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This article was published in 1979
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The Epidemiology of Nardoo Poisoning in Sheep
B.F. Chick, Veterinary Research Officer, Armidale; G.W. Eggleston, Veterinary Inspector, Moree; B.M. McCleary, Biochemist, Biological and Chemical Research Institute, Rydalmere.
Paper presented by B.F. Chick
Richard Roe has outlined the role epidemiology plays in the veterinary profession today with particular emphasis on the role of the Bureau of Animal Health.
I would like to take a particular disease investigation, Nardoo Poisoning, and follow through the steps taken in attempting to define the factors involved in the distribution and occurrence of this disease over time.
In this talk I will cover the characteristic features of Nardoo Poisoning, expand it to include an identical condition, Polioencephalomalacia, and then discuss the steps we have taken in defining the disease interactions.
Nardoo (Marsilea drummondii) is a member of the fern family, being related to Bracken fern and Rock fern. Marsilea sp. and particularly Marsilea drummondii are common in inland areas of Australia often growing on flood prone flats or in depressions holding water for some time after rain. They have been recorded from all mainland states being particularly plentiful in north western New South Wales, central Queensland and south-western Western Australia.
The flood plains of the Gwydir River watercourse west of Moree is a favourable habitat. In certain years Nardoo may constitute almost 100% of available pasture in certain areas.
Mortalities in sheep grazing Nardoo have been recorded since early this century (Henry and Massy 1911). Since then, sporadic losses have been reported in sheep grazing Nardoo in the north western area, generally following periods of inundation (Hurst 1942, Clarke 1979).
During 1974-19[?] several deaths, apparently associated with the ingestion of Nardoo were reported from the watercourse area. On 13 properties running a total of 57,000 sheep, 2200 deaths were reported, the highest incidence being 600 dead of a total of 4500 on one property (Pritchard et al. 1978).
Pathological examination of material from these cases showed that the gross and microscopic lesions seen in this condition were indistinguishable from those seen in natural cases of Polioencephalomalacia.
Polioencephalomalacia is an acute neurological disorder of ruminants characterised clinically by depression, coma and convulsions and pathologically by necrosis of the cerebral cortex and deeper structures. In Australia under extensive management conditions individual outbreaks of up to 10% mortality have been reported (Gabbedy and Richards 1977).
Polioencephalomalacia (P.E.) was first described by Jensen et al. (1956) in the United States of America. It was then reported in Britain by Terlecki and Markson (1959). Since then P.E. has been reported from most countries where it has been diagnosed histologically in sheep, cattle and goats.
In 1965 thiamine (Vitamin B.) was incriminated in the pathogenesis of the condition when Davies et al. working in Britain treated 11 clinical cases with this vitamin. All 11 recovered, however 3 were left with residual nervous signs - obviously these were the severely affected ones. Since then response to treatment with thiamine therapy (50-200 mg) has been well documented, showing that P.W. is a thiamine responsive disease.
Edwin et al. (1968) detected an enzyme thiaminase I in ruminal fluids and the faeces of sheep suffering from P.E. This enzyme catalyses the fission of the methylene group in thiamine in the presence of an amine, thus splitting the thiamine molecule into its two moities. Since then thiaminase I enzyme has consistently been isolated from ruminal fluids and faeces of sheep suffering from P.E. Thus it appears that the disease P.E. is an induced thiamine deficiency precipitated by an enzyme, thiaminase I, which destroys the normally available thiamine in the rumen.
With this background we initiated an epidemiological study of the condition Nardoo Poisoning. We were particularly interested in the following factors and interactions for any common findings:
plant - stage of growth
- composition of pasture
- thiaminase I activity
animals - age, type, class
- previous grazing strategy
seasonal conditions - over previous 12 months
husbandry practices - drenches
- normal procedures
This study consisted of 4 phases.
1. A Retrospective Study of previously documented reports of the condition, looking particularly for mention of the epidemiological factors above.
Other than a classic clinical documentation of the condition in 1911, much of this aspect of the study was unrewarding. It seemed, principally, from unpublished Department of Agriculture disease reports, that the condition was seen in all classes of sheep, in all age groups and although generally following periods of inundation, was not necessarily restricted to these times. Deaths were also reported on actively growing Nardoo, 'hayed off' Nardoo and what was apparently almost dead plant material.
It is worth repeating the 1911 clinical description of the disease as reported by Henry and Massy...
'Feed at the time of the investigation was scarce, and what was available was burnt and dry consisting principally of Nardoo. The disease attacks animals of all ages from 2 weeks upwards, wethers, ewes and rams.... The first symptoms observed were pricking and trembling of the ears, raising of the tail to some slight extent in lambs, and trembling of the limbs when standing still. As the disease progresses the sheep stands apart from the flock, standing rigid with the head held high; appetite is lost; the eyes are half shut, but attention can be attracted and the head turned and the eyes opened. The animal moves with rather jerky action and some loss of control mostly in the hindquarters.... In a more advanced stage the sheep stand with head outstretched, champing of the jaws, and will not move until a hand is placed on them, when they move away showing evident lack of control over the hind quarters, and will run into any obstacles...and stand against them with head held high, breathing quickly and with twitching of the muscles of the nose and face. They appear later to lose the power of standing and lean against fences and posts etc., but at last lie down with legs stretched out, head drawn back and sometimes a little to one side, the breathing is rapid and often jerky and noisy. At intervals they kick and struggle convulsively, the ground all round being greatly disturbed.... No notice is taken of a threatened blow and the eyes are kept wide open. The convulsive fits become gradually less and less intensive and the animal dies usually stretched out with the head back.'
