Isolation, characterization, and pathogenic mechanisms of a novel Lawsonia intracellularis train from Guangdong, China: impacts on digestive enzymes and gut microbiota.

INTRODUCTION

Lawsonia intracellularis causes Porcine Proliferative Enteritis (PPE), leading to significant economic losses, yet obtaining isolates for vaccine development remains challenging.

METHODS

In this study, a novel L. intracellularis strain, designated LIGD01, was isolated from the ileum of a pig with acute hemorrhagic enteritis in Guangdong, China. The strain was stably passaged in McCoy cells for 40 generations.

RESULTS

Phylogenetic analysis of the 16S rRNA gene confirmed its identity, and indirect immunofluorescence assay (IIFA) and scanning electron microscopy (SEM) demonstrated characteristic intracellular colonization and curved rod-shaped morphology. LIGD01 induced intermittent fecal shedding starting at 3 days post-infection (dpi), with seroconversion in all challenged pigs by 21 dpi. Necropsy revealed distinct ileal hyperplasia. Histopathology showed villous blunting, epithelial exfoliation, and inflammatory infiltration. Crucially, infection significantly reduced Average Daily Gain (ADG) (252.21 ± 17.07 g/day vs. 300.98 ± 19.39 g/day in controls, p < 0.05) and suppressed the activities of key digestive enzymes (trypsin, lipase, amylase) in the pancreas and intestine. Furthermore, Lawsonia intracellular infection characterized by a reduction in beneficial genera (Lactobacillus, Christensenellaceae) and an increase in opportunistic pathogens (Streptococcus, Enterococcus), concomitant with upregulated pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1α).

DISCUSSION: This study not only provides a new candidate strain for vaccine development but also elucidates the physiological and microbial mechanisms underlying growth retardation in PPE.