scholarly journals Incidence of Latent Infection of Immature Peach Fruit by Monilinia fructicola and Relationship to Brown Rot in Georgia

Plant Disease ◽  
2000 ◽  
Vol 84 (8) ◽  
pp. 853-857 ◽  
Author(s):  
K. M. Emery ◽  
T. J. Michailides ◽  
H. Scherm

Peach fruit are most susceptible to infection by Monilinia fructicola during the preharvest ripening stage. Although various sources of inoculum for preharvest infection have been characterized, the role of latent infection of immature fruit in the carryover of M. fructicola from the spring (blossom blight phase) to the preharvest period (fruit rot phase) is unknown for the southeastern United States. From 1997 to 1999, immature peach fruit were collected at 14-day intervals from orchards in middle and northern Georgia. Fruit were surface disinfested and treated with paraquat (1997) or frozen overnight (1998 and 1999) to induce tissue senescence and activate latent infections. Across sites and years, the incidence of latent infection remained low until the final sampling date 7 to 12 days before harvest. The incidence of latent infection on the final sampling date ranged from 0 to 22.0% and correlated significantly with both the incidence of blossom blight earlier in the season (r = 0.9077, P = 0.0332) and the incidence of fruit rot at harvest (r = 0.9966, P = 0.0034). There also was a significant association between the incidence of latent infection at the onset of pit hardening (between 7 and 10 weeks before harvest) and subsequent fruit rot incidence (r = 0.9763, P = 0.0237). Weather variables (cumulative rainfall or rainfall frequency) alone did not correlate with fruit rot incidence (P > 0.05), whereas combined latent infection-rainfall variables did. The results suggest that latent infections can serve as a source of inoculum for subsequent fruit rot in peach orchards in Georgia. Despite its significant association with fruit rot incidence, the potential for using latent infection incidence as a biological indicator of disease risk at harvest may be limited; the assessment of latent infection during the fruit ripening stage (similar to the timing of the final sampling date in this study) would not provide sufficient lead time for preharvest disease management decisions, whereas an earlier assessment (e.g., at the onset of pit hardening) would require large sample sizes due to the low incidence of latent infection present during that period.

Plant Disease ◽  
2001 ◽  
Vol 85 (9) ◽  
pp. 999-1003 ◽  
Author(s):  
Yong Luo ◽  
Zhonghua Ma ◽  
Themis J. Michailides

Two studies were conducted to determine the effects of water content (WC) on sporulation on thinned fruit and the effects of wetness duration, inoculum density, and temperature on secondary infection of prune fruit by Monilinia fructicola, the main causal pathogen of brown rot in California. In the first study, sporulation intensity and duration of sporulation of the pathogen were tested on inoculated thinned fruit with five levels (67.2, 53.8, 40.3, 26.9, and 13.4%) of WC. Regression analyses showed that both sporulation intensity and duration of sporulation increased as WC of thinned fruit increased. The predicted difference in duration of sporulation between fruit with 13.4 and 67.2% WC was about 3 days. In the second study, three inoculum concentrations (8,000, 16,000, and 24,000 conidia per milliliter) of M. fructicola were atomized onto prune fruit on trees in an orchard. Inoculated fruit and shoots were covered with plastic bags to maintain wetness duration for 4, 8, 12, or 16 h. An overnight freezing and incubation technique was used after harvest to determine the proportion of fruit with latent infection. Regression analysis demonstrated that inoculum concentration and wetness duration were significant factors affecting secondary infection. Temperature was less important. Increased inoculum concentration and wetness duration increased the percentage of fruit with latent infections. Increased temperature decreased the percentage of fruit with latent infections.


Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1166-1166 ◽  
Author(s):  
A. Munda ◽  
M. Viršček Marn

