scholarly journals First Report of Race 3 of Fusarium oxysporum f. sp. lycopersici in Southeastern Florida

Plant Disease ◽  
2000 ◽  
Vol 84 (2) ◽  
pp. 199-199
Author(s):  
R. C. Ploetz ◽  
J. L. Haynes

Race 3 of Fusarium oxysporum f. sp. lycopersici, cause of Fusarium wilt of tomato, Lycopersicon esculentum, was first recognized in Florida in 1982 on the west coast (Hillsborough and Manatee counties) (2). Approximately 10 years later, race 3 was reported in northeastern production areas of the state (Gadsden County) (1) and was observed on the east coast (Ft. Pierce area) (D. O. Chellemi, personal communication). During the 1998 to 1999 season, mature plants of Sanibel, a commercial tomato cultivar with resistance to races 1 and 2, were observed with symptoms of Fusarium wilt at the University of Florida's Tropical Research and Education Center in Homestead. Approximately 20% of the plants were conspicuously wilted, chlorotic, and necrotic in all or unilateral portions of the canopy. Internal, vascular discoloration in affected plants extended far into the canopy, distinguishing the disease from Fusarium crown rot, caused by F. oxysporum f. sp. radicis-lycopersici. Pure colonies of fungi were isolated from surface-disinfested (10 s with 70% ethanol, 2 min with 10% bleach) stem segments on potato dextrose agar (PDA) amended with streptomycin (100 mg/liter), rifamycin (50 mg/liter), and a commercial miticide (Danitol 2EHC [4 drops/liter]). Isolates were identified as F. oxysporum due to their production of typical falcate macroconidia with foot-shaped basal cells, microconidia borne in false heads only on mono-phialides, and chlamydospores. In replicated (three) greenhouse trials, six single-spore isolates were used to root-dip inoculate (107 conidia per ml) seedlings of differential tomato cultivars (Bonnie Best, no resistance; Manapal, race 1 resistance; Walter, race 1 and race 2 resistance). All isolates were pathogenic on each of the differential cultivars, and one isolate, 2-1, caused severe damage on Walter (mean rating of 3.5 on a 1 to 5 scale). The results were repeated in a second trial with the most virulent isolate. In both trials, pure colonies of F. oxysporum were recovered from symptomatic seedlings. Southeastern Florida is the last major tomatoproduction area in Florida to be affected by race 3 of F. oxysporum f. sp. lycopersici. References: (1) D. O. Chellemi and H. A. Dankers. Plant Dis. 76:861, 1992. (2) R. B. Volin and J. P. Jones. Proc. Fla. State Hortic. Soc. 95:268, 1982.

Plant Disease ◽  
2014 ◽  
Vol 98 (10) ◽  
pp. 1326-1332 ◽  
Author(s):  
Anthony P. Keinath ◽  
Richard L. Hassell

Fusarium wilt of watermelon, caused by the soilborne fungal pathogen Fusarium oxysporum f. sp. niveum race 2, is a serious, widespread disease present in major watermelon-growing regions of the United States and other countries. ‘Fascination,’ a high yielding triploid resistant to race 1, is grown in southeastern states in fields that contain a mixture of races 1 and 2. There is some benefit to using cultivars with race 1 resistance in such fields, even though Fascination is susceptible to Fusarium wilt caused by race 2. Experiments in 2012 and 2013 were done in fields infested primarily with race 2 and a mixture of races 1 and 2, respectively. Fascination was grafted onto four rootstock cultivars: bottle gourd (Lagenaria siceraria) ‘Macis’ and ‘Emphasis’ and interspecific hybrid squash (Cucurbita maxima× C. moschata) ‘Strong Tosa’ and ‘Carnivor.’ Nongrafted and self-grafted Fascination were used as susceptible control treatments. In both experiments, mean incidence of plants with symptoms of Fusarium wilt was ≥52% in the susceptible control treatments and ≤6% on the grafted rootstocks. Disease incidence did not differ between rootstock species or cultivars. In both years, Fascination grafted onto Strong Tosa and Macis produced more marketable-sized fruit than the susceptible control treatments. Grafted Emphasis and Carnivor also produced more fruit than the control treatments in 2012. The cucurbit rootstocks suppressed Fusarium wilt caused by race 2 and increased marketable yield of triploid watermelon grown in infested soil.


