scholarly journals First Report of Fusarium Wilt of Exacum affine Caused by Fusarium oxysporum

Plant Disease ◽  
2001 ◽  
Vol 85 (10) ◽  
pp. 1120-1120 ◽  
Author(s):  
W. Elmer ◽  
E. O'Dowd

Wilting Persian violets (Exacum affine) were observed in a Connecticut retail outlet. Diseased stems developed a dark coloration at the nodes, while the foliage turned papery, whitish tan. The vascular tissue in affected stems was reddish brown and extended from the base of the stem upward in a unilateral pattern. Fusarium grew from the discolored stem tissue when placed on Komada's medium (2). Single spores were cultured on carnation leaf agar and identified as F. oxysporum (2). Koch's postulates were completed by growing 12 2-month-old seedlings of E. affine ‘Midget’ in potting mix amended with ground dried millet seed (2.0 g/liter of soil) that had been colonized for 2 weeks by the fungus. Symptoms appeared slowly after 8 weeks, and F. oxysporum was re-isolated from the vascular tissue. Plants grown in soil mix with sterile millet remained healthy. Similar tests at different times of the year produced the same results. Other tests examined host specificity with two new isolates on seedlings of Persian violet, carnation, lisianthus, and basil. Both isolates caused symptoms only on Persian violets. Although Haematonectria haematococca (synonym Nectria haematococca, anamorph F. solani) causes Nectria canker of Persian violet (1), this is the first report of F. oxysporum causing Fusarium wilt of Persian violet. We propose the formae specialis be F. oxysporum f. sp. exaci. An isolate has been deposited at the Fusarium Research Center at The Pennsylvania State University, University Park, under Accession No. O-2282. References: (1) M. Daughtrey et al. Compendium of Flowering Potted Plant Diseases. American Phytopathological Society, St. Paul, MN, 1995. (2) Nelson et al. Fusarium species: An Illustrated Manual for Identification. The Pennsylvania State University Press, University Park, PA, 1983.

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 ◽  
2005 ◽  
Vol 89 (3) ◽  
pp. 341-341 ◽  
Author(s):  
C. E. Windels ◽  
J. R. Brantner ◽  
C. A. Bradley ◽  
M. F. R. Khan

In 2002, somel sugar beet (Beta vulgaris L.) fields in the Red River Valley (RRV) of Minnesota and North Dakota had symptoms characteristic of Fusarium yellows (4). In 2004, ≈5% of fields in the RRV had symptomatic plants. Interveinal yellowing of older leaves typically began in mid-July and as the disease progressed, younger leaves turned yellow. Sometimes, one side of the leaf was yellow or necrotic while the other side remained green. As leaves died, they remained attached to the crown. Transverse sections of roots revealed a light gray-brown discoloration of the vascular tissue but no external rotting of roots. Isolations from 35 symptomatic roots collected in eight fields yielded 25 isolates identified as F. oxysporum (from single conidia grown on homemade potato dextrose agar and carnation leaf agar) (3). Pathogenicity was determined by dipping roots of 5-week-old sugar beet plants (cv. ACH 9363) in a suspension of 104 conidia per ml for 8 min (12 isolates, 10 to 12 plants per isolate). Plants were planted in Cone-tainers (3.8 cm diameter × 21 cm; Stuewe and Sons, Inc. Corvallis, OR) containing sterile soil. Three known cultures of F. oxysporum Schlecht. emend. Snyd. & Hans. f. sp. betae Stewart (= F. conglutinans var. betae Stewart [4]) also were included (13 and 216c from L. Hanson, USDA-ARS, Fort Collins, CO; 0-1122 from The Pennyslvania State University Fusarium Research Center). The control was sterile water. Plants were placed in a greenhouse at 24 to 27°C with natural light supplemented with illumination from high-pressure sodium-vapor lamps for 16 h daily and lightly fertilized biweekly to avoid chlorosis from nutrient deficiency. After 6 to 7 weeks, plants were rated for disease on a 0 to 4 scale: 0 = no disease; 1 = slight to extreme plant stunting, leaves may be wilted; 2 = chlorotic leaves, some with necrosis at margins; 3 = tap root dried and brown to black in color, leaves dying; and 4 = plant dead (1). The experiment was repeated. Disease severity differed between trials, but all isolates of F. oxysporum and F. oxysporum f. sp. betae resulted in disease ratings statistically (P < 0.05) greater than that of the water control. In Trial 1, isolates of F. oxysporum averaged a rating of 2.1 (range of 1.8 to 3.3) and F. oxysporum f. sp. betae averaged 2.1 (range of 2.0 to 2.2) compared with 0.1 for the water control. One isolate of F. oxysporum had a statistically higher rating than did the cultures of F. oxysporum f. sp. betae. In Trial 2, isolates of F. oxysporum averaged a rating of 3.3 (range of 2.7 to 3.7) and F. oxysporum f. sp. betae averaged 3.1 (range of 2.7 to 3.4) compared with 0.2 for the water control. Cultures of F. oxysporum (8 of 12) resulted in ratings statistically higher than that of the least pathogenic culture of F. oxysporum f. sp. betae. Cultures of F. oxysporum and F. oxysporum f. sp. betae recovered from inoculated plants were identical to those used to inoculate plants. To our knowledge, this is the first report of F. oxysporum f. sp. betae on sugar beet in the Red River Valley of Minnesota and North Dakota. The disease has been reported in California, Colorado, Montana, Nebraska, Oregon, Texas, and Wyoming (1,2). References: (1) R. A. Cramer et al. J. Phytopathol. 151:352, 2003. (2) G. A. Fisher and J. S. Gerik. Phytopathology 84:1098, 1994. (3) P. E. Nelson et al. Fusarium Species: An illustrated Manual for Identification. The Pennsylvania State University Press. University Park, 1983. (4) D. Stewart. Phytopathology 21:59, 1931.


