scholarly journals First Report of Fusarium Rot Caused by Fusarium oxysporum on Lemon in Tucumán, Argentina

Plant Disease ◽  
2013 ◽  
Vol 97 (7) ◽  
pp. 989-989 ◽  
Author(s):  
G. M. Fogliata ◽  
C. V. Martínez ◽  
M. E. Acosta ◽  
M. L. Muñoz ◽  
L. D. Ploper

Fusarium rot is considered a minor disease of citrus fruits. Several Fusarium species have been associated with fruit decay, most commonly F. lateritium Nees, F. moniliforme J. Sheld., F. oxysporum Schltdl., and F. solani (Mart.) Sacc. (2,3). In the winters of 2007, 2009, 2010, and 2011, lemon [Citrus limon (L.) Burm. f.] fruit with white mycelium covering the peduncle were submitted to the Phytopathology Lab at the Estación Experimental Agroindustrial Obispo Colombres. All fruit samples from Tucumán, Argentina, were stored in boxes kept in packinghouse for more than 1 month. In 2007 only, light to dark brown flavedo around the peduncle was observed in less than 1% of the sample fruit received. No internal breakdown was visible. No change in rind color was observed in the samples received in remaining years. Abundant Fusarium sp. conidia were observed on the mycelium. Colonies with white to violet fluffy aerial mycelium developed on potato dextrose agar (PDA) and produced abundant ovoid or oblong microconidia (1.9 to 3.6 × 4.8 to 10.8 μm), usually unicellular, borne in false heads on short monophialides, and loculated slightly falcate macroconidia were mostly three to five septate (2.4 to 4.8 × 19.2 to 31.2 μm). Unbranched and branched-monophialidic conidiophores were observed. Simple or paired chlamydospores developed on synthetic nutrient agar (1 g KH2PO4, 1 g KNO3, 0.5 g MgSO4.7H2O, 0.5 g KCl, 0.2 g sucrose, and 20 g agar/liter distilled water). On the basis of morphological and cultural criteria, 22 isolates were identified as F. oxysporum (4) designated as D1 to D22. Morfological identification was confirmed by PCR (1) using genomic DNA extracted from the mycelium of pure culture, and an amplified product of 70 bp, specific for the species F. oxysporum, was obtained. The internal transcribed spacer (ITS) region of rDNA was amplified using the primers ITS4/ITS5 and secuenced. BLAST analysis of the 600 bp segment showed a 100% indentity with F. oxysporum, strains CCF 4362 and 1166 (GenBank Accession Nos. HE974454 and FR731133, respectively). Pathogenicity tests were conducted twice by inoculating 10 surface-disinfected wounded lemon fruit. A rind disc (5 mm in diameter and 1 mm deep) near the stem end was removed and a 5-mm-diameter agar disc of D2 isolate (grown at 25°C for 5 days on PDA) was attached to the wound replacing the rind disc. The inoculation site was covered with moistened cotton wool and the fruit were wrapped in plastic bags to prevent the inoculum from drying out. Ten control fruit were inoculated with uncultured PDA plugs (5 mm in diameter). All fruit were maintained in a growth chamber at 25°C under humid conditions. After 5 to 6 days, all inoculated fruit showed white aerial mycelium, initially on the inoculation site and then on the peduncle, similar to that observed on naturally infected fruit. After 20 days, two fruit developed stem end dry rot and showed peduncle fall but no internal breakdown was visible. Control fruit developed any symptom as described above. F. oxysporum was consistently reisolated from infected tissues, completing Koch's postulates. To our knowledge, this is the first report of Fusarium rot caused by F. oxysporum on lemon in Tucumán, Argentina. References: (1) V. Edel et al. Mycol. Res. 104:518, 2000. (2) H. S. Fawcett. Citrus Diseases and Their Control, 1936. (3) A. Z. Joffe and M. Schiffmann-Nadel. Fruits 27:117, 1972. (4) P. E. Nelson et al. Fusarium species: An Illustrated Manual for Identification, 1983.

Plant Disease ◽  
2013 ◽  
Vol 97 (12) ◽  
pp. 1657-1657 ◽  
Author(s):  
J. H. Wang ◽  
Z. H. Feng ◽  
Z. Han ◽  
S. Q. Song ◽  
S. H. Lin ◽  
...  

