Abstract

The phenomenon of melon wilting dueto Monosporascus infection (Fig. 1) isknown in many regions around the worldand has been referred to as melon collapse(13,27,32,38), sudden wilt (2,6,8,26,29),root rot (17,39), vine decline (1,3,36), androot rot and vine decline (21–23,41,42).This disease is known also in the ’AravaRift Valley of southern Israel (8,19,26,31;Fig. 2), and the major causal agent isMonosporascus cannonballus Pollack &Uecker (Fig. 3). This pathogen is commonin hot, semiarid melon-growing areas ofIndia (22), southern Spain (13), southwest-ern regions of the United States (23,24,36),Saudi Arabia (15), Central America (1),Japan (40), Taiwan (37), and Tunisia (21).This disease in the ’Arava can be verysevere, capable of destroying the entirecrop (26), and will be referred to here asMonosporascus wilt. To date, disease man-agement in the ’Arava (38) has beenmainly based on methyl bromide fumiga-tion of the soil prior to planting. Sincemethyl bromide use will be prohibited inthe near future (33), there is an urgent needto develop alternative strategies for diseasemanagement.Melon root rot and vine decline causedby M. cannonballus has been reviewed in afeature article by Martyn and Miller (22),which describes the biology, pathology,and epidemiology of the disease, as well asmolecular methods for detecting variationin the pathogen population. In this article,we discuss approaches for the control ofMonosporascus wilt, with an emphasis onthe potential for integrated management, inview of the coming phaseout of methylbromide. These approaches include breed-ing for resistance, grafting melon plantsonto resistant Cucurbita and melon root-stocks, changes in irrigation schemes, im-proved soil solarization, chemical controlwith fungicides, and the use of other fumi-gants, alone or combined with soil solari-zation, to improve disease control.In field trials conducted by Reuveni andKrikun in the Jordan Valley and southern’Arava region in Israel (Fig. 2) in the early1980s, it was shown that Monosporascuseutypoides (apparently synonymous withM. cannonballus) is the primary agent ofmelon collapse (19,31). Pathogenicity testsperformed in 1995 and 1996 suggested thatthe most virulent species involved in themelon collapse syndrome in the ’Arava(Fig. 2) is M. cannonballus, although otherpathogens might also be involved (26).Monosporascus appears to be adapted tohot climates. This can be inferred from theclimatic conditions in the areas in whichthe fungus has been found and by itsgrowth temperature optimum. Vegetativemycelial growth is extensive in the rangeof 25 to 35°C, and perithecia formation invitro is optimal at 25 to 30°C (22).In commercial fields in Israel, the meloncrop can be totally destroyed by Monospo-rascus wilt in the autumn cropping season,whereas disease incidence and severity in acrop raised in the same plot during thefollowing winter–spring season can bemuch lower (2). Differences in soil tem-perature between crop seasons have beensuggested as a possible cause for such aphenomenon (17,28). This idea has beensupported by enhanced wilting obtainedfollowing artificial heating of the soil dur-ing the winter–spring crop season (28).Soil fumigation with methyl bromidebefore planting is the most common ap-proach for controlling Monosporascus wiltof melons in Israel. Methyl bromide haslethal exposure periods as short as 2 daysand can be applied at relatively low tem-peratures. The aeration period to eliminatevolatile residues before planting is short inmost soils, 3 to 10 days, allowing plantingshortly after treatment (18). In fact, meloncultivation in the ’Arava region is ex-tremely risky without methyl bromidefumigation prior to planting, due to theubiquity of M. cannonballus in ’Aravasoils that results in severe yield losses. Thephaseout of methyl bromide in developed

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