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This article was published in 1961
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Survey of Avian Tuberculosis
W. B. Harding, B.V.Sc., Veterinary Inspector, Tamworth
Avian tuberculosis may be defined as a contagious disease caused by Mycobacterium tuberculosis avium. The disease is characterised by its insidious chronicity, its long continuation in a flock once it becomes established and by its tendency to induce in affected birds lowered egg production, unthriftiness and eventually death.
The Causative Agent
There are three main strains of Mycobacterium tuberculosis: avian, bovine and human. The disease in poultry is caused by the avian strain. The bovine strain mainly affects cattle and to a lesser extent pigs, humans, dogs, cats and occasionally birds. The human strain affects mainly humans but may affect dogs, cattle, cats and occasionally caged birds. The avian strain, besides being responsible for the disease in poultry, readily affects pigs, occasionally sheep and rabbits and very rarely humans.
Pathogenicity for Other Birds
All species of birds are capable of being infected with avian tubercle bacilli, but domesticated birds are affected more frequently than those living in a wild or free state. Among domesticated birds other than fowls in which tuberculosis may occur are turkeys, ducks, geese, swans and peacocks. Pigeons are more resistant than fowls. Parrots and canaries are less susceptible to avian tubercle bacilli than to the mammalian forms of the organism.
Among wild fowl, tuberculosis is infrequent. However, pheasants are markedly susceptible. Overseas the disease has been observed in the sparrow, crow, barn owl, cowbirds, blackbird, sparrow hawk, black headed gull, and the jackdaw. In Australia it has been found in a brown hawk and a wild duck.
Tuberculosis is common in birds in zoological gardens and usually the infectious agent is the avian tubercle bacillus.
Pathogenicity for Mammals
Under conditions of natural exposure it is very exceptional for aggressive, extensive tuberculosis to develop in mammals (other than rabbits and swine) as a consequence of avian tubercle bacilli. However, the organisms may multiply in the tissues for some time and may induce a state of sensitivity to tuberculin, even though no apparent alterations in the tissues can be found. Although natural infection of mammals fails in most cases to produce a serious disease condition similar to that in fowls, it is possible to produce extensive changes in some mammals by introducing the agent artificially.
Cattle
Avian tubercle bacillus has a limited pathogenicity for cattle. The morbid changes produced are inclined to remain localised and show the histological changes recognised as tuberculosis. Following natural exposure to avian tubercle bacilli, cattle may become sensitised to avian tuberculin, and some of the animals may react to mammalian tuberculin also. This makes the interpretation of the tuberculin test more difficult and uncertain.
Swine
Swine are readily infected naturally with avian tubercle bacilli. In those states of U.S.A. where the incidence of tuberculosis in fowls is high there is a parallel incidence in swine. Despite the fact that tuberculosis has practically been eliminated in cattle in that country, in 1954 3.9% of pigs slaughtered were affected. Undoubtedly the vast proportion of these affected pigs had contracted the disease from infected fowls. In U.S.A. probably 90% of the tuberculosis lesions in swine are caused by the avian organism.
Humans
Man is very resistant to avian tuberculosis. Fewer than 100 cases of tuberculosis reputed to be caused by the avian type of tubercle bacillus have been reported from all over the world. Apparently man can resist this type of infection, or sufficient exposure to produce the disease is lacking. We do not eat raw poultry meat. Eggs from tuberculosis hens sometimes contain tubercle bacilli, but as a rule diseased hens lay few or no eggs. Further, eggs usually are cooked; so few virulent tubercle bacilli are thus eaten.
Incidence and Geographic Distribution
1. Overseas. Tuberculosis in fowls is spread widely over the civilised countries of the world, although it occurs more frequently in the North Temperate Zone than elsewhere.
The highest incidence in fowls appears to be in the U.S.A.; where it was first recognised about 1900. but not known to be distributed widely until 1920. There is an extremely high incidence in the corn belt, or the north central States, where 50% of the fowl population is located. The incidence of Avian Tuberculosis is indicated by the following summary of testing of poultry in 1946-49. in Iowa, one of the States in the Corn Belt:—
| Flocks (No.) | Birds (No.) | Positive (No.) | Positive (%) | Flocks Positive (No.) | Flocks Positive (%) |
|---|---|---|---|---|---|
| 468 | 97,323 | 3,926 | 4.03 | 211 | 45.08 |
In Canada the incidence in the various Provinces varies from one to 26%. It occurs to a limited extent in the Panama Canal Zone and has been observed infrequently in Chile, Cuba and Puerto Rico.
The condition occurs also in most European countries. It is rather prevalent in England, Germany and certain of the Baltic States.
