Basic Biology of Herp Color
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
Yellow xanthophores - 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 "washed out."
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 biochemically.
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.
Melanism / 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 blocked.
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 weird."
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 chromatophores without loss of chromatophores. Chromatophores are present in the skin, but are not able to produce pigment or fully formed pigment.