The Komodo dragon (Varanus komodoensis) is the world’s largest lizard, with a mass up to 90 kg and a length of 3 m. It is restricted to five small islands in Eastern Indonesia where it is an apex predator, with adult lizards killing the largest ungulate prey found on the island – water buffalo, pigs and Timor deer – that often equal or exceed its own body mass. Individual dragons often kill their prey directly but also feed on carcasses of prey killed by other lizards or other agents. A large carcass enables multiple dragons to feed on one carcass at the same time.
In some cases, the ultimate demise of a prey is purportedly due to more than just direct bite induced trauma, involving bacterial sepsis acquired from the lizard’s bite or envenomation. Whilst direct bite inflicted injury is the most intuitive and oft observed mechanism to rapidly dispatch prey, the role of bacteria or venom to aid prey death is poorly known. In a study of multiple lizards, 58 species of bacteria were identified from the saliva and oral cavities, 93% of which are classified as potentially pathogenic. At least one species, tentatively identified as Pastuerella multocida, caused high mortality among mice injected with Komodo dragon saliva. Thus, the potential exists for bite-induced sepsis to contribute to prey mortality, but the bacteria may instead be coincidental to any effect on prey. Or are they?
Deathly Drool: Evolutionary and Ecological Basis of Septic Bacteria in Komodo Dragon Mouths. 2010 PLoS ONE 5(6): e11097. doi:10.1371/journal.pone.0011097
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.