114.  [Google Scholar]). This is similar to the situation in the rat and the guinea-pig (Spector and Willoughby, 1965 Spector, W. G. and Willoughby, D. A. 1965. The Inflammatory Process, Edited by: Zwiefach, B. W., Grant, L. and Mc-Cluskey, R. T. 427–427. New York: Academic Press. In [Google Scholar]). In contrast to the situation in the rat and the guinea-pig, various nucleosides (Vegad, 1970c Vegad, J. L. 1970c. Effect of hyaluronidase and nucleosides on vascular permeability in sheep and its suppression by mepyramine maleate. Indian J. exp. Biol., 8: 141–142.  [Google Scholar]), hyaluronidase (Vegad, 1970c Vegad, J. L. 1970c. Effect of hyaluronidase and nucleosides on vascular permeability in sheep and its suppression by mepyramine maleate. Indian J. exp. Biol., 8: 141–142.  [Google Scholar]), 5-hydroxytryptamine, turpentine-induced pleural exudates and the lymph node cell extracts also release histamine in the sheep skin (Vegad, 1967 Fischel, E. E. and Kabat, E. A. 1947. Quantitative study of Arthus phenomenon induced passively in rabbit. J. Immun., 55: 337–343.  [Google Scholar]). From these results it was thought possible that cutaneous antigen-antibody reactions might also release histamine in the sheep, and this possibility has been investigated in the present experiments.     

Toxicity of zinc in ruminants in relation to facial eczema

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The toxicity of zinc salts to ruminants has been studied by Ott et al (4) Ott, E. A., Smith, W. H., Harrington, R. B. and Beeson, W. M. 1966. Zinc toxicity in ruminants. I. Effect of high levels of dietary zinc on gains, feed consumption and feed efficiency of lambs. J. Anim. Sci., 25: 414–481. [Web of Science ®] , [Google Scholar] (5) Ott, E. A., Smith, W. H., Harrington, R. B. and Beeson, W. M. 1966. Zinc toxicity in ruminants. II. Effects of high levels of dietary zinc on gains, feed consumption and feed efficiency of beef cattle. J. Anim. Sci., 25: 419–423. [Web of Science ®] , [Google Scholar] (6) Ott, E. A., Smith, W. H., Harrington, R. B., Stob, M., Parker, E. H. and Beeson, W. M. 1966. Zinc toxicity in ruminants. III. Physiological changes in tissues and alterations in rumen metabolism in lambs. J. Anim. Sci., 25: 424–431. [Web of Science ®] , [Google Scholar] (7) Ou, E. A., Smith, W. H., Harrington, R. B., Parker, H. E. and Beeson, W. M. 1966. Zinc toxicity in ruminants. IV. Physiological changes in tissues of beef cattle. J. Anim. Sci., 25: 432–428.  [Google Scholar] and others (3) Miller, W. J., Clifton, C. M., Fowler, P. R. and Perkins, H. F. 1965. Influence of high levels of dietary zinc on zinc in milk, performance and biochemistry of lactating cows. J Dairv Sci., 48: 450–453.  [Google Scholar] (16) Zurcher, T. D. 1970. “A study of the zinc requirement of beef cattle”. In PhD Thesis, Purdue University.  [Google Scholar] (2) Feaster, J. P., Hansard, S. L., McCall, J. T., Skipper, F. H. and Davis, G. K. 1954. Absorption and tissue distribution of radio zinc in steers fed high-zinc rations. J Anim. Sci., 13: 781–788.  [Google Scholar] (12) Thompson, A., Hansard, S. L. and Bell, M. C. 1959. The influence of aluminium and zinc upon absorption and retention of calcium and phosphorous in lambs. Anim. Sci., 18: 187–197.  [Google Scholar] (9) Rosenberger, G. and Gruender, H. D. 1975. “Experiments on the toxicity of zinc dusts in cattle”. In 20th World Veterinary Congress Summaries Vol. 2 Thessaloniki Greece 920–921.  [Google Scholar]. In much of this work zinc has been incorporated in the feed, a situation more applicable to intensive feedlot farming rather than the New Zealand pastoral situation, or the zinc has been fed for limited periods of time with the possibility that the full potential of zinc for causing toxicity has not been realised.     

