RESUMO
Citrus Sudden Death (CSD), a new, graft-transmissible disease of sweet orange and mandarin trees grafted on Rangpur lime rootstock, was first seen in 1999 in Brazil, where it is present in the southern Triângulo Mineiro and northwestern São Paulo State. The disease is a serious threat to the citrus industry, as 85% of 200 million sweet orange trees in the State of São Paulo are grafted on Rangpur lime. After showing general decline symptoms, affected trees suddenly collapse and die, in a manner similar to trees grafted on sour orange rootstock when affected by tristeza decline caused by infection with Citrus tristeza virus (CTV). In tristeza-affected trees, the sour orange bark near the bud union undergoes profound anatomical changes. Light and electron microscopic studies showed very similar changes in the Rangpur lime bark below the bud union of CSD-affected trees: size reduction of phloem cells, collapse and necrosis of sieve tubes, overproduction and degradation of phloem, accumulation of nonfunctioning phloem (NFP), and invasion of the cortex by old NFP. In both diseases, the sweet orange bark near the bud union was also affected by necrosis of sieve tubes, and the phloem parenchyma contained characteristic "chromatic" cells. In CSD-affected trees, these cells were seen not only in the sweet orange phloem, but also in the Rangpur lime phloem. Recent observations indicated that CSD affected not only citrus trees grafted on Rangpur lime but also those on Volkamer lemon, with anatomical symptoms similar to those seen in Rangpur lime bark. Trees on alternative rootstocks, such as Cleopatra mandarin and Swingle citrumelo, showed no symptoms of CSD. CSD-affected trees did recover when they were inarched with seedlings of these rootstocks, but not when inarched with Rangpur lime seedlings. These results indicate that CSD is a bud union disease. In addition, the bark of inarched Rangpur lime and Volkamer lemon seedlings showed, near the approach-graft union, the same anatomical alterations as the bud union bark from the Rangpur lime rootstock in CSD-affected trees. The dsRNA patterns from CSD-affected trees and unaffected trees were similar and indicative of CTV. CSD-affected trees did not react by immunoprinting-ELISA using monoclonal antibodies against 11 viruses. No evidence supported the involvement of viroids in CSD. The potential involvement of CTV and other viruses in CSD is discussed.
RESUMO
ABSTRACT Three field experiments were conducted in 1997, 1998, and 1999 to investigate the effects of angular leaf spot and rust, separately or combined, on host growth and yield of individual bean plants (Phaseolus vulgaris). In each experiment, three treatments were established by inoculating cv. Carioca with Phaeoisariopsis griseola, Uromyces appendiculatus, or with both pathogens. An additional control treatment was not inoculated, but was sprayed with a fungicide. In the 1997 and 1999 experiments, angular leaf spot reached higher disease levels than rust, whereas in 1998, rust was more severe than angular leaf spot. Host growth, expressed as healthy leaf area duration (HAD), and yield were the highest in 1997 and lowest in 1998. In each experiment, the treatments did not differ significantly to the area under leaf area progress curve, HAD, and healthy leaf area absorption (HAA). All inoculated treatments had significantly more severe disease and less yield than the control treatment. Based on the analysis of 60 plants in each experiment, yield was not related to the areas under disease progress curve for either or both diseases. In 1997 and 1999, yield was related to HAD (R(2) = 0.57 and 0.43) and HAA(R(2) = 0.60 and 0.55). Based on the combined analysis of all 36 plots, angular leaf spot reduced the leaf area because of defoliation, whereas rust did not affect the leaf area. Rust reduced yield more than four times that of angular leaf spot, although the decrease in photosynthesis to angular leaf spot was twice that of rust.