Pepper (Capsicum annuum L.) is an important vegetable crop worldwide. Some Fusarium species can cause pepper fruit rot, leading to significant yield losses of pepper production and, for some Fusarium species, potential risk of mycotoxin contamination. A total of 106 diseased pepper fruit samples were collected from various pepper cultivars from seven provinces (Gansu, Hainan, Heilongjiang, Hunan, Shandong, Shanghai, and Zhejiang) in China during the 2012 growing season, where pepper production occurs on approximately 25,000 ha. Pepper fruit rot symptom incidence ranged from 5 to 20% in individual fields. Symptomatic fruit tissue was surface-sterilized in 0.1% HgCl2 for 1 min, dipped in 70% ethanol for 30 s, then rinsed in sterilized distilled water three times, dried, and plated in 90 mm diameter petri dishes containing potato dextrose agar (PDA). After incubation for 5 days at 28°C in the dark, putative Fusarium colonies were purified by single-sporing. Forty-three Fusarium strains were isolated and identified to species as described previously (1,2). Morphological characteristics of one strain were identical to those of F. concentricum. Aerial mycelium was reddish-white with an average growth rate of 4.2 to 4.3 mm/day at 25°C in the dark on PDA. Pigments in the agar were formed in alternating red and orange concentric rings. Microconidia were 0- to 1-septate, mostly 0-septate, and oval, obovoid to allantoid. Macroconidia were relatively slender with no significant curvature, 3- to 5-septate, with a beaked apical cell and a foot-shaped basal cell. To confirm the species identity, the partial TEF gene sequence (646 bp) was amplified and sequenced (GenBank Accession No. KC816735). A BLASTn search with TEF gene sequences in NCBI and the Fusarium ID databases revealed 99.7 and 100% sequence identity, respectively, to known TEF sequences of F. concentricum. Thus, both morphological and molecular criteria supported identification of the strain as F. concentricum. This strain was deposited as Accession MUCL 54697 (http://bccm.belspo.be/about/mucl.php). Pathogenicity of the strain was confirmed by inoculating 10 wounded, mature pepper fruits that had been harvested 70 days after planting the cultivar Zhongjiao-5 with a conidial suspension (1 × 106 spores/ml), as described previously (3). A control treatment consisted of inoculating 10 pepper fruits of the same cultivar with sterilized distilled water. The fruit were incubated at 25°C in a moist chamber, and the experiment was repeated independently in triplicate. Initially, green to dark brown lesions were observed on the outer surface of inoculated fruit. Typical soft-rot symptoms and lesions were observed on the inner wall when the fruit were cut open 10 days post-inoculation. Some infected seeds in the fruits were grayish-black and covered by mycelium, similar to the original fruit symptoms observed at the sampling sites. The control fruit remained healthy after 10 days of incubation. The same fungus was isolated from the inoculated infected fruit using the method described above, but no fungal growth was observed from the control fruit. To our knowledge, this is the first report of F. concentricum causing a pepper fruit rot. References: (1) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Ames, IA, 2006. (2) K. O'Donnell et al. Proc. Nat. Acad. Sci. USA 95:2044, 1998. (3) Y. Yang et al. 2011. Int. J. Food Microbiol. 151:150, 2011.


Plant Disease ◽  
2021 ◽  
Author(s):  
Laikun Xia ◽  
Yanyong Cao ◽  
Jie Wang ◽  
Jie Zhang ◽  
Shengbo Han ◽  
...  

