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Aetiology of food-related oral lesions in chickens
Research in Veterinary Science 1986, 40, 219-224
Aetiology of food-related oral lesions in chickens M. J. GENTLE, Agricultural and Food Research Council's Poultry Research Centre, Roslin, Midlothian EH259PS
Brown Leghorn chickens fed on a mash diet developed ulcerated oral lesions with extensive epithelial erosion and large colonies of bacteria. Some birds had lesions by six weeks old and by 30 weeks oral lesions were present in all birds fed on a mash diet. These lesions occur infrequently in birds fed a pelleted diet and the relatively extensive lesions shown by birds on a mash diet heal quickly (in many cases within two weeks) when the birds are transferred to a pelleted diet. The cause of the lesion is unknown but there was no evidence for food impaction, mechanical damage to the epithelium, specific dietary constituents or blocked salivary ducts. The lesions may be due to poor oral hygiene which results from the lack of mechanical stimulation of the oral epithelium to which fine particles of mash adhere. THE presence of oral lesions in flocks of chickens are usually noticed when the lesions become so large that the swollen tissue is visible from an external examination of the bird. They are usually considered to be caused by food impaction. In a series of recent experiments to measure taste sensitivity of adult hens great difficulty was found in selecting birds without signs of oral lesions. A brief survey of some of the adult hens kept at the Poultry Research Centre (White Leghorn type, Brown Leghorn, Brown Medium hybrid) showed that the lesions were present in all the strains examined. It also appeared that the condition was more prevalent in birds fed on a mash diet than on a pelleted diet. A search of the literature (Hungerford 1970, Sainsbury 1980, Gordon and Jordan 1981, Hofstad et al 1984) failed to produce any references to the condition. It was therefore decided to investigate the pathology of the lesions, their onset and development and the effects of dietary manipulation. Materials and methods
Pathology Ten adult Brown Leghorn hens with oral lesions at various stages of development were killed by cervical dislocation. The damaged areas of the buccal epithelium were removed and fixed in 10 per cent formol
saline. After fixation the tissue was embedded in paraffin wax and cut vertically at 8/-1m. Serial sections were taken through the lesions and all sections were stained with haematoxylin and eosin (H&E).
Experimental procedure Sixty-three Brown Leghorn chicks of both sexes which had been bred at the Poultry Research Centre were used. They were allowed access to food and water ad libitum. Of these chicks 45 were fed on a chick starter mash up to six to eight weeks old, when they were transferred to a grower mash. The diet was changed again at 16 weeks old to a layer mash. The composition of these mash diets are shown in Table 1 and a particle size analysis of the layers' mash is shown in Table 2. The remaining 18 chicks were fed on the same diet which had been steam pelleted. They were fed small pellets (4 mm in diameter) as chicks and larger pellets (6 mm diameter) as the birds grew older (at six to eight weeks of age). The oral cavities of all the birds were examined at six, 16,21,23,26,27 and 30 weeks old. The presence and position of any oral lesions were noted. At 32 weeks old all of the birds which had been fed on a mash diet were transferred to the pelleted diet
TABLE 1: Composition of the diets used (kg 1000 kg- 1)
Barley Maize Wheat Herring meal Soya Meat and bone meal Grass meal Limestone Dicalcium phosphate 'Vitamin mix number 3 'Vitamin mix number 4 • Mineral mix number 5 Salt Pancoxin! amprolmix • Bolton and Blair 11974)
219
Chick starter
Grower
100
300
300
200
245 50 220
o
50 5·3 21·7 2·5 2·5 2·5 2·5
0·454
280 35 100
o
50 10·0 17·5 2·5 2·5 2·5 2·5 0·368
Layer! breeder
255 242 193 48
104 19
50 68 14
2·5 2·5 2·5 2·0 0·556
220
M. J. Gentle
\1/ .
.~
De
-Oe"
b
.'
."
e
and their mouths were examined for lesions at 34· 5 and 37 weeks old. Ten of the birds which had been fed on the pelleted diet up to 32 weeks old were transferred to the mash diet and were also examined at 34· 5 and 37 weeks.