Plant Disease ◽  
2010 ◽  
Vol 94 (2) ◽  
pp. 277-277 ◽  
Author(s):  
D. Palmero ◽  
M. De Cara ◽  
C. Iglesias ◽  
M. M. Moreno ◽  
N. González ◽  
...  

In October of 2008, decayed garlic bulbs (Allium sativum L. cv. Blancomor de Vallelado) were received from a producer in Segovia, Spain. In November of 2009, similar symptoms were observed on stored bulbs (cvs. Blancomor de Vallelado and Garcua) from each of 30 municipalities in northwest Segovia and Valladolid. A minimum of one sample was collected from 12 localities. Pieces of symptomatic bulbs were surface disinfested for 2 to 3 min in 0.5% NaOCl and transferred to potato dextrose agar (PDA) and Komada's media. Colonies had catenate microconidia and curved macroconidia that were usually three to five septate. Microconidia were club shaped with a flattened base, aseptate, and were produced on both mono- and polyphialides. On the basis of morphological features, the fungus was identified as Fusarium proliferatum (T. Matsushima) Nirenberg (2,3). Pathogenicity tests were conducted with 12 isolates of the fungi following the method of Dugan et al. (1). Each assay with an isolate consisted of six cloves (cv. Blancomor de Vallelado) disinfested in 0.5% NaOCl for 45 s, rinsed with sterile water, and injured to a depth of 4.5 mm with a probe 1 mm in diameter. The wound was filled with PDA colonized by the appropriate isolate. Six cloves for each tested isolate received sterile agar as a control. The cloves were incubated at 25°C for 5 weeks. The test was repeated once with cv. Garcua. All isolates produced water-soaked, tan lesions. An isolate of the fungus was deposited in the collection of the Plant Production Department of the University of Almeria. No fungi were recovered from the control cloves. F. proliferatum has been reported on garlic in the northwestern United States (1) and Serbia (4). To our knowledge, this is the first report of a Fusarium sp. in the section Liseola attacking garlic in Spain. The fungus seems to be well established on this host in Spain. References: (1) F. M. Dugan et al. Phytopathology 155:437, 2007. (2) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. Pennsylvania State University Press, University Park, 1983. (3) H. Nirenberg et al. Mycologia 90:434, 1998. (4) S. Stankovic et al. Eur. J. Plant Pathol. 118:165, 2007.


