I have had several questions of late regarding pigmentation and
chromatophores. There is a lot of information out on the
misinformation super highway about chromatophores, but it is highly
confusing. Part of the reason for this is many people take information
from studies done in mammals and think that can be lumped into one big
pot with studies done in reptiles. I would even argue that lumping
mainstem reptile studies with studies in archosaurs might be a
mistake. The fact is they do not function in the same way, they do not
go through the same development and they do not even have the same
cells. Mammals lack xanthophores (and the subclass erythrophores) and
iridophores. Mammals also lack dermal melanophores. Mammals (some
argue) do not even have melanophores, but instead have melanocytes.
The point is that the misinformation super highway (MiSH - not to
confuse with MSH which is melanophore (melanocyte) stimulating hormone)
is full of people that do not do the proper research and do not fully
understand the subject they are writing about. Some in the
misinformation super highway's drunk lane (abbreviated 'wikipedia') do
much more than confuse the issues, they actually write things that are
incorrect and when it is corrected, change it back the the incorrect
information (see the wikipedia article on leucism that a colleague of
mine at another college tried to correct and wound up getting his stuff
changed back to the incorrect information and told that he did not
offer credible citations when he used research papers, peer reviewed
literature and expert's text books as references).
The result is that there is a mass of confusion and it stems from the
MiSH and wikipedia. For an entry level of understanding about reptile
and amphibian chromatophores you should start with the following three
Reptile and amphibian variants - Bechtel, 1995 (book).
Dermal Chromatophores - Taylor and Bagnara, Am. Zoologist, 122:43-62(1972)
The Dermal Chromatophore Unit - Bagnara, Taylor and Hadley, The J of Cell Bio, 38:67-79(1968)
I will have a more thorough discussion on this topic later in the semester.
In brief, mammalian melanocytes do not appear to be the same as the
melanophores in reptiles and amphibians. Indeed, they do not appear to
be the same as the chromatophores of invertebrates or fish either. The
chromatophore is a neural crest cell in its typical origin, though
chromatophores not from neural crest develop in the eye. They start
out as a protochromatophore or chromatoblast. They then differentiate
into one of three, or four, types.
Chromatophore Subtypes - xanthophores, iridophores and melanophores
contain all elements of all the chromatophore types. Thus,
melanophores contain pterinosomes and the iridophore plates (called
reflecting platelets), but what makes them distinctly one type or
another is the degree to which they contain the other structures.
Melanophores are melanophores because they contain around 99.9%
melanosomes and only a small percentage of the other structures. This
is important to note, because this fact is what gave rise to the single
progenitor theory for chromatophres.
Melanophores - contain mostly
melanosomes and are capable of two forms of pigment production.
Eumelanin is brown to black and pheomelanin is orange to rust or rusty
brown. Melanophores, unlike melanocytes in mammals, generally do not
inject their melanosomes into keratinocytes. They are also usually
able to move their melanosomes into their dendrites or into the
perikaryon depending on neurohormonal stimulation. The melanins are
contained within the melanosomes.
Xanthophores - contain two
major pigment bodies the pterinosomes containing pteridines and
vesicles that contain fats with stored carotenoids. Another class of
organelle may exist in which the pteridines are converted to
drosopterins and some people have suggested the name drosopterinosome.
However, since drosopterins are made from pteridines, this may be a bit
of a splitter attitude, and really may not be valid. But it cannot be
denied that yellow pteridine rich cells occur within microns of orange
or red drosopterin rich cells, so there may be something to the
separation. At any rate, xanthophores can be divided into at least two
- contain organelles called pterinosomes that are pterinidine rich and range from creamy yellow to orange. Since these cells are yellow to yellow
orange and the term xanthophore can apply to the red xanthophores as
well, there is a good argument to refer to this subtype as luteophores,
but that term has yet to catch on.
Red xanthophores (erythrophores) - pterinosomes (drosopterinosomes) are rich in drosopterins which range from orange to red and even violet. These cells are more easily seen on histology than their yellow counterparts and can be seen in the pictures at the top of this page.
while possessing all the organelles of the other chromatophores, the
iridophores primarily use refractile platelets formed by crystals of
the uric acid based DNA components called purines. Specifically the
purines hypoxanthine, guanine and possibly adenine. Basically theses
platelets act as prisms and refract light to form certain colors and interact with different pigment bearing chromatophores to vary the
Here is a list of color abnormality definitions so
you can see why color abnormalities are a group of conditions that are problematic to name.
Erythrism /Erythristic - excessive production and deposition, or distribution of red pigments (orange possibly).
Anerythrism /Anerythristic - lack of production of pigments in the darker orange to red range.
Hypoerythrism /Hypoerythristic -
reduction in the amount of darker orange to red pigments so that the
appearance of this color is largely absent except for traces or appears
Xanthism / Xanthic - excessive production and deposition, or distribution of yellow pigments (orange possibly).
Axanthism /Axanthic - lack of yellow and
lighter orange pigments, depending on the point in the pigment cascade,
this mutation can also cause corresponding anerythrism since erythric
pigments (drosopterins) appear to come from the more yellow pteridines
Hypoxanthism / Hypoxanthic - reduction in the amount of yellow or lighter orange pigments so that
the appearance of this color is only found in trace amounts or appears
"washed out." This may also result in hypoerythrism since the red pigments appear to be made from the yellow pteridines.
/ Melanistic - excessive producution and deposition, or distribution of
melanin pigments (may be orange if pheomelanin to black if eumelanin).
Amelanism / Amelanistic - lack of melanin
production. At least three basic forms are possible, though whether all
forms have been observed is questionable. 1) amelanism where the
chemical cascade is defected before eumelanin and pheomelanins take
separate biochemical routes, resulting in a complete lack of melanin
production. 2) aeumelanism - where only eumelanin production is
blocked. 3) apheomelanism where only production of pheomelanins is
Hypomelanism / Hypomelanistic
- condition resulting in the reduced production of melanins. At least
three types are possible by restriction of production at the initial
stages of melanin production, at the eumalnin production cascade or at
the pheomelanin cascade.
Iridism / Iridistic - excessive production and deposition, or distribution of
iridophore platelets (this is, as yet, only a theoretical condition).
Aniridism / Aniridistic - (again theoretical - I have not heard this reported) lack of the formation of refractile platelets in iridophores.
Hypoiridism / Hypoiridistic - (theoretical) reduction in the number of refractile platelets formed in iridophores.
Only if a reptile, amphibian or similar polychromatic animal
lacks melanin, drosopterins (red) and pteridines (yellow) -- is
amelanistic, anerythristic and axanthic-- is it really an albino.
Remember albino means "white."
Mammals, which have only melanin, are albino if they lack melanin. This is not true of multipigmented animals like reptiles.
If a reptile lacks melanin it is amelanistic.
In animals with more than just melanin the word albino is often used incorrectly.
LEUKISM or LEUCISM
Also means white and is discussed below.
Pronunciation Problems to Ponder
Many questions have been asked of me as a herpetologist and
veterinarian. One of these is the nature of leucism. First of all, it is NOT pronounced "loo-si-zm"
saying that immediately identifies a person as poorly educated in
scientific and medical terminology. The correct pronunciation is "loo-ki-zm." In Classical Latin the C is always
pronounced like K - the so called hard C sound. You do not call a
neoplasm of blood cells "loo-see-mee-ah" it is pronounced
"loo-kee-mee-ah." The rule is the same for the prefix leuc- or leuk-
across the board. White blood cells are pronounced "loo- ko- site" not
"loose- o- site" (which incidentally, is spelled leukocyte or leucocyte
with the k form being more common, but both correct). It is "loo-
ko-" in the words leucoencephalomalacia and all other words with the
prefix. Arrogant as it sounds, in many medical circles the mispronunciation
of basic words like that makes people think of you as poorly educated
and without a firm grasp of scientific or medical language. In fact, one
colleague of mine once heard another doctor say "loo-sis-tic" and said "did
you hear that? Where did he get his doctorate? From an online college staffed by trailer trash?" Ok, I agree that is harsh, but similar (though more tactfully expressed sentiments ) are frequently found in the halls of academia. So
mispronouncing words can make people dismiss you as a rube, so make an
effort not to do it.
