A population genetic survey of over 200 structural loci previously revealed that the South African cheetah (Acinonyx jubatus jubatus) has an extreme paucity of genetic variability, probably as a consequence of a severe population bottleneck in its recent past. The genetic monomorphism of the species is here extended to the major histocompatibility complex, since 14 reciprocal skin grafts between unrelated cheetahs were accepted. The apparent consequences of such genetic uniformity to the species include (i) great difficulty in captive breeding, (ii) a high degree of juvenile mortality in captivity and in the wild, and (iii) a high frequency of spermatozoal abnormalities in ejaculates. The species vulnerability of the cheetah was demonstrated by an epizootic of coronavirus-associated feline infectious peritonitis in an Oregon breeding colony in 1983. Exposure and spread of the coronavirus, which has a very low morbidity in domestic cats (approximately 1 percent), has decimated a heretofore productive and healthy captive population. The extreme genetic monomorphism, especially at the major histocompatibility complex, and the apparent hypersensitivity of the cheetah to a viral pathogen may be related, and provide a biological basis for understanding the adaptive significance of abundant genetic variation in outbred mammalian species.

Analysis of 40 semen samples collected by electroejaculation from 18 cheetahs revealed no major differences in seminal traits among Transvaal, South West (Namibia) or hybrid (Transvaal X South West) males. However, mean spermatozoal concentration (14.5 X 10(6) spermatozoa/ml of ejaculate) and percent motility (54.0%) were less in cheetahs than in domestic cats (147.0 X 10(6) spermatozoa/ml of ejaculate, 77.0% motility) subjected to the same electroejaculation regimen. On the average, cheetah ejaculates contained 71.0% morphologically abnormal spermatozoa compared to 29.1% aberrant spermatozoal forms in the domestic cat. These results indicate that seminal characteristics in the cheetah are markedly inferior compared to the domestic cat, particularly with respect to the incidence of pleiomorphic spermatozoa. Because a recent parallel study demonstrates that the cheetah lacks genetic variation, it appears likely that spermatozoal abnormalities are a genetic consequence of genomic homozygosity characteristic of this endangered species.

The extent and progression of exposure to feline infectious peritonitis (FIP) virus in the cheetah, Acinonyx jubatus, was monitored by a worldwide serological survey with indirect fluorescent antibody titers to coronavirus. The indirect fluorescent antibody assay was validated by Western blots, which showed that all indirect fluorescent antibody-positive cheetah sera detected both domestic cat and cheetah coronavirus structural proteins. There was a poor correlation between indirect fluorescent antibody results and the presence of coronaviruslike particles in cheetah feces, suggesting that electron microscopic detection of shed particles may not be an easily interpreted diagnostic parameter for FIP disease. Low, but verifiable (by Western blots [immunoblots]) antibody titers against coronavirus were detected in eight free-ranging cheetahs from east Africa as well as from captive cheetahs throughout the world. Of 20 North American cheetah facilities screened, 9 had cheetahs with measurable antibodies to feline coronavirus. Five facilities showed patterns of an ongoing epizootic. Retrospective FIP virus titers of an FIP outbreak in a cheetah-breeding facility in Oregon were monitored over a 5-year period and are interpreted here in terms of clinical disease progression. During that outbreak the morbidity was over 90% and the mortality was 60%, far greater than any previously reported epizootic of FIP in any cat species. Age of infection was a significant risk factor in this epizootic, with infants (less than 3 months old) displaying signfficantly higher risk for mortality than subadults or adults. Based upon these observations, empirical generalizations are drawn which address epidemiologic concerns for cheetahs in the context of this lethal infectious agent.

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The de Wildt Cheetah and Wildlife Centre was established in 1971 and the first cheetah cubs were born in 1975. During the period 1975-2005, 242 litters were born with a total of 785 cubs. Mean cub survival from 1 to 12 months and greater than 12 months of age was 71.3 and 66.2%, respectively. The majority of losses (84.9%) occurred during the first month postpartum whereas only 15.1% deaths took place between 1 and 12 months of age. Females were first bred at an age of approximately 3 years, reached maximum reproductive age at 6-8 years, where after fertility declined. Males reached peak reproduction at 6 and maintained this for up to 12 years of age. Male fertility was best correlated with sperm morphology. During recent years, for practical purposes, males were allocated to 'good' (>or=70% normal), 'fair' (40-70% normal) and 'poor' (<40% normal) categories according to sperm morphology count. The breeding males were selected from the good (preferably) and fair categories but poor category males were also used at times. Average litter sizes for 'good', 'fair' and 'poor' males were 3.44 (n = 21), 3.14 (n = 18) and 2.28 (n = 18), respectively. In females the heritability for litter size was high at 0.5848 (532 progeny, 1975-2007) and the maternal heritability for cub mortality was estimated to be 0.596. The data from the de Wildt Cheetah and Wildlife Centre and two other centres in the world (Kapama and Wassenaar) demonstrate that cheetah can be bred successfully in captivity.