Preliminary study of mucosal IgA in the equine small intestine: specific IgA in cases of acute grass sickness and controls.
BACKGROUND
There is much evidence to suggest that group III Clostridium botulinum (types C and D) are involved in the aetiology of equine grass sickness (EGS). Antibodies have been detected previously in the blood and high levels associated with resistance to disease. Specific mucosal antibodies in the gastrointestinal (GI) tract are likely to be important in protection, and this study was performed to ascertain if such antibodies could be detected and if their levels were related to disease state.


OBJECTIVE
To develop a method for quantifying IgA antibodies to C. botulinum types C and D in the GI tract of horses and to relate antibody levels to disease status.


METHODS
Samples of tissue (n = 25: 6 duodenum, 7 jejunum and 12 ileum) were taken from acute grass sickness (AGS) cases and from control horses (n = 12; 4 samples from each site) at post mortem. They were extracted with the detergent saponin in the presence of protease inhibitors and assayed for total IgA, for specific IgA against botulinum neurotoxins types C and D (BoNT/C or BoNT/D), and against surface antigens of a BoNT/C negative strain of C. botulinum type C (SA) and of Clostridium tetani (TetSA), as a control. Specific IgA was expressed as percentage total IgA.


RESULTS
Compared to controls, significantly higher levels of specific IgA against BoNT/C were detected in the jejunum (P = 0.04) and ileum (P = 0.02) of AGS cases. Similarly, higher specific levels against BoNT/D were demonstrated in duodenum (P = 0.01) and jejunum (P = 0.02). Significantly higher levels of IgA against SA were demonstrated only in duodenal samples (P = 0.01).


CONCLUSIONS
Levels of IgA antibody to BoNTs in control horses were at near undetectable levels, suggesting no recent exposure to toxins. In AGS cases, significantly higher levels of specific IgA were detected predominantly in jejunum and ileum.


CONCLUSIONS
If specific IgA is protective then any successful vaccine for EGS should induce a mucosal response.
Nunn
F G
FG
Medical Microbiology, Centre for Infectious Diseases, University of Edinburgh College of Medicine and Veterinary Medicine, The Chancellor's Building, 49 Little France Crescent, Edinburgh EH16 4SB, UAE.
Pirie
R S
RS
McGorum
B
B
Wernery
U
U
Poxton
I R
IR
D000818:Animals; D000907:Antibodies, Bacterial / Q000032:analysis / Q000097:blood; D001342:Autonomic Nervous System Diseases / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control / Q000662:veterinary*; D001905:Botulinum Toxins / Q000276:immunology*; D001906:Botulism / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control / Q000662:veterinary*; D016022:Case-Control Studies; D003014:Clostridium botulinum / Q000276:immunology / Q000472:pathogenicity; D004797:Enzyme-Linked Immunosorbent Assay / Q000662:veterinary; D006734:Horse Diseases / Q000276:immunology* / Q000382:microbiology / Q000517:prevention & control; D006736:Horses; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000032:analysis* / Q000097:blood; D007421:Intestine, Small / Q000276:immunology*; D006109:Poaceae / Q000382:microbiology; D014611:Vaccination / Q000662:veterinary
D000907:Antibodies, Bacterial; D007070:Immunoglobulin A; C096325:botulinum toxin type D; D001905:Botulinum Toxins; C096324:botulinum toxin type C