Comparative genomics of two Leptospira interrogans serovars reveals novel insights into physiology and pathogenesis.

Leptospira species colonize a significant proportion of rodent populations worldwide and produce life-threatening infections in accidental hosts, including humans. Complete genome sequencing of Leptospira interrogans serovar Copenhageni and comparative analysis with the available Leptospira interrogans serovar Lai genome reveal that despite overall genetic similarity there are significant structural differences, including a large chromosomal inversion and extensive variation in the number and distribution of insertion sequence elements. Genome sequence analysis elucidates many of the novel aspects of leptospiral physiology relating to energy metabolism, oxygen tolerance, two-component signal transduction systems, and mechanisms of pathogenesis. A broad array of transcriptional regulation proteins and two new families of afimbrial adhesins which contribute to host tissue colonization in the early steps of infection were identified. Differences in genes involved in the biosynthesis of lipopolysaccharide O side chains between the Copenhageni and Lai serovars were identified, offering an important starting point for the elucidation of the organism's complex polysaccharide surface antigens. Differences in adhesins and in lipopolysaccharide might be associated with the adaptation of serovars Copenhageni and Lai to different animal hosts. Hundreds of genes encoding surface-exposed lipoproteins and transmembrane outer membrane proteins were identified as candidates for development of vaccines for the prevention of leptospirosis.

Comparative analyses of the complete genome sequences of Pierce's disease and citrus variegated chlorosis strains of Xylella fastidiosa.

Xylella fastidiosa is a xylem-dwelling, insect-transmitted, gamma-proteobacterium that causes diseases in many plants, including grapevine, citrus, periwinkle, almond, oleander, and coffee. X. fastidiosa has an unusually broad host range, has an extensive geographical distribution throughout the American continent, and induces diverse disease phenotypes. Previous molecular analyses indicated three distinct groups of X. fastidiosa isolates that were expected to be genetically divergent. Here we report the genome sequence of X. fastidiosa (Temecula strain), isolated from a naturally infected grapevine with Pierce's disease (PD) in a wine-grape-growing region of California. Comparative analyses with a previously sequenced X. fastidiosa strain responsible for citrus variegated chlorosis (CVC) revealed that 98% of the PD X. fastidiosa Temecula genes are shared with the CVC X. fastidiosa strain 9a5c genes. Furthermore, the average amino acid identity of the open reading frames in the strains is 95.7%. Genomic differences are limited to phage-associated chromosomal rearrangements and deletions that also account for the strain-specific genes present in each genome. Genomic islands, one in each genome, were identified, and their presence in other X. fastidiosa strains was analyzed. We conclude that these two organisms have identical metabolic functions and are likely to use a common set of genes in plant colonization and pathogenesis, permitting convergence of functional genomic strategies.

Xanthomonas albilineans Haplotype B Responsible for a Recent Sugarcane Leaf Scald Disease Outbreak in Cuba.

Over the past 3 years, the incidence of sugarcane leaf scald disease (LSD) caused by Xanthomonas albilineans has increased at alarming rates in some Caribbean countries. LSD was in latent phase since 1978, when the disease was reported in Cuba, until February 1998 when typical symptoms were observed in germ plasm collections and in some commercial plantings. More than 150 bacterial isolates from different sugarcane varieties and from different localities were isolated on Wilbrink agar medium and characterized. All isolates had shown similar cultural and biochemical patterns. However, serological differences between isolates from the recent outbreak and the ones obtained prior to 1998 were detected by indirect ELISA testing. Differences between Cuban isolates obtained prior to 1998 and those from the recent outbreak were confirmed by analysis of repetitive DNA sequences dispersed throughout the genome. According to the pattern obtained, the newer isolates were similar to reference strains classified as haplotype B by pulsed field gel electrophoresis (1). It is concluded that the recent outbreak of LSD was caused by a strain different than the ones previously detected in Cuba. Reference: (1) M. J. Davis et al. Phytopathology 87:316, 1997.