Where does this come from? Leuc- is the Latin form of the Greek
Leukos. Thus, technically any word that is spelled with the leuc-
prefix can be spelled with the Greek prefix instead and spelled leuk-.
An example is the word leukocyte. The Greek is used, but it is
acceptable (though more rare) to spell it with the Latin to form
leucocyte. In the case of leucism the opposite has become true. The
Latin form has become more widespread, but the Greek is equally valid.
Thus, leukism is correct. In fact, I have increasingly begun to spell
it with the Greek spelling because of the pronunciation issue.
Some have suggested that the S sound is apt since it comes from Greek and is transformed into the Latin, but this is a form of grasping at straws in order to garner some reason to preserve the incorrect pronunciation. The scientific terms are based (ideally) on the Latin pronunciation. Even the scientific names of animals come from various languages (Gopherus the genus of the gopher tortoise actually comes from French), but they are "latinized." The standard Latin in science is Classical Latin. That is the Latin that was the Emperor's Latin during the Pax Romana. Another Latin did exist called the Vulgate (Vulgar Latin) which was the Latin spoken by the commoners, mostly illiterate and lower class Romans. This Latin is what ultimately spreads and becomes the common Latin after the fall of Rome, and the so called Church Latin. Think of it this way, the difference is like the difference between the Queen's English and Cockney. The ideal pronunciation in science was decided to be based on the "higher" form of Latin, Classical Latin. Thus, any C is pronounced as a C not an S. The use of an S sound is Vulgate - Vulgar Latin. So if you want to be vulgar you can be, but it is better to sound like you are educated.
Unfortunately, most people that pronounce it "loo-si-zm" are hobbyists
that are poorly trained in medical terminology, if they are trained at
all. Most know nothing about science beyond their high school biology
and chemistry classes. It is very difficult to correct people that
have formed an entire community which is equally badly educated. You
fall into a form of peer pressure to be wrong. If you pronounce a word
correctly when everybody else is pronouncing it wrong you are looked at
as a jerk or a wierdo. Veterinarians and some herpetologists then adopt the incorrect pronunciation so they will not offend their clients.
This is what scientists and medical
professionals have to combat. Peer ignorance pressure is difficult to
overcome. I can remember speaking to a group of hobbyists not long ago
and someone asked me a question about leukism. I corrected their
pronounciation very politely, but you should have seen the looks from
the whole room. I said, "I'm sorry, do you mean leukism?" The person
looked a little puzzled. I continued by saying "the condition is
called leukism, it comes from the Greek leukos meaning white." The
whole room smiled and looked rather odd. I asked several people
afterward why they looked odd. They laughed and said "everybody says
'leusism'." When I pointed out that was not correct, they replied
"maybe, but if you say it like you say it, people will think you are
For that reason (as I mentioned before) I still tend to write using the
more common spelling with a C, but I have increasingly begun to spell
it with a k when dealing with hobbyists.
Concepts to Consider
There is a great deal of bad information out there (hence the new term
"wikipedian information"). If you have not run across that term, you
will eventually. One of the greatest sources of misinformation is
wikipedia. I have read the article on leucism there and there is a
great deal of misunderstanding. One of the things that is not
understood is the fact that the words leucism (or leukism) and albinism
are essentially the same in their roots. They both mean white. The
medical field is what delineated a difference between them. Those not
in the medical field rarely use the distinction correctly. Just because
something looks white does not mean it is either leukistic or albino.
There are other genetic mutations out there that cause feathers or hair
to be white which have to do with deposition of melanin or other
pigments (carotenoids in many avian species for example) that have
nothing to do with leukism or albinism. Many PhD's (and I am one as
well as a DVM) have a very poor concept of what constitutes these
conditions. So I will break them down in the most basic forms.
The first thing we must remember is the definitions are artificial.