Plant Disease ◽  
2018 ◽  
Vol 102 (9) ◽  
pp. 1820-1827 ◽  
Author(s):  
Anthony P. Keinath ◽  
Paula A. Agudelo

Interspecific hybrid squash (Cucurbita maxima × C. moschata ‘Strong Tosa’) and bottle gourd (Lagenaria siceraria ‘Macis’) rootstocks are resistant to Fusarium oxysporum f. sp. niveum but susceptible to Meloidogyne incognita (Southern root-knot nematode). Coinfection of Early Prolific Straightneck summer squash (C. pepo) with root-knot nematode and F. oxysporum f. sp. niveum has been reported to increase susceptibility to Fusarium wilt. The objectives of this study were to determine whether such an interaction occurred between M. incognita and F. oxysporum f. sp. niveum races 1 and 2 on Strong Tosa, Macis, and watermelon cultivars Fascination (resistant to race 1) and Tri-X 313 (susceptible to both races). Hosts were inoculated in a greenhouse with one of four pathogen treatments: F. oxysporum f. sp. niveum, M. incognita, both pathogens, or neither pathogen. Galling was present on ≥10% of the root systems of 90% of the plants inoculated with M. incognita. Bottle gourd had less galling than interspecific hybrid squash. Plants not inoculated with F. oxysporum f. sp. niveum did not wilt. Four weeks after inoculation, incidence and severity of Fusarium wilt and recovery of F. oxysporum did not differ for any hosts inoculated with F. oxysporum f. sp. niveum alone and F. oxysporum f. sp. niveum plus M. incognita (host–treatment interactions not significant). In general, Early Prolific Straightneck grouped with the F. oxysporum f. sp. niveum-resistant rootstocks when inoculated with F. oxysporum f. sp. niveum race 2 and with the susceptible watermelon when inoculated with race 1, regardless of inoculation with M. incognita. Recovery of F. oxysporum from stems of inoculated watermelon was greater than recovery from the other three hosts, regardless of nematode inoculation. In conclusion, our experiments do not support the hypothesis that resistance to F. oxysporum f. sp. niveum in cucurbit rootstocks or resistant watermelon cultivars would be compromised when M. incognita infects the roots.


2003 ◽  
Vol 83 (2) ◽  
pp. 377-379 ◽  
Author(s):  
S. Neumann and A. G. Xue

Reactions of the 117 field pea cultivars available in Canada were evaluated to the four common races (1, 2, 5, and 6) of Fusarium oxysporum Schl. f. sp. pisi (van Hall) Sny. and Hans, the causal agent of fusarium wilt, in growth chambers. Based on the visual assessment of foliar wilt symptoms, 49 cultivars were resistant to at least one of the four races, and the remaining 68 cultivars were susceptible to all four races. Of these resistant cultivars, Ascona and 44 other cultivars were resistant to race 1; Impala to race 2; Aladin to races 1 and 2; and Radley and Princess to races 2, 5, and 6. In an effort to standardize the methodology for screening field pea for resistance to the pathogen, other quantitative parameters including shoot length, vascular discoloration, and shoot and root dry weights were evaluated on selected cultivars. Correlation analysis revealed that foliar wilt symptoms and the reduction in shoot length were highly correlated (r = -0.90, P < 0.01). The result suggests that the reduction in shoot length could be used to supplement the visual severity rating for fusarium wilt in field pea. Key words: Field pea, Pisum sativum, fusarium wilt, Fusarium oxysporum f. sp. pisi, resistance


HortScience ◽  
2005 ◽  
Vol 40 (3) ◽  
pp. 529-531 ◽  
Author(s):  
James D. McCreight ◽  
Michael E. Matheron ◽  
Barry R. Tickes ◽  
Belinda Platts

