scholarly journals First Report of Fusarium oxysporum f. sp. lycopersici Race 2 on Tomato in Italy

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.

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 ◽  
2008 ◽  
Vol 92 (6) ◽  
pp. 983-983 ◽  
Author(s):  
B. D. Bruton ◽  
W. W. Fish ◽  
D. B. Langston

Watermelon (Citrullus lanatus (Thunb.) Matsum. & Nakai) is the number one specialty crop grown in Georgia, a state that ranks fourth nationally in watermelon production. In the last 5 years, Fusarium wilt caused by Fusarium oxysporum f. sp. niveum (Fon) has been the greatest yield-limiting disease of watermelon in Georgia. In 2004, a seedless-watermelon field of ‘Regency’ and ‘Tri-X 313’ in Berrien County, GA exhibited approximately 40% of wilted plants. Affected plants also exhibited strong discoloration in the crown xylem. Plant samples (cultivars unknown) from a similarly affected field were also tested from Crisp County, GA. Xylem tissue was excised from the main stem of eight diseased plants in the area between the second and third internode, surface sterilized for 1 min in 1% NaOCl, rinsed with 80% ethanol, and plated onto water agar amended with 100 μg/liter of streptomycin sulfate. Fungi with the morphological characteristics of Fusarium oxysporum (4) were consistently recovered from the diseased tissue of all eight plants. The isolates were hyphal tipped and maintained in vials of sterile artificial potting mix until ready for use (1). Isolates were grown on Esposito and Fletcher medium (2) for 10 days, filtered through cheesecloth, and adjusted to 1 × 106 spores/ml. Reference isolates of race 1 and 2 were used as comparisons for race determination of the unknowns. In each of four studies, plants at the two-leaf stage were removed from potting mix, washed gently, and their roots were uniformly trimmed to 2.5 cm. Before repotting, the seedlings were subjected to a 2-min root-dip in the respective spore-containing media. In each study, approximately 40 plants of each watermelon differential were inoculated with the respective isolates. In disease scoring, each plant was considered a rep. ‘Black Diamond’ is susceptible to races 0, 1, and 2; ‘Charleston Gray’ is resistant to race 0; ‘Calhoun Gray’ is resistant to races 0 and 1, and PI-296341-FR (3) is resistant to races 0, 1, and 2 of Fon. Four plants were planted per 15-cm plastic pot, maintained in an air-conditioned headhouse for 24 h, and then placed in the greenhouse in a randomized complete block design. After 30 days, all plants were rated as to healthy, wilted, or dead plants. From eight isolates tested, one isolate from each county was determined to be Fon race 2 on the basis of its ability to wilt/kill a high percentage of the race 1 resistant differential, i.e., ‘Calhoun Gray’. Mean disease percentages for the isolates from each of the two counties on the watermelon differentials were 95 and 100% on ‘Black Diamond’, 68 and 80% on ‘Charleston Gray’, and 70 and 86% on ‘Calhoun Gray.’ Because of apparent genetic drift within our PI-296341-FR population, we determined that these data were not useful for identifying race 2. In fact, we observed a range of 17 to 80% wilt/death in the PI-296341-FR over a total of four studies that included a known race 2 isolate (Calg 13(15); E. Vivoda). To our knowledge, this is the first report of race 2 in Georgia and it increases the number of states to seven in which race 2 has been identified. Five of the top 10 watermelon-producing states have now reported race 2 of Fon for which there is no genetic resistance within commercial cultivars. References: (1) B. D. Bruton et al. Plant Dis. 84:907, 2000. (2) R. Esposito and A. Fletcher. Arch. Biochem. Biophys. 93:369, 1961. (3) R. D. Martyn and D. Netzer. HortScience 26:429, 1991. (4) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. Pennsylvania State University Press, University Park, 1983.


