Several models have shown that virulence varies from one strain of Listeria monocytogenes to another, but little is known about the cause of low virulence. Twenty-six field L. monocytogenes strains were shown to be of low virulence in a plaque-forming assay and in a subcutaneous inoculation test in mice. Using the results of cell infection assays and phospholipase activities, the low-virulence strains were assigned to one of four groups by cluster analysis and then virulence-related genes were sequenced. Group I included 11 strains that did not enter cells and had no phospholipase activity. These strains exhibited a mutated PrfA; eight strains had a single amino acid substitution, PrfAK220T, and the other three had a truncated PrfA, PrfA⌬174-237. These genetic modifications could explain the low virulence of group I strains, since mutated PrfA proteins were inactive. Group II and III strains entered cells but did not form plaques. Group II strains had low phosphatidylcholine phospholipase C activity, whereas group III strains had low phosphatidylinositol phospholipase C activity. Several substitutions were observed for five out of six group III strains in the plcA gene and for one out of three group II strains in the plcB gene. Group IV strains poorly colonized spleens of mice and were practically indistinguishable from fully virulent strains on the basis of the above-mentioned in vitro criteria. These results demonstrate a relationship between the phenotypic classification and the genotypic modifications for at least group I and III strains and suggest a common evolution of these strains within a group.

A different transcription pattern of P. gingivalis genes was observed, depending on the stimulus of oxidative stress. We present new evidence that the expression of tpx, encoding a thiol peroxidase, is partially OxyR-dependent and is induced after atmospheric oxygen exposure.

Several reports have described Listeria monocytogenes strains which were nonpathogenic or weakly pathogenic, but little is known about these low-virulence strains. We found that 9 field L. monocytogenes strains were hypovirulent and 17 were avirulent, based on the number of mice contaminated and the colonization of their spleens after subcutaneous inoculation. All these strains possessed the known virulence genes. We have now assessed the low virulence of these strains in other assays before determining how they differ from virulent strains. We have shown that the low-virulence strains exhibited a phenotypic stability and were not a mixture of virulent and avirulent bacteria. They did not recover virulence after many passages in mice and colonized the spleens of mice more poorly than virulent strains after i.v. inoculation. Their lethal capacities, determined by 50% lethal dose (LD 50 ), were lower than those of virulent strains. Like Listeria innocua, 14 of 17 avirulent strains had no LD 50 and were eliminated by the lymph nodes after subcutaneous inoculation. The virulent, hypovirulent, and avirulent strains were always significantly different, whatever the tests of virulence used, confirming the importance of these low-virulence field strains in identifying the proteins involved in virulence.Listeria monocytogenes organisms are ubiquitous gram-positive bacteria. They are widespread in the environment and have been isolated from many sources, including soil, sewage, decaying vegetation, and food. They are responsible for human diseases characterized by meningitis, meningoencephalitis, septicemia, abortion, and gastroenteritis. Through contaminated food, bacteria reach the gastrointestinal tract and can translocate the intestinal barrier to infect lymph nodes. Then, through lymph and blood, a fraction of the bacteria reach the spleen and liver. Apoptosis, neutrophils, and phagocytic cells contribute to the rapid clearing of the bacteria before complete abolition by the specific immune response. In some cases, such as the immunocompromised host, bacteria multiply unrestrictedly in the hepatocytes from which they disseminate through blood to the brain and placenta. Although L. monocytogenes is also present in the environment and is probably frequently ingested by humans (2), listeriosis is very rare. The incidence is very low, around two to eight sporadic cases annually per million people in Europe and the United States (16). If we exclude the susceptibility of the host, another reason for this conflicting evidence may lie in the variability of virulence in the L. monocytogenes strains. Serotypes of L. monocytogenes could also be linked to the level of virulence, as only three serotypes (1/2a, 1/2b, and 4b) have been implicated in human cases. However, no bacterial genes related to the serotype have yet been found. Studies using different assays have shown that virulence varies from one strain of L. monocytogenes to another. The mouse assays are extremely sensitive assays for evaluating the pathogenicity of L. mo...

In 6/16 subjects the same P. gingivalis isolate was found in the blood and in oral cavity. P. gingivalis heterogeneity suggests no association of a unique clonal type with transient bacteremia.