2. Survey of Affected Properties
A standard questionnaire was drawn up and all owners experiencing losses due to suspect Nardoo Poisoning over the preceding 12 months were interviewed. Once again emphasis in these interviews was placed on the four principle areas previously mentioned.
All interviews were conducted by either Graeme Eggleston or myself in an effort to standardise follow-up questions. All interviews were conducted on a face-to-face basis allowing any interesting information to be followed up immediately.
This survey confirmed
a. That all classes and age groups of sheep were affected although there appeared to be some bias towards the older animals. Young lambs (less than 6 weeks) were not affected.
b. Mortalities were limited to sheep which had had access to Nardoo a minimum of 2 weeks; in almost all cases this was longer and often for the lifetime of the animal.
c. Mortalities followed a period of rapid growth and multiplication of the fern in the watercourse country. 1973 and 1974 were favourable for the growth of Nardoo and in certain areas this plant dominated the available pasture.
d. Mortalities were reported on actively growing plant as well as drier plant material.
e. A significant number of sheep, treated intravenously with 200 mg thiamine HCl responded to treatment, confirming that this was a 'thiamine responsive disorder'.
f. Pathological examination of typical cases revealed lesions diagnostic of P.E. confirming that Nardoo Poisoning and P.E. were a similar entity.
3. Ongoing Field Study
Because of the similarities of the conditions, Nardoo Poisoning and P.E., it was decided to study these conditions concurrently.
A. Polioencephalomalacia Study (State Wide)
i. A retrospective study of all confirmed cases of P.E. in sheep over the previous 5 years was made throughout the state.
ii) Four Pastures Protection Board districts were selected, three of which had previously had P.E. diagnosed in their area and one which had not.
From each of these four districts faecal samples were collected for thiaminase I enzyme estimation.
One hundred and ninety separate outbreaks of P.E. in sheep were confirmed histologically throughout the state between 1972-1977. Once again there appeared to be few trends perceptible although as can be seen from Table I there was an apparent seasonal factor.
Approximately half of all cases occurred whilst the animals were on an abnormal feeding regime - viz drought feeding, show feeding or dry feed conditions without supplementary feeding.
Animals of all ages and classes were involved with the exception of young lambs.
The two monthly faecal sampling in the four Pastures Protection Board districts has not yielded any significant trends. Low non-significant levels of thiaminase I enzyme activity have been detected in all districts with no apparent difference between districts and/or time of collection.
B. Nardoo Study
Night observation sites were selected on the watercourse country and sampled monthly. Nardoo growth, state of maturation, percentage composition of the pasture, seasonal conditions are recorded and thiaminase I enzyme activity estimated.
We have consistently recorded high thiaminase I enzyme levels in plant material, at all stages of growth, although the highest level (460 mg thiamine hydrolysed/hour/gram dry weight) was obtained during the active growth of the plant (McCleary and Chick 1977).
4. Experimental Laboratory Work
Small animal feeding trials were initiated being chickens, guinea pigs and rabbits.
In chickens we were able to consistently reproduce clinical signs of thiamine deficiency in 8-10 days of feeding the test diet consisting of active Nardoo, balanced chicken feed and various amines. Using these small animals as an experimental model we have conducted numerous feeding trials of varying levels of
- thiaminase I enzyme
- levels of amine
- various amines.
From the work outlined to you, we have shown that
1. Nardoo Poisoning and Polioencephalomalacia are clinically and pathologically similar.
2. Epidemiologically, Nardoo Poisoning has a seasonal distribution apparently associated with the level of thiaminase I activity in the plant at that time.
3. We have also shown by small animal studies that there is another factor, other than thiaminase I activity which needs to be present to precipitate the clinical condition.
4. This second factor has been shown to be groups of amines. In small animal feeding trials certain amines are more effective in this action. Further work is being undertaken to define which anines are present in both natural cases of P.E. and Nardoo Poisoning.
It is therefore by the means outlined above using retrospective and current in-depth surveys, as well as ongoing investigational work that we have studied the epidemiology of this particular disease.
Acknowledgements
We would like to thank the Wool Research Trust Fund of the Australian Wool Board who provided financial support for this project.
REFERENCES
Clarke, F.L. (1979) personal communication
Davies, E.T., Pill, A.H., Collings, D.F., and Venn, J.A.J. (1965) Vet. Rec. 77, 290
Edwin, E.E., Lewis, G., and Allcroft, R., (1968) Vet. Rec. 83, 196
Gabbedy, B, & Richards, R.B. (1977) Aust. Vet. J. 53, 36
Henry, M. & Massey, A.E. (1912) Agric. Gazette N.S.W. 22, 109
Hurst, E. (1942) 'Poison Plants of N.S.W.' 428-432
Jensen, R., Griner L.A. & Adams, O.R. (1956) J.A.V.M.A. 12, 312
McCleary, B.V., & Chick, B.F. (1977) Phytochem. 16, 307
Pritchard, D., Eggleston, W., & Macadam, J., (1978) Aust. Vet. J. 34, 204
Terlecki, S. & Markson, L.M. (1959) Vet. Rec. 21, 508.
FIG. 2.
FIG. 1.
