## 1 Introduction  
Lethal bronzing (LB) is a fatal phytoplasma disease affecting over 20 different species of palm (Arecaceae) [1]. It is widespread in Florida, USA, causing significant economic losses throughout the entire state [2]. Symptoms of LB involve an initial necrosis of the infloresence and/or premature fruit drop, a browning or bronzing of oldest fromds that rapidly progresses to younger fronts, and the eventual death of the plant, as evidenced by collapse of the spear leaf. Recently, the vector of LB was identified as the planthopper _Haplaxius crudus_ (Hemiptera: Cixiidae) [3], which is a very widespread and abundant species in Florida and the Caribbean basin (including Mesoamerica and northern South America) [4]. During survey work in Florida in areas with active disease spread, it was demonstrated that populations of _H. crudus_ were higher in areas of LB incidence and appeared to preferentially feed on LB-infected palms over healthy individuals [5]. Furthermore, the difference between LB-infected and healthy trees was demonstrated using a low-cost electronic nose (eNose) [6]. These findings indicate that there is likely one or several volatiles emitted from LB-infected palms that may cause _H. crudus_ to orient towards them, thus utilizing this chemical queue. Plants generally respond to stress through releasing volatile organic compounds (VOCs). Green-leaf volatiles (GLVs) are C6 compounds of alcohols, esters, and aldehydes that attract or repel insects, as well as activate plant defenses, that can possess antimicrobial properties via the hydroperoxide lyase pathway of oxylipin metabolism. As such, GLVs serve as a means of plant-to-plant communication for warning of mechanical damage, herbivory, fungal or bacterial infection, abiotic stress such as drought, heat, and high light [7; 8]. The GLVs released can provide precise information about the location of an attacking herbivore, demonstrating that plants can evolve to recognize a pest or microbe (fungi, virus, or bacteria) and initiate their defense mechanisms [9; 10]. There are reports that the piercing/sucking behavior of some hemipteran insects showed a lower concentration of GLVs when compared to chewing insects [11; 12]. Recently, the vector (_Diaplorina citri_) of '_Candidatus Liberobacter_ asiaticus_' (causal agent of citrus greening) was shown to prefer non-infected hosts (_Citrus sinensis_), while vectors that were not carrying the pathogen preferred infected citrus [13]. In this study, it was demonstrated that Z-3-hexenyl and methyl salicate were the principal compounds involved in vector-vector interactions. This suggests that VOCs can influence pathogen-vector interactions, ultimately influencing the epidemiology of a given plant disease. Another study revealed that tobacco (_Nicotiana occidentalis_), apple (_Malus domestica_), and pear (_Pyrus communis_), infected with the phytoplasma '_Candidatus phytoplasma_ mail' demonstrated a significant increase in ethyl benzoate concentrations relative to non-infected plants [14]. In addition, for the infected plants, the VOC profile differed from that of the healthy plants and showed high concentrations of unidentified sesquiterpene in tobacco and methyl salicate in apple trees. The interaction between GLVs and plant hormones, such as salicylic and jasmonic acids, induces or stimulates plant defenses that are regulated through a complex communication network located between hormonal pathways that influences the plant-pathogen-vector interaction. This system allows plant-to-plant communication about an insect or microbe attack [15; 16; 17]. A common phenomenon in plants and insects is the ability to convert Z-3-hexenal to its E-2-hexenal isomer after fungal infection or herbivory. However, many questions are yet to be clarified regarding this conversion relation to wound induction or insect derivatives introduced into the wound during feeding. However, the main function and the benefits of this increase in the concentration of E-2-hexenal are yet to be fully elucidated [8].