Vesico-ureteral reflux in the dog

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Recent interest in the subject of vesicoureteral reflux (regurgitation of the vesical contents into the ureters) in man has lead to many experimental investigations of this phenomenon in dogs (Ross and Thompson, 1963 Ross, G. and Thompson, I. M. 1963. The relationship of non-obstructive reflux and chronic pyelonephritis: An experimental study. J. Urol., 90: 391–394.  [Google Scholar]; Schoenberg et al, 1963 Schoenberg, H. W., Beisswanger, P., Howard, W., Walter, C. F. and Murphy, J. J. 1963. Effect of lower urinary tract infection upon ureteral function. Amer. Coll. Surgeons Surgical Forum, 14: 483–484.  [Google Scholar]; Levers and Metcalfe, 1964 Levers, P. E. and Metcalfe, J. O. 1964. Urethral resistance measurement: Vesicoureteral reflux and age. J. Urol., 91: 368–375.  [Google Scholar]; Schoenberg et al, 1964 Schoenberg, H. W., Beisswanger, P., Howard, W., Walter, C. F. and Murphy, J. J. 1964. Effect of lower urinary tract infection on ureteral function. J. Urol., 92: 107–108.  [Google Scholar]; Scott, 1964(a) Scott, J. E. S. 1964a. An experimental investigation into the effects of prolonged vesico-ureteric reflux. Brit. J. Urol., 36: 391–398.  [Google Scholar]; Scott, 1964(b) Scott, J. E. S. 1964b. An experimental study of urinary infection and vesico-ureteric reflux. Brit. J. Urol., 36: 501–509.  [Google Scholar]; Cass and Lenaghan, 1965 Cass, A. S. and Lenaghan, D. 1965. The influence of posture on the occurrence of vesico-ureteral reflux. Invest. Urol., 2: 523–529.  [Google Scholar]; Mori and Hara, 1965 Mori, Y. and Hara, T. 1965. Vesicoureteral reflux. Part I. Experimental observation on the mechanism of the prevention of vesicoureteral reflux. Mio. Med. Med. J., 14: 245–249.  [Google Scholar]; Sommer and Roberts, 1966 Sommer, J. L. and Roberts, J. A. 1966. Ureteral reflux resulting from chronic urinary infection in dogs: Long term studies. J. Urol., 95: 502–510.  [Google Scholar]; King and Idriss, 1967 King, L. R. and Idriss, F. S. 1967. The effect of vesicoureteral reflux on renal function in dogs. Invest. Urol., 4: 419–427.  [Google Scholar]). Little, however, has been written on the naturally-occurring condition seen in canine clinical practice. In fact, apart from isolated reports from experimental workers (Barksdale and Baker, 1930 Barksdale, E. S. and Baker, W. W. 1930. The effect of denervation of the lower ureter upon the incidence of ureteral reflux in the dog. J. Urol., 24: 263–268.  [Google Scholar]; Scott and de Luca, 1960 Scott, J. E. S. and de Luca, F. G. 1960. Further studies on the uretero-vesical junction of the dog. Brit. J. Urol., 32: 320–323.  [Google Scholar]) it has rarely been seriously considered as a complication of urinary disorders by practising veterinarians.     

