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Disease Cycle
Disease cycle of Monosporascus root rot and vine decline.
A) Mature ascospores in soil; B) Germinated ascopsore in the rhizosphere and attachment to the root; C) Necrotic lesions on melon roots; D) Above ground symptoms of vine decline and death; E) Perithecia formed in infected root tissue; F) Mature perithecium releasing ascospores into soil. (Courtesy R. Cohen)
The disease cycle of M. cannonballus appears to be relatively simple. Infection of the roots can occur from either mycelium that has survived in the soil or plant debris or from germinating ascospores (A-B in disease cycle & Figure 10). The fungus invades the fine feeder roots (B-C in disease cycle & Figure 11) colonizes the cortex and xylem, and kills the rootlet.
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Figure 10 |
Figure 11. |
Figure 12. |
The infection advances to the next root via the root junction or perhaps from new infections. Smaller roots die while lesions are formed predominantly on larger roots. The fungus continues to colonize the root tissue and invades the xylem causing the plant to form tyloses. While the fungus invades the xylem, it does become systemic in the plant and, as such, is not a true vascular wilt pathogen, such as Fusarium oxysporum or Verticillium spp. Infection is favored by warm soil temperatures (25 to 35 °C). In climates where double cropping of melons occurs (two crops per year), disease typically is more severe in the late-summer or autumn-planted crop than the spring or winter-planted crop. Perithecia are formed on the roots most abundantly late in the season but may form throughout the life cycle. When mature, the perithecia rupture, discharging the ascospores into the soil (F, Figures 4, 5). Several hundred ascospores may form in a single perithecium (Figure 12) and a single mature melon plant root system is capable of producing 400,000 or more ascospores.
External stresses, both biotic and abiotic, may exacerbate disease symptoms and speed up wilting and vine collapse. One aspect that has been investigated in this regard is fruit load. Vine collapse usually occurs during fruit maturation and several studies have noted that removal of developing fruit from infected plants delays symptom expression and, in some cases, prevents wilting and death of the plant.
Above ground disease symptoms involve a gradual decline of the leaves, typically beginning with the crown leaves and progressing outward. By late in the season, many of the leaves are dead, exposing the developing fruit to intense solar radiation and heat. The combination of tyloses in the root tissue and the loss of most of the secondary and tertiary roots causes the vines to collapse quickly, often appearing as though they collapsed “overnight”. Entire fields of plants may collapse resulting in near total economic loss. This rapid collapse resulted in disease names such as 'sudden wilt' and 'sudden death'. Fruits on infected plants are of low quality due to reduced size and sugar content, as well as, sunburned and cracked rinds.
A PCR-based protocol using species-specific ITS primers has been developed for the early detection of M. cannonballus in root tissue. Similarly, a quantitative real-time PCR protocol has been developed, also based on the ITS1 region of the rDNA. This later technique has been used along with color image analysis to phenotypically score melon root responses to M. cannonballus.
Epidemiology
No aerial stage of the disease is known, and no asexual spore stage of the fungus has been observed. Thus, ascospores are considered the primary inoculum and can survive in the soil or plant debris until the next planting season or, in the absence of a host, may survive for many years in a dormant state. Mycelium from infected crop debris can serve as a source of inoculum, although it is not known how long mycelium survives in the soil. The disease is considered monocyclic.
Ascospores can build up to high numbers in fields cropped successively to melons; however, the minimum threshold level for disease development is not known. Severe disease has occurred in fields with as few as one to two ascospores per gram of dry soil and as high as 15 spores per gram of dry soil. In the few cases studied, ascospores appear uniformly distributed throughout the fields, with the highest concentration in the upper 10 inches (25 cm). There is some evidence that the fungus may colonize and reproduce on roots of other plants (monocots and dicots) without causing noticeable disease, providing another means of survival and reproduction. Additionally, ascospores have been found in soil from noncultivated land and in native desert soils in Texas and Arizona in the U.S. and in Brazil. Thus, M. cannonballus appears to be an indigenous soilborne fungus and the epidemiology of this disease may be more complex than we currently understand.
The spread of the pathogen can be by any method that displaces contaminated soil or crop debris e.g. cultivation, flooding, wind, erosion, etc. Airborne spread of the pathogen is not likely because of the large size of the ascospores and the lack of a known conidial stage. There is no evidence that the pathogen is seedborne or systemic in the plant. Colonization appears to be limited to the roots. Fruit and foliage are not infected directly, although they manifest symptoms related to root infection, water stress, and plant decline.
Copyright © 2002
by The American Phytopathological Society