Equine grass sickness is associated with low antibody levels to Clostridium botulinum: a matched case‐control study

Abstract

Summary Reasons for performing study: 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. Hypothesis: 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. Potential relevance: Increasing anticlostridial antibody levels by vaccination and appropriate managemental interventions may decrease the risk of EGS occurring.;

Why are certain premises at increased risk of equine grass sickness? A matched case‐control study

“…We speculate that increased levels of soil total nitrogen influence the amount of herbage available to horses through increased growth and yield (rather than influencing nitrogen levels found in herbage). Such an alteration in pasture yield may be analogous to dietary change, which we have previously reported to be a significant risk factor for EGS (McCarthy et al 2004). We speculate that dietary change plays a role in the alteration of digestive fermentation which, in turn, could contribute to disease development in susceptible horses.…”

“…This was a companion study to the case-control study described by McCarthy et al (2004). Premises were identified between March 1999 and May 2001 that gave rise to histologically confirmed cases of EGS.…”

“…The questionnaire described in McCarthy et al (2004) included questions seeking information on the following aspects of pasture management during the previous year; fertilisation, ploughing, reseeding, harrowing, mixed species grazing, pasture excavation/disturbance (deeper layers of soil being brought to the surface by digging, burrowing or other means) and previous EGS in horses grazing the pasture. Questionnaire information related to the particular pasture that the EGS case was grazing during onset of disease.…”

“…A matched analysis was performed as described by McCarthy et al (2004). Conditional logistic regression (EGRET, version 2.0.3) 2 was used to calculate univariable odds ratios and 95% confidence intervals for both continuous and categorical variables that may be associated with the occurrence of EGS.…”

Evaluation of Formalin-Fixed Ileum as the Optimum Method to Diagnose Equine Dysautonomia (Grass Sickness) in Simulated Intestinal Biopsies

“…The etiology is unknown, but recent research has focused on the hypothesis that ED is a toxicoinfection with Clostridium botulinum type C that is acquired from soil while grazing. 4,5 Equine dysautonomia is characterized by neuronal degeneration resembling chromatolysis and a reduction in the number of neurons in the prevertebral and paravertebral autonomic ganglia and the enteric plexuses. 3,6 Neuronal damage in the gastrointestinal tract is not uniform, and although the ileum is usually the most severely affected, 8 the jejunum can be more severely affected than the ileum in a minority of cases.…”