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Observations of Xanthomatosis in Chickens
Observations of Xanthomatosis in Chickens C. F. MEINECKE, A. I. FLOWERS AND J. N. BEASLEY
Department of Veterinary Microbiology, Texas Agricultural Experiment Station, The Agricultural and Mechanical College of Texas, College Station, Texas (Received for publication December 11, 1961)
X
ANTHOMATOSIS, a tumor-like condition affecting primarily the skin and wattles of chickens, apparently has increased in incidence in recent years. Nieberle (1949) reported a xanthoma in a parrot but failed to describe the condition. A localized lesion in a horse was reported by Nitsche (1930). Jarmai (1938) described a generalized case in a horse. The literature contains several reports in which xanthomatosis in humans was apparently related to hepatic involvement, as for example, jaundice (Stolzer, 1950) or hepatic damage (Chanutin and Ludewig, 1937). The first report of this condition in chickens was that of Peckham (1955). He observed the condition in two strains of White Leghorns in the same pen. There were equal numbers of strains A and B, but 40 percent morbidity occurred in the birds of Strain A, whereas, only 2 percent morbidity was observed in birds of Strain B. Birds of varying ages in adjoining pens were not affected. Peckham was unable to correlate the condition in chickens to the disease in man or other animals, nor was he able to determine the etiology. Corner et al. (1959) reported xanthomatosis in two flocks of White Leghorns in Canada. The flocks were widely separated and the etiology was not determined. Additional evidence that xanthomatosis is restricted to no particular area is contained in reports from Alabama (Roberts, 1960) and Georgia (Morris, 1961).
outbreaks in the field. The first recognized case was presented to the laboratory on April 6, 1959. Observations were made on birds from 19 owners, representing 23 flocks. Four strains of White Leghorns and one broiler breed were represented. Thirty-one affected birds have been presented to the laboratory and examined. They ranged in age from five weeks to eighteen months at the time signs of xanthomatosis were first observed. The morbidity varied from less than 1 percent to 33 percent. Standard procedures were used in an attempt to isolate bacterial or viral agents from lesions and body organs. In an effort to transmit the disease, fluid from the lesions of xanthomatosis was applied to the cornea or conjunctiva of ten-week-old White Leghorn males. Serum cholesterol determinations were made by the method of Bloor (1922) modified for use with Hycel cholesterol reagent.* The readings were made on a Bausch and Lomb Spectronic-20. Tissue sections for histopathological studies included the lesions in the skin or subcutaneous tissues, liver, spleen, pancreas, lungs, heart, brain, kidneys, and intestine. These were fixed in 10 percent formalin and stained with Mayer's hemalum and eosin. Frozen sections of selected tissues were stained with Sudan IV. RESULTS AND DISCUSSION
Figure 1 shows the condition as it most frequently is observed. There is a gelat-
PROCEDURE
The cases of xanthomatosis reported in this study were from naturally occurring
* Scientific Products, Division of American Hospital Supply Corporation, Evanston. Illinois.
1207
1208
C. F. MEINECKE, A. I. FLOWERS AND J. N. BEASLEY
edly, the amount of cholesterol in the tissues continues to increase and there is an increasing thickness of skin as the birds grow older. Numerous mononuclear cells with vacuolated cytoplasm were observed in the dermis and subcutaneous tissue, and granulocytes were also present. Cholesterol clefts and multinucleated cells occurred in the more chronic cases. Fat stains revealed the presence of lipids in the cytoplasm of the mononuclear cells. In chronic cases, the occurrence of birefrigent crystals in association with the multinucleated cells was observed when sections were examined with polarized light. While specific lesions in the parenchymatous organs were not observed, a few individual birds did have visceral lymphomatosis. The findings were compatible with the findings of Peckham (1955). No infectious agent was isolated and the disease was not transmitted; however, fluids FIG. 1. The affected areas of the breast, leg and wattles can be seen showing the nature of the lesions.
inous edema of the submandibular region. The skin of the breast or legs or both and the wattles are also involved. All of the lesions may appear simultaneously or singly in a particular bird. The skin lesions in the earlier stages consisted of edema with some thickening and wrinkling. The lesions of the submandibular area may be observed in figure 2 and the skin lesions are apparent in Figure 3. As the disease progresses, the skin adheres to underlying muscles. It becomes dimpled at the feather follicles, rather nodular and tumorous and continues to thicken as the bird grows older. There is a yellow color in all these lesions which Peckham (1955) ascribes as being due to a high cholesterol content. The deepness of the yellow color and, suppos-
FIG. 2. A close-up of the submandibular area which illustrates the glistening nature of the edematous tissue.