Three races of Fusarium oxysporum f.sp. lactucae, cause of fusarium wilt of lettuce, are known in Japan, where the pathogen was first observed in 1955. Fusarium wilt first affected commercial U.S. lettuce production in 1990 in Huron, Calif., but did not become a serious problem in the U.S. until 2001 when it reappeared in Huron and appeared in the Yuma, Arizona lettuce production area. Reactions of three fusarium wilt differentials (`Patriot', susceptible to races 1, 2 and 3; `Costa Rica No. 4', resistant to race 1, and susceptible to races 2 and 3; and `Banchu Red Fire', susceptible to races 1 and 3, and resistant to race 2) in a naturally-infected commercial field test and artificially-inoculated greenhouse tests, indicated presence of race 1 in the Yuma lettuce production area. Reactions of these differentials to an isolate from Huron confirmed the presence of race 1 in that area. Consistent with previous results from the U.S. and Japan, `Salinas' and `Salinas 88' were resistant to the Yuma and Huron isolates of race 1, whereas `Vanguard' was highly susceptible. Limited F1 and F2 data indicate that resistance to race 1 in `Costa Rica No. 4' and `Salinas' is recessive. `Calmar' is the likely source of resistance in `Salinas' and `Salinas 88'.


Plant Disease ◽  
2010 ◽  
Vol 94 (11) ◽  
pp. 1376-1376 ◽  
Author(s):  
P. Sánchez-Peña ◽  
S. O. Cauich-Pech ◽  
J. Núñez-Farfán ◽  
R. D. Núñez-Cebreros ◽  
S. Hernández-Verdugo ◽  
...  

Sinaloa State is the main producer of tomatoes (Solanum lycopersicum L) in Mexico where production attained 15,784 ha in 2008 (3). Fusarium wilt of tomato caused by Fusarium oxysporum f. sp. lycopersici (Sacc) Snyder & Hansen causes significant yield losses in Sinaloa each year (2). Three pathotypes or races of F. oxysporum f. sp. lycopersici have been described: races 1, 2, and 3 (1). The purpose of this study was to determine the races of F. oxysporum f. sp. lycopersici present in Sinaloa and distribution of these races in the region. F. oxysporum f. sp. lycopersici isolates were obtained from plants showing symptoms of yellowing and necrosis of vascular bundles. Plants were sampled from 50 fields throughout the production area in Sinaloa from November 2008 to March 2009. Four differential cultivars were used to identify the races of 26 F. oxysporum f. sp. lycopersici isolates collected across Sinaloa: Bonny Best (susceptible to all races), UC-82-L (susceptible to races 2 and 3), F1 MH-1 (susceptible to race 3), and IR-3 (resistant to all races). A microconidial suspension was prepared for each isolate (1 × 106 CFU/ml) from cultures grown in potato dextrose broth with constant agitation (110 rpm) at 28°C for 7 days. Five 25-day-old seedlings (three fully expanded true leaves) from each differential cultivar were immersed in the appropriate microconidial suspension for 10 min, then individually transplanted into a pot containing 1 kg of sterilized commercial potting mix, and grown in a growth chamber at 25 to 28°C and 60 to 75% relative humidity for 5weeks with 14-h light/10-h darkness. Control plants (root dipped for 10 min in sterile water) were grown similarly and remained asymptomatic. Susceptible cv. Bonny Best showed typical symptoms of Fusarium wilt including epinasty, yellowing, defoliation, vascular necrosis, and wilt. None of these plants survived 25 days postinoculation for any of the isolates. All UC-82-L plants inoculated with each of the 26 isolates died before 35 days, indicating that none of the isolates was of race 1. F1 MH-1 plants only survived inoculation with 3 of the 26 isolates (11.5%), indicating that the 23 isolates that killed these plants (88.5% of the 26 isolates) were of race 3, and only 3 isolates were of race 2. All IR-3 plants inoculated with the 26 isolates survived. The isolates showed variation in response to the differential cultivar UC-82L in duration from inoculation to when the plants died (variation in isolate aggressiveness). The three F. oxysporum f. sp. lycopersici race 2 isolates were restricted to the Culiacan Valley, whereas the 23 F. oxysporum f. sp. lycopersici race 3 isolates were widely distributed across Sinaloa. Koch's postulates were confirmed by reisolating the fungus from the roots and stem base of each dead, inoculated plant (4). This study provides baseline data for future surveys to monitor changes in distribution of F. oxysporum f. sp. lycopersici races in Sinaloa, Mexico. References: (1) G. Cai et al. Phytopathology 93:1014, 2003. (2) P. Sánchez-Peña. Programa de Fomento y Apoyo a Proyectos de Investigación (PROFAPI), Universidad Autónoma de Sinaloa, México, 2007. (3) Secretaría de Agricultura, Ganadería, Desarrollo Rural, Pesca y Alimentación, Servicio de Información Agroalimentaria y Pesquera, México. www.siap.gob.mx , 2009. (4) B. A. Summerell et al. Plant Dis. 87:117, 2003.


