Differences in Immune Defense Evasion of Selected Inbred Lines of Heterorhabditis Bacteriophora in Two White Grub Species

Abstract

We determined virulence of seven Heterorhabditis bacteriophora strain GPS11 inbred lines possessing superior infective juvenile longevity, and heat and ultra violet radiation tolerance against white grubs Popillia japonica and Cyclocephala borealis. At 1 and 2 weeks after treatment, inbred line A2 was significantly more virulent towards P. japonica compared to the parent strain GPS11 and inbred lines A7, A8, A12 and A21; and line A2 caused significantly higher C. borealis mortality than lines A6 and A12. Penetration, encapsulation and survival of two inbred lines, A2 and A12, that showed the highest and lowest virulence against both grub species were then assessed. There were no differences between the two lines for the total number of nematodes penetrated in either P. japonica or C. borealis within the first 24 h, but a significantly higher percentage of penetrated nematodes were alive in line A2 compared to the line A12 in both grub species. P. japonica immune response over time to hemocoel-injected nematodes of A2, A12 and the parent strain was further investigated. While all injected nematodes were encapsulated at 6 h post injection, non-encapsulated living nematodes were detected at 12 and 24 h post injection, showing the breakage out of encapsulation. A higher percentage of non-encapsulated living nematodes and a lower percentage of dead nematodes were found in line A2 as compared to the line A12 after 12 h post injection. These data suggest that virulence differences in the studied H. bacteriophora inbred lines are not due to differences in nematode penetration or recognition by the grub immune system, but are related to the ability of the infective juveniles to break out of encapsulation.

Virulence of Native EPN Strains and their Symbionts alone to Polyphagous Lepidopteran Pests vis a vis Model Insect Galleria melonella along with in vivo Production

“…Once inside the host insect, the nematodes and the multiplying bacteria in the hemocoel produce virulence factors resulting in insect death [8]. Developing nematodes feed on the bacteria by disintegrating host tissues, produce 1-3 generations and when the food resources are exhausted; nematodes emerge as IJs to seek new hosts [9]. During host invasion, the bacteria release several toxins and exoenzymes that play a role in insect death.…”

Cellular reactions of the white grub larvae, Polyphylla adspersa, against entomopathogenic nematodes

“…Therefore, IJ were likely to escape from the capsule by releasing the bacteria that eventually cause host death. An et al (2012) stated that differences between the virulence of H. bac teriophora inbred lines were related to the ability of ne matodes to break out of encapsulation. Similarly, Li et al (2007) indicated that the immune suppression ability of EPN (S. glaseri in Manduca sexta and H. bacteriophora in Immunity response of Polyphylla adspersa larvae against entomopathogenic nematodes G. mellonella) is correlated with their escape from encap sulation leading to successful infection by nematodes.…”

“…Currently, the salient management tool for P. adspersa is the ap plication of chemical insecticides, mainly organophosphates (Radjabi, 1991). Due to concerns related to chemi cal control, an effective, safe and environmentally friendly biocontrol alternative, based on entomopathogenic nema todes (EPN) such as Steinernema scarabaei, S. arenarium, S. glaseri, S. kushidai, Heterorhabditis bacterio phora and H. megidis, is being considered (Klein, 1990;Poinar, 1990;Koppenhofer & Fuzy, 2003;Klein et a l, 2007;An et al, 2012). Among these species, S. glaseri and H. bacteriophora are natu ral pathogens of white grubs (Glaser & Fox, 1930;Poinar, 1990) including P. adspersa .…”

Susceptibility variation to different entomopathogenic nematodes in Strategus aloeus L (Coleoptera: Scarabaeidae)

“…The bacteria can subsequently proliferate in the host causing septicemia, permitting the nematode to develop its life cycle. (An et al 2012 ; Bisch et al 2015 ). Collectively, reports describe some bacteria are capable of eliciting a pathogenic reaction, therefore the host’s immune response acts by encapsulation, phagocytosis, among others.…”

“…Contrary to that reported in the literature, S teinernema sp3 JCL027 had a greater susceptibility compared with Heterorhabditis efficacy against S. aloeus third instar larvae. We suggest S teinernema sp3 JCL027 IJs were able to overcome the host’s barriers and physiological mechanisms to evade an immune response or digestive tract acidity, permitting the subsequent nematode-bacteria infective cycle development (An et al 2012 ; Demir et al 2014 ). Taking into account Scarabaeidae and Melolonthidae immune response defense, in particular during their third instar (Griffin et al 2005 ), we expected S. aloeus would be more susceptible to Heterorhabditis than Steinernematids based on certain advantages (Khatri-Chhetri et al 2011 ; Vashisth et al 2013 ).…”