Results
Pathology When they first appeared the lesions were small pinhead-sized areas sometimes light yellow in colour but more often black. They occurred in the buccal epithelium throughout the entire oral cavity including
FIG 1: Photomicrographs of 8 I'm section of the buccal epithelium stained with haematoxylin and eosin. Ep Epidermis, De Dermis, PI Plug of tissue debris, Bc Bacterial colonies. Oe Lakes of oedema. la) Section 18 I'm) through a lesion at an early stage in its development and showing Slight thinning of the epithelium and accumulated tissue debris. H&E x 26. Ib) This shows a more advanced lesion and considerable thinning of the epithelium. The plug of tissue debris is much thicker and there are numerous bacterial colonies present. H&E x 26. (c) The epithelium has been completely eroded and bacterial colonies are present adjacent to the dermal tissue. H&E x 26. td) In this case the lesion has extended into the dermal tissue and lakes of oedema are present. H&E x 60. (e) This is a higher magnification of part of section b (as shown by the box) and shows heterophils in the epithelial and subepithelial tissue. H&E x 142. If I This is a higher magnification of part of section c (as shown by the box) where it can be seen that as well as heterophils being present there are reactive fibroblasts and proliferating capillaries. H&E x 142
the tongue. In the more advanced condition there were characteristically two large lesions, one on each side of the buccal epithelium of the lower jaw (Fig 3), with numerous smaller lesions elsewhere in the mouth. In the early development of the lesions the epithelial damage was slight (Fig la). The epithelium
Oral lesions in chickens TABLE 2: Particle size analysis of layers mash diet British Standards mesh number
% mash retained 1-62 4·63 8·23 12·33 13·15 14·00
8 12 16 22 30
44 60 85 Base
9'38 8·42 25,02
20
Discussion
'#. 60
'iii
2 s:
.§
Dietary manipulation
40
80
The percentage of the birds fed on a mash diet exhibiting oral lesions at the age examined is shown in Fig 2. By 16 weeks, 16 per cent of the birds had developed lesions. At this stage, however, the lesions were very small. By 21 weeks, 29 per cent of the birds had lesions and the number of birds developing lesions increased in almost a linear fashion up to 30 weeks old when all birds had oral lesions present. Though all birds had lesions present by 30 weeks, the size and distribution of the lesions varied considerably. Some birds had a few pinhead sized lesions, while others had large lesions similar to those shown in Fig 3 together with large numbers of smaller lesions throughout the entire oral cavity. At 30 weeks none of the birds fed a pelleted diet had any oral lesions. Though oral lesions were occasionally observed in the birds fed on a pelleted diet, they were always small and apparently healed quickly. Thus at 28 weeks 10 per cent of the birds had lesions but these had disappeared by 30 weeks old.
All the birds which had been fed on the mash diet up to 32 weeks of age showed lesions before being transferred to the pelleted diet. After 2· 5 weeks on the pelleted diet only 34 per cent still showed lesions and only 6 per cent still had lesions present after five weeks. The 6 per cent which still had lesions at five weeks were those birds which had had the largest lesions. Fig 3, IlIa, b, IVa and b compares the mouth of two birds before they were transferred to pellets and after five weeks of being fed the pelleted diet. Transferring 32-week-old birds from the pelleted diet to the mash diet resulted in the birds rapidly developing oral lesions. After 2· 5 weeks 78 per cent of the birds had developed lesions and 2· 5 weeks later 80 per cent of the birds had developed lesions (Fig 3, IlIa, b, IVa and b) .
100
c:
In three birds the bacteria in the lesions were cultured and they were found to consist mainly of streptococci, staphylococci and, in one bird, Pasteurella multocida. There was no sign of any fungal infection.
