scholarly journals Semi-selective culture medium for Exserohilum turcicum isolation from corn seeds

2014 ◽  
Vol 40 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Roberto Luis De Rossi ◽  
Erlei Melo Reis

Northern corn leaf blight, caused by Exserohilum turcicum (Et), is a disease of widespread occurrence in regions where corn, sweetcorn and popcorn are grown. This disease has great potential to cause damage and has been studied for years, but the association of its causal agent with seeds remains unconfirmed. Thus, the availability of a sensitive method to detect and quantify the inoculum in seeds, even at low incidence, is essential. The aim of this study was to develop a method to detect and quantify the presence of the fungus infecting and infesting corn and popcorn seeds. Artificially and naturally infected seeds were employed to develop the medium. The semi-selective medium was composed of carbendazim (active ingredient) (60 mg/L), captan (30 mg/L), streptomycin sulfate (500 mg/L) and neomycin sulfate (600 mg/L) aggregated to the medium lactose casein hydrolysate agar medium. By using this, Et was detected in naturally infected corn seeds, showing 0.124% incidence, in four out of ten analyzed samples. In addition, 1.04 conidia were detected per infested seed. By means of isolation, pathogenicity test, morphological characterization and comparison with descriptions of the species in the literature, the fungus isolated from the seeds was confirmed to be Et. Both infection and infestation were considered low; thus, for studies of Et detection in corn seeds, the use of semi-selective medium and more than 1,200 seeds/sample is suggested.

Plant Disease ◽  
2014 ◽  
Vol 98 (2) ◽  
pp. 282-282 ◽  
Author(s):  
Y. Li ◽  
L. D. Chi ◽  
L. G. Mao ◽  
D. D. Yan ◽  
Z. F. Wu ◽  
...  

Ginger (Zingiber officinale Roscoe) is an important commercial crop that is planted in 60,000 to 70,000 ha every year in Shandong Province, China. In 2010, rotted rhizomes of cultivar Laiwu Big Ginger were reported on 20 ha in Anqiu, Shandong Province, and yield losses of up to 70% were reported. The aboveground symptoms were the water-conducting portion of symptomatic rhizomes was discolored brown and had a black dry rot of the cortex tissues (3). Thirty symptomatic rhizomes were sampled from six fields in six farms. Komada's method (1) was used to isolate the pathogen. Ten pieces from each rhizome were washed with sterile distilled water and plated on Komada selective medium at 25°C. White fungal colonies turned orchid after 7 days of incubation. Two types of asexual spores were associated with the colonies: microconidia and macroconidia. The microconidia were the most abundantly produced spores and were oval, elliptical or kidney shaped, and produced on aerial mycelia. Macroconidia had three to five cells and gradually pointed or curved edges, varied in size from 3 to 5 × 19 to 36 μm. The rDNA of the internal transcribed spacer regions 1 and 2 and the 5.8S gene in five isolates were amplified using primers ITS1 and ITS4, and the nucleotide sequence was the same as isolate no. 3, which was deposited in GenBank (Accession No. KC594035). A BLAST search showed 99% identity with the strain Z9 of Fusarium oxysporum (EF611088). Pathogenicity tests of five isolates were carried out in a greenhouse and the pathogenicity test of isolate no. 3 was selected for the method description. Ten 1-month-old ginger plants (cv. Laiwu Big Ginger) were grown in plastic pots (diameter 20 cm) with sandy soil and inoculated. Ten plants were used as untreated controls. Isolate no. 3 was grown on casein hydrolysate medium (4) for 72 h and the spores were harvested in sterile distilled water. Aqueous spore suspensions of isolate no. 3 were adjusted with deionized water to 1 × 108 CFU/ml as the inoculum. The prepared inoculum was injected with a syringe into the soil around the rhizome of ginger plants. Inoculated plants were placed in the greenhouse at 24 to 26°C and assessed for rhizome rot on the 14th day after inoculation. Disease severity was recorded based on a scale in which – = no symptoms; 1 = small lesions on seedlings, no rot; 2 = seedling rot; and 3 = plant dead. Similar rhizome rot symptoms were observed after inoculation. The inoculated isolate was re-isolated from diseased rhizomes, confirming its pathogenicity. To our knowledge, this is the first report of rhizome rot of ginger caused by F. oxysporum in China. Rhizome rot of ginger caused by Fusarium spp. is well known in Asian countries such as India (2). References: (1) H. Komada. Rev. Plant Prot. Res. 8:114, 1975. (2) V. Shanmugam et al. Biol Control. 66:1, 2013. (3) E. E. Trujillo. Diseases of Ginger (Zingiber officinale) in Hawaii, Circular 62, Hawaii Agricultural Experiment Station, University of Hawaii, December, 1964. (4) G. E. Wessman. Appl. Microbiol. 13:426, 1965.


