Skeletal changes in hemochromatosis of Salers cattle

Hemochromatosis is an inherited defect in Salers cattle, characterized by increased iron absorption and wasting in young animals. Loss of teeth and soft bones has been reported. This study details bone changes in a prospective study of an affected Salers heifer and an age-matched, half-sibling control. The heifer fell 2 weeks before euthanasia, developed non-weight bearing lameness, and then became recumbent. At necropsy, the heifer was smaller than the control and had fractures of the humerus, femur, and ribs. Distinctive circumferential laminations in the outer third of the cortex were seen radiographically as layers of variably decreased density. In midshaft cross sections, the cortex was wider in some long bones, and fluorescent labeling revealed irregular and intermittent mineralization in the outer cortical layers. Mineral apposition rates in osteons of the inner cortex were decreased as compared with the control, and longitudinal bone formation at the growth plate was markedly decreased. Histologically, there were buried layers of osteopenic, poorly mineralized plexiform bone in outer circumferential lamellae. There was stainable iron in woven bone cores of the matrix. Iron was found in occasional osteoclasts as well. The mandible was severely affected, with loss of cortical bone as well as trabecular bone around the teeth and resorption of dental roots. Bone analysis revealed iron levels in the affected calf that were 30-50 times greater than the control and decreased percent ash in the outer cortex. These results indicate that periosteal dysplasia and osteopenia are responsible for pathologic fractures and tooth loss.     

beta-Mannosidosis in a Salers calf: a new storage disease of cattle

A storage disease characterised by widespread vacuolation of cells throughout the body was diagnosed in a newborn calf of the Salers breed. Extraction and analyses of water soluble material showed that the storage material was oligosaccharide in nature and was probably derived from the core region of the heterosaccharide moiety of glycoproteins. Glycosidase analyses showed that the disease was due to a deficiency of acidic beta-mannosidase.     

Hepatic tyrosine aminotransferase and glucocorticoid abuse in meat cattle

Bertarelli, D., Balbo, A., Carletti, M., Cannizzo, T., Girolami, F., Nebbia, C. Hepatic tyrosine aminotransferase and glucocorticoid abuse in meat cattle. J. vet. Pharmacol. Therap.  35 , 596–603. Besides being extensively applied as therapeutical remedies, glucocorticoids (GCs) – most notably dexamethasone or prednisolone – are also illegally used in livestock for growth‐promoting purposes. This study was designed to assess the suitability of liver tyrosine aminotransferase (TAT), a gluconeogenic enzyme known to be induced by GCs, to act as a reliable candidate biomarker to screen for GC abuse in cattle. Enzyme activity was measured spectrophotometrically in liver cytosols or in cell extracts, and TAT gene expression was determined by real‐time PCR. Compared with untreated veal calves, a notable scatter (20‐fold) and much higher median values (3‐fold) characterized TAT specific activity in liver samples from commercially farmed veal calves. A time‐related increase in both enzyme activity and gene expression was detected in rat hepatoma cell lines treated with dexamethasone concentrations (10^?8 or 10^?9 m ) in the range of those recorded in noncompliant samples from EU official controls. In experimental studies in which finishing bulls were administered GCs at growth‐promoting dosages, however, no such changes were recorded in dexamethasone‐treated animals; a statistically significant rise in liver TAT activity (+95%) only occurred in prednisolone‐treated bulls. Although further research is needed to characterize the GC‐mediated response in cattle liver, TAT does not appear to be a specific and sensitive biomarker of GC abuse in the bovine species.     

Right ventricular heart failure of Montana cattle

Congestive right ventricular heart failure of Montana cattle is characterized clinically by an accumulation of edematous fluid in the brisket region and ventral portions of the body but not of the legs. A well developed jugular pulse is first observed followed by a watery diarrhea and usually by the accumulation of excessive fluid in the pleural and peritoneal cavities. As the case develops over a period of two to three weeks, the ventral edema becomes more marked (Fig. 1) and straw-colored fluid may accumulate in the body cavities until the abdomen is distended and breathing labored. Death may occur as a result of respiratory failure due to the large volume of pleural fluid or from general debilitation as a result of the right ventricular failure. The incidence of this type of heart failure in Montana cattle is highest on moist mountain valleys. Eighty-one of 113 cases observed over a seven year period occurred in cattle that were maintained at altitudes of 1525 m or below. This paper describes the conditions under which the disease occurs in Montana and compares the hemograms of clinically ill and healthy cattle.     

Hepatic ultrasonography and blood changes in cattle with experimentally induced hepatic abscesses.

