(a) In both susceptible and resistant cultivars of sorghum, spores (S) germinated to produce appressoria (A). At the base of the appressoria a pore develops, the penetration pore (PP) which is surrounded by highly thickened cell walls (arrows). An infection peg (IP) emerges through the pore and penetrates the cuticle and epidermal cell wall (CW). Once inside the epidermal cell the infection peg enlarges to form the infection vesicle (Ve). Note the infection peg has a very small diameter where it passes through the cell wall and there is very little, if any, cell wall dissolution. In susceptible cultivars the host plasmalemma and cell cytoplasm (C) is invaginated around the infection vesicle.

(b) Primary hyphae (PH) begin to branch out from the infection vesicle approx. 42 hours after inoculation. The primary hyphae grow intracellularly with the host plasmalemma (P) invaginated around them. Note the fungal cell wall (FCW) is very thin and there is no significant matrix between it and the host. The cell organelles, such as the nucleus (N), remain intact and the cell cytoplasm (C) appears normal.

(c) As the primary hyphae (PH) advance from cell to cell, the previously infected cells gradually lose their viability, the host plasmalemma (P) becomes fragmented, the cell cytoplasm (C) becomes disorganised and the cell organelles disappear. The fungal cell wall also starts to become thicker.

(d) Approximately 66 hours after inoculation narrow secondary hyphae (SH) start to branch out from primary hyphae (PH) within epidermal cells and radiate into adjacent epidermal and mesophyll cells. Note that the cell appears void of cytoplasm with just a few fragments of plasmalemma (P) remaining. Note also that where the primary hyphae passes from one cell to the next it is highly constricted.

(e) The secondary hyphae (SH) proliferate throughout the tissue growing both intra and inter-cellularly. They also grow within cell walls causing massive damage with extensive dissolution of the cell wall (CW). (Cu) Cuticle.

(f) After 90 hours the secondary hyphae start to form swellings beneath the leaf cuticle (Cu). These then rupture the cuticle forming acervuli which contain the setae (Se) and conidiophores (Co) which produce fungal spores (S).

(a) As noted previously (Fig. 3) pigmented inclusions accumulate in infected epidermal cells around the site of penetration. These inclusions (In) are densely stained by lead citrate/uranyl acetate under the electron microscope. Note that the cytoplasm of the cell (C) is still mainly intact although it is starting to disintegrate and the plasmalemma(P) is starting to fragment.

(b) In some cases, during penetration varying amounts of wall apposition material were deposited outside the plasmalemma (P) around the infection peg (IP), forming a papilla (Pa). Most hyphae were not restricted by this material, but occasionally the hypha became completely encased, and further development was prevented. Papillae are formed in both compatible and incompatible interactions.

(c) As the infection progressed the papillae become impregnated with the host defense compounds which also accumulate inside the infection vesicles (Ve). The infection vesicle appears empty and devoid of cytoplasm with only the darkly staining compounds present.

(d) By 42 hours after inoculation the inclusions have coalesced and what little cytoplasm (C) remains in the cells appears foamy in nature.