Maize stalk rot has become one of the most important diseases in maize production in China. From 2017 to 2019, a survey was conducted to determine the population diversity of Fusarium species associated with maize diseases in 18 cities across Henan Province. Maize stalk rot with an incidence of more than 20% that caused yield losses up to 30% was observed on maize variety Zhengdan958, which was grown in two continuous maize fields in Zhumadian City, Henan Province. The stem tissues from the boundary between diseased and healthy pith were chopped into small pieces (3 × 8 mm), disinfected (70% ethanol for 1 min) and then placed onto potato dextrose agar (PDA) amended with L-(+)-Lactic-acid (1 g/L) and incubated at 25°C for 4 days. Colonies on PDA produced fluffy, light yellow aerial mycelium and purple to deep brick red pigment at 25°C (Fig 1A, 1B). On carnation leaf agar (CLA), macroconidia in orange sporodochia formed abundantly, but microconidia were absent. Macroconidia were short and thick-walled, had 3 to 5 septa, a poorly developed foot cell and rounded apical cell (Fig 1C). These characteristics matched the description of Fusarium culmorum (Leslie and Summerell 2006) and isolates DMA268-1-2 and HNZMD-12-7 were selected for further identity confirmation. Species identification was confirmed by partial sequences of three phylogenic loci (EF1-α, RPB1, and RPB2) using the primer pairs EF1/EF2, CULR1F/CULR1R, and CULR2F/CULR2R, respectively (O'Donnell et al., 1998). The consensus sequences from the two isolates were deposited in GenBank (MZ265416 and MZ265417 for TEF, respectively; MZ265412 and MZ265414 for RPB1, respectively; MZ265413 and MZ265415 for RPB2). BLASTn searches indicated that the nucleotide sequences of the three loci of the two isolates revealed 99% to 100% similarity to those of F. culmorum strains deposited in the GenBank, Fusarium-ID, and MLST databases (Supplementary Table 1~3). Pathogenicity test was conducted at the flowering-stage using Zhengdan958 and Xundan20 plants according to previously described method (Zhang et al., 2016; Cao et al., 2021; Zhang et al., 2021). The second or third internodes of thirty flowering plants were drilled to make a wound approximately 8 mm in diameter using an electric drill. Approximately 0.5 mL inoculum (125 mL colonized PDA homogenized with 75 mL sterilized distilled water) was injected into the wound and sealed with Vaseline and Parafilm to maintain moisture and avoid contamination. Sterile PDA slurry was used as a control. Thirty days after inoculation, the dark-brown, soft rot of pith tissues above and below the injection sites were observed, and some plants were severely rotten and lodged (Fig 1D, 1E). These symptoms were similar to those observed in the field. No symptoms were observed on control plants. The same pathogen was re-isolated from the inoculated stalk lesions but not from the control, thereby fulfilling Koch's postulates. To our knowledge, this is the first report of F. culmorum as the causal agent of stalk rot on maize plants in China. Also, this fungus has been reported to cause maize ear rot in China (Duan et al. 2016) and produce mycotoxins such as trichothecenes, nivalenol, and zearalenone that cause toxicosis in animals (Leslie and Summerell 2006). The occurrence of maize stalk rot and ear rot caused by F. culmorum should be monitored due to the potential risk for crop loss and mycotoxin contamination.


Plant Disease ◽  
2001 ◽  
Vol 85 (9) ◽  
pp. 1030-1030 ◽  
Author(s):  
R. D. Peters ◽  
I. K. Macdonald ◽  
K. A. MacIsaac ◽  
S. Woodworth

Fusarium dry rot is a significant postharvest disease of potato (Solanum tuberosum L.) and is often controlled by applying thiabendazole to tubers prior to storage. However, thiabendazole-resistant isolates of Fusarium spp. have been reported from Europe (2), the United States (1), and Canada (1,4). To address concerns, samples of potato tubers showing symptoms of dry rot caused by Fusariumspp. were collected from three storage bays in a commercial storage facility in Nova Scotia, Canada, in February 2001. All tubers had been treated with thiabendazole after harvest and prior to storage. Tubers were cut longitudinally, and small tissue samples (10 × 5 × 3 mm) were taken from the margins of internal necrotic regions with a sterile scalpel, surface-sterilized in 0.6% sodium hypochlorite for 15 s, rinsed twice in sterile distilled water (SDW), and blotted dry on sterile filter paper. Tissue pieces were plated on 0.5-strength potato dextrose agar (PDA) amended with tetracycline (0.05 g/liter) and streptomycin sulfate (0.1 g/liter). Petri dishes were incubated in the dark at 22°C for 4 to 7 days. After incubation, hyphal tips from the margins of actively growing isolates were removed with a sterile probe and plated on 0.5-strength PDA to generate pure cultures. Of 35 potato tubers examined, 10 (29%) yielded Fusarium isolates for further study. All 10 isolates were identified as F. sambucinum Fuckel according to Nelson et al. (3). Agar plugs (5 mm diameter) taken from the margins of 7- to 10-day-old cultures of F. sambucinum isolates were transferred to petri dishes containing 0.5-strength PDA amended with thiabendazole at 0, 1, 5, 10, 20, 50, or 100 mg/liter. Thiabendazole was prepared as a stock solution in SDW and added to molten agar after autoclaving. Cultures were grown in the dark for 7 days at 22°C, after which mycelial growth diameter was measured using digital calipers. Two measurements, along orthogonal diameters, were taken from each of three replicate plates for a total of six measurements per thiabendazole concentration. Means were calculated, and the diameter of the inoculation plug was subtracted from each mean. Calculated EC50 values (thiabendazole concentration inhibiting pathogen growth by 50%) were obtained by regression of the log of the chemical concentration against the corresponding probit of percent fungal inhibition. All isolates of F. sambucinum were resistant to thiabendazole, with EC50 values ranging from 7 to 82 mg/liter. Six isolates had EC50 values between 40 and 82 mg/liter. Control isolates of F. sambucinum, F. avenaceum, F. solani, and F. oxysporum were sensitive to thiabendazole, with EC50 values of <1 mg/liter. Although isolates of F. sambucinum resistant to thiabendazole have been recovered from eastern Canada (1,4), this is the first report of thiabendazole resistance in F. sambucinum isolates from tubers in commercial storage in the Annapolis Valley of Nova Scotia, Canada, a production region that concentrates on growing processing potatoes for the potato chip industry and is several hundred kilometers from other potato-growing regions of Prince Edward Island and New Brunswick. References: (1) A. E. Desjardins. Am. Potato J. 72:145, 1995. (2) G. A. Hide et al. Plant Pathol. 41:745, 1992. (3) P. E. Nelson et al. 1983. Fusarium Species: An Illustrated Manual for Identification . Pennsylvania State University Press, University Park, PA. (4) H. W. Platt. Phytoprotection 78:1, 1997.


