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documented lengths up to (and possibly exceeding) 3.4 m], 18 has caused human
fatalities. 19 As a result of the discovery of toxins in the oral secretions of these liz-
ards, they have been prematurely labeled “venomous.” This information has been
sensationalized and accepted by the press (and some of the established scientific
community) without further verification. Consideration must be given to the current
consensus definition of venom (see p. 32), and the need for evidence supporting the
use of venom in the subjugation/capture of prey and/or as an antipredator strategy.
Although there are toxins of several classes common to venomous snakes present in
the oral secretions of these lizards, there is no evidence verifying the use of these in
prey capture. Their function may be a result of “preadaptation” (also referred to as
“exaptation”; Gould and Vrba, 1982), an evolutionary phenomenon that assigns pre-
vious characters of ancestors in one biological role being co-opted to new biological
roles in later descendants (Gould, 2002). Toxins that occur in oral secretions, when
biochemically documented in colubroid snakes and basal squamates, do not automat-
ically qualify the reptile as venomous. Instead, these toxins may play different bio-
logical roles in basal groups, later to be co-opted into a new role in the true venom
system of derived snakes (Weinstein et al., 2010). Therefore, these genes and their
products (in these cases, toxins) are “exapted” (adapted at a later date) from earlier
phylogenetic roles into new derived roles (Arthur, 2002). The only way to confirm
a toxin's biological role in basal squamates is by experimental confirmation and/or
extensive, well-documented field observations.
There is also no evidence of medical significance of these saurian secretions. While
it is agreed that the oft proposed and popular theory of V. komodoensis prey capture via
sepsis 20 is most likely incorrect, to date the few well-documented cases of bites inflicted
on human victims by this endangered species have only included infection, physical
trauma, and blood loss. In the most recent documented attack (the first fatality docu-
mented in approximately 33 years), an 8-year-old boy was tragically killed after being
bitten on the “waist,” and “tossed viciously from side-to-side,” he “died from mas-
sive bleeding half an hour later” ( The Guardian , Monday, June 4, 2007). Auffenberg
(1981) reported two uncomplicated aseptic bites inflicted by 1.0-1.2 m specimens.
Interestingly, a recent consideration of the potential role of oral bacterial flora of
V. komodoensis contemplated a new model (“lizard-lizard epidemic”), partly based
on field observations, in which bacteria spread epidemically among lizards via oral
18 According to the US National Zoological Park, Smithsonian Institution ( http://nationalzoo.si.edu ), the
largest verified specimen reached a length of 3.13 m and weighed 166 kg (this may have included the
weight of a recent undigested meal). More typical weights for the largest wild dragons are about 70 kg. A
recent study found average snout-vent lengths (SVL) ranged between 74.7 and 92.1 cm and mass between
7.9-23.5 kg among a significant sampling of specimens from four islands in the Komodo National Park.
Maximal V. komodoensis SVL and mass were strongly correlated with prey density [specifically, Timor
deer ( Cervus timorensis )] on a given island (Jessop et al., 2006).
19 See Auffenberg (1981) for a detailed, fascinating discussion of the biology and predatory behavior of
V. komodoensis and historical examples of fatal attacks by this imposing species of giant lizard.
20 Multiple taxa of pathogenic bacteria have been identified and cultured from the oropharynx of V. komo-
doensis . These included several taxa of Streptococcus , Staphylococcus , Pasteurella multocida , and a num-
ber of other organisms. The colonizing flora between captive and wild lizards was notably different, with
wild specimens containing a preponderance of potential pathogens (see Montgomery et al., 2002).
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