In the natural environment, Caenorhabditis elegans and closely related nematodes are thought to associate with invertebrate hosts for transport (phoresy) or for food (necromeny) (Kiontke and Sudhaus, 2006). Recently, Abebe et al. (Abebe et al., 2010) showed that by feeding C. briggsae (and other Caenorhabditis species) Serratia marcescens (Serratia sp. SCBI), they could turn a normally benign nematode into a lethal entomopathogen capable of infecting and killing wax moths (Galleria mellonella). This behavior is similar to entomopathogenic nematodes (EPNs) from the genera Steinernema and Heterorhabditis, which have formed a mutualistic symbiosis with the bacteria Xenorhabdus and Photorhabdus, respectively (Forst et al., 1997). These bacteria are released by nematodes upon penetration into the insect host and cause death within 24–48 hours as a result of bacterial toxin production (Ciche, 2007). The nematodes reproduce prolifically on the dead host and, once the food source is depleted, new infective juveniles are produced that then search for new hosts.
Can Caenorhabditis spp. become pathogenic insect killers similar to EPNs by feeding on Serratia sp. SCBI? Abebe et al. showed that C. briggsae fed Serratia sp. SCBI and then injected into insects caused toxicity (Abebe et al., 2010). Serratia sp. SCBI is extremely toxic to G. mellonella and causes 100% mortality when injected with 100 cells per insect. The authors state that the nematodes were “transformed to become entomopathogenic.” However, both “nematodes and associated bacteria” were injected into G. mellonella and so Serratia sp. SCBI killed G. mellonella and the nematodes reproduced on the cadaver. In a second experiment, Caenorhabditis spp. were grown on Serratia sp. SCBI and exposed to G. mellonella for 7 days. Unfortunately, there was no surface sterilization procedure to eliminate bacteria from the nematode cuticle and therefore it is impossible to discount the possibility that residual transfer of Serratia sp. SCBI on the nematode epidermis or in the gut or bacterial proliferation in the prepared plate caused G. mellonella to die. The pathogenicity shown in Abebe et al. (Abebe et al., 2010) is simply the effect of C. briggsae inadvertently introducing Serratia sp. SCBI into and/or onto G. mellonella. In addition, C. briggsae and other Caenorhabditis species lack specific morphological adaptations that allow genuine symbiosis between nematodes and bacteria such as EPNs (Martens and Goodrich-Blair, 2005). Therefore, the authors have failed to demonstrate the pathogenicity of Caenorhabditis species and the symbiotic nature of this association.
All known EPNs can only reproduce on one bacterium, inside a parasitized host, and only infective stage juveniles, not adults, are found in soil. Abebe et al. tried to isolate adult C. briggsae from soil or rotting fruits to further show similarities to EPNs (Abebe et al., 2010). The sampling had a negative outcome and no adults were obtained, although the authors argue that this “clearly points towards the true entomopathogenic nature of the strain.” We feel that this proves nothing about the life history of C. briggsae. It is rare to find adults from a range of phoretic and necromenic nematodes in soil; e.g. C. elegans and Pristionchus pacificus are generally only found as third-stage infective (dauer) juveniles and are not parasitic (Weller et al., 2010). It is thus overstating the case to say that C. briggsae or any other Caenorhabditis species are actually entomopathogenic nematodes.
