Adaptations for marine habitat and the effect of Triassic and Jurassic predator pressure on development of decompression syndrome in ichthyosaurs

Decompression syndrome (caisson disease or the “the bends”) resulting in avascular necrosis has been documented in mosasaurs, sauropterygians, ichthyosaurs, and turtles from the Middle Jurassic to Late Cretaceous, but it was unclear that this disease occurred as far back as the Triassic. We have examined a large Triassic sample of ichthyosaurs and compared it with an equally large post-Triassic sample. Avascular necrosis was observed in over 15?% of Late Middle Jurassic to Cretaceous ichthyosaurs with the highest occurrence (18?%) in the Early Cretaceous, but was rare or absent in geologically older specimens. Triassic reptiles that dive were either physiologically protected, or rapid changes of their position in the water column rare and insignificant enough to prevent being recorded in the skeleton. Emergency surfacing due to a threat from an underwater predator may be the most important cause of avascular necrosis for air-breathing divers, with relative frequency of such events documented in the skeleton. Diving in the Triassic appears to have been a “leisurely” behavior until the evolution of large predators in the Late Jurassic that forced sudden depth alterations contributed to a higher occurrence of bends.     

Did ice-age bovids spread tuberculosis?

Pathognomonic metacarpal undermining is a skeletal pathology that has been associated with Mycobacterium tuberculosis in bovids. Postcranial artiodactyl, perissodactyl, and carnivore skeletons were examined in major university and museum collections of North America and Europe for evidence of this and other pathology potentially attributable to tuberculosis. Among nonproboscidean mammals from pre-Holocene North America, bone lesions indicative of tuberculosis were restricted to immigrant bovids from Eurasia. No bone lesions compatible with diagnosis of tuberculosis were found in large samples of other pre-Holocene (164 Oligocene, 397 Miocene, and 1,041 Plio–Pleistocene) North American mammals, including 114 antilocaprids. Given the unchanged frequency of bovid tubercular disease during the Pleistocene, it appears that most did not die from the disease but actually reached an accommodation with it (as did the mastodon) (Rothschild and Laub 2006). Thus, they were sufficiently long-lived to assure greater spread of the disease. The relationships of the proboscidean examples need further study, but present evidence suggests a Holarctic spread of tuberculosis during the Pleistocene, with bovids acting as vectors. While the role of other animals in the transmission of tuberculosis could be considered, the unique accommodation achieved by bovids and mastodons makes them the likely “culprits” in its spread.