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Disease Cycle and Epidemiology

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Disease Cycle

Bacteria propagate in lesions in leaves, stems, and fruit. When there is free moisture on the lesions, the bacteria ooze out and can be dispersed to infect new growth. Wind-driven rain is the main dispersal agent and wind ≥ 8 m/s (18 mph) aids in the penetration of bacteria through the stomatal pores (Drawing of the disease cycle) or wounds made by thorns (Figure 20), insects (leafminer) (Figure 11), and blowing sand. Pruning causes severe wounding and can lead to infection. Multiplication of bacteria occurs mostly while the lesions are still expanding and numbers of bacteria produced per lesion is related to general host susceptibility (Figure 22 graph of growth).

Figure 20	Figure 12
Figure 22

The bacteria remain alive in the margins of the lesions in leaves and fruit until they abscise and fall to the ground. Bacteria have also been reported to survive in lesions on woody branches up to a few years of age (Figure 23). Bacteria that ooze onto plant surfaces do not survive and begin to die upon exposure to rapid drying. Death of bacteria is also accelerated by exposure to direct sunlight. Survival of exposed bacteria is limited to a few days in soil and to a few months in plant refuse that is incorporated into soil. On the other hand, the bacteria can survive for years in infected plant tissues that have been kept dry and free of soil.

Figure 23

Epidemiology

Infection: Leaves, stems, and fruit become resistant to infection as they mature unless they are wounded. Almost all infections occur on leaves and stems within the first 6 weeks after initiation of growth. The most critical period for fruit rind infection is during the first 90 days after petal fall. Any infection that occurs after this time results in the formation of only small and inconspicuous pustules. Because the fruit are susceptible over longer periods compared to leaves, infections can result from more than one dispersal event resulting in lesions of different age on the same fruit (Figure 8). Fruit can also act as an indicator of time of infection. Lesion age can be estimated on fruit and help determine when infection occurred and this information can be related to meteorological events, such as storms, that occurred at that time (Figure 24).

Figure 8

Figure 24

Pathogen Dispersal: Most spread of canker by wind and rain is for short distances, i.e., within trees or to neighboring trees. Canker develops more severely on the side of the tree exposed to wind-driven rain. Spread over longer distances, up to several miles, can result from severe meteorological events such as tropical storms, hurricanes, and tornadoes (Figure 25) (Figure 26). A recent study determined that 99% of infections that occur within a 30-day period are located within 594 m (1950 ft) of prior infected trees during normal weather conditions, i.e., when normal rain storms occur but tropical storms and hurricanes do not.. Hurricanes and tropical storms greatly increase citrus canker infection and can spread the bacteria over many miles. During 2004, Florida was subjected to three hurricanes that crossed and affected the majority of the commercial citrus industry. Bacterial dispersal gradients of up to 53 km (32 mi) were recorded and hundreds of new out breaks were subsequently discovered. However, long-distance spread more often occurs with the movement of diseased propagating material, such as budwood, rootstock seedlings, or budded trees. There is no record of seed transmission. Commercial shipments of diseased fruit are potentially a means of long-distance spread, but there is no authenticated record of this ever having happened. Nursery workers can carry bacteria from one nursery to another unless hands, clothes, and equipment are disinfected. Such spread can also result from contaminated budwood or contaminated budding equipment. Pruning, hedging (Figure 27), and spray equipment (Figure 28) have been demonstrated to spread the disease within and among plantings. Wooden harvesting boxes that contained diseased fruit and leaves and are later taken to disease-free orchards have also been implicated in long-distance spread (Figure 29).

Figure 25	Figure 26
Figure 27	Figure 28
Figure 29

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