The term albino and leucistic actually literally mean the same thing -
white. The artificial division between them began in the veterinary and herpetological
communities, and rather recently too. In fact the word leucism has not
made it (as of this writing) into most dictionaries. Among those that
study chromatophore biology and pigment mutations there are a set of
definitions for these words that are accepted as the standard.
1) ALBINISM- genetic mutations that alter the pigment cells of the skin
and other tissues in such a way that the pigments themselves are not
formed in their final, normal biological form. NOTE I said skin and
other tissues. If the skin and rest of the body is not devoid of
pigment, but the hair or feathers are white, that does not equate to
albino. Also albinism is a derangement of pigment formation, not
deposition. There are numerous forms of albinism. In humans, there are
two pigments. Eumelanin is brown to black and pheomelanin is rusty or
even orange or red. They travel along a similar cascade when being
formed but differ in the amount of sulfur in the final melanin
compound. Any disruption along the cascade can cause a form of
albinism. Some albinos have red hair because they have a gene that is
faulty for the formation of eumelanin, so they are really only
eumelanistic albinos. Other pigments found in reptiles can also have
faulty genes. The pteridines and drosopterins in the other cells
(xanthophores and a subset of xanthophores called erythrophores) can
cause other forms of albinism. Currently the iridophores (which use
crystals and refraction to cause color instead of pigment) are not
really known to be faulty in the same way since there are not pigments but crystals;
so iridophoric albinism is something that simply does not occur, at least so far as is known in the literature.
2)LEUKISM (LEUCISM)- medically defined this is a defect in the skin,
not the pigment cells. There are other derangements of pigment that can
cause a whitening effect, but they are not classical leukism. Classical
leukism is caused by a faulty gene, or set of genes, that causes the
skin to be unable to support pigment cells. Experiments have been done
that illustrate this. In one set of experiments normal pigment cells
from a normal animal were placed in albino skin and the cells were
normal and produced pigment. This demonstrated that the albino defect
was in the pigment cells of the albino but not in the skin itself. The
same experiment done in leukistic skin caused the normal pigment cells
to die. Some have claimed that the reason eyes are pigmented in
leukistic animals is because the pigment in the eye comes from another
origin (the non-neural crest theory). This is really not the case. In
fact some (unfortunately as yet unpublished research that really needs
to get published) experiments were done transplanting RPE eye pigment
cells into the skin and they died. Conclusion? Well nothing. The eye
pigment cells can't survive out of the eye is all that proved. So
melanophores from the iris were transplanted and they died in leukistic
skin but survived in albino skin. Conclusion? The defect has to do with
the skin, not the origin of the pigment cells. Further evidence of
this can be found in numerous species that have melanin or other
pigments present in other tissues such as the peritoneum but are
typical of leukistic animals on the outside when alive.
However, some leukistic animals are also leukistic internally. What does this mean? At present it is unknown. It might reflect a subtype of leukism where there is agenesis, dysgenesis or complete necrosis embryologically of the chromatophores. This could represent another branch on the leukism scheme and might indicate a disorder we might call Complete Leukism. Where forms just limited to the skin might be termed Cutaneous Leukism. One thing is clear, the definition of leukism is only semi set. There is room for other forms, but it should be understood that there must be a standard definition defined in pathological terms.
So are there other forms of leukism? Possibly, but one must not confuse leukism with dysregulation of dysfunction of chromatophores. For example, if the chormatophore cannot produce pigments, but is otherwise functional, that is albinism. However, what about a mutation in a
receptor that causes the pigment cell to be unable to receive signals
(a MSH receptor for example) to produce pigment? That situation is more
closely related to albinism since the pigment cells are present but not
functioning, though they are dysfunctional from a different cause. Thus it is probably better call the condition something
else in order to eliminate confusion. I personally refer to these
potential disorders as receptor mediated chromatophoropathies (or chromatopathy) or
RMC's. I first coined the term RMC back in 2003, but have had no real case
where this could be proven. Since many of the immunohistochemical
markers for mammal receptors do not work in reptiles and leukistic or
RMC mammals are much harder to come by, I have not been able to publish
the term in the mainstream literature. But published or not, it is
useful for this discussion.
