Enteric dysganglionosis resembling intestinal neuronal dysplasia in a foal with bacterial colitis.
Authors: Giri D K, Quist E M, Ambrus A, Gold J, Porter B F, Bratton G R, Storts R W
Journal: Veterinary pathology
Summary
# Enteric Dysganglionosis in a Neonatal Foal: A Rare Developmental Abnormality A five-day-old Quarter Horse colt presented with hypothermia, respiratory distress, and diarrhoea before being euthanased; post-mortem examination revealed an unusual developmental pathology affecting the enteric nervous system. Microscopic analysis of tissue samples from the small intestine and colon identified discrete submucosal nodules containing abnormally distributed neurons and ganglia—32% of these neuronal clusters contained 8 or more neurons compared with just 6% in age-matched controls—along with areas of inflammation, bacterial infection, and vascular damage. The histopathological findings were consistent with intestinal neuronal dysplasia, a condition previously documented in human medicine but exceptionally rare in equine cases. This condition likely disrupted normal intestinal motility and barrier function, predisposing the foal to secondary bacterial colitis and systemic complications. Whilst such severe dysganglionosis appears incompatible with long-term survival, recognition of this pathology in neonatal foals presenting with intractable diarrhoea and early deterioration may help clinicians understand underlying developmental abnormalities and inform discussions around prognosis and intervention in similar cases.
Read the full abstract on PubMed
Practical Takeaways
- •Recognize that severe, treatment-resistant neonatal diarrhea with hypothermia may indicate congenital neuronal dysplasia rather than infectious colitis alone.
- •This rare developmental condition currently has no clinical diagnostic test available in live horses; diagnosis requires post-mortem histopathology.
- •Understanding this pathology helps explain why some foals with apparent bacterial colitis do not respond to antimicrobial therapy—the primary defect is neuronal architecture, not infection.
Key Findings
- •A 5-day-old foal presented with intestinal neuronal dysplasia characterized by expanded submucosal mesenchyme with excessive neuronal proliferation (32% of ganglia contained ≥8 neurons versus 6% in age-matched controls).
- •Histologic changes included necrosuppurative inflammation, vasculitis, thrombosis, and bacterial colonization within submucosal nodules throughout the colon and small intestine.
- •This is the first reported case of intestinal neuronal dysplasia in an equine species, a condition previously described only in humans.