- Email: [email protected]
The Effect of Vitamin A Deficiency on Malposition of the Chick Embryo*
T h e Effect of Vitamin A Deficiency on Malposition of the Chick Embryo* H. D. POLK AND G. R. SiPEf
Poultry Department, Mississippi State College, State College, Mississippi (Received for publication March 11, 1940)
M
ALPOSITION and mortality of the chick embryo has received a great deal of attention in recent years by research workers. The purpose of this research has been to determine the exact cause of mortality and malposition. Results to date are not in complete agreement as to whether mortality and malposition are due to environmental, nutritional, or inherited factors, or a combination of these sources. H u t t and Pilkey (1932) classified malposition of the chick embryo into six types, and made a study of 18 days' incubation with eggs placed horizontally as compared with eggs with the large end raised 45 degrees. In eggs incubated horizontally, the frequency of malposition was 10.1 percent in embryos alive at 18 days, or 60.4 percent in those dying after that age. In eggs with the large end raised, the frequency of malposition was 10.7 percent in embryos alive at 18 days, or 65.9 percent in those dying after that age. The frequency of position head between thighs was twice as great in the tilted as in the horizontal, and beak over wing was 25 percent higher in tilted than in horizontal. Head in small end was * Contribution from the Department of Poultry Husbandry, Mississippi Agricultural Experiment Station, State College, Mississippi. Published with the approval of the director, Mississippi Agricultural Experiment Station. Paper No. 30, New Series, February, 1940. t Assistant poultry husbandman and poultry husbandman.
twice as common, and embryos rotated from air cell thrice as common in horizontal as in tilted eggs. Over a three-year period these differences were consistent in eggs, and were significant. They further pointed out that by combining the desirable features of both positions mortality could be reduced approximately 6 to 8 percent. Waters (1935) states that "The evidence is conclusive that embryonic change in position takes place within the eggs after the eighteenth day of incubation, and that certain of previously designated malpositions are but a natural occurrence in the normal development of the chick embryo." Asmundson (1938) examined embryos that failed to hatch from turkeys, chickens, pheasants, and partridges, and from 5,000 embryos that were examined he found the position of the turkey, partridge, and pheasant comparable to those of the chick, and that species differences were not significant. He also suggests that the difference of the incidence of embryos with head to the left from different species and hens may be due to hereditary factors. Cavers and Hutt (1934) said that mortality for embryos normally oriented was significantly lower than those abnormally oriented. Abnormal orientation apparently did not affect the vitality of the embryo until the last four days of incubation. The occurrence of embryos upside down and head in small end of the egg was five times as frequent in those which had been oriented towards the small end of the eggs on
[396]
VITAMIN A DEFICIENCY AND MALPOSITION OF THE CHICK EMBRYO
'
the fourth day as among those normally oriented. Eggs oriented within 37.5 degrees of the small end of the egg were incubated in a tilted position with the large end up; the frequency of malposition was reduced to 1.9 percent, but for those eggs in a horizontal position the frequency was 9 percent. Tilting the eggs did not materially reduce malposition of the embryo having the original orientation. Dove (1934) is of the opinion that defective embryos are associated with nutrition of the dam, thus-the correlation between embryo position and mortality is in part due to effect of breeding, of feeding, and of incubation methods. Many of the embryos started the normal shift in position as a secondary effect of the true lethal factor. Upp (1934) reported that of 4,180 dead embryos, 63.79 percent showed abnormalities of various types. Of 14.54 percent leg malformation, chondrodystrophy made up 6.55 percent of the dead embryos or 1.79 percent of all eggs incubated, hemorrhage accounted for 6.67 percent, edema 3.17 percent, and malposition, 22.94 percent of all embryos dying in the shell. He agreed with Dove (1934) that the method of feeding and breeding has a definite bearing on the number of abnormalities. He suggests that >some abnormalities of the chick embryo are due to the sex linked factor, and that sons were found to be carriers. Landauer (1936) reported abnormalities in chick embryos due to a restricted calcification of the periphery of the bone, low and irregular cartilage columns, and small cartilage cells. The long bones of the wings and legs were shortened, and the wings were also affected. This condition was contributed to a prenatal nutritional deficiency. Lyons and Insko (1937) found hens on rations low in manganese produced eggs with low hatchability, with a peak of embryo mortality on the twentieth and
