Relationship between the incidence of latent infections caused by Monilinia spp. and the incidence of brown rot of peach fruit: factors affecting latent infection

2008 ◽  
Vol 121 (4) ◽  
pp. 487-498 ◽  
Author(s):  
Iray Gell ◽  
Antonieta De Cal ◽  
Rosario Torres ◽  
Josep Usall ◽  
Paloma Melgarejo
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 ◽  
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.


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.


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

2020 ◽  
Vol 6 (4) ◽  
pp. 266
Author(s):  
Carlos Garcia-Benitez ◽  
Carla Casals ◽  
Josep Usall ◽  
Ismael Sánchez-Ramos ◽  
Paloma Melgarejo ◽  
...  

Latent infections caused by Monilinia spp. in nectarines cause great economic losses since they are not detected and rejected at harvest and can appear at any time post-harvest, even at the consumer’s home. The effect of a pre-cooling chamber, water dump operation, and cold-storage chamber on the activation and/or development of preharvest latent infections caused by Monilinia spp. on nectarines were studied under different postharvest conditions: (a) cold storage for 0, 1, or 3 d at 4 °C at either 75% relative humidity (RH) or 100% RH before water dumping, (b) water dumping for 10 minutes at 15 °C, and (c) cold storage for 0, 3, or 10 d at 4 °C at either 75% RH or 100% RH after water dumping. These storage conditions were transformed to fungal physiological time. For visualization of the latent infections caused by Monilinia spp., the nectarines were placed in sterile paper bags and frozen at −20 °C for 48 h in order to damage the epidermis. To compare different handling scenarios, the incidence of latent infection was modelled for physiological time description by a modified Gompertz model. The activation and/or development of preharvest natural latent infections caused by Monilinia spp. at postharvest was mainly related to temperature and incubation time at postharvest. Storing nectarines with any postharvest handling less than 11 days at 4 °C avoids brown rot symptoms and reduced the activation and/or development of pre-harvest latent infections caused by Monilinia spp., while more cold days caused the exponential phase of latent infection activation and/or development. The Gompertz model employed could be used for predicting the activation and/or development of latent infection caused by Monilinia spp. at postharvest conditions and looks at the postharvest life. To our knowledge, this is the first time that the effects of post-harvest handling on latent infections in fruit have been studied.


Revista CERES ◽  
2018 ◽  
Vol 65 (6) ◽  
pp. 517-526
Author(s):  
Elizandra Pivotto Pavanello ◽  
Magno Roberto Pasquetti Berghett ◽  
Erani Eliseu Schultz ◽  
Fabio Rodrigo Thewes ◽  
Suele Fernanda Prediger Schmidt ◽  
...  

ABSTRACT The peach brown rot, caused by Monilinia fructicola, is the main disease of the crop, causing significant losses during preharvest and postharvest. This study aimed to evaluate the performance of preharvest fungicide application on brown rot control and verify the role of latent infection and external contamination in postharvest disease. An experiment was carried out in the years 2014 and 2015 in order to evaluate the performance of six active ingredients (captan, iprodione, iminoctadine, tebuconazole, difenoconazole and azoxystrobin) during preharvest on brown rot control and the effect on latent infection. A second experiment was carried out to monitor the latent infection during growth and ripening of the fruit and in order to correlate it with the postharvest disease incidence. The data were submitted to analysis of variance (Anova) and the means were grouped by the Scott-Knott test (p < 0.05), using statistical software Sisvar. The active ingredients iprodione, tebuconazole and difenoconazole were the most efficient in controlling brown rot on the field, while iminoctadine has higher efficiency during postharvest control, acting on latent infections. The incidence of latent infections during fruit growth and ripening has a positive correlation with brown rot incidence at postharvest. The highest disease incidence after storage is due to the latent infections manifestation. Effective chemical control in the field, throughout the growing and ripening of fruit, is an important approach to postharvest brown rot control, even after cold storage and during shelf life at 20 °C.


2003 ◽  
Vol 77 (13) ◽  
pp. 7696-7701 ◽  
Author(s):  
Scott A. Tibbetts ◽  
Joy Loh ◽  
Victor van Berkel ◽  
James S. McClellan ◽  
Meagan A. Jacoby ◽  
...  

ABSTRACT Gammaherpesviruses such as Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus are important human pathogens that establish long-term latent infections. Understanding of the initiation and maintenance of latent infections has important implications for the prevention and treatment of gammaherpesvirus-related diseases. Although much is known about gammaherpesvirus pathogenesis, it is unclear how the infectious dose of a virus influences its ability to establish latent infection. To examine the relationship between the infectious dose and gammaherpesvirus latency, we inoculated wild-type mice with 0.01 to 106 PFU of murine gammaherpesvirus 68 (γHV68) and quantitatively measured latency and acute-phase replication. Surprisingly, during latency, the frequencies of ex vivo reactivation were similar over a 107-fold range of doses for i.p. infection and over a 104-fold range of doses for intranasal infection. Further, the frequencies of cells harboring viral genome during latency did not differ substantially over similar dose ranges. Although the kinetics of acute-phase replication were delayed at small doses of virus, the peak titer did not differ significantly between mice infected with a large dose of virus and those infected with a small dose of virus. The results presented here indicate that any initiation of infection leads to substantial acute-phase replication and subsequent establishment of a maximal level of latency. Thus, infections with doses as small as 0.1 PFU of γHV68 result in stable levels of acute-phase replication and latent infection. These results demonstrate that the equilibrium level of establishment of gammaherpesvirus latency is independent of the infectious dose and route of infection.


1956 ◽  
Vol 7 (6) ◽  
pp. 504 ◽  
Author(s):  
GC Wade

Evidence is presented that infection of apricot fruit with Sclerotinia fructicola may occur early in the fruit's development but remain latent until ripening commences. Evidence from culturing from green fruit is supported by the results of spraying experiments with fungicides and by inoculation experiments. Latent infection is confined to the epidermis and is not associated with any particular position on the fruit surface. Histological studies indicate that infection takes place through the stomata. It is tentatively suggested that an inhibitory substance is present in green fruit, and maintains infections in a latent condition. The presence of a substance inhibitory towards a species of Histoplasma is demonstrated. This substance begins to disappear as ripening commences.


Neurology ◽  
2019 ◽  
Vol 93 (13) ◽  
pp. 584-594 ◽  
Author(s):  
Mauricio F. Farez ◽  
Jorge Correale ◽  
Melissa J. Armstrong ◽  
Alexander Rae-Grant ◽  
David Gloss ◽  
...  

ObjectiveTo update the 2002 American Academy of Neurology (AAN) guideline regarding immunization and multiple sclerosis (MS).MethodsThe panel performed a systematic review and classified articles using the AAN system. Recommendations were based on evidence, related evidence, principles of care, and inferences according to the AAN 2011 process manual, as amended.Major recommendations (Level B except where indicated)Clinicians should discuss the evidence regarding immunizations in MS with their patients and explore patients' opinions, preferences, and questions. Clinicians should recommend that patients with MS follow all local vaccine standards, unless there are specific contraindications and weigh local vaccine-preventable disease risks when counseling patients. Clinicians should recommend that patients with MS receive the influenza vaccination annually. Clinicians should counsel patients with MS about infection risks associated with specific immunosuppressive/immunomodulating (ISIM) medications and treatment-specific vaccination guidance according to prescribing information (PI) and vaccinate patients with MS as needed at least 4–6 weeks before initiating patients' ISIM therapy. Clinicians must screen for infections according to PI before initiating ISIM medications (Level A) and should treat patients testing positive for latent infections. In high-risk populations, clinicians must screen for latent infections before starting ISIM therapy even when not specifically mentioned in PI (Level A) and should consult specialists regarding treating patients who screen positive for latent infection. Clinicians should recommend against using live-attenuated vaccines in people with MS receiving ISIM therapies. Clinicians should delay vaccinating people with MS who are experiencing a relapse.


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