scholarly journals Contribution of Mid-Season Cover Sprays to Management of Peach Brown Rot at Harvest

Plant Disease ◽  
2017 ◽  
Vol 101 (5) ◽  
pp. 794-799 ◽  
Author(s):  
N. Lalancette ◽  
L. L. Blaus ◽  
J. D. Gager ◽  
K. A. McFarland

Four protectant fungicides applied as midseason cover sprays were quantitatively assessed for their ability to reduce brown rot caused by Monilinia fructicola during the preharvest fruit ripening periods in the 2012 through 2015 growing seasons. No fungicides were applied during bloom or during the preharvest period. Treatment programs consisted of captan, sulfur, ziram, and thiram applications beginning at early shuck-split stage and ending with the final cover spray at 23 to 26 days before harvest. The incidence of brown rot at harvest was determined by examining 41 to 91 fruit for symptoms of rot on each of four replicate trees for each treatment. The incidence of sporulating blossom blight cankers was assessed during the preharvest period at 8, 15, and 22 days after the final cover spray. An in vivo bioassay was also conducted at 7, 14, and 21 days after the final cover spray to ascertain the level of fungicide residue during the preharvest period. The bioassay uses conidia germination as a quantitative indicator of effective residue. Results of the harvest assessment showed that captan cover sprays significantly reduced brown rot incidence in all years of the study. Furthermore, results of the bioassay demonstrated that fungicide residue was the mechanism by which this control occurred. None of the other fungicide cover spray programs contributed significantly to brown rot control at harvest in any year, and bioassay results showed insufficient residue to inhibit conidial germination. Antisporulant activity against blossom blight cankers was not observed for any fungicide program, indicating that reducing inoculum production from this source was not a mechanism for brown rot control. The captan and sulfur programs provided very good control of peach scab incidence and severity, caused by Fusicladium carpophilum, while the ziram and thiram programs failed to control this disease. These findings demonstrated that captan cover sprays can contribute significantly to control of brown rot at harvest, thereby augmenting the efficacy and consistency of management by preharvest fungicide programs. Furthermore, any reduction of the M. fructicola population by the captan cover sprays should reduce selection pressure against the site-specific fungicides commonly used during the preharvest period, thereby prolonging their useful life for brown rot control.

2005 ◽  
Vol 95 (10) ◽  
pp. 1132-1136 ◽  
Author(s):  
Yong Luo ◽  
Themis J. Michailides ◽  
David P. Morgan ◽  
William H. Krueger ◽  
Richard P. Buchner

Brown rot, caused by Monilinia fructicola, is a destructive disease of stone fruit in California. Disease management requires information on inoculum dynamics and development of latent and visible fruit infections during the season to help make decisions on timing of fungicide treatments and choice of cultural practices. In this study, the daily spore concentration (ascospores and conidia) of M. fructicola in the air was monitored with spore traps in two prune orchards during the growing seasons in 2001 and 2002. The spore concentrations were low to moderate at early bloom, increased at full bloom, and decreased to the lowest level at the end of bloom. Improper timing of fruit thinning and irrigation in midseason increased spore concentration in the air and fruit infections late in the season. Artificial fruit inoculations were conducted periodically in 10 prune orchards in 2002 and 2004, and incidence of fruit rot at different inoculation dates was assessed. Fruit rot development rate increased linearly with inoculation date during the growing season. Natural blossom and fruit infections were monitored periodically in 10 prune orchards, and incidence of latent fruit infection was determined by using the overnight freezing-incubation technique. Incidence of fruit rot also was assessed 2 weeks before harvest in these orchards. The incidence of latent fruit infection at the pit hardening stage significantly correlated with that at the late stages and with the incidence of fruit rot at harvest.


Plant Disease ◽  
2010 ◽  
Vol 94 (8) ◽  
pp. 1048-1054 ◽  
Author(s):  
M. Villarino ◽  
P. Melgarejo ◽  
J. Usall ◽  
J. Segarra ◽  
A. De Cal

Immediately following the identification of Monilinia fructicola in a Spanish peach orchard in the Ebro Valley in 2006, this orchard and two other orchards in the same valley were intensively sampled for potential tree and ground sources of primary Monilinia inoculum before and during three growing seasons between 2006 and 2008. Overwintered Monilinia spp. produced inoculum from only mycelium, and no apothecia were found in any of the three orchards over the three growing seasons. Mummies on trees were the main source of primary inoculum. More than 90% of Monilinia isolates on all fruit mummies were M. laxa. Positive relationships were found between (i) the number of mummified fruit and the incidence of postharvest brown rot (P = 0.05, r = 0.75, n = 8), and (ii) the number of mummified fruit and nonabscised aborted fruit in the trees and the number of conidia on the fruit surface (P = 0.04, r = 0.71; P = 0.01, r = 0.94, respectively, n = 8) and the incidence of latent infection (P = 0.03, r = 0.75; P = 0.001, r = 0.99; respectively, n = 8). In addition, the numbers of mummified fruit and pruned branches on the orchard floor were correlated with the number of airborne conidia in the orchard. Based on the results of these surveys, the control of brown rot in stone fruit orchards is discussed.


