During the Dutch National Budgerigar Symposium of april 15th 1989, an interesting lecture was presented by a well known judge. The lecture was entitled "Pied is Beautifull". He mentioned a possible new pied mutation from Australia called the mottle [3]. It appeared that similar mutations also did occur in The Netherlands.
A few years earlier a bird was shown to him which was obviously pied in appearance, but unlike any pied form known at that time. This bird looked like a recessive pied but did have normal white irisses. The wingmarkings were quite remarkable because the wingcovert feathers were white whereas all flightfeathers were normally pigmented. This bird developed normally pigmented juvenile feathering after hatching and during the first year, however it became more and more pied in the second year of age. There were more reports of such birds coming from the same area later on. Also during the Dutch Grand National Show in 1989 a cinnamon greygreen was showed which had become pied at age. This bird also showed white wingcovert feathers with normally pigmented flight feathers.

Such pigmentary disorders have been known for a long time in fowls [6] and also in humans, as well as in a number of other species including chimpanzees, elephants, horses, swine, dogs, guinea pigs, cats and mice [9,10].
Different causes have been found for this phenomenon such as malfunction of the thyroid gland or disorders of the gonads. The mutation described by the former mentioned judge shows great resemblance with the DAM (delayed amelanosis) chicken line, especially developed, by selective breeding, for their ability to depigment progressively [1,2,13]. These DAM chickens hatch with normal pigmentation and afterwards develop irregular amelanotic (pied) areas in their plumage. The incidence of feather amelanosis in newly hatched DAM chickens is 39%. One bird did not develop amelanotic feathers before 36 weeks of age [1]. The number of DAM chickens which became blind after some time was 68,7%. This is caused by degenerative processes in the choroid and the retina related to the same trait. Although the inheritance of this kind of "pied" appears to be dominant, there is evidence that it is controlled by multiple autosomal genes (polygenic). This is probably the explanation that less than 40% of the offspring is affected by the trait.
Many hypothesis have been offered for these symptoms and at present this mutation is still under investigation. In humans this trait has also been found and is called vitiligo. The obvious manifestations are asymptomatic white spots on the skin [12]. About 1% of the world population suffers from this trait [9].

The different mechanisms for amelanosis are:
1.) The melanoblasts (pigment cell precursers) do not succeed in reaching their destination (the skin). The explanation for classical piebaldness and white domestic chickens to be amelanotic and yet having black eyes [8].
2.) A general enzyme defect resulting in albinism [15].
3.) The elimination of melanocytes in a functional competent system like in vitiligo [9,12].

Melanocytes can also be destroyed by the basic products necessary for melanin production like tyrosine and dopa [5,6]. It appears that melanocytes under normal conditions do have an effective mechanism to protect themselves against destruction by these products. If this protective mechanism is lost by mutation, melanocytes are easely destroyed (selfdestruction). Feather loss during moult or plucking, stimulates the featherpapilla to reorganize after about three days, and epidermal cells to proliferate and give rise to the epidermal collar. Subsequently melanoblasts residing at the base of the feather germ are initiated to migrate to the base of the dermal papilla [4]. At the base of the feather papilla, melanoblasts differentiate into melanocytes which immediately start melanosome synthesis. These melanosomes (pigment granules) are transferred into feather barbules and eventually become incorporated into the keratinized feather as it emerges.
In DAM (vitiligo) birds which still are normally pigmented, melanoblasts differentiate into more and more abnormal melanocytes during each moult. During the development of amelanotic feather areas, a hyperactive immune system eventually eliminates the reserve pool of melanoblasts residing at the base of the feather papilla and thus prevent migration and/or differentiation of melanoblasts in regenerating feathers.
In vitro (testtube) developed melanocytes, partially imitate the same defects seen in degenerating melanocytes found in vitiligo subjects and might indicate a genetical defect separate from the immune system [2]. It is known in literature that eyesight in fowls is affected by alterations in pigmentsynthesis [11,14]. Sex-linked albinism in the Japanese quail (couturnix couturnix japonica) is involved in bad eyesight caused by alterations of the optic nerve, the cornea and the retina. Sex-linked albinism in the fowl (gallus gallus) also leads up to bad eyesight in contrast with parrot- and finch-like birds.

Lightmicroscopical examinations of cross-sections made from amelanotic feathers plucked from affected Budgerigars (mottles) showed seriously degenerated melanosomes opposite the amelanotic feathers taken from Australian pieds in which no melanosomes have been found at all due to the lack of melanosomes in the unpigmented (skin) areas. This phenomenon is called leukism.

Consulted and cited literature:

[1] Boissy R.E., Smyth J.R., Fite K.V.
    Progressive Cytologic Changes During the Development of Delayed
    Feather Amelanosis and Associated Choroidal Defects in the DAM
    Chicken Line
    Am.Journ.Path. Vol.111 no.2 (1983); p.p.197-212
[2] Boissy R.E., Moellmann G., Trainer A.T.
    Delayed-Amelanotic (DAM or Smyth) Chicken: Melanocyte
    Dysfunction in Vivo and in Vitro
    Journ.Invest.Derm. Vol.86 no.2 (1986); p.p.149-156
[3] Dobie E.J.
    The 'Mottled' Variety
    Budgerigar World Issue 64 (1987); p.p.27-28
[4] Foulks J.G.
    An Analysis of the Source of Melanophores in Regenerating Feathers
    Physiological Zoology (1943); p.p.351-380
[5] Graham D.G., Tiffany S.M., Vogel S.F.
    The Toxicity of Melanin Precursors
    Journ.Invest.Derm. Vol.70 no.2 (1978); p.p.113-116
[6] Hill H.Z., Hill G.J.
    Eumelanin causes DNA Strand Breaks and Kills Cells
    Pigment Cell Research Vol.1 (1987); p.p.163-170
[7] Hutt F.B.
    Genetics of the Fowl
    McGraw-Hill Book Company, Inc Nw York (1949); p.p.1-577
[8] Jimbow K., Szabo G., Fitzpatrick T.B.
    Ultrastructural Investigations of Autophagocytosis of Melanosomes
    and Programmed Death of Melanocytes in White Leghorn Feathers:
    a Study of Morphogenetic Events Leading to Hypomelanosis
    Dev.Biol. Vol.36 (1974); p.p.8-23
[9] Lerner A.B., Nordlund J.J.
    VITILIGO What is it? Is it Important?
    JAMA Vol.239 no.12 (1978); p.p.1183-1187
[10]Lerner A.B., Shiohara T., Boissy R.E.
    A Possible Mouse Model for Vitiligo
    Journ.Invest.Derm. Vol.87 no.3 (1986); 299-304
[11]Mueller C.D., Hutt F.B.
    Genetics of the Fowl- Sex-linked imperfect albinism
    Journal of Heredity Vol.32 (1941); p.p.71-80
[12]Nordlund J.J., Lerner A.B.
    VITILIGO: It is Important
    Arch.Derm.Vol.118 (1982); p.p.5-8
[13]Smyth J.R., Boissy R.E., Fite K.V.
    The DAM Chicken: A Model for Spontaneous Postnatal Cutaneous and
    Ocular Amelanosis
    Journal of Heredity Vol.72 (1981); p.p.150-156
[14]Takatsuji K., Ito H., Watanabe M.
    Histopathalogical Changes of the Optic Nerve in the Albino Mutant
    (couturnix couturnix japonica)
    Journ.Comp.Path. Vol.94 (1984); p.p.387-404
[15]Witkop C.J.Jr.
    Albinism
    Adv.Hum.Genetics Vol.2 (1971); p.p.61-142