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This article was published in 1980
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Crofton Weed Poisoning in Horses
D.B. Unger, B.V.Sc. . Veterinary Inspector, Casino
Reports of a respiratory condition in horses linked with the appearance of crofton weed date back to the early 40's. Due to the geographical locations of its incidence, it has been variously called 'Tallebudgera Horse Disease' and 'Numinbah Horse Sickness'.
Under the latter name, one of our earlier colleagues N.L.C. Jones, Stock Inspector with the Tweed-Lismore Pastures Protection Board, published one of the earliest references, (1954).
Increased running of horses in danger areas coincident with the inflow of new settlers or members of the alternate society has seen numerous equine mortalities due to crofton weed in recent years.
Some recent examples of mortalities are 11 ex 12 over 4 year period, 2 ex 8 over 2 years, 3 ex 6 over 1 year. One local, newly established stud lost 12 horses in one year.
The Plant
Crofton Weed (Eupatorium adenophorum) is a native of Central America. Naturalised in Australia, it can be found along the east coast from Brisbane to Sydney, growing mainly in shady slopes and gullies and along creeks.
It is an aggressive weed and now covers hundreds of acres in the hill country of north eastern N.S.W., particularly on properties adjoining rainforest.
A full botanical description is provided by Everist (1974).
It is to be distinguished from E. riparium, (Mist Flower or Creeping Crofton Weed), by the latter's sprawling growth and narrower leaves. E. riparium is not involved in poisonings.
Incidence
Reports of this disease are almost entirely restricted to south-east Queensland and north-east New South Wales, although McBarron (1976) mentions Kurnell and Newcastle areas of central coast of New South Wales. A similar condition is reported by Jones (1954) for Hawaii.
Aetiology
The poisonous principle of crofton weed is unknown at this stage. Whether there is an allergic reaction to the heavy pollen production in spring as some suggest, has yet to be determined.
However, O'Sullivan (1979) managed to reproduce the disease in feeding trials using E. adenophorum.
Occurrence
The disease occurs only when crofton weed dominates the pasture or is preferentially grazed. Horses frequently fit the latter category and have been observed to select the plant, even in paddocks in which there is ample feed and only scattered clumps of crofton weed.
The disease effects animals of all ages and both sexes, although work sometimes precipitates death.
The youngest field case examined was a 13 month old colt reared on the property from 1 month old.
The oldest was a 20 year old draught mare which had been introduced from clean country one year previously.
Symptoms and mortalities commonly are reported in summer following spring flowering.
Pathogenesis
The very early stages of the disease have not been elucidated. However, as noted by O'Sullivan (1979),
'the presence of proteinaceous fluid in the alveoli together with the vascular damage seen in natural and experimental cases of the disease in horses and rabbits suggest capillary integrity is lost in the early development of the disease'.
Severe infection and abscessation noted in only a proportion of cases appears to be a secondary part of the disease due to impaired defence mechanisms of debilitated lung tissue.
Two cases examined had massive pericardial haematoma and one case, enlargement of the right ventricle.
Hypertrophy of the right ventricle in the horse has been associated with chronic pulmonary emphysema or chronic interstitial pneumonia, both similar to lesions of crofton weed poisoning.
Spontaneous rupture of the heart, usually affecting the right side in animals, is due to abnormal pressure relationships determined by the coincidence of violent cardiac contractions, (e.g. as demanded in forced exercise, work, parturition) and obstruction to the outflow of blood (e.g. pulmonary hypertension).
Conditions causing pulmonary hypertension include emphysema, multiple pulmonary embolism, thrombosis, and widespread pulmonary fibrosis. All of these changes are found in crofton weed cases.
Cardiac rupture quickly leads to acute circulatory failure through cardiac tamponade (i.e. not due to blood loss but because the heart is unable to dilate during diastole).
Failure of the respiratory and/or cardio-vascular system would account for those horses in apparent good health which die suddenly, especially related to work or other stress (e.g. parturition).
Clinical Findings
The earliest sign usually is coughing related to exercise. Later, a persistent cough may be noted even at rest. Forced exercise produces severe dyspnoea and affected animals gradually lose stamina to the point of being unfit for work. Severely affected horses sometimes refuse to ascend slopes even when grazing undisturbed.