Ovine Johne's disease in New Zealand

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Cambendazole, isopropy1 2-(4-thiazoly1)-5-benzimidazolecarbamate, has been reported to be a highly efficient anthelmintic against gastro-intestinal nematodes of cattle (Egerton et al., 1970 Egerton, J. R., Eary, C. H., Lanza, G. R., Wombolt, T. H. and Campbell, W. C. 1970. The efficacy of cambendazole against gastro-intestinal nematodes of cattle. Res. vet. Sci., 11: 495–499.  [Google Scholar]; Baker and Walters, 1971 Baker, N. P. and Walters, G. T. 1971. Anthelmintic efficacy of cambendazole in cattle. Ant. J. vet. Res., 14: 29–33.  [Google Scholar]; Ciordia and McCampbell, 1971 Ciordia, J. and McCampbell, H. C. 1971. Anthelmintic efficacy of four dose levels of cambendazole in cattle. Proc. helm. Soc. Wash., 38: 40–42.  [Google Scholar]; Benz, 1971a Benz, G. W. 1971a. Anthelmintic activities of cambendazole in calves. Am. J. vet. Res., 32: 399–403.  [Google Scholar], b Benz, G. W. 1971b. Activity of cambendazole against gastro-intestinal nematodes of calves: Single vs. two therapeutic treatments. J. Parasit., 57: 286–288.  [Google Scholar]; Restani, 1971 Restani, R. 1971. Research on the anthelmintic activity of cambendazole against some nematodes of cattle. Vet. Italiana, 22: 137–139.  [Google Scholar]). Efficacy against the cattle lungworm, Dictyocaulus viviparus, has also been reported as high (Rubin, 1972 Rubin, R. 1972. Efficacy of cambendazole against lungworm (Dictyocaulus vivipams) of cattle. Am. J. vet. Res., 33: 425–426.  [Google Scholar]; Gibbs and Gupta, 1972 Gibbs, H. C. and Gupta, R. P. 1972. The anthelmintic activity of cambendazole in calves and lambs. Can. J. comp. Med., 36: 108–115.  [Google Scholar]; Baker et al., 1972 Baker, N. F., Walters, G. T., Hjerp, G. A. and Fisk, R. A. 1972. Experimental therapy of Dictyocaulus viviparis infection in cattle with cambendazole. Am. J. vet. Res., 33: 1127–1130.  [Google Scholar]). This paperreports the results of four controlled critical efficacy trials with cambendazole against naturally acquired nematode infections in cattle.     

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]).     

Potentiated trimethoprim for the therapy of calf scours

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Trimethoprim became generally available 3 years ago, following its original discovery as a unique antibacterial agent for combating diseases of both man and animals (Hitchings and Bushby, 1961 Hitchings, G. H. and Bushby, S. R. M. 5-Benzyl-2, 4-diaminopyrimidines a new class of systemic anti-bacterial agents. 5th Int. Congr. Biochem. Moscow. pp.165–165.  [Google Scholar]; Pugsley et al., 1969 Pugsley, D. G., Mwanje, L., Pearson, C and Blowers, R. 1969. Use of trimethoprim and sulphamethoxazole in tropical Africa: Typhoid fever; Salmonella typhi carriage and Staphylococcus aureus sepsis. Postgrad, med. J., 45: 95–99. Nov. 1969, Suppl. [Google Scholar]; McGuinness, 1969 McGuinness, B. W. 1969. A combination of trimethoprim and sulphamethoxazole in upper respiratory infection. Postgrad, med. J., 45: 99–101. Nov. 1969, Suppl. [Google Scholar]; McCaig, 1970 McCaig, J. 1970. A clinical trial using trimethoprim-sulphadiazine in dogs and cats. Vet. Rec., 87: 265–265.  [Google Scholar]; Barnett and Bushby, 1970 Barnett, Margaret and Bushby, S. R. M. 1970. Trimethoprim and the sulphonamides. Vet. Rec., 87: 43–51.  [Google Scholar]; Rehm and White, 1970 Rehm, W. F. and White, G. 1970. A field trial with trimethoprim and sulphadoxine in bacterial diseases of cattle and pigs. Vet. Rec., 87: 39–42.  [Google Scholar]; Craig 1972 Craig, G. R. 1972. The place of potentiated trimethoprim in the therapy of diseases of the skin in dogs and cats. J. small Anim. Pract., 13: 65–70.  [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.     

Genital infection of ram hoggets associated with a gram-negative pleomorphic organism

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An acute epididymitis affecting mainly young rams and associated with a gram-negative pleomorphic organism was first reported in New Zealand in 1955 (1) Dodd, D. C. and Hartley, W. J. 1955. A specific suppurative epididymitis of rams. N.Z. vet. J., 3: 105–110. [Taylor &; Francis Online] , [Google Scholar]. Subsequently a similar syndrome attributed to Actinobacillus seminis has been reported in Border Leicester and other rams in Australia (2) Baynes, I. D. and Simmons, G. C. 1960. Ovine epididymitis caused by Actinobacillus seminis. N.Sp. Aust. vet. J., 36: 454–459.  [Google Scholar] (3) Simmons, G. C., Baynes, I. D. and Ludford, C. G. 1966. Epidemiology of Actinobacillus seminis in a flock of Border Leicester sheep. Aust. vet. J., 42: 183–187.  [Google Scholar] (4) Baynes, I. D. and Simmons, G. C. 1968. Clinical and pathological studies of Border Leicester rams naturally infected with Actinobacillus seminis. Aust. vet. J., 44: 339–343.  [Google Scholar]. A like condition also described in Australia in a single crossbred ram was causally attributed to Histophilus ovis (5) Claxton, P. D. and Everett, R. E. 1966. Recovery of an organism resembling Histophilus ovis from a ram. Aust. vet. J., 42: 457–458.  [Google Scholar]. Actinobacillus seminis was isolated from an epididymal infection in a Rambouillet ram in America (6) Livingston, C. W. and Hardy, W. T. 1964. Isolation of Actinobacillus seminis from ovine epididymitis. Am. J. vet. Res., 25: 660–663.  [Google Scholar] and from a Dorper ram in South Africa(7) Worthingron, R. W. and Bosman, P. P. 1968. Isolation of Actinobacillus seminis in South Africa. J I. S. Aft. vet. med. Ass., 39: 81–85.  [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.     