Onset and development
showed some thinning and accumulated tissue debris was seen attached to the outer layers but there was no evidence of accumulating vegetable matter. While some of the lesions were connected with the pores of the salivary glands, lesions were also observed in areas not adjacent to these pores. At this early stage of the development of the lesion a careful examination of the serial sections did not produce any evidence of any mechanical injury to the epithelium. Fig Ib shows a more advanced lesion. The epithelium was still intact but considerably thinner and the plug of tissue debris was much thicker. There were numerous colonies of bacteria present and heterophils were clearly seen in the epithelium and subepithelial tissue (Fig l e). Again the plug was composed primarily of necrotic cells and tissue debris with little vegetable matter. In the more advanced lesions the epithelium was eroded and numerous bacterial colonies were present adjacent to the dermis tissue (Fig lc). In some cases the damage extended into the dermis and considerable oedema was present (Fig Id) together with heterophils, reactive fibroblasts and proliferating capillaries (Fig I f).
0
221
"E iii
Age of birds (weeks)
26
30
FIG 2: Percentage of Brown Leghorn chickens showing oral lesions when fed on a mash diet recorded at intervals from six to 30 weeks old
When chickens were fed a fine mash diet, food was often seen adhering to the buccal epithelium but the almost total absence of vegetable matter within the plug of tissue debris of the lesion would indicate that the lesions were not caused by food impaction. There was also no evidence of food particles damaging the epithelium and blocked salivary ducts did not appear
222
M. J. Gentle
b
b FIG 3: Oral cavity showing the development and regression of oral lesions following dietary manipulation. I and II are two birds photographed at 32 weeks of age after having been fed on a pelleted diet (a) and after five weeks on a mash diet Ibl. III and IV are two birds of a similar age which had been on a mash diet (a) and after five weeks on a pelleted diet (bl
223
Oral lesions in chickens
Ilia
b
IVa
b
25mm
224
M. J. Gentle
to be the prime cause of the lesion. The bacterial colonies present were those which would normally be present in the environment and although P multocida was identified it was only present in one of the three birds examined. No lesions were seen in chicks and although some lesions were present at 16 weeks old they were small. There was a rapid increase in the number of animals with oral lesions after 16 weeks of age, with the biggest increase from 20 to 30 weeks. Birds fed on a pelleted diet of the same composition as the mash diet did not develop extensive lesions and this would argue against any specific dietary component being responsible. The lesions healed quickly when the birds were transferred to a pelleted diet. Although birds fed on a pelleted diet sometimes developed small lesions, these usually healed quickly and did not get progressively worse. While there is no data concerning oral lesions in commercial flocks of poultry a recent article (Anon 1984) on the work of Eldridge and Engster reported that of 100 white-egg layers 25 per cent had lesions in the roof of the oral cavity and all feed samples were negative for T-2 toxin. It would therefore appear that oral lesions are present in commercial flocks and the results presented here would suggest that particle size of the food is a major factor; however, the minimum particle size necessary for their prevention has not yet been determined. It is difficult to know the cause for the development of oral lesions but it is possible that in birds fed on a fine mash diet food particles cling to the epithelium,
and also that the lack of hard food particles of the correct size may prevent mechanical stimulation of the buccal epithelium. These two factors may result in a build up of pockets of oral bacteria which lead to subsequent epithelial erosion. This problem may therefore be, in many respects, one of oral hygiene. Acknowledgements I wish to thank Mr C. J. R. Randall, Ministry of Agriculture, Fisheries and Food, Veterinary Laboratory, Lasswade, who identified the bacteria and Dr P. A. L. Wight for his help with pathological interpretation of the lesions. Thanks are also due to Miss L. Hunter for her technical assistance and Mr N. Russell for his photographic skills. References ANON (1984) Feedstuffs 56, 18 BOLTON, W. & BLAIR, R. (1974) Poultry Nutrition, 4th edn. Bulletin of the Ministry of Agriculture, Fisheries and Food GORDON, R. F. & JORDAN, F. T. W. (1982) Poultry Diseases, 2nd edn. London, Bailliere, Tindall HOFSTAD, M. S., BARNES, H. J., CALNEK, B. W., REID, W. M. & YODER, JR., H. W. (1984) Diseases of Poultry, 8th edn. Ames, Iowa State University Press HUNGERFORD, T. G. (1970) Diseases of Poultry. Sydney, Angus and Robertson SAINSBURY, D. (1980) Poultry Health and Management. London, Granada