Plant Disease ◽  
2012 ◽  
Vol 96 (12) ◽  
pp. 1823-1823 ◽  
Author(s):  
A. Garibaldi ◽  
P. Martini ◽  
L. Repetto ◽  
M. Odasso ◽  
D. Bertetti ◽  
...  

During fall 2011, symptoms of a wilt disease were observed in a commercial nursery near Ventimiglia as well as in the Research Center of Floriculture of Sanremo (northern Italy) on plants of Papaver nudicaule (Iceland poppy) of a local unnamed cultivar. In the commercial nursery, 15 to 20% of plants were affected, while about 3% of plants were affected at the Research Center. Symptoms consisted of chlorosis, premature leaf drop, and foliar wilting, followed by the stem wilting, bending, and eventually rotting from the base. Brown discoloration was observed in the stem vascular tissue. Using Komada's Fusarium-selective agar medium (2), a fungus was consistently and readily isolated from symptomatic vascular tissue of plants collected from both sites. The isolates were purified and subcultured on potato dextrose agar (PDA), on which medium both isolates produced pale violet, abundant, aerial mycelium, felted in old cultures, with pale purple pigments in the agar medium. The isolate generated short monophialides with unicellular, ovoid-elliptical microconidia of 3.9 to 6.7 × 1.4 to 3.0 (average 5.4 × 2.3) μm. On carnation leaf agar (CLA) (1), isolates produced pale orange sporodochia with macroconidia that were 3-septate, slightly falcate with a foot-shaped basal cell and a short apical cell, and 26.0 to 43.5 × 3.1 to 4.4 (average 35.3 × 3.7) μm. Chlamydospores were abundant, terminal, and intercalary, rough walled, mostly singles but sometime in short chains or clusters, and 5.2 to 10.1 μm in diameter. Such characteristics are typical of Fusarium oxysporum (3). The internal transcribed spacer (ITS) region of rDNA was amplified from the isolates using the primers ITS1/ITS4 (4), and sequenced. BLASTn analysis of the 507-bp ITS sequence of one isolate from P. nudicaule collected from the commercial nursery (GenBank Accession No. JX103564) showed an E-value of 0.0 and 100% identity with the ITS sequence of F. oxysporum (HQ649820). To confirm pathogenicity of one of the Iceland poppy isolates, tests were conducted on 2-month-old plants of the same cultivar on which symptoms were first observed. Plants (n = 14) were inoculated by dipping roots in a 1 × 107 CFU/ml conidial suspension of the isolate of F. oxysporum prepared from 10-day-old cultures grown in potato dextrose broth (PDB) on a shaker (90 rpm) for 10 days at 22 ± 1°C (12-h fluorescent light, 12-h dark). Non-inoculated control plants (n = 14) were dipped in sterilized water. All the plants were transplanted into pots filled with steamed potting mix (sphagnum peat/perlite/pine bark/clay at 50:20:20:10), and maintained in a glasshouse at 24 to 28°C. Inoculated plants showed typical symptoms of Fusarium wilt after 10 days. The stems then wilted and plants died. Non-inoculated plants remained healthy. F. oxysporum was reisolated from inoculated plants but not from control plants. The pathogenicity test was conducted twice with the same results. Since Fusarium wilt has not previously been described on Iceland poppy at any location, this is first report of F. oxysporum on P. nudicaule in Italy and anywhere in the world. References: (1) N. L. Fisher et al. Phytopathology 72:151, 1982. (2) H. Komada. Rev. Plant Prot. Res. 8:114, 1975. (3) J. F. Leslie and B.A. Summerell. The Fusarium Laboratory Manual, Blackwell Professional, IA, 2006. (4) T. J. White et al. PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, San Diego, CA, 1990.