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]).     

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]).     

The microflora of the cervix of the thoroughbred mare: A clinical and bacteriological survey in a large-animal practice in Hastings

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Many reports concerned with the microflora of the genital tract in thoroughbred mares stress the potential pathogenic significance of the haemolytic streptococci. Many years ago, Dimock (1929 Dimock, W. W. 1929. Breeding diseases of the horse. J. Am. vet. med. Ass., 74: 327–335.  [Google Scholar], 1939 Dimock, W. W. 1939. Equine breeding hygiene. J. Am. vet. med. Ass., 94: 469–478.  [Google Scholar]) and Dimock and Edwards (1928) Dimock, W. W. and Edwards, P. R. 1928. The pathology and bacteriology of the reproductive organs of mares in relation to sterility. Ky agric. exp. Stn Bull., 286: 287–339.  [Google Scholar] associated the haemolytic streptococci with persistent endometritis, sterility and deaths in foals up to 2 to 4 weeks after birth. In Holland, Ressang (1954) Ressang, A. 1954. “Sterility in Mares. A clinical, bacteriological and histopathological investigation”. In Thesis, State University of Utrecht.  [Google Scholar] isolated haemolytic streptococci of Lancefield's Group C from 34 of 153 (22%) mares offered for examination because of poor breeding performance. Ressang noted that mares with streptococcal endometritis were not likely to show satisfactory fertility even after the infection had apparently been eliminated. Haemolytic streptococci have also been associated with infertility in mares in Turkey (Pusat, 1955 Pusat, M. M. 1955. Kisraklarin sikit amili streptococlarin tipleri ve streptococcus genitalium uzerinde bir munakasa. Turk vet. Hekim. Dern. Derg., 24: 2,039–2,047.  [Google Scholar]), in the United Kingdom (Moran and Cronin, 1957 Moran, A. B. and Cronin, M. T. 1957. Organisms isolated from the uteri of thoroughbred mares. J. comp. Path., 67: 106–109.  [Google Scholar]) and in Ireland (Farrelly and Mullaney, 1964 Farrelly, B. T. and Mullaney, P. E. 1964. Cervical and uterine infection in thoroughbred mares. Ir. vet. J., 18: 201–212.  [Google Scholar]). In Australia, Bain (1966) Bain, A. M. 1966. The role of infection in infertility in the thoroughbred mare. Vet. Rec., 78: 168–173.  [Google Scholar] noted that 12% of infected mares at stud in the Hunter district of New South Wales harboured beta-haemolytic strepotcocci in the genital tract. This organism was considered the most serious pathogen encountered as only 40% of these mares infected with haemolytic streptococci produced a live foal in the first year following infection: 35% had still not completed a successful pregnancy within the subsequent 3-year period.     

Congestive heart failure in broilers,resembling toxic heart degeneration and chick oedema disease

