Chloride and lactate as prognostic indicators of calf diarrhea from eighty-nine cases.

IMPORTANCE: Deaths due to neonatal calf diarrhea are still one of the most critical problems of cattle breeding worldwide. Determining the parameters that can predict diarrhea-related deaths in calves is especially important in terms of prognosis and treatment strategies for the disease. OBJECTIVE: The primary purpose of this study was to determine mortality rates and durations, survival status, and predictive prognosis parameters based on vital signs, hematology, and blood gas analyses in neonatal diarrheic calves. METHODS: The hospital automation system retrospectively obtained data from 89 neonatal diarrheic calves. RESULTS: It was found that 42.7% (38/89) of the calves brought with the complaint of diarrhea died during hospitalization or after discharge. Short-term and long-term fatalities were a median of 9.25 hours and a median of 51.50 hours, respectively. When the data obtained from this study is evaluated, body temperature (°C), pH, base excess (mmol/L), and sodium bicarbonate (mmol/L) parameters were found to be lower, and hemoglobin (g/dL), hematocrit (%), lactate (mmol/L), chloride (mmol/L), sodium (mmol/L) and anion gap (mmol/L) parameters were found to be higher in dead calves compared to survivors. Accordingly, hypothermia, metabolic acidosis, and dehydration findings were seen as clinical conditions that should be considered. Logistic regression analysis showed that lactate (odds ratio, 1.429) and CI- (odds ratio, 1.232) concentration were significant risk factors associated with death in calves with diarrhea. CONCLUSIONS AND RELEVANCE: According to the findings obtained from this study, the determination of lactate and Cl- levels can be used as an adjunctive supplementary test in distinguishing calves with diarrhea with a good prognosis.

Efficacy of pomades containing different percentages of enilconazole in the treatment of bovine dermatophytosis.

BACKGROUND: Enilconazole is a broad-spectrum topical antimycotic agent used for the management of bovine dermatophytosis. HYPOTHESIS/OBJECTIVES: To investigate the efficacy of pomades containing different concentrations of enilconazole for the treatment of bovine dermatophytosis. METHODS: Dermatophytosis was confirmed in 120 cattle from farm in Gole region of Turkey. Animals were divided into six groups (n = 20 in each). Pomades containing 1%, 2%, 3%, 4% and 5% enilconazole were applied topically to individual lesions in groups I-V, respectively, once a day for 3 days. Group VI animals were used as a control group. Animals were monitored clinically once a week for a two month period. RESULTS: Cows treated with pomades containing 4% and 5% enilconazole recovered; adverse topical reactions occurred in 40% and 55% of animals, respectively. The success rate for cows treated with pomades containing 3% enilconazole was 95% and they recovered with no adverse reactions. Success rates for treatment were 25% and 50% for cows treated with pomades containing 1% and 2% enilconazole, respectively. No improvement was observed in the control group. CONCLUSIONS AND CLINICAL IMPORTANCE: Pomades containing 3% enilconazole are recommended for the treatment of bovine dermatophytosis.

Investigation of protective effect of L-carnitine on L-asparaginase-induced acute pancreatic injury in male Balb/c mice.

INTRODUCTION: The present analysis deals with the biochemical and histopathological effects of L-carnitine in mice with L-asparaginase (ASNase)-induced experimental acute pancreatic injury (API). METHODS: A total of 32 male Balb/c mice were divided into four groups as follows. Group I (control) was injected with single saline via the intraperitoneal route. Group II received 500 mg/kg of L-carnitine daily with the injected volume of 62.5-75 µl for 25-30 g mice using a Hamilton microinjector applied for 5 days. Group III received a single 10,000 IU Escherichia coli ASNase/kg body weight dose of ASNase at a dose of 500 mg/kg. Group IV received 500 mg/kg of L-carnitine daily and a single dose of 500 mg/kg of ASNase and were decapitated on the fifth day following the injection. Blood and pancreatic tissue samples were obtained for evaluation of histopathological structure and levels of malondialdehyde (MDA), reduced glutathione (GSH), total sialic acid (TSA), glucose, amylase and triglyceride. RESULTS: In group III, compared to group IV and group I it was determined that levels of GSH and amylase were significantly lower while levels of MDA, TSA, glucose and triglyceride were higher. Levels of GSH, MDA, TSA, glucose, triglyceride and amylase, especially in group IV, approached that of group I. As a result, L-carnitine for ASNase-induced API mice may be protective against pancreatic tissue degeneration and oxidative stress or lipid peroxidation.

The effects of dexmedetomidine on mesenteric arterial occlusion-associated gut ischemia and reperfusion-induced gut and kidney injury in rabbits.