Hepatic abscesses were induced experimentally in 5 steers by inoculating Fusobacterium necrophorum via ultrasonography-guided, percutaneous catheterization of the portal vein. Hepatic ultrasonography was performed to determine the onset and progression of abscessation. Blood samples were collected before and after inoculation for performing leukocyte counts and hepatic function tests. Ultrasonographic evidence of liver abscesses was observed as early as 3 days after inoculation. Abscesses appeared as hyperechoic centers (cellular debris and pus) surrounded by hypoechoic or anechoic areas (fluid). Increases in rectal temperature, leukocyte counts, fibrinogen, globulin, bilirubin, gamma-glutamyltransferase, and sorbitol dehydrogenase concentrations were detected. Hepatic dysfunction was evidenced by decrease in serum albumin concentration and low sulfobromophthalein clearance. The ultrasonographic diagnosis of abscesses correlated well with necropsy findings.     

Fertilization failure and embryonic mortality in parous and nonparous beef cattle

One hundred and two nonparous females, 18 to 24 mo old, and 55 parous or multiparous beef females, 3 to 12 yr old, were mated naturally (d 0) and slaughtered on d 2 to 5, 6 to 8 or 14 to 16 of gestation. Each reproductive tract was flushed with phosphate-buffered saline, and the flushings were searched for an oocyte or embryo. Parous females had a higher (P less than .05) fertilization rate than nonparous females. In nonparous females, reproductive failure was attributed equally to fertilization failure and embryonic mortality, which had occurred or was occurring by d 8 of gestation. In parous females, reproductive failure was attributed entirely to embryonic death. About 67% of this embryonic mortality had occurred or was occurring by d 8 of gestation; the other 33% occurred between d 8 and 16 of gestation. These findings show that in both nonparous and parous beef females, a large portion of the reproductive failure occurs by d 8 of gestation and would not have any noticeable influence on length of the estrous cycle.     

Hepatic biotransformation pathways and ruminal metabolic stability of the novel anthelmintic monepantel in sheep and cattle

Monepantel (MNP) is a new amino‐acetonitrile derivative anthelmintic drug used for the treatment of gastrointestinal (GI) nematodes in sheep. The present work investigated the main enzymatic pathways involved in the hepatic biotransformation of MNP in sheep and cattle. The metabolic stability in ruminal fluid of both the parent drug and its main metabolite (monepantel sulphone, MNPSO₂) was characterized as well. Additionally, the relative distribution of both anthelmintic molecules between the fluid and particulate phases of the ruminal content was studied. Liver microsomal fractions from six (6) rams and five (5) steers were incubated with a 40 μm of MNP. Heat pretreatment (50 °C for 2 min) of liver microsomes was performed for inactivation of the flavin‐monooxygenase (FMO) system. Additionally, MNP was incubated in the presence of 4, 40, and 80 μm of methimazole (MTZ), a FMO inhibitor, or equimolar concentrations of piperonyl butoxide (PBx), a well‐known general cytochrome P450 (CYP) inhibitor. In both ruminant species, MNPSO₂ was the main metabolite detected after MNP incubation with liver microsomes. The conversion rate of MNP into MNPSO₂ was fivefold higher (P < 0.05) in sheep (0.15 ± 0.08 nmol/min·mg) compared to cattle. In sheep, the relative involvement of both FMO and CYP systems (FMO/CYP) was 36/64. Virtually, only the CYP system appeared to be involved in the production of MNPSO₂ in cattle liver. Methimazole significantly reduced (41 to 79%) the rate of MNPSO₂ production in sheep liver microsomes whereas it did not inhibit MNP oxidation in cattle liver microsomes. On the other hand, PBx inhibited the production of MNPSO₂ in liver microsomes of both sheep (58 to 98%, in a dose‐dependent manner) and cattle (almost 100%, independently of the PBx concentration added). The incubation of MNP and MNPSO₂ with ruminal contents of both species showed a high chemical stability without evident metabolism and/or degradation as well as an extensive degree of adsorption (83% to 90%) to the solid phase of the ruminal content. Overall, these results are a further contribution to the understanding of the metabolic fate of this anthelmintic drug in ruminants.     

Locoweed (Oxytropis sericea) poisoning and congestive heart failure in cattle

Locoweed (Oxytropis sericea), when fed to calves at high elevations, increased the prevalence and severity of congestive heart failure. Forced exercise did not increase the prevalence of congestive heart failure, but it did increase severity. Calves consuming locoweed at high elevations developed signs and gross lesions of congestive heart failure and microscopic lesions of congestive heart failure and locoweed poisoning. Calves fed locoweed at low elevations developed only signs and lesions of locoweed poisoning.     

