Enquiry has shown that in the Department of Agriculture's library there is no record of Salmonella infection in sheep and consequently this paper is an introduction to something new to us. On this account the subject matter has deliberately been set out in rather full detail, and also because of the considerable variations noted in symptoms and lesions.
The organisms believed to be responsible for the mortalities were Salmonella morbificans bovis, which has not been recorded in Australia, and Salmonella typhimurium, probably a new strain, var. Narrabri.
At the end of September, 1938, more than 100 sheep died in a fortnight on a property K. of 23,000 acres, out of 2,000 fat Corriedale ewes of mixed ages. The country was very heavy, black, open plain, and at the time was carrying a good growth of winter herbage, composed largely of Trefoils, Lamb's Tongue (Chenopodium atriplicinum), Barley Grass (Hordeum murinum), and Variegated thistle (Silybum marianum). No typical case was seen or examined, but from the history of sudden deaths and the fact that this disease was very prevalent at that time, the trouble was diagnosed as enterotoxaemia.
One very fat ewe had been sick for 24 hours, dull, with slight scouring and inability to stand except with difficulty. It was destroyed for post-mortem examination. The lesions were swollen mesenteric lymphatic glands, friable liver, distended gall bladder and slightly congested kidneys. There was excess fluid in the pericardial sac, but the serous surfaces all appeared to be normal. The contents of the omasum were hard and dry. Prior to death, 30m1. of ten per cent. calcium gluconate were administered without effect.
The Director of Veterinary Research considered that smears were not suggestive of enterotexaemia, but it was considered that the mortality as a whole was due to enterotoxaemia, which was very prevalent at the time. Losses ceased, and no opportunity offered for further post-mortem examinations. In some respect this one sheep examined was very similar to those dead from Salmonella infection, and it is possible that losses which were reported in December actually began at this time.
On the same holding in mid-December, losses in all paddocks in 17,000 sheep of all ages and sexes were reported. This had been going on for at least six weeks. Feed was not very fresh at the time, being mainly Mitchell Grass (Astrebla spp.) with a mixture of Minder's Grass (Iseilemma sp.), Tah Vine (Boerrhavia diffusa), Sida sp. and Solanum esuriale in fair quantity. In some of the paddocks the Mitchell Grass was seeding and almost the only plant growing, but in others was grazed down to such an extent that Hard Roley Poley was almost the only plant remaining. In one other paddock there were numerous Oxalis corniculata butts.
From about July to October the losses were 360, and October to March 420, counts being taken at shearing and crutching. These losses include losses at lambing, crow-pick, fly strike and other odd causes. Watering was from bore drains which badly needed delving, and in which the water was stagnating and becoming foul.
On another property S, in mid-February, 1939, seventeen sheep died in a mob of 1,700 fat Merino wethers of mixed ages carrying seven months wool. They had been watering at a small ground tank into which a short bore drain emptied in a 2,300 acre paddock on heavy black open country, with no shade of any consequence, the feed being composed of fresh mixed herbage; Tah Vine, Roley Poley, Solanum esuriale, a fresh growth of Oxalis corniculata which had come as a result of a storm three weeks previously, grasses and other insignificant herbage in small quantity. No losses occurred in any other paddocks.
On another property M. in 3,000 acres (all one paddock) from 10th February to 28th February, 1938, about 180 sheep out of 2,500 Xbred wether hoggets with symptoms and lesions similar to those in the other outbreaks. Outstanding lesions were oedema, congestion and ulceration of the abomasum, congestion of the small intestine, caecum and colon, and erosion of the rectum in areas about an eighth of an inch in diameter one foot or so from the anus. Mesenteric lymphatics were oedematous and one was congested.
No organimns were found in the smears, but from pipettes of spleen and liver a heavy growth of coliformbacilli was obtained. (Were these Salmonella sp.?).
In the second post-mortem ulcerative colitis and gastro-enteritis were found. The gall bladder was distended and its wall was thickened.
