Introduction

Oculocutaneous albinism has been observed in the American alligator and appears to be similar to the condition seen in humans. A second condition of hypopigmentation, leucism, has also been documented in alligators and appears to be similar to piebaldism in humans. The medical term "albinism'' defines disorders with congenital reduction in melanin synthesis and is associated with specific ocular changes in the developing eye. These include: reduction in iris pigment, foveal hypoplasia, misrouting of optic fibers at the chiasm, nystagmus, and alternating strabismus (1). These abnormalities are common to all types of albinism and are necessary for the diagnosis of albinism (1). Albinism is associated with: deformed scales in snakes, neurological defects in humans, and hematologic disorders in mice. Immune system failures have also been reported in humans. In the present report, we describe the necropsy of an alligator with oculocutaneous albinism with apparent immune system failure, and lesions in the liver, pancreas and ovaries.

Results

A dead American alligator with oculocutaneous albinism was presented to the University of Florida Veterinary Medicine Teaching Hospital in November 1995 for necropsy. The animal had been "off feed" since the middle of May 1995 and had been treated with Baytril. Aeromonas Sp had been isolated from the throat and cloaca. Clinical examinations were essentially normal except for a dense mass on the right side of the abdomen. Gross and microscopic lesions were observed in the liver, lungs, pancreas and ovaries. The most severe lesions were those in the liver and pancreas although the pneumonia and congestion of the lungs may have been the actual cause of death. Clinical values support severe liver damage (ALT, Alkaline phosphatase and uric acid). We believe that the chronic liver damage (of unknown origin but probably genetic based on the absence of a gall bladder) was a primary cause of Eve's problems. A lowered immunocompetence, as indicated by significantly decreased globulin levels, apparently allowed the opportunistic Aeromonas infection to fulminate. Aeromonas infection was confirmed by isolation from the blood, liver, kidney and lungs. Eve's clinical values paralleled values obtained from previous acute Aeromonas infections (2).

Discussion

Oculocutaneous albinism type 1 (OCA1) is caused by mutations in the tyrosinase gene. The malfunctioning gene cannot convert tyrosine to dihydroxyphenylalanine, the rate limiting step in pigment production. Both eye and skin pigment are absent in OCA1. OCA1 then can be subdivided into mutations associated with no residual enzyme activity (OCA1A), residual enzyme activity (OCA1B and OCAlMP), and temperature-sensitive enzyme activity (OCAlTS). In leucistic alligators, cutaneous pigment is decreased, but ocular pigment is intact. Current evidence on leucism indicates that: 1) there is some pigment of the skin, 2) the gene is not dominant because offspring produced leucistic males and normal-colored females are normal-colored, 3) leucism affects both males and females, 4) there has been no indication of organ deformities as seen in the albino alligators, 5) leucistic alligators have normal globulin levels which appear to be depressed in albino alligators and, 6) male leucistic alligators have normal sperm concentrations, morphology, and motility (3,4).

References

1.  King R.A., Hearing,V.J., Creel,D.J., Oetting,W.S. Albinism in The Metabolic and Molecular Bases of Inherited Disease. 7th Ed Vol 3 McGraw Hill 1993.

2.  Barnett,J.D. and Cardeilhac P.T. IAAAM Proceedings 22, 1995.

3.  Larsen R. and Cardeilhac P.T. IAAAM Proceedings 23, 1996.

4.  Atkinson R. and Agular R. Pers. Com. Audubon Park Zoo New Orleans La.