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 ◽  
2005 ◽  
Vol 89 (10) ◽  
pp. 1130-1130 ◽  
Author(s):  
S. T. Koike ◽  
T. R. Gordon

Cilantro, or coriander (Coriandrum sativum), is a leafy vegetable in the Apiaceae and is grown commercially in California primarily for use as a fresh herb. During 2002 and 2003 in coastal California (Santa Barbara County), commercial cilantro fields showed symptoms of a wilt disease. Affected plants grew poorly and were stunted. Lower foliage turned yellow with reddish tinges, and plants wilted during warmer times of the day. The main stem, crown, and taproot exhibited vascular discoloration that was reddish to light brown. As disease progressed, plants eventually died. For both years, the disease distribution was limited to isolated small patches (each patch measuring less than 1 m2 in area). A fungus was consistently isolated from symptomatic vascular tissue in crowns and taproots. On the basis of colony and conidial morphology, the isolates were identified as Fusarium oxysporum (2). No other fungi or bacteria were recovered from these plants. To test pathogenicity, suspensions containing 1 × 106 conidia/ml were prepared for five isolates. The roots of 30-day-old cilantro plants of four cultivars (30 plants each of Festival, Leisure, Santo, and LSO 14) were clipped and then soaked in the suspensions for 20 min. The roots of 30 plants of each cultivar were soaked in water as a control. Plants were repotted into new redwood bark + peat moss rooting medium and maintained in a greenhouse setting at 24 to 26°C. After 1 month, 95% or more of the inoculated plants showed yellowing and vascular discoloration symptoms similar to those seen in the field. F. oxysporum was reisolated from all inoculated plants. The four cilantro cultivars did not show differences in disease severity. Control plants showed no symptoms, and the fungus was not recovered from these plants. The experiment was repeated and the results were the same. Experiments also were conducted to determine if cilantro isolates could cause disease in celery (Apium graveolens var. dulce). Celery transplants and cilantro seedlings were prepared and inoculated as described above. However, after 2 months, celery plants did not show any disease symptoms, while the cilantro developed wilt symptoms and eventually died. A Fusarium wilt disease has been reported on coriander in Argentina and India where the pathogen was named F. oxysporum f. sp. coriandrii (1,3). To our knowledge, this is the first report of Fusarium wilt of cilantro in California. References: (1) M. Madia et al. Fitopatologia 34:155, 1999. (2) P. E. Nelson et al. Fusarium species: An Illustrated Manual for Identification. Pennsylvania State University Press, University Park, 1983. (3) U. S. Srivastava. Indian Phytopathol. 22:406, 1969.


Plant Disease ◽  
2021 ◽  
Author(s):  
Maria Luz Herrero ◽  
Nina Elisabeth Nagy ◽  
Halvor Solheim

