EPIDEMIOLOGY

Although northeast Scotland has the highest incidence of grass sickness, with a rate estimated at 1% to 2% of horses per annum, the disease has been recognized throughout the United Kingdom (UK) and most other Northern European countries. Grass sickness also affects animals in Chile, Argentina, the Falkland Islands (where it is called mal del seco), and Colombia (tambora).

Only a handful of cases have been diagnosed in North America and Ireland despite substantial movement of horses from the UK to these regions. This suggests that development of grass sickness is more dependent on the presence or absence of an environmental factor than on direct transmission of a contagious agent between horses. Clustering of cases in both space and time has been reported, suggesting that contagious or other spatially and temporally localized processes play a role, including local climate or pasture management practices. Many of the risk factors for grass sickness (Box 81-1) are consistent with it being a toxicoinfection with a soil-borne organism such as C. botulinum, against which horses may develop immunity. Although attempts to eliminate many of these risk factors theoretically should reduce the statistical probability of a horse developing grass sickness, prevention of the condition on high-risk premises is probably achieved only by permanently stabling horses and avoiding feeding of freshly cut grass. This control measure, however, is rarely used because of practical, economic, and welfare considerations.

ETIOLOGY

Since grass sickness was first reported as a specific disease entity in central Scotland around 1907, it has been the subject of extensive research. The definitive cause remains unknown despite investigations into possible mineral deficiencies, toxic plants, mycotoxins, insect vectors, viruses, oxidative stress, streptococcal infection, Clostridium perfringens enterotoxicity, and C. botulinum toxicoinfection. Transmission studies have revealed a toxin in serum from horses with acute grass sickness that is either a protein exceeding 30 kDa in mass or a molecule with smaller mass that is bound to serum proteins. Although retrograde axonal spread of this toxin has been demonstrated experimentally, the anatomic distribution of neuronal lesions in horses with grass sickness is consistent with hematogenous spread of toxin, probably following absorption from the gastrointestinal tract.

There is historical and recent evidence to suggest that grass sickness is a toxicoinfectious form of botulism whereby a dietary trigger induces intestinal bacterial overgrowth and in vivo production of botulinum neurotoxins C (BoNT/C), D (BoNT/D), or both. This proposed pathogenesis contrasts with that of neuroparalytic botulism (forage poisoning), which is most commonly caused by ingestion of preformed botulinum neurotoxins. This etiopathogenesis was first proposed in 1923, when a large spore-forming bacterium with morphology and toxin characteristics similar to those of C. botulinum was cultured from affected horses. Subsequent in vivo challenge of horses with the C. botulinum organism or its toxins induced clinical and gross pathologic features considered by the investigators to be consistent with grass sickness. However, the conclusions of those authors can be questioned because grass sickness was not confirmed histologically, and the reported clinical and gross pathologic findings were more consistent with neuroparalytic botulism than with grass sickness. Bolstering this concern is the fact that in a recent study, oral challenge with broth cultures of C. botulinum type C, in combination with various putative trigger factors, induced neuroparalytic botulism and not grass sickness.

More convincing support for the botulinum hypothesis was, however, obtained in the 1920s from a large, well-controlled intervention study, which revealed that administration of an antitoxin-neutralized botulinum toxin vaccine conferred significant and dose-dependent protection against grass sickness. Furthermore, recent work identified an association between grass sickness and the presence of C. botulinum type C and BoNT/C1 within the intestinal tract of affected horses. Increased concentrations of serum antibodies specific for botulinum surface antigens and for BoNT/C1 have been detected in horses recently exposed to affected horses, and increased levels of these antibodies are associated with increased protection against grass sickness. The presence of botulinum type C–specific antibodies in colostrum and milk from horses in grass-sickness–endemic areas may explain the low prevalence of grass sickness in foals younger than 6 months of age.

Although the aforementioned data support an association between C. botulinum

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