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This article was published in 1954
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.

"Numinbah Horse Sickness"

A PULMONARY DISEASE IN HORSES

N. L. C. JONES, Inspector of Stock, Tweed-Lismore

About 1941 a disease in horses in the Numinbah Valley in the Tweed district came under notice. This disease appears to have made its appearance about the same time as Crofton Weed began its spread throughout the valley. Two specimens of this noxious weed have been identified as Eupatorium glandulosum "Giant Hemp Agrimony" — and Eupatorium riparium — "Hemp Agrimony". At the present time hundreds of acres of farm land are covered with this weed, both species of which are native of Mexico.

The area in which this disease occurs is a somewhat isolated one and it has not been easy to maintain the necessary contact with the farmers concerned; to a considerable extent due to the shortage of veterinary staff. The disease occurs only in the extreme northern part of New South Wales and a small area in southern Queensland; both areas being infested with Crofton Weed. No such disease of horses is recorded elsewhere in veterinary literature as far as can be ascertained. Occurrence has been at erratic intervals, and during the months following an outbreak as many cases as the staff position would permit, have been investigated. From time to time cases which had recovered from the acute sickness and were in the chronic stage were seen, and where possible post-mortem examinations were held and material obtained and submitted to Glenfield Research Station.

The laboratory examinations indicated that the disease commenced as an acute oedema of the lungs, followed by haemorrhage. In some cases where recovery occurred a considerable portion of the lung tissue was destroyed and the lung in the area was solid. In the very acute cases seen the oedema of the lung was so severe and the out-pouring of fluid into the lung so great as actually to cause death by drowning. Once investigations were started, reported cases became more numerous, and from 1948 onwards reports continued to increase. It will be of great interest to summarise some of these very briefly:

(a) Reported the loss of seven horses in the last few years, following the exhibition of typical symptoms of the above disease. In all cases the affected animals had shown slight symptoms over a fairly lengthy period and then had suddenly shown advanced symptoms, followed by rapid death. This property was infested with Crofton Weed.

(b) This owner had lost four horses in two years and another draught horse was in a "bad way". The latter died within a few days, but owing to flood conditions the property could not be reached in time for a post-mortem. The property was found heavily infested with Crofton Weed.

(c) Farmers on one creek stated they had lost twenty-two horses in twelve months. All of these farms were heavily infested with Crofton Weed.

(d) This owner lost six horses over a period of seven years. These horses had access to Crofton Weed, but had been fed some maize and chaff.

(e) An owner reported that he had lost five horses, and that since the last horse died he had mechanised the property. It was stated that the previous owners had lost eleven horses. This property was heavily infested with Crofton Weed.

Many more such cases could be quoted, and over the last ten years hundreds of horses have died from this disease. A large number of owners gave up maintaining horses; one man complaining that he had to push his cream cans two miles to the roadside in a wheelbarrow because he was unable to maintain a horse on the property.

Up to this period laboratory examination of specimens had failed to reveal the presence of any infective agent; while the few transmission experiments carried out had given negative results.

Arrangements were made to forward weekly supplies of Crofton Weed for the purpose of feeding experiments at Glenfield Research Station; such supplies going forward for a period of two months. One horse consumed a total of 105½ lbs. of Eupatorium riparium, the fine leafed creeping plant. No ill-effects were produced, and it was decided to discontinue feeding. In light of further knowledge it would appear that either the weed underwent some change during transit or the feed trial would be required to be carried on for several months.

In spite of the limited staff position a considerable amount of investigation into this horse mortality had been carried out up to this time. However, the research staff was handicapped by the fact that it was dealing with a condition not previously known to veterinary workers and therefore it had to start "off scratch" in the investigation.

