The infection cycle of Beauveria bassiana in invertebrates bodies has been depicted by Mascarin and Jaronski (2016) Asexual spores (conidia) are dispersed by wind, rain splashing or even by arthropod vectors facilitating the fungus to establish infection on susceptible hosts (OrtizUrquiza and Keyhani 2013).
The host infection by the fungus occurs in four steps: adhesion, germination and differentiation, penetration, and dissemination.
- 1st step: adhesion.
It is characterized by recognition and compatibility mechanisms of conidia of the host cuticle cells (Vey et al. 1982 reported by De Kouassi 2001). Conidia (or in some cases blastospores) were attached to insect’s cuticle by electrostatic and chemical forces (Mascarin and Jaronski 2016). Then, through the production of mucilage, they induced epicuticular modification (Wraight and Roberts 1987) leading to conidia germination.
- 2nd step: germination-differentiation.
Germination is a process that depends on environmental conditions, host physiology (biochemical composition of the host cuticle) as well. Such conditions can stimulate or inhibit it (Butt et al. 1995; Butt and Beckett 1994; Smith and Grula 1982; St Leger et al. 1989b). When conditions are suitable, conidia or blastospores germination leads to germ tubes formation. In fact, conidia germinate and form a germ tub with rehydration and chemical stimuli (Mascarin and Jaronski 2016). Differentiation is characterized by the appressoria or penetration peg establishment, which serves as inking point, softening the cuticle and promoting penetration. For this purpose, the germ tub may form a specialized structure, namely appressorium (i.e., an enlarged cell expression bearing key hydrolytic cuticle-degrading enzymes) or penetration peg enabling hyphae growth to breach the host integument (De Kouassi 2001; Mascarin and Jaronski 2016). However, appressoria production is highly dependent on nutritional value of the host cuticle (Magalhaes et al. 1988; St Leger et al. 1989a). A nutritious cuticle may stimulate mycelial growth rather than penetration (St Leger et al. 1989a).
- 3rd step: penetration.
From the appressorium or penetration peg and with the hydrolytic action of enzymes (proteases, chitinases, lipases: the most important being proteases), mechanical pressure, and other factors (such as oxalate), the fungus is able to penetrate all cuticle layers until reaching a nutrient-rich environment, i.e. the insect hemolymph.
- 4th step: dissemination within the host and to another host.
In the hemolymph, the fungus undergoes a morphogenetic differentiation from filamentous growth to single-celled, yeast-like hyphal bodies or blastospores that strategically exploit nutrients, colonize internal tissues, and disturb the host immune system. During this stage of the infection, the fungus can also secrete toxic metabolites that help to overcome the insect’s immune defense mechanisms for successfully colonization. Some strains produce non-enzymatic toxins such as beauvericin, beauverolides, bassianolides, and isarolides increasing the speed of the infection process (Hajeck and StLeger 1994; Roberts 1981). These events eventually lead to the death of host that became mummified. When the infected insect dies, the fungus produces an antibiotic called “Oosporin” that is used to overcome bacteria competition in insect gut (De Kouassi 2001). Then, B. bassiana hyphae cross the insect integument preferentially at the inter-segmental level and then become cottony white. Finally, conidiophores appear on the mummified cadavers after a few days and bear newly infection conidia (sporulation) for dispersal (passive dissemination).
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