1209
XANTHOMATOSIS IN CHICKENS
FIG. 3. The thickened adhesions between the skin and muscle are evident in the plaque-like area on the muscle.
from the lesions did cause an irritation of the eye in inoculated birds. Mortality appears over a prolonged period but is apparently negligible. Hens with xanthomatosis may survive for as much as a year or more while slowly declining in production and condition. Results of analysis for serum cholesterol are inconclusive. A seasonal variation appears to be present since there was a drop in September as compared to August and a rise again in January of the following year (Table 1). However, Peckham (1955) reports his findings were well within normal limits. The average of the cholesterol values for the affected birds was higher than those of the highest of the two controls. The controls in the pens with the affected hens were males. Dukes (1955) gives a total serum cholesterol range from 58 to 94 milligrams per 100 milliliters of serum in laying hens and from 23 to 121 milligrams in nonlayers. No values are given for males.
Published reports and our observations indicate that laying breeds are most often affected and usually these are white birds. It must be realized, however that many breeds of layers are white and that broilers do not live to an age at which the condition would normally be seen. Peckham (1955) was of the opinion that arsenicals may be involved but he was unable to reproduce the disease. His report indicates that there may be a genetic resistance to the condition. Since the liver is an important factor in cholesterol metabolism, it may be that substances or factors causing hepatic damage are a contributing etiological agent. There may be no direct relationship; however, one must observe that xanthomatosis in chickens has appeared with the advent of feed additives and increased in direct correlation with their use. SUMMARY
Xanthomatosis in chickens is being diagnosed with increasing frequency. The paucity of reports in the literature on this conTABLE 1.—Total serum cholesterol levels Milligrams percent of total cholesterol in serum
Affected Birds 1366 1367 1368 1369 1370 1371 1372 1373 1374 1375 1376 1377 1378 1379 1380 1175 1176 1172
F F F F F F F F F F F F F F F F F F
Control Control
M M
Average
August 9, 1960
September 15, I960
January 5, 1961
531.0 286.4 376.2 382.3 361.4 724.9
174.0 127.0 136.0 226.0 177.0 177.0
336.0 355.0
—t
-t 286.0
450.7 76.6 241.4 90.5 297.2 257.7 489.2 441.0
-t —t -t —t
-t
357.6
81.5 195.0 72.5 159.0
-t
163.0 172.0 204.0 186.0 195.0
-t -t 170.7 ( - )
—t
222.0
-t
283.0 328.0 345.0
—t —t 257.0 —t 301.0
222.0 318.0 443.0 363.0
-t 266.0* 310.0* 314.4 ( + )
* N o t included in average. Normal male average was 288 mg.% f No determination made.