I have also seen, but could not prove, another condition. A client of a colleague has a snake that went white like a "snow corn" over a few months. It suddenly died. Upon necropsy there was a tumor in the brain. I suspect, but without immunohistochemistry that would work on reptiles could not prove that the MSH producing cells were destroyed by the tumor. Because of this case I had to also add another possible disorder. Whether acquired or through genetic mutation, a deficiency in the hormone stimulating the chromatophores is possible. I refer to this possible disease as Hormone Mediated Pesudoalbinism or Pesudoleukism. In the case I described, my colleague failed to notice if the eyes retained any pigment, so I am not sure what the presentation would be. But with all the confusion these classifications can separate some of the confusion like
Classic leukism is due to chromatophore necrosis, apoptosis, dysgenesis or agenesis - and is the the absence of recognizable
chromatophore cells on histopathology.
Receptor Mediated Chromatophoropathy (RMC) is a white state due to chromatophores not receiving signals or are receiving only low level signals to produce pigment due to a mutation in some
receptor or signaling pathway, but chromatophores are present in the skin on histopathology.
Hormone Mediated Pseudoalbinism or Pseudoleukism (HMP complex) is a white state due to a deficiency of stimulatory hormone, but the chromatophores are present in the skin on histopathology. In this case the chromatophores are completely normal. They are reacting normally to an abnormal condition (lack of stimulatory hormone), so they are neither leukistic, nor albino. The appearance of these animals might mimic leukism or albinism.
Albinism is a defect of pigment production within the chromatophoreswithout loss of chromatophores. Chromatophores are present in the skin, but are not able to produce pigment or fully formed pigment.
3)Any white animals with pigmented eyes are leukistic? NO. Particularly in those animals where their color or percieved color comes from keratin structures like hair or feathers. There are other
mutations out there where the pigment cells are working but the (in the
case of mammals for example) melanocytes are prevented from injecting
their melanosomes into hair shafts. This causes white coats, but
pigmented skin. Some white haired horses are an example of this. They may have
black skin, but white hair. They are not leukistic. Other
animals have this kind of situation too and it can arise as a mutation
in a population. Birds may also have a condition like this where they are really normal as far a pigment production, but not in terms of deposition in the feathers.
4)Animals with patterns are leukistic, right? NO. Leukistic animals
should be all white. There was a picture of a giraffe circulating about
the internet a few years ago that was black and white. No brown. People
started calling it leukistic. NO. It had black, so it was not
leucistic. It may have had a pheomelanin defect or other mutation, but
it was definitely not leukistic. On the wikipedia website under leucism
there is (as of this writing) even a picture of several avians with black feathers but white
feathers also. That is NOT leukism. Pattern mutations are something
separate as is piebaldism. Piebaldism was believed to be a related condition to leukism,
but it is often a progressive condition over time in animals, though
may be static. Animals that are born with a pattern that is maintained
over the course of their life may not be piebald, that is often
something else, like mosaicism or a pattern mutation it depends on the nature of the color pattern. Too often I have had someone show me an animal with a clear case of pattern mutation where the normally white bands (kingsnakes are a good example) are wider than usual and less neat, and they call it piebald. It is not so.
progressive piebald animals start out normal then loose patches of
pigment over time until they reach or get near maturity when it often
stops progressing, though some can progress to complete loss of
pigment. However, some species have static piebaldism too, but
whatever the type, piebaldism is random, not patterned. Thus animals
with white patches that form a symmetrical pattern are not piebald, but
are suffering from a pattern mutation. One must also be careful not to
throw the word around carelessly. A spotted horse is not piebald just
because it is spotted. Horses are not piebald just because they have white. If the skin under the white spots is also devoid of pigment, then that may be considered piebald. But caution must be used with piebald too.
What exactly consititues a piebald? Piebald is where normal pigmented skin and structures (hair, feathers) are randomly distributed around the body with non-pigmented skin and structures. If the skin under the coat is normal, it is not piebald. Some argue that there is also another condition to piebald and that it must be an abnormal condition.
