Intestinal bacterial overgrowth includes potential pathogens in the carbohydrate overload models of equine acute laminitis.
Carbohydrate overload models of equine acute laminitis are used to study the development of lameness. It is hypothesized that a diet-induced shift in cecal bacterial communities contributes to the development of the pro-inflammatory state that progresses to laminar failure. It is proposed that vasoactive amines, protease activators and endotoxin, all bacterial derived bioactive metabolites, play a role in disease development. Questions regarding the oral bioavailability of many of the bacterial derived bioactive metabolites remain. This study evaluates the possibility that a carbohydrate-induced overgrowth of potentially pathogenic cecal bacteria occurs and that bacterial translocation contributes toward the development of the pro-inflammatory state. Two groups of mixed-breed horses were used, those with laminitis induced by cornstarch (n=6) or oligofructan (n=6) and non-laminitic controls (n=8). Cecal fluid and tissue homogenates of extra-intestinal sites including the laminae were used to enumerate Gram-negative and -positive bacteria. Horses that developed Obel grade2 lameness, revealed a significant overgrowth of potentially pathogenic Gram-positive and Gram-negative intestinal bacteria within the cecal fluid. Although colonization of extra-intestinal sites with potentially pathogenic bacteria was not detected, results of this study indicate that cecal/colonic lymphadenopathy and eosinophilia develop in horses progressing to lameness. It is hypothesized that the pro-inflammatory state in carbohydrate overload models of equine acute laminitis is driven by an immune response to the rapid overgrowth of Gram-positive and Gram-negative cecal bacterial communities in the gut. Further equine research is indicated to study the immunological response, involving the lymphatic system that develops in the model.
Rutgers Equine Science Center, Rutgers University New Brunswick, NJ 08901 , USA. onishi@aesop.rutgers.edu
Janet C
JC
Onishi
Joong-Wook
JW
Park
Julio
J
Prado
Susan C
SC
Eades
Mustajab H
MH
Mirza
Michael N
MN
Fugaro
Max M
MM
Häggblom
Craig R
CR
Reinemeyer
D000818:Animals; D001419:Bacteria; D001424:Bacterial Infections / Q000662:veterinary; D058491:Bacterial Load; D002432:Cecum / Q000382:microbiology*; D003106:Colon / Q000382:microbiology*; D004731:Endotoxins / Q000378:metabolism; D005534:Foot Diseases / Q000382:microbiology / Q000473:pathology / Q000662:veterinary*; D005630:Fructans; D006724:Hoof and Claw / Q000378:metabolism / Q000473:pathology; D006734:Horse Diseases / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D006736:Horses; D007249:Inflammation / Q000662:veterinary; D007794:Lameness, Animal / Q000139:chemically induced / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D008198:Lymph Nodes / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D013213:Starch
D004731:Endotoxins; D005630:Fructans; D013213:Starch