A clinical case in Belgium demonstrated that feeding a feed concentrate containing considerable levels of deoxynivalenol (DON, 1.13 mg/kg feed) induced severe liver failure in 2-to 3-month-old beef calves. Symptoms disappeared by replacing the highly contaminated corn and by stimulating ruminal development via roughage administration. A multi-mycotoxin contamination was demonstrated in feed samples collected at 15 different veal farms in Belgium. DON was most prevalent, contaminating 80% of the roughage samples (mixed straw and maize silage; average concentration in positives: 637 ± 621 µg/ kg, max. 1818 µg/kg), and all feed concentrate samples (411 ± 156 µg/kg, max. 693 µg/kg). In order to evaluate the impact of roughage provision and its associated ruminal development on the gastro-intestinal absorption and biodegradation of DON and its acetylated derivatives (3-and 15-ADON) in calves, a toxicokinetic study was performed with two ruminating and two non-ruminating male calves. Animals received in succession a bolus of DON (120 µg/kg bodyweight (BW)), 15-ADON (50 µg/kg BW), and 3-ADON (25 µg/kg) by intravenous (IV) injection or per os (PO) in a cross-over design. The absolute oral bioavailability of DON was much higher in non-ruminating calves (50.7 ± 33.0%) compared to ruminating calves (4.1 ± 4.5%). Immediately following exposure, 3-and 15-ADON were hydrolysed to DON in ruminating calves. DON and its acetylated metabolites were mainly metabolized to DON-3-glucuronide, however, also small amounts of DON-15-glucuronide were detected in urine. DON degradation to deepoxy-DON (DOM-1) was only observed to a relevant extent in ruminating calves. Consequently, toxicity of DON in calves is closely related to roughage provision and the associated stage of ruminal development.Keywords Biodegradation · Calf · Deoxynivalenol · 3-and 15-Acetyldeoxynivalenol · Mycotoxin · Toxicokinetics Bonnie Valgaeren and Léonard Théron contributed equally to this work.Alfons Callebaut: Deceased. Electronic supplementary materialThe online version of this article (https ://doi.

The aim of this study was to identify the species and antimicrobial susceptibility of bacteria involved in parietal fibrinous peritonitis (PFP). We studied 156 peritoneal fluid samples from cows presenting PFP after caesarean section. Bacteria were cultured in selective media and their antimicrobial susceptibility was tested by disk diffusion assay. Bacteria were isolated in the majority (129/156; 83%) of samples. The majority (82/129; 63%) of positive samples contained one dominant species, while two or more species were cultured in 47/129 (36%) samples. Trueperella pyogenes (T. Pyogenes) (107 strains) was the most identified species, followed by Escherichia coli (E. coli) (38 strains), Proteus mirabilis (P. mirabilis) (6 strains), and Clostridium perfringens (C. perfringens) (6 strains). Several other species were sporadically identified. Antimicrobial susceptibility was tested in 59/185 strains, predominantly E. coli (38 strains) and P. mirabilis (6 strains). Antibiotic resistance, including resistance to molecules of critical importance, was commonly observed; strains were classified as weakly drug resistant (22/59; 37%), multidrug resistant (24/59; 41%), extensively drug resistant (12/59; 20%), or pan-drug resistant (1/59; 2%). In conclusion, extensive antibiotic resistance in the isolated germs might contribute to treatment failure. Ideally, antimicrobial therapy of PFP should be based upon bacterial culture and susceptibility testing.

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This study aimed to describe the inflammation, hydro-electrolyte and acid-base imbalances caused by generalised peritonitis (GP) and parietal fibrinous peritonitis (PFP) after caesarean section. After clinical examination, blood was sampled from 11 cows with PFP, 30 with GP and 14 healthy cows. Serum and plasma refractometry and glutaraldehyde tests were used to evaluate the inflammation level, while hydro-electrolytes and acid-base parameters were assessed using an EPOC® device. In addition to clinical signs of dehydration (>10%), blood analysis showed a high fibrinogen concentration (PFP: 8.64 ± 8.82 g/L; GP: 7.83 ± 2.45 g/L) and fast glutaraldehyde coagulation (<3 min) indicative of severe inflammation in both diseases compared to the control group (p < 0.05). Moreover, a severe decrease in electrolytes concentration (Na+: 126.93 ± 5.79 mmol/L; K+: 3.7 ± 1.3 mmol/L; Ca++: 0.89 ± 0.12 mmol/L; Cl−: 82.38 ± 6.45 mmol/L) and a significant increase in bicarbonate (30.87 ± 8.16 mmol/L), base excess (5.71 ± 7.42 mmol/l), L-lactate (8.1 ± 4.85 mmol/L) and creatinine (3.53 ± 2.30 mg/dL) were observed in cows with GP compared to the control group (p < 0.05). In contrast, few major perturbations were noticed in PFP, where only K+ (3.64 ± 0.25 mmol/L) and Ca++ (1.06 ± 0.09 mmol/L) were significantly modified (p < 0.05). In conclusion, a high dehydration and severe inflammation are induced by PFP and GP. Nevertheless, GP causes more electrolytes and acid-base disturbances than PFP.