Diseases of captive cheetahs (Acinonyx jubatus): Results of the cheetah research council pathology survey, 1989–1992

Knowledge of the diseases of cheetahs is essential to prevent and treat conditions that can modulate fertility and longevity. Toward this aim, a comprehensive pathology survey was conducted under a directive from the Cheetah Species Survival Plan. To date, 31 adult cheetahs and nine cubs from 16 zoological parks have been evaluated. Also, liver biopsies from 67 female cheetahs from 22 zoological parks were examined. Veno-occlusive disease (VOD) affected 82% of deceased cheetahs and 51% of live female cheetahs, and was the cause of death in nine cheetahs. Glomerulosclerosis and nephrosclerosis affected 84% and 39% of the population, respectively, and caused renal failure in eight cheetahs. The severity of VOD and glomerulosclerosis increased with age, and was not associated with infertility. Chronic gastritis was noted in 91% of the study population, and 95% of these cases also had spiral bacteria. Feline infectious peritonitis caused the death of two cheetahs. Male cheetahs had testicular degeneration, atrophy, and/or spermatogenic arrest, but these cheetahs also had severe systemic illness. Most females did not have reproductive tract lesions that would cause infertility, including those with parovarian cysts. Ovarian histology suggested that infertile cheetahs were not ovulating. Most cubs died from pneumonia or other systemic infections. The results of this study indicate that serious diseases are prevalent in the North American cheetahs, but these diseases do not appear to be the cause of infertility in the population. However, these diseases do limit the life span and well-being of cheetahs in captivity. Further research is needed to elucidate the causes of these diseases. © 1993 Wiley-Liss, Inc.     

Watching proteins in motion

A report of the 23rd Protein Symposium 'Proteins in Motion', Boston, USA, 23-27 July 2009.     

Biosynthesis of lipid A. Enzymatic incorporation of 3-deoxy-D-mannooctulosonate into a precursor of lipid A in Salmonella typhimurium.

The cell envelope fraction of Salmonella typhimurium contains an enzyme system which catalyzes transfer of 3-deoxyoctulosonate (KDO) from CMP-KDO to an incomplete, KDO-deficient precursor of lipid A. The enzyme system is firmly membrane-bound, but has been solubilized by treatment with nonionic detergent at alkaline pH and partially purified. Both the particulate and partially purified fractions catalyzed formation of a single reaction product containing 2 residues of KDO. Periodate oxidation of the purified product permitted tentative identification of the KDO disaccharide structure as KDO2-4KDO.     

MTOR,PIK3C3, and autophagy: Signaling the beginning from the end

A key point in starvation-induced autophagy occurs at the end of the process, where lysosomes are regenerated from autolysosomes through a pathway termed autophagic lysosome reformation (ALR). ALR occurs when autolysosomal MTOR becomes reactivated by amino acids derived from the autophagic delivery of protein cargo. This activation not only turns off autophagosome formation but also leads to reformation of lysosomes, ready for the next round of autophagy, through a series of events involving autolysosomal tubulation. We have now found that MTOR regulates multiple steps of ALR including direct activation of the PIK3C3-UVRAG lipid kinase complex to enable autolysosomal tubules to break away and regenerate lysosomes.