Plant Disease ◽  
2006 ◽  
Vol 90 (1) ◽  
pp. 111-111 ◽  
Author(s):  
Z. M. Sheu ◽  
T. C. Wang

Fusarium wilt caused by Fusarium oxysporum Schlechtend.:Fr. f. sp. lycopersici (Sacc.) W.C. Snyder & N.H. Hans. is a destructive disease of tomato crops worldwide. The use of resistant varieties is the best strategy for disease control. There are three reported races of the pathogen. Recent surveys indicated that many of the commercial cultivars with resistance to F. oxysporum f. sp. lycopersici race 1 planted in Taiwan displayed Fusarium wilt symptoms. Yellowing on the older leaves was observed on one side of the stems close to fruit maturity. The yellowing gradually affected most of the foliage and was accompanied by wilting of the plants. The vascular tissue was usually dark brown and discoloration extended to the apex. The wilting became more extensive until plants collapsed and died. A total of 87 isolates obtained from typical diseased plants throughout Taiwan from 2002 to 2005 were analyzed to determine the race and distribution of this pathogen in Taiwan. Isolates were confirmed at the species level using F. oxysporum-specific primers FOF1 and FOR1 (4). Subsequently, isolates were characterized for pathogenicity, race and restriction fragment length polymorphisms of the intergenic spacer region of rDNA (IGS-RFLP) with two reference isolates, Fol 11A (race 1) and Fol 34-1 (race 2). Pathogenicity tests and race determination were conducted using root-dip inoculation (3) on 2-week-old seedlings of host differentials Bonny Best (no resistance), UC82-L (resistant to race 1), and Florida MH-1 (resistant to races 1 and 2). Thirty-six seedlings of each cultivar were arranged into three replications and inoculated with each isolate. Disease reaction was evaluated 3 weeks after inoculation. The disease severity rating (DSR) was determined on individual plants according to the following scale: 0 = plant healthy without external symptoms; 1 = slight vascular discoloration with or without stunted growth; 2 = severe vascular discoloration usually with stunted growth; and 3 = plant wilted beyond recovery or dead. The presence of severe vascular discoloration indicated a susceptible reaction. All isolates were race 2, and over 70% of the isolates showed strong virulence with a DSR >2 on cvs. Bonny Best and UC-82L. This result was different from a previous report of race 1 from Taiwan (2). Two IGS-RFLP haplotypes generated by EcoRI, RsaI, and HaeIII digestions (1) were identified. Eighty-six isolates displayed one banding pattern, and one unique isolate displayed a second banding pattern. The results demonstrated the predominance of race 2 and low diversity within the Taiwan population. To our knowledge, this is the first report regarding the predominant race and IGS-RFLP haplotype identification of F. oxysporum f. sp. lycopersici in Taiwan. Our study indicates that tomato varieties in Taiwan should possess resistance to race 2. References: (1) G. Cai et al. Phytopathology 93:1014, 2003. (2) K. S. Elias and R. W. Schneider. Phytopathology 82:1421, 1992. (3) J. W. Gerdemann and A. M. Finley. Phytopathology 41:238, 1951. (4) P. K. Mishra et al. FEMS Microbiol. Lett. 218:329, 2003.