It has been observed, too, in Indonesia: but is rare in the Philippines. Also noted in the Union of South Africa and in New Zealand.
2. Australia. It appears that the first record of Avian Tuberculosis in this country was in Victoria in 1927. Generally in Australia it is not of economic importance in the recognised poultry districts; apparently the reason being that the only introductions to commercial poultry farms are day-old chickens. Similarly in the U.S.A., it is not a problem on the large commercial poultry farms.
It has been found in ducks in Victoria and in turkeys in New South Wales.
The disease exists in pigs in New South Wales, Victoria, South Australia and Tasmania. The position has not been surveyed closely but it is believed not to be widespread in pigs except in North-western Victoria, South Australia and Tasmania.
South Australia is the only State in which it is believed that Avian Tuberculosis has occurred in cattle: though sensitivity to Avian tuberculin has been detected in dairy cattle in New South Wales.
Avian Tuberculosis is not prevalent in the main dairying districts of Australia and is therefore not considered to be of great economic importance in cattle. Further, only very occasionally has it been a complicating factor in the tuberculin testing of cattle.
It has been recorded twice in wild birds in Australia - in a brown hawk and a wild duck; taken from areas where the disease is enzootic in domestic poultry. However, Avian Tuberculosis often is seen in all classes of birds in zoological gardens in Australia.
The position in the various States:—
New South Wales - Avian Tuberculosis was first diagnosed in the Corowa district in 1940, but it apparently had been present there in 1937. Three outbreaks occurred in the next five years; all being in the Riverina. It appeared that the infection had spread from Victoria. Then, in 1946, the disease was detected on two farms in the Grafton District; without any history of birds having been introduced from Victoria.
By 1960, Avian Tuberculosis had broken out in eighteen additional flocks of fowls and three flocks of turkeys. Between then and 1952 several further outbreaks occurred; again mainly in the Riverina.
Up till 1953 no outbreaks had occurred in the main poultry farming areas; viz:— around Sydney, Tamworth and Young. In that year an outbreak occurred in the outer Metropolitan area at Casula. Since then two outbreaks have occurred in Cumberland, two in Tamworth and one in the Young district.
From 1952 until 1959 outbreaks have occurred as follows:—
| 1952 | 1953 | 1954 | 1955 | 1956 | 1957 | 1958 | 1959 | Tl. | |
|---|---|---|---|---|---|---|---|---|---|
| Albury | 2 | 1 | 1 | 4 | 3 | 3 | 3 | 1 | 18 |
| Condobolin | — | — | 1 | — | — | — | — | — | 1 |
| Corowa | 1 | — | — | — | — | — | 1 | — | 2 |
| Cumberland | — | — | — | — | 1 | — | 1 | — | 2 |
| Forbes | — | — | — | — | 1 | — | — | — | 1 |
| Jerilderie-Deniliquin | 2 | — | 2 | — | — | — | — | — | 4 |
| Goulburn | — | — | — | 1 | — | — | — | — | 1 |
| Gundagai | — | — | 1 | — | — | — | — | — | 1 |
| Moss Vale | — | 2 | — | — | — | 1 | — | — | 3 |
| Narrandera | — | 1 | — | — | — | — | — | — | 1 |
| Moulamein | — | — | — | — | — | — | — | 1 | 1 |
| Tamworth | — | — | — | 1 | — | — | 1 | — | 2 |
| Wagga | 3 | 3 | 3 | 2 | 5 | 1 | 1 | — | 18 |
| Young | — | — | — | — | 1 | — | — | — | 1 |
| TOTAL | 8 | 7 | 8 | 8 | 11 | 5 | 7 | 2 | 56 |
In all, approximately 90 outbreaks were recorded from 1940 to 1959. Very few of these occurred on commercial poultry farms; that is, where the owner has relied on poultry as his only source of income.
Very little is known about the incidence of Avian Tuberculosis in pigs in this State. It was first recorded in a pig in July, 1951; this animal being from the Forbes District. The outbreak in fowls at Loomberah, Tamworth, in 1958 was discovered following a check as a result of a pig being condemned for tuberculosis. There was no evidence of bovine tuberculosis on this property and it is reasonable to suspect that the avian type organism was present in the pig.
Victoria — Between 1927 and 1950, Avian Tuberculosis became widespread and was found in poultry on 320 farms, but was known to have occurred on more. As in N.S.W., the disease has been found on only a few commercial poultry farms.
The incidence of Avian Tuberculosis in pigs is not known fully. There was a report in 1952 of 559 pigs tested with avian tuberculin showing 45 reactors. Lesions were found in thirty-one (5.5%) of the reactors, and avian type organisms were recovered.
South Australia — Avian Tuberculosis was first encountered in 1934, but not seen again until 1945. The disease is fairly widespread but the majority of the outbreaks have occurred in the densely settled areas within a 50 miles radius of Adelaide. Again only a few outbreaks have occurred on large commercial poultry farms.
Clapp carried out a survey on swine in 1955; when he examined 420 glands from pigs. These glands were believed by Meat Inspectors to be showing lesions of Tuberculosis. From 167 of these glands mycobacteria were isolated. Of these, six were of the bovine type, 18 were saprophytic mycobacteria, and the remaining 143 were strains of the avian type.
Only five of the pigs examined had generalised tuberculosis and from these the bovine strain was isolated. The conclusion was reached that in South Australia almost all the cases of Tuberculosis in swine are due to the avian type; the bovine strain being found rarely.
Tasmania — Avian Tuberculosis is widespread in that State, but again is seen infrequently in commercial flocks.
Tuberculosis in pigs is confined mostly to the avian type. This is due to the fact that poultry are allowed free range and pigs and poultry freely intermingle. Also, Bovine Tuberculosis has been reduced to a very low level in Tasmania.
Age in Relation to Incidence
The incidence of infection is considerably higher in birds over one year of age, than in birds under one year. This is well illustrated by the following data:— 28 flocks in one county in Illinois were tuberculin tested and 14 (or 50%) contained tuberculous birds. In these flocks of 1,476 hens more than one year old, 11.1% were infected. In 1056 pullets less than one year old in the same flocks, the incidence determined by the tuberculin test was 0.19%. In Nebraska, on testing 40,073 fowls the incidence was found to be 9.3%. Of these, 77.6% of the infected birds were more than one year, and 22.4% were one year of age or less.
Tuberculosis is less prevalent in young birds, not because they are more resistant than older birds, but because in older birds the disease has had greater opportunity to become established as a consequence of longer exposure to infection.
Sources of Infection
Undoubtedly in most instances the disease commences in a healthy flock due to the introduction of diseased birds. However, there have been many outbreaks of Tuberculosis in poultry where this explanation apparently does not apply. Just what part infected native birds play in the spread of infection is not known; since opportunities to examine carcases of the latter seldom occur.
Another possible source of infection is the feeding of uncooked garbage, which may contain offal from tuberculous fowls.
There is no evidence that chickens hatched from eggs laid by infected hens may contract the disease and so introduce it into a healthy flock. Providing they are reared in a non infected environment they should remain tubercle-free.
Symptoms
Affected birds are languid and depressed. A white diarrhoea is often evident. A striking loss of weight becomes apparent and there may be complete atrophy of the pectoral muscles.
The feathers have a dull ruffled appearance. The comb and wattles usually become thinner and anaemic. Icterus, indicating hepatic changes. is often a striking symptom.
In many cases the bird reveals a unilateral lameness which is due to tuberculous involvement of bone marrow of a leg.
In Australia, affected birds usually die within a few weeks of the appearance of the first symptoms. Overseas reports indicate that the disease often takes a more protracted course. Death finally occurs from exhaustion or haemorrhage as a result of rupture of the liver or spleen.
Diagnosis
Convincing proof of a tuberculous infection can be obtained by necropsy. There are two pathological findings which are characteristic:
(i) character and distribution of lesions in the abdomen; associated in many cases with lesions in the bone marrow, and
(ii) the presence in the tissues of acid fast bacilli. The latter are very significant as they do not occur in any other spontaneous disease of fowls.
The Tuberculin Test
(1) Technique of test — The bird is restrained so that the head is completely immobile. Using a Dr. Raison's all-metal dental syringe as used for tuberculin testing of cattle, about 0.05 ml. of avian tuberculin is injected into the dermis of the wattle; which is held between the thumb and forefinger of one hand.
(2) The reaction — Examination is made 48 hours later. Using the uninjected wattle for comparison, a positive reaction is indicated by an oedematous swelling at the site of injection. The reactions are of variable magnitude, some are small while others increase the thickness of the wattle one to five times.
The reliability of the test can be illustrated best by quoting Robin's results in South Australia. They show that 623 positive reactors were obtained from 3,052 birds tested on 16 farms. No visible lesions were detected in 45 reactors (13.8%). Only 1078 non-reactors were examined; 54 had lesions (19.9%); 23 of the birds being grossly infected cases.
The general opinion of the test is that, although it is relatively high in its efficiency, it is not reliable enough to be employed solely as a procedure for the eradication of the disease from infected flocks.