1210
C. F. MEINECKE, A. I. FLOWERS AND J. N.
dition indicates that it is relatively new. The birds in this study represent 23 flocks. The incidence of affected birds in the flocks ranges from less than 1 percent to 33 percent. Fluid from the xanthomatosis lesions causes severe irritation to the eyes of tenweek-old cockerels. Attempts to isolate a bacterial or viral agent were unsuccessful. No direct correlation could be made between this condition in chickens and similar conditions in other animals or man. No conclusion can be drawn concerning serum cholesterol levels since no control birds were kept with affected birds and only a few birds were available. According to values given by Dukes (1955) there is some indication that high serum cholesterol may be correlated with the condition. The histopathological studies of tissues from affected birds agree with the findings previously reported. REFERENCES Bloor, W. R., K. F. Pelkam and D. M. Allen, 1922. Determination of fatty acids (and cho-
BEASLEY
lesterol) in small amounts of blood plasma. J. Biol. Chem. 52: 191-205. Chanutin, A., and S. Ludewig, 1937. Blood lipid studies in a case of xanthomatosis associated with hepatic damage. J. Lab. Clin. Med. 22: 903-911. Corner, H. H., J. M. Isa and G. L. Bannister, 1959. Xanthomatosis in White Leghorns in Canada. Can. J. Comp. Med. 23: 6: 199-202. Dukes, H. H.. 1955. The Physiology of Domestic Animals. Seventh Edition. Comstock Publishing Associates, a division of Cornell University Press: 49. Jarmai, K., 1938. Uber Einen Fall von Generalisierter Lipoidose Beim Pferd Archiv. f. Tierheilk. 72: 115-133. Abs. 1938 Vet. Bull. 8: 457. Morris, 1961. Personal communication. Nitsche, O., 1930. Riesenzellen fuhrendes xanthom in der Unterhaut eines Pferdes. Archiv. f. Tierheilk. 62: 97-102. Peckham, M. C , Xanthomatosis in chickens. Am. J. Vet. Res. 16: 6 1 : 580-583. Roberts, C , 1960. Personal communication. Stolzer, O. L., G. Miller and W. A. White, 1950. Post-arsenical obstructive jaundice complicated by xanthomatosis and diabetes mellitus. Am. J. Med. 8: 675. Von Nieberle, K., 1949. Lehrbuch der Speiziellen Pathologischen Anatomie der Haustiere P. Cohrs: 703.
Growth and Feed Utilization of Turkeys as Affected by Reserpine W.
D.
MORRISON
Master Feeds, Division of Maple Leaf Mills Limited, Toronto, Ontario, Canada (Received for publication December 12, 1961)
AORTIC rupture in turkeys was first -**• discussed by Durrell, Pomeroy, Carr and Jerstad in 1952 but was first adequately described by McSherry et al. (1954). Within recent years the severity of the problem has markedly increased. Various changes in management and rations have not altered the course of the condition, Ringer (1959), Morrison (1960). Ringer (1959) suggested that the high
blood pressure of turkeys, particularly males, might account for the incidence of aortic rupture. Carlson (1959), Barnett (1960), Morrison (1960) and Slinger et al. (1961) reported that various levels of reserpine in the diet reduced losses from spontaneously appearing aortic rupture. The effect of reserpine on growth and feed efficiency when fed during the time when losses due to aortic rupture are most
Department of Veterinary Microbiology, Texas Agricultural Experiment Station, The Agricultural and Mechanical College of Texas, College Station, Texas (Received for publication December 11, 1961)
X
ANTHOMATOSIS, a tumor-like condition affecting primarily the skin and wattles of chickens, apparently has increased in incidence in recent years. Nieberle (1949) reported a xanthoma in a parrot but failed to describe the condition. A localized lesion in a horse was reported by Nitsche (1930). Jarmai (1938) described a generalized case in a horse. The literature contains several reports in which xanthomatosis in humans was apparently related to hepatic involvement, as for example, jaundice (Stolzer, 1950) or hepatic damage (Chanutin and Ludewig, 1937). The first report of this condition in chickens was that of Peckham (1955). He observed the condition in two strains of White Leghorns in the same pen. There were equal numbers of strains A and B, but 40 percent morbidity occurred in the birds of Strain A, whereas, only 2 percent morbidity was observed in birds of Strain B. Birds of varying ages in adjoining pens were not affected. Peckham was unable to correlate the condition in chickens to the disease in man or other animals, nor was he able to determine the etiology. Corner et al. (1959) reported xanthomatosis in two flocks of White Leghorns in Canada. The flocks were widely separated and the etiology was not determined. Additional evidence that xanthomatosis is restricted to no particular area is contained in reports from Alabama (Roberts, 1960) and Georgia (Morris, 1961).