Plant Disease ◽  
2012 ◽  
Vol 96 (6) ◽  
pp. 914-914 ◽  
Author(s):  
D. Fernández-Ortuño ◽  
X. P. Li ◽  
F. Wang ◽  
G. Schnabel

Gray mold caused by Botrytis spp. is one of the most economically important diseases of cultivated strawberry (Fragaria × ananassa) worldwide. In June 2011, strawberry fruit that was symptomatic of gray mold disease was collected from High Point county in North Carolina. Fruit had brown lesions that enlarged quickly and were covered with green-gray masses of spores followed by a soft rot. To isolate the causal agent, conidia were scraped off the fruit, suspended in 1% Tween 20, spread on water agar amended with 0.1% lactic acid, and emerging colonies were then transferred onto potato dextrose agar (PDA) medium. All but one single-spore colony (designated HP33) were at first colorless and later became gray to brown when the conidiphores and conidia developed on PDA. Isolate HP33 was white to pale gray with short, tufted aerial mycelium, black sclerotia in concentric rings, and did not produce conidia on PDA. Conidia were subhyaline to light brown, smooth, ellipsoid, ovoid or obovoid, and were on average 11.7 × 8.6 μm. The conidiophores were erect, septate, and brown to subhyaline from the base to apex, with swollen basal cell and multiple inflated conidiogenous cells. These morphological features were consistent with Botrytis caroliniana X. P. Li & G. Schnabel sp. nov., a new species isolated recently from blackberry fruit in South Carolina (2). All other single-spore isolates were confirmed to be B. cinerea as described previously (1). To confirm the identity of isolate HP33 to the species level, the necrosis and ethylene-inducing protein 1 (NEP1) was PCR amplified and sequenced by primer pairs NEP1for/NEP1rev as described previously (3). The nucleotide sequence matched the ones published for B. caroliniana (GenBank Accession Nos. JF811593, JF811594, and JF811595). Pathogenicity tests were conducted by inoculating 10 surface-sterilized strawberry fruit with single agar plugs (6 mm in diameter) containing actively growing mycelium; 10 control fruit received agar plugs without mycelium. The inoculated fruit were incubated for 3 days at room temperature in airtight plastic bags and after that developed typical gray mold symptoms. Koch's postulates were fulfilled by the reisolation of B. caroliniana from symptomatic fruit. Control fruit remained healthy. To our knowledge, this is the first report of B. caroliniana on strawberry. It is uncertain whether the new species requires management strategies different from those that control gray mold caused by B. cinerea. References: (1) D. Fernández-Ortuño et al. Plant Dis. 95:1482, 2011. (2) X. P. Li et al. Mycologia 2012, doi:10.3852/11-218. (3) M. Staats et al. Fungal Genet. Biol. 44:52, 2007.


Plant Disease ◽  
2013 ◽  
Vol 97 (3) ◽  
pp. 427-427 ◽  
Author(s):  
G. D. Sinniah ◽  
N. K. B. Adikaram ◽  
I. S. K. Vithanage ◽  
C. L. Abayasekara ◽  
M. Maymon ◽  
...  

