Why Are Some Listeria monocytogenes Genotypes More Likely To Cause Invasive (Brain, Placental) Infection?

Abstract

Although all isolates of the foodborne pathogen Listeria monocