Biomedical Engineering Reference
In-Depth Information
breaches is mainly constituted by chitin fi brils embedded in a protein matrix
the quantity and type of proteins varying between insect species, tissue
and growth stages (Andersen 1974). The infection begins with adhesion of
the fungal spore to the insect cuticle. Though technically a single conidium
should be suffi cient to induce infection, it is observed that successful
infection of the insect does not take place unless the insect is infected by
several conidia. Surpassing a threshold dose of conidia is required for
inducing infection. This is dubbed as “Allee effect” (Devi and Rao 2006).
The entry of the fungus into the insect body is mediated both by mechanical
pressure and enzymatic processing of the insect cuticle. The conidiospores
germinate on the surface of the cuticle. Mucilage is secreted from the
conidium—a process assumed to result from utilization of lipids in the outer
layer of the insect cuticle (Boucias and Pendland 1991). A germ tube, also
called infection peg, emerges from the conidium. After about 4-8 hours,
the germ tube stops growing and begins to swell at the tip due to building
up of water (turgor) pressure. The resultant swollen structure is called an
appressorium (
Figs. 1a and b)
(fi gure legend: Formation of infection peg and
appressorium (a) germinating conidium with appressorium (b) Scanning
electron micrograph showing appressoria (1) in and around a setal socket
(2) on the insect cuticle). It is designed to exert enough pressure to force
the germ tube into the insect. Thus, formation of the appressorium plays a
pivotal role in establishing a pathogenic interaction with the host. Adjunct to
mechanical force of the appressorium, a wide range of extracellular enzymes
secreted from the germ tube are supposed to facilitate the aggression of
the fungus into the insect. The infection peg penetrates the cuticle (Fig.
1c) (fi gure legend: diagrammatic representation of conidial germination
on an insect cuticle) gaining access to the nutrient rich hem lymph. In the
insect hemocoel, the fungal hypha breaks into multinucleate fragments.
These fragments produce naked protoplasts to evade immune response
of the insect (Tanada and Kaya 1993). Fungi are termed hyphal bodies
(Alexopoulos et al. 1996). The infection process is depicted in fi gure 1d
(fi gure legend: diagrammatic representation of structure of insect cuticle and
mode of penetration (according to Clarkson and Charnley 1996). The hyphal
bodies multiply through budding and spread systemically in the insect body
depleting its nutrients. The infected insect loses appetite and also develops
fever. The hyphal bodies secrete toxins in the hemocoel. Multiple factors—
weakening of insect due to aggressive colonization of the fungus in its body
and the toxins lead to fi nal succumb of the insect. Death occurs suddenly
due to the paralyzing effect of the neurotoxins secreted by the fungus such
that insect cadavers are seen in
in situ
movement postures. The dead insect
is mummifi ed. Following the death of the host, fungal growth reverts back
to the typical hyphal form (the saprotrophic stage).The mycelium grows
out of the cuticle and proliferates on it leading to a cottony covering on
