Characterization of Soybean, Tomato, and Nicandra physalodes as Sources of Inoculum of Tomato Severe Rugose Virus to Tomato Crops.

Tomato severe rugose virus (ToSRV) is one of Brazil's main begomoviruses infecting tomato (Solanum lycopersicum). Recent studies indicate that soybean (Glycine max) crops harboring the whitefly Bemisia tabaci Middle East-Asia Minor 1 (MEAM1) may have epidemiological significance by acting as an asymptomatic amplifier host for the virus. In this study, we gathered experimental greenhouse and field evidence of the role of soybean in the epidemiology of the disease caused by ToSRV. Tomato and Nicandra physalodes, known as good sources of inoculum of this begomovirus, were used as references. The infection rates of soybean, tomato, and N. physalodes with ToSRV in greenhouse no-choice transmission tests with B. tabaci MEAM1 were 50, 71.4, and 64.2%, respectively. The transmission efficiencies of ToSRV to tomato when B. tabaci MEAM1 acquired the virus in ToSRV-infected soybean, tomato, and N. physalodes were 43, 33, and 20%, respectively. Leaves of ToSRV-infected soybean, tomato, and N. physalodes used as sources of inoculum had similar virus titers. In the host preference assay, viruliferous whiteflies preferred to land on tomato rather than soybean and N. physalodes, whereas aviruliferous whiteflies landed indistinctly on these plants. Under experimental field conditions, the transmission efficiency of ToSRV to tomato was higher when tomato was used as a source of inoculum, followed by N. physalodes and soybean. Considering that soybean is extensively cultivated in several Brazilian states that also grow tomato, it can serve as an efficient asymptomatic source of inoculum and support the recent hypothesis that it can also play, under certain conditions, a relevant role as an amplifier host in the epidemiology of the disease caused by ToSRV.

Amplifier Hosts May Play an Essential Role in Tomato Begomovirus Epidemics in Brazil.

Current control of tomato golden mosaic disease, caused in Brazil predominantly by tomato severe rugose virus (ToSRV), is dependent on both, planting resistant/tolerant hybrids and intensive insecticide sprays (two to three per week) for controlling Bemisia tabaci, the vector of ToSRV. Resistant hybrids only confer moderate resistance to infection by ToSRV and some tolerance to the disease. Insecticide sprays, although widely used, have failed in most tomato production areas in Brazil, as they are unable to reduce primary spread, i.e., infection caused by the influx of viruliferous whiteflies coming from external sources of inoculum. Severe epidemics are recurrently observed in some tomato fields in several Brazilian regions, which prompted us to postulate the existence in the agroecosystem, in some places and time, of amplifier hosts that provide the necessary force of infection for epidemics to occur, even in the absence of secondary spread in the target crop. Amplifier hosts are ideally asymptomatic, occur in high density near the target crop, and support growth of both virus and vector. Soybean and common bean are potential amplifier hosts for begomovirus in tomato crops. Our results support the hypothesis that soybean plants may play an important role as an amplifier host of ToSRV for tomato crops in the field, although this does not seem to be a frequent phenomenon. Successful amplification will depend on several factors, including the soybean cultivar, the soybean stage of development at the moment of infection, the ToSRV isolate, and the perfect synchrony between the beginning of a soybean field and the end of a ToSRV-infected crop, and, later, between the senescence of the ToSRV-infected soybean plants and the new tomato crop. The concept of amplifier hosts has been widely used in ecology of zoonoses but, to our knowledge, has never been used in botanical epidemiology.

Spatial and temporal analyses of citrus sudden death as a tool to generate hypotheses concerning its etiology.

ABSTRACT Citrus sudden death (CSD), a new disease of unknown etiology that affects sweet orange grafted on Rangpur lime, was visually monitored for 14 months in 41 groves in Brazil. Ordinary runs analysis of CSD-symptomatic trees indicated a departure from randomness of symptomatic trees status among immediately adjacent trees mainly within rows. The binomial index of dispersion (D) and the intraclass correlation (k) for various quadrat sizes suggested aggregation of CSD-symptomatic trees for almost all plots within the quadrat sizes tested. Estimated parameters of the binary form of Taylor's power law provided an overall measure of aggregation of CSD-symptomatic trees for all quadrat sizes tested. Aggregation in each plot was dependent on disease incidence. Spatial autocorrelation analysis of proximity patterns suggested that aggregation often existed among quadrats of various sizes up to three lag distances; however, significant lag positions discontinuous from main proximity patterns were rare, indicating a lack of spatial association among discrete foci. Some asymmetry was also detected for some spatial autocorrelation proximity patterns, indicating that within-row versus across-row distributions are not necessarily equivalent. These results were interpreted to mean that the cause of the disease was most likely biotic and its dissemination was common within a local area of influence that extended to approximately six trees in all directions, including adjacent trees. Where asymmetry was indicated, this area of influence was somewhat elliptical. Longer-distance patterns were not detected within the confines of the plot sizes tested. Annual rates of CSD progress based on the Gompertz model ranged from 0.37 to 2.02. Numerous similarities were found between the spatial patterns of CSD and Citrus tristeza virus (CTV) described in the literature, both in the presence of the aphid vector, Toxoptera citricida. CSD differs from CTV in that symptoms occur in sweet orange grafted on Rangpur lime. Based on the symptoms of CSD and on its spatial and temporal patterns, our hypothesis is that CSD may be caused by a similar but undescribed pathogen such as a virus and probably vectored by insects such as aphids by similar spatial processes to those affecting CTV.