Post-mortem Lesions
Pathological changes are those of infectious granuloma, but while lesions have a general similarity to those of Tuberculosis of mammals there are certain characteristic distinctions.
Distribution of Lesions
Infection of the majority of fowls occurs via the digestive tract. Lesions are seen most frequently on the liver, spleen, intestines and bone marrow. The lungs are affected frequently, but not as often as the liver and spleen. The tuberculous bacillaemia, which probably occurs early in most infected birds, provides opportunity for widespread distribution of lesions. The only tissues which appear to be immune from possible infection are those of the central nervous system.
Anatomy of Lesions
In the organs of predilection occur irregular nodules, varying in size from those hardly discernible to those up to an inch or so in diameter. The colour of these nodules is usually yellowish, but may be greyish-yellow or greyish-white. The liver and spleen usually undergo considerable hypertrophy.
The nodules are easily enucleated from the liver and spleen. They are firm but incise readily as no mineral salts are present. On cross section the nodule is fibrous and there may be a number of small yellowish foci, or a single soft, yellowish central region which is frequently caseous. The latter is surrounded by a fibrous capsule, the continuity of which often is interrupted by small circumscribed necrotic foci.
The number of lesions is variable; ranging from a few to innumerable. Usually a few large nodular lesions occur in the liver or spleen; associated with an enormous number of lesions of minute to moderate size.
Spread of Infection
An infected environment is the most important factor in the perpetuation of the disease. The occurrence of ulcerated tuberculous lesions in the intestines leads to the constant voiding in the faeces of tremendous numbers of virulent bacteria. Organisms from the liver lesions also enter the faeces via the common duct. Consequently infected faecal material is mainly responsible for the setting up of an infected environment.
Elimination of bacteria from the respiratory tract, especially if lesions are present in the tracheal mucosa, in addition to the lungs will also lead to contamination of the environment.
Vectors. There is a possibility that vectors have a role in the dissemination of avian tubercle bacilli from infected to healthy flocks. However, it is not considered that they are responsible for the considerable amount of infection that exists in an infected flock.
Eggs. There is no clear evidence that Tuberculosis can be transmitted through the eggs from tuberculous hens. On the contrary, it appears that day-old chickens hatched from eggs from infected hens, if reared out of possible contact with infection, will remain tubercle-free.
Control of Avian Tuberculosis
It is considered generally that the tuberculin test is not reliable enough to be used to eradicate the disease from a flock.
Overseas the recommendation has been made to restock each year with day-old chickens and only maintain a pullet flock; the assumption being that very few birds develop a generalised form of tuberculosis whilst they are pullets. Thus they do not become faecal excretors of the causal organism. This method means living with the disease and could be advocated only where the disease is widespread.
In areas where the incidence is low the policy should be complete eradication of the disease. The procedure should be:—
(a) Dispose of the entire infected flock.
(b) Set up new premises on clean ground, well away from the infected environment — if that is possible. Care should be taken to see that this area will not become contaminated by drainage, or the wind blowing infected material from the old site.
(c) Only day-old chickens should be used to start the new flock.
(d) Infected premises or contaminated ground should not be used for two years on account of the longevity of the avian bacillus.
If it is not practicable to set up new premises on clean ground the new flock should be:—
(i) Preferably housed in cages, or
(ii) Run on deep litter in houses with concrete floors
In areas where the disease is widespread, or in the case of commercial poultry farms, where for economic reasons the above recommendation may not be feasible, the following modified scheme is suggested:—
(i) Dispose of for slaughter any birds older than pullets.
(ii) Tuberculin test the pullets.
(iii) Keep the flock in cages or on deep litter.
(iv) Restock only with day-old chickens.
(v) Dispose of the remainder of the original flock at the end of the laying period. Then sheds and floors should be thoroughly disinfected; also cages, if used. Or, if on deep litter, the old litter should be removed completely.
References:
- Clapp, K. N. (1956) — Aust. vet. J., 32: 110
- Division of An. Ind., N.S.W. — Personal communication
- Edgar, G. (1950) — Aust. vet. J., 26: 278
- Feldman, W. H. (1944) — Biester and Deuvies, Diseases of Poultry: 271
- Lee, C. D. (1955) — Proceedings Book, Am. Vet. Med. Assn.: 420
- Luke, D. (1954) — Vet. Rec., 66: 448
- Rae, R. (1951) — Aust. vet. J., 27: 209
- Robin, A. H. (1950) — Aust. vet. J., 26: 274
- Seddon, H. R. (1953) — Diseases of Domestic Animals in Australia, Part 5: 1: 154
- United States Department of Agriculture, The Yearbook of Agriculture (1956) — 219