Pathogen Biology

Fusarium oxysporum f. sp. niveum (FON) has no known sexual reproductive stage. Asexual reproductive structures include both micro- and macroconidia (Figures 4-6). Microconidia are abundant, oval to kidney-shaped, generally one-celled and are formed on short conidiophores. Microconidia are capable of infecting roots but probably play little role in initial infection in the field because of their ephemeral nature. Macroconidia are fusiform (‘canoe-shaped’), typically having three to five cells (Figures 5 & 6) and are produced in large numbers, often in clumps known as sporodochia. Macroconidia also may infect roots but their primary role may be survival as they have the ability to form chlamydospores (asexual resting structures). Chlamydospores are the primary means of survival and typically form under conditions of suboptimal growth for the fungus or death of the plant. F. oxysporum forms two types of chlamydospores; one within the macroconidium (Figure 6) and one from within the mycelium. Those formed from mycelia tend to occur singly or in pairs and may be either intercalary (within the mycelium) or terminal (occurring at the ends). Disease results from infection of the root or hypocotyls by hyphae resulting from either the macroconidia or chlamydospores. Once infection has occurred the fungus penetrates and grows within the xylem. Microconidia are produced within the vessel (Figure 7), dislodge, and are carried up the xylem with the transpiration stream, sporadically germinating and producing more mycelia and microconidia. Wilting occurs as a result of the formation of tyloses within the xylem by the host. Tyloses are ‘balloon-like’ invaginations of the xylem parenchyma cells that block the vessel (Figures 8-12). Tyloses serve to slow the spread of the pathogen through the plant but also restrict water flow, resulting in wilting. In addition, the pathogen causes a general breakdown of the xylem parenchyma cells resulting in various types of gums that add to the blockage. The extent to which fungal toxins are involved in pathogenesis is not known. Once infection has occurred, FON is limited to the xylem and generally emerges only after death of the plant.

Figure 4	Figure 5	Figure 6
Figure 7	Figure 8	Figure 9
Figure 10	Figure 11	Figure 12

Fusarium oxysporum is a cosmopolitan soilborne fungus with both saprophytic and pathogenic members. Pathogenic strains (formae speciales) are somewhat specialized and are defined on the basis of the host they predominantly infect. Currently, there are over 100 different formae speciales described, causing disease in a wide range of dicot and monocot plant species. Many are further divided into pathological races based on their pathogenicity to a set of differential host cultivars, each with a unique set of resistance genes. Six different formae speciales have been described that cause wilt in curcurbits: F. o. f. sp. niveum (watermelon); F. o. f. sp. melonis (muskmelon); F. o. f. sp. cucumerinum (cucumber) are the most economically important. While there are reports of cross infection between some formae speciales, these are mostly laboratory and greenhouse phenomena and, in the field, the cucurbit wilt fusaria are host-specific and rarely cross-infect. The biology, pathology, epidemiology, and control are very similar among all of the cucurbit-infecting formae speciales.

Three races of F. o. f. sp. niveum have been described – race 0, 1, and 2. A recent report of a possible fourth race awaits further confirmation. Races are described based on their ability to overcome specific resistance genes in a set of differential cultivars (Table 1). Race 0, first detected in Florida in 1963, is pathogenic only on watermelon cultivars with no resistance genes and, therefore, is of little economic importance. Race 1 is the predominant race throughout commercial watermelon regions in the U.S. and world. Thanks to plant breeding programs initiated over a hundred years ago, most commercial diploid cultivars have a high degree of resistance to race 0 and 1. Triploid (seedless) cultivars are generally more susceptible to Fusarium wilt since there has been less time to breed resistance. There is growing speculation, however, that the distinction between race 0 and race 1 may be more quantitative than qualitative and, consequently, race 0 and race 1 may all be strains of race 1 varying in aggressiveness. On the other hand, race 2 is highly aggressive to all current commercial watermelon cultivars and hybrids and clearly is a distinct race. Race 2 was first observed in Israel in 1973 and now occurs in at least six U.S. states (Florida, Texas, Oklahoma, Maryland, Delaware, Indiana) and several countries. No commercial genotypes have high resistance to race 2; however, an improved plant introduction line from South Africa (PI-296341-FR) has high resistance to all three races. A second PI line, PI-272769, also is reported to have resistance to race 2.

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by The American Phytopathological Society