Plant Disease ◽  
2008 ◽  
Vol 92 (4) ◽  
pp. 655-655 ◽  
Author(s):  
A. Garibaldi ◽  
A. Minuto ◽  
M. Shiniti Uchimura ◽  
M. L. Gullino

In 2006, gerbera (Gerbera jamesonii) plants, cvs. Basic, Xena, and Olimpia grown for cut flower production in two greenhouse farms in the region of Guarapuava, Paraná, Brazil, exhibited symptoms of a wilt disease. Affected plants (approximately 20, 60, and 50% on cvs. Basic, Xena, and Olimpia, respectively) were stunted and developed yellow leaves unilaterally with initially brown and eventually black streaks in the vascular system. The first symptoms occurred 2 months after transplanting during the hottest period of the summer with an average air temperature of 27°C. Vascular streaks in the yellow leaves were continuous with a brown discoloration in the vascular system of the crown and upper taproot. Occasionally, the leaves of affected plants turned red. A Fusarium sp. was consistently and readily isolated onto a Fusarium-selective medium from symptomatic vascular tissue sampled from the crown of infected plants. Colonies were identified as Fusarium oxysporum on the basis of colony and conidia morphology (1) after subculturing on potato dextrose agar. Since F. oxysporum f. sp. chrysanthemi has been previously reported on Chrysanthemum morifolium, Argyranthemum frutescens, and gerbera (4), pathogenicity tests were carried out by using one monoconidial isolate obtained from wilted plants and one Italian isolate (F. oxysporum f. sp. chrysanthemi MASS 6). The isolates of F. oxysporum were grown in casein hydrolysate in shake culture (90 rpm) for 10 days at 25°C with 12 h of fluorescent light per day. Healthy rooted plants of 30-, 20-, and 45-day-old C. morifolium (cv. Captiva), A. frutescens (cv. Stella 2000), and gerbera (cvs. Jaska, Dalma, and Excellence), respectively, were inoculated by separately dipping roots into a conidial suspension (5 × 107 conidia/ml) of the two isolates of F. oxysporum. Plants were transplanted (one plant per pot) into pots (3.5 liter vol). Noninoculated plants served as control treatments. Plants (15 per treatment) were grown in a glasshouse at an average day temperature of 32°C and night temperature of 23°C (minimum 21°C and maximum 43°C). Wilt symptoms and discoloration of the vascular system in roots, crown, and petioles developed within 29 days on C. morifolium, 26 days on A. frutescens, and 14 days on gerbera. Noninoculated plants remained healthy. F. oxysporum was consistently reisolated from infected plants. The pathogenicity test was carried out twice. Gerbera wilt caused by F. oxysporum f. sp. chrysanthemi was recently reported in Italy (2) and Spain (3). Currently, the wilt of gerbera in the area of Paraná is limited to two farms. To our knowledge, this is the first report of the disease in Brazil as well as in South America. References: (1) C. Booth. Fusarium. CMI, Kew, UK, 1977. (2) A. Garibaldi et al. Plant Dis. 88:311, 2004. (3) A. Garibaldi et al. Plant Dis. 91:638, 2007. (4) A. Minuto et al. J. Phytopathol. 155:373, 2007.


Plant Disease ◽  
2007 ◽  
Vol 91 (5) ◽  
pp. 638-638 ◽  
Author(s):  
A. Garibaldi ◽  
A. Minuto ◽  
A. M. Prados-Ligero ◽  
J. M. Melero-Vara ◽  
M. L. Gullino