Accepted July 4, 1985
Aetiology of food-related oral lesions in chickens M. J. GENTLE, Agricultural and Food Research Council's Poultry Research Centre, Roslin, Midlothian EH259PS
Brown Leghorn chickens fed on a mash diet developed ulcerated oral lesions with extensive epithelial erosion and large colonies of bacteria. Some birds had lesions by six weeks old and by 30 weeks oral lesions were present in all birds fed on a mash diet. These lesions occur infrequently in birds fed a pelleted diet and the relatively extensive lesions shown by birds on a mash diet heal quickly (in many cases within two weeks) when the birds are transferred to a pelleted diet. The cause of the lesion is unknown but there was no evidence for food impaction, mechanical damage to the epithelium, specific dietary constituents or blocked salivary ducts. The lesions may be due to poor oral hygiene which results from the lack of mechanical stimulation of the oral epithelium to which fine particles of mash adhere. THE presence of oral lesions in flocks of chickens are usually noticed when the lesions become so large that the swollen tissue is visible from an external examination of the bird. They are usually considered to be caused by food impaction. In a series of recent experiments to measure taste sensitivity of adult hens great difficulty was found in selecting birds without signs of oral lesions. A brief survey of some of the adult hens kept at the Poultry Research Centre (White Leghorn type, Brown Leghorn, Brown Medium hybrid) showed that the lesions were present in all the strains examined. It also appeared that the condition was more prevalent in birds fed on a mash diet than on a pelleted diet. A search of the literature (Hungerford 1970, Sainsbury 1980, Gordon and Jordan 1981, Hofstad et al 1984) failed to produce any references to the condition. It was therefore decided to investigate the pathology of the lesions, their onset and development and the effects of dietary manipulation. Materials and methods
Pathology Ten adult Brown Leghorn hens with oral lesions at various stages of development were killed by cervical dislocation. The damaged areas of the buccal epithelium were removed and fixed in 10 per cent formol
saline. After fixation the tissue was embedded in paraffin wax and cut vertically at 8/-1m. Serial sections were taken through the lesions and all sections were stained with haematoxylin and eosin (H&E).
Experimental procedure Sixty-three Brown Leghorn chicks of both sexes which had been bred at the Poultry Research Centre were used. They were allowed access to food and water ad libitum. Of these chicks 45 were fed on a chick starter mash up to six to eight weeks old, when they were transferred to a grower mash. The diet was changed again at 16 weeks old to a layer mash. The composition of these mash diets are shown in Table 1 and a particle size analysis of the layers' mash is shown in Table 2. The remaining 18 chicks were fed on the same diet which had been steam pelleted. They were fed small pellets (4 mm in diameter) as chicks and larger pellets (6 mm diameter) as the birds grew older (at six to eight weeks of age). The oral cavities of all the birds were examined at six, 16,21,23,26,27 and 30 weeks old. The presence and position of any oral lesions were noted. At 32 weeks old all of the birds which had been fed on a mash diet were transferred to the pelleted diet
TABLE 1: Composition of the diets used (kg 1000 kg- 1)
Barley Maize Wheat Herring meal Soya Meat and bone meal Grass meal Limestone Dicalcium phosphate 'Vitamin mix number 3 'Vitamin mix number 4 • Mineral mix number 5 Salt Pancoxin! amprolmix • Bolton and Blair 11974)
219
Chick starter
Grower
100
300
300
200
245 50 220
o
50 5·3 21·7 2·5 2·5 2·5 2·5
0·454
280 35 100
o
50 10·0 17·5 2·5 2·5 2·5 2·5 0·368
Layer! breeder
255 242 193 48
104 19
50 68 14
2·5 2·5 2·5 2·0 0·556
220
M. J. Gentle
\1/ .
.~
De
-Oe"
b
.'
."
e
and their mouths were examined for lesions at 34· 5 and 37 weeks old. Ten of the birds which had been fed on the pelleted diet up to 32 weeks old were transferred to the mash diet and were also examined at 34· 5 and 37 weeks.
