Infections of fruit are associated with rainfall and occur from fruitset until harvesting, with dead leaves entangled in the tree canopy, defoliated branch terminals, mummified inflorescences and flower bracts constituting the main source of inoculum, (Dodd et al., 1992). Conidia spread throughout the orchard by means of heavy dew, irrigation and light rain, with rainy weather being conducive to conidium production, dispersal and infection (Prusky, 1994). Once effectively attached, the conidium germinates and the germ tube grows a short distance before forming a terminal appressorium (Jeffries et al., 1990). Infection pegs are produced, but their structure depends on the stage of development of fruit at the time of infection (Coates et al., 1993).

Before forming infection hyphae, the appressoria undergo a stage of dormancy or quiescence (Jeffries et al., 1990). Suppression of fungal development is mainly by physical barriers such as surface waxes and cuticles, which inhibit germination and/or penetration. Preformed inhibitors in the mango peel are a combination of resorcinols can also further inhibit infection (Prusky & Plumbley, 1992). As the fruit ripens, these inhibitors decline to sub-fungitoxic levels, and fungal activity resumes. Cells within the peel tissue are then rapidly colonised inter- or intracellularly and subsequently degraded (Coates et al., 1993).

Since C. gloeosporioides remains quiescent in the cuticle of unripe fruit, infections can be prevented either with protective treatments or by treatment with post-harvest fungicides that penetrate the infection site, restraining further development (Prusky, 1994). Pre-harvest treatments include spraying with copper oxychloride, benomyl and mancozeb for mangos (Nel et al., 2003). Recently, azoxystrobin was also registered as a pre-harvest treatment for anthracnose. Registered post-harvest treatments are limited and include packhouse treatments with heated benomyl or prochloraz solutions (Nel et al., 2003). Alternative chemistries are currently under evaluation for post-harvest treatment of anthracnose and stem-end rot and show a great deal of promise, particularly when combined with a sound pre-harvest strategy. Other pre-harvest control strategies comprise cultural and sanitation practices, including pruning of tree canopies and insect control (Prusky, 1994). Alternative control strategies include the use of antagonistic microorganisms. Bacillus subtilis isolated from the avocado phylloplane has been successfully exploited for control of pre-harvest (Korsten et al., 1994) and post-harvest (Korsten et al., 1989) avocado diseases. This biocontrol agent also controlled pre- (Korsten et al., 1992) and post-harvest (De Villiers & Korsten, 1994) diseases of mangos.

To date, there has been a great of confusion surrounding the etiological agent of soft brown rot. However, a great deal of this was resolved in a study done by Jacobs (2002), who described and characterised the Botryosphaeria species involved. Susceptible cultivars include Irwin, Sensation, Zill, Haden and Tommy Atkins (Lonsdale, 1993b).

The pathogen is able to infect the host during any stage between flowering and harvest (Lonsdale, 1992). However, fruit is usually infected approximately six weeks after flowering by the endophytic colonization of the inflorescence, peduncle and pedicels of fruit (Johnson & Sangchote, 1994). Further infection is restricted by host defence mechanisms until the fruit are harvested, wounded or begin to ripen (Johnson and Sangchote, 1994). The exact mode of entry has not been conclusively determined. However, wounds caused by pruning, insects and sunburn seem to be the most likely route of infection (Lonsdale, 1992).

Initial stages of infection can be observed as blossom blight. Later, the infected axes, florets and fruitlets shrivel up, blacken and die. Under favourable conditions, the pathogen may move down the main axis and colonise stem tissue, resulting in die back. When fruit is infected in the orchard, the infection can remain latent until after harvest. At this stage, the pathogen colonises fruit tissue, resulting in the characteristic soft brown rot symptom during ripening (Lonsdale, 1993a). This is therefore an important mango disease since it results not only in post-harvest decay, but also poor fruit set with subsequent yield reduction (Lonsdale, 1993a).

Soft brown rot most probably originates from endophytic colonisation of the peduncle and pedicle tissue as well as from infection and colonisation of peel tissue. Fruit invasion by the pathogen is continued by growth through the stem end, colonisation of the inflorescence and systemic spread to cause a latent infection of the fruit (Lonsdale, 1993b, Saaiman, 1996). Saaiman (1996) confirmed that rainfall plays an important role in the spread of the pathogen. The initial systemic infection plays a crucial role in establishing blossom blight infection. However, secondary infection is apparently an even more important factor in soft brown rot development and incidence. With secondary infection, spores are washed away by rain from various inoculum sources such as leaves and stems on the tree (Saaiman, 1996).

Spread of the pathogen is very quick and when infected fruit come into contact with healthy fruit, they can contaminate the entire carton (Kruger et al., 1995). This causes significant problems for exporters which usually only detect rotten fruit at the end of the fruit export chain, resulting in significant financial losses (Lonsdale, 1993; Saaiman, 1996). Export mango fruit have to be transported over long distances often under specified cooling conditions, making the effective pre- and post-harvest control of the pathogen essential to minimise losses due to soft brown rot (Kruger et al., 1995).

In many cases, disease is due to mismanagement and neglect of orchards. It was confirmed by Cooke and co-workers (1998) that levels of endophytic organisms, such as Botryosphaeria spp., are reduced significantly when implementing a commercial pruning program in mango orchards as a pre-harvest control measure. Fluctuations of disease incidence would appear to relate to variation in the extent of latent infection that takes place in orchards. Latent infections can be influenced by orchard fungicide spraying, sanitation, climate and tree age (Saaiman, 1995, Sangchote, 1998a). To date, there are no registered fungicides for control of soft brown rot, although azoxystrobin applications at critical stages have been shown to significantly reduce disease incidence.

Different post-harvest practices can be used to delay disease development. These include low-temperature storage and modified or controlled atmosphere storage. A combined treatment of wax and hot water (55ºC) give very effective control of most post-harvest pathogens (Sangchote, 1998). Considerable potential exists for improving the presently utilized packhouse treatments and storage procedures (Kruger et al., 1995). Alternative chemistries are also currently under evaluation for post-harvest treatment of soft brown rot and show a great deal of promise, particularly when combined with a sound pre-harvest strategy.

While most of the diseases can be cured or controlled by techniques such as chemical spraying or dusting, prevention is still better than cure (Singh, 1960). Control of post-harvest diseases may be achieved by preventing infection, eradicating infection or delaying symptom development so that the fruit can be marketed and consumed before disease appears (Johnson & Sangchote, 1994). The best strategy is not to rely entirely on a single measure of control, but to implement a continuous integrated control strategy (Saaiman & Lonsdale, 1994). The need for effective pre- and post-harvest control measures for SBR from orchard to market cannot be emphasized enough (Darvas, 1991).