A Heritable Crippling Anomaly in the Fowl

A Heritable Crippling Anomaly in the Fowl

64 G . V . MOREJOHN chickens suffering from "hemorrhagic disease" in Israel. Response to a massive dose of injectable menadione sodium bisulfite, i.e...

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G . V . MOREJOHN chickens suffering from "hemorrhagic disease" in Israel. Response to a massive dose of injectable menadione sodium bisulfite, i.e. 1-2 mg. per chick, occurred in a matter of hours. Response to 5 % alfalfa meal in the diet was not as rapid, but was nonetheless complete over a period of days. In an addendum to their paper these authors point to the effect of sulfa drugs as possible causative agents and cite one field case wherein drinking water treatment with sulfamethazine produced characteristic symptoms of the disease. The comprehensive report by T. M. Goldhaft and N. Wernicoff (Tenth World's Poultry Congress, Edinburgh, p. 278, 1954) describes the field results with menadione sodium bisulfite mentioned above. These authors state "The only product which gave any uniform results was menadione bisulfite added to the drinking water at a level of 10 mg. per gallon of water and given continuously to the birds for a period of 48 to 72 hours."

ADDENDUM

ACKNOWLEDGMENT

Attention is called to the paper by Bornstein, S. and Y. Samberg, Poultry Sci., 33: 831-836, 1954, on the correction of abnormal clotting times in

Animal care and conduct of clotting time determinations by Albin Junnila, Burton Main, and Adolph Glabowicz is gratefully acknowledged.

A Heritable Crippling Anomaly in the Fowl G. VICTOR M O R E J O H N

University of California, Davis (Received for publication April 3, 1954)

T

HE present paper describes a new crippling abnormality involving the pelvis and the joints of the leg in the domestic fowl and persents genetic evidence for its inheritance. Many heritable anomalous conditions of the fowl have been reported (reviewed by Hutt, 1949, and Jull, 1952) including several affecting the legs. The abnormalities more closely resembling the one described herein are: Perosis or "slipped tendon," neurolymphomatosis and congenital perosis. Polygenic inheritance of perosis was first demonstrated by Serfontein and Payne (1934). In this abnormality the Achilles tendon slips from the intercondylar groove of the tibial metatarsal joint and the latter bends inward.

The effect of neurolymphomatosis on the sciatic and femoral nerves of the legs causes partial or complete paralysis. An inherited susceptibility to this disease (commonly called "range paralysis") has been shown by Asmundson and Biely (1932), Gildow el al. (1940), Taylor el al. (1943), Hutt and Cole (1947) and many others. Congenital perosis, which is caused by an autosomal recessive gene in homozygous state, is lethal to chicks within a few days after hatching (Bohren, 1951, in Jull, 1952, p. 214). Another condition which resembles the anomaly to be described is "curled toe paralysis," but the inheritance of this defect has not been demonstrated. It is caused by a dietary deficiency of riboflavin

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1954. Vitamin K requirements of adult dogs and the influence of bile on its absorption from the intestine. Am. J. Physiol. 176: 239-242. Reynolds, W. M., W. K. Warden and H. G. Luther, 1953-1954. Antibiotics, vitamin K and bloodclotting time in poultry. Antibiotics Annual, 380-385. Sorbye, O., I. Kruse and H. Dam, 1953. Activity of cosmene and alloocimene as coagulation factors. Acta. Chem. Scan. 7: 1015-1016. Stamler, F. W., R. T. Tidrick and E. D. Warner, 1943. Vitamin K and prothrombin levels with special reference to the influence of age. J. Nutrition, 26: 95-103. Sweet, G. B., L. R. Romoser and G. F. Combs, 1954. Further observations on the effect of sulf aquinoxaline, p-aminophenylarsonic acid, and oxytetracycline on blood-clotting in chicks. Poultry Sci. 33:430432.

