Frontiers in veterinary science · 2026
Intestinal overgrowth of Clostridium perfringens and reduced cadA gene copy number characterize fatal diarrhea in captive corn snakes (Pantherophis guttatus).
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Hung You-Chen, Yang Wen-Yuan
Аннотация
INTRODUCTION: Fatal diarrhea has recently emerged as a significant health problem in captive-bred corn snakes (Pantherophis guttatus), particularly among juveniles under 6 months of age. Affected snakes typically present with watery diarrhea, anorexia, dehydration, and high mortality.
METHODS: To clarify the etiological basis of this syndrome, we investigated bacterial pathogens associated with fatal diarrhea and characterized virulence gene profiles of predominant isolates. Rectal swabs were collected from healthy and diarrheic snakes, and pathogen detection and bacterial loads were quantified.
RESULTS: Clostridium perfringens demonstrated a significantly higher detection rate and rectal bacterial load in diarrheic snakes compared with healthy individuals (p = 0.0007; p < 0.0001), whereas Salmonella spp. and Escherichia coli were not associated with disease status. Toxinotyping of 24 C. perfringens isolates identified toxinotypes A, B, D, and G without a disease-specific distribution, suggesting that toxinotype alone is insufficient to explain outbreak occurrence. Quantitative analysis of five virulence-associated genes, including cell-wall-anchored extracellular nuclease (cadA), collagen adhesion protein (cna), sialidase (nanI), necrotic enteritis B-like toxin (netB), and toxin C. perfringens large cytotoxin (tpeL) genes, revealed a significantly lower cadA gene copy number in isolates from diarrheic snakes (p = 0.0343), while no significant differences were observed for the other genes.
DISCUSSION: Fatal diarrhea in captive corn snakes is associated with increased intestinal colonization by C. perfringens, rather than with toxinotype variation. The reduced cadA gene copy number observed in isolates from diarrheic snakes suggests a potential role for biofilm-related mechanisms in disease expression, although functional studies are required for confirmation. These findings provide field-based evidence supporting the involvement of C. perfringens overgrowth in reptile enteric disease and may inform future disease monitoring and management strategies in intensive breeding systems.
METHODS: To clarify the etiological basis of this syndrome, we investigated bacterial pathogens associated with fatal diarrhea and characterized virulence gene profiles of predominant isolates. Rectal swabs were collected from healthy and diarrheic snakes, and pathogen detection and bacterial loads were quantified.
RESULTS: Clostridium perfringens demonstrated a significantly higher detection rate and rectal bacterial load in diarrheic snakes compared with healthy individuals (p = 0.0007; p < 0.0001), whereas Salmonella spp. and Escherichia coli were not associated with disease status. Toxinotyping of 24 C. perfringens isolates identified toxinotypes A, B, D, and G without a disease-specific distribution, suggesting that toxinotype alone is insufficient to explain outbreak occurrence. Quantitative analysis of five virulence-associated genes, including cell-wall-anchored extracellular nuclease (cadA), collagen adhesion protein (cna), sialidase (nanI), necrotic enteritis B-like toxin (netB), and toxin C. perfringens large cytotoxin (tpeL) genes, revealed a significantly lower cadA gene copy number in isolates from diarrheic snakes (p = 0.0343), while no significant differences were observed for the other genes.
DISCUSSION: Fatal diarrhea in captive corn snakes is associated with increased intestinal colonization by C. perfringens, rather than with toxinotype variation. The reduced cadA gene copy number observed in isolates from diarrheic snakes suggests a potential role for biofilm-related mechanisms in disease expression, although functional studies are required for confirmation. These findings provide field-based evidence supporting the involvement of C. perfringens overgrowth in reptile enteric disease and may inform future disease monitoring and management strategies in intensive breeding systems.