References 5 and 6 Abstracted in Vet Notes N.S.W. Department of Agriculture, Vol. 10, No. 1 March 1974 p. 28-29 as follows:
1. Epizootiology: The data from 32 outbreaks of kikuyu grass poisoning on farms in the Northland Province of New Zealand were analysed. The grass was introduced into New Zealand from Rhodesia in 1920 and has become the dominant grass on affected farms in Northland Province.
The data shows that mortalities have occurred from February to June with a peak incidence in April. A feature of all outbreaks has been the occurrence of a precursory period of warm wet weather within 10 days preceding the mortalities. This precursory period has mostly lasted for at least two days during which total rainfall has generally exceeded 20 mm and the daily grass minimum temperatures have usually been over 14°C. No convincing correlation between meteorological conditions before the precursory period and the subsequent development of kikuyu grass poisoning was found. However, mortalities did appear more likely if the rains followed a prolonged dry spell.
Most outbreaks were on coastal sandy country but some were on inland volcanic soils. Most mortalities followed the transfer of cattle to a paddock which had been previously rested to allow regrowth of pasture. Symptoms were usually apparent about 48 hours after transfer to the new paddock. However, this period varied from less than 24 hours to more than 96 hours.
There appeared to be a consistent relationship between the occurrence of poisoning and previous invasion of the pasture with army caterpillars. On one farm where mortality occurred though these caterpillars had not been seen, pastures had been previously damaged by black beetles.
Mostly toxic paddocks have remained in that state for only a few days. However, on one property an affected paddock was found still capable of causing symptoms of poisoning ten days after the first signs of trouble were noted. Information from farmers indicated that the danger period could sometimes extend for as long as three weeks.
2. Symptoms and Pathology: The incidence of clinical cases has varied from less than 5 per cent to over 90 per cent of cattle placed on toxic pastures. Mortality has mostly involved up to 50 per cent of affected cattle. Breed and sex differences in susceptibility have not been detected. But cattle two years of age and younger appear more susceptible than older animals. Severe cases have usually become recumbent in 24 to 72 hours with death occurring after a further 12 to 24 hours. Those which recover usually do so within a few days of being removed from toxic pasture.
Symptoms have consisted of depression, ataxia and evidence of abdominal pain. Affected animals tend to surround water troughs with their mouths near the surface of the water but water intake is less than normal. Occasional transient diarrhoea has been observed. Severe cases invariably show marked dehydration.
A characteristic necropsy finding is a rumen overloaded with sloppy contents. Some of this frequently spills over into the abomasum whose contents frequently resemble that of the rumen. By contrast, intestinal contents are usually scanty. That of the small intestine is whitish-grey and mucoid and in the large intestine, abnormally dry. There is frequently diffuse reddening of the mucosa of the omasum and occasionally of the reticulum and rumen. Subepicardial ecchymotic haemorrhages are also commonly seen.
3. Histopathological Findings
The fore-stomach mucosal lesions are similar to those seen in the chemical rumenitis of grain engorgement and in certain experimental mycotoxicoses (Martinovich et al.. 1972). There is a superficial necrotising rumenitis, reticulitis and omasitis with minimal sub-epithelial changes (hyperaemia and oedema) unless necrosis of the full thickness of the stratified squamous epithelium has occurred, when a marked suppurative response is apparent. Mucosal damage is frequent, more severe and more visible in the omasum and examination of that organ is indicated at all times.
Abomasal and intestinal lesions were quite variable. Hyperaemia, localised superficial necrosis (erosions or gross ulceration) and some haemorrhage and/or early inflammatory response were observed together with mild toxic degenerative lesions in kidney and liver.
A CHRONOLOGICAL BIBLIOGRAPHY OF 'KIKUYU GRASS POISONING'
1. Busch, J., Harris, G.H., Coup, M.R. and Cordes, D.O. (1969). Acute ruminal indigestion, alkalosis and death of cattle glazing kikuyu. New Zealand Veterinary Journal 17:182. (Vet. Notes NSW Dept. Agriculture, Vol. 5, No. 3, Sept. 1969, p. 30.)
2. Cordes, D.O., Coup, M.R., Harris, G.H., Devenport, P.G. and Busch, J. (1969). Acute ruminal indigestion, alkalosis and death of cattle grazing kikuyu grass. New Zealand Veterinary Journal 17:77
3. Martinovich, D., Mortimer, P.H. and Margaret di Menna L. (1972). Similarities between so-called kikuyu poisoning of cattle and two experimental mycotoxicoses. New Zealand Veterinary Journal 20:57. (Vet. Notes NSW Dept. Agriculture, Vol. 9, No. 2, June 1973, p. 38-39).
4. Martinovich, D. and Smith, B. (1972). Kikuyu poisoning in sheep. New Zealand Veterinary Journal 20:169
5. Martinovich, D. and Smith, B. (1973). Kikuyu poisoning of cattle. 1. Clinical and Pathological Findings, New Zealand Veterinary Journal. 21:55. (Vet. Notes, NSW Dept. Agriculture, Vol. 10, No. 1, March 1974, p. 28-29)
6. Smith, D. and Martinovich, D. (1973). Kikuyu poisoning of cattle. 2. Epizootiological Aspects. New Zealand Veterinary Journal 21:85 (Vet. Notes, NSW Dept. Agriculture, Vol. 10, No. 1, March 1974, p. 28-29)
7. Vet. Notes, NSW Dept. Agriculture, Vol. 9, No. 4, Dec 1973, p. 26 - CLINICAL CASE REPORT IN NSW
8. Gabbedy, B.J., Gwynn, R., Hopkinson, WI and Kay, B.E. (1974). Kikuyu poisoning of cattle in Western Australia. Australian Veterinary Journal 50:369
9. Van Heerden, J., Williams, M.C., Van Rensburg, I.B . and Ipland, F.F. (1978). An outbreak of 'Kikuyu poisoning' in Western Transvaal. J. Sth. Afr. Vet. Assoc. 49(1):27-30
10. Schalm, C.W., Jain, N.C., Carroll, E.J. (1978). Veterinary Haematology 3rd ed Philadelphia, Lea & Fabiger