Abstract

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Between November 1972 and February 1973, severe outbreaks of a disease in broilers, characterized by congestive heart failure,, hydropericardium, liver shrinkage, ascites, and sometimes subcutaneous oedema were observed in the North Island. The disease resembled enzootic fatal syncope (toxic heart degeneration) described earlier in laying hens in New Zealand (Fischel, 1946 Fischel, W. E. 1946. Enzootic Fatal Syncope (Toxic Heart Degeneration) in fowls. Aust. vet. J., 22: 144–149.  [Google Scholar]), chick edema disease seen in the U.S.A. (Schmittle et al., 1958 Schmittle, S. C., Edwards, H.M. and Morris, D. 1958. A disorder of chickens probably due to toxic feed — preliminary report. J. Am. vet. med. Ass., 152: 216–219.  [Google Scholar]; Sanger et al., 1958 Sanger, V. L., Scott, L., Hamdy, A., Gale, C. and Pounden, W. D. 1958. Alimentary toxemia in chickens. J. Am. vat. med. Ass., 33: 172–176.  [Google Scholar]), possible fat intoxication in chickens reported from Britain (Wannop and Chubb, 1961 Wannop, C. C. and Chubb, L. G. 1961. Possible fat intoxication in chickens. Vet. Rec., 75: 586–586.  [Google Scholar]), and alimentary toxaemia or water belly ascites experienced in Australia (Sinkovic, 1961 Sinkovic, B. 1961. Cited by Hungerford (1969) [Google Scholar]).     

Diarrhoeal diseases of the calf: Observations on treatment and prevention

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During the past two decades intestinal absorptive and secretory functions and the intestinal flora have been significantly clarified. Important concepts of intestinal dysfunction have emerged which have proved of immense clinical value(32) Moon, H. W. 1974. Pathogenesis of Enteric Diseases Caused by Escherichia coli. Adv. Vet. Sci. Comp. Med, 18: 179–211. [PubMed] , [Google Scholar] (39) Phillips, S. F. 1972. Diarrhoea: A Current View of the Pathophysiology. Gastroenterology, 63: 495–518.  [Google Scholar] (46) Smith, H. W. 1965. Observations on the Flora of the Alimentary Tract of Animals and Factors Affecting its Composition. J. Pathol, 89: 95–122.  [Google Scholar] (47) Smith, H. W. 1971. The Bacteriology of the Alimentary Tract of Domestic Animals Suffering from E. coli Infection. Ann. N. Y. Acad Set, 176: 110–125.  [Google Scholar] (51) Soergel, K. H. 1973. New Concepts of Intestinal Function. Hepatogaslroenterol, 20: 351–358.  [Google Scholar]. Despite this, the medical and economic consequences of diarrhoea continue to beset the cattle industry(1) Barnum, D. A., Glantz, P. J. and Moon, H. W. 1967. Colibacillosis. CI_RV_eterinary Monograph Series/Two, : 5–44.  [Google Scholar] (18) Hubbert, W. T. 1974. Factors Affecting Survival of the Bovine Fetus and Neonate. Theriogenology, 1: 15–34.  [Google Scholar] (30) Marsh, H. 1968. Prenatal and Postnatal Mortality in Cattle. National Academy of Science. Pub. No. 1685,, : 1–6.  [Google Scholar] (56) Vollmar, R. E. 1974. Diarrhoea Control in a Dairy Operation. Mod Vet. Pract., 55: 509–512.  [Google Scholar] (57) White, R. G. Scours-The Calf Killer. Presented at the California Livestock Symposium. An. Nut. Health, pp.14–18.  [Google Scholar]. Diarrhoeal disease of the calf occurs at a time of complex developmental, environmental and functional change. The surface defences and enzyme systems of the neonatal gut are maturing in a protective film of maternal antibody, while undergoing increasing stimulation from environmental microbial challenge. The precarious nature of this defence system is not surprising. It is contingent upon a balance of such changing conditions as maternal antibody quantity, quality and delivery(5) Bush, L. J., Aguilera, M. A., Adams, G. D. and Jones, E. W. 1971. Absorption of Colostral Immunoglobulins by Newborn Dairy Calves. J. Dairy Sci., 54: 1547–1549.  [Google Scholar], environmental microbial challenge(46) Smith, H. W. 1965. Observations on the Flora of the Alimentary Tract of Animals and Factors Affecting its Composition. J. Pathol, 89: 95–122.  [Google Scholar] (47) Smith, H. W. 1971. The Bacteriology of the Alimentary Tract of Domestic Animals Suffering from E. coli Infection. Ann. N. Y. Acad Set, 176: 110–125.  [Google Scholar] and neonatal immunological and intestinal epithelial maturation(7) Corley, L. D., Staley, T. E., Bush, L. J. and Jones, E. W. 1977. Influence of Colostrum on Transepithelial Movement of E. coli 055. J. Dairy Sci., in press [Google Scholar] (52) Staley, T. E., Corley, L. D., Bush, L. J. and Jones, E. W. 1972. The Ultra-structure of Neonatal Calf Intestine and Absorption of Heterologous Proteins. A rial. Rec, 172: 559–579. [Crossref], [PubMed] , [Google Scholar]. While both infectious and non-infectious etiologic factors are involved(1) Barnum, D. A., Glantz, P. J. and Moon, H. W. 1967. Colibacillosis. CI_RV_eterinary Monograph Series/Two, : 5–44.  [Google Scholar] the former (Escherichia coli, Saltiionsllci and Shigella spp., and reo and corona viruses) is the more significant. Enteropathogenic E. coli (EPEC), a major contributor to neonatal diarrhoeal disease, will be discussed primarily. Four syndromes, septicaemia, enteric-toxaemia, local invasive and enterotoxic have been described(32) Moon, H. W. 1974. Pathogenesis of Enteric Diseases Caused by Escherichia coli. Adv. Vet. Sci. Comp. Med, 18: 179–211. [PubMed] , [Google Scholar] and ad verseoutcomes may result from endotoxic shock and/or hypovolemic shock, from systemic infection and from malnutrition. The clinician is thus faced with the selection of a multi-faceted approach to the problem. Avenues of attack, in addition to prophylactic husbandry, include: passive and active immunization, reduction of challenge, specific antimicrobial therapy, and resolution of fluid and electrolyte loss and shock. This presentation includes a resumé of the calf scour syndrome, together with observations concerning treatment and control. These observations include active and passive immunization, antimicrobial therapy, and modification of intestinal fluid loss.     