397
twenty-first day of incubation. Embryos that died after 10 days of incubation were chondrodystrophic, characterized by short thickened legs, short wings, parrot beaks, protruding abdomens, and retarded down and body growth. Normal embryonic development occurred within 15 days after hens on a deficient ration were supplied with manganese, sunlight, range, and green feed. Taylor (1932) states "There was no relationship between orientation and other common malposition." Smith (1930) made a study with animal proteins alone, and in combinations with and without cod liver oil for the summer and winter hatching season. The study involved five malpositions covering a period of over two years. The percentage of malpositions for the summer and winter seasons were practically identical except in the case of position 1, which showed a marked decrease durng the summer months. The results secured suggest a genetic and possibly a dietary influence on the abnormal condition of dead chicks in the shell. EXPERIMENTAL
The experiment covered the period from May 15, 1936, to May 15, 1939. Rhode Island Red yearling hens were carefully selected, equalized, and divided into two lots. Lot 1, vitamin A deficient, and lot 2, vitamin A adequate, were further subdivided into four pens, so that one male could be alternated every other day between vitamin A deficient and vitamin A adequate pens. The object of alternating the males between pens and rations was to equalize breeding as much as possible. All males used throughout the test were closely related. The hens were confined in two 18 by 20 feet shed type, open front, 100 hen size, Mississippi laying houses. Each house wasdivided into four pens, each 5 by 18 feet,
398
H. D. POLK AND G. R.
with an average of seven birds to each pen per year. Pine needles and servall litter were used to prevent the birds from picking up any source of vitamin A from the litter. It was necessary to replace part or all of the hens used in the test at the end of each year. The replacement of hens was followed with the same precautions as carried out in the initial selection. No eggs were incubated until the hens had been on feed for a period of three months. The hens were trapped, and each egg numbered, so that an accurate record could be kept on each individual of each lot. Feed consumption, mortality, and egg production records were kept for each pen for the duration of the test. TABLE 1.—Rations used in experiment in pounds Vitamin A adequate Yellow corn meal White corn meal Wheat shorts Wheat bran Shrimp meal Cod liver oil Oyster shell Salt Tobacco dust
30 20 20 20 10 .33 Ad lib. .5 2
Vitamin A deficient 30 20 20 20 10 Ad lib. .5 2
Table 1 gives the rations used in the test. The rations were all mash and identical except the vitamin A adequate ration carried 0.33 pound of cod liver oil per 100 pounds of mash. The cod liver oil carried 3,000 units of vitamin A per gram. The vitamin A deficient ration was equivalent to the ration used by Sherwood (1932), except the test conducted at the Texas Station was a mash and grain ration and the ration used in this test was an all mash ration. Sherwood and Frapps (by the Sherman-Munsell unit method with rats) determined the daily intake of vitamin A on this ration to be 120 units. The vitamin A potency of the egg yolk was shown to decrease from 20 units per gram
SIPE
of egg yolk to S units per gram of egg yolk over a period of 6.5 months, which clearly indicates a deficiency of vitamin A in the ration. They found the normal vitamin A potency of the egg yolk to be 20 units to the gram of yolk, or 300 units for an egg of standard size. They further estimated each unit in the egg represented 6.3 units in the feed. Therefore, a hen laying IS eggs per month with 10 units of vitamin A to the gram would require approximately 450 units per day above maintenance requirements. The vitamin A adequate ration contained 120 units of vitamin A plus 1,120 units from cod liver oil, or a maximum of 1,240 units daily. The requirements for a 150 egg hen was estimated by the Texas Station to be 600 units per day. Due to the evidence presented by the work conducted at the Texas Station, rat feeding trials were not considered as essential in this test. The eggs were incubated at 100°F. in a forced air draft incubator, and turned three times per day, morning, noon, and night. The incubation covered all seasons of the year, and in no instance were the eggs over 12 days old when set. All eggs were candled on the eighteenth day of incubation to remove the infertile eggs and dead germs. All embryos showing considerable development, the lives of which were in doubt, were left in the incubator. All eggs which failed to hatch were carefully broken, and the position of the embryo determined and recorded. A record was also kept of all malformed chicks and the dam from which they came. There was no attempt to determine the cause of death of any embryo which died prior to the eighteenth day; such embryos were classified as dead germs. The malpositions were classified as follows: (1) head between legs, (2) head in small end of egg, (3) beak under left wing, (4) head away from air cell,