Mannosidosis — A cause of neonatal mortality in angus calves

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Mannosidosis, a lethal inherited neurological disease associated with a deficiency of the lysosomal enzyme α-mannosidase (Hocking et al., 1972 Greene, H. J., Leipold, H. W., Hibbs, C. M. and Kirkbridge, C. A. 1974. Congenital osteopetrosis in Angus calves. J. Am. vet. med. Ass., 164: 389–395.  [Google Scholar]) has been described clinically as affecting Angus calves usually in their firstyear of life (Whittem and Walker, 1957 Hocking, J. D., Jolly, R. D. and Batt, R. D. 1972. Deficiency of α-mannosidase in Angus cattle. Biochem. J., 128: 69–78.  [Google Scholar]; Jolly, 1970 Jolly, R. D. 1970. Diagnosis and control of pseudolipidosis of Angus calves. N.Z. vet. J., 13: 228–229.  [Google Scholar], 1975 Jolly, R. D. 1975. “Mannosidosis of Angus cattle: A prototype control program for some genetic diseases”. In Advances in Veterinary Science and Comparative Medicine, Edited by: Brandly, C. A. and Cornelius, C. E. Vol. 19, London and New York: Academic Press. In [Google Scholar]). Although it has been suspected as a significant cause of neonatal mortality in herds at risk, figures and diagnosis supporting such an hypothesis have not been available.     

Experimental Ostertagia infection of sheep: Pathology following a single high dose of larvae

