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Mechanism and treatment of acidosis in neonatal diarrhea

Posted on:2005-10-06Degree:Ph.DType:Dissertation
University:The University of Saskatchewan (Canada)Candidate:Ewaschuk, Julia BethFull Text:PDF
GTID:1454390008985150Subject:Agriculture
Abstract/Summary:
The D-isomer of lactate contributes to metabolic acidosis in diarrheic calves, and is hypothesized to originate from microbial fermentation in the gastrointestinal tract. This study aimed to identify whether D-lactate is produced in the rumen, the colon, or both and to quantify urinary excretion of D-lactate. Further objectives were to determine whether Lactobacillus GG (LGG) is a suitable treatment of D-lactic acidosis in calves and to investigate the prevalence of D-lactic acidosis in monogastrics with diarrhea.;To determine if the LGG reduces D-lactic acidosis or fecal water %, 40 diarrheic calves were randomized into 2 groups. The experimental group was fed LGG, the other served as a control group. Fecal and serum samples were collected at admission, and at 24 and 48 h after the first LGG dose, and analyzed for D-lactate. No difference in D-lactate was detected in either matrix, but fecal water was significantly lower in experimental calves at 24 h. D-lactic acidosis was absent in all calves remaining in the clinic at 48 h. Serum was also collected from 17 diarrheic foals, 30 piglets and 14 infants. Only one case of mild D-lactic acidosis was detected in a foal (3.2 mmol/L).;Collectively, these studies contribute to the currently limited knowledge of D-lactic acidosis in diarrhea by confirming the gastrointestinal origin of D-lactate in diarrheic calves, revealing the efficacy of current therapy, and the lower incidence of D-lactic acidosis in monogastrics compared with ruminants.;High performance liquid chromatographic methods were validated for the separation of D- and L-lactate, DL-lactate, pyruvate and acetate in calf feces, rumen fluid and urine. Fecal, rumen, serum and urine samples were then obtained from 15 diarrheic and 10 healthy calves and analysed for D- and L-lactate, pyruvate and acetate. Neither pyruvate, acetate or L-lactate contributed significantly to acidemia in any case. L-lactate was significantly higher in the rumen contents and feces of diarrheic calves compared to healthy controls but not different in serum or urine. Rumen, fecal, serum and urine D-lactate concentrations were all significantly higher (p < 0.05) in diarrheic calves than in healthy calves. Colonic fermentation contributed more to acidosis than did ruminal fermentation.
Keywords/Search Tags:Acidosis, Diarrheic calves, Fermentation, LGG
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