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.

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A deficiency of protein C (PC), antithrombin, or protein S is strongly associated with deep-vein thrombosis in selected patients and their families. However, the strength of the association with venous thrombosis in the general population is unknown. This study was a population-based, patient-control study of 474 consecutive outpatients, aged less than 70 years, with a first, objectively diagnosed, episode of venous thrombosis and without an underlying malignant disease, and 474 healthy controls who matched for age and sex. Relative risks were estimated as matched odds ratios. Based on a single measurement, there were 22 (4.6%) patients with a PC deficiency (PC activity, less than 0.67 U/mL or PC antigen, less than 0.33 U/mL when using coumarins). Among the controls, the frequency was 1.5% (seven subjects). Thus, there is a threefold increase in risk of thrombosis in subjects with PC levels below 0.67 or 0.33 U/mL [matched odds ratio, 3.1; 95% confidence interval (CI), 1.4 to 7.0]. When a PC deficiency was based on two repeated measurements, the relative risk for thrombosis increased to 3.8 (95% CI, 1.3 to 10); when it was based on DNA-confirmation, the relative risk increased further to 6.5 (95% CI, 1.8 to 24). In addition, there was a gradient in thrombosis risk, according to PC levels. The results for antithrombin are similar to those for PC, although less pronounced (relative risk, 2.2; 95% CI, 1.0 to 4.7). We could not find an association between reduced total protein S (relative risk, 0.7; 95% CI, 0.3 to 1.8) or free protein S levels (relative risk, 1.6; 95% CI, 0.6 to 4.0) and thrombosis risk. Although not very frequent, PC and antithrombin deficiency are clearly associated with an increase in thrombosis risk.

No abstract

In making the diagnosis of deep-vein thrombosis in symptomatic outpatients, serial compression ultrasonography is preferable to impedance plethysmography, in view of its superior performance in detecting venous thrombosis.