Mango malformation disease (MMD) is one of the most devastating diseases causing severe economic losses to this crop worldwide. MMD has not been reported in Sri Lanka although the disease was reported in neighboring India over a century ago. Abnormal, thick, and fleshy mango panicles (40%) and proliferating stunted shoots (<1%) showing characteristic malformation symptoms were observed in Peradeniya-Kandy area (7°17'4.15” N, 80°38′14.08” E). Malformed inflorescences and vegetative shoots were collected during January to March and September to November, in 2008 through 2012. Pieces of malformed tissues were surface sterilized in 1% sodium hypochlorite and transferred to potato dextrose agar (PDA). The plates were incubated at 26 ± 2°C for 7 days. Monoconidial cultures of 41 isolates that resembled Fusarium spp. were obtained. Colonies showed white sparse aerial mycelium and magenta-dark purple pigmentation on the underside. Growth rate of the isolates averaged 3.67 mm/day in the dark at 25°C on PDA. To stimulate conidia development, Fusarium isolates were transferred to carnation leaf agar (CLA). Sympodially branched conidiophores bearing mono- and polyphialides with 2 to 3 conidiogenus openings originated erect and prostrate on aerial mycelium. Oval to allontoid, abundant microconidia were produced in false heads on mono- and polyphialides. Dimensions of aseptate conidia were 2.5 to 12.5 (6.47) × 1.25 to 3.8 (2.29) μm. Macroconidia were long and slender, 3 to 5 celled and 27.5 to 47.5 (38.59) × 2.5 to 5 (2.94) μm. Chlamydospores were absent. These characters are consistent for F. mangiferae. DNA was extracted from 30 monoconidial Fusarium isolates (1) and amplified with species-specific PCR primers 1-3F/R (forward: 5′-TGCAGATAATGAGGGTCTGC-3′; reverse: 5′-GGAACATTGGGCAAAACTAC-3′) (3). Eight isolates from malformed inflorescences (I6, I13, I15, and I16) and malformed vegetative tissues (V1, V2, V3, and V4), were identified as F. mangiferae based on a 608-bp species-specific amplified DNA fragment. Pathogenicity of F. mangiferae isolates, I15 and V2, was tested on 1-year-old seedlings cv. Willard planted in 10-liter plastic pots. Conidia suspensions (107 conidia/ml of 0.1% water agar) were obtained from 10-day-old monoconidial cultures. Each isolate was inoculated onto 15 apical buds by placing drops (20 μl) of conidia (2). Both F. mangiferae isolates, I15 and V2, on artificial inoculation produced typical floral malformation symptoms in 40% of the buds, up to 10 weeks after inoculation. The Fusarium isolates recovered were identical in colony and mycelia morphology and conidia dimensions to the original F. mangiferae isolates. No Fusarium species were recovered from control flower buds. To our knowledge, this is the first report of MMD in the inflorescence and the vegetative shoots caused by F. mangiferae in Sri Lanka. Isolation of other Fusarium spp. that were not identified as F. mangiferae in this study suggests that additional Fusarium spp. may be associated with the MMD in Sri Lanka. Further studies are needed to confirm the identity of these Fusarium isolates, their role in MMD, and the distribution over the island. Since the disease is likely to drastically reduce productivity, measures will be required to protect 12,160 ha of mango cultivation from this devastating disease. References: (1) S. Freeman et al. Exp. Mycol. 17:309, 1993. (2) S. Freeman et al. Phytopathology 89:456, 1999. (3) Q. I. Zheng and R. C. Ploetz. Plant Pathol. 51:208, 2002.


Plant Disease ◽  
2013 ◽  
Vol 97 (2) ◽  
pp. 284-284 ◽  
Author(s):  
I. H. Al Mahmooli ◽  
F. Al Balushi ◽  
O. Doyle ◽  
A. M. Al Sadi ◽  
M. L. Deadman

Hybrid gladiolus varieties have potential as a major ornamental crop in Oman. Grown for the cut-flower industry, their production has increased significantly in recent years. In 2010, during a field trial of two hybrid varieties (Red Majesty and Mascagni) grown in sandy soil at Al Moballah, Muscat, approximately 3% of Red Majesty plants and 12% of Mascagni plants showed signs of wilting and yellowing prior to plant death. In all cases, tissue taken from 20 diseased corms yielded Fusarium-like colonies on potato dextrose agar (PDA). Colonies were light to dark purple in color with dense and abundant aerial mycelium; macroconidia were 33.8 × 4.8 μm with 3 to 5 septa per spore; microconidia were 13.5 × 4.8 μm with 0 to 1 septa per spore and were in chains (mean of 50 spores in both cases). No chlamydospores were observed. In vitro characters and spore measurements conformed to previously described features of Fusarium proliferatum (Matsushima) Nirenberg (2). Mycelial plugs (5 mm in diameter) were taken from 5-day-old cultures of F. proliferatum grown on 2.5% PDA and wrapped on the base of Gladiolus corms using Parafilm and wet cotton. The Parafilm was removed after 7 days of inoculation. The corms were kept in moistened polythene bags for and symptoms were recorded. Control corms were inoculated using PDA (1). Artificial inoculations resulted in rot symptoms on all corms within 14 days and fungal colonies identical to initial isolations were recovered from artificially infected corms. Rotting was not observed in corms inoculated using PDA alone. Identification of F. proliferatum was confirmed using sequences of the internal transcribed spacer (ITS) of the ribosomal DNA (ITS1 and ITS4 primers) and sequences of the translation elongation factor alpha (TEF-1) gene (EF-1-986 and EF-728 primers). The ITS and TEF-1 sequences were found to share 99.8% and 99.6% nucleotide similarity to previously published sequences of the ITS (HQ113948) and EF (JN092351) regions of F. proliferatum in GenBank, respectively. The ITS sequence of one isolate was assigned GenBank Accession No. JN86006. To our knowledge, this is the first report of the occurrence of F. proliferatum in Oman or in the Arabian Peninsula. References: (1) C. Linfield. Ann. Appl. Biol. 121:175, 1983. (2) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. Pennsylvania State University Press, USA, 1983.


