The biggest problem for Tyrannosaurus rex could have been a single-celled parasite in a paleolithic turn on the tiny-fells-mighty, War of the Worlds story.
A relative of lowly Trichom*onas, a microbe commonly found today in pigeons, may have killed off Sue, the famous T. rex skeleton at the Chicago Field Museum, and many other tyrannosaurids, too.
Paleontologist Ewan Wolff of the University of Wisconsin-Madison and colleagues use evidence from modern predatory bird species to argue that the protozoan parasite could have formed lesions along the tyrannosaur mandible, eroding the bone away.
In some cases, the illness might have been bad enough to prevent the animals from feeding, leading to their death from starvation, and creating telltale holes in the jaws of the great beasts.
"I think it's very tempting when you see a hole in a bone to say it's bite marks, but there are innumerable disease you could list that cause holes in bones that have nothing to do with bite wounds," said Ewan Wolff, lead author of a new paper describing the work published Sept. 29 in PLoS One.
There are three pieces of evidence against the bite-wound hypothesis, Wolff said. First, the holes are generally nicely circular or ovoid, not obviously tooth-shaped. Second, dinosaurs obviously had many teeth, not just one, and the holes don't seem to come in groups. Third, there are no smaller marks or scrapes on the bone surrounding the holes.
"We're definitely familiar with what predation traces look like from tooth marks in tyrannosaurus," Wolff said. "And this is not it."
Furthermore, they found evidence in predatory birds that trichom*onosis can cause holes in the mandible that look quite similar to those found in nine tyrannosaurid specimens.
The disease could have been passed to dinosaurs from their prey or from tyrannosaur to tyrannosaur during combat, mating, or cannibalism.
"Head or face-biting behavior relating to intraspecific territoriality, social dominance, courtship, feeding or some other unknown aspect of tyrannosaurid behavior would have provided the ideal mechanism for the transmission of this trichom*onosis-like disease," Wolff and colleagues wrote.
Other researchers, notably dinosaur anatomy expert Elizabeth Rega of Western University of Health Sciences in Pomona, California, have argued the holes were disease-induced. But Rega's culprit was a bacteria on the model of actinomyces.
Wolff, however, argued that much of the damage that actinomycosis causes in humans is due to pus. Birds don't actually create puss, and the same was likely true of dinosaurs. It's not part of the avian immune response. Instead, birds coat invading organisms with a fibrous protein.
"So instead of getting puss, you get this very cheesy inflammatory area," Wolff said. "You get chronic infection that just doesn't go away."
He said that the actinomycosis-trichom*onosis debate showed how his team's approach differed from other paleopathologists.
"In the past, a lot of comparisons of paleopathological specimens have been made to humans or domesticated animals," Wolff said, instead of with dinosaurs' closer relatives, birds and reptiles. "It makes a lot of sense to look at animals that share a close evolutionary relationship to each other and the diseases that they have. The approach in this article is to do just that and that's relatively novel in the paleopathological community."