In 2004, gerbera (Gerbera jamesonii cv. Excellence) plants, grown for cut flowers, were observed in a soilless cultivation system (coconut fiber substrate) in one farm in the Cadiz area (southwestern Spain) exhibiting symptoms of a wilt disease. Gerbera represents a relevant crop for the industry in the region, after rose and carnation. Affected plants were stunted and developed yellow leaves with initially brown and eventually black streaks in the vascular system. The vascular streaks in the yellow leaves were continuous with a brown discoloration in the vascular system of the crown and upper taproot. In some cases, the leaves of affected plants turned red. Fusarium spp. was consistently and readily isolated from symptomatic vascular tissue of infected plants onto a Fusarium-selective medium (3). Colonies were identified as F. oxysporum after subculturing on potato dextrose agar on the basis of morphological observations. Pathogenicity tests were carried out by using two monoconidial isolates, compared with an Italian one, obtained from wilted gerbera plants. Each isolate of F. oxysporum was grown in shake culture (90 rpm) for 10 days on casein hydrolysate at 25°C with 12 h of fluorescent light per day. Healthy rooted 30-day-old plants (cv. Jaska), were inoculated by dipping roots into a conidial suspension (5 × 107 conidia/ml) in one of the three test isolates of F. oxysporum. Plants were transplanted (1 plant per pot) into pots (3.5 liter vol.) containing rockwool-based substrate. Noninoculated plants served as control treatments. Plants (15 per treatment) were grown in a glasshouse at an average day temperature of 30°C and night temperature of 24°C (minimum of 22°C and maximum of 41°C). Wilt symptoms and vascular discoloration in the roots, crown, and veins developed within 30 days on each inoculated plant, while noninoculated plants remained healthy. F. oxysporum was consistently reisolated from infected plants. The pathogenicity test was conducted twice. A wilt of gerbera was described in the Netherlands in 1952 (1) but its presence was not confirmed in further observations (4). Gerbera wilt was recently reported in Italy (2) and identified as F. oxysporum f. sp. chrysanthemi (A. Garibaldi, personal communication). Currently, the wilt of gerbera in Spain is limited to a few farms and a very limited percent (2 to 3%) of plants. References: (1) J. Arx and J. A. von Tijdschr. PlZiekt. 58:5, 1952. (2) A. Garibaldi et al. Plant Dis. 88:311, 2004. (3) H. Komada. Rev. Plant Prot. Res. 8:114, 1975. (4) G. Scholten. Neth. J. Plant Pathol. 76:212, 1970.


Plant Disease ◽  
2005 ◽  
Vol 89 (6) ◽  
pp. 684-684 ◽  
Author(s):  
A. Garibaldi ◽  
G. Gilardi ◽  
M. L. Gullino

During the spring of 2004, bitterroot (Lewisia cotyledon (S. Wats.) B.L. Robins), a flowering perennial of interest for rock gardens, showed symptoms of a wilt disease in several commercial nurseries located in Piedmont (northern Italy). Ten to thirty percent of plants from several different nurseries were affected. Wilted plants were first observed approximately 20 days after being transplanted into containers when outside temperatures ranged from 15 to 22°C. Symptomatic plants were stunted with yellowed leaves and brown-to-black veins. The vascular browning extended into the crown and was continuous with a brown discoloration in the vascular system of the crown and upper taproot. Fusarium oxysporum, identified on the basis of colony and conidia morphology (1), was consistently and readily isolated from symptomatic vascular tissue onto a Fusarium-selective medium (2). Three isolates were transferred to casein hydrolysate and grown for 10 days to produce conidial inoculum. Healthy 30-day-old plants were inoculated by dipping roots into a (1 × 106 CFU/ml) conidial suspension. Plants were then transplanted into pots filled with steam-sterilized soil. Noninoculated plants served as a control. Plants (12 per treatment) were placed in a climatic chamber at 25°C. Wilt symptoms and vascular discoloration in the roots, crown, and veins developed within 20 days on each inoculated plant, while noninoculated plants remained healthy. F. oxysporum was consistently reisolated from symptomatic plants. The pathogenicity test was conducted twice with the same result. One isolate of the pathogen has been deposited in the ATCC culture collection. To our knowledge, this is the first report of F. oxysporum on L. cotyledon in Italy and elsewhere in the world. Currently, this disease is present in several nurseries in the Piedmont Region of Italy. References: (1) C. Booth. Fusarium. CMI, Kew, UK, 1977. (2) H. Komada. Rev. Plant Prot. Res. 8:114, 1975.


