title: Equine grass sickness is associated with low antibody levels to Clostridium botulinum: a matched case-control study.
abstract: BACKGROUND
  Equine grass sickness is a high mortality disease which, despite many years of investigation, is of unknown aetiology. Recent findings indicating that the disease is associated with Clostridium botulinum require support from an epidemiological study that recognises and controls for potential confounders, e.g. age, time of year and premises.
  
  
  OBJECTIVE
  EGS is associated with low antibody levels to C. botulinum antigens.
  
  
  METHODS
  A matched case-control study was conducted. Data were collected from 66 histologically confirmed cases of EGS and 132 premises-matched control horses. The probability of EGS in horses was modelled using conditional logistic regression.
  
  
  RESULTS
  EGS was significantly associated (age-adjusted P < 0.005) with low antibody levels to each of 3 clostridial antigens; C. botulinum type C and C. novyi type A surface antigens and a C. botulinum type C toxin complex toxoid. These serological risk factors for EGS remained highly significant when entered into multivariable models. This study also identified new horse-level risk factors for EGS; feeding hay or haylage was associated with a decreased risk of disease, change of feed type or quantity during the 14 days prior to disease was associated with increased risk, and the use of an ivermectin anthelmintic at both the ultimate and penultimate treatments was also associated with a significantly increased risk of EGS.
  
  
  CONCLUSIONS
  This study provides strong support for the role of C. botulinum in the aetiology of EGS and identifies managemental risk factors for the disease.
  
  
  CONCLUSIONS
  Increasing anticlostridial antibody levels by vaccination and appropriate managemental interventions may decrease the risk of EGS occurring.
authors.affiliation: Faculty of Veterinary Science, University of Liverpool, Leahurst, Neston, Wirral CH64 7TE, UK.
authors.forename: H E
authors.initials: HE
authors.lastname: McCarthy
authors.forename: N P
authors.initials: NP
authors.lastname: French
authors.forename: G B
authors.initials: GB
authors.lastname: Edwards
authors.forename: I R
authors.initials: IR
authors.lastname: Poxton
authors.forename: D F
authors.initials: DF
authors.lastname: Kelly
authors.forename: C E
authors.initials: CE
authors.lastname: Payne-Johnson
authors.forename: K
authors.initials: K
authors.lastname: Miller
authors.forename: C J
authors.initials: CJ
authors.lastname: Proudman
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000276:immunology; D000954:Antigens, Surface / Q000276:immunology; D001342:Autonomic Nervous System Diseases / Q000097:blood / Q000209:etiology / Q000382:microbiology / Q000662:veterinary*; D001905:Botulinum Toxins / Q000276:immunology; D016022:Case-Control Studies; D003014:Clostridium botulinum / Q000276:immunology*; D005260:Female; D006734:Horse Diseases / Q000097:blood / Q000209:etiology* / Q000382:microbiology; D006736:Horses; D016015:Logistic Models; D008297:Male; D006109:Poaceae / Q000382:microbiology; D012307:Risk Factors; D014611:Vaccination / Q000662:veterinary
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D000954:Antigens, Surface; D001905:Botulinum Toxins; C096324:botulinum toxin type C