<i>Lawsonia intracellularis</i> associated equine proliferative enteropathy in Danish weanling foals

Abstract Background Lawsonia intracellularis, an obligate intracellular bacterium, causes equine proliferative enteropathy, mainly in horses around weaning. This disease is rarely reported in the Scandinavian countries. Results Five cases of equine proliferative enteropathy were diagnosed between 2008–2016 at the University of Copenhagen Large Animal Teaching Hospital. Cases were Danish Warmbloods and a Friesian horse, aged 6–7 months, presenting with typical clinical signs of lethargy, poor body condition, pyrexia and diarrhea. Clinical pathology was consistent with previous reports of severe hypoalbuminemia and leukocytosis. Diagnosis was confirmed by fecal polymerase chain reaction, serum immunomonolayer peroxidase assay and/or immunofluorescence and fluorescence in situ hybridization performed on formalin-fixed ileum samples. Concurrent intestinal parasitism was present in all five cases. Treatment consisted of antimicrobial therapy, anti-inflammatories, intravenous crystalloids and plasma. Three foals were euthanised due to deterioration and poor response to treatment, one with complications of septic arthritis and Strongylus vulgaris associated intestinal infarct. The other two foals survived and were reported by the owners to be healthy on long-term follow-up. Conclusions Equine proliferative enteropathy is a disease to consider in young horses presenting with diarrhea and hypoproteinemia in Denmark

Serum amyloid A as a marker to detect sepsis and predict outcome in hospitalized neonatal foals

Background Serum amyloid A (SAA) has been reported to hold promise as diagnostic and prognostic marker in foals. This has not been investigated thoroughly. Objectives Evaluate admission SAA concentrations as predictor of sepsis and outcome. Animals Five hundred and ninety hospitalized foals <14 days old. Methods Retrospective multicenter study. Foals were scored with sepsis and survival scores, grouped according to health category (septic, sick but nonseptic, uncertain sepsis status) and outcome; septic foals were further categorized according to severity (normal sepsis, severe sepsis, and septic shock). SAA was compared between groups using Mann-Whitney test and Kruskal-Wallis test. Receiver operating characteristic curves identified optimal SAA cut off values for detecting sepsis and predicting outcome. Results Admission SAA concentrations differed significantly between sick nonseptic foals (312.1 +/- 685.4 mg/L) and septic foals (1079.7 +/- 1254.5 mg/L) and increased with increasing sepsis score. SAA did not differ between sepsis severity groups. The optimal cut off for sepsis detection was 1050 mg/L (sensitivity 30.2%, specificity 90.7%). Admission SAA concentrations were lower in surviving (435.0 +/- 723.6 mg/L) compared to nonsurviving foals (1062.7 +/- 1440.1 mg/L) and decreased with increasing survival score. The optimal cut off for nonsurvival prediction was 1250 mg/L (sensitivity 22.1%, specificity 90.8%). Conclusions and Clinical Importance SAA concentration was higher in septic foals and nonsurviving foals. Even though optimal cut offs for SAA to detect sepsis and predict outcome had low sensitivity, they had good specificity. SAA can therefore be used as a marker to rule out sepsis and nonsurvival