Monilinia fructicola, the causal agent of brown rot, is a destructive fungal pathogen that affects mainly stone fruits (Prunoideae). It causes fruit rot, blossom wilt, twig blight, and canker formation and is common in North and South America, Australia, and New Zealand. M. fructicola is listed as a quarantine pathogen in the European Union and was absent from this region until 2001 when it was detected in France. In August 2009, mature peaches (Prunus persica cv. Royal Glory) with brown rot were found in a 5-year-old orchard in Goriška, western Slovenia. Symptoms included fruit lesions and mummified fruits. Lesions were brown, round, rapidly extending, and covered with abundant gray-to-buff conidial tufts. The pathogen was isolated in pure culture and identified based on morphological and molecular characters. Colonies on potato dextrose agar (PDA) incubated at 25°C in darkness had an average daily growth rate of 7.7 mm. They were initially colorless and later they were light gray with black stromatal plates and dense, hazel sporogenous mycelium. Colony margins were even. Sporulation was abundant and usually developed in distinct concentric zones. Limoniform conidia, produced in branched chains, measured 10.1 to 17.7 μm (mean = 12.1 μm) × 6.2 to 8.6 μm (mean = 7.3 μm) on PDA. Germinating conidia produced single germ tubes whose mean length ranged from 251 to 415 μm. Microconidia were abundant, globose, and 3 μm in diameter. Morphological characters resembled those described for M. fructicola (1). Morphological identification was confirmed by amplifying genomic DNA of isolates with M. fructicola species-specific primers (2–4). Sequence of the internal transcribed spacer (ITS) region (spanning ITS1 and ITS 2 plus 5.8 rDNA) of a representative isolate was generated using primers ITS1 and ITS4 and deposited in GenBank (Accession No. GU967379). BLAST analysis of the 516-bp PCR product revealed 100% identity with several sequences deposited for M. fructicola in NCBI GenBank. Pathogenicity was tested by inoculating five mature surface-sterilized peaches with 10 μl of a conidial suspension (104 conidia ml–1) obtained from one representative isolate. Sterile distilled water was used as a control. Peaches were wounded prior to inoculation. After 5 days of incubation at room temperature and 100% relative humidity, typical brown rot symptoms developed around the inoculation point, while controls showed no symptoms. M. fructicola was reisolated from lesion margins. Peach and nectarine orchards in a 5-km radius from the outbreak site were surveyed in September 2009 and M. fructicola was confirmed on mummified fruits from seven orchards. The pathogen was not detected in orchards from other regions of the country, where only the two endemic species M. laxa and M. fructigena were present. To our knowledge, this is the first report of M. fructicola associated with brown rot of stone fruits in Slovenia. References: (1) L. R. Batra. Page 106 in: World Species of Monilinia (Fungi): Their Ecology, Biosystematics and Control. J. Cramer, Berlin, 1991. (2) M.-J. Côté et al. Plant Dis. 88:1219, 2004. (3) K. J. D. Hughes et al. EPPO Bull. 30:507, 2000. (4) R. Ioos and P. Frey. Eur. J. Plant Pathol. 106:373, 2000.


2001 ◽  
Vol 91 (9) ◽  
pp. 864-872 ◽  
Author(s):  
Yong Luo ◽  
Themis J. Michailides

Experiments were conducted in three prune orchards in California. In each orchard, inoculations with Monilinia fructicola, the causal agent of brown rot of stone fruits, were performed on branches of trees at bloom and fruit developmental stages. Five inoculum concentrations were used in each inoculation. Six and four wetness durations were created for each inoculum concentration at bloom and fruit developmental stages, respectively. Fruit were harvested 3 weeks before commercial harvest. The overnight freezing incubation technique was used to promote sporulation and to determine incidence of latent infection (ILI) of fruit brown rot. No differences in ILI among locations were found. A seasonal pattern of bloom and fruit susceptibility to latent infection was determined. Susceptibility to latent infection at bloom stage was at a moderate level and increased to reach the highest level at pit hardening stage. Subsequently, fruit susceptibility to latent infection decreased, reaching the lowest level in early June at embryo growth stage. Thereafter, the susceptibility increased again with fruit development and maturity until harvest. Linear relationships between ILI and inoculum concentration were obtained for most combinations of growth stage and wetness duration. Incidence of latent infection increased linearly with increased wetness duration at bloom stage and increased exponentially with increased wetness duration at early and late fruit developmental stages. The optimum temperatures for latent infection at pit hardening stage ranged from 14 to 18°C, but the effect of temperature on latent infection was reduced at resistant stages. The temperature range favorable to latent infection varied for different wetness durations.


1969 ◽  
Vol 20 (2) ◽  
pp. 317 ◽  
Author(s):  
PF Kable

Blossom blight is of economic importance in apricots on the Murrumbidgee Irrigation Areas (MIA), but fruit rot is not. Monilinia fructicola generally does not overwinter effectively in apricot trees in the MIA, the inocula for primary infections coming from nearby peach plantations. Blighted blossoms in apricot trees, which flower a week before peaches, may provide inoculum for blighting of flowers in the latter crop. In apricot trees, unlike peach, there is a continuous infection chain from flowering till harvest. Inoculum may pass from apricot to peach in December and January, thus bridging a gap in the infection chain in peach. The infection chain in apricot is described. Latent and quiescent infections were observed. The implications of the exchange of inoculum between peach and apricot are discussed.


2012 ◽  
Vol 13 (1) ◽  
pp. 28 ◽  
Author(s):  
S. E. Everhart ◽  
A. Askew ◽  
L. Seymour ◽  
T. C. Glenn ◽  
H. Scherm

To better understand the fine-scale spatial dynamics of brown rot disease and corresponding fungal genotypes, we analyzed three-dimensional spatial patterns of pre-harvest fruit rot caused by Monilinia fructicola in individual peach tree canopies and developed microsatellite markers for canopy-level population genetics analyses. Using a magnetic digitizer, high-resolution maps of fruit rot development in five representative trees were generated, and M. fructicola was isolated from each affected fruit. To characterize disease aggregation, nearestneighbor distances among symptomatic fruit were calculated and compared with appropriate random simulations. Within-canopy disease aggregation correlated negatively with the number of diseased fruit per tree (r = −0.827, P = 0.0009), i.e., aggregation was greatest when the number of diseased fruit was lowest. Sixteen microsatellite primers consistently amplified polymorphic regions in a geographically diverse test population of 47 M. fructicola isolates. None of the test isolates produced identical multilocus genotypes, and the number of alleles per locus ranged from 2 to 16. We are applying these markers to determine fine-scale population structure of the pathogen within and among canopies. Accepted for publication 23 May 2012. Published 23 July 2012.


