Crooked Beaks

Fowls with various abnormalities of the beak are seen in many different breeds and have been reported from several countries. The most common of these is probably the non-genetic condition associated with unilateral icrophthalmia or anophthalmia in chick embryos, but the majority of these are never seen because they die during the later stages
of incubation. A few hatch. This abnormality probably results, as do other teratological conditions, from an accident in development, sometimes induced by an unfavorable environment.

The most common kind of crooked beak in older chickens is probably that which develops between 3 and 8 weeks of age in chicks which were normal at hatching. The lower beak is unaffected except that,since it is not used for pecking, the end is not worn down as much as in normal fowls and one side is worn more than the other. At maturity the tip of the upper beak tends to curl downward. In the skulls of affected birds there is a marked asymmetry of the maxillae, nasals, and pre-maxillae, which is probably responsible for the condition of the beak. Birds with the upper beak straight but much shortened are sometimes found in families showing crooked beaks, and the two forms are probably genetically identical.

Genetics. This type of crooked beak is hereditary, but the manifestation of the character is so irregular that a definite genetic basis for it is as yet unknown. In extensive studies by Landauer (1938) the condition was clearly recessive to the normal, but no Mendelian ratios were observed. Some matings of normal parents produced only a single cross-beak in 21, 30, and 48 chicks. From four matings of cross-beaked birds inter se the ratio in the progeny was 91 normal: 53 cross-beaked. Apparently only a small proportion of the birds homozygous for crooked beak are visibly affected. Mercier and Poisson (1925) suggest that in their stock the character was even manifested by heterozygotes. Birds with crooked beaks survive, especially if the beaks are trimmed and if the feed is supplied in a deep hopper. The variation in which the upper beak is straight but shortened is more likely to be fatal before maturity, because of the difficulty in feeding.

Other Types. In some birds the upper beak is normal, but the lower one is twisted. Little is known of this condition or its causes. In the authors experience it reduces viability more than the hereditary type just described. Mercier and Poisson (1927) found that in such birds the cornifled region at the tip of the tongue is extended and somewhat up-curved. Cornification increases with age and use, till fragments at the end fall off and the tongue is eventually so shortened that birds 2 to 3 years old can no longer feed even from dishes.

Another kind of crooked beak, reported by Landauer (1938), is a hereditary condition in which the beaks are crossed at hatching, some becoming normal later on. This was found only in White Leghorns. Its manifestation was just as irregular as that of the type discussed above.

Seven matings of cross-beaked fowls yielded 113 normal:155 affected. One mating of normal parents produced a single cross-beaked chick of this type among 59 offspring. Although the genetic basis for both these types of crooked beak is unknown, they are apparently different. Apart from the difference in the ages at which the defect appears, Landauer found that crosses of the two types yielded only normal progeny.

Abnormal or Missing Maxillae, mx A defect of the skeleton that is lethal to homozygotes was found by Asmundson (1936) in a flock of inbred Single-comb White Leghorns

Morphology. The character is recessive, and heterozygotes are normal. In homozygous embryos the maxillae in the upper beak are either absent or much reduced. The premaxillae are normal in many cases but smaller than usual in some embryos. The nasals are present but sometimes reduced in size, and other bones of the face are sometimes affected. The upper beak is frequently bent to one side, and in some cases the eyes appear to be slightly smaller than normal. Affected embryos can be distinguished easily from normals by the twelfth day of incubation. The condition appears to have little or no effect on the viability of the embryo up to the time of hatching, but of 53 such embryos observed by Asmundson only 1 was able to hatch unaided. The defect of the beak apparently prevents most of the chicks from pipping the shell. Seven that were helped out of their shells all died within 1 week.

Genetics. A ratio of 173 normal :58 abnormal in matings of heterozygotes showed clearly that a single recessive gene in homozygous condition was responsible for the abnormality. Since short names are desirable in linkage studies, and elsewhere, this character, which Asmundson called abnormal upper mandible, might be known as amaxilla. The symbol mx is proposed. Short Upper Beak, su

Another mutation affecting the beak, in this case semi-lethal, i~ras studied by Landauer (1941).
Morphology. The upper beak is shortened by amounts varying from abotit a millimeter up to half its normal length. The lower beak is apparently unaffected. This defect was evident in some embryos as early as the ninth day of incubation. In some of those which hatched, the beak became normal during growth. In others it twisted to one side, more frequently to the right than to the left. The mutation also reduces the length of the long bones in the wing and leg, particularly in the latter. Embryos of 18 and 20 days with short upper beaks were somewhat smaller than normal ones. t~enetics. Embryos thus affected are homozygous for an autosomal, recessive gene for which the symbol su (short upper) is proposed. In an F2 population of 652 embryos at least 18 days old and in 250 progeny from the backcross of heterozygotes to a homozygote, the ratios of normal to abnormal were very close to those of 3:1 and 1:1 expected for a simple recessive character. This not only confirmed the genetic basis for short upper beak but also showed that, prior to 18 days of incubation, mortality among the defective embryos was no higher than in normal ones. About two thirds of the embryos with short upper beak apparently died on the twenty-first and twenty-second days of incubation, but one third were still alive at the end of the latter day. Although about 13 per cent of the embryos with short upper beak that were alive on the eighteenth day eventually hatched, mortality among these was high, presumably because of difficulties in eating. In 5 years of selection against these lethal effects of the mutation, Landauer (1946) raised hatchability of homozygotes practically to normal (77 per cent), and among those hatched the proportion with normal beaks was raised from zero in 1941 to 71 per cent in 1945. Those still abnormal at hatching usually became normal before maturity.

Missing Mandible, md Morphology. This abnormality differs from the two previous ones in that the mandible, or lower beak, is reduced to a mere vestige. The upper beak is also reduced but remains from one-quarter to two-thirds of normal size. It is frequently pointed upward or even curved over the front part of the head. There is always some degree of cerebral hernia. The abnormality is recognizable in young embryos as soon as the beak begins to form.

Genetics. This mutation was found by Marble et at. (1944) in White Leghorns and shown to be a simple, recessive autosomal character. It was lethal to all homozygotes, but some of them were still alive at 21 days of incubation. Genetic tests yielded 378 normal: 134 lethal from heterozygotes mated inter se. The expected ratio of carriers to non-carriers among normal chicks from such matings is 2:1. In tests of 31 females the actual numbers found were 22 carriers and 9 lacking the gene, a close fit to expectation. The symbol md is proposed. Short Mandible, sm

Morphology. Somewhat similar to the missing mandible just described is the short lower beak studied by McGibbon (1946) in White Leghorns. In affected chicks and embryos the lower beak is seldom more than half the normal length; in extreme cases the rami are buckled up or down, almost at right angles to the normal plane, and sometimes cause the mouth to be propped open. Other parts of the skeleton are apparently normal. In extreme cases the tip of the tongue is curled under. Only half the affected embryos hatch, and few of the chicks survive. In those still alive at 5 to 6 months of age, the lower beak is about normal in length, but unless the upper beak be trimmed, the bird cannot close its mouth because of the downward curvature of the upper beak.

Genetics. This abnormality segregated in F2 and backcross populations as a simple recessive autosomal character. When birds that had survived were mated together, they produced 2 normal offspring and 37 with the defect. The 2 exceptions suggest that some birds may not show the character though homozygous for it. Short mandible must be classified as a semi-lethal mutation.