Author(s):  
Barbara Ludwig Navarro ◽  
Lucia Ramos Romero ◽  
María Belén Kistner ◽  
Juliana Iglesias ◽  
Andreas von Tiedemann

AbstractNorthern corn leaf blight (NCLB) is one of the most important diseases in maize worldwide. It is caused by the fungus Exserohilum turcicum, which exhibits a high genetic variability for virulence, and hence physiological races have been reported. Disease control is based mainly on fungicide application and host resistance. Qualitative resistance has been widely used to control NCLB through the deployment of Ht genes. Known pathogen races are designated according to their virulence to the corresponding Ht gene. Knowledge about of E. turcicum race distribution in maize-producing areas is essential to develop and exploit resistant genotypes. Maize leaves showing distinct elliptical grey-green lesions were collected from maize-producing areas of Argentina and Brazil, and 184 monosporic E. turcicum isolates were obtained. A total of 66 isolates were collected from Argentina during 2015, 2018 and 2019, while 118 isolates from Brazil were collected during 2017, 2018 and 2019. All isolates were screened on maize differential lines containing Ht1, Ht2, Ht3 and Htn1 resistance genes. In greenhouse experiments, inoculated maize plants were evaluated at 14 days after inoculation. Resistance reaction was characterized by chlorosis, and susceptibility was defined by necrosis in the absence of chlorosis. The most frequent race was 0 in both Argentina (83%) and Brazil (65%). Frequencies of race 1 (6% and 24%) and race 23N (5% and 10%) were very low in Argentina and Brazil, respectively. The high frequency of race 0 isolates provides evidence that qualitative resistance based on the tested Ht genes is not being used extensively in Argentina and Brazil to control NCLB. This information may be relevant for growers and breeding programs as the incidence of NCLB is increasing in both countries.


Plant Disease ◽  
2003 ◽  
Vol 87 (2) ◽  
pp. 203-203 ◽  
Author(s):  
D. De Merlier ◽  
A. Chandelier ◽  
M. Cavelier

In the past decade, a new Phytophthora species inducing shoot canker on Rhododendron and dieback of Viburnum has been observed in Europe, mainly in Germany and the Netherlands, and California. This new pathogen has been named Phytophthora ramorum (3). In May 2002, a diseased Viburnum plant (Viburnum bodnantense) from the Plant Protection Service (Ministry of Agriculture, Belgium) was submitted to our laboratory for diagnosis. Symptoms included wilting, leaves turning from green to brown, discolored vascular tissues, and root necrosis. The plant came from a Belgian ornamental nursery that obtained supplies of stock plants from the Netherlands. Pieces of necrotic root tissue were excised, surface-disinfected, and transferred aseptically to a Phytophthora selective medium. P. ramorum was identified based on morphological characteristics, including the production of numerous, thin-walled chlamydospores (25 to 70 µm in diameter, average 43 µm) and deciduous, semi-papillate sporangia arranged in clusters. Radial growth after 6 days at 20°C on V8 juice agar was 2.8 mm per day. Random amplified microsatellite markers (RAMS) (2) from the total genomic DNA of the Belgian strain (CBS 110901) were similar to those of P. ramorum reference strains (CBS 101330, CBS 101332, and CBS 101554). Using PCR primers specific for P. ramorum, the identification was confirmed by W. A. Man in't Veld (Plantenziektenkundige Dienst, Wageningen, the Netherlands) (1). A pathogenicity test was carried out on three sterile cuttings of Rhododendron catawbiense (3). Brown lesions were observed on the inoculated cuttings after 6 to 7 days. None of the three uninoculated cuttings showed symptoms of infection. P. ramorum was reisolated from lesion margins on the inoculated cuttings. To our knowledge, this is the first report of the fungus from Belgium. Since our initial observation, we have found P. ramorum in other Belgian nurseries on R. yakusimanum. References: (1) M. Garbelotto et al. US For. Ser. Gen. Tech. Rep. PSW-GRT. 184:765, 2002. (2) J. Hantula et al. Mycol. Res. 101:565, 1997. (3) S. Werres et al. Mycol. Res. 105:1155, 2001.


Plant Disease ◽  
2019 ◽  
Vol 103 (7) ◽  
pp. 1450-1457 ◽  
Author(s):  
Krishan K. Jindal ◽  
Albert U. Tenuta ◽  
Tsegaye Woldemariam ◽  
Xiaoyang Zhu ◽  
Dave C. Hooker ◽  
...  