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Poisoning of cattle and sheep with superphosphate where the fertilizer was stored within reach of the animals has been reported by Romanenko (1954 Romanenko, K. L. 1954. Poisoning of farm animals with superphosphate. Veterinariya, 31(8): 52–52.  [Google Scholar]). In New Zealand losses of pregnant and lactating ewes grazing pastures topdressed with phosphatic fertilizers have been recognixed for several years, and records kept since 1965 show that 39 outbreaks have been reported to Ruakura Animal Health Laboratory (P. J. O'Hara, pers. comm.). Swan and McIntosh (1952 Swan, J. B. and Mcintosh, I. G. 1952. The toxicity of North African phosphate and superphosphate to milking cows. Proc. N.Z. Soc. Anim. Prod., 12: 83–88.  [Google Scholar]) have described the toxicity to dairy cows of grazing pasture topdressed with North African phosphate and superphosphate. The toxic factor was later identified as fluorine (Animal Research Division of the New Zealand Department of Agriculture Reports 1952–3, p. 28; 1953–4, p. 34; 1954–5, p. 35). Phosphatic fertilizers are known to contain 1 to 4% fluorine (Caro, 1964 Caro, J. H. 1964. Superphosphate. Its History, Chemistry and Manufacture, Washington, D.C.: USDA arid TVA. In [Google Scholar]), and the danger of poisoning stock with fluorine in untreated phosphates used as feed supplements has been described by many authors (Emmerling, 1902 Emmerling, A. 1902. Warning against the use of toxiccalcium phosphate in feed. Milchzeitung, 31: 728–728.  [Google Scholar]; Dammann and Manegold, 1904 Dammann, C. and Manegold, O. 1904. Poisonings by fluorine-containing calcium phosphate used as a feed supplement. Dt tierarztl. Wscht., 12: 129–131.  [Google Scholar]; Gardiner, 1930 Gardner, U. R. 1930. Agricultural Experiment Station Report, 201–201. Michigan State College. June 30 [Google Scholar]; Phillips et al., 1934 Phillips, P. H., Hart, E. B. and Bohstedt, G. 1934. Chronic toxicosis in dairy cows due to the ingestion of fluorine. Wisconsin Univ. Agric. Exp. Sta. Res. Bull., 123: 1–3.  [Google Scholar]; Hatfield et al., 1942 Hatfield, J. D., Shrewsbury, C. L. and Doyle, L. P. 1942. The value of rock phosphate as a supplement for sheep. J. Anim. Sci., 1: 59–59.  [Google Scholar]; Udall, 1947 Udall, D. H. 1947. The Practice of Veterinary Medicine, 5th ed., 724–725. Ithaca, New York: Udall.  [Google Scholar]; Fincher, 1952 Fincher, M. G. 1952. Fluorine Poisoning in Cattle. Report of the New York State Veterinary College of Cornell University 1950–51, : 34–34.  [Google Scholar]; Harris et al., 1952 Harris, L. E., Baird, G. T., Bateman, G. Q., Binns, W., Draper, C. I., Greenwood, D. A., Henderson, G. R., Jenkins, W. R., Rich, L. H., Thorne, D. W. and Wann, F. B. 1952. Recommended practices to reduce fluorosis in livestock and poultry. Utah State Agric. Coll. Agric. Exp. Sta. Circ., : 130–130.  [Google Scholar]; Crampton, 1954 Crampton, E. W. 1954. Fluorosis in dairy cows traced to rations. Can. Milling and Feed, 35(12): 24–26.  [Google Scholar]; Dale and Crampton, 1955 Dale, G. D. and Crampton, E. W. 1955. Observations on chronic fluorosis in dairy cattle. Can. J. comp. Med., 19: 6–16.  [Google Scholar]; Snook, 1962 Snook, L. C. 1962. Rock phosphate in stock feeds. The fluorine hazard. Aust. vet. J., 38: 42–47.  [Google Scholar]; Rek, 1967 Rek, L. 1967. Tolerance to dietary fluorine by farm animals. Agrochemia, 7: 334–336.  [Google Scholar]; Agarwala et al, 1971 Agarwala, O. N., Nath, K. and Mahadevan, V. 1971. Use of superphosphate as a phosphorus supplement for lambs — effect on calcination or supplementation with oral cobalt or parenteral vitamin B₁₂. J. agric. Sci., Camb., 77: 467–471.  [Google Scholar]).     

Polio-encephalomalacia of sheep

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Increasing references have been made in the recent veterinary literature to malacic diseases of the nervous system in sheep and other animals. Plowright (1954 Cordy, D. R. 19S4. J. Neuropath., 13: 330–330.  [Google Scholar]) and Innes and Plowright (1955 Hartley, W. J. 1956. N.Z.vet.J., 4: 129–129. [Taylor &; Francis Online] , [Google Scholar]) have described a focal symmetrical spinal poliomalacia of unknown aetiology in sheep in Kenya. In the U.S.A., Cordy (1954 Haymaker, W., Ginzler, A. M. and Ferguson, R. L. 1952. Military Surgeon, 111: 231–231.  [Google Scholar]) has described a focal symmetrical encephalomalacia of horses following the ingestion of a species of thistle, and Jensen et al. (1956 Hurst, E. W. 1940. Aust. J. exp. Biol. med. Sci., 18: 201–201.  [Google Scholar]) have described an idiopathic polio-encephalomalacia in cattle and sheep. In New Zealand, Hartley (1956 Innes, J. R. M. and Plowright, W. 1955. J. Neuropath., 14: 185–185.  [Google Scholar]) has described a focal symmetrical encephalomalacia (F.S.E.) of lambs that may be related to the sublethal effects of the toxin of Clostridium perfringens (welchii) Type D. Smith (1957 Jensen, Rue, Griner, L. A. and Adams, O. R. 1956. J. Amer. vet. med. Ass., 129: 311–311. [PubMed] , [Google Scholar]) has described widespread lesions of polio-encephalomalacia together with eosinophilic meningoencephalitis in sodium chloride poisoning of swine.     

