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Ovine White-Liver Disease (OWLD). Pathology

Kvitleversjuke (kobolt/vitamin B12 mangel) hos lam. Patologi

Abstract

Microscopic liver changes could earliest be found after 1 month on OWLD pasture, and included extensive fatty change with large spherical vacuoles in hepatocytes, varying size of hepatocytes and nuclei, and formation of Councilman bodies. Later came ceroid deposits, biliary hyperplasia and mesenchymal proliferation. Changes occurred in all lambs which died or were killed due to OWLD, and altogether 83% of the lambs grazing OWLD pastures showed typical or suspect changes. Widespread haemosiderosis of the spleen was common. In severely affected lambs, sclerosis of the Peyer’s patches and of the germinative centres of the intestinal lymph nodes were seen, as were neuronal atrophy and patchy microcavitation of areas in the brain stem. Four had polyvasculitis.

Cobalt/vitamin B12 supplemented lambs showed no specific changes. Lambs which grew well on other pastures (H lambs), but which were subclinically Co/B12 deficient some years, showed no fulminant hepatic OWLD, but 15% developed some features seen in OWLD. They showed no extensive fatty change.

Results indicate that OWLD is a manifestation of B12 deficiency worsened by factors triggering early hepatic fatty change resulting in a more severe liver damage with loss of intracellular homeostasis rendering the hepatocytes vulnerable to other elements, like copper.

Sammendrag

Mikroskopiske leverforandringer ble tidligst funnet etter 1 måned på sjukdomsbeitet, og omfattet utbredt fettinfiltrasjon i form av store vakuoler i levercellene, anisocytoseAnucleose og dannelse av Councilman-legemer. Senere kom ceroidavleiring, gallegangshyperplasi, Kupffercellehypertrofi, og infiltrasjon av betennelsesceller.

Totalt 83% av alle undersøkte lam som gikk på sjukdomsbeitene hadde typiske eller suspekte leverforandringer. Økt hemosiderinavleiring i milten var vanlig. Hos alvorlig affiserte dyr var det en viss lymfocyttuttømning og fibrose i de germinative sentra i peyerplettene i tarmen og i tarmlymfeknutene, samt neuronal atrofi og mikroaviteringer i hjernestammen. Fire hadde polyvasculitt.

Kobolt/vitamin B12 doserte lam viste ingen spesifikke forandringer.

Lam som gikk på andre beiter (H lam), og som noen år var subklinisk Co/B12 deficitte, viste ingen fulminante OWLD forandringer. Et år hadde 3 av 7 lam moderate forandringer suspekte for OWLD, men uten særlig fettinfiltrasjon. Resultatene viser at OWLD er en vitamin B12 mangel intensiven av samvirkende faktorer som forårsaker fettavleiring i levercellene og større leverskade, som resulterer i at den intracellulære homeostasen ødelegges og levercellene blir mer sårbare for f.eks. kopper.

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Ulvund, M.J. Ovine White-Liver Disease (OWLD). Pathology. Acta Vet Scand 31, 309–324 (1990). https://doi.org/10.1186/BF03547543

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