Of 830 Neisseria meningitidis isolates obtained from healthy carriers in Bavaria, Germany, 136 (164 %) lacked the operons necessary for the synthesis, lipid modification, and transport of capsular polysaccharide. These operons were replaced by a non-coding intergenic region either 113 or 114 bp in length, termed here the capsule null locus (cnl). Comparisons of the nucleotide sequence of this region in the meningococcus and its acapsulate relatives, Neisseria gonorrhoeae and Neisseria lactamica, revealed six distinct sequence variants (cnl-1 to cnl-6), with a total of 10 nucleotide substitutions and three indels. With the exception of one 4 bp insertion, which was unique to a gonococcal isolate, all of the individual sequence changes were present in the N. lactamica isolates examined. The meningococcal isolates with a cnl belonged to one of four otherwise genetically diverse genetic groupings : the ST-53 and ST-1117 complexes (75 isolates) ; the ST-845 complex (12 isolates) ; the ST-198 and 1136 complexes (46 isolates), and the ST-44 complex (one isolate).These data demonstrated that a substantial proportion of carried meningococci were incapable of capsule production, that the cnl circulated within Neisseria populations by horizontal genetic exchange, and that the expression of a polysaccharide capsule was not a requirement for person-to-person transmission of certain meningococcal lineages.Keywords : Neisseria meningitidis, multilocus sequence typing, transmission, capsule null locus INTRODUCTIONThe causative organism of meningococcal disease, Neisseria meningitidis, is primarily a commensal bacterium which can be cultured from up to 40 % of human nasopharyngeal swab samples (Broome, 1986). This figure, which is likely to be an underestimate of the actual carriage rate (Sim et al., 2000), is dependent on a number of factors particular to the individuals sampled, including age and social status, together with population factors such as geographical location and climatic conditions (Rosenstein et al., 2001 The GenBank accession number for the sequence of the cnl-1 allele is AJ308327.species being harmless inhabitants of the mucosal surfaces of animals and humans (Morse & Knapp, 1992). Within the genus, the expression of a capsular polysaccharide is unique to N. meningitidis, and it is tempting to speculate that the acquisition of the genetic material necessary for the expression of a capsule was an important step in the evolution of the meningococcus from other Neisseria species.Immunochemical differences among meningococcal capsules define the serogroups of the organism (Vedros, 1987). Five of the 13 recognized capsular polysaccharides, those conferring serogroups A, B, C, W-135 and Y, can be thought of as virulence determinants, as virtually all meningococcal disease is caused by organisms expressing one of these capsular antigens (Poolman et al., 1995). These capsules are capable of protecting the bacterium against opsonophagocytosis during disseminated infection (Kahler et al., 1998 ; Masson & Holbein, 1985...

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Explanation of pathophysiology and benign nature of the condition.

Thus, somatosensory profiling in male patients with painful extremities may be useful in the detection of FD.

In Fabry disease, no linear relationship exists between pain and small nerve fibre function. With older age and more severe disease pain may abate as nerve fibre function further deteriorates.