outbreaks in the field. The first recognized case was presented to the laboratory on April 6, 1959. Observations were made on birds from 19 owners, representing 23 flocks. Four strains of White Leghorns and one broiler breed were represented. Thirty-one affected birds have been presented to the laboratory and examined. They ranged in age from five weeks to eighteen months at the time signs of xanthomatosis were first observed. The morbidity varied from less than 1 percent to 33 percent. Standard procedures were used in an attempt to isolate bacterial or viral agents from lesions and body organs. In an effort to transmit the disease, fluid from the lesions of xanthomatosis was applied to the cornea or conjunctiva of ten-week-old White Leghorn males. Serum cholesterol determinations were made by the method of Bloor (1922) modified for use with Hycel cholesterol reagent.* The readings were made on a Bausch and Lomb Spectronic-20. Tissue sections for histopathological studies included the lesions in the skin or subcutaneous tissues, liver, spleen, pancreas, lungs, heart, brain, kidneys, and intestine. These were fixed in 10 percent formalin and stained with Mayer's hemalum and eosin. Frozen sections of selected tissues were stained with Sudan IV. RESULTS AND DISCUSSION
Figure 1 shows the condition as it most frequently is observed. There is a gelat-
PROCEDURE
The cases of xanthomatosis reported in this study were from naturally occurring
* Scientific Products, Division of American Hospital Supply Corporation, Evanston. Illinois.
1207
1208
C. F. MEINECKE, A. I. FLOWERS AND J. N. BEASLEY
edly, the amount of cholesterol in the tissues continues to increase and there is an increasing thickness of skin as the birds grow older. Numerous mononuclear cells with vacuolated cytoplasm were observed in the dermis and subcutaneous tissue, and granulocytes were also present. Cholesterol clefts and multinucleated cells occurred in the more chronic cases. Fat stains revealed the presence of lipids in the cytoplasm of the mononuclear cells. In chronic cases, the occurrence of birefrigent crystals in association with the multinucleated cells was observed when sections were examined with polarized light. While specific lesions in the parenchymatous organs were not observed, a few individual birds did have visceral lymphomatosis. The findings were compatible with the findings of Peckham (1955). No infectious agent was isolated and the disease was not transmitted; however, fluids FIG. 1. The affected areas of the breast, leg and wattles can be seen showing the nature of the lesions.
inous edema of the submandibular region. The skin of the breast or legs or both and the wattles are also involved. All of the lesions may appear simultaneously or singly in a particular bird. The skin lesions in the earlier stages consisted of edema with some thickening and wrinkling. The lesions of the submandibular area may be observed in figure 2 and the skin lesions are apparent in Figure 3. As the disease progresses, the skin adheres to underlying muscles. It becomes dimpled at the feather follicles, rather nodular and tumorous and continues to thicken as the bird grows older. There is a yellow color in all these lesions which Peckham (1955) ascribes as being due to a high cholesterol content. The deepness of the yellow color and, suppos-
FIG. 2. A close-up of the submandibular area which illustrates the glistening nature of the edematous tissue.
1209
XANTHOMATOSIS IN CHICKENS
FIG. 3. The thickened adhesions between the skin and muscle are evident in the plaque-like area on the muscle.
from the lesions did cause an irritation of the eye in inoculated birds. Mortality appears over a prolonged period but is apparently negligible. Hens with xanthomatosis may survive for as much as a year or more while slowly declining in production and condition. Results of analysis for serum cholesterol are inconclusive. A seasonal variation appears to be present since there was a drop in September as compared to August and a rise again in January of the following year (Table 1). However, Peckham (1955) reports his findings were well within normal limits. The average of the cholesterol values for the affected birds was higher than those of the highest of the two controls. The controls in the pens with the affected hens were males. Dukes (1955) gives a total serum cholesterol range from 58 to 94 milligrams per 100 milliliters of serum in laying hens and from 23 to 121 milligrams in nonlayers. No values are given for males.
Published reports and our observations indicate that laying breeds are most often affected and usually these are white birds. It must be realized, however that many breeds of layers are white and that broilers do not live to an age at which the condition would normally be seen. Peckham (1955) was of the opinion that arsenicals may be involved but he was unable to reproduce the disease. His report indicates that there may be a genetic resistance to the condition. Since the liver is an important factor in cholesterol metabolism, it may be that substances or factors causing hepatic damage are a contributing etiological agent. There may be no direct relationship; however, one must observe that xanthomatosis in chickens has appeared with the advent of feed additives and increased in direct correlation with their use. SUMMARY
Xanthomatosis in chickens is being diagnosed with increasing frequency. The paucity of reports in the literature on this conTABLE 1.—Total serum cholesterol levels Milligrams percent of total cholesterol in serum
Affected Birds 1366 1367 1368 1369 1370 1371 1372 1373 1374 1375 1376 1377 1378 1379 1380 1175 1176 1172
F F F F F F F F F F F F F F F F F F
Control Control
M M
Average
August 9, 1960
September 15, I960
January 5, 1961
531.0 286.4 376.2 382.3 361.4 724.9
174.0 127.0 136.0 226.0 177.0 177.0
336.0 355.0
—t
-t 286.0
450.7 76.6 241.4 90.5 297.2 257.7 489.2 441.0
-t —t -t —t
-t
357.6
81.5 195.0 72.5 159.0
-t
163.0 172.0 204.0 186.0 195.0
-t -t 170.7 ( - )
—t
222.0
-t
283.0 328.0 345.0
—t —t 257.0 —t 301.0
222.0 318.0 443.0 363.0
-t 266.0* 310.0* 314.4 ( + )
* N o t included in average. Normal male average was 288 mg.% f No determination made.