Under this definition with abnormality being required, paint horses are not piebald since their color is normal for the breed. Calico cats are
not piebald, though they have a random arrangement of color. I personally do not accept this definition. I do, however, accept the prerequisite that the distribution of piebaldness is random.
bi-colored crow or grackle that is symmetrical and has a distinct
pattern is not piebald or leukistic, but has a pattern mutation. White
pigeons with black speckles are not piebald or leukistic, they have a
speckled pattern mutation. The list goes on. If you want to see
misidentified pictures just look at any number of websites - they will
often have a spotted pigeon and call it leukistic or piebald.
I must also bring a point of standardization here. A sparrow with a white patch around its head is more in keeping with piebaldness than leukism. Leukism is complete lack of pigment over the body. Not patches. Not blotches. Not stripes. Random patches of depigmentation are due to a pathologic disease resulting in depigmentation or due to something like piebaldism. The purity of the term leukism must be preserved for the sake of standardization. The way the current use is (especially in birding circles) if you say something is leukistic, you do not know if it is piebald, hypomelanistic, has autoimmune depigmentation, been burnt and has a depigmented white area, has a birth mark causing the hair or feathers to be white, or is completely white with pigmented eyes. This is simply UNACCEPTABLE, ASININE AND INTOLERABLE. Especially in the scientific community, which should know better than allow this kind of confusion.
5) For lack of a better term... DIETARY PSEUDOLEUKISM - I choose to coin the
term dietary pseudoleukism to identify the condition of false leukism seen in those animals (birds particularly) where pigment is dietary. Picture
a flamingo which is stark white and has pigmented eyes. It is
leukistic! Wrong! In point of fact this condition is common in avians.
Many avian species do not deposit the classical pigments in their
feathers. Many dispose of excess pigment from their diet by excreting
it into the feathers as they are forming. Carotenoids are a common one.
You would be surprised how many people have told me they have seen
leukistic flamingos at the zoo. If flamingos, cocks of the rock or
other species are not provided carotenoids in their diet, they go
white. They are not leukistic or albino.
I added the following because of
some questions generated by some of you. You e-mailed me some places
to visit that were birding sites where they claim that washed out birds
with low levels of pigment are leukistic. I hope this explanation
6)HYPOMELANISM - another source of confusion out there is the really
bad tendency of the literature particularly the non-peer reviewed
literature of mammal and bird color morphs to call those with lower
than normal levels of pigment (not absence) leukistic. The problem
with that is that there is a wholly different pathogenesis going on
there. I have had the opportunity to examine some of these birds at
necropsy and I examined their skin and feathers. The ones I have
examined were very similar to hypomelanistic reptiles. The
melanophores are present but have a reduced level of melanin
production. The exact pathogenesis of hypomelanism is not worked out
but it is known that in some species it is a Mendelian recessive gene.
It is not classical leukism, nor should it be referred to as leukism
So there is a brief run down on leukism (leucism). Be careful what you read out
there. Some explanation on leukism can be found in the book "Reptile
and Amphibian Variants" by H. Bernard Bechtel. He talks about the skin
micro-environment defect briefly and the transplant experiments. Keep
your questions coming and I will try to answer. I hope my students have
found my new blog. I will be e-mailing you all again to update you
since it is now up. I will try to post my old posts eventually, but
necropsy has been heavy lately and I am swamped with cases.
Concerning Birding Sites and the Ornithology Books
You have to be careful about many of the birding books and sites. Most
PhD's in ornithology know very little about chromatophore biology and
they throw words around carelessly. To be fair, ornithologists are not
physiologists, cell biologists or pathologists and have most of their
education in behavior, ecology and taxonomy. So they can perhaps be
forgiven for not really understanding the finer points of pathological
conditions and the need for consistency within the scientific community
that deals with these issues. Hobbyists are really bad about using
terms incorrectly and that comes from much misinformation on the net
and from reading books by those who are not really qualified to make a
diagnosis of albinism or leucism (leukism). There are several sites
with really weird definitions out there that have no pathological
basis. One site that has been brought to my attention:
This one does a fairly good job at pointing out the inconsistencies in the birding literature regarding leukism.