The prevalence of Mycoplasma ovipneumoniae and Mycoplasma arginini in the respiratory tract of sheep

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In an initial study of mycoplasmas of the respiratory tract of New Zealand sheep a number of strains of mycoplasma were recovered and identified as either M. ovipneumoniae or M. arginini (Clarke et al., 1974 Clarke, J. K., Brown, V. G. and Alley, M. R. 1974. Isolation and identification of mycoplasmas from the respiratory tract of sheep in New Zealand. N.Z. vet. J., 22: 117–121. [Taylor &; Francis Online] , [Google Scholar]). Investigations in Australia have produced evidence that M. ovipneumoniae is associated with a proliferative interstitial pneumonia in Queensland sheep (Sullivan et al., 1973 Sullivan, N. D., St. George, T. D. and Horsfall, N. 1973. A proliferative interstitial pneumonia of sheep associated with mycoplasma infection. I. Natural history of the disease in a flock. Aust. vet. J., 49: 57–62.  [Google Scholar]) and for this reason the present survey was undertaken to investigate the prevalence of mycoplasmas in the respiratory tract of sheepin New Zealand.     

Caprine arthritis encephalitis

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Caprine arthritis encephalitis (CAE) is a disease of goats of any breed, sex and age, caused by a retrovirus related to, but distinct from, the maedi-visna virus which affects sheep.(4) Gazit, A., Yaniv, A., Divr, M., Perk, K., Irving, S.G. and Dahlberg, J.E. 1983. The caprine arthritis-encephalitis virus is a distinct virus within the lentivirus group. Virology, 124: 192–195.  [Google Scholar] (10) Roberson, Susan M., McGuire, T.C., Klevjer-Anderson, Paula, Gorham, J.R. and Cheevers, W.P. 1982. Caprine arthritis-encephalitis virus is distinct from visna and progressive pneumonia viruses as measured by genome sequency homology. J. Virol., 44: 755–758. [PubMed], [Web of Science ®] , [Google Scholar] Both infections are included among the so-called slow virus diseases which are characterised by a long incubation period, protracted clinical course and persistent infection. Maedi-visna is not present in New Zealand but CAE has been detected in a number of goat flocks.     

Response of cobalt deficient lambs to cobaltic oxide pellets

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In New Zealand, cobalt-containing drenches are recommended for the field diagnosis of cobalt deficiency, but find little use as a routine method of controlling the disease. For the latter purpose, cobaltized licks have a place on extensively-grazed untopdressed hill country. Otherwise, topdressing pastures annually with cobalt sulphate, usually as cobaltized superphosphate, has proved the best method of prevention (N.Z. Dept. Agric, 1954 N.Z. Dept. Agric. 1954. N.Z. Dept. Agric. Bull.,  [Google Scholar]; Andrews, 1956 Andrews, E. D. 1956. N.Z. J. Agric., 92: 239–239.  [Google Scholar]). In Australia, however, greater reliance has been placed on drenches and licks, partly because cobalt topdressing is regarded as uneconomic on the extensive undeveloped holdings usually associated with cobalt deficiency in that country, and partly because the effects of cobalt applied to the land have often proved ephemeral, particularly on the acutely-deficient calcareous coastal sands (Lee, 1950 Lee, H. J. 1950. Aust. vet. J., 26: 152–152. [Crossref], [PubMed] , [Google Scholar]; Bennetts, 1955 Bennetts, H. W. 1955. J. Agric. West Ami., 4: 42–42.  [Google Scholar]). However, recent work in South Australia opens up an entirely new approach to the control of cobalt deficiency disease. Dewey et al. (1958 Dewey, D. W., Lee, H. J. and Marston, H. R. 1958. Nature (Lond), 181: 1367–1367.  [Google Scholar]) report that when semi-porous pellets containing cobaltic oxide are administered to sheep they are retained in the reticulum, or less commonly in the rumen, and release a continuous and adequate supply of cobalt to the animal. Phalaris staggers and cobalt deficiency disease can be prevented in this way.     