OBJECTIVE: We assessed the antioxidant activity of dexmedetomidine (Dex) administered during the ischemic period in a rabbit model of mesenteric ischemia/reperfusion (I/R) injury using biochemical and histopathological methods. METHODS: A total of 24 male New Zealand white rabbits weighing between 2.5 and 3.0 kg were randomly divided into three groups: the sham group (Group S, n = 8), the I/R group (Group I/R, n = 8), and the I/R plus Dex treatment group (Group Dex, n = 8). In the I/R group, ischemia was achieved with 60 min of mesenteric occlusion. The sham group provided normal basal values. The rabbits in Group I/R were operated to achieve I/R. Group Dex received intravenous Dex 30 min after the commencement of reperfusion (10 µg/kg Dex was infused within 10 min, and then a maintenance dose of 10 µg/kg/h Dex was infused intravenously). For the measurement of tissue malondialdehyde, total antioxidant status, total oxidant status, lipid hydroperoxide levels, superoxide dismutase, catalase, and myeloperoxidase activity levels in the renal tissue samples of animals, the rabbits in each group were sacrificed 3 h after reperfusion. The histopathological examination scores were determined using the intestinal and renal tissues. RESULTS: The mean malondialdehyde, total oxidant status, myeloperoxidase, and lipid hydroperoxide levels were significantly higher in Group I/R than in Groups S and Dex (P < 0.05). There also were significant decreases in the mean total antioxidant status, catalase, and superoxide dismutase activities in Group I/R compared with Groups S and Dex (P < 0.05). The histopathological examination scores of the intestinal and renal tissues were significantly higher in Group I/R compared with Groups S and Dex (P < 0.05). CONCLUSION: Dex treatment may have biochemical and histopathological benefits by preventing I/R-related cellular damage of intestinal and renal tissues as shown in an experimental mesenteric ischemia model. The preference to use Dex for anesthesia during the mesenteric ischemia procedure may attenuate I/R injury in intestinal and renal tissues.

Detection of myocardial degeneration with point-of-care cardiac troponin assays and histopathology in lambs with white muscle disease.

The aim of this study was to evaluate the use of human cardiac troponin-I (cTn-I) and cardiac troponin-T (cTn-T) kits for the determination of myocardial degeneration in lambs suffering from white muscle disease (WMD). Cardiac troponin (cTn) analyses and necropsy were performed on 12 lambs with acute WMD. Only cTn analyses were tested in six healthy lambs. cTn-I and cTn-T tests were positive for all lambs with WMD, but negative in healthy lambs. Necropsy revealed that the cardiac and skeletal muscles of lambs with WMD had chalky white lesions, which appeared as necrosis and calcification in histopathology. The histopathological findings of the heart muscle and increased cTn in lambs with WMD suggested that marked myocardial degeneration may be detected by point-of-care cTn assays in lambs.

Pyridine induction of cytochrome P450 1A1, iNOS and metallothionein in Syrian hamsters and protective effects of silymarin.

An in vivo assessment for the protective effects of silymarin for pyridine toxicity was investigated through cytochrome P450 isoform CYP1A1 and inducible nitric oxide synthase (iNOS) activity prevention. Moreover, the effect of pyridine-induced oxidative stress on metallothionein I-II (MT), a scavenger of oxygen-derived free radicals, was investigated. Forty Syrian hamsters were allocated into 4 groups. Syrian hamsters were dosed with pyridine (400mg/kg) intraperitoneally with and without silymarin (200mg/kg daily by gavage) for 4 days. Pyridine induced diffuse degeneration and necrosis of the proximal and distal renal tubular cells; cloudy swelling, necrosis and hepatocellular atypia of the liver; and degenerative changes in the myocardium. The degree of pathological alterations was less severe with simultaneous silymarin application. CYP1A1, iNOS and MT expression levels were elevated in liver, kidney and heart in response to acute pyridine toxicity. Silymarin application abolished or significantly suppressed the induction of CYP1A1, iNOS and MT expressions in liver, kidney and heart of the pyridine-treated Syrian hamsters. Enhanced synthesis of MT by pyridine possibly implies a purposive cellular response to prevent damage caused by oxygen radicals. However, silymarin significantly reduced the oxidative-stress-inducing effect of pyridine as reflected by decreased synthesis of MT. These results suggest that through oxidant generation, pyridine may cause alteration of the metabolic ways, including nitric oxide-mediated CYP1A1 activity.

Determination of cardiac troponin I in the blood and heart of calves with foot-and-mouth disease.

The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 +/- 1.9 ng/ml) concentration and CK (573 +/- 407 U/l), CK-MB (238 +/- 37 U/l), AST (84 +/- 7), and LDH (298 +/- 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.

Hepatoprotective effect of L-carnitine against acute acetaminophen toxicity in mice.