Lettuce (Lactuca sativa L.) is produced in Norway both in field and greenhouses. In Norway, greenhouse lettuce is one of the most important vegetables grown year-round. In winter 2018, wilting symptoms were observed on soil-grown lettuce of the cultivar Frillice in a greenhouse in south east Norway (Buskerud county). Affected plants showed stunted growth, wilting of outer leaves, and brownish discoloration of vascular tissues of taproots and crowns. According to the producer, the disease led to an estimated 10% of yield losses. Fungal isolates were obtained from crowns and roots of diseased plants collected from the greenhouse in 2018 and 2019. Two single spore isolates, 231274 from 2018 and 231725 from 2019, were used in further studies. The isolates were incubated on synthetic nutrient-poor agar (SNA) at 18-20 ⁰C, and a 12 hours dark, 12 hours UV light cycle. Isolate 231274 produced abundant macro- and microconidia characteristics of Fusarium oxysporum while macroconidia were never observed in isolate 231725. On potato dextrose agar (PDA), colonies of isolate 231274 were purple in color and colonies of isolate 231725 were pinkish with abundant aerial mycelium. For PCR-assay, DNA from mycelia was extracted using Easy-DNA kit (Invitrogen). A portion of the translation elongation factor 1-α (EF1-α) gene was amplified using primers F-728F (Carbone and Kohn. 1999) and EF2 (O'Donnell et al. 1998) as described by Aas et al. 2018. Blast analysis of both sequences (accession no. MW316853 for 231274 and MW316854 for 231275) obtained a 99% homology with the sequence of Fusarium oxysporum f.sp. lactucae (FOL) race 1 strain S1 (accession no. DQ837657)(Mbofung et al. 2007). Both isolates were identified as race 1 by using specific primers Hani3’ and Hanilatt3rev (Pasquali et al. 2007) as described by Cabral et al. 2014. To complete Koch’s postulate, lettuce plants of the cultivar Frillice were used. Race identity was confirmed using the differential lettuce cultivars Costa Rica No.4 (resistant to FOL race 1), Banchu Red Fire (resistant to FOL races 2 and 4) and Romana Romabella (resistant to FOL races 1 and 2) (Gilardi et al. 2017) provided by the breeding company Rijk Zwaan (De Lier, The Netherlands). For inoculation, roots of six 2-weeks old seedlings per cultivar were dipped in a spore suspension (1 x 106 CFU/ml) for 1 min, while controls were dipped in distilled water. Seedlings were planted in 250 ml pots containing fertilized potting substrate, and were placed in a greenhouse with temperature ranging from 15 to 35 ⁰C and an average of 23 ⁰C. After 10 days reduced growth was observed in cultivars Frillice and Banchu Red Fire for both fungal isolates. After 25 days wilting was observed in both cultivars. Affected plants presented discoloration of vascular tissue. No difference in growth was observed between cultivars Romana Romabella and Costa Rica No. 4 and their respective controls. FOL was re-isolated from all inoculated cultivars but not from controls. The colony patterns of the recovered isolates were the same than those of the isolates used for inoculation. These results confirm that the isolate belongs to race 1. Greenhouse lettuce in Norway is mainly produced in hydroponics. FOL is here reported to cause damages in soil- grown lettuce. Nevertheless FOL in hydroponic systems has been reported in Japan (Fujinaga et al. 2003) and Thailand (Thongkamngam and Jaenaksorn 2017). Thus, the possibility of infections in hydroponics remain a big concern for lettuce production in Norway.


Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1163-1163 ◽  
Author(s):  
K. Perveen ◽  
N. Bokhari

In November 2008, a wilt of lavender (Lavandula pubescens) seedlings was observed in the greenhouse at King Saud University, Riyadh, Saudi Arabia. Affected seedlings were wilted and the root system was poorly developed. Diseased stems developed a dark coloration that extended down to the roots. Vascular tissue of the affected seedlings appeared red or brown. Isolations consistently yielded a fungus growing from the discolored stem tissue when placed on potato dextrose agar. The macroscopic characteristics of the colony, as well as microscopic structures, were used to identify the fungus as Fusarium oxysporum (2). Oval to elliptical microconidia without septa and originating from short phialides were used to distinguish the species from F. solani (1). The fungus was authenticated by the ITCC (Indian Type Collection Centre), Indian Agricultural Research Institute, New Delhi, India, and given I.D. No. 7532.09. For conducting further experiments, healthy seedlings of L. pubescens were obtained from the botanical garden of the King Saud University and grown in steam-sterilized soil. Healthy seedlings of lavender were inoculated using a root-dip method with a conidial suspension (1 × 107 CFU/ml) of one strain of F. oxysporum obtained from infected plants. Inoculated seedlings were then transplanted into steam-sterilized soil. Plants inoculated with sterilized water (1 ml per plant) served as control treatments. Wilt symptoms and vascular discoloration in the roots and crown developed within 20 days on all plants inoculated with the pathogen, while control plants remained asymptomatic. F. oxysporum was consistently reisolated from symptomatic plants. The pathogenicity test was conducted twice. To our knowledge, this is the first report of F. oxysporum on L. pubescens in Saudi Arabia or elsewhere in the world, and this newly identified disease may be a potential threat to commercial production of lavender. References: (1) J. F. Leslie and B. A. Summerell. Page 212 in: The Fusarium Laboratory Manual. Blackwell Publishing Professional, Hoboken, NJ, 2006. (2) P. C. Nelson et al. Clin. Microbiol. Rev. 7:479, 1994.


