Abstract
Siberian tigers (Panthera tigris altaica) are a critically endangered species. Poaching and loss of habitat have drastically reduced the number of wild tigers. Captive reproduction is integral to conserving the species.
Klinefelter syndrome is any chromosomal anomaly with multiple X-chromatin genotypes.5 In humans, the most common anomaly is 47 XXY.3,4 In domestic felines, 39 XXY is commonly demonstrated by male calico and tortoise shell cats, of which more than two-thirds are sterile.1 Testicular hypoplasia, azoospermia, hyalinization and fibrosis of the seminiferous tubules, and clumping of Leydig cells are demonstrated during clinical and histopathologic evaluations.1,4
A 13-year-old intact male Siberian tiger, weighing 195 kg, housed as a single adult at the Kansas City Zoological Park (KCZP), was immobilized for annual examination during the winter of 1999. As part of the examination, a routine skin biopsy was obtained, and forwarded to the Center for the Reproduction of Endangered Species for processing (C.R.E.S., Cytogenetics Division Zoological Society of San Diego, P.O. Box 120551, San Diego, CA 92112 USA). In addition, testicular measurements and physical examination of the reproductive tract were performed.
Fibroblast cultures of the biopsy were established by tissue dissociation in 0.5% collagenase B (Boehringer Mannheim). Metaphase chromosomes were obtained from heparinized blood and fibroblasts following general protocols.3 Standard and G-banded karyotypes indicated an abnormal diploid chromosome number as the result of an additional sex chromosome. Contrary to the expected 2n=38 XY, this tiger demonstrated 2n=39 XXY.
The tiger demonstrated normal libido, often initiating mating with various enrichment items in his exhibit. However, numerous evaluations of ejaculates revealed no evidence of spermatozoa.
Approximately 1 year later, the tiger was euthanatized because of multiple intervertebral disc disease (IVDD), confirmed with myelography. Blood obtained prior to euthanasia for a complete blood count and select serum profile revealed no abnormalities other than frequent “drumsticks”1 observed in neutrophils. Histopathologic examination of formalin-fixed tissue specimens from the reproductive tract revealed a paucity of seminiferous tubules and expansion of the fibrous interstitium in the testes. Remaining tubules were devoid of spermatogonia and contained moderate numbers of sustentacular (Sertoli) cells. An increase in interstitial fibrous connective tissue was noted in sections of the prostate and epididymis.
No other histologically significant findings of the reproductive tract were demonstrated. A degenerative myelopathy, compatible with IVDD was demonstrated in the spinal cord.
In domestic cats, 39 XXY is most commonly observed in male calico and tortoise cats. The coat colors (black and orange) are controlled by allelic genes on the X chromosome and usually coexist only in individuals with two X chromosomes.2 Normal male cats have only one X chromosome, which carries the gene for orange.2 The second X chromosome in XXY individuals allows for the expression of black.
The relationship of the tiger’s normal coat colors (black, white and orange) to the XXY syndrome is undetermined at this time. Genetic lineage of this tiger is currently being evaluated.
In conclusion, we believe this finding in an SSP managed, critically endangered species mandates all institutions holding Siberian tigers to obtain skin biopsies for karyotype evaluation. Hopefully select breeding based on genetic lineage will eliminate this abnormality from the population and lead to the continued success of reproducing Siberian tigers in captivity.
Acknowledgments
The authors would like to thank the KCZP animal care staff for their care of the tiger, Dr. Doug Armstrong, Omaha’s Henry Doorly Zoo, and G. McDowell for technical assistance.
Literature Cited
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2. Chastain, C.B., Guilford, W.G., Schmidt D. 1988. The 38, XX/39, XXY genotype in cats. Compendium 2:75–87.
3. Conen P.E., Sergovich F. 1979. Chromosomal Studies in Endocrinology, 2nd ed. Hagerstown, Maryland, Harper and Row Publications, Pp. 332–381.
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5. Klinefelter H.F., Reifenstein E.C., Albright F. 1942. Syndrome characterized by gynecomastia, aspermatogenesis without aleydigism, and increased excretion of follicle stimulating hormone. J. Clin. Endocrinol. Metab. 2:615–627.