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Many cobalt-deficient sheep develop liver lesions known as ovine "white liver" disease, but the etiology of these changes is controversial. It has been suggested that cofactors are required for development of liver damage in cobalt-deficient sheep. In this study, one group of lambs (n = 5) was fed a diet low in cobalt (4.5 micrograms/kg) while a group of control lambs (n = 4) received the same diet after it had been supplemented with cobalt (1000 micrograms/kg). All cobalt-depleted lambs had reduced growth rate, anorexia, lacrimation, and alopecia, and they eventually became emaciated (mean body weight at end of study: 83% of initial body weight). Plasma concentrations of bilirubin and serum activity of glutamate-oxaloacetate transferase were elevated in these animals, while plasma concentrations of vitamin B12 were reduced (less than 220 pmol/L from day 42). Fatty degeneration of the liver associated with reduced concentrations of vitamin B12 (14.5 pmol/g) was seen in these animals at necropsy at 196 days. Microscopic liver lesions included accumulation of lipid droplets and lipofuscin particles in hepatocytes, dissociation and necrosis of hepatocytes, and sparse infiltration by neutrophils, macrophages, and lymphocytes. Ultrastructural hepatocytic alterations included swelling, condensation and proliferation of mitochondria, hypertrophy of smooth endoplasmic reticulum, vesiculation and loss of arrays of rough endoplasmic reticulum, and accumulation of lipid droplets and lipofuscin granules in cytoplasm of hepatocytes. No liver lesions were seen in control lambs. The results of this study indicate that cofactors are not a prerequisite to development of hepatic damage in cobalt-deficient sheep. Reduced activities of the vitamin B12-dependent enzymes, methylmalonyl CoA mutase and methionine synthase, and lipid peroxidation are of likely pathogenetic importance in the development of the lesions.

Materials and MethodsR SV a t b ronchi ol a r a nd a lveo la r level s. Thi s paper d escrib es ultra structural cha nges in th e bronchi ol ar e pitheliu m of eigh t yo u ng calv e s in o culated w ith R SV. U ltra structura l cha nges within al veoli will be d escribed in a se parate report.Vet Pathol 28: 293-299 (1991) Abstrac t. Ultrastruc tural cha nges were obs er ved in bron ch ioles in acute and repai r stages of respira tory syncy tial virus pneum oni a induced in eight yo ung calves (calf No s. 1-8) using a bov ine stra in of respira tory syncytial virus. Five of th e calves were Friesians and th ree were Hereford x Friesians and all were male. Ti ssues from three mock-infected contro l calves (two Fr iesian , one Hereford x Friesian) were also exam ined. Calves were fro m 3 to 6 days old at the tim e of first inoculati on , with the exception o f calf No .8 , which was 2 weeks old . In th e acute stage o f the ind uced pneum oni a, ev idence of resp ira tory syncytial viru s replicatio n and release was demonstrable in both ciliated and non -ciliated bron ch iolar epithelial cells, with the virus -releas ing process most obv ious at 4 and 5 days after infection. Respiratory syncytial virus infection of bron ch iolar epithelium was associated wit h var ious changes, includi ng hypert rophy, hyper plasia, and formation of syncytia. Necro sis o f epithelial cell struc tures usually appear ed to be preceded by their desquamati on from bronch iolar walls. Respiratory syncytial virus infection resulted in co nside rable damage to the bronchiolar ciliary appa ratus. Such damage was seen as early as I day post-in fection and was sti ll obv ious at 10 da ys post-in fection . Neutro phils were closely associated with resp ira tor y syncytial viru s infected epithelial cells and ev ide nce o f neutro phil fusion with infected epithelial cells was seen. T hese obs ervat ions suggest that neut rophi ls may be inv olved in killing respi rat or y syncytia l virus infected cells and th at neutrophi ls m ight play an im por tant role in early antiv ira l de fense against respiratory syncytial virus at a time when antib od y levels are low and other cellular defen ses are not fully in play. Bro nch iolar repa ir was evide nt from 6 days after infection an d was well advanced at 10 and 13 da ys after in fection .Key words: Bron chiolitis; cow; pneum on ia; respira tory syncytial virus. R espirato ry sy nc yt ia l v irus (R SV) is a co m mon ca use o f severe bronchiol it is a nd pneum onia in yo u ng ca ttle. IA.II.ISSurprisingly, howe ver, m o st ex pe r imen ta l infection s with RSV result in m ild or s u bcl in ica l disease w ith minimal lung lesio n s. In only two reports.v ? exten sive lung lesions o f co m pa ra b le seve rity to tho se seen in field cases were induced b y ex peri men tal R SV in fec tion of ca lv es .Eight calves (calf Nos . 1-8) were inoculat ed with a bovine Several reports are a vaila ble o n light m icro scopic stra in of respiratory syncytial virus (RSY). Five of the calves feature s o...

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