Prevalence of antibodies to infectious laryngotracheitis virus in poultry in New Zealand

Abstract

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Infectious laryngotracheitis (ILT) is an acute respiratory disease of fowls which was first reported from the U.S.A. by May and Tittsler (1925) Adlakha, S. C. 1966. A serological investigation to determine respiratory infections of poultry in India. Avian Dis., 10: 401–404.  [Google Scholar]. Both severe acute forms with high mortality and chronic enzootic forms with low mortality have been described, and the earlier literature was reviewed by Jordan (1966) Chang, P. W., Yates, V. J., Dardiri, A. H. and Fry, D. E. 1960. Some observations of the propagation of infectious laryngotracheitis virus in tissue culture. Avian Dis., 4: 384–390.  [Google Scholar]. In New Zealand ILT virus was first isolated in 1957 (Webster, 1959 Hitcher, S. B., Shea, C. A. and White, P. G. 1958. Studies on a serum neutralization test for the diagnosis of laryngotracheitis in chickens. Avian Dis., 2: 258–269.  [Google Scholar]).     

Successful treatment of suspected thoracic nocardiosis in a dog

Abstract

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Sir, — The leptospiral serovars that have been cultured in New Zealand are pomona, copenhageni, ballum and hardjo. (Anon., 1951 Anon. N.Z. Dept Agric. A. Rep. 1950–1 1951 28 28  [Google Scholar]; Kirschner and Gray, 1951 Kirsch, W. 1974. Clinical observations in infection with L. tarassovi. Proc. int. Symp. on Leptospiroses, Smolenice, : 277–279. Czechoslovakia, September 11 to 13, 1973 [Google Scholar]; Anon., 1967a Anon. Leptospiral Serotype Distribution Listsaccording to Host and Geographical Area U.S. Dept of Health, Education and Welfare. Public Health Service 1966  [Google Scholar]; Lake, 1973 Kirschner, L. and Gray, W. G. 1951. Leptospirosis in New Zealand. N.Z. med. J., 50: 342–351.  [Google Scholar], respectively.) Serological evidence of serovar tarassovi has been published (Russell and Hansen, 1958 Rogers, R. J., Flanagan, M. and Hill, M. W. M. 1972. A survey of infectious causes of reproductive failure in beef cattle in north-eastern Australia. Aust. vet. J., 48: 203–207.  [Google Scholar]) but it is believed that until now no members of this serogroup have been isolated in New Zealand.     

