Komodo dragons are fascinating creatures – they are huge, they are aggressive and dangerous, and they are venomous! But they also have bacteria in their mouths and it was hypothesized, especially before the venom was discovered, that the bacteria play a role in killing the prey that managed to escape the first time it is attacked.
In last week’s PLoS ONE article, Deathly Drool: Evolutionary and Ecological Basis of Septic Bacteria in Komodo Dragon, authors Bull, Jessop and Whiteley investigate the mouth bacteria in Komodo dragons, the different species found in mouths of different individuals, and the way bacteria get transmitted from one individual to another.
By outfitting Komodo dragons with radio-collars, observing their behavior and identifying bacteria in their saliva and on their killed prey, they concluded that large pray carcasses act as giant petri dishes for bacteria. It takes a long time for a large animal to get eaten by the lizards, and each such carcass is eaten by multiple individual lizards over time. This is sufficient time for bacteria from the first lizard’s saliva to grow on the carcass and then ‘infect’ the mouths of subsequent lizards. The large carcasses are thus a means for bacteria to spread from one individual to another. And this mostly happens in large Komodo dragons, as small individuals tend to kill small prey that is eaten too rapidly for any bacteria to get established.
Of course, the photographs of Komodo dragons chasing the pray, and then eating the kill, are fascinating:
From the article’s Abstract:
Komodo dragons, the world’s largest lizard, dispatch their large ungulate prey by biting and tearing flesh. If a prey escapes, oral bacteria inoculated into the wound reputedly induce a sepsis that augments later prey capture by the same or other lizards. However, the ecological and evolutionary basis of sepsis in Komodo prey acquisition is controversial. Two models have been proposed. The “bacteria as venom” model postulates that the oral flora directly benefits the lizard in prey capture irrespective of any benefit to the bacteria. The “passive acquisition” model is that the oral flora of lizards reflects the bacteria found in carrion and sick prey, with no relevance to the ability to induce sepsis in subsequent prey. A third model is proposed and analyzed here, the “lizard-lizard epidemic” model. In this model, bacteria are spread indirectly from one lizard mouth to another. Prey escaping an initial attack act as vectors in infecting new lizards. This model requires specific life history characteristics and ways to refute the model based on these characteristics are proposed and tested. Dragon life histories (some details of which are reported here) prove remarkably consistent with the model, especially that multiple, unrelated lizards feed communally on large carcasses and that escaping, wounded prey are ultimately fed on by other lizards. The identities and evolutionary histories of bacteria in the oral flora may yield the most useful additional insights for further testing the epidemic model and can now be obtained with new technologies.