[PNEUMOCOCCAL BIOFILMS AS A FORM OF PERSISTENCE: FORMATION, STRUCTURE, ROLE IN PATHOGENESIS, IMMUNE RESPONSE].

A review of studies on pneumococcal biofilms as a form of persistence is presented. The following provisions are examined: formation of pneumococcal biofilm on abiotic and mucosal surfaces, pathogenetic significance of biofilm pneumococci, their immunogenicity, as well as resistance to antibiotics and unfavorable environmental factors. Differences between biofilm properties, that are formed in vivo and in vitro, are shown. The significance of pneumococcal biofilm formation as means of survival for a long time is underscored.

A In Vitro and In Vivo Study of the Ability of NOD1 Ligands to Activate the Transcriptional Factor NF-kB.

Pattern-recognition receptors (PRR) play a crucial role in the induction of the defense reactions of the immune system against pathogenic bacterial and viral infections. The activation of PRR by specific, highly conserved pathogen-associated molecular patterns (PAMPs) induces numerous immune reactions related both to innate and adaptive immunity. In addition to the well-studied Toll-like receptors, pathogens can be recognized by the receptors belonging to the other PRR families; including NOD-like receptors (NLR). Stimulation of members of NOD-like receptors (NOD1, 2) and Toll-like receptors results in the activation of the transcriptional factor NF-kB regulating gene expression in numerous molecules implicated in the development of proinflammatory reactions. As opposed to Toll-like receptors, the NF-kB-activating ability of NLRs has not been fully studied. In this work, we examine the ability of one member of the NLR family - NOD1 - to activate the main proinflammatory transcriptional factor NF-kB. We also compare the NF-kB-activating ability of NOD1 ligands of a different structure with TLR4,5 ligandsin vitroandin vivo.

Molecular epidemiology of serogroup a meningitis in Moscow, 1969 to 1997.

Molecular analysis of 103 serogroup A Neisseria meningitidis strains isolated in Moscow from 1969 to 1997 showed that four independent clonal groupings were responsible for successive waves of meningococcal disease. An epidemic from 1969 to the mid-1970s was caused by genocloud 2 of subgroup III, possibly imported from China. Subsequent endemic disease through the early 1990s was caused by subgroup X and then by subgroup VI, which has also caused endemic disease elsewhere in eastern Europe. A 1996 epidemic was part of the pandemic spread from Asia of genocloud 8 of subgroup III. Recent genocloud 8 epidemic disease in Moscow may represent an early warning for spread of these bacteria to other countries in Europe.

A study of pathogenic factors of Streptococcus pneumoniae strains causing meningitis.

Pneumococcal meningitis in St. Petersburg in the period 1985-1991 occurred in 1.7-2.3 children per 100,000 annually. The most common serotypes among pneumococcal strains isolated from patients with meningitis were 19, 1, 6, 15, and 2, whereas, among the capsulated strains isolated from carriers, type 3 predominated. Only one third of strains from cases of meningitis were highly virulent for mice (types 1, 2, 3). Hyaluronidase was produced by all the 39 studied strains, 22 (84.6 +/- 7.1%) out of 26 strains from patients with otitis media, and only by 15 (11.5 +/- 2.8%) out of 130 strains isolated from carriers. Non-capsulated strains lacked this enzyme. Results of intranasal inoculation of pneumococcal strains with different hyaluronidase activity and addition of exogenous hyaluronidase to strains which did not produce the enzyme confirm the hypothesis that this enzyme plays an important role in bacterial dissemination and breaching of the blood brain barrier by pneumococci. It was concluded that high hyaluronidase activity, presence of capsule, and pneumolysin or serotype (1, 2, and 19) despite hyaluronidase titer, are the most important factors contributing to the development of pneumococcal meningitis. The role of the mouse toxic factor is unclear.

The study of agglutination of trypsin-treated sheep red cells by Corynebacterium diphtheriae strains.

620 Corynebacterium diphtheriae strains from 472 sick and healthy persons were studied for their adhesive activity (AA) in direct agglutination of trypsin-treated sheep erythrocytes. Toxigenic strains had more active AA than non-toxigenic ones which was not dependent on the presence of toxin in the culture. Neither biotype nor serotype of the strains correlated with their AA. Several lysotypes among toxigenic and non-toxigenic strains were more active than others. Toxigenic strains from patients had higher AA than those from carriers. Both toxigenic and non-toxigenic strains isolated from the prolonged carriers possessed the highest AA. It was concluded that AA measured in this way was an important colonization factor for all diphtheria strains and a pathogenicity factor for toxigenic strains.

Pathogenesis of diphtheria carrier state from the immunological point of view.

Results of a comparative investigation of diphtheria antitoxin and type-specific antibacterial antibodes in 264 carriers of diphtherial bacteria, 41 diphtheria patients and 263 non-infected subjects are presented. A high level of antitoxin did not prevent the development of toxigenic-strain carrier state. A basically similar immunological antibacterial response was observed in patients with manifest forms of diphtheria and in carriers of toxigenic strains; such a response could not as yet be detected in carriers of non-toxigenic strains. It has been suggested that the infectious process in the toxigenic-strain carrier state is due to factors of the virulence responsible for infectivity and invasiveness of the diphtherial microbe. The toxin plays no pathogenic role in carrier state.