The occurrence of antibodies to bovine virus diarrhoea,infectious bovine rhinotracheitis and parainfluenza 3 viruses in sera from New Zealand cattle

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Despite many viruses having been isolated from bovine respiratory and intestinal tracts, only those of bovine virus diarrhoea (BVD), bovine parainfluenza 3 (PI 3) and infectious bovine rhinotracheitis-infectious pustular vulvovaginitis (IBR) have so far been associated with specific clinical complexes. Serological surveys have demonstrated the wide geographical distribution of all three viruses (Huck, 1962 Hack, R. A. 1962. Some recently isolated viruses from cattle. Vet. Bull., 32: 493–504.  [Google Scholar]; Paterson, 1962 Paterson, A. B. 1962. Virus diseases in calves. Vet. Rec., 74: 1384–1389.  [Google Scholar]; French and Snowdon, 1964 French, E. L. and Snowdon, W. A. 1964. Mucosal disease in Australian cattle. Aust. vet. J., 40: 99–105.  [Google Scholar]; Dawson and Darbyshire, 1964 Dawson, P. S. and Darbyshire, J. H. 1964. The occurrence and distribution in the United Kingdom of antibodies to parainfluenza 3 and infectious bovine rhinotracheitis viruses in bovine sera. Vet. Rec., 76: 111–115.  [Google Scholar]), although so far only IBR has been confirmed as being present in New Zealand (Webster and Manktelow, 1959 Webster, R. G. and Manktelow, B. W. 1959. Some observations on bovine rhinotracheitis in New Zealand. N.Z. vet. J., 7: 143–148. [Taylor &; Francis Online] , [Google Scholar]). However, in view of a previous outbreak of a mucosal-like disease (Salisbury etal., 1961 Salisbury, R. M., Hartley, W. J., Mcintosh, I. G., Hansen, N. F., Te Punga, W. A. and Jamieson, S. 1961. A mucosal disease-like syndrome of cattle in New Zealand. Bull. Off. int. Epiz., 56: 62–79.  [Google Scholar]) together with the frequent occurrence of upper respiratory tract symptoms, it seemed most unlikely that other members of this virus trio would be absent from cattle in this country.     

Rhinitis and sinusitis involving Aspergillus fumigatus in a dog

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Fungi of the genus Aspergillus are ubiquitous, but their involvement in clinical disease in man and other mammals is relatively uncommon. When involved in a disease process they are generally considered to be a secondary complicating factor to other underlying local or systemic conditions (Zimmerman, 1955 Zimmerman, L. E. 1955. Fatal fungus infections complicating other diseases. Am. J. clin. Path., 25: 46–65.  [Google Scholar]; Smith, 1962 Smith, D. T. 1962. Symposium Summation. Lab. Invest., 11: 1239–1241.  [Google Scholar]; Cordes and Shortridge, 1968 Cook, W. R., Campbell, R. S. F. and Dawson, C. 1968. The pathology and aetiology of guttural pouch mycosis in the horse. Vet. Rec., 83: 422–438.  [Google Scholar]; Kilman et al, 1969 Kilman, T. W., Ahn, C., Andrews, M. C. and Klassen, K. 1969. Surgery for pulmonary aspergillosis. J., thorac. cardiovasc. Surg., 57: 642–647.  [Google Scholar]; McCausland, 1972 McCausland, I. P. 1972. Systemic mycoses in two cats. N.Z. vet. J., 20: 10–12. [Taylor &; Francis Online] , [Google Scholar]).     

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.     

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.).     

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]     

Magnesium status of dairy cows

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Madam:– Magnesium has been identified as an important mineral in the nutrition of dairy eows and reeent findings in New Zealand(1 Young, P.W., Rys, G. and O'Connor, M.B. 1981. Hypomagnesemia and dairy production. Proc. N.Z. Soc. An. Prod., 41: 61–67.  [Google Scholar]) emphasize this importance. For example, a large survey of dairy animals(2 Young, P.W., O'Connor, M.B. and Feyter, C. 1979. Importance of magnesium in dairy production. 30th Ruakura Farmers Conf. Proc. MAP, : 110–120.  [Google Scholar]) showed one-third of almost one million cows could be suffering from hypomagnesemia. A separate survey (3 1984. Surveillance. Bovine hypomagcsemia, 11: 5–7. Published by the Ministry of Agriculture and Fisheries Private Bag, Wellington [Google Scholar])> involving 76 farms estimated that supplementing with magnesium to prevent hypomagnesemia would have produced a net benefit of between $1,600 and $4,250 per farm. The cost/benefit ratio was remarkably high and ranged from 11–28.