Appetite and body weight are often unaffected except in cases with secondary infection and toxaemia.
The respiration is of the forced expiration, abdominal type.
Sibilant and crepitant rales are heard in some cases; others have surprisingly little sound or slight wheezing only on auscultation, even though subsequent autopsy findings in these may be marked.
Heart and respiration rate are usually elevated e.g. H.R. 50-100 (normal 30-40), R.R. 30-80 (normal 8-10).
Occasional animals show oedema of the ventral abdominal and thoracic walls.
In summary, main signs are coughing, dyspnoea and low exercise tolerance.
Clinical Pathology
Haematology of 3 field cases revealed one anaemic with haemoglobin levels of 8.75 g/dl, Haematocrit 27% (others 12.75 g/dl and 71.0 g/dl and Haematocrit 37 and 32%).
All animals had a mild Leukocytosis (10.89, 11.88 and 16.61 WBC x 103 / cmm). The anaemic animal was showing a degenerative shift to the left and died a fortnight later.
Serum enzymology was not fruitful with results for SGOT, CPK and GT within normal ranges.
This is to be expected as lung tissue doesn't contain any organ specific enzymes.
Similar results were obtained by O'Sullivan (1979).
Autopsy Findings
These are almost exclusively confined to the thorax.
The most consistent finding is generalised fibrosis and yellow-pink consolidation of the lungs.
The lungs of chronic cases were pale to white, fibrous and denser than normal.
The degree of pleuritis varied greatly from mild roughening and little or no fibrin tags and adhesions through to extremely severe hydrothorax, severe adhesions, haemorrhages and abscessation.
Two animals had massive pericardial haematoma and one an enlarged right ventricle. Mild to severe hydropericardium was a feature of other autopsies.
The cut surface of the lung almost invariably showed a yellow-pink consolidation, except for one long standing case which had not had access to crofton weed for 12 months. This one showed diffuse pallor and fibrosis of the lung.
Other acute cases showed pleural and interlobular oedema and sometimes emphysema.
Approximately 50% of cases show focal areas of liquefactive necrosis and cavitation up to 10 cm. diameter in some cases containing small, caseous cores.
One animal which showed extreme pleuritis and hydrothorax also had the worst secondary infection with two large thoracic abscesses, one of which measured 20 x 30 cm.
Histopathology
Extensive interstitial fibrosis, alveolar pseudomembranisation, proliferative pneumonia and accumulation of proteinaceous material and mononuclear cells in alveoli are common features.
Pleuritis of varying degrees of congestion, oedema, fibrosis, fibrin tagging and adhesions between parietal and visceral pleura is a constant feature. In some cases bacterial colonies and suppurative lesions are seen. A few showed alveolar and interstitial emphysema, generally though the picture is moderate alveolar emphysema, if at all.
Diagnosis
This is based on knowledge of the district, a history of the property and the horse with particular reference to access to crofton weed and clinical signs, particularly respiration and loss of stamina.
Treatment
Early removal from contact with the plant is essential.
Use of antibiotics, antihistamines and corticosteroids of acute cases and other members of the mob combined with restriction from grazing crofton weed, has saved horses.
However, many are left permanently useless for work.
Control
Control is based on preventing horses ingesting the plant and in some cases from excessive exposure to the pollen, (based on the assumption that the disease in an allergic reaction to inhaling plant particles).
The most effective control methods to date have been hand clearing of small areas or slashing, followed by spraying of the regrowth with 2.4-D (sic) of larger areas.
Follow-up seeding and fertilising of infested areas is recommended
Confinement and hand feeding of horses is often the only short term solution on heavily infested properties.
References
Everist, S.L. (1974) - Poisonous Plants of Australia Angus and Robertson, Sydney
Jones, N.L.C. (1954). Institute of Inspectors of Stock of N.S.W. Year Book [ Numingah Horse Sickness, Flock & Herd Archive - ed. ]
McBarron, E.J. (1976) - Medical and Veterinary Aspects of Plant Poisons of New South Wales, Department of Agriculture, New South Wales
O'Sullivan, B.M. (1979) - Aust. Vet. J. 55:19