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 ◽  
2011 ◽  
Vol 95 (7) ◽  
pp. 877-877 ◽  
Author(s):  
G. Polizzi ◽  
D. Aiello ◽  
V. Guarnaccia ◽  
A. Vitale ◽  
G. Perrone ◽  
...  

Philotheca myoporoides (DC.) M.J. Bayly (previously known as Eriostemon myoporoides), commonly called long-leaf waxflower and native to eastern Australia (Rutaceae family), is a hardy compact shrub or small tree occurring in subtropical to cool temperate regions. P. myoporoides is cultivated in Sicily (Italy) for its ornamental appeal. During April of 2010, a widespread wilting was observed on approximately 80% of 2,000 1-year-old, potted long-leaf waxflower plants grown in a commercial nursery near Catania (eastern Sicily, Italy). Internally, symptomatic plants had conspicuous vascular brown discoloration from the crown to the canopy. Diseased crown and stem tissues of 20 plants were surface disinfested for 30 s in 1% NaOCl, rinsed in sterile water, plated on potato dextrose agar (PDA) amended with 100 mg/liter of streptomycin sulfate, and incubated at 25°C. A Fusarium sp. was consistently isolated from affected plant tissues. Colonies with white or light purple aerial mycelia and violet pigmentation on the underside of the cultures developed after 9 days. On carnation leaf agar, 20 single-spore isolates produced microconidia on short monophialides, macroconidia that were three to five septate with a pedicellate base, and solitary and double-celled or aggregate chlamydospores. A PCR assay was conducted on one representative isolate (ITEM 13490) by analyzing sequences of the benA gene (coding β-tubulin protein) and CaM gene (coding calmodulin protein) using the primers reported by O'Donnell et al. (1). The benA gene sequences of ITEM 13490 (GenBank No. FR828825) exhibited an identity of 100% to Fusarium oxysporum f. sp. radicis-lycopersici strain ATCC 52429 (GenBank No. DQ092480). CaM gene sequences of ITEM 13490 (GenBank No. FR828826) exhibited an identity of 99.6% to F. oxysporum strain ITEM 2367 (GenBank No. AJ560774). Morphological characteristics of the 20 isolates, as well as the PCR assay on a representative strain, identified the isolates associated with disease symptoms as F. oxysporum Schlechtend.:Fr. A pathogenicity test was performed by placing two 1-cm2 plugs of PDA from 9-day-old mycelial cultures near the crown on potted, healthy, 2-month-old cuttings of P. myoporoides. Thirty plants were inoculated with strain ITEM 13490 and the same number of plants served as noninoculated controls. All plants were enclosed for 4 days in plastic bags and placed in a growth chamber at 25 ± 1°C. Plants were then moved to a greenhouse where temperatures ranged from 23 to 27°C. First symptoms, which were identical to those observed in the nursery, developed on one plant 15 days after inoculation. Wilting was detected on all plants after 30 days. Control plants remained symptomless. F. oxysporum was successfully reisolated from symptomatic crown and stem tissues and identified as described above, fulfilling Koch's postulates. To our knowledge, this is the first report of F. oxysporum causing disease of P. myoporoides worldwide. Moreover, this pathogen was recently reported in the same nursery on Eremophila sp. (2), confirming the presence of Fusarium wilt as a potential threat to ornamental plant production in this area, and necessitates the innovation and development of disinfection methods for alveolar trays, greenhouses, and various propagation materials to reduce future disease outbreaks. References: (1) K. O'Donnell et al. Mycoscience 41:61, 2000. (2) G. Polizzi et al. Plant Dis 94:1509, 2010.


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