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Yellow Fungus or Flesh Eating Fungus - Nannizziopsiosis in Bearded Dragons
Photo of clinical Nanizziopsiosis. Note the yellow coloration of the infected area giving the disease its common name, yellow fungus.
GMS with Hematoxylin counter stain of skin. Black filaments (arrows) are fungal hyphae. Note the invasion of the alpha keratin layers of the stratum corneum. Red arrow = mass of fungal hyphae in interscalar space.
Chrysosporium anamorph of Nannizziopsis vriesii
Nannizziopsiosis (Nan-eezee-opsee-osees or Nan-izi-opssee-osis where the first is the more correct Classical Latin pronunciation and the second is the Anglicized pronunciation) is a fungal disease of bearded dragons that has clinically been on the rise in recent years. I have seen at least 70 cases of this disease in the past year (2008) and only 20 cases the year before that. In 2006 I saw four cases of the disease. I did a presentation on the disease at one of the national pathology meetings in 2005, but the cases have been so common and questions so frequent of late, that I have decided to post this information.
The causative agent of the disease (called necrotizing mycotic dermatitis) is the Chrysosporium anamorph of Nannizziopsis vriesii. This fungus has been associated with fatal necrotizing dermatitis in crocodiles and with infections in numerous species of lizards. The same fungus that has been identified in numerous lizards (including identification through culture by a professional laboratory from cases I have seen) has even turned out to be potentially zoonotic. In 2005, Emerging Infectious Diseases volume 11, number 2, pages 349-350, reported brain abscesses in a human patient from this fungus. The patient was immunosuppressed due to HIV disease and had the fungus in the lungs as well as the brain.
In reptiles the disease is often called "yellow fungus." This is a poor and inexact name, since I have seen several cutaneous fungal infections (that were not this species) turn the skin yellow as it consumed the tissue. I therefore do not like to use the term. The correct disease name is necrotizing mycotic dermatitis (NMD) if the agent is not known. If the agent is known to be the Chrysosporium anamorph of Nannizziopsis vriesii, the correct etiologic diagnosis is Nannizziopsiosis. Nannizziopsis is the genus. According to the rules of naming a disease the terminus of the word is dropped and the suffix -osis or -iosis is added. Remember that the suffixes -asis, -iasis, -esis, -isis and -sis only mean that something is present. They do not mean that there is clinical disease.
STRANGE BUT TRUE SECTION: The rules of the suffixes is why dogs with heartworm disease do not have dirofilariasis. They have dirofilariosis. Dirofilariasis only means that heartworms are present, with or without clinical disease. Unfortunately, this is sometimes messed up even by primary care doctors because of erroneous usage and failure to distinguish between the two terms in Ettinger and Feldman's Textbook of Veterinary Internal Medicine which is extensively used by many veterinarians.
The fungus is a common soil fungus and is normally a saprophyte, that is a cleaner. It lives in the soil and digests the detritus and dead material and acts as a decomposer. However, whether there is a new strain or if the fungus is simply responding to a food source with no defenses is unclear. Yet, the fungus has been causing problems. I have generally noted that those farms growing lizards that are very healthy have few cases with Nannizziopsiosis. Most cases are sporadic and usually involve geriatric or highly stressed individuals. This observation gives credence to the hypothesis that the fungus is attacking a food source that has no defenses. Immunosupression may be the key to understanding the nature of the infection. Those poorly managed farms I have seen with high stress and poor management practices often have numerous cases of this disease. Combine that with the fact that once management improves the cases drop to a minimal level, again usually among the stressed or geriatric, then the pattern becomes more convincing.
Symptoms of Nannizziopsiosis
Reluctance to move.
Patchy yellowing of the skin followed by fragility of the yellow patches and/or dysecdysis.
Yellow skin goes from thick and dry with adhered dead skin to moist and macerated in appearance, especially when upper layers of dead tissue are removed.
Yellow areas begin to slough or turn brown or black and slough.
Spread of the yellow and subsequent necrosis until the animal dies of secondary infections and/or shock.
Understanding the nature of the infection and the problems with topical antifungals is paramount to knowing how to treat the disease. The skin of most reptiles consists of several layers. The outermost layer is the dead layer called the stratum corneum or horny layer. The stratum corneum is made of several layers as well. The outermost is the oberhautchen and is compressed, waterproof beta keratin. The next layer is the beta layer, also waterproofing and made from beta keratin. The next layer is about 2-3 cell layers thick and is made from alpha keratin and is called the meso. The deepest layer of the statum corneum is the alpha layer, made of alpha keratin like a mammal's stratum corneum. Below the stratum corneum is the living layers of the skin consisting inconsistently of the stratum granulosum (this may be only one cell layer thick or largely absent in reptiles), and consistently of the stratum spinosum and stratum germinativum (stratum basale).
In brief here is an outline of the layers.
Stratum granulosum (+/-)
The fungus infects the skin, presumably from some break in the skin, and infects the deeper layer first. This is observed from the histopathology. It travels along the meso and alpha layer digesting them and prompting hyperkeratosis and dysecdysis. The beta keratin layers apparently take longer to break down and these are only invaded toward the center of the lesion where the fungus has been longest. The outer margins are completely within the alpha layers. This makes some sense. The alpha layers are softer and presumably easier to digest. The problem is that the beta keratin layers remain intact over the advancing wave of fungal hyphae. This prevents topical antifungals from reaching the fungus efficiently. As the disease advances the fungus moves inward into the living layers of the skin and then into the underlying muscle tissue. In some severe cases, I have seen the entire body wall open up to expose the coelomic cavity.
How then is the fungus treated? Oral itraconazole at the recommended dose (about 25mg/kg) is often effective, but must be given over a period of weeks to months. This drug is toxic and can cause toxicity if carelessly administered, thus consultation with your exotics veterinarian and explanation of how to properly administer it is advised. Other drugs have been used, but in my experience itraconazole is the only one I have had consistent efficacy with. That being said, the degree of infection is important. Those with small lesions or isolated large lesions have often responded well, but widespread infection or multiple coalescing large lesions are often too advanced and the animal often too debilitated to survive. The potential zoonotic risk should also be evaluated.
Those with poor immune system function should be careful when dealing with animals suffering from nannizziopsiosis. Though the reports of immunosupressed people infected are few, the potential is present. If you are immunosuppressed from AIDS, steroids for transplants or immune mediated disease, you should consult your MD or Osteopath (DO) before you handle animals infected with this fungus.