2003 ◽  
Vol 93 (1) ◽  
pp. 102-111 ◽  
Author(s):  
Yong Luo ◽  
Themis J. Michailides

Inoculations were performed six to eight times in each of 10 prune orchards located in nine counties of California. In each inoculation, branches that bore 40 to 60 blossoms or 30 to 40 fruit were inoculated with conidial suspensions of Monilinia fructicola. Three inoculum concentrations and 14 to 16 h of humidity were used for each inoculation. All inoculated fruit were maintained on trees and harvested separately 2 weeks before commercial harvest. The incidence of latent infection (ILI) and percentage of branches with fruit rot (PBFR) were determined for each inoculation in each orchard. As the ILI increased, the PBFR also increased linearly. Five conditions that lead latent infection to fruit rot include (i) latent infection level; (ii) fruit developmental stage; (iii) inoculum concentration; (iv) total hours of relative humidity greater than 90% (hRH); and (v) total hours of dew period (hDEW) from mid-July to mid-August. Three levels of PBFR, 1, 5, and 10% were assigned, and threshold conditions that lead to these levels were determined based on the experimental results. The relative probabilities that lead latent infection to fruit rot (r_PBFR) at different fruit developmental stages were calculated. A preliminary decision support model to guide fungicide application was developed based on the above results. One of the four recommendations, safe, wait, check historical weather as a reference, and apply a fungicide immediately, could be provided based on the level of latent infection and the decision process developed through this study.


Plant Disease ◽  
2017 ◽  
Vol 101 (6) ◽  
pp. 1002-1008 ◽  
Author(s):  
C. Garcia-Benitez ◽  
P. Melgarejo ◽  
A. De Cal

Most stone fruit with a latent brown rot infection caused by Monilinia do not develop visible signs of disease until the arrival of fruit at the markets or the consumer’s homes. The overnight freezing-incubation technique (ONFIT) is a well-established method for detecting latent brown rot infections, but it takes between 7 to 9 days. In this report, we inform on the advantages of applying a qPCR-based method to (i) detect a latent brown rot infection in the blossoms and fruit of nectarine trees (Prunus persica var. nucipersica) and (ii) distinguish between the Monilinia spp. in them. For applying this qPCR-based method, artificial latent infections were established in nectarine flowers and fruit using 10 Monilinia fructicola isolates, 8 M. fructigena isolates, and 10 M. laxa isolates. We detected greater amounts of M. fructicola DNA than M. laxa and M. fructigena DNA in latently infected flowers using qPCR. However, greater DNA amounts of M. laxa than M. fructicola were detected in the mesocarp of latently infected nectarines. We found that the qPCR-based method is more sensitive, reliable, and quicker than ONFIT for detecting a latent brown rot infection, and could be very useful in those countries where Monilinia spp. are classified as quarantine pathogens.


2008 ◽  
Vol 123 (4) ◽  
pp. 415-424 ◽  
Author(s):  
Iray Gell ◽  
Antonieta De Cal ◽  
Rosario Torres ◽  
Josep Usall ◽  
Paloma Melgarejo

2015 ◽  
Vol 105 (4) ◽  
pp. 542-549 ◽  
Author(s):  
S. E. Everhart ◽  
H. Scherm

The purpose of this study was to determine the fine-scale genetic structure of populations of the brown rot pathogen Monilinia fructicola within individual peach tree canopies to better understand within-tree plant pathogen diversity and to complement previous work on spatiotemporal development of brown rot disease at the canopy level. Across 3 years in a total of six trees, we monitored disease development, collected isolates from every M. fructicola symptom during the course of the season, and created high-resolution three-dimensional maps of all symptom and isolate locations within individual canopies using an electromagnetic digitizer. Each canopy population (65 to 173 isolates per tree) was characterized using a set of 13 microsatellite markers and analyzed for evidence of spatial genetic autocorrelation among isolates during the epidemic phase of the disease. Results showed high genetic diversity (average uh = 0.529) and high genotypic diversity (average D = 0.928) within canopies. The percentage of unique multilocus genotypes within trees was greater for blossom blight isolates (78.2%) than for fruit rot isolates (51.3%), indicating a greater contribution of clonal reproduction during the preharvest epidemic. For fruit rot isolates, between 54.2 and 81.7% of isolates were contained in one to four dominant clonal genotypes per tree having at least 10 members. All six fruit rot populations showed positive and significant spatial genetic autocorrelation for distance classes between 0.37 and 1.48 m. Despite high levels of within-tree pathogen diversity, the contribution of locally available inoculum combined with short-distance dispersal is likely the main factor generating clonal population foci and associated spatial genetic clustering within trees.


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