Plant Disease ◽  
2005 ◽  
Vol 89 (1) ◽  
pp. 108-108 ◽  
Author(s):  
D. S. Egel ◽  
R. Harikrishnan ◽  
R. Martyn

Fusarium oxysporum f. sp. niveum race 1 is uniformly distributed throughout watermelon (Citrullus lanatus (Thunb.) Matsum. & Nakai) growing regions, but F. oxysporum f. sp. niveum race 2 has a limited known distribution in the United States (Texas, Florida, Oklahoma, Maryland, and Delaware) (3,4). Since the spring of 2001, commercial watermelon fields in Knox and Gibson counties in southwestern Indiana have been observed with symptoms of one-sided wilt and vascular discoloration typical of Fusarium wilt. Race 2 of F. oxysporum f. sp. niveum was suspected as the casual agent since the diseased watermelon cultivars are considered resistant to races 0 and 1. Two isolates of F. oxysporum obtained from wilted watermelon plants in two different commercial fields and one isolate obtained from a wilted seedling in a transplant house were compared for pathogenicity in a greenhouse assay. Known isolates of F. oxysporum f. sp. niveum races 0, 1, and 2 were obtained from Don Hopkins (University of Florida, Apopka), Kate Everts (University of Maryland/University of Delaware, Salisbury, MD), and Ray Martyn (Purdue University, West Lafayette, IN), respectively, and were used for comparison. All isolates were grown in shake cultures in a mineral salts liquid medium. (1). After 72 hr, the predominately microconidal suspensions were filtered through cheesecloth and adjusted to 1 × 105 conidia/ml with the aid of a hemacytometer. A concentration of 1 × 105 condia/ml was shown previously to cause the desired disease reaction in the standard cultivars. Seedlings of the differential cvs, Black Diamond (universal susceptible), Charleston Gray (race 0 resistant), and Calhoun Gray (race 0 and 1 resistant) were grown in a 1:1, (v:v) sand/ vermiculite mixture to the first true-leaf stage after which the plants were uprooted and the roots carefully washed prior to root dip inoculation. Subsequent to inoculation, seedlings were planted in a sand/vermiculite/ peat mixture (4:1:1, [v:v:v]) with four seedlings to a 15-cm-diameter pot. The experimental design was a randomized complete block with five replications. Two isolates from the commercial field plants caused an average of 100% wilt on cv. Black Diamond, 95% wilt on cv. Charleston Gray, and 80% wilt on cv. Calhoun Gray, resulting in a designation of race 2. The isolate from a commercial transplant house resulted in 100, 60, and 15% wilt, respectively, on the three standard cultivars resulting in a race 1 designation. The presence of F. oxysporum f. sp. niveum race 2 in Indiana is significant because Indiana currently ranks fifth in the United States in watermelon production and there are no commercially available cultivars that possess resistance to race 2. To our knowledge, this is the first report of F. oxysporum f. sp. niveum race 2 in Indiana and the first report of race 2 from the Midwest region of the United States. Race 2, first described from the United States in 1985 (2), has now been confirmed in six states. References: (1) R. Esposito and A. Fletcher. Arch. Biochem. Biophys. 93:369, 1961. (2) R. Martyn, Plant Dis. 69:1007, 1985. (3) R. Martyn, Plant Dis. 71:233, 1987. (4) X. Zhou and K. Everts. Plant Dis. 87:692, 2003.


Plant Disease ◽  
2003 ◽  
Vol 87 (6) ◽  
pp. 692-698 ◽  
Author(s):  
X. G. Zhou ◽  
K. L. Everts

A survey was conducted to determine races and inoculum density of Fusarium oxysporum f. sp. niveum, the causal agent of Fusarium wilt of watermelon in Maryland and Delaware. Virulence on six differential cultivars was tested for each of 63 isolates of F. oxysporum f. sp. niveum, obtained from 25 commercial watermelon fields. Thirteen isolates (21%) were identified as race 0, 36 isolates (57%) as race 1, and 14 isolates (22%) as race 2. Races 0 and 1 were present in 12 (48%) and 10 (40%) of the fields, respectively. The highly aggressive race 2 was identified from five fields in two counties in Maryland and from one field in Delaware, representing 24% of the fields. Race 2 was copresent with one or two other races. Race 2 (19 isolates) predominated among the 25 isolates obtained from a research field in Maryland. Nineteen commercial fields had inoculum densities of F. oxysporum f. sp. niveum ranging from 100 to 1,200 CFU/g of soil at harvest. Within this range of inoculum densities, >20% incidence of wilt was observed when the susceptible watermelon cv. Sugar Baby was planted in samples of soil collected from these fields. The relationship (P < 0.0001) between inoculum density of F. oxysporum f. sp. niveum (X) and incidence of Fusarium wilt (Y) on Sugar Baby was best described using the monomolecular equation, Y = 1 - exp[-0.0013 (X + 166)]. The ratio of pathogenic to total population of F. oxysporum in the fields linearly increased with increasing inoculum density of F. oxysporum f. sp. niveum (R 2 = 0.4; P < 0.0009).