This was associated with large numbers of Gram-negative bacilli. It is now considered that this mortality was most probably due to some type of Salmonella infection.
On K the malady was invariably fatal, a few young rams being the exception. The mob generally was perfectly healthy, there being no scouring or other evidence of sickness in any but definitely affected sheep. Sick sheep separated from the mob were depressed, and some were scouring a little. In later stages they stayed at the water and had a mania for going into it, quite a proportion having to be pulled from it.
Symptoms noted by the manager of S were slight muscular tremors, lassitude, and disinclination to move. In one sheep at least there was a hypocalcaemia and hypermagnesaemia, which was perhaps associated with ingestion of Oxalis corniculata. Some had a stilted gait. No scouring was present, but in one destroyed for post-mortem there was some scouring, due in the opinion of the manager, to the young Camel Melon in the paddocks into which the sheep had been moved in hopes of checking the losses. Sheep did not have the same tendency to stay on the water. So far as is known, no sheep recovered, death occurring in from one to three days.
In a sheep destroyed the symptoms were personally observed to be lassitude, scouring, a humped back and a stilted proppy gait, almost amounting to loss of use of the hindquarters. Loss of condition was marked. The faeces were dark, green, fluid, and contained a small amount of mucoid material.
Sheep were dead on their sides, had struggled a little, with no discharges from any of the external orifices, the eyes and mucosa of the mouth being normal.
On K. in one sheep found dead a short time, the skin was congested, the lungs slightly congested, some excess fluid in the pericardial sac, pinpoint petechiae on the pericardial surface mainly confined to the longitudinal grooves. The endocardial surfaces were normal, the heart rather large and of normal consistency. On opening the abdomen the obvious abnormality was enlargement of the mesenteric lymphatic glands, which were white and oedematous. The abomasum was slightly congested, but otherwise the alimentary tract was normal. The liver was slightly greasy (probably a condition of cloudy swelling) and there were a few petechial spots on its surface. The gall bladder was full though not distended, and its inner surface was covered with some dark deposit, whilst its outer surface was oedematous.
In another, bled to death, the lungs, heart and gall bladder were quite normal. The liver was greasy, the mesenteric lymphatic glands were much enlarged and oedematous and the omasum was small and compact. The abomasum was slightly congested and its mucous membrane thickened; the small intestines were apparently normal but ingesta in them very fluid. The caecum was definitely congested, the mucosa much thickened and the contents very fluid. The colon and rectum were normal but empty. Very small, numerous red spots were visible throughout the cortex of the kidney.
During February, 1938, losses in the vicinity of 300 sheep each occurred on this and an adjoining property. The owner considers that this was identical with the more recent outbreak, though in a slightly more acute form. Lesions, symptoms and history confirm this. No bacteriological examination was made and Solanum esuriale was suspected as the cause in both cases.
On the property S. lesions in an old wether which was destroyed were briefly; there was a greasy liver, full gall bladder with thickened wall, the cortex of the kidneys was marked with numerous, very minute red spots, the ingesta was fluid, the mucosa of the duodenum appeared to be thinner than normal, and the jejunum and ileum were thickened and slightly congested. There was oedema of the mesenteric attachment of the ileum and the mucosa of the caecum was very much thickened, with well marked congestion in an area about four inches by five inches. The mesenteric lymphatics were oedematous nnd considerably swollen.
For the purposes of routine diagnosis in sheep, this type of infection seems to be associated with lesions in any part of the gastrointestinal tract, inflammation being constant and erosion of the mucous membranes not infrequent. The gall bladder, liver, spleen and blood stream appear to be sites of infection.