Plant Disease ◽  
2005 ◽  
Vol 89 (1) ◽  
pp. 106-106 ◽  
Author(s):  
A. Belisario ◽  
M. Maccaroni ◽  
A. Coramusi

Cultivation of hazelnut (Corylus avellana L.) has considerable economic potential in Italy, in particular, in the northern Lazio Region. Since early summer of 2000, cankered twigs have been observed on hazelnut trees that were severely affected by gray necrosis, which is a disease complex causing fruit drop (1). In subsequent years, sunken areas were observed on 1-year-old shoots from late April through May. The resulting cankers had reddish brown margins and the death of the cambium in the infected area and produced an L-shaped malformation of twigs. Girdling of the twig by the canker resulted in death of the foliage. Yellow-to-orange sporodochia were evident on cankers by early June. Isolations were made from the margins of young cankers from 20 twigs collected from 10 trees. Tissue pieces were plated onto potato dextrose agar (PDA) after surface disinfection with 1% sodium hypochlorite. Slow-growing, cream-to-reddish brown colonies with sparse aerial mycelium emerged from 80% of diseased tissue pieces within 10 days of incubation at 20 to 22°C. Conidial production was induced by keeping pure cultures at 22 to 25°C under natural light but out of direct sunlight. Within 1 month, sporodochia bearing ellipsoidal, spindle-shaped, commonly 1 to 3 septate macroconidia developed. Intercalary chlamydospores were often present in chains. Single conidia were subcultured on carnation leaf agar (CLA). On the basis of morphological and cultural characteristics, the fungus was identified as Fusarium lateritium Nees. (2). Pathogenicity tests were conducted outdoors on the current year's shoots of hazelnut trees with four isolates derived from single conidia of F. lateritium. Inocula used were either mycelial plugs cut from the margin of actively growing cultures or small (10 × 10 mm) pieces of sterile cheesecloth soaked in 1 × 106 conidia per ml suspension. The mycelial plugs were placed under the bark, while the soaked cheesecloth pieces were wrapped around an area that had been wounded by gently scraping off a length of the bark (approximately 10 mm) with a sterile needle. All the inoculations were wrapped with Parafilm to prevent desiccation. Six inoculations per isolate were performed. In a similar manner, controls were inoculated with agar plugs or water only. After 3 months, the length and width of each canker were measured. For both inoculation methods, cankers were similar to those observed in nature and averaged 20.6 × 5 mm, while the controls did not show any symptoms. F. lateritium was consistently reisolated from the canker margins of the inoculated shoots. To our knowledge, this is the first report of F. lateritium causing twig cankers on hazelnut. The fungus has been reported to cause cankers on several tree species, including Malus domestica (apple), Morus spp. (mulberry), Sophora japonica (Japanese pagoda tree), Robinia pseudoacacia (black locust), Citrus spp., and Pyrus pyrifolia (Asian pear). References: (1) A. Belisario et al. Inf. Agrario 59(6):71, 2003. (2) P. E. Nelson et al. Fusarium Species: An Illustrated Manual for Identification. Pennsylvania State University, University Park, 1983.


Plant Disease ◽  
2010 ◽  
Vol 94 (8) ◽  
pp. 1069-1069 ◽  
Author(s):  
J. C. Bienapfl ◽  
D. K. Malvick ◽  
J. A. Percich

