R. solanacearum Race 3 biovar 2, which causes potato brown rot and Southern wilt of geranium, is a high-consequence quarantine pathogen in Europe and North America and causes large crop losses in tropical highlands. This practical review emphasizes prevention, detection, diagnosis, and effective management of diseases caused by this destructive pathogen. Accepted for publication 17 January 2009. Published 13 March 2009.

Three separate field trials were established in Guadeloupe under different agronomic and rainfall conditions to study phyllosphere contamination and infection of sugarcane plants by Xanthomonas albilineans, the causal agent of sugarcane leaf scald. Disease-free and leaf scald susceptible cv. B69566 was planted and monitored during three 1-year crop cycles. Presence of leaf scald contaminated sugarcane fields in the proximity of the disease-free trials appeared critical in early contamination of the sugarcane phyllosphere. Later on, particular meteorological events, such as tropical storms, were also important in aerial spread of the pathogen. A positive correlation was found between epiphytic populations of X. albilineans and severity of leaf necrotic symptoms, but occurrence of leaf symptoms was not always related to subsequent stalk infection. However, when the data of the three crop seasons were considered together, a high correlation was found between rainfall and maximum epiphytic populations of X. albilineans, and between rainfall and subsequent stalk infections. Consequently, rainfall is a key factor to be considered in evaluation of risks of leaf scald epidemics, and protocols for propagation of healthy sugarcane material and screening methods for leaf scald resistance may have to be revised in humid tropical locations.

Pathogenicity of 75 strains of Xanthomonas albilineans from Guadeloupe was assessed by inoculation of sugarcane cv. B69566, which is susceptible to leaf scald, and 19 of the strains were selected as representative of the variation in pathogenicity observed based on stalk colonization. In vitro production of albicidin varied among these 19 strains, but the restriction fragment length polymorphism pattern of their albicidin biosynthesis genes was identical. Similarly, no genomic variation was found among strains by pulsed-field gel electrophoresis. Some variation among strains was found by amplified fragment length polymorphism, but no relationship between this genetic variation and variation in pathogenicity was found. Only 3 (pilB, rpfA, and xpsE) of 40 genes involved in pathogenicity of bacterial species closely related to X. albilineans could be amplified by polymerase chain reaction from total genomic DNA of all nine strains tested of X. albilineans differing in pathogenicity in Guadeloupe. Nucleotide sequences of these genes were 100% identical among strains, and a phylogenetic study with these genes and housekeeping genes efp and ihfA suggested that X. albilineans is on an evolutionary road between the X. campestris group and Xylella fastidiosa, another vascular plant pathogen. Sequencing of the complete genome of Xanthomonas albilineans could be the next step in deciphering molecular mechanisms involved in pathogenicity of X. albilineans.

Total genomic DNA from 137 strains of Xanthomonas albilineans from worldwide locations was hybridized with two DNA probes that together harbor the entire 49-kb albicidin biosynthesis gene cluster and two additional 3-kb genomic regions required for albicidin production. Fourteen haplotypes and two major genetic groups (albicidin [ALB]-restriction fragment length polymorphism [RFLP] A and ALB-RFLP B) were identified, and strains that were isolated after recent outbreaks of leaf scald disease belonged to group ALB-RFLP B. Albicidin genetic diversity was very similar to the previously described genetic diversity of the pathogen based on the whole genome. No relationship was found between variability of albicidin biosynthesis genes and the amount of albicidin produced in vitro by X. albilineans. Leaf scald-susceptible sugarcane cv. H70-144 was inoculated with 20 strains of the pathogen belonging to different ALB-RFLP haplotypes. Among them, 10 strains from Guadeloupe belonged to the same ALB-RFLP group but differed in the amount of albicidin produced in vitro. Strains were distributed in at least three different pathogenicity groups based on symptom severity and pathogen population density in the stalk. These two pathogenicity factors varied concurrently; however, no relationship between variation in albicidin biosynthesis genes, variation in the amount of albicidin produced in vitro, and variation in pathogenicity of X. albilineans was found. Further investigation is necessary to identify other genes involved in pathogenicity of X. albilineans.

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