Virulence genes of pathogenic and clinical treatment in floppy kid syndrome

Floppy kid syndrome (FKS) is a metabolic disorder disease in newborn goats caused by intestinal dysbiosis. In this study, pathogens were isolated from the intestinal contents of FKS-affected goats (8 Escherichia coli isolates and 2 Staphylococcus aureus isoates), and virulence gene detection showed that Escherichia coli predominantly expressed HlyD (62.5 %) and K88 (37.5 %), with 37.5 % of isolates co-expressing HlyD/K88; all Staphylococcus aureus isolates carried the nuc, sea, sed, and FnbA. Antibiotic susceptibility testing revealed that amikacin exhibited the highest sensitivity against both pathogens, with sensitivity rates of 87.5 % in Escherichia coli and 100 % in Staphylococcus aureus. By combining virulence gene detection and antimicrobial susceptibility tests, a comprehensive treatment regimen (amikacin + sodium bicarbonate + glucose) was designed, and clinical trial indicated that the 3-day cure rate in the treatment group reached 100 % (24/24), significantly higher than 14.3 % (2/14) in the control group. This study revealed a synergistic pathogenic mechanism between Escherichia coli HlyD/K88 and Staphylococcus aureus enterotoxins, confirming that an amikacin-based combined treatment regimen can effectively alleviate FKS symptoms, thereby providing a theoretical basis for precision medication in FKS.