Plant Disease ◽  
2013 ◽  
Vol 97 (10) ◽  
pp. 1377-1377 ◽  
Author(s):  
H.-W. Choi ◽  
S. K. Hong ◽  
Y. K. Lee ◽  
H. S. Shim

In July 2010, fusarium wilt symptoms of tomato (Lycopersicon esculentum Mill.) plants were found in two commercial greenhouses in the Damyang area of Korea. Approximately 1% of 7,000 to 8,000 tomato plants were wilted and chlorotic in each greenhouse. The vascular tissue was usually dark brown and the discoloration extended to the apex. Fragments (each 5 × 5 mm) of the symptomatic tissue were surface-sterilized with 1% NaOCl for 1 min, then rinsed twice in sterilized distilled water (SDW). The tissue pieces were placed on water agar and incubated at 25°C for 4 to 6 days. Nine Fusarium isolates were obtained from four diseased plants, of which three isolates were identified as F. oxysporum based on morphological characteristics on carnation leaf agar medium and DNA sequences of the translation elongation factor 1-alpha (EF-1α) gene (2). Macroconidia were mostly 3- to 5-septate, slightly curved, and 28 to 53 × 2.8 to 5.2 μm. Microconidia were abundant, borne in false heads or short monophialides, generally single-celled, oval to kidney shaped, and 5 to 23 × 3 to 5 μm. Chlamydospores were single or in short chains. The EF-1α gene was amplified from three isolates by PCR assay using ef1 and ef2 primers (3), and the amplification products were sequenced. The nucleotide sequences obtained were deposited in GenBank (Accession Nos. KC491844, KC491845, and KC491846). BLASTn analysis showed 99% homology with the EF-1α sequence of F. oxysporum f. sp. lycopersici MN-24 (HM057331). Pathogenicity tests and race determination were conducted using root-dip inoculation (4) on seedlings of tomato differential cultivars: Ponderosa (susceptible to all races), Momotaro (resistant to race 1), Walter (resistant to races 1 and 2), and I3R-1 (resistant to all races). A spore suspension was prepared by flooding 5-day-old cultures on potato dextrose agar with SDW. Plants at the first true-leaf stage were inoculated by dipping the roots in the spore suspension (1 × 106 conidia/ml) for 10 min. Inoculated plants were transplanted into pots containing sterilized soil, and maintained in the greenhouse at 25/20°C (12/12 h). Twenty-four seedlings of each cultivar were arranged into three replications. An equal number of plants of each cultivar dipped in water were used as control treatments. Disease reaction was evaluated 3 weeks after inoculation, using a disease index on a scale of 0 to 4 (0 = no symptoms, 1 = slightly swollen and/or bent hypocotyl, 2 = one or two brown vascular bundles in the hypocotyl, 3 = at least two brown vascular bundles and growth distortion, 4 = all vascular bundles brown and the plant either dead or very small and wilted). All isolates caused symptoms of fusarium wilt on all cultivars except I3R-1, indicating that the isolates were race 3. The pathogen was reisolated from the discolored vascular tissue of symptomatic plants. Control plants remained asymptomatic, and the pathogen was not reisolated from the vascular tissue. Fusarium wilt of tomato caused by isolates of F. oxysporum f. sp. lycopersici races 1 and 2 has been reported previously; however, race 3 has not been reported in Korea (1). To our knowledge, this is the first report of isolates of F. oxysporum f. sp. lycopersici race 3 on tomato in Korea. References: (1) O. S. Hur et al. Res. Plant Dis. 18:304, 2012 (in Korean). (2) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Ames, IA, 2006. (3) K. O'Donnell et al. Proc. Nat. Acad. Sci. 95:2044, 1998. (4) M. Rep et al. Mol. Microbiol. 53:1373, 2004.