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H E R I T A B L E ANOMALY

DESCRIPTION AND INHERITANCE

One D a r k Cornish cockerel and two Dark Cornish pullets were purchased from a breeder of commercial crossbred poultry for use in other genetic and anatomic studies. One pullet died of visceral lymphomatosis before being used. Eggs were taken subsequently for hatching from the remaining pullet (C308) mated to the cockerel (ClOO). These two birds and their descendents proved to be extremely susceptible to lymphomatosis and to have very low fecundity. Crippled chicks appeared in the offspring of these two birds and their descendents. Table 1 lists the matings made and presents evidence of inheritance of this crippled condition. While the totals for normal and crippled progeny from Cornish matings suggest a single autosomal recessive gene, the totals for the F 2 generation out of Cornish c ? X N e w Hampshire 9 9 suggest a more complex mode of inheritance. Further investigation of the genetics involved are desirable, b u t unfortunately all the Cornish (ClOO, C6, C9, C15) with the exception of C308 died of visceral lymphomatosis and the remaining birds had to be discarded.

TABLE 1.—Summary 0} matings P rogeny (18 days incubation or older)

Parents

Normal Sire

Sire's parents

C100» C6

C6

Dam

C308* CIOO X C308

Dam's parents

Dark Cornish — 13

C308*

cioo X C308

C15

cioo C6

X C308

C9

CIOO X C308

cioo X

Crippled

UnHatched h a t c h e d ! Hatched

3

1

1

2

2

2

2

2

13

C308

29 5 7 F5 (Original cross: Cornish c^XNew Hampshire 9 9 ) . The 13 Fi progeny were normal. CIOO CIOO 359 (F,) X 307 (Fi) X 28 11 1 H24 H24 359 (F,)

CIOO X H24

341 (F,)

CIOO X H22

25

3

2

53

14

3

t No abnormalities were observed in unhatched chicks. * Foundation birds—ancestry unknown.

gained use of one of their legs, although the toes were still curled inward or outward. The tibia of the most severely affected leg underwent an outward and posterior rotation presumably caused by an unnatural twisting of its proximal end. The distal end of the tibia (anterior side) faced dorsally and the tarso-metatarsus extended upward. This peculiar position of the legs (Fig. 1) resembled t h a t which'

In most cripples, restricted flexion of" the tibial metatarsal joints affected both FIG. 1. Crippled Dark Cornish female (79 days legs equally in the newly hatched chick. old) weighing 570 grams, approximately two-thirds Within three days most crippled chicks normal weight.

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(vitamin B2) and results in a partially crippled condition (Stokstad and Manning, 1938). Birds suffering from this deficiency typically sit on the tibial metatarsal joints, and toes of both legs curl inward. Genetic differences have been found in the ability of fowl to survive, grow and reproduce on diets deficient in riboflavin and other nutrients ( H u t t , 1949; Jull, 1952). The anomaly described herein m a y involve an inherited inability to use one or more nutritional elements.

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G. V. MOREJOHN

is found in birds afflicted with neurolymphomatosis, but autopsies revealed no internal symptoms of visceral lymphomatosis or neurolymphomatosis or other pathological conditions. In other crippled birds, the tibial metatarsal joint lost its re-

T h e entire process of flexion, rotation and extension was more or less completed before the chick was sixty days old. Only in one case did the Achilles tendon slip

FIG. 3. Pelves of perosis-afflicted Brown Leghorn (left) 89 days old, normal Dark Cornish-New Hampshire F2 (center) 85 days old; and crippled Dark Cornish (right) 74 days old. Distortion of left ilium on cripple has displaced relative position of acetabula. Differences in degree of calcification are probably due to age and breed.