A mass screening programme of angus cattle for the mannosidosis genotype — A prototype programme for control of inherited diseases in animals

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Recent research has shown that the gene frequency for mannosidosis (pseudolipidosis) may approximate 0.05 in pedigree Angus herds (Jolly, unpublished data). As epidemiological studies suggest an equal frequency in commercial non-pedigree herds, the disease is elf economic importance to the national beef industry. Mannosidosis is an inherited lysosomal storage disease associated with a defect in catabolism, of the heterosaccharide fractioln of glycoproteins (Whittem and Walker, 1957 Donnelly, W. J. C., Sheahan, B. J. and Rogers, T. A. 1973a. GM₁ gangliosidosis in Friesian calves. J. Path., 111: 173–179.  [Google Scholar]; Jolly 1971 Donnelly, W. J. C., Sheahan, B. J. and Kelly, M. 1973b. Bet α-galactosidase deficiency in GM₁ gangliosidosis of Friesian calves. Res. vet. Sci., 15: 139–141.  [Google Scholar]; Hocking et al., 1972 Hocking, J. D., Jolly, R. D. and Batt, R. D. 1972. Deficiency of α-mannosidase in Angus cattle. Biochem. J., 128: 69–78.  [Google Scholar]; Phillips et al., 1974 Jolly, R. D. 1971. The pathology of the central nervous system in pseudolipidosis of Argus cattle. J. Path., 103: 113–121.  [Google Scholar]). Whereas animals with mannosidosis have negligible tissue sand plasma levels of α-mannosidase, heterozygotes having one normal gene and one defective gene have approximately half the normal level of enzyme in their tissues and plasma. This observation forms the basis for a control programme in which heterozygotes are identified by their plasma α-mannosidase 1evels (Jolly et al., 1973 Jolly, R. D., Tse, C. A. and Greenway, R. M. 1973. Plasma α-mannosidase activity as a means of detecting mannosidosis heterozygotes. N.Z. vet. J., 21: 64–69. [Taylor &; Francis Online] , [Google Scholar], 1974a Jolly, R. D., Thompson, K. G., Tse, C. A., Munford, R. E. and Merrall, M. 1974a. Identification of mannosidosis heterozygotes — factors affecting normal plasma α-mannosidase levels. N.Z. vet. J., 22: 155–162. [Taylor &; Francis Online] , [Google Scholar], b Jolly, R. D., Thompson, K. G. and Tse, C. A. 1974b. Evaluation of a mass screening programme for identification of mannosidosis heterozygotes in Angus cattle. N.Z. vet. J., 22: 185–190. [Taylor &; Francis Online] , [Google Scholar]).     