Northern corn leaf blight (NCLB) caused by Exserohilum turcicum is the most common and economically significant fungal leaf disease of corn in Ontario, Canada. During the past 10 years in Ontario, severity and incidence of NCLB have increased, possibly owing to the appearance of new races. Several races have been identified in various parts of the world; however, information on occurrence and distribution of races in Ontario is lacking. In the current study, 677 single conidial isolates of E. turcicum were isolated from 687 symptomatic leaf samples collected between 2012 and 2016. These isolates were evaluated for pathogenicity on six corn differential inbreds (A619, A619Ht1, A619Ht2, A619Ht3, A632Htn1, and H102Htm1) under controlled environmental conditions and then grouped into 17 physiological races (0, 1, 2, 3, M, N, 12, 1M, 1N, 3M, 13M, 12N, 13N, 1MN, 12MN, 13MN, 123MN) based on the reaction of the inbreds to infection (resistant or susceptible). Four races (0, 1M, 1N, and 1MN) were most frequent, with an isolation frequency of 13, 10, 12, and 41%, respectively. Seventy-six percent of the isolates were virulent on more than one Ht resistance gene, with 2.4% (16 isolates) virulent on all five Ht resistance genes used in this study. Further analysis of the distribution of races in four regions over the years revealed that the occurrence and distribution of the races changed with time in Ontario. Overall, the frequency of virulence of the 677 isolates screened on the differentials with resistance genes Ht1, Ht2, Ht3, Htm1, and Htn1 varied from 6 to 81% (Ht1 81%, Ht2 6%, Ht3 12%, Htm1 64%, and Htn1 64%). Virulent isolates produced fewer lesions on the Htm1 differential, and smaller lesions that were slower and having less sporulation on the Htn1 differential, compared with infection of the differentials with Ht1, Ht2, and Ht3 resistance genes. Virulence frequency also changed within the four geographical regions of Ontario, with fewer isolates virulent on all resistance genes in eastern Ontario compared with southern and western Ontario. Isolates from southern Ontario had greater virulence frequency against Ht1 and Htm1, whereas isolates from western Ontario were more frequently virulent on Ht1 and Htn1. The information generated in this study on the distribution of E. turcicum races in Ontario corn will help growers to select appropriate hybrids with required resistance genes and will assist seed companies in deploying resistance genes in corn hybrids across the province or within a particular region.


Plant Disease ◽  
2012 ◽  
Vol 96 (12) ◽  
pp. 1826-1826 ◽  
Author(s):  
M. Lazarotto ◽  
M. F. B. Muniz ◽  
T. Poletto ◽  
C. B. Dutra ◽  
E. Blume ◽  
...  

Conspicuous leaf spots in combination with fruit spots were observed for the first time in April and May 2010 on a 30-ha pecan [Carya illinoensis (Wangenh.) K. Koch] orchard in the state of Rio Grande do Sul, Brazil. Initially, tiny grey spots were observed on leaves and, over time, the spots expanded to become gray to light brown circles surrounded by a dark brown border, followed by leaves falling. Eventually, fruits were also attacked, with typical symptoms beginning with tiny water soaked spots which then became necrotic. The disease was also observed in pecan nursery and field seedlings. Isolation of the pathogen from symptomatic leaves and morphological identification by conidia characters (number of cells, color, hyaline terminal cells, number of appendages) revealed Pestalotiopsis sp. (2) as the causal agent of the disease. Conidia constituted of transverse septa with four dark intermediate sections and two hyaline terminal sections. One of the terminal sections presented two or three apical appendages. Conidia averaged 6.88 μm wide × 31.00 μm long, not considering the apical appendages. Primers ITS 1 and ITS 4 were used to amplify the internal transcribes spacer ITS 1-5.8S-ITS 2 region. Nucleotide sequences were 99% similar to Pestalotiopsis clavispora (G.F. Atk.) Steyaert. Conidia produced on potato dextrose agar medium were used to inoculate 8 plants with a spore suspension of 2.0 × 106 conidia/ml. Eight additional plants were used as control (non-inoculated). The inoculation was performed by spraying the suspension onto the leaves of Pecan seedlings and the plants were incubated for 72 h in a humid chamber (1). All inoculated plants showed symptoms 25 days after inoculation and the fungus was reisolated. The pathogenicity test was repeated once. Ten more isolates collected from four different cities in the same state were identified as Pestalotiopsis spp. by morphological characterization and pathogenicity was confirmed. Because this disease causes losses on production of nuts indirectly by reducing photosynthetically active area when the pathogen attacks leaves and directly when attacking fruits, it may restrict the production where the pathogen occurs. On some orchards in the state of Rio Grande do Sul, the attack rate reached 80% of the plants. P. clavispora has been reported causing stem end-rot of avocado in Chile (3), but this note constitutes the first report, to our knowledge, of P. clavispora causing leaf spot on C. illinoensis in Brazil. References: (1) A. C. Alfenas and F. A. Ferreira. Page 117 in: Métodos em Fitopatologia. A. C Alfenas and R. G. Mafia (eds.). Editora: UFV, Viçosa, 2007. (2) S. S. N. Maharachchikumbura et al. Fungal Diversity 50:167, 2011. (3) A. L. Valencia et al. Plant Dis. 95:492, 2011.


