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Leucism, Albinism and Similar Conditions - Understanding Reptile Color and Correct Color Terminology


Unstained histopathology slide from a Chameleon.  Melanophores (black arrow) and erythrophores (red arrow) are clearly visible.  The iridophores appear in this section as golden brown and there are two distinct rows.  Deep margin on left.

Unstained histopathology slide from a Chameleon. Melanophores (black arrow) and erythrophores (red arrow) are clearly visible. The iridophores appear in this section as golden brown and there are two distinct rows. Deep margin on left.

Same section as above under polarized light microscopy.  The polarized light reveals the birefringence of the iridophore platelets and makes the two distinct rows of iridophores even more distinct.

Same section as above under polarized light microscopy. The polarized light reveals the birefringence of the iridophore platelets and makes the two distinct rows of iridophores even more distinct.

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 resources:

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 subtypes.

  • 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.

Iridophores - 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 colors.

Color Abnormalities

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.

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  • 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.


  • Also means white and is discussed below.

Leukism (Leucism)

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.

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 this:

  1. Classic leukism is due to chromatophore necrosis, apoptosis, dysgenesis or agenesis - and is the the absence of recognizable chromatophore cells on histopathology.

  2. 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.

  3. 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.

  4. 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.

Typical 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.

A 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 helps.

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 (leucism).

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 folks:

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 here).

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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