Experimental Eperythrozoon ovis infection of sheep

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Eperythrozoon ovis is an epi-erythrocytic sheep parasite of uncertain classification with a world-wide distribution (Sutton, 1970 Sutton, R. H. 1970. Eperythrozoon ovis — a blood parasite of sheep. N.Z vet. J., 18: 156–164. [Taylor &; Francis Online] , [Google Scholar]), but whether eperythrozoonosis is a disease of economic importance remains unresolved. In Scotland, Foggie and Nisbet (1964 Foggie, A. and Nisbet, D. I. 1964. Studies on Eperythrozoon infection in sheep. J. comp. Path., 74: 45–61.  [Google Scholar]), found that experimentally E. ovis caused a clinical anaemia, occasionally with jaundice, but there was no significant difference in weight gain between infected and control sheep. Similar observations in naturally infected sheep were recorded in Norway by Overas (1969 Overas, I. 1969. Studies on Eperythrozoon ovis infection in sheep. Acta vet. Scand., Suppl. 28 [Google Scholar]), and in Australia by Harbutt (1969b Harbutt, R. Patricia. 1969b. The effect of Eperythrozoon ovis infection on body weight gain and haematology of lambs in Victoria. Aust. vet. J., 45: 500–504.  [Google Scholar]), Other Australian authors have found infection by this parasite; associated with outbreaks of ill-thrift in lambs (Sheriff et al., 1966 Sheriff, D., Clapp, K. H. and Reid, A. Marjorie. 1966. Eperythrozoon ovis infection in South Australia. Aust. vet. J., 42: 169–176.  [Google Scholar]) and severe anaemia with some mortality (Littlejohns, 1960 Littlejohns, I. R. 1960. Eperythrozoon ovis in sheep. Aust. vet. f., 36: 260–265.  [Google Scholar]; Maxwell, 1969 Maxwell, J. A. L. 1969. Eperythrozoon ovis infection in Western Australia. Ausf. vet. J., 45: 436–436.  [Google Scholar]; Campbell et al., 1971 Campbell, R. W., Sloan, C. A. and Harbutt, R. Patricia. 1971. Observations on mortality in lambs in Victoria associated with Eperythrozoon ovis. Aust. vet. J., 47: 538–541.  [Google Scholar]). Although the presence of strains of different pathogenicity has been suggested (Foggie and Nisbet, 1964 Foggie, A. and Nisbet, D. I. 1964. Studies on Eperythrozoon infection in sheep. J. comp. Path., 74: 45–61.  [Google Scholar], 1966 Foggie, A. and Nisbet, D. I. 1966. Eperyihrozoon ovis. Vet. Rec., 79: 297–298.  [Google Scholar]; Harbutt, 1969a Harbutt, R. Patricia. 1969a. The incidence and clinical significance of Eperythrozoon ovis infections of sheep in Victoria. Ausf vet. J., 45: 493–499.  [Google Scholar]), other factors influencing the disease should also be considered (Littlejohns, 1960 Littlejohns, I. R. 1960. Eperythrozoon ovis in sheep. Aust. vet. f., 36: 260–265.  [Google Scholar]).     

Cobalt deficiency in sheep and diagnostic reference ranges

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In the last 2 years, two papers have been published suggesting that current New Zealand reference criteria for diagnosing cobalt deficiency should be reviewed (Grace et al 2003), and they are conservatively high and lead to the over-diagnosis of vitamin B₁₂ deficiency and ill-thriftiness in sheep (Gruner et al 2004). The comments refer to reference ranges cited by animal health diagnostic laboratories. These reference ranges were derived from the paper by Clark et al (1989 Clark, RG, Wright, DF, Millar, KR and Rowland, JD. 1989. Reference curves to diagnose cobalt deficiency in sheep using liver and serum vitamin B₁₂ levels.. New Zealand Veterinary Journal, 37: 7–11. [Taylor &; Francis Online], [Web of Science ®] , [Google Scholar]), which reviewed data from published and unpublished weight gain response trials preceding that date. The review included all published trials in New Zealand and as many unpublished trials that the authors could obtain. They involved serum vitamin B12 data from 54 trials and liver vitamin B₁₂ data from 21 trials. It was stated that more data from trials conducted in autumn were required to reliably determine an autumn response curve. In addition, it was envisaged that as other trial data became available the reference curves could be upgraded (Clark et al 1985 Clark, RG, Wright, DF and Millar, KR. 1985. A proposed new approach and protocol to defining mineral deficiencies using reference curves. Cobalt deficiency in young sheep is used as a model.. New Zealand Veterinary Journal, 33: 1–5. [Taylor &; Francis Online], [Web of Science ®] , [Google Scholar]).     