Plant Disease ◽  
2011 ◽  
Vol 95 (12) ◽  
pp. 1587-1587
Author(s):  
B. Singh ◽  
C. S. Kalha ◽  
V. K. Razdan ◽  
V. S. Verma

While screening newly introduced cultivars of walnut (Juglans regia) at Bhaderwah (Mini Kashmir), Jammu and Kashmir, India in September 2008, 60% of grafted plants were found to be dying because of a cankerous growth observed on seedling stems. Later, these symptoms extended to lateral branches. In the surveyed nurseries, cvs. SKU 0002 and Opex Dachaubaria were severely affected by the disease. Cankers were also observed in all walnut nurseries in the area with several wild seedlings also being observed to be exhibiting similar cankerous symptoms on stem and branches. Necrotic lesions from cankerous tissues on seedling stems were surface disinfested with 0.4% NaOCl for 1 min and these disinfected cankerous tissues were grown on potato dextrose agar (potato-250 g, dextrose-15 g, agar-15 g, distilled water-1 liter). A Fusarium sp. was isolated consistently from these cankerous tissues, which was purified using single-spore culture. Carnation leaf agar was used for further culture identification (2,3). The fungal colony was floccose, powdery white to rosy in appearance when kept for 7 days at 25 ± 2°C. Macroconidia were straight to slightly curved, four to eight septate and 30 to 35 × 3.5 to 5.7 μm. These are characteristics consistent with Fusarium incarnatum (3). Pathogenicity was confirmed by spraying a conidial suspension (1 × 106 conidia/ml) onto bruised branches of 1-year-old walnut plants (cv. Opex Dachaubaria) while sterile distilled water sprays were used for the controls. Inoculated plants were incubated at 20 ± 2°C and 85% relative humidity for 48 h. Fifty days following inoculation, branch dieback followed by canker symptoms developed on inoculated plants. Control plants remained healthy with no symptoms of canker. F. incarnatum (Roberge) Sacc. was repeatedly isolated from inoculated walnut plants, thus satisfying Koch's postulates. Infected plant material has been deposited at Herbarium Crytogamae Indiae Orientalis (ITCC-6874-07), New Delhi. To our knowledge, this is the first report of walnut canker caused by F. incarnatum (Roberge) Sacc. from India. This fungus was previously reported to be affecting walnut in Italy (1) and Argentina (4). References: (1) A. Belisario et al. Informatore Agrario 21:51, 1999. (2) J. C. Gilman. A Manual of Soil Fungi. The Iowa State University Press, Ames, 1959. (3) P. E. Nelson et al. Fusarium Species. An Illustrated Manual for Identification. The Pennsylvania State University Press, University Park, 1983. (4) S. Seta et al. Plant Pathol. 53:248, 2004.


Plant Disease ◽  
2007 ◽  
Vol 91 (11) ◽  
pp. 1519-1519 ◽  
Author(s):  
W. H. Elmer ◽  
M. Daughtrey ◽  
K. Rane ◽  
M. M. Jimenez-Gasco

Disease symptoms were observed in a commercial nursery in the midwest on Coreopsis verticillata ‘Moonbeam’ during the summer of 2006. Plants in a roughly circular area in one field showed foliar necrosis, stem basal cankers, root rot, and eventually plant death. Vascular discoloration was noted in stems of affected plants. Sporulation typical of Fusarium oxysporum was observed on the surface of cankers. Five isolates of F. oxysporum (KR1, KR2, KR4, MDU, and MDL) were taxonomically identified from monosporic cultures obtained from surface-disinfested stems and roots. All five isolates were vegetatively compatible with each other. Two methods of inoculation were used. Method one (conidial drench) involved pouring 100 ml of conidial suspension (106 conidia per ml) into 10-cm pots containing one healthy 2-month-old division of the same cultivar that was obtained from a different nursery. Method two (millet infestation) involved mixing autoclaved millet seed that had been colonized by each isolate into potting mix (2.5 g/L of mix) prior to transplanting. Four plants were tested per isolate per method and controls received distilled water or autoclaved millet. After 3 months, only two isolates (KR1 and KR2) inoculated by conidial drench caused root rot, whereas all isolates inoculated by millet infestation caused wilt, root rot, and vascular discoloration, and all inoculated plants died after 3.5 months Controls remained healthy. The fungus was recovered and was vegetatively compatible with the original F. oxysporum isolates. The tef-α gene from two F. oxysporum isolates was sequenced, submitted to the Blast ID search at Pennsylvania State University (1), and found to belong to the F. oxysporum species complex. Two isolates (KR1 and KR 2) have been deposited at the Fusarium Research Center at Pennsylvania State University under deposition numbers O-2437 and O-2438. Because of the popularity of this coreopsis cultivar, this disease has the potential to cause significant economic loss in nurseries and landscape businesses. The affected nursery, however, has taken all precautions to avoid disseminating the pathogen. Reference: (1) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004.


