Observations on the Coeliaco-Mesenteric Ganglia of Horses with and without Grass Sickness

Howell, J. M.; Baker, J. R.; Ritchie, H.E.

doi:10.1016/s0007-1935(17)35892-x

Cited by 19 publications

(7 citation statements)

References 4 publications

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“…In acute cases of equine grass sickness the number of degenerate chromatolytic neurons can vary between 23 and 90% (Brownlee, 1959). However the additional changes of fine vacuolation of neuronal cytoplasm (Howell et al, 1974), large numbers of dead neurons, marked neuronal loss and the presence of spheroids (Mahaffey, 1959;Pogson et al, 1992;Uzal et al, 1992) was not evident in the present case. In addition, three other cattle (C9, C16 and C35) of the study population had marked central chromatolysis (>20% of neurons affected) in the cranial cervical ganglion without exhibiting megaoesophagus.…”

Section: Discussioncontrasting

confidence: 49%

“…Dysautonomia is the most frequently diagnosed condition affecting autonomic ganglia and the disease has been reported in horses (equine grass sickness), cats (Key-Gaskell syndrome), dogs, rabbits, hares and sheep with common clinical signs of oesophageal dysfunction, inappetence and gut stasis (Key and Gaskell, 1982;Pollin and Griffiths, 1992;Griffiths and Whitwell, 1993;Pruden et al, 2004;Hahn et al, 2005;Niessen et al, 2007;Wylie and Proudman, 2009). Histopathological changes associated with dysautonomia are central chromatolysis and fine vacuolation of neuronal cytoplasm, variable numbers of dead neurons, marked neuronal loss and the presence of spheroids (Mahaffey, 1959;Howell et al, 1974;Pogson et al, 1992;Uzal et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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A Histopathological Study of Bovine Ganglia

Jahns

Fast

2014

Journal of Comparative Pathology

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One hundred and sixty-eight ganglia from 54 cattle aged 10 days to 10 years were examined microscopically. Samples from six autonomic ganglia and one sensory ganglion were represented. Thirteen animals were clinically normal and 41 were submitted for post-mortem examination. Neuronal vacuolation, spheroid formation, lipofuscin accumulation and central chromatolysis were observed sporadically and were of varying magnitude. Neuronal vacuolation and spheroid formation were not age-related changes, while lipofuscin accumulation was more common in older animals and central chromatolysis was more common in younger cattle. Non-suppurative inflammation and neuronophagia were also common findings (23 out of 54 animals, 42.6%) in autonomic ganglia that did not contain herpesvirus DNA as determined by polymerase chain reaction. Renaut bodies, features of peripheral nerves, were most commonly noted in the vagus. None of the histopathological findings were related to any particular disease in which loss of autonomic nervous system function might be expected. Furthermore, all changes were as common in clinically normal animals as in animals with disease.

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Section: Discussioncontrasting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

A Histopathological Study of Bovine Ganglia

Jahns

Fast

2014

Journal of Comparative Pathology

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“…The choice of the sympathetic ganglion for analysis was, however, a curious one, when one assumes that the majority of parotid secretomotor fibres may project to the otic (parasympathetic) ganglion. In the naturally occurring disease, there is an interesting observation on the time course of events by Howell et al 43 who found that lesions in the coeliaco‐mesenteric ganglion may not be seen within the first few days of acute cases, which may support the hypothesis that there is a primary gut lesion with retrograde transport of neurotoxin or secondary degeneration involved. The absence of lesions in dorsal root ganglia observed by Barlow 38 may also be explained in this way.…”

Section: Neuropathologymentioning

confidence: 93%

The neurology and enterology of equine grass sickness: a review of basic mechanisms