VITAMIN TABLE 1 .—Egg
A
D E F I C I E N C Y AND M A L P O S I T I O N
OF T H E
CHICK
399
EMBRYO
production, feed consumption, mortality, and number of birds on vitamin A adequate and vitamin A deficient rations from May 15, 1936, to May 15, 1939 Vitamin A adequate
Vitamin A deficient
Years
Number of hens
Production
Feed consumed
Mortality
Number of hens
Production
Feed consumed
Mortality
1936 1937 1938
28 24 32
2971 2349 3046
2223.75 1953 2050
4 4 8
28 24 32
2679 1428 1992
2316.75 1824.50 1934
4 6 15
Total
84
8366
6226.75
16
84
6099
6075.25
25
(5) feet over head, and (6) beak over right wing. By comparison of the results presented in Table 2 it will be noted that the hens receiving the vitamin A adequate ration produced 8,366 eggs as compared to 6,099 eggs produced by the hens on vitamin A deficient ration, or a difference of 2,267
dition and general health of the birds receiving cod liver oil as a source of vitamin A was good, while the birds on the ration deficient in vitamin A showed several cases of nutritional roup, especially during the latter part of the year. Tables 3 and 4 summarize the incubation results, giving the number of mal-
TABLE 3.—Incubation results, number and kind of malposition for vitamin A deficient ration from May 15, 1936, to May 15,1939 Eggs set
Chicks
1936 1937 1938
883 576 882
Total
2,341
Years
Malposition
Years
Eggs set
Normal unhatched
Dead germs
53 43 51
332 104 160
33 31 30
80 38 118
147
596
94
236
1
2
3
4
5
6
Total
385 360 520
0 0 3
16 13 11
6 2 6
11 7 12
0 3 2
0 0 0
20 18 20
1,265
3
40
14
30
5
0
58
eggs. Mortality was nine birds less in the vitamin A adequate ration. The difference in feed consumption was not as significant between the two lots of birds, being only 151.5 pounds. The difference in feed consumption could be easily due to the greater number of birds surviving and egg production in the vitamin A adequate group. ConTABLE 4.-
Infertile
Malformed
formed and malposition embryos by years for a three year period. It is interesting to note that there is very little difference over a three-year period between the number of the respective types of malpositions for vitamin A adequate and vitamin A deficient rations. From a total of 3,156 eggs set from hens receiving an adequate amount
-Incubation results, number and kind of malposition for vitamin A adequate ration from May 15, 1936 to May 15, 1939 MalChicks formed
Malposition 1
2
3
4
5
6
Total
Infertile
Normal Dead unhatched germs
1936 1937 1938
857 946 1,354
380 551 707
0 0 3
8 6 17
2 6 3
7 7 11
0 0 0
0 0 1
8 7 27
25 26 59
335 245 361
25 33 57
92 91 167
Total
3,157
1,638
3
31
11
25
0
1
42
110
941
115
350
400
H. D. POLK AND G. R. SIPE
of vitamin A, 31 chicks were in type 1, head between legs; 11 in type 2, head in small end of the egg; 25 in type 3, beak under left wing; none in type 4, head away from air cell; 1 in type 5, feet over head; and 42 in type 6, beak over right wing. From a total of 2,341 eggs set from the hens receiving a ration deficient in vitamin A, 40 chicks were in type 1, 14 were in type 2, 30 were in type 3, 5 were in type 4, none were in type S, and 58 were in type 6. It will be noted that in all types but one, hens receiving a ration deficient in vitamin A produced a greater number of malposition than hens fed an adequate amount of vitamin A. The one exception was type 5. Types 1, 3, and 6 constituted the majority of all embryos showing malposition for both rations. Out of a total of 226 malpositions occurring in both rations for types 1,3, and 6, the vitamin A deficient ration produced 30 more than did the vitamin A adequate ration. For all types there was a total of 110 for the ration adequate in vitamin A and 147 for the ration deficient in vitamin A, or a difference of 37. A percentage analysis of the data involving the total number of malpositions from the vitamin A adequate and the vitamin A deficient rations may be applied. This analysis, based on the fertile eggs set, shows that 4.9 percent of the eggs from the vitamin A adequate ration developed embryos in malposition as compared to 8.4 percent from the vitamin A deficient ration. The difference of the percentages divided by the standard error of the difference, gives value of 4.37 which is significant. ^ A similar analysis of the differences of the six types gave a significant value of 3.1 for type 6. The number of malformed embryos was small and identical in both rations, and occurred during the third year of the test. The cause of the malformed embryos, while not definitely apparent, was probably due to a deficiency of vitamin G.
