Jeanne Lofstedt

White muscle disease of foals.

White muscle disease (nutritional myodegeneration) of foals is a peracute to subacute myodegenerative disease affecting skeletal and cardiac muscle. It is caused by a dietary deficiency of selenium and vitamin E, usually in association with predisposing factors such as a high intake of dietary unsaturated fats or unaccustomed exercise. White muscle disease has been observed in foals from birth to 1 year of age, particularly those foals born to dams fed selenium-deficient diets during gestation. The disease in foals may present as an acute, fulminant syndrome, which is rapidly fatal, or a subacute syndrome characterized by profound muscular weakness. Failure of passive transfer, aspiration pneumonia, and stunting are frequent complications. Markedly increased muscle enzyme and low glutathione peroxidase activities are common findings in affected foals. Foals with the subacute form of the disease may survive if they are supplemented early with selenium; however, mortality rates ranging from 30% to 45% have been reported, even for this form of the disease.

Model to predict septicemia in diarrheic calves

The difficulty in distinguishing between septicemic and nonsepticemic diarrheic calves prompted a study of variables to predict septicemia in diarrheic calves, 28 days old that were presented to a referral institution. The prevalence of septicemia in the study population was 31%. Variables whose values were significantly different (P < .10) between septicemic and nonsepticemic diarrheic calves were selected using stepwise, forward, and backward logistic regression. Variables identified as potentially useful predictors were used in the final model‐building process. Two final models were selected: 1 based on all possible types of predictors (laboratory model) and 1 based only on demographic data and physical examination results (clinical model). In the laboratory model, 5 variables retained significance: serum creatinine > 5.66 mg/dL (> 500 μmol/L) (odds ratio [OR] = 8.63, P = .021), toxic changes in neutrophils ≥ 21 (OR = 2.88, P = .026), failure of passive transfer (OR = 2.72, P = .023), presence of focal infection (OR = 2.68, P = .024), and poor suckle reflex (OR = 4.10, P = .019). Four variables retained significance in the clinical model: age ≤ 5 days (OR = 2.58, P = .006), presence of focal infection (OR = 2.45, P = .006), recumbency (OR = 2.98, P = .011), and absence of a suckling reflex (OR = 3.03, P = .031). The Hosmer—Lemeshow goodness‐of‐fit chi‐square statistics for the laboratory and clinical models had P‐values of .72 and .37, respectively, indicating that the models fit the observed data reasonably well. The laboratory model outperformed the clinical model by a small margin at a predictabilty cutoff of 0.5, however, the predictive abilities of the 2 models were quite similar. The low sensitivities (39% and 40%) of both models at a predicted probability cutoff of 0.5 meant many septicemic calves were not being detected by the models. The specificity of both models at a predicted probability cutoff of 0.5 was .90%, indicating that .90% of nonsepticemic calves would be predicted to be nonsepticemic by the 2 models. The positive and negative predictive values of the models were 66–82%, which indicated the proportion of cases for which a predictive result would be correct in a population with a prevalence of septicemia of 31%.

Contribution of Unmeasured Anions to Acid–Base Disorders and its Association with Altered Demeanor in 264 Calves with Neonatal Diarrhea

Background The quantitative effect of strong electrolytes, unmeasured anions (UAs), p CO 2, and plasma protein concentrations in determining plasma pH and bicarbonate (HCO 3 −) can be demonstrated using the physicochemical approach. Demeanor of calves with diarrhea is associated with acidemia, dehydration, and hyper‐d‐lactatemia. Hypothesis Unmeasured anions are a major factor influencing changes in plasma pH and HCO 3 − of calves with diarrhea and UAs and strong UAs, estimated by anion gap (AG) and strong ion gap (SIG), respectively, are more strongly associated with alteration of demeanor compared to other acid–base variables. Animals A total of 264 calves with diarrhea from two data sets (DS1 and DS2). Methods Retrospective study. Forward stepwise regression was performed to determine the relationship between measured pH or HCO 3 −, and physicochemical variables. A two‐way ANOVA was performed to investigate the association between acid–base variables and attitude (bright, obtunded, and stuporous), posture (standing, sternal or lateral recumbency), and strength of suckling reflex (strong, weak, or absent). Results Increased strong UAs estimated by SIG was the most important contributor to changes in measured pH and HCO 3 − (DS1: r 2 66 and 59%, DS2: 39 and 42%, P < .0001). SIG and AG were correlated to deteriorating calf demeanor for all three clinical scoring categories: attitude, posture, and suckle reflex (P < .0001). Conclusion and Clinical Relevance Elevated concentrations of strong UAs were the primary cause of acidemia and had an important influence on the demeanor of calves with diarrhea. These findings emphasize the importance of the calculation of UAs when evaluating acid–base abnormalities in calves.