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FIG. 2. The wrinkled eyelid is usually found in birds showing extreme crippling as shown in Fig. 1.

stricted flexion and the tarso-metatarsus gradually extended downward and backward bending at the tibial metatarsal joint in the opposite direction, describing in the process an arc of about 200 degrees and rotating at the tibial metatarsal joint. Thus, the morphologically anterior side of the tarso-metatarsus faced posteriorly. This extreme condition, however, was not found in all the affected chicks and in some did not persist. Most of them showed some degree of this condition; one regained use of its legs and otherwise was normal except for its toes which curled inward and outward on both legs, resembling "curled toe paralysis."

POULTRY SCIENCE INDEX

67

POULTRY SCIENCE INDEX A subject matter index and an author index of volumes 21 to 30 inclusive, together with an author index of volumes 1 to 20 inclusive, is available from

C. B. Ryan, Secretary-Treasurer, Poultry Science Association, Texas A and M College System, College Station, Texas at $2.00 per copy.

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SUMMARY from the intercondylar groove as in perosis. The most severely affected chicks usuA crippled anomaly in the domestic ally had peculiar wrinkled eyelids which fowl is described which affects the pelvis, were not found in normal or known car- joints of the legs and in some cases rier birds (Fig. 2) and lacked many feath- the eyelids. This anomaly somewhat reers of the ocular region. sembles other abnormalities in the fowl, Attempts were made to raise cripples namely, perosis, neurolymphomatosis, to maturity. They were isolated in com- congenital perosis and curled toe paralypartments with wood shavings as litter in sis. Genetic evidence is presented which order to prevent excessive bruising in their demonstrates that this anomaly is inviolent attempts to move. Of the ten crip- herited. ples studied, seven were lost by natural Pelves of crippled and perosis-afflicted deaths before ninety days of age; two birds were compared and were found to were destroyed before ninety days of age, resemble each other in their asymmetry. and one lived to 104 days before being No significant deviation from normal was destroyed because of infection of bruises found in bone ash of cripples or perosison wings and legs. afflicted birds. Pelves of normal, crippled and unrelated perosis-afflicted birds were compared (Fig. REFERENCES 3). Aside from smaller total body size of Asmundson, V. S., and J. Biely, 1932. Inheritance crippled birds, the pelves of cripples and of resistance to fowl paralysis {Neurolymphoperosis-afflicted birds resembled each other malosis gallinarum). I. Differences in susceptiin their asymmetry. The side of the pelvis bility. Can. J. Research, 6:171-175. to which the normal or least affected leg Gildow, E. M., J. K. Williams and C. E. Lampman 1940. The transmission and resistance to fowl articulated showed a greater degree of paralysis (lymphomatosis). Idaho Agr. Expt. asymmetry than the side which had the Sta. Bull. 235. more severely affected leg. This reciprocal Hutt, F. B., 1949. Genetics of the Fowl. McGrawrelationship may be caused by compensaHill Book Co., New York. tory muscular forces attempting to main- Hutt, F. B., and R. K. Cole, 1947. Genetic control tain the bird in an upright position. of lymphomatosis in the fowl. Science, 106: 379— 384. Femurs of normal, crippled and perosisafflicted birds were ashed to compare de- Jull, M. A., 1952. Poultry Breeding. John Wiley and Son, Inc., 3d. ed., New York. gree of mineralization, but no significant Serfontein, P. J., and L. F. Payne, 1934. Inheritance differences were found. Percentages of dry of abnormal anatomical condition in the tibial fat-free weights were as follows: Normal metatarsal joints. Poultry Sci. 13: 61-63. 54.9%; crippled 56.6%; perosis-afflicted Stokstad, E. L. R., and P. D. V. Manning, 1938. Curled toe paralysis in chicks. J. Nutrition, 16: 54.6%. 279-283. Grateful acknowledgments are made to Taylor, L. W., I. M. Lerner, K. B. DeOme and J. R. the Division of Poultry Pathology, School Beach, 1943. Eight years of progeny-test selecof Veterinary Medicine, and to Dr. H. tion for resistance and susceptibility to lymphoGoss, Department of Animal Husbandry. matosis. Poultry Sci. 22:339-347.