Dr. Came gives an excellent outline of the pathogenesis of acute infections by Salmonellae in general. He states: "Infection occurs by ingestion. The fact that acute enteritis is one of the outstanding features of most of these infections led to the original belief that the causative bacilli passed through the stomach, proliferated in the intestine giving rise to primary intestinal lesions, and from thence often escape into the blood stream. More recent evidence, however, indicated that the bacilli penetrate in relatively small numbers through the lymphoid tissues of the pharynx, and possibly also the lymphoid tissues of the intestinal canal, and reach the blood stream via the lymphatics, causing a transitory bacteraemia. The circulating organisms are removed from the blood by reticulo-endothelial phagocytes, especially of the liver, spleen and bone marrow, and then multiply in these situations. At this stage, the blood may be sterile. Following the continued multiplication of the bacilli in these foci, they escape into the blood stream, leading to a secondary bacteraemia with generalisation of organisms throughout the tissues. In typical enteric infections there now follows invasion of the intestine, principally via the bile duct and gall bladder, with the subsequent development of characteristic intestinal lesions.
In the early stages the infecting organisms can usually be cultured from the blood, whereas they may be absent from the faeces at this stage. Later on faecal cultures become positive; finally, about a fortnight after the initial infection, specific agglutinins appear in the circulating blood and can be demonstrated by agglutination tests."
Some special features which may be of significance, and were common to the outbreaks, are:
1. Solanum esuriale was present in fair quantity on all the properties.
2. The coincidence of outbreaks with the extreme heat of summer.
3. Lack of shade.
4. Bore water the water supply.
The constant association of Solarium esuriale with these mortalities and the fact that it has been suspected on many other occasions gives one cause to wonder whether Salmonella infection may not have been the cause of all such mortalities.
It is suggested that the ingestion of this plant may lower the resistance of the bowel wall and thus render the animal susceptible to infection in the same fashion that Bracken Fern (Pteridium aquilinum) is reputed to render cattle susceptible to infection by B. coli and Pasteuralla spp.). It must be borne in mind, however, that this plant is common to the majority of paddocks in the North-West, and grows the whole year round.
The outbreaks have consistently occurred in the hot weather, sheep carrying six to eight months wool at the time, and being subjected to extreme temperatures in the total absence of shade, or else with shade which is quite inadequate to offer appreciable protection. Conditions such as these would lower the resistance of any animal.
Water supplies are probably the means of spread of the organisms. On the property K. the bore drains were stagnant and needed cleaning; on S they watered from a short bore drain emptying into a small ground tank, and on M from a very large waterhole filled by a bore drain. At this time of the year water supplies are at their lowest and therefore infecting doses would most likely be greatest. It is almost certain that infection of any kind would live most probably for a very short time on the ground, where it would be exposed to the efficient sterilising of extreme heat, sunlight and drying.
In preparing this paper and that on Oxalis corniculata poisoning, reference to old files continually impresses the necessity for a complete recording of observations. Information which was observed may have been deliberately omitted from reports as being of no consequence, and this later may have been valuable. Memory may serve to bring back some unrecorded details, but it cannot be trusted far. Consequently I would try to impress on you the necessity for complete recording. Next year you may not be in the same office and preliminary investigations you may have carried out lose much of their value to another officer unless complete in detail. Your District Veterinary officer has, no doubt, brought this to your notice on occasion, but you will find that a shortage of information is just as important to you or your successor as it is to him. It may seem impertinent for me to advise in this way, but admission of one of my own shortcomings may assist you in avoiding it yourselves.
1. History, symptoms and lesions in mortality due to Salmonellae in sheep are described.
2. Previous similar mortalities are outlines.
3. The pathogenesis of acute Salmonella infection is outlined.
4. Possible predisposing factors are outlined:
(a) Lowered resistance due to climatic factors—especially heat.
(b) Ingestion of Solanum esuriale—a suspected poisonous plant.
I have to thankfully acknowledge the permission of Dr. H. R. Carne, Lecturer in Pathology and Bacteriology, Veterinary School, Sydney University, for permission to quote verbatim from his notes, and the permission of Mr. C. C. Blumer, B.V.Sc., District Veterinary Officer for the North, and Mr. W. L. Hindmarch, B.V.Sc., M.R.C.V.S., D.V.H., the Director of Veterinary Research, Glenfield, for permission to use information contained in official reports.