Results
Pathology When they first appeared the lesions were small pinhead-sized areas sometimes light yellow in colour but more often black. They occurred in the buccal epithelium throughout the entire oral cavity including
FIG 1: Photomicrographs of 8 I'm section of the buccal epithelium stained with haematoxylin and eosin. Ep Epidermis, De Dermis, PI Plug of tissue debris, Bc Bacterial colonies. Oe Lakes of oedema. la) Section 18 I'm) through a lesion at an early stage in its development and showing Slight thinning of the epithelium and accumulated tissue debris. H&E x 26. Ib) This shows a more advanced lesion and considerable thinning of the epithelium. The plug of tissue debris is much thicker and there are numerous bacterial colonies present. H&E x 26. (c) The epithelium has been completely eroded and bacterial colonies are present adjacent to the dermal tissue. H&E x 26. td) In this case the lesion has extended into the dermal tissue and lakes of oedema are present. H&E x 60. (e) This is a higher magnification of part of section b (as shown by the box) and shows heterophils in the epithelial and subepithelial tissue. H&E x 142. If I This is a higher magnification of part of section c (as shown by the box) where it can be seen that as well as heterophils being present there are reactive fibroblasts and proliferating capillaries. H&E x 142
the tongue. In the more advanced condition there were characteristically two large lesions, one on each side of the buccal epithelium of the lower jaw (Fig 3), with numerous smaller lesions elsewhere in the mouth. In the early development of the lesions the epithelial damage was slight (Fig la). The epithelium
Oral lesions in chickens TABLE 2: Particle size analysis of layers mash diet British Standards mesh number
% mash retained 1-62 4·63 8·23 12·33 13·15 14·00
8 12 16 22 30
44 60 85 Base
9'38 8·42 25,02
20
Discussion
'#. 60
'iii
2 s:
.§
Dietary manipulation
40
80
The percentage of the birds fed on a mash diet exhibiting oral lesions at the age examined is shown in Fig 2. By 16 weeks, 16 per cent of the birds had developed lesions. At this stage, however, the lesions were very small. By 21 weeks, 29 per cent of the birds had lesions and the number of birds developing lesions increased in almost a linear fashion up to 30 weeks old when all birds had oral lesions present. Though all birds had lesions present by 30 weeks, the size and distribution of the lesions varied considerably. Some birds had a few pinhead sized lesions, while others had large lesions similar to those shown in Fig 3 together with large numbers of smaller lesions throughout the entire oral cavity. At 30 weeks none of the birds fed a pelleted diet had any oral lesions. Though oral lesions were occasionally observed in the birds fed on a pelleted diet, they were always small and apparently healed quickly. Thus at 28 weeks 10 per cent of the birds had lesions but these had disappeared by 30 weeks old.
All the birds which had been fed on the mash diet up to 32 weeks of age showed lesions before being transferred to the pelleted diet. After 2· 5 weeks on the pelleted diet only 34 per cent still showed lesions and only 6 per cent still had lesions present after five weeks. The 6 per cent which still had lesions at five weeks were those birds which had had the largest lesions. Fig 3, IlIa, b, IVa and b compares the mouth of two birds before they were transferred to pellets and after five weeks of being fed the pelleted diet. Transferring 32-week-old birds from the pelleted diet to the mash diet resulted in the birds rapidly developing oral lesions. After 2· 5 weeks 78 per cent of the birds had developed lesions and 2· 5 weeks later 80 per cent of the birds had developed lesions (Fig 3, IlIa, b, IVa and b) .
100
c:
In three birds the bacteria in the lesions were cultured and they were found to consist mainly of streptococci, staphylococci and, in one bird, Pasteurella multocida. There was no sign of any fungal infection.