In 1948 a Research Officer spent several days in the area and was able to see several cases. A two-year-old colt which had been affected with the disease for about ten days was examined. This horse showed a temperature of 102.5 degrees F. with marked distress on moving. The respiration was laboured and abdominal in type. Auscultation of the thorax revealed excess thoracic fluid. A week earlier the affected horse had been placed in a paddock in which there was no Eupatorium, but no clinical improvement had been observed. The animal was killed and the only macroscopic lesions were confined to the thorax. The heart showed marked petechial haemorrhages and hydropericardium. The lungs showed marked oedema, with areas of intense thickening of the interlobular septa. Throughout both lungs was a number of sequestra containing necrotic lung tissue. Subsequent bacteriological examination of the carcase failed to reveal the presence of any organisms.

There seems to be little doubt that the occurrence of the disease bears a close relationship to the presence of Eupatorium. Properties on which there is little or none of the plant have had no experience of the disease. Before interviewing owners one could say of various properties which were badly infested with Eupatorium, that they had no horses or had lost horses from the particular disease; frequently both alternatives were found to be the case.

Another owner had an eleven-year-old mare which had been on the property for seven years, this being the tenth horse that this owner had had affected from the same condition. The horse showed a slight cough nine days previously and since then had paroxysms of coughing followed by fairly normal periods when allowed to rest. When first affected the horse had been working, but during the last few days it had been too badly affected to be worked at all. At the time of the inspection the animal was standing in a depressed attitude and showed a marked disinclination to move; being in effect partially paralysed.

This case had a temperature of 104.6 degrees. This temperature was somewhat high, but the horse was standing in the hot sun and subsequent postmortem examination showed that there would have been very poor air circulation through the lungs. The pulse rate varied from 110 to 120 per minute and the pulse was very shallow. The respiration was very laboured and of a double-action, abdominal type. The respiratory rate averaged 50 per minute; being intermittently faster and slower than this rate. There were a number of areas of "scalded" skin; these being slightly oedematous, somewhat raised areas. Similar lesions had been noticed by the owner in other affected horses.

The mare was killed by shooting through the brain. Post-mortem examination showed slight oedema of the mammary glands and the ventral abdominal wall. The thorax showed an intense oedema and some ecchymoses of each lung; while there were several small areas of acute congestion in the lungs. The pulmonary oedema was so intense that even when the thoracic walls were opened the lungs showed no tendency to collapse. When the lungs were cut, large quantities of frothy fluid flowed from the cut surface. The heart showed marked dilation, there was slight hydropericardium, but no evidence of pleurisy. There were some fibrinous adhesions to the peritoneal surface of the diaphragm, liver, spleen and kidneys. The gastro-intestinal tract showed comparatively little ingesta. There was a heavy parasitic infestation causing a patchy congestion of the intestinal mucosa. The kidneys showed slight congestion. There were a number of yellow caseous and calcareous nodules throughout the liver, and particularly along the margin of the organ. These lesions obviously had been present for a long time and appeared to be of parasitic origin.

The history of the disease on this property dates back to about 1940, when the owner purchased a number of horses from Toowoomba. During the following three months, four of the purchased horses and one of those previously on the property had died from a pulmonary disease. Following this mortality the owner was without horses for about six years, but during the last three years a further five horses have been lost from the same condition.

On this property there is a close association of the disease with Crofton Weed. When the first mortality occurred in 1939 there was comparatively little of the plant growing, but since that time it has become much more plentiful and has taken possession of large areas of the country. The owner considers that the shortest time from the introduction of horses (from an area free from Crofton Weed) to death from the pulmonary condition was two months. It has been his experience that six-year-old horses are more susceptible to the disease. There appears to be some evidence that horses which are affected and which are not worked may live for six weeks after showing symptoms. When horses are continued working after showing symptoms, death usually ensues in slightly more than a week.

Post-mortem examination has suggested that deaths would be due primarily to the intense pulmonary oedema: resulting either in drowning or in cardiac failure following dilation and inability to pump blood through the oedematous lungs. The post-mortem findings do not suggest that the condition is due to an infective agent. It is suggested tentatively that the pulmonary oedema may be an allergic response rather than a local oedema due to cardiac insufficiency, In this respect it would appear that the affected animals have become sensitised to some particular plant.