CONCLUSIONS
1. In this study of relationship between vitamin A and malposition of embryo, there / were more malpositions in five types from ' birds on vitamin A deficient ration. 2. The difference in number of malpositions in respective types on vitamin A adequate and deficient- rations was significant-, for type 6.(^4^ f-^"* /^<^tv<3. The difference between tire totals of malpositions from birds on vitamin A adequate and deficient rations was 37 more V from deficient. The percentage difference was significant and definitely suggests a relationship between vitamin A and malposition. 4. The incidence of malformation was apparently not associated with the quantity of vitamin A in the ration. r ( ( _, £
Xjsj
VYREttimcEiV
(^H^-^
"''
'"•)•
Asmunds^h, V. S.M938. The position of turkey,^" chicken, pheasant^ and partridge embryos that fail to hatch. Poultry Sci. vol. 17, no. 6. Cavers, J. R., and F. B. Hutt, 1934. The relationship between abnormal orientation of 4-day embryo and position of the chick at hatching. Journal Agr. research. 48:517-531. Dove, W. F., 1934. Poultry investigations in Maine. Maine Sta. Bui. 377, pp. 369-374, fig. I. Hutt, F. B., and A. M. Pilkey, 1930, 31, 32. Studies in embryonic mortality in fowls vs. relationship between position of the egg and frequencies of malposition. Poul. Sci. 13(1):3-13. Landauer, W., 1936. Micromelia of chicken embryos and newly hatched chicks caused by nutritional deficiency. Anat. Rec. 64(2) :267-276. Lyons, M., and W. M. Insko, Jr., 1937. Chondrodystrophy in the chick embryo produced by manganese deficiency in the diet of the hen. Ky. Sta. Bui. No. 371. pp. 61-75, fig. 2. Sherwood, R. M., and G. S. Frapps, 1932. The quantities of vitamin A required by pullets for maintenance and for egg production. Texas Agri. Exp. Sta. Bui. 468. Smith, J. B., 1930. Malposition a factor in hatchability. Proceedings Poul. Sci. 22 Annual meeting, pp. 66-71. Taylor, Lewis W., 1932. Early orientation of the chick embryo in relation to malposition and hatchability abstract and notes presented 24th annual meeting, Poul. Sci. Asso.
Poultry Department, Mississippi State College, State College, Mississippi (Received for publication March 11, 1940)
M
ALPOSITION and mortality of the chick embryo has received a great deal of attention in recent years by research workers. The purpose of this research has been to determine the exact cause of mortality and malposition. Results to date are not in complete agreement as to whether mortality and malposition are due to environmental, nutritional, or inherited factors, or a combination of these sources. H u t t and Pilkey (1932) classified malposition of the chick embryo into six types, and made a study of 18 days' incubation with eggs placed horizontally as compared with eggs with the large end raised 45 degrees. In eggs incubated horizontally, the frequency of malposition was 10.1 percent in embryos alive at 18 days, or 60.4 percent in those dying after that age. In eggs with the large end raised, the frequency of malposition was 10.7 percent in embryos alive at 18 days, or 65.9 percent in those dying after that age. The frequency of position head between thighs was twice as great in the tilted as in the horizontal, and beak over wing was 25 percent higher in tilted than in horizontal. Head in small end was * Contribution from the Department of Poultry Husbandry, Mississippi Agricultural Experiment Station, State College, Mississippi. Published with the approval of the director, Mississippi Agricultural Experiment Station. Paper No. 30, New Series, February, 1940. t Assistant poultry husbandman and poultry husbandman.