Plant Disease ◽  
2015 ◽  
Vol 99 (12) ◽  
pp. 1727-1731 ◽  
Author(s):  
N. Lalancette ◽  
J. Gager ◽  
K. A. McFarland

Recent fungicide efficacy studies indicated that brown rot fruit rot at harvest, caused by Monilinia fructicola, was being controlled by residual activity from protectant fungicides applied during the time between bloom and the preharvest fruit ripening period. To determine the extent of this residue, a simple in vivo bioassay was developed by assaying M. fructicola spore germination directly on sampled fruit. A 1.5-cm section of clear flexible tubing was placed upright on harvested fruit to create a small incubation well. After the tubing–fruit interface was sealed using silicon grease, a suspension of M. fructicola conidia was pipetted into the well. The spores were suspended in a buffer-substrate medium consisting of 0.025 M potassium phosphate, 0.1% sucrose, and 0.1% yeast extract. A rubber stopper with an aeration hole was inserted into the well’s top and the fruit was placed in an incubator at 25°C. Results of a time-course study indicated that the optimal conidial incubation time was 6 h. Bioassay sensitivity was evaluated by examining test results from varying concentrations of captan fungicide. Results indicated that captan residue levels as low as one-thousandth the standard field rate could be detected using spore germination as the predictor. Fitting of the logistic decline model to the data created a standard curve to allow quantitative estimation of fungicide residue based on observed level of spore germination. A modified version of the bioassay, which can be used to detect carbohydrate or nutrient sources on the fruit surface, was also demonstrated.


Plant Disease ◽  
2010 ◽  
Vol 94 (6) ◽  
pp. 737-743 ◽  
Author(s):  
A. Amiri ◽  
P. M. Brannen ◽  
G. Schnabel

Quinone outside inhibitor (QoI) and succinate dehydrogenase inhibitor (SdhI) fungicides are respiration inhibitors (RIs) used for preharvest control of brown rot of stone fruit. Both chemical classes are site-specific and, thus, prone to resistance development. Between 2006 and 2008, 157 isolates of Monilinia fructicola collected from multiple peach and nectarine orchards with or without RI spray history in South Carolina and Georgia were characterized based upon conidial germination and mycelial growth inhibition for their sensitivity to QoI fungicides azoxystrobin and pyraclostrobin, SdhI fungicide boscalid, and a mixture of pyraclostrobin + boscalid. There was no significant difference (P = 0.05) between EC50 values for inhibition of conidial germination versus mycelial growth. The mean EC50 values based upon mycelial growth tests for 25 isolates from an orchard without RI-spray history were 0.15, 0.06, 2.23, and 0.09 μg/ml for azoxystrobin, pyraclostrobin, boscalid, and pyraclostrobin + boscalid, respectively. The respective mean EC50 values for 76 isolates from RI-sprayed orchards in South Carolina were 0.9, 0.1, 10.7, and 0.13 μg/ml and for 56 isolates from RI-sprayed orchards in Georgia were 1.2, 0.1, 8.91, and 0.17 μg/ml. Overall, mean EC50 values of populations from RI-sprayed orchards increased three-, two-, five-, and twofold between 2006 and 2008 for azoxystrobin, pyraclostrobin, boscalid, and pyraclostrobin + boscalid, respectively. A subset of 10 M. fructicola isolates representing low and high EC50 values for azoxystrobin, boscalid, and boscalid + pyraclostrobin was selected for a detached fruit assay to determine disease incidence and severity following protective treatments of formulated RI fungicides at label rates. Brown rot incidence was greater than 50% when fruit were inoculated with isolates having EC50 values of 2, 4, and 0.6 μg/ml for azoxystrobin, boscalid, and pyraclostrobin + boscalid, respectively. Pyraclostrobin failed to control any of the isolates tested in detached fruit assays. Based on minimum inhibitory concentration and brown rot incidence data, we recommend using 3 and 0.75 μg/ml as discriminatory doses to distinguish between sensitive isolates and those with reduced sensitivity to azoxystrobin and pyraclostrobin + boscalid, respectively. Results from our in vitro and in vivo assays indicate a shift toward reduced sensitivity in M. fructicola from the southeastern United States. No cross-resistance was observed between the QoI and the SdhI fungicides, which implies that rotation or tank mixtures of these two chemical classes can be used as a resistance management strategy.


2000 ◽  
Author(s):  
Anne K. Kowal ◽  
Caroline Kohrer ◽  
Uttam L. RajBhandary

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 428
Author(s):  
Emma Renard ◽  
Estel Collado Camps ◽  
Coline Canovas ◽  
Annemarie Kip ◽  
Martin Gotthardt ◽  
...  

Variable domains of heavy chain only antibodies (VHHs) are valuable agents for application in tumor theranostics upon conjugation to both a diagnostic probe and a therapeutic compound. Here, we optimized site-specific conjugation of the chelator DTPA and the photosensitizer IRDye700DX to anti-epidermal growth factor receptor (EGFR) VHH 7D12, for applications in nuclear imaging and photodynamic therapy. 7D12 was site-specifically equipped with bimodal probe DTPA-tetrazine-IRDye700DX using the dichlorotetrazine conjugation platform. Binding, internalization and light-induced toxicity of DTPA-IRDye700DX-7D12 were determined using EGFR-overexpressing A431 cells. Finally, ex vivo biodistribution of DTPA-IRDye700DX-7D12 in A431 tumor-bearing mice was performed, and tumor homing was visualized with SPECT and fluorescence imaging. DTPA-IRDye700DX-7D12 was retrieved with a protein recovery of 43%, and a degree of labeling of 0.56. Spectral properties of the IRDye700DX were retained upon conjugation. 111In-labeled DTPA-IRDye700DX-7D12 bound specifically to A431 cells, and they were effectively killed upon illumination. DTPA-IRDye700DX-7D12 homed to A431 xenografts in vivo, and this could be visualized with both SPECT and fluorescence imaging. In conclusion, the dichlorotetrazine platform offers a feasible method for site-specific dual-labeling of VHH 7D12, retaining binding affinity and therapeutic efficacy. The flexibility of the described approach makes it easy to vary the nature of the probes for other combinations of diagnostic and therapeutic compounds.


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