L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing the beta-oxidation of fatty acid in the mitochondria. It is also a known antioxidant with protective effects against lipid peroxidation. In this study, hepatoprotective effect of L-carnitine was investigated against acetaminophen (AA)-induced liver toxicity where mitochondrial dysfunction and oxidative stress are thought to be involved in AA hepatotoxicity. Sixty-four Balb/C mice were divided into eight groups. Mice were dosed with single-AA injection (500 mg/kg via the intra peritoneal route) with or without L-carnitine (500 mg/kg for 5 days starting 5 days before AA injection via intra peritoneal route) and sampled at 4, 8 and 24 h following AA injection. AA increased serum AST, ALT, total sialic acid (TSA) and MDA as well as tissue TSA and MDA levels significantly with the highest increase observed at 4 h, but there was a decrease in blood and tissue GSH level. Administration of L-carnitine significantly reduced AA-induced elevations in AST, ALT, TSA and MDA concentrations and increased GSH levels at all sampling points. AA also induced necrosis, hyperemia, sinusoidal congestion and hemorrhage with time-dependent increase in severity, but the degree of necrosis and histopathologic alterations were most severe at 24 h following AA administration. However, the degree of pathologic alterations was less severe with simultaneous L-carnitine application. These results suggest that AA results in oxidative damage in the liver with an acute effect. L-carnitine also has a prominent protective effect against AA toxicity and may be of therapeutic value in the treatment of AA-induced hepatotoxicity.

Effect of time delay and storage temperature on blood gas and acid-base values of bovine venous blood.

The aim of this study was to investigate possible changes in the gas composition and acid-base values of bovine venous blood samples stored at different temperatures (+4, 22 and 37 degrees C) for up to 48 h. Five healthy cattle were used in the study. A total of 15 blood samples collected from the animals were allocated into three groups, which were, respectively, then stored in a refrigerator adjusted to +4 degrees C (Group I, n=5), at a room temperature of about 22 degrees C (Group II, n=5) and in an incubator adjusted to 37 degrees C (Group III; n=5) for up to 48 h. Blood gas and acid-base values were analysed at 0 (baseline), 1, 2, 3, 4, 5, 6, 12, 24, 36 and 48 h of storage. A significant decrease (p<0.001) was found, in the pH of the refrigerated blood after 5 h and its maximum decrease was recorded at 48 h as 0.04 unit. There were also significant alterations (p<0.001) in the blood pH of the samples stored at room temperature and in the incubator after 2 and 3 h, respectively. The maximum mean alteration in pCO(2) value for Group I was -0.72 kPa during the assessment, while for groups II and III, maximum alterations in pCO(2) were detected as +2.68 and +4.16 kPa, respectively. Mean pO(2) values increased significantly (p<0.001) for Group I after 24 h and for Group II after 6 h, while a significant decrease was recorded for Group III after 24 h (p<0.001). Base excess (BE) and bicarbonate (HCO(3)) fractions decreased significantly for all the groups during the study, compared to their baseline values. In conclusion, acid-base values of the samples stored at 22 and +4 degrees C were found to be within normal range and could be used for clinical purposes for up to 12 and 48 h, respectively, although there were small statistically significant alterations.

[Concentrations of carnitine and further biochemical parameters in the blood serum of healthy dairy cows and cows with abomasal displacement (dislocatio abomasi) and puerperal disorders]. / Carnitinkonzentrationen und weitere biochemische Parameter im Blutserum von gesunden Milchkühen und Kühen mit Dislocatio abomasi sowie Puerperalstörungen.

It was the aim of this study to compare the concentrations of total (TC) and free L-carnitine (FC) in blood serum of different groups of lactating cows. The animals were allotted into three groups, a) control animals (N = 11), b) cows with abomasal displacement (AD) (N = 5) and c) cows with puerperal disorders (PD) (N = 5). TC and FC were measured with an radioenzymatic assay. Blood samples were collected from 5 to 0 d before parturition (a. p.) and from 0 to 28 d after parturition (p. p.). It was of interest to examine whether L-carnitine might be limiting under certain conditions of metabolic stress which are typical for high yielding lactating cows. Concentrations of TC and FC (mumol/l) in control cows before and after parturition were 10.0* and 8.6* and 6.0-8.9 and 3.7-4.9, respectively. The corresponding TC and FC values for cows with AD were 19.6* and 8.9* and 10.5-20.7 and 4.8-6.9, respectively. Cows with PD showed TC and FC concentrations a. p. and p. p. of 15.7* and 9.2* and 10.3-13.0 and 4.8-6.3, h other puerperal disorders PD respectively (* only one value). TC and FC concentrations in serum of normal cows were higher before than after parturition. Cows, which developed post partal puerperal disorders had a higher prepartum concentrations of TC and CE, on the other hand, serum concentrations of FC was lower. Post partum cows with metabolic disorders showed higher CE levels than control animals. Cows which developed DA had significantly higher concentrations of TC and CE in serum only on d 7 p.p. than animals with other PD. It appeared that increased fat mobilization was regularly associated with responsive increases of CE concentrations in blood serum.