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Streptococcus bovis infections in pigeons: virulence of different serotypes.

In a first experiment, the relative virulence for pigeons of 5 strains of S. bovis was assessed by experimental inoculations. Two S. bovis serotype 1 strains, one serotype 2 strain and two serotype 3 strains were examined. One of the serotype 1 strains and the serotype 2 strain were isolated from pigeons that died from septicaemia. The other strains were isolated from cloaca samples of healthy pigeons. For each strain, 10-20 pigeons were intravenously inoculated with 1 x 10(9) CFU. Morbidity after infection with the serotype 1 and 2 strains varied between 75% and 90%. Disease signs included inability to fly, lameness, emaciation, production of slimy, green droppings, polyuria and sudden death. In groups of pigeons inoculated with the serotype 3 strains, morbidity was 0% and 6%, respectively. Results demonstrate that serotype 3 strains are less virulent for pigeons than serotype 1 and 2 strains. In a second experiment, bacteriological and histological examinations were performed on organs of pigeons serially killed between 1 and 10 days after experimental inoculation with an S. bovis serotype 3 strain of low virulence. Results were compared with results of studies carried out with a highly virulent serotype 1 strain. Notwithstanding bacterial spread and replication in various organs of inoculated pigeons, clinical disease was not observed and histological lesions were scarce and of limited extent.

Animals↗

The interleukin-6 -174 promoter polymorphism is associated with extrapulmonary bacterial dissemination in Streptococcus pneumoniae infection.

Interleukin-6 (IL-6) is required for the clearance of bacteria in pneumococcal pneumonia. The abundance of endogenous IL-6 production on infectious stimuli is associated with genotypic differences in the -174 promoter region of IL-6 (-174 G-->C), showing increased IL-6 levels in patients carrying the GG genotype. One hundred patients with culturally proven pneumococcal disease were analyzed for distribution of the G-/C-alleles in the IL-6 -174 promoter region in comparison to 50 age-matched controls. Extrapulmonary pneumococcal dissemination, including septic metastasis, endocardial and meningeal infection, was used as parameter for impaired clearance of the bacteria. No significant differences in the allele distribution were observed between patients and controls. Within the patient group, the interleukin-6 GG homozygous carriers were less likely to develop extrapulmonary pneumococcal infection (10.3% versus 30.9%; OR 0.26, 95% CI 0.07-0.94, p=0.04). The IL-6 GG genotype, encoding for enhanced IL-6 secretion on bacterial stimuli, reduces the risk of bacterial spread to extrapulmonary sites in pneumococcal infection, possibly due to a more effective clearance of the pathogen from the blood and the respiratory tract.

Genotype↗

Epidemiology of invasive Streptococcus pneumoniae infections in adults in Finland.

Laboratory-based surveillance of invasive pneumococcal infections in adults in Finland from 1983 to 1992 identified 862 episodes of pneumococcal bacteraemia and 97 episodes of meningitis. The overall incidence of invasive pneumococcal infections was 9.1 per 100,000 for all adults per year, but 27.1, 35.8, and 44.5 per 100,000 in those aged 65 years or over, 75 years or over, and 85 years or over, respectively. Most (99.7%) of the pneumococcal strains were sensitive to penicillin. Ninety-five percent of the strains belonged to serogroups/types present in the 23-valent pneumococcal polysaccharide vaccine. Group/type distribution was different in patients aged 16-64 years compared to those 65 years or over (P < 0.001), in bacteraemia compared to meningitis (P < 0.001), and in the years 1983-7 compared to 1988-92 (P < 0.05).

Adolescent↗

Vascular dysfunction and ischemic destruction of tissue in Streptococcus pyogenes infection: the role of streptolysin O-induced platelet/neutrophil complexes.

Rapid tissue destruction in group A streptococcal (GAS) necrotizing fasciitis/myonecrosis often necessitates extensive debridement to ensure survival. The mechanisms responsible for this fulminant process remain unknown; we hypothesized that toxin-induced ischemia contributes to necrosis. In a rat model, Doppler flowmetry was used to measure local blood flow at the site of the intramuscular injection of exotoxins from an invasive M-type 1 GAS, which caused a rapid, dose-dependent decrease in perfusion that was irreversible at the highest toxin concentration tested. Videomicroscopic results revealed that blood flow was impeded by occlusive intravascular cellular aggregates. Flow-cytometric results confirmed that GAS toxins induced the coaggregation of platelets and neutrophils, that this activity was attributable to streptolysin O, and that platelet/neutrophil complex formation was largely mediated by platelet P-selectin (CD62P). Strategies that target platelet adherence molecules may prevent vascular occlusion, maintain tissue viability, and reduce the need for amputation in necrotizing GAS infections.

Animals↗