The association of Clostridium botulinum type C with equine grass sickness: a toxicoinfection?

The cause of grass sickness, an equine dysautonomia, is unknown. The diseas e usually results in death. Gastrointestinal (GI) dysfunction is a common c linical manifestation in all forms of the disease. It is generally thought that equine grass sickness (EGS) is caused by an ingested or enterically pr oduced neurotoxin which is absorbed through the GI tract. Clostridium botul inum was first implicated as a causative agent when it was isolated from th e GI tract of a horse with EGS in 1919, The aim of the present study was to investigate the hypothesis that EGS results from toxicoinfection with C. b otulinum type C: growth of the bacterium in the GI tract with production of toxin (BoNT/C), Ileum contents and faeces from horses with EGS were invest igated for BoNT/C, and indirectly for the presence of C, botulinum type C, and compared with control samples from horses without EGS. BoNT/C was detec ted directly by ELISA in the ileum of 45% (13/29) of horses with EGS compar ed to 4% (1/28) of controls, and in the faeces of 44% (20/45) of horses wit h EGS compared to 4% (3/77) of controls. Levels of up to 10 mu g toxin/g we t weight of gut contents were observed, The one control horse with detectab le toxin in the ileum had been clinically diagnosed as having acute EGS, bu t this was not confirmed by histopathology, The organism was detected indir ectly by assaying for BoNT/C by ELISA after enrichment in culture medium. C , botulinum type C was shown to be present in 48% (14/29) of ileum samples and 44% (20/45) of faecal samples from horses with EGS, compared with 7% (2 /27) of ileum samples and 8% (6/72) of faecal samples from controls. These results support the hypothesis that EGS results from a C, botulinum type C toxicoinfection.