Plant Disease ◽  
2014 ◽  
Vol 98 (5) ◽  
pp. 694-694 ◽  
Author(s):  
F. García-Bastidas ◽  
N. Ordóñez ◽  
J. Konkol ◽  
M. Al-Qasim ◽  
Z. Naser ◽  
...  

Fusarium wilt or Panama disease of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), is among the most destructive plant diseases (3). Race 1 ravaged ‘Gros Michel’-based export trades until the cultivar was replaced by resistant Cavendish cultivars. However, a new variant of Foc, tropical race 4 (TR4), was identified in Southeast Asia in 1992 and has spread throughout the region (3). Cavendish clones, which are most important in subsistence and export production, are among the wide range of cultivars that are affected, and there is a huge concern that TR4 will further disseminate in Africa since its presence was announced in November 2013 and move into Latin America, thereby threatening other vital banana-growing regions. In Jordan, Cavendish bananas are produced on 1,000 to 1,500 ha in the Jordan Valley (32°N, 35.5°E). In 2006, symptoms of Fusarium wilt were observed and sampled for the isolation of Foc. On half-strength PDA amended with 100-ppm streptomycin sulfate, pale salmon-colored colonies with floccose mycelia developed consistently from surface-disinfested xylem. Single microconidia from these colonies were transferred to half-strength PDA, and conidia and mycelia from these monospore colonies were stored at –80°C in 15% glycerol. On banana leaf agar (Co60-irradiated leaf tissue on water agar), isolates resembled F. oxysporum phenotypically by producing infrequent three- to five-celled macroconidia, copious, usually aseptate microconida on monophialides, and terminal and intercalary chlamydospores after 2 weeks (2). With nitrate-nonutilizing (nit) mutants and testers for different vegetative compatibility groups (VCGs), each of seven examined monospore isolates were placed in VCG 01213, which contains only strains of TR4 (3). Total DNA was extracted from six isolates and PCR analyses, which confirmed their identity as TR4 (1). Subsequently, one of the isolates (JV11) was analyzed for pathogenicity. Inoculum production and inoculation were according to (1) by dipping (30 min) root-wounded 10-week-old plants of the Cavendish cv. Grand Naine in 2 liters of spore suspension (1.0 × 106 spores/ml). Inoculated plants were then placed in sand in 3-liter pots under 28°C, 70% relative humidity, and a 16/8-h light/darkness photoperiod. Sets of three plants were each treated with either JV11 or two TR4 controls (isolate II-5 and a strain isolated from an affected Cavendish plant in Mindanao, Philippines, both of which were diagnosed as TR4 by PCR and pathogenicity analyses). Control sets were either treated with race 1 originating from Cruz das Almas, Bahia, Brazil (1), or water. After 2 weeks, plants inoculated with JV11 and TR4 controls produced typical symptoms of Fusarium wilt. After 4 weeks, tissue was collected from all plants and plated on Komada's medium. TR4 was directly confirmed by PCR (1), either directly from symptomatic plants (JV11 and TR4 controls), or from isolates that were recovered from these plants. Nothing was re-isolated from race 1 inoculated plants and water controls, which remained asymptomatic. This is the first report of TR4 affecting Cavendish outside Southeast Asia, is its northernmost outbreak, and represents a dangerous expansion of this destructive race. Currently, 80% of the Jordan Valley production area is affected by Fusarium wilt, and 20 to 80% of the plants are affected in different farms. References: (1) M. A. Dita et al. Plant Pathol. 59:348, 2010. (2) J. F. Leslie and B. A. Summerell. The Fusarium Lab Manual. Blackwell, Ames, 2006. (3) R. C. Ploetz. Phytopathology 96:653, 2006.