twice as common, and embryos rotated from air cell thrice as common in horizontal as in tilted eggs. Over a three-year period these differences were consistent in eggs, and were significant. They further pointed out that by combining the desirable features of both positions mortality could be reduced approximately 6 to 8 percent. Waters (1935) states that "The evidence is conclusive that embryonic change in position takes place within the eggs after the eighteenth day of incubation, and that certain of previously designated malpositions are but a natural occurrence in the normal development of the chick embryo." Asmundson (1938) examined embryos that failed to hatch from turkeys, chickens, pheasants, and partridges, and from 5,000 embryos that were examined he found the position of the turkey, partridge, and pheasant comparable to those of the chick, and that species differences were not significant. He also suggests that the difference of the incidence of embryos with head to the left from different species and hens may be due to hereditary factors. Cavers and Hutt (1934) said that mortality for embryos normally oriented was significantly lower than those abnormally oriented. Abnormal orientation apparently did not affect the vitality of the embryo until the last four days of incubation. The occurrence of embryos upside down and head in small end of the egg was five times as frequent in those which had been oriented towards the small end of the eggs on
[396]
VITAMIN A DEFICIENCY AND MALPOSITION OF THE CHICK EMBRYO
'
the fourth day as among those normally oriented. Eggs oriented within 37.5 degrees of the small end of the egg were incubated in a tilted position with the large end up; the frequency of malposition was reduced to 1.9 percent, but for those eggs in a horizontal position the frequency was 9 percent. Tilting the eggs did not materially reduce malposition of the embryo having the original orientation. Dove (1934) is of the opinion that defective embryos are associated with nutrition of the dam, thus-the correlation between embryo position and mortality is in part due to effect of breeding, of feeding, and of incubation methods. Many of the embryos started the normal shift in position as a secondary effect of the true lethal factor. Upp (1934) reported that of 4,180 dead embryos, 63.79 percent showed abnormalities of various types. Of 14.54 percent leg malformation, chondrodystrophy made up 6.55 percent of the dead embryos or 1.79 percent of all eggs incubated, hemorrhage accounted for 6.67 percent, edema 3.17 percent, and malposition, 22.94 percent of all embryos dying in the shell. He agreed with Dove (1934) that the method of feeding and breeding has a definite bearing on the number of abnormalities. He suggests that >some abnormalities of the chick embryo are due to the sex linked factor, and that sons were found to be carriers. Landauer (1936) reported abnormalities in chick embryos due to a restricted calcification of the periphery of the bone, low and irregular cartilage columns, and small cartilage cells. The long bones of the wings and legs were shortened, and the wings were also affected. This condition was contributed to a prenatal nutritional deficiency. Lyons and Insko (1937) found hens on rations low in manganese produced eggs with low hatchability, with a peak of embryo mortality on the twentieth and
397
twenty-first day of incubation. Embryos that died after 10 days of incubation were chondrodystrophic, characterized by short thickened legs, short wings, parrot beaks, protruding abdomens, and retarded down and body growth. Normal embryonic development occurred within 15 days after hens on a deficient ration were supplied with manganese, sunlight, range, and green feed. Taylor (1932) states "There was no relationship between orientation and other common malposition." Smith (1930) made a study with animal proteins alone, and in combinations with and without cod liver oil for the summer and winter hatching season. The study involved five malpositions covering a period of over two years. The percentage of malpositions for the summer and winter seasons were practically identical except in the case of position 1, which showed a marked decrease durng the summer months. The results secured suggest a genetic and possibly a dietary influence on the abnormal condition of dead chicks in the shell. EXPERIMENTAL
The experiment covered the period from May 15, 1936, to May 15, 1939. Rhode Island Red yearling hens were carefully selected, equalized, and divided into two lots. Lot 1, vitamin A deficient, and lot 2, vitamin A adequate, were further subdivided into four pens, so that one male could be alternated every other day between vitamin A deficient and vitamin A adequate pens. The object of alternating the males between pens and rations was to equalize breeding as much as possible. All males used throughout the test were closely related. The hens were confined in two 18 by 20 feet shed type, open front, 100 hen size, Mississippi laying houses. Each house wasdivided into four pens, each 5 by 18 feet,