Multiple Fusarium species have been found in association with soybean (Glycine max) plants exhibiting root rot in the United States (3). Soybean plants that lacked apparent foliar symptoms, but exhibited 2- to 5-mm brown, necrotic taproot lesions and lateral root necrosis were observed in Minnesota in one field each in Marshall and Otter Tail counties in July of 2007, as well as in one field in Marshall County in July of 2008. Sampling was conducted as part of a study investigating root rot in major soybean-production areas of Minnesota. Plants were arbitrarily dug up at the R3 growth stage. Root systems were washed, surface disinfested in 0.5% NaOCl for 3 min, rinsed in deionized water, and dried. Fusarium isolates were recovered from root sections with necrotic lesions embedded in modified Nash-Snyder medium (1). One resulting Fusarium colony from one plant per county was transferred to half-strength acidified potato dextrose agar (PDA) and carnation leaf agar (CLA) to examine morphological characteristics (4). Culture morphology on PDA consisted of flat mycelium with sparse white aerial mycelium. On CLA, thick-walled macroconidia with a hooked apical cell and a foot-shaped basal cell were produced in cream-colored sporodochia. Macroconidia ranged from 32.5 to 45.0 μm long. Microconidia were oval to cylindrical with 0 to 1 septa, ranged from 7.5 to 11.25 μm long, and were produced on monophialides. Chlamydospores were produced abundantly in chains that were terminal and intercalary in the hyphae of 4-week-old cultures. Morphological characteristics of the three isolates were consistent with descriptions of F. redolens (2,4). The identity of each isolate was confirmed by sequencing the translation elongation factor 1-α (TEF) locus (4). BLAST analysis of the TEF sequences from each isolate against the FUSARIUM-ID database resulted in a 100% match for 17 accessions of F. redolens (e.g., FD 01103, FD 01369). Each F. redolens isolate was tested for pathogenicity on soybean. Sterile sorghum grain was infested with each isolate and incubated for 2 weeks. Sterile sorghum was used for control plants. Soybean seeds of cv. AG2107 were planted in 11.4-cm pots ~1 cm above a 25-cm3 layer of infested sorghum or sterile sorghum. Two replicate pots containing four plants each were used per treatment and the experiment was repeated once. Root rot was assessed 28 days after planting. Each F. redolens isolate consistently caused taproot necrosis on inoculated plants, whereas control plants did not exhibit root necrosis. Isolations were made from roots of inoculated and control plants and the isolates recovered from inoculated plants were identified as F. redolens based on morphological characteristics and TEF sequences. Fusarium species were not isolated from control plants. To our knowledge, this is the first report of F. redolens causing root rot of soybean; however, it is possible F. redolens has been found previously and misidentified as F. oxysporum (2,4). Results from inoculations suggest that F. redolens may be an important root rot pathogen in Minnesota soybean fields. References: (1) J. C. Bienapfl et al. Acta Hortic. 668:123, 2004. (2) C. Booth and J. M. Waterston. No. 27 in: CMI Descriptions of Pathogenic Fungi and Bacteria. CMI, Kew, England, 1964. (3) G. L. Hartman et al. Compendium of Soybean Diseases. 4th ed. The American Phytopathological Society, St. Paul, MN, 1999. (4) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Ames, IA, 2006.


Plant Disease ◽  
2021 ◽  
Author(s):  
Anam Moosa ◽  
Ayaz Farzand ◽  
Sajid Aleem Khan ◽  
Tanvir Ahmad ◽  
Hafiz Muhammad Usman Aslam ◽  
...  

Citrus reticulata cv. ‘Kinnow’ mandarin is the most popular and widely grown fruit crop in Pakistan. During 2017, a survey was conducted to the local citrus fruit markets of Faisalabad, Pakistan. Citrus fruits (n=50) exhibiting stem end rot and fruit rot were collected with 15% disease incidence. The stem end region showed light to dark brown lesions and white fungal growth was also observed in the severely infected fruit. Infected fruit were excised into 2mm2 segments, surface disinfected with 1% NaClO, rinsed with sterilized water and dried. Later, these tissues were placed on potato dextrose agar (PDA) medium and subsequently incubated at 25 °C. Purified isolates produced white colonies with beige pigmentation. The frequency of fungal isolation was 47%. Microscopic observations revealed that macroconidia (n=50) had 5 to 6 septations, with a prominent dorsiventral curvature, tapered and elongated apical cell, and a foot shape basal cell. The macroconidia were measuring 22 to 45 × 2.9 to 4.3 µm with an average of 31 × 3.6 µm. However, microconidia were not observed. Chlamydospores were globose, intercalary, solitary, or in pairs, appearing in chains (Leslie and Summerell 2006). For molecular identification, DNA was extracted from all isolates. The internal transcribed spacer region (ITS) ITS1/4 (White et al. 1990), translation elongation factor-1 alpha (TEF) EF1/2 (O’Donnell et al. 1998), and RNA polymerase II subunit 1 (RPB1) (O'Donnell et al. 2013) were amplified using PCR and the product was subsequently sequenced. Based on BLAST analysis, the isolate was identified as Fusarium equiseti (FUS-21). The sequences of the representative isolate FUS-21 were deposited in the GenBank with accession numbers (ITS, MH581300), (TEF, MK203749), and (RPB1, MW596599) showing more than 99% similarity with ITS accession GQ505683, TEF accession GQ505594, and 100% to RPB1 accession JX171481. To determine the pathogenicity, 40 healthy surface disinfested citrus fruit were taken. The fruit were inoculated by creating artificial wounds on the surface with a sterilized needle and 10 μL of 105 spores/mL was deposited in the wounds. In case of control fruit were inoculated with 10 μL sterilized distilled water only, and incubated at 25 °C. All fruit inoculated with the putative pathogen, developed symptoms like the original fruit from which they were isolated. The pathogenicity test was repeated twice. Visible white mycelium appeared at the stem end region and the fruits became dried as the infection progressed. However, the control fruit remained asymptomatic. The pathogen was re-isolated from infected fruit and identified based on morphometric and molecular analysis. Previously we have reported F. oxysporum causing citrus fruit rot in Pakistan (Moosa et al. 2020). This is the first report of F. equiseti causing post-harvest rot of citrus fruits in Pakistan. Kinnow is an important fruit crop of Pakistan with huge export value the management of Fusarium rot is quite important to save the loss of fresh produce.


