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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.
Samples from the "Case Book"
K. V. BYRNE, B.V.Sc., Formerly Inspector of Stock, Young.
COLIBACILLOSIS IN POULTRY
In June, 1952, a veterinary practitioner brought to this office some viscera from a Black Orpington hen which he had obtained from a property in the Young district; the bird having been brought to him by a landholder for the purpose of determining the cause of mortality in his fowls. In the post-mortem examination carried out by the veterinarian, creamy white growths were seen in the liver and on the surface of the peritoneum and intestines. He formed the opinion that the bird was affected with tuberculosis and therefore brought specimens to the writer. This disease so far has not been recorded in poultry in the Young district.
On examination of the viscera, one concurred in the diagnosis and the specimens were despatched for laboratory examination. A visit was made to the property where it was found that the losses were occurring in a lot of 50 Black Orpington pullets which had been purchased as day-old chicks from a Sydney hatchery in the previous November. These birds had thrived until laying commenced, but a mortality then started, and continued slowly until 12 months after purchase, none of the 50 birds was left. The only symptom was that the affected birds wasted away for a week or more before dying.
Subsequently, a report from Glenfield Veterinary Research Station stated that no acid-fast organisms were detected in the nodules and that it was considered that the birds probably had been affected with colibacillosis. However, in a further effort to make sure that Tuberculosis was not present, all in-contact birds were subjected to a test with avian tuberculin; with negative results.
The disease Colibacillosis, which results from infection with E. coli, has not been encountered previously by the writer, and so far as is known is not common in this State. The disease has an acute and chronic type, the former having considerable similarity to fowl cholera. In it the bird becomes dopey, loses appetite and shows all the symptoms of a severe septicaemia; darkening of the comb and wattles, ruffling of the feathers, increased thirst and exhaustion. Post-mortem appearances in the acute form have a septicaemic character. In this outbreak, however, the disease took the form to which the term Coligranuloma is applied and the particular significance of this manifestation is that the granulomae present are morphologically indistinguishable from the tubercles of Avian Tuberculosis. These granulomae are found in the caeca, liver and intestinal tract; and in the particular bird examined in this mortality the liver lesions especially were quite characteristic of those seen in tuberculosis.
ASPERGILLOSIS IN TURKEYS
Recently a turkey raiser from an adjoining P.P. Board District brought to this office a turkey pullet about 5 weeks old, stating that 20 such birds had died during the previous 2 weeks and that 15 were sick. The symptoms shown by the sick birds were respiratory distress and constant chirping. On post-mortem examination numerous yellowish hard nodules of caseous consistency and varying in size from 1 to 4 millimetres in diameter were found scattered throughout the lung tissue. Cultural and microscopic examination at Glenfield showed the presence of Aspergillus species.
At the time of carrying out the post-mortem examination it was considered the birds were affected with Brooder Pneumonia and to pay attention to hygiene. However, the owner was most emphatic that hygiene was satisfactory, and from his description it appeared likely that this was so.
At a later date, though, he returned and said that the only fault he could find with his arrangements was that the watering troughs were leaking and keeping portion of the sanded floor on which the birds were running in a wet condition. He had therefore moved them to new premises, the result being that the mortality had ceased.
This owner's experience fits in with observations made elsewhere that Aspergillosis infection usually is acquired from bedding, and that the major move in control is attention to hygiene.
POST-DRENCHING MORTALITY IN SHEEP
Mortality in sheep following drenching with Bluestone-nicotine sulphate associated with ulceration of the mouth is well recognised. However, since being in the Young P.P. Board District, the writer has seen two mortalities in sheep following the use of this drench in which no lesions were to be seen in the buccal cavity. In each of these the appearances have been the same. Affected sheep develop a large submaxillary swelling, which in many cases extends down the central line of the neck and arm to the brisket. This swelling develops within 24 hours of drenching and mortality commences within 48 hours of that operation.
As has been mentioned, when a post-mortem examination is conducted nothing abnormal is to be seen inside the mouth. Externally, the throat swelling shows a dark discolouration of the skin and when it is incised one sees large blood clots which have the appearance of haematomata. These latter are of bright red colour: the appearance not being suggestive of a gas gangrene infection. Pipettes from them and from affected animals generally have shown the presence of various bacteria, but none considered to be of any significance.
In the first mortality investigated the sheep concerned were stud merinos in good condition and the owner made determined efforts to reduce the mortality without any observable success. Out of the 400 drenched, 35 eventually died despite treatment with sulpha drugs and penicillin. Not all affected sheep died, but those which did not suffered severely in condition and took a long time to recover. In most of the sheep which did not die the swellings broke; in some instances the break taking place into the mouth. In all these latter cases the owner noted the break into the mouth was on the left-hand side and as this was the side on which the sheep were drenched it seems likely that the mortality was due to damage done at drenching which allowed the entry of infection. Nevertheless, as has been said, no evidence of damage was to be seen on the buccal membrane prior to the break developing and any such damage, therefore, must have been of a very minor nature.