HortScience ◽  
1990 ◽  
Vol 25 (9) ◽  
pp. 1068f-1068 ◽  
Author(s):  
J.W. Scott ◽  
J.P. Jones

Forty-two Lycopersicon pennellii Corr. D'Arcy accessions, from the Tomato Genetics Stock Center, were inoculated for resistance to Fusarium wilt race 3 at the 3-leaf and cotyledon stage. All were over 90% healthy when inoculated at the 3-leaf stage but had greater disease incidence at the cotyledon stage. Crosses were made between healthy plants within each accession. Using this seed, 39 accessions were 100% healthy and 3 were over 96% healthy when inoculated at either stage. Seventeen F1's with susceptible parents were tested for race 3 and all had over 80% healthy plants. Twenty-two accessions were tested for Fusarium wilt race 1 and race 2. For race 1, 21 were 100% healthy and 1 was 91% healthy, For race 2, 20 were 100% healthy, 1 was 96% healthy, and 1 was 75% healthy. Forty accessions were screened for Fusarium crown rot and Verticillium wilt. For crown rot, LA 1277, LA 1367, and LA 1657 were over 95% healthy, 6 other accessions were over 68% healthy and several others had over 50% healthy plants, All 40 were susceptible to Verticillium wilt race 1. L. pennellii appears to be a good source of resistance to Fusarium sp. but not to Verticillium wilt.


Plant Disease ◽  
1999 ◽  
Vol 83 (10) ◽  
pp. 967-967 ◽  
Author(s):  
V. M. Stravato ◽  
R. Buonaurio ◽  
C. Cappelli

During the summer of 1997, symptoms of Fusarium wilt were observed on tomato (Lycopersicon esculentum Mill.) cvs. Monica F1 and PS 110, which bear the I gene for resistance to race 1 of Fusarium oxysporum Schlechtend.:Fr. f. sp. lycopersici (Sacc.) W.C. Snyder & H.N. Hans., in two commercial production greenhouses in Latium (Fondi) and one greenhouse in Sardinia (Oristano). Infected plants showed yellowing, stunting, vascular discoloration, and premature death. A fungus from tomato stems with discolored vascular tissue was consistently isolated on potato dextrose agar (PDA) and, based on morphological features, was identified as F. oxysporum. To verify the pathogenicity of four fungal isolates, cv. Bonny Best tomato plants, which do not carry genes for Fusarium wilt resistance, were inoculated by dipping roots of 2-week-old seedlings in a suspension of 105 microconidia per ml for 30 s. Inocula were obtained from 1-week-old fungal cultures grown on PDA. Roots of control plants were dipped in water. Seedlings were transplanted to pots containing peat and river sand (1:1, vol/vol) and placed in a greenhouse at 20 to 25°C. One month after inoculation, all fungal isolates provoked wilting of inoculated plants. No symptoms were observed on control plants. The morphological features of the fungus reisolated from diseased plants were similar to those of the original isolates. Based on the pathogenicity test, we concluded that the fungal isolates belong to F. oxysporum f. sp. lycopersici. To determine the races of the fungal isolates, differential tomato lines VFN8 (I gene for resistance to race 1), Florida MH-1 (I and I2 genes for resistance to races 1 and 2), and I3R (I, I2, and I3 genes for resistance to races 1, 2, and 3) were inoculated with the four fungal isolates, using the same procedure described for the pathogenicity test. Because disease symptoms were detected on VFN8 but not on Florida MH-1 and I3R, we deduced that the fungal isolates belong to F. oxysporum race 2. This is the first report of F. oxysporum f. sp. lycopersici race 2 in Italy. Previous research indicated that race 1 is present in Italy (1). Currently, many commercially acceptable cultivars resistant to races 1 and 2 are available to Italian greenhouse growers. Reference: (1) M. Cirulli. Phytopathol. Mediterr. 4:63, 1965.


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