Bovine virus diarrhoea (mucosal disease): Case report and virus isolation

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Madam:—Out of season (autumn/winter) lambing is expanding in northern areas. These lambs need to grow at moderate rates through the late winter feed trough so they can fully utilise the spring flush to reach heavy weights before summer. Autumn-born lambs are likely to face high parasite roundworm challenge pre- and post-weaning. Strongyle faecal egg counts of autumn and spring-born lambs at weaning averaged 2000 and 400 eggs/g respectively (n=30) under an all-sheep, splitseason lambing policy near Kaikohe. ⁽⁷⁾ McSporran, K.D. and Andrewes, W.G.K. 1987. Field study of the post-parturient rise in faecal egg counts of lactating ewes. The effects of season, genotype of ewe and number of lambs born per ewe. Inter. J. Parasit., (pers. comm) [Google Scholar] Roundworm infestation can also reduce selenium concentration in the liver. ⁽²⁾ Andrews, E.D., Hogan, K.G. and Brunsdon, R.V. 1971. Some effects of anthelmintic dosing on the mineral status of hoggets. Proc. N.Z. Soc. Anim. Prod., 31: 65–65.  [Google Scholar] Although Se level in pasture tends to be higher in autumn/winter than in spring/summer ^(l) Andrews, E.D., Grant, A.B. and Stephenson, B.J. 1964. Weight responses of sheep to cobalt and selenium in relation to vitamin B12 and selenium concentrations in liver and kidney. N.Z. J. agric. Res., 13: 17–27.  [Google Scholar] this could be offset by lower pasture availability. Better winter growth rates have been recorded in weaned calves from a combination anthelmintic/selenium drench than from either of these alone. ⁽⁵⁾ McLeod, C.C., Wolff, J.E. and Schwarz, G. 1975. Effect of anthelmintic and selenium drenching on liveweight gain in young beef cattle. N.Z. J. exp. Agric., 4: 219–225.  [Google Scholar]     

Malignant hyperthermia in a crossbred landrace-large white pig

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Malignant hyperthermia is a rare and usually fatal complication of general anaesthesia. It occurs in man (Britt and Kalow, 1970 Britt, B. A. and Kalow, W. 1970. Malignant hyperthermia: a statistical review. Can. Anaesth. Soc. J., 17: 293–315. [Crossref], [PubMed] , [Google Scholar]) and in certain breeds of pigs, the, Landrace (Hall et al., 1966 Hall, L. W., Woolf, N., Bradley, J. W. P. and Jolly, D. W. 1966. An unusal reaction to suxamethonium chloride. Br. med. J., 3: 594–594.  [Google Scholar]; Berman et at, 1970 Berman, M. C., Harrison, G. G. and Bull, A. B. 1970. Changes underlying halothane-induced malignant hyperpyrexia in Landrace pigs. Nature. Lond., 225: 653–655.  [Google Scholar]; Harrison et al., 1970 Harrison, G. G., Berman, M. C., Heekman, R., Bull, A. B., Terblanche, J. and Kench, J. E. 1970. “Anaesthetic induced malignant hyperpyrexia — Some observations of the syndrome in Landrace pigs”. In Ill Asian Australasian Congress of Anesthesiology, Canberra. Butterworths 158–166.  [Google Scholar]) the Poland China (Jones et al., 1972 Jones, E. W., Nelson, T. E., Anderson, I. L., Kerr, D. D. and Burnap, T. K. 1972. Malignant hyperthermia in swine. Anesthesiology, 36: 42–51.  [Google Scholar]), the Pietrain (Allen et al., 1970 Allen, W. M., Harding, J. D. J. and Paterson, D. S. P. 1970. Experimentally induced acute stress syndrome in Pietrain pigs. Vet. Rec., 87: 64–69.  [Google Scholar]) and the Large White (Mawdesley-Thomas, 1969 Mawdesley-Thomas, L. E. 1969. Cited by Allen, W. M. et al. (1970) [Google Scholar]).     