Another problem with the bird literature is the superficial examination
of the animals themselves with no real scientific scrutiny. The
tendency to throw the word leucism (leukism) around is rather
frightening. Any animal with a messed up patch of feathers that have
gone white is called leucism by these people. Just look at the Cornell
SCARY for anyone concerned with accuracy and precision, the way scientists are supposed to be.
The problem with this "bird brained" approach to the question is they
are examining feathers. These are structures composed of keratin and
they have no idea whether or not there is a lack of pigment, reduction
of pigment or if there is an impairment of pigment transfer to the
keratin. Transfer impairment would constitute a whole new pigment
disorder not leukism, which has already been established as a defect involving the survival or migration from the
neural crest of chromatophores. To date this has not been examined.
What is more, is that many birds called leukistic are not really
leukistic. They have pigment on most of their feathers, they just have
patches of white. That is not really classical leukism. Pattern
mutations, piebaldism, or some other disorder should be considered
before the diagnosis of leukism is applied. To make a diagnosis of a disorder without understanding the basic pathogenesis is at the least VERY BAD FORM, and MALPRACTICE at worst!
Furthermore all you have to do is look at a calico cat as a good
example. Due to the X chromosomes having different color genes you get
two colors, right? No, you get three. One color on calicos is white.
Tuxedo cats also have black and white. This is not leucism. It is a
pattern mutation. The abnormal patchy distribution of white in the
feathers of birds may be something similar, and this must be ruled out
before they can be called leukisitc.
Regarding pigments, other sites which are not so good, I will not
mention. But several of you have asked about another birding term,
that really has no pathological authority. Xanthochroism is
an odious term to be frank about it. It really has no real biological
basis. It often is seen in psittacines and in aquarium fish. The
cause is generally a lack of the melanins and other pigments that cause
the yellow pigments to be all that is left, so yellow predominates. There is a problem with
this term. First the term means yellow skin. Not a good term for
birds, since we are talking about the feathers not the skin itself. Also it is a lack of pigments that causes the problem, not
excess of yellow. To understand the
pathogenesis, it is necessary to understand the proper name to give the
condition. By the way, xanthism is also used for this and that is a
really poor choice.
So if the condition in psittacines is caused by reduced melanin for
example it is really a hypomelanism or amelanism not xanthism or
xanthocroism. Furthermore, many birds have blue in the feathers as a
structural color, that means it is not caused by pigments but by
structural design of the feather causing the reflection of blue light
back toward your eye. If yellow pigment and blue structures are
combined then you will perceive green. In this case if the feathers
turn yellow it is a structural change in the feather, and that is
another defect entirely. That may be a good condition to use
xanthocroism for, or perhaps another name (I am open to suggestions
A Word on Blue
Blue is generally a structural color and is the result of the interaction of iridophores and other chromatophores. There should be a note here that some species possess other forms of chromatophores. Leukophores (leucophores) are described in fish, but they are really iridophores that have platelets reflecting white back at the observer's eye. Being a bit of a lumper, I really do not consider leukophores a separate cell line, but some people do. I must also admit to and point out a bit of hypocrisy here, since I tend to talk about xanthophores and erythrophores, but lump iridophores and leukophores.
Among the other cells out there are some that have been called cyanophores. No they do not produce lethal cyanide. Cyan = blue. "Bluephores" then are cells that would contain blue pigments. This has thus far been unusual. Most animals do not have blue pigments, but use iridophores and other chromatophores to produce blue. However, that does not mean that cyanophores do not exist. They have been demonstrated in fish, and I strongly suspect they are present in cephalopods and would be surprised if they are not. Are they present in amphibians and reptiles? No, not so far as I can find, but that does not mean they are not present in some species and just have not been described. I do not look to find them in any known reptile species (though I would be pleased if I was surprised), but hope to find a paper one day where they have found them is some rain forest amphibian.
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