Plant Disease ◽  
2004 ◽  
Vol 88 (2) ◽  
pp. 222-222 ◽  
Author(s):  
T. J. Michailides ◽  
D. P. Morgan ◽  
K. R. Day

In early July 2001, samples of nectarine and peach fruit were brought from orchards in northern Tulare County or from packinghouses to our laboratory for diagnosis of an unusual decay. When the decay lesions originated close to the stylar end, leaking juice streamed from it. When the decay lesion was on the stem end of the fruit and touched the packing box, it developed a decay consisting of a ring of 0.5 to 2.0 cm (inner diameter) and 1.0 to 3.0 cm (outer diameter). The leaking juice dissolved the cuticle, epidermis, and some of the flesh, creating distinct furrows in the tissue. Samples with similar decay lesions were examined in 2001, 2002, and 2003. In each year, isolations from these fruit consistently yielded two or three different yeasts that were identified as Geotrichum candidum Link, Issatchenkia scutulata (Phaff et al.) Kurtzman et al., and Kloeckera apiculata (Reess emend. Klocker) Janke. All three yeasts were isolated from most of the samples, although sometimes, different combinations of two of the yeasts recovered. To complete Koch's postulates, each yeast was single spored and cultured on acidified potato dextrose agar at 25°C to prepare a dense (108) cell suspension. Eight, mature, ‘Elegant Lady’ peach fruit were surface disinfested in 0.1% sodium hypochlorite for 3 min, allowed to dry, and wounded once with a sterile nail (3 × 5 mm) on the fruit cheek. A 50-µl drop of the cell suspension was placed in each wound, and the peaches were incubated in containers with >95% relative humidity at 27°C. Fruit inoculated similarly with a 50-µl drop of sterile water served as controls. In 2001, two containers containing eight fruit each were used for each yeast, and lesions started developing within 1 week after inoculation. The diameter of the decay lesion was measured after 10 days of incubation of the fruit. The diameter of decay lesions ranged from 21 to 68 mm for G. candidum, 30 to 55 mm for I. scutulata, and 9 to 39 mm for K. apiculata inoculations. The inoculation experiment was repeated with two containers of eight ‘Red Glo’ nectarine fruit per treatment yeast, under the same conditions as described above. Organisms recovered from the decay lesions were the same yeasts used for inoculating the peaches or nectarines. All three yeasts caused similar decay lesions in peaches, and the leaking effect was reproduced in both types of fruit. Symptoms were similar to those observed on fruit samples brought to our laboratory. Control fruit did not develop the characteristic decay lesions, although brown rot caused by Monilinia fructicola developed on a few of the control fruit. We concluded that each isolated yeast had the capacity to cause sour rot decay on stone fruit. From samples and reports, the disease has been found on ‘Red Glo’, ‘Ruby Diamond’, ‘Zee Grand’, ‘Spring Bright’, and ‘Honey Blaze’ nectarines and ‘Elegant Lady’ and ‘Fire Red’ peaches. G. candidum was isolated from peaches and other fruit in California and incited rot of ‘Paloro’ peach in 1960 (2) and caused postharvest sour rot of peaches originating from Georgia, Pennsylvania, New Jersey, and North Carolina (1). However, to our knowledge, this is the first report of G. candidum, I. scutulata, or K. apiculata causing sour rot of commercial peaches and nectarines in the field and postharvest situations in California. References: (1) C. L. Burton and W. R. Wright. Plant Dis. Rep. 53:580, 1969. (2) E. E. Butler. Phytopathology 50:665, 1960.


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