1210
C. F. MEINECKE, A. I. FLOWERS AND J. N.
dition indicates that it is relatively new. The birds in this study represent 23 flocks. The incidence of affected birds in the flocks ranges from less than 1 percent to 33 percent. Fluid from the xanthomatosis lesions causes severe irritation to the eyes of tenweek-old cockerels. Attempts to isolate a bacterial or viral agent were unsuccessful. No direct correlation could be made between this condition in chickens and similar conditions in other animals or man. No conclusion can be drawn concerning serum cholesterol levels since no control birds were kept with affected birds and only a few birds were available. According to values given by Dukes (1955) there is some indication that high serum cholesterol may be correlated with the condition. The histopathological studies of tissues from affected birds agree with the findings previously reported. REFERENCES Bloor, W. R., K. F. Pelkam and D. M. Allen, 1922. Determination of fatty acids (and cho-
BEASLEY
lesterol) in small amounts of blood plasma. J. Biol. Chem. 52: 191-205. Chanutin, A., and S. Ludewig, 1937. Blood lipid studies in a case of xanthomatosis associated with hepatic damage. J. Lab. Clin. Med. 22: 903-911. Corner, H. H., J. M. Isa and G. L. Bannister, 1959. Xanthomatosis in White Leghorns in Canada. Can. J. Comp. Med. 23: 6: 199-202. Dukes, H. H.. 1955. The Physiology of Domestic Animals. Seventh Edition. Comstock Publishing Associates, a division of Cornell University Press: 49. Jarmai, K., 1938. Uber Einen Fall von Generalisierter Lipoidose Beim Pferd Archiv. f. Tierheilk. 72: 115-133. Abs. 1938 Vet. Bull. 8: 457. Morris, 1961. Personal communication. Nitsche, O., 1930. Riesenzellen fuhrendes xanthom in der Unterhaut eines Pferdes. Archiv. f. Tierheilk. 62: 97-102. Peckham, M. C , Xanthomatosis in chickens. Am. J. Vet. Res. 16: 6 1 : 580-583. Roberts, C , 1960. Personal communication. Stolzer, O. L., G. Miller and W. A. White, 1950. Post-arsenical obstructive jaundice complicated by xanthomatosis and diabetes mellitus. Am. J. Med. 8: 675. Von Nieberle, K., 1949. Lehrbuch der Speiziellen Pathologischen Anatomie der Haustiere P. Cohrs: 703.
Growth and Feed Utilization of Turkeys as Affected by Reserpine W.
D.
MORRISON
Master Feeds, Division of Maple Leaf Mills Limited, Toronto, Ontario, Canada (Received for publication December 12, 1961)
AORTIC rupture in turkeys was first -**• discussed by Durrell, Pomeroy, Carr and Jerstad in 1952 but was first adequately described by McSherry et al. (1954). Within recent years the severity of the problem has markedly increased. Various changes in management and rations have not altered the course of the condition, Ringer (1959), Morrison (1960). Ringer (1959) suggested that the high
blood pressure of turkeys, particularly males, might account for the incidence of aortic rupture. Carlson (1959), Barnett (1960), Morrison (1960) and Slinger et al. (1961) reported that various levels of reserpine in the diet reduced losses from spontaneously appearing aortic rupture. The effect of reserpine on growth and feed efficiency when fed during the time when losses due to aortic rupture are most