There is no doubt that the disease caused considerable losses of horses, but one gained the impression that the general management of horses in the area is bad. These animals frequently are turned out for long periods into paddocks containing little apart from Eupatorium; and until recent times there appears to have been no thought given to hand feeding, and few owners have made any attempt to combat the particular weed.

It appears that horses must graze on the weed for about three months before symptoms are likely to be seen. The plant seems to contain a toxin which increases the permeability of the pulmonary endothelium and causes the typical lung picture. There is some evidence that hand-feeding may assist in warding off the disease if only by reducing the intake of Eupatorium.

It was recommended that two horses be brought from outside the Numinbah area and placed in a paddock containing large quantities of Eupatorium; the fences on the selected property being such that there would be no contact with other horses. The staff position in this area improved during 1949 by the appointment of a veterinary officer and he was able to make regular inspections of the two horses in this feeding trial on the property at Numinbah. The first of these experimental animals died in October, after being on the holding approximately twelve months; while the second death took place a few months later. In both instances the horses died suddenly and it was not possible for an officer to examine the carcases until some degree of post-mortem decomposition had set in. Nevertheless, it was possible to determine from the post-mortem examination, that in each instance death was due to the typical "Numinbah horse sickness".

Staff changes at this period again left the area without close veterinary supervision, and very little further investigation could be made until 1951; when a veterinary officer was stationed in this vicinity.

Many owners now were attempting to prevent horses gaining access to the plant, but some properties had become so heavily infested that this measure was not possible.

Cases of the disease continued to be reported and a practitioner treated a number of sick horses by the administration of sulphanilamide. He claimed that a big percentage had recovered and he was of the opinion that the condition was due to an infection. Although we have not been able to check up to any great extent from the owners concerned the outcome of this practitioner's treatment, no owner yet has been encountered to report a recovery following sulphanilamide therapy, and we know of several instances in which death ensued despite this, line of treatment.

With the improved staff position it was decided that further investigation as many cases as possible should be carried out in the field, with the collection of case histories and the submission of further specimens for examination. It was suggested also that trial therapy of affected horses with Anthisan might be undertaken. Cases were treated with a course of Anthisan (5 per cent.) and regular examinations were made. Some appeared to respond for a time but deteriorated sharply and died. From all the specimens submitted the lung showed the intense pulmonary oedema typical of that seen in cases of Nurninbah horse sickness. No bacterial growth was obtained from pipettes of lung tissue and fluid.

Considerable time was devoted to the examination of all reported cases and it was hoped that it would be possible to push to a conclusion investigations commenced ten years ago, earlier. However, late in 1953, owing to the resigna tion of the veterinary officer, this area again was left without close supervision, and very little time could be given to continue the work.

Observations to date would indicate that if the condition is the result of ingestion of Eupatorium spp. it is clear that it has to be eaten over a period of at least several months, and possibly longer. It would appear also that cases of the condition are more likely after the plant has been in flower in September; though it might be mentioned that there have been instances of horses eating the plant over a period of many years without developing symptoms. If the plant is the prime cause of the condition it could act in one of the following ways:

1. Through the action of a cumulative toxic principle.

2. A principle within the plant which after prolonged ingestion provokes an allergic reaction on the part of the animal; resulting in death.

3. A principle within the plant which predisposes the animal to the action of an infective agent.

There is evidence that the disease of horses referred to as probably due to ingestion of Eupatorium was of considerable importance in Hawaii during the 1920's (but not reported now for a number of years), although no diagnosis was ever proven.