398
H. D. POLK AND G. R.
with an average of seven birds to each pen per year. Pine needles and servall litter were used to prevent the birds from picking up any source of vitamin A from the litter. It was necessary to replace part or all of the hens used in the test at the end of each year. The replacement of hens was followed with the same precautions as carried out in the initial selection. No eggs were incubated until the hens had been on feed for a period of three months. The hens were trapped, and each egg numbered, so that an accurate record could be kept on each individual of each lot. Feed consumption, mortality, and egg production records were kept for each pen for the duration of the test. TABLE 1.—Rations used in experiment in pounds Vitamin A adequate Yellow corn meal White corn meal Wheat shorts Wheat bran Shrimp meal Cod liver oil Oyster shell Salt Tobacco dust
30 20 20 20 10 .33 Ad lib. .5 2
Vitamin A deficient 30 20 20 20 10 Ad lib. .5 2
Table 1 gives the rations used in the test. The rations were all mash and identical except the vitamin A adequate ration carried 0.33 pound of cod liver oil per 100 pounds of mash. The cod liver oil carried 3,000 units of vitamin A per gram. The vitamin A deficient ration was equivalent to the ration used by Sherwood (1932), except the test conducted at the Texas Station was a mash and grain ration and the ration used in this test was an all mash ration. Sherwood and Frapps (by the Sherman-Munsell unit method with rats) determined the daily intake of vitamin A on this ration to be 120 units. The vitamin A potency of the egg yolk was shown to decrease from 20 units per gram
SIPE
of egg yolk to S units per gram of egg yolk over a period of 6.5 months, which clearly indicates a deficiency of vitamin A in the ration. They found the normal vitamin A potency of the egg yolk to be 20 units to the gram of yolk, or 300 units for an egg of standard size. They further estimated each unit in the egg represented 6.3 units in the feed. Therefore, a hen laying IS eggs per month with 10 units of vitamin A to the gram would require approximately 450 units per day above maintenance requirements. The vitamin A adequate ration contained 120 units of vitamin A plus 1,120 units from cod liver oil, or a maximum of 1,240 units daily. The requirements for a 150 egg hen was estimated by the Texas Station to be 600 units per day. Due to the evidence presented by the work conducted at the Texas Station, rat feeding trials were not considered as essential in this test. The eggs were incubated at 100°F. in a forced air draft incubator, and turned three times per day, morning, noon, and night. The incubation covered all seasons of the year, and in no instance were the eggs over 12 days old when set. All eggs were candled on the eighteenth day of incubation to remove the infertile eggs and dead germs. All embryos showing considerable development, the lives of which were in doubt, were left in the incubator. All eggs which failed to hatch were carefully broken, and the position of the embryo determined and recorded. A record was also kept of all malformed chicks and the dam from which they came. There was no attempt to determine the cause of death of any embryo which died prior to the eighteenth day; such embryos were classified as dead germs. The malpositions were classified as follows: (1) head between legs, (2) head in small end of egg, (3) beak under left wing, (4) head away from air cell,
VITAMIN TABLE 1 .—Egg
A
D E F I C I E N C Y AND M A L P O S I T I O N
OF T H E
CHICK
399
EMBRYO
production, feed consumption, mortality, and number of birds on vitamin A adequate and vitamin A deficient rations from May 15, 1936, to May 15, 1939 Vitamin A adequate
Vitamin A deficient
Years
Number of hens
Production
Feed consumed
Mortality
Number of hens
Production
Feed consumed
Mortality
1936 1937 1938
28 24 32
2971 2349 3046
2223.75 1953 2050
4 4 8
28 24 32
2679 1428 1992
2316.75 1824.50 1934
4 6 15
Total
84
8366
6226.75
16
84
6099
6075.25
25
(5) feet over head, and (6) beak over right wing. By comparison of the results presented in Table 2 it will be noted that the hens receiving the vitamin A adequate ration produced 8,366 eggs as compared to 6,099 eggs produced by the hens on vitamin A deficient ration, or a difference of 2,267
dition and general health of the birds receiving cod liver oil as a source of vitamin A was good, while the birds on the ration deficient in vitamin A showed several cases of nutritional roup, especially during the latter part of the year. Tables 3 and 4 summarize the incubation results, giving the number of mal-
TABLE 3.—Incubation results, number and kind of malposition for vitamin A deficient ration from May 15, 1936, to May 15,1939 Eggs set
Chicks
1936 1937 1938
883 576 882
Total
2,341
Years
Malposition
Years
Eggs set
Normal unhatched
Dead germs
53 43 51
332 104 160
33 31 30
80 38 118
147
596
94
236
1
2
3
4
5
6
Total
385 360 520
0 0 3
16 13 11
6 2 6
11 7 12
0 3 2
0 0 0
20 18 20
1,265
3
40
14
30
5
0
58