Onset and development
showed some thinning and accumulated tissue debris was seen attached to the outer layers but there was no evidence of accumulating vegetable matter. While some of the lesions were connected with the pores of the salivary glands, lesions were also observed in areas not adjacent to these pores. At this early stage of the development of the lesion a careful examination of the serial sections did not produce any evidence of any mechanical injury to the epithelium. Fig Ib shows a more advanced lesion. The epithelium was still intact but considerably thinner and the plug of tissue debris was much thicker. There were numerous colonies of bacteria present and heterophils were clearly seen in the epithelium and subepithelial tissue (Fig l e). Again the plug was composed primarily of necrotic cells and tissue debris with little vegetable matter. In the more advanced lesions the epithelium was eroded and numerous bacterial colonies were present adjacent to the dermis tissue (Fig lc). In some cases the damage extended into the dermis and considerable oedema was present (Fig Id) together with heterophils, reactive fibroblasts and proliferating capillaries (Fig I f).
0
221
"E iii
Age of birds (weeks)
26
30
FIG 2: Percentage of Brown Leghorn chickens showing oral lesions when fed on a mash diet recorded at intervals from six to 30 weeks old
When chickens were fed a fine mash diet, food was often seen adhering to the buccal epithelium but the almost total absence of vegetable matter within the plug of tissue debris of the lesion would indicate that the lesions were not caused by food impaction. There was also no evidence of food particles damaging the epithelium and blocked salivary ducts did not appear
222
M. J. Gentle
b
b FIG 3: Oral cavity showing the development and regression of oral lesions following dietary manipulation. I and II are two birds photographed at 32 weeks of age after having been fed on a pelleted diet (a) and after five weeks on a mash diet Ibl. III and IV are two birds of a similar age which had been on a mash diet (a) and after five weeks on a pelleted diet (bl
223
Oral lesions in chickens
Ilia
b
IVa
b
25mm
224
M. J. Gentle
to be the prime cause of the lesion. The bacterial colonies present were those which would normally be present in the environment and although P multocida was identified it was only present in one of the three birds examined. No lesions were seen in chicks and although some lesions were present at 16 weeks old they were small. There was a rapid increase in the number of animals with oral lesions after 16 weeks of age, with the biggest increase from 20 to 30 weeks. Birds fed on a pelleted diet of the same composition as the mash diet did not develop extensive lesions and this would argue against any specific dietary component being responsible. The lesions healed quickly when the birds were transferred to a pelleted diet. Although birds fed on a pelleted diet sometimes developed small lesions, these usually healed quickly and did not get progressively worse. While there is no data concerning oral lesions in commercial flocks of poultry a recent article (Anon 1984) on the work of Eldridge and Engster reported that of 100 white-egg layers 25 per cent had lesions in the roof of the oral cavity and all feed samples were negative for T-2 toxin. It would therefore appear that oral lesions are present in commercial flocks and the results presented here would suggest that particle size of the food is a major factor; however, the minimum particle size necessary for their prevention has not yet been determined. It is difficult to know the cause for the development of oral lesions but it is possible that in birds fed on a fine mash diet food particles cling to the epithelium,
and also that the lack of hard food particles of the correct size may prevent mechanical stimulation of the buccal epithelium. These two factors may result in a build up of pockets of oral bacteria which lead to subsequent epithelial erosion. This problem may therefore be, in many respects, one of oral hygiene. Acknowledgements I wish to thank Mr C. J. R. Randall, Ministry of Agriculture, Fisheries and Food, Veterinary Laboratory, Lasswade, who identified the bacteria and Dr P. A. L. Wight for his help with pathological interpretation of the lesions. Thanks are also due to Miss L. Hunter for her technical assistance and Mr N. Russell for his photographic skills. References ANON (1984) Feedstuffs 56, 18 BOLTON, W. & BLAIR, R. (1974) Poultry Nutrition, 4th edn. Bulletin of the Ministry of Agriculture, Fisheries and Food GORDON, R. F. & JORDAN, F. T. W. (1982) Poultry Diseases, 2nd edn. London, Bailliere, Tindall HOFSTAD, M. S., BARNES, H. J., CALNEK, B. W., REID, W. M. & YODER, JR., H. W. (1984) Diseases of Poultry, 8th edn. Ames, Iowa State University Press HUNGERFORD, T. G. (1970) Diseases of Poultry. Sydney, Angus and Robertson SAINSBURY, D. (1980) Poultry Health and Management. London, Granada
Accepted July 4, 1985