Plant Disease ◽  
2008 ◽  
Vol 92 (7) ◽  
pp. 1132-1132 ◽  
Author(s):  
L. Riccioni ◽  
A. Haegi ◽  
M. Valvassori

Lentil (Lens culinaris Medik.) is a traditional crop in Sicily, Italy. Near Villalba (Caltanissetta), a local lentil landrace, “Lenticchia di Villalba”, is commonly grown. From 2002 to 2004, wilt was observed in five lentil fields (≈1 ha each) at rates from 5 to 20%. Affected plants were yellow and stunted with discoloration in the vascular tissue of stems and crowns. Pieces of brown vascular tissue from stems were disinfested in 2% sodium hypochlorite for 2 min, rinsed with sterile distilled water, placed on potato dextrose agar, and incubated at 23°C. Isolates with morphological characteristics of Fusarium oxysporum Schlecht.:Fr. (2) were consistently recovered from affected plants. For molecular identification of five isolates, the rDNA internal transcribed spacer (ITS) region and a portion of the elongation factor EF-1α were sequenced using ITS5/4 and EF1/2 primers, respectively (1). Two sequences of the ITS region were obtained: a 468-bp sequence from isolates ER1259, ER1260, and ER1275 (submitted as GenBank Accession No. EU159118) and a 483-bp sequence from isolates ER1274 and ER1276 (submitted as GenBank Accession No. EU281661). The two sequences shared 93% similarity. A sequence homology search using the NCBI BLAST program revealed that the first sequence had 100% homology with the ITS sequences of more than 50 F. oxysporum isolates of various formae speciales in GenBank and the second shared 100% homology with the ITS sequences of five isolates of F. redolens Wollenw. (e.g., GenBank Accession No. X94169 of the strain CBS 360.87). Amplification of the EF-1α produced a sequence from isolates ER1274 and ER1276 (submitted as GenBank Accession No. EU281660) with 99 to 100% homology to sequences of F. redolens and a sequence from strains ER1259, ER1275, and ER1260 (submitted as GenBank Accession No. EU281659) with 100% homology to that of more than 50 F. oxysporum strains in GenBank. Although F. redolens and F. oxysporum are morphologically similar, recent molecular studies have shown that they are distinct and phylogenetically distant species (3). On the basis of genetic sequences, isolates ER1274 and ER1276 were identified as F. redolens. These isolates were evaluated for pathogenicity on lentil. For each isolate, 10 2-week-old seedlings of “Lenticchia di Villalba” were inoculated by submerging roots in a suspension of 2.5 × 106 conidia/ml for 10 min. Plants were put into separate tubes containing 70 ml of a nutritional liquid medium (7 ml of HydroPlus Olikani per liter; Yara, Nanterre, France) and incubated in a growth chamber at 20°C with 12 h of light per day. Seedlings dipped in sterile water served as the control treatment. The pathogenicity test was repeated twice. Inoculated seedlings started to wilt 1 week after inoculation and developed root rot and vascular discoloration. After 2 weeks, 70% of the inoculated plants were affected by both isolates and 40 and 10% died when inoculated with ER1274 and ER1276 isolates, respectively. F. redolens was consistently reisolated from the stems of wilted plants. Noninoculated plants remained healthy. Currently, only F. oxysporum f. sp. lentis Vasud. and Sriniv. has been reported as the cause of Fusarium wilt of lentil. To our knowledge, this is the first report of F. redolens as a pathogen on lentil. References: (1) R. P. Baayen et al. Phytopathology 91:1037, 2001. (2) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. The Pennsylvania State University Press, University Park, 1983. (3) K. O'Donnell et al. Mycologia 90:465, 1998.