Cottrell

McGorum

Pearson

1999

Neurogastroenterology Motil

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Autonomic dysfunction constitutes a prominent clinical feature of equine grass sickness (EGS). Significant injury to the nervous control of the alimentary system is life threatening, partly because of dysphagia but also because of the failure of the unique regulatory mechanisms in equine digestion involving water and electrolyte balance. The neuropathology also indicates the presence of a somatic polyneuropathy. The morphological features of EGS are similar to those of excitotoxic neuronal degeneration, which resembles neuronal apoptosis. It is difficult to ascertain from published accounts the degree of damage to central neurones: the distribution is well documented and selective but the proportion of damage is poorly quantified. If lesions involve a significant number of regulatory neurones they should produce functional deficits. Any clinical assessment of horses, especially those with chronic EGS, should include a thorough neurological examination. Although this will not necessarily improve the outcome of the case, it may enable the rational selection of animals with a reasonable prognosis for recovery which is partly determined by the extent of CNS lesions. The evidence supports the following pathogenesis. There is an initial lesion in the enteric nervous system of susceptible horses. In the acute form of EGS, massive enteric neuronal damage occurs first functionally, then structurally leading to generalized alimentary smooth muscle atony, enhanced secretions and altered fluid fluxes. Severe distension of the stomach and small intestines rapidly develops, which augments the intestinal ileus by intersegmental inhibitory reflexes and causes colic and dehydration. In subacute cases, failure of intestinal bicarbonate buffer together with alimentary stasis rapidly reduces caecal-colonic fermentation. Thus the osmolality of large intestinal digesta reduces and water travels out of the bowel along osmotic gradients. Water returns to the circulation, but is eventually lost in the gastric and small intestinal secretions. The observation that pathological lesions may not be seen in the prevertebral ganglia within the first few days of acute cases supports the view that a functional deficit precedes structural lesions which may be secondary to a retrograde degeneration. It is therefore possible to resolve the observations that less damage may be seen in prevertebral ganglia and elsewhere in peracute and acute cases with the more common finding that greater neuronal damage is present in acute than in chronic cases. These different observations are probably time dependent. Chronic EGS occurs when there is less initial enteric nerve damage which may lead to less secondary prevertebral ganglionic pathology, and more time for functional and structural compensatory mechanisms to develop. Denervation hypersensitivity develops at target sites both in the gut and in peripheral somatic nerves which may account, in part, for the clinical signs of patchy sweating and muscle tremors. Raised circulating adrenaline levels may also ac...

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“…Both the topographical distribution of damage and the nature of the lesion are very similar to equine grass sickness. The involvement of autonomic ganglia is well known in this latter condition (Mahaffey, 1959;Barlow, 1969;Gilmour, 1973;Howell, Baker & Ritchie, 1974). Changes in dorsal root ganglia, identical cranial nerve nuclei and spinal cord have been demonstrated in grass sickness (Barlow, 1969;Gilmour, 1973), although not every location is involved in each case.…”

Section: Discussionmentioning

confidence: 99%

Feline Dysautonomia (The Key‐gaskell Syndrome): An Ultra Structural Study of Autonomic Ganglia and Nerves

Griffiths

Sharp

McCulloch

1985

Neuropathology Appl Neurobio

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Recently a feline dysautonomia of unknown aetiology, the Key-Gaskell syndrome, has caused widespread morbidity in the UK. This report describes the ultrastructural appearances of the autonomic ganglia and axons of the sympathetic chain in this condition. Nuclei of affected neurones were eccentric and abnormally crenated. Nucleolar abnormalities such as increased electron density (due to loss of the intranucleolar vacuoles), nucleolar segregation and ring nucleoli were observed in a proportion of neurones. There was marked loss of ribosomes, both bound and unbound, and cisternae of the rough endoplasmic reticulum were distended with a floccular electron dense material. Numerous smooth-walled cisternae were also present and complex stacks of smooth semi-parallel membranes were observed, probably derived from the smooth endoplasmic reticulum or Golgi apparatus. No normal Golgi formations were seen. Frequent autophagic vacuoles and membranous dense bodies were present in some cells. Many unmyelinated fibres in the sympathetic chain were swollen and contained vesiculo-tubular profiles, disordered neurotubules and filaments and various degenerating membranous organelles. Myelinated fibres within the sympathetic chain were also degenerating. These studies indicate that the organelles involved with protein biosynthesis are severely affected by the disease.

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Observations on the Coeliaco-Mesenteric Ganglia of Horses with and without Grass Sickness

Cited by 19 publications

References 4 publications

A Histopathological Study of Bovine Ganglia

A Histopathological Study of Bovine Ganglia

The neurology and enterology of equine grass sickness: a review of basic mechanisms

Feline Dysautonomia (The Key‐gaskell Syndrome): An Ultra Structural Study of Autonomic Ganglia and Nerves

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