Hepatic steroid inactivating enzymes,hepatic portal blood flow and corpus luteum blood perfusion in cattle

Production from the corpus luteum (CL) and/or hepatic steroid inactivation impacts peripheral concentrations of P4, which can alter reproductive performance. Our primary objective was to examine hepatic steroid inactivating enzymes, portal blood flow, and luteal blood perfusion at 10 days post‐insemination in pregnant versus non‐pregnant beef and dairy cows. Twenty early lactation Holstein cows and 20 lactating commercial beef cows were utilized for this study. At day 10 post‐insemination, hepatic portal blood flow and CL blood perfusion were measured via Doppler ultrasonography. Liver biopsies were collected and frozen for later determination of cytochrome P450 1A (CYP1A), 2C (CYP2C), 3A (CYP3A), uridine diphosphate‐glucuronosyltransferase (UGT) and aldo‐keto reductase 1C (AKR1C) activities. Pregnancy was determined at day 30 post‐insemination and treatment groups were retrospectively assigned as pregnant or non‐pregnant. Data were analyzed using the mixed procedure of SAS. Steroid metabolizing enzyme activity was not different (p > .10) between pregnant versus non‐pregnant beef or dairy cows. Hepatic portal blood flow tended (p < .10) to be increased in pregnant versus non‐pregnant dairy cows. Luteal blood perfusion was increased (p < .05) in pregnant versus non‐pregnant dairy cows. Pregnant dairy cows appear to have an increased rate of hepatic clearance of P4 in combination with increased synthesis from the CL. This could account for the lack of difference in peripheral P4 concentrations between pregnant and non‐pregnant dairy cows. This study highlights the relevance of further investigation into steroid secretion and inactivation and their impact on the maintenance of pregnancy in cattle.     

The failure of genus specific serological tests to detect leptospirosis in cattle and rabbits

Abstract

Extract

In New Zealand, Leptospirosis of cattle is an important zoonosis. Human leptospirosis, one of the most common of the) notifiable diseases (Christmas et al., 1974 Christmas, B. W., Tennent, R. B. and Lindsay, P. G. 1974. Dairy farm fever in New Zealand: A local outbreak of human leptospirosis. N.Z. med. J., 79: 901–904.  [Google Scholar]) is almost exclusively a disease of dairy farmers. Clinical signs of bovine Leptospira infections are frequently not observed (Sullivan, 1974 Sullivan, N. D. 1974. Leptospirosis in animals and man. Aust. vet. J., 50: 216–223.  [Google Scholar]). Consequently, serological tests are often used to detect leptospirosis in cattle. The microscopic agglutination (MA) test is fairly serotypespecific, but it is tedious to perform and requires potentially hazardous living cultures. The complement fixation (CF) test is less serotype-specific, uses killed organisms, and may be a better indicator of recent infection (Hodges and Ris, 1974 Hodges, R. T. and Ris, D. R. 1974. Complement fixing and agglutinating antibody responses and leptospiruria in calves inoculated with Leptospira serotypes pomona, hardjo, copenhageni or ballum. N.Z. vet. J., 22: 25–30. [Taylor &; Francis Online] , [Google Scholar]). Both tests require a variety of serotypes to identify those causing the infection.     

Heart disease in cattle with clinical signs of heart failure: 59 cases

This retrospective study identified clinical signs, underlying cardiac conditions, blood findings, echocardiographic findings, and prognosis for 59 cattle with clinical signs of congestive heart failure. Signalment; history; clinical signs; clinicopathologic, echocardiographic, and radiographic findings; and treatment were determined by reviewing medical records. Follow-up information was obtained by telephone conversation with owners. Most patients were tachycardic (n = 50), and tachypneic (n = 55). Pericarditis of traumatic origin (n = 21), by extension from pleuritis (n = 3), or of idiopathic origin (n = 1) was diagnosed in 25 cases. Other diagnoses were congenital heart defect (n = 13), cardiomyopathy (n = 9), bacterial endocarditis (n = 7), and neoplasm (n = 5). Twelve cases (20%) were discharged. Long-term survival was good in 2 out of 3 cases treated by pericardiostomy. The prognosis is poor in cases of heart failure in cattle and deaths within 1 mo (n = 3) or between 1 to 3 mo after discharge (n = 3) were common in cases for which follow-up was available (n = 8).