2021 ◽  
pp. 1-8
Author(s):  
Ravi Bika ◽  
Fulya Baysal-Gurel

The cut flower growers of the eastern and southern United States are threatened with postharvest meltdown of zinnia (Zinnia elegans), which reduces yield and income as well as limiting opportunities for production expansion. Disease symptoms such as bending of the stem just below the flower were visually apparent on zinnia cut flowers. The objective of this study was to identify the causal agent related to zinnia meltdown. A total of 20 symptomatic zinnia cut flower stems were collected from Tennessee. Several Fusarium-like colonies with micro and macroconidia were isolated from the base and bend area of stems on potato dextrose agar (PDA) and Fusarium-selective media. Morphological characterization, polymerase chain reaction, and sequencing of three representative isolates, FBG2020_198, FBG2020_199, and FBG2020_201, were conducted to confirm pathogen identification. The sequence identity of the isolates was >99% identical to Fusarium commune, and a combined phylogenetic tree grouped the isolates with the clade of F. commune from different host and geographical locations. To accomplish Koch’s postulates, a pathogenicity test was performed on ‘Benary’s Giant Golden Yellow’, ‘Benary’s Giant Lime’, and ‘Benary’s Giant Pink’ zinnia plants at vegetative (2 weeks after transplantation) or flower bud stage (1 month after transplantation) by drench, stem injection, and foliar spray of conidial suspension (1 × 105 conidia/mL). Similar symptoms of meltdown (floral axis bending just below the flower) were observed on inoculated zinnia cultivars 2 days after harvesting. Fusarium commune was re-isolated from the infected flower stems of all three cultivars but not from the noninoculated zinnia flower stems. Zinnia stem colonization by F. commune was statistically similar in all three tested cultivars regardless of plant growth stage and method of inoculation. This study confirms F. commune as being the causal agent of postharvest zinnia flower meltdown issue in Tennessee. In the future, possible sources of pathogen will be screened, and disease management recommendations will be developed.


Plant Disease ◽  
2004 ◽  
Vol 88 (3) ◽  
pp. 309-309 ◽  
Author(s):  
A. Garibaldi ◽  
A. Minuto ◽  
M. L. Gullino

During the fall of 2002, African daisy (Osteospermum sp.) plants showing symptoms of a wilt disease were observed in a commercial, nonheated glasshouse in Albenga in northern Italy. Wilted plants were first observed when outside temperatures were between 15 and 28°C. Symptoms were first observed on seedlings 40 days after they had been transplanted into pots. The vascular tissues of affected plants appeared brown. These plants were stunted and developed yellowed leaves with brown or black streaks in the vascular system. The vascular streaks in the yellow leaves extended from the crown and were continuous with a brown discoloration in the vascular system of the crown and upper taproot. Fusarium oxysporum was consistently and readily isolated from symptomatic vascular tissue onto a Fusarium-selective medium (1). Healthy, rooted, 40-day-old plants were inoculated by root-dip with a conidial suspension (1 × 107 CFU/ml) of three isolates of F. oxysporum obtained from infected plants and transplanted into pots filled with steam-sterilized soil. Noninoculated plants served as control treatments. Plants (10 per treatment) were grown in a glasshouse at an average temperature of 25°C (minimum of 12°C and maximum of 39°C). Wilt symptoms and vascular discoloration in the roots, crown, and veins developed within 20 days on each inoculated plant, while noninoculated plants remained healthy. F. oxysporum was consistently reisolated from infected plants. The pathogenicity test was conducted twice. To our knowledge, this is the first report of F. oxysporum on Osteospermum sp. in Italy or elsewhere in the world. Reference: (1) H. Komada. Rev. Plant Prot. Res. 8:114, 1975.


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