Microbial pathogenesis
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Microbial pathogenesis · Jul 2004
Borrelia burgdorferi outer surface protein (osp) B expression independent of ospA.
The outer surface proteins (Osp) A and B are two important lipoproteins of Borrelia burgdorferi, the Lyme disease spirochete. Extensive in vitro studies indicate that ospB shares a common promoter with ospA and thus these two lipoprotein genes are coordinately transcribed. ⋯ The ratio of ospA and ospB mRNA transcripts was 3.5:1 in tick-adapted spirochetes while B. burgdorferi matched every ospA mRNA with up to 70 ospB transcripts during murine infection. This was consistent with the analysis of antibody responses to the two lipoproteins, which showed a more frequent OspB response than OspA during chronic murine infection.
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Microbial pathogenesis · Jan 2004
Mycobacterium bovis infection of vitamin D-deficient NOS2-/- mice.
Vitamin D deficiency is associated with an increased risk for tuberculosis infection. Studies using in vitro systems indicate that 1,25-dihydroxyvitamin D(3) [i.e. 1,25(OH)(2)D(3)], the most active form of the vitamin, enhances mycobacterial killing by increasing nitric oxide (NO) production. To evaluate concurrently the role of 1,25(OH)(2)D(3) and NO on the host response to tuberculosis infection, mice deficient in NO synthase 2 (NOS2(-/-)) and/or vitamin D were aerosol-challenged with Mycobacterium bovis and subsequently evaluated for mycobacterial colonization and lesion formation. ⋯ However, effects of vitamin D on colonization, but not lesion area, were more pronounced in NOS2(+/+) mice than in NOS2(-/-) mice. These findings are consistent with the current hypothesis that 1,25(OH)(2)D(3) enhances mycobacterial killing through a NO-dependent mechanism. As responses of NOS2(-/-) mice were affected by 1,25(OH)(2)D(3) deficiency, albeit to a lesser extent than were those of NOS2(+/+) mice, NO-independent actions of 1,25(OH)(2)D(3) also likely exist.
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Microbial pathogenesis · Sep 1997
Establishment of a Streptococcus pneumoniae nasopharyngeal colonization model in adult mice.
Human nasopharyngeal carriage of Streptococcus pneumoniae constitutes the major natural reservoir of pneumococci and is thought to be the prelude to virtually all pneumococcal disease. If carriage could be greatly reduced, pneumococcal transmission and disease could be largely eliminated. To facilitate the studies of mechanisms important in carriage and to identify immunogens that can elicit protection against carriage, we characterized an adult mouse model of nasopharyngeal carriage. ⋯ To ensure carriage in the largest percentage of mice, without causing sepsis or death, inoculations of 10(7) colony forming units (cfu) should be used. In this model, carriage was generally observed without concomitant bacteremia or sepsis and carriage was observed even with strains that were avirulent when injected i.v. The model should be useful for the identification of protection-eliciting antigens, since intranasal immunization with heat-killed pneumococci or lysates of pneumococci protected against carriage.
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Microbial pathogenesis · May 1997
Role of bacteria in the pathogenesis of short bowel syndrome-associated D-lactic acidemia.
Previously, we have demonstrated that short bowel syndrome (SBS) patients suffer daily from D-lactic acidemia; in these patients rather high amounts of (bacterial) D-lactate emerge in blood and urine with a circadian rhythm. The aim of this study was to establish the microbial basis of D-lactic acidemia in SBS. Therefore, faecal flora of (young and adult) SBS-patients was analysed qualitatively and quantitatively, and compared to that of controls. ⋯ Use of oral antibiotics in two SBS-children did not reduce the total numbers of lactobacilli, but caused shifts within the intestinal populations of at least lactobacilli. It is concluded that the strongly reduced intestinal capacity for carbohydrate absorption and the oral consumption of easily fermentable carbohydrates form the physiological basis for D-lactic acidemia in SBS, and that the fermentative D-lactate production by intestinal bacteria, especially the abundant, resident lactobacilli, forms its microbial basis. In these patients the antimicrobial and therapeutic effects of antibiotics are unpredictable.
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Microbial pathogenesis · Jun 1987
Role of exotoxin A and elastase in the pathogenicity of Pseudomonas aeruginosa strain PAO experimental mouse burn infection.
We examined the virulence of Pseudomonas aeruginosa strain PAO and xcp (extracellular proteins deficient) and xch (extracellular proteins hyperproducing) mutants derived from strain PAO in an experimental mouse burn infection model. The results showed that xcp mutants, which produced little or no extracellular elastase and exotoxin A, were as virulent as their corresponding xcp+ strains. ⋯ Neither elastase nor exotoxin A seem to play any role in burn infections with P. aeruginosa strain PAO. However, ability for iron uptake is an important virulence factor.