The Territorial Veterinarian, Hawaii (in a communication to the C.D.A.L.). states: "One of the most complete descriptions that I have found is in an undated communication from J. C. Fitzgerald, M.R.C.V.S., who was district veterinarian on Maui, the only place the disease was found. It is entitled "Notes on held observation made on a disease resembling Pestis Equinus." This obscure disease has existed for some years without any investigation, until a few months ago. It occurs on the slopes of the Mountain Haleakala at elevations from 2,000 to 7,000 feet, is never seen below 2,000; is common among horses of all ages, rarely noticed in mules and then only mild attacks, and never in donkeys. This is authentic, as all three are well represented in the afflicted district. Broken and un-broken horses are like affected, but not seen in stabled animals unless just brought in from pasture a few days previous to the attack. The locality is usually dry and well drained, with fair rainfall in the winter and spring months; in the latter the disease is most prevalent, rarely occurring in the summer drought. Mosquitoes are present and include the small night mosquito (Culex pipiers), the striped night mosquito and the day mosquitoes: the cattle horn fly are also present in great numbers. The local flora extraordinary include "paamakani" (Hawaiian) Eupatorium glandulosum, a native of Mexico which is a pest throughout this district. Yorkshire Fog which is heavily infested with fust (penicillium) is common in the pastures. I am informed by the botanists that there are no poisonous weeds or plants.

The disease has two forms, acute and chronic; in the former there are practically no premonitory symptoms. If being worked at the onset of the attack difficult respiration with muscular tremors will come on quite suddenly and if pressed by an ignorant rider the animal will fall dead in a few minutes, asphyxiated; whereas if pulled up the stertorous breathing may continue for a few hours, after which the animal will die. The pulse is usually rapid, soft, and often running; a jugular pulse is usually quite visible. The temperatures are rarely elevated. In the chronic cases the animal may go for months or even years if not worked or exerted. In the majority of cases the following points have been noted: There is either immunity at the lower altitude, or the causative factor is not present, as no cases are on record below 2,000 feet.

The predominating symptoms in all cases is the condition of emphysema in the lungs, which resemble a rubber sponge in consistency and which do not collapse but rather expand on opening the thorax. The spleen is normal in all cases. Few if any horses recover if attacked, or the condition may exist in the earlier stages without any inconvenience. The greatest difficulty in respiration is in the expiratory effort, which appears to require great muscular force; bringing the intercostal and abdominal muscles visibly into play to an abnormal extent. Local lay opinions are unamimous in that it is rarely seen in animals that do daily work. The appetite is hardly ever impaired, many animals eating to the end. Many efforts to transmit and to reproduce the disease were undertaken but failed in each instance. Dr. K. V. Jeyer of the Hooper Foundation was brought down here in 1926 to study the disease but as far as can be determined he too failed to reach a diagnosis. It was told by Dr. Fitzgerald, many years ago, that the hand-cleaning of the affected horse pastures of Paamakani (Eupatorium glandulosum) would prevent the disease. Then if at times economic conditions forced discontinuance of the weeding the disease would again be noticed. However, feeding trials were negative; as were pollen inhalation trials on a previously sensitised horse. The practical solution to the problem, if we accept the Paamakani theory, is to rid the pastures of the plant. With this in mind our entomologists introduced a gall fly which has been very successful in the control of the weed".

This communication from the Territorial Veterinarian, Hawaii, is most interesting and the main points seem to confirm our theory as to the cause of the condition. Although there is no suggestion here of an altitude factor there can be little doubt that the described disease in Hawaii is identical with our Numinbah Horse Sickness. The following features are in common with the Hawaiian disease:

1. Affects all ages and classes of horses except those stabled and hand-sed.

2. Few, if any, recover (although temporary remission of symptoms is not uncommon).

3. Jugular pulse in acute form.

4. Temperature normal (except when pneumonia is superimposed).

5. Appetite often normal.

6. Marked abdominal respiration.

7. Chronic cases may last months or years.

8. Rubber sponge consistency of lungs.

The Stem Gall Fly recently has been released in the Numinbah area and although it is too early to predict the outcome, present indications are encouraging. Will the Stem Gall Fly be the solution to the problem?

Acknowledgment: It is desired to thank the Chief, Division of Animal Industry, for approval to publish; and to acknowledge the assistance of official reports, quoted freely, from the Director of Veterinary Research, the DVO, Grafton and the VO, Murwillumbah.

 


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