eggs. Mortality was nine birds less in the vitamin A adequate ration. The difference in feed consumption was not as significant between the two lots of birds, being only 151.5 pounds. The difference in feed consumption could be easily due to the greater number of birds surviving and egg production in the vitamin A adequate group. ConTABLE 4.-
Infertile
Malformed
formed and malposition embryos by years for a three year period. It is interesting to note that there is very little difference over a three-year period between the number of the respective types of malpositions for vitamin A adequate and vitamin A deficient rations. From a total of 3,156 eggs set from hens receiving an adequate amount
-Incubation results, number and kind of malposition for vitamin A adequate ration from May 15, 1936 to May 15, 1939 MalChicks formed
Malposition 1
2
3
4
5
6
Total
Infertile
Normal Dead unhatched germs
1936 1937 1938
857 946 1,354
380 551 707
0 0 3
8 6 17
2 6 3
7 7 11
0 0 0
0 0 1
8 7 27
25 26 59
335 245 361
25 33 57
92 91 167
Total
3,157
1,638
3
31
11
25
0
1
42
110
941
115
350
400
H. D. POLK AND G. R. SIPE
of vitamin A, 31 chicks were in type 1, head between legs; 11 in type 2, head in small end of the egg; 25 in type 3, beak under left wing; none in type 4, head away from air cell; 1 in type 5, feet over head; and 42 in type 6, beak over right wing. From a total of 2,341 eggs set from the hens receiving a ration deficient in vitamin A, 40 chicks were in type 1, 14 were in type 2, 30 were in type 3, 5 were in type 4, none were in type S, and 58 were in type 6. It will be noted that in all types but one, hens receiving a ration deficient in vitamin A produced a greater number of malposition than hens fed an adequate amount of vitamin A. The one exception was type 5. Types 1, 3, and 6 constituted the majority of all embryos showing malposition for both rations. Out of a total of 226 malpositions occurring in both rations for types 1,3, and 6, the vitamin A deficient ration produced 30 more than did the vitamin A adequate ration. For all types there was a total of 110 for the ration adequate in vitamin A and 147 for the ration deficient in vitamin A, or a difference of 37. A percentage analysis of the data involving the total number of malpositions from the vitamin A adequate and the vitamin A deficient rations may be applied. This analysis, based on the fertile eggs set, shows that 4.9 percent of the eggs from the vitamin A adequate ration developed embryos in malposition as compared to 8.4 percent from the vitamin A deficient ration. The difference of the percentages divided by the standard error of the difference, gives value of 4.37 which is significant. ^ A similar analysis of the differences of the six types gave a significant value of 3.1 for type 6. The number of malformed embryos was small and identical in both rations, and occurred during the third year of the test. The cause of the malformed embryos, while not definitely apparent, was probably due to a deficiency of vitamin G.
CONCLUSIONS
1. In this study of relationship between vitamin A and malposition of embryo, there / were more malpositions in five types from ' birds on vitamin A deficient ration. 2. The difference in number of malpositions in respective types on vitamin A adequate and deficient- rations was significant-, for type 6.(^4^ f-^"* /^<^tv<3. The difference between tire totals of malpositions from birds on vitamin A adequate and deficient rations was 37 more V from deficient. The percentage difference was significant and definitely suggests a relationship between vitamin A and malposition. 4. The incidence of malformation was apparently not associated with the quantity of vitamin A in the ration. r ( ( _, £
Xjsj
VYREttimcEiV
(^H^-^
"''
'"•)•
Asmunds^h, V. S.M938. The position of turkey,^" chicken, pheasant^ and partridge embryos that fail to hatch. Poultry Sci. vol. 17, no. 6. Cavers, J. R., and F. B. Hutt, 1934. The relationship between abnormal orientation of 4-day embryo and position of the chick at hatching. Journal Agr. research. 48:517-531. Dove, W. F., 1934. Poultry investigations in Maine. Maine Sta. Bui. 377, pp. 369-374, fig. I. Hutt, F. B., and A. M. Pilkey, 1930, 31, 32. Studies in embryonic mortality in fowls vs. relationship between position of the egg and frequencies of malposition. Poul. Sci. 13(1):3-13. Landauer, W., 1936. Micromelia of chicken embryos and newly hatched chicks caused by nutritional deficiency. Anat. Rec. 64(2) :267-276. Lyons, M., and W. M. Insko, Jr., 1937. Chondrodystrophy in the chick embryo produced by manganese deficiency in the diet of the hen. Ky. Sta. Bui. No. 371. pp. 61-75, fig. 2. Sherwood, R. M., and G. S. Frapps, 1932. The quantities of vitamin A required by pullets for maintenance and for egg production. Texas Agri. Exp. Sta. Bui. 468. Smith, J. B., 1930. Malposition a factor in hatchability. Proceedings Poul. Sci. 22 Annual meeting, pp. 66-71. Taylor, Lewis W., 1932. Early orientation of the chick embryo in relation to malposition and hatchability abstract and notes presented 24th annual meeting, Poul. Sci. Asso.