Epidermal langerhans cellsin the oppossum,Trichosurus vulpecula

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Madam:-Langerhans cells (LC) are dendritic cells of bone marrow origin found above the basal cell layer of the epidermis and in mucous membranes. ⁽⁹⁾ Silberberg-Sinakin, I. and Thorbecke, G.J. 1980. “The Langerhans cells”. In The Reticuloendothelial System: A Comprehensive Treatise, Edited by: Carr, I. and Daems, W.T. 555–605. New York: Plenum Press. In, Vol. 1 [Google Scholar] They are the only epidermal cells that have Fc and C3b receptors ⁽¹¹⁾ Stingl, G., Wolff-Schreiner, E.C.H., Pichler, W.J., Gschnait, F., Knapp, W. and Wolff, K. 1977. Epidermal Langerhans cell bears Fc and C3b receptors. Nature, 268: 245–246.  [Google Scholar] and express class II histocompatibility structures. ⁽¹⁾ Klareskog, L., Tjernlund, U.M., Forsum, U. and Peterson, P.A. 1977. Epidermal Langerhans cells express la antigens. Nature, 268: 248–250.  [Google Scholar] ⁽⁵⁾ Rowden, G., Lewis, M.G. and Sullivan, A.K. 1977. Ia antigen expression on human epidermal Langerhans cells. Nature, 268: 247–248.  [Google Scholar] These features suggest that LC are the epidermal equivalent of macrophages but the relationship between these two types of cells is uncertain. ⁽⁹⁾ Silberberg-Sinakin, I. and Thorbecke, G.J. 1980. “The Langerhans cells”. In The Reticuloendothelial System: A Comprehensive Treatise, Edited by: Carr, I. and Daems, W.T. 555–605. New York: Plenum Press. In, Vol. 1 [Google Scholar] LC are involved in the induction of contact hypersensitivity [CHS], ⁽⁶⁾ Shelley, W.B. and Juhlin, L. 1977. Selective uptake of contact allergens by the Langerhans cell. Arch. Dermatol., 113: 187–194.  [Google Scholar] ⁽⁷⁾ Silberberg, I. 1973. Apposition of mononuclear cells to Langerhans cells in contact allergic reactions. Acta. Derma. Venerol., 53: 1–9.  [Google Scholar] ⁽⁸⁾ Silberberberg, I., Baer, R.L. and Rosenthal, S.A. 1976. The role of Langerhans cells in allergic contact hypersensitivity. A review of findings in man and guinea pigs. J. invest. Dermatol., 66: 210–217.  [Google Scholar] ⁽¹⁰⁾ Stingi, G., Katz, S.I., Clement, L., Green, O. and Shevach, E.M. 1980. “Langerhans cell — lymphocyte interactions”. In Macrophage Regulation of Immunity, Edited by: Unanue, E.R. and Rosenthal, A.S. 285–295. New York: Academic Press. In [Google Scholar] their density determining whether CHS or immunological tolerance follows skin painting with haptens. ⁽¹²⁾ Toews, B.G., Bergstresser, P.R. and Streilein, J.W. 1980. Epidermal Langerhans cell density determines whether contact hypersensitivity or unresponsiveness follows skin painting with DNFB. J. Immuno., 124: 445–453.  [Google Scholar]     

Colitis X in the horse

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Colitis X is a peracute, sporadic noncontagious disease affecting horses of all ages, characterized by sudden onset of shock, dehydration and foetid diarrhoea (Rooney et al., 1963 Rooney, J. R., Bryan's, J. T. and Doll, E. R. 1963. Colitis “X” of horses. J. Am. vet. Med. Ass., 142: 510–511.  [Google Scholar]; Pickrell, 1968 Pickrell, J. W. 1968. Equine killer: Colitis X. Med. vet. Pract., 49: 63–66.  [Google Scholar]). Rooney et al. (1966 Rooney, J. R., Bryans, J. T., Prickett, M. E. and Zent, W. W. 1966. Exhaustion shock in the horse. Cornell Vet., 56: 220–235. [PubMed] , [Google Scholar]) have described a form of colitis X without diarrhoea. Otubreaks of the disease which affected numerous horses under the same conditions of management have been described (Rooney et al., 1963 Rooney, J. R., Bryan's, J. T. and Doll, E. R. 1963. Colitis “X” of horses. J. Am. vet. Med. Ass., 142: 510–511.  [Google Scholar]; W. P. C. Richards, pers. comm.).