Abstract
Black-footed cats (Felis nigripes) are native to arid grassy habitats in southern Africa and are currently listed in Appendix I of CITES. They are the smallest of the felid species, weighing approximately 1–2 kg. In contrast to many species that tend to live longer in captive settings, black-footed cats tend to have shorter life-spans in captivity than in the wild. The average life-span of black-footed cats in captivity is three to five years while free-ranging cats have been estimated to live approximately five to six years. A retrospective review of necropsy records identified amyloidosis as a significant cause of mortality within the captive population (N. Lamberski, unpublished data).
The amyloidoses are a group of diseases that are characterized by intracellular or extracellular deposition of insoluble fibrillar protein.2 Over 20 different precursor proteins have been identified in the various forms of amyloidosis, with each disease having a specific amyloidogenic protein. Amyloidosis may be classified as systemic (involving multiple organs) or localized (affecting a single organ or tissue). The most severe clinical form of systemic amyloidosis in both mammals and birds is AA amyloidosis, which often results in hepatic or renal failure. In this condition, amyloid fibrils are derived from serum protein AA (SAA) that is produced predominantly in the liver. Production of this protein by the liver is increased in response to inflammation and, therefore, AA amyloidosis is often seen secondary to chronic inflammatory processes. Among non-domestic species, cheetahs (Acinonyx jubatus),10 dorcas gazelles (Gazella dorcas),11 and Anseriformes3,6,8 appear to be uniquely susceptible to develop AA amyloidosis secondary to chronic infections. Familial or breed specific forms of AA amyloidosis occur in dogs4,7 and catsl and may be associated with chronic stress5. In the Abyssinian cat, amino acid sequence variations in the SAA protein may render it more amyloidogenic, but additional factors affecting production or processing of the precursor protein may also be involved in the pathogenesis of familial AA amyloidosis.
To better characterize the pathogenesis of amyloidosis in black-footed cats, necropsy samples from 33 black-footed cats representing the North American, European, and Southern African captive populations were reviewed. In addition, necropsy samples from one free-ranging juvenile were examined. Amyloidosis was present in 88% of animals and was the cause of death in a percentage of all cases. Amyloid was present in the kidneys, gastrointestinal tract, spleen, lymph nodes, adrenal, and/or thyroid glands. Within the kidneys, amyloid deposition occurred both in the glomeruli and the medullary interstitium. All eight facilities had at least one affected animal, and the free-ranging animal was also affected. Average age of affected animals was 4.67 years, while the average age of unaffected animals was 11.5 years. There was no apparent sex predilection. Concurrent inflammation was prevalent among affected animals, but inflammation was generally mild and, in some cases, only acute. Adrenal hyperplasia was also prevalent among affected animals. If the amyloid in black-footed cats is AA, then these concurrent conditions (chronic inflammation and chronic stress) may be the underlying cause. Ongoing studies are utilizing immunohistochemistry9,12,13 to determine the type of amyloid in tissues of black-footed cats. Additionally, pedigree information from the International Studbook will be used to evaluate a familial basis for amyloidosis in black-footed cats. This information will be combined with the results of the necropsy survey to identify potential risk factors for the development of amyloid in black-footed cats. The results of these continuing studies will be critical for improved medical management of this species and may, if familial tendencies are determined, dramatically impact captive breeding recommendations.
Acknowledgments
This study was funded through a grant from the American Association of Zoo Veterinarians Mazuri Fund. The authors wish to thank Dr. Alex Sliwa and Gea Olbricht for contributing samples from the European captive population and the samples from a free-ranging black-footed cat, as well as Dr. Lorna Bolton for providing samples and information from the South African captive population.
Literature Cited
1. Boyce JT, DiBartola SP, Chew DJ, Gasper PW. Familial renal amyloidosis in Abyssinian cats. Vet Pathol. 1984;21:33–38.
2. Cotran RS, Kumar V, Collins T. Robbins Pathologic Basis of Disease. Philadelphia, PA: WB Saunders; 1999.
3. Cowan DF, Johnson WC. Amyloidosis in the white Pekin duck. I. Relation to social environmental stress. Lab Invest. 1970;23:551–555.
4. DiBartola SP, Tarr MJ, Webb DM, Giger U. Familial amyloidosis in Chinese Shar Pei dogs. JAVMA. 1990;197:483–487.
5. Germann PG, Kohler M, Ernst H, Baumgart H, Mohr U. The relation of amyloidosis to social stress induced by crowding in the Syrian hamster (Mesocricetus auratus). Z Versuchstierkd. 1990;33:271–275.
6. Guo JT, Aldrich CE, Mason WS, Pugh JC. Characterization of serum amyloid A protein mRNA expression and secondary amyloidosis in the domestic duck. In: Proceedings from the National Academy of Sciences. 1996.25:14,548–553.
7. Johnson KH, Sletten K, Hayden DW, O’Brien TD, Tossow KD, Westermark P. AA Amyloidosis in Chinese shar-pei dogs: immunohistochemical and amino acid sequence analysis. Amyloid: Int J Exp Clin Invest. 1995;2:92–99.
8. Kramer JM, Montali RJ, Strandberg JD, Fortner JH. Avian amyloidosis. In: Montali RJ, Migaki G, eds. The Comparative Pathology of Zoo Animals. Washington, DC: Smithsonian Institution Press; 1980:317–325.
9. Ma Z, Westennark GT, Johnson KH, O’Brien TD, Westennark P. Quantitative immunohistochemical analysis of islet amyloid polypeptide (IAPP) in normal, impaired glucose tolerant, and diabetic cats. Amyloid. 1998;5:255–261.
10. Papendick RE, Munson L, O’Brien TD, Johnson KH. Systemic AA amyloidosis in captive cheetahs (Acinonyx jubatus). Vet Pathol. 1997;34:549–556.
11. Rideout BA, Montali RJ, Wallace RS, Bush M, Phillips LG Jr., Antonovych TT, Sabnis SG. Renal medullary amyloidosis in dorcas gazelles. Vet Pathol. 1989;26:129–135.
12. Roertgen KE, Lund EM, O’Brien TD, Westennark P, Hayden DW, Johnson KH. Apolipoprotein AI-derived pulmonary vascular amyloid in aged dogs. Am J Pathol. 1995;147:1311–1317.
13. Westennark P, Johnson KH, Sletten K, Hayden DW. AA-amyloidosis in dogs: partial amino acid sequences of protein AA and cross-reactivity with human and cow AA-amyloid. Compo Biochem Physiol. 1985;82:211–215.