Thoracic sympathetic chain ganglion neuronal abnormalities that may explain some of the clinical signs of grass sickness

John, Huw A.; Creighton, A. J.; Baird, Andrew

doi:10.1136/vr.148.6.180

Cited by 9 publications

(10 citation statements)

References 23 publications

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“…Clinical signs of grass sickness are characterised as either acute, subacute or chronic according to the duration and severity of signs (Doxey et al 1991a) and are attributable to histologically evident disruption of the autonomic nervous system, particularly of the gastrointestinal tract (Obel 1955;Mahaffey 1959;Barlow 1969;Scholes et al 1993;Doxey et al 2000;John et al 2001). Clinical presentation of EGS is typically characterised by signs of mild colic, increased heart rate, muscle tremors, patchy sweating, difficulty in swallowing, reduced intestinal motility, weight loss and, occasionally, sudden death (Tocher et al 1923;Tocher 1924;Greig 1942;Doxey et al 1991a;Milne 1996).…”

Section: Introductionmentioning

confidence: 99%

An epidemiological study of risk factors associated with the recurrence of equine grass sickness (dysautonomia) on previously affected premises

Newton

Hedderson

Adams

et al. 2004

Equine Veterinary Journal

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Summary Reasons for performing study: The reasons why equine grass sickness (EGS) recurs on premises are unknown and, consequently, practical methods for reducing the risk of recurrence are not available. Objectives: To identify risk factors associated with recurrence of EGS on premises and to gain possible insights into the pathogenesis of the disease. Methods: Data on disease history and risk factors were collected by postal questionnaire from premises with EGS cases between 1st January 1997 and 31st December 2001. Data on variation in rates of recurrence of EGS for different risk factors were analysed using Poisson regression analysis. Results: Of 509 premises contacted, 305 (60%) returned useable questionnaires and 100 of these (33%) were classified as ‘recurrent’ premises. An overall median incidence rate for EGS of 2.1 EGS incidents/100 horses/premises/year was recorded. There was an increased rate of recurrence with higher numbers of horses, presence of younger animals, stud farms and livery/riding establishments, loam and sand soils, rearing of domestic birds and mechanical droppings removal. The rate of recurrence decreased with chalk soil, cograzing ruminants, grass cutting on pastures and removal of droppings by hand. Several statistically significant interactions were identified. Conclusions: Many of the findings are consistent with the theory that EGS is a toxico‐infectious form of botulism. Several of the significant factors identified may directly or indirectly relate to soil disturbance and consequent soil contamination of grass, thereby increasing the rate of exposure of grazing horses to Clostridium botulinum, which resides in soil. Potential relevance: Identification of potentially modifiable risk factors may, ideally following validation in appropriately designed, controlled and randomised intervention studies, lead to practical measures to reduce the incidence of EGS on previously affected premises.

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Section: Introductionmentioning

confidence: 99%

An epidemiological study of risk factors associated with the recurrence of equine grass sickness (dysautonomia) on previously affected premises

Newton

Hedderson

Adams

et al. 2004

Equine Veterinary Journal

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“…The sympathetic innervation is of interest both because of its possible involvement in pathology (John et al, 2001) and because knowledge of the organization of sympathetic innervation of the gastrointestinal tract derives almost entirely from small laboratory animals and the carnivores, cat and dog. The innervation in this large herbivore, the horse, is largely unknown.…”

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confidence: 99%

Sympathetic innervation of the ileocecal junction in horses

Russo

Bombardi

Grandis

et al. 2010

J of Comparative Neurology

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The distribution and chemical phenotypes of sympathetic and dorsal root ganglion (DRG) neurons innervating the equine ileocecal junction (ICJ) were studied by combining retrograde tracing and immunohistochemistry. Immunoreactivity (IR) for tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), neuronal nitric oxide synthase (nNOS), calcitonin gene-related peptide (CGRP), substance P (SP), and neuropeptide Y (NPY) was investigated. Sympathetic neurons projecting to the ICJ were distributed within the celiac (CG), cranial mesenteric (CranMG), and caudal mesenteric (CaudMG) ganglia, as well as in the last ganglia of the thoracic sympathetic chain and in the splanchnic ganglia. In the CG and CranMG 91 +/- 8% and 93 +/- 12% of the neurons innervating the ICJ expressed TH- and DBH-IR, respectively. In the CaudMG 90 +/- 15% and 94 +/- 5% of ICJ innervating neurons were TH- and DBH-IR, respectively. Sympathetic (TH-IR) fibers innervated the myenteric and submucosal ganglia, ileal blood vessels, and the muscle layers. They were more concentrated at the ICJ level and were also seen encircling myenteric plexus (MP) and submucosal plexus (SMP) descending neurons that were retrogradely labeled from the ICJ. Among the few retrogradely labeled DRG neurons, nNOS-, CGRP-, and SP-IR nerve cells were observed. Dense networks of CGRP-, nNOS-, and SP-IR varicosities were seen around retrogradely labeled prevertebral ganglia neurons. The CGRP-IR fibers are probably the endings of neurons projecting from the intestine to the prevertebral ganglia. These findings indicate that this crucial region of the intestinal tract is strongly influenced by the sympathetic system and that sensory information of visceral origin influences the sympathetic control of the ICJ.

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“…Clinical signs of grass sickness are characterised as acute, subacute or chronic according to the duration and severity of signs (Doxey et al 1991) and are attributable to histologically evident disruption of the autonomic nervous system, particularly of the gastrointestinal tract (Obel 1955;Brownlee 1959;Mahaffey 1959;Barlow 1969;Gilmour 1973aGilmour , 1975Scholes et al 1993a;Doxey et al 2000;John et al 2001). Clinical presentation of EGS is typically characterised by signs of mild colic, increased heart rate, muscle tremors, patchy sweating, difficulty in swallowing, alimentary stasis, abdominal distension, oesophageal ulceration, ptosis, rhinitis sicca, weight loss and, occasionally, sudden death (Tocher et al 1923;Tocher 1924;Greig 1942;Doxey et al 1991;Milne 1996).…”

Section: A Review Of Historical Clinical and Geographical Aspects Bmentioning

confidence: 99%

Prospects for vaccination against equine grass sickness

Hedderson

Newton

2004

Equine Veterinary Journal

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Thoracic sympathetic chain ganglion neuronal abnormalities that may explain some of the clinical signs of grass sickness

Cited by 9 publications

References 23 publications

An epidemiological study of risk factors associated with the recurrence of equine grass sickness (dysautonomia) on previously affected premises

An epidemiological study of risk factors associated with the recurrence of equine grass sickness (dysautonomia) on previously affected premises

Sympathetic innervation of the ileocecal junction in horses

Prospects for vaccination against equine grass sickness

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