Plant Disease ◽  
1997 ◽  
Vol 81 (7) ◽  
pp. 830-830 ◽  
Author(s):  
N. G. Wenner ◽  
W. Merrill ◽  
J. T. Moody

In August 1996, several 4- to 6-m-tall Abies fraseri (Pursh) Poir. in Adams County, PA, were found bearing numerous dead branches and/or dead tops. The trees had been severely stressed by being ball-and-burlapped and replanted in 1993. Distinct cankers occurred between the living and dead portions of stems and branches. Associated with these cankers were abundant, reddish-orange, erumpent stroma, each bearing three to 10 similarly colored cupulate ascomata. The latter contained asci bearing two to four large, muriform ascospores that, as they matured, formed large numbers of small ascoconidia, indicating the pathogen was Thyronectria balsamea (Cooke & Peck) Seeler (= Nectria balsamea Cooke & Peck). In September 1996, cankered dead stems and branches from affected A. frasrei Christmas tree plantations in Avery County, NC, were found bearing the same pathogen. This fungus is known on A. bal-samea (L.) Mill. from northern Minnesota east through Canada to northern New York and Newfoundland (2). Funk (1) reported it from A. lasio-carpa (Hook.) Nutt. in (presumably) British Columbia, but gave no details. This is the first report of it in the eastern United States south of northern New York, a considerable extension of its known range, and the first report of it from A. fraseri. Voucher specimens are in PACMA (Pennsylvania State University Mycologica Herbarium, Mont Alto Campus). References: (1) A. Funk. Can. For. Serv. BC-X-222:142, 1981. (2) E. V. Seeler, Jr. J. Arnold Arbor. 21:442, 1940.


Plant Disease ◽  
1998 ◽  
Vol 82 (12) ◽  
pp. 1405-1405 ◽  
Author(s):  
G. Lori ◽  
S. Wolcan ◽  
C. Mónaco

During the summer of 1995-1996, an 80-ha field of 6-year-old asparagus plants (cv. UC 72) in Saladillo (Province of Buenos Aires) was affected by a decline syndrome (1). The plants showed a decline in vigor and approximately 60 to 70% of the plants died. The symptomatic plants were chlorotic, stunted, with stem lesions and crown and root rot. Fusarium moniliforme and F. proliferatum were isolated from vascular and epidermal tissues of roots, crowns, and stems. Identification of Fusarium to species was made by examining conidiogenous cells from colonies cultured on KCl medium (2). Microconidia were born in long and short chains and false heads. The isolates were identified based on the the presence of polyphialides in F. proliferatum and their absence in F. moniliforme, which produces monophialides only (2). In two separate trials, asparagus seeds (cv. UC 72) were surface sterilized and placed in steamed soil infested with a conidial suspension of each species. The viable propagules in the soil (CFU per g) were estimated by soil plate dilutions on Nash & Snyder-PCNB (pentachloronitrobenzene) medium. The F. moniliforme and F. proliferatum soil densities were 19.2 × 103 and 23 × 103 CFU per g of soil, respectively. The pots were placed in the greenhouse on different benches to avoid cross-contamination. After 4 months, inoculated plants showed root and crown discoloration. F. moniliforme and F. proliferatum were reisolated (64 and 75%, respectively) from discolored portions of internal and external root and crown tissues. Although the stems did not show symptoms, F. moniliforme and F. proliferatum were also recovered (27 and 38%, respectively) from asymptomatic tissues. Six months after inoculation the plants developed chlorotic symptoms with crown and root rot, and then wilted. F. moniliforme and F. proliferatum were reisolated from root systems, crowns, and stems of all inoculated plants. F. moniliforme and F. proliferatum are involved in corn stalk and ear rot in Argentina. Corn and asparagus are frequently grown in close proximity and often follow one another at a particular site. Airborne and soil debris carrying F. moniliforme and F proliferatum from corn may be an additional source of inoculum for asparagus in Argentina. The results indicate that the presence of F. moniliforme and F. proliferatum is a factor that contributes to asparagus decline in Argentina. References: (1) W. H. Elmer et al. Plant Dis. 80:117, 1996. (2) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. Pennsylvania State University, University Park, 1983.


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