|Bassanezi, R. b.|
|Bergamin filho, A.|
Submitted to: Phytopathology
Publication Type: Abstract only
Publication Acceptance Date: 11/9/2002
Publication Date: 4/1/2003
Citation: Bassanezi, R. B., Bergamin-Filho, A., Amorim, L., Gimenes-Fernandes, N., Gottwald, T. R. 2003. Spatial and Temporal Analysis of Citrus Sudden Death as a Tool to Generate Hypotheses Concerning its Etiology. Phytopathology. Interpretive Summary: Citrus Sudden Death (CSD) is a serious disease new disease of citrus that has not been completely characterized nor is the cause of the disease known. The disease is attacking citrus in Sao Paulo state of Brazil and is both serious and rapidly spreading in the Brazilian citrus industry, and thus a concern to the US citrus industry because of possible introduction. This paper describes the disease and what is known of its pathology. Through a series of epidemiological/statistical analysis of the spread and patterns of the disease, the authors have determined that both the patterns of disease and the way it spreads is very similar to citrus tristeza virus. The conclusion of the paper is that because of these similarities, the disease is likely insect transmitted and is probably caused by a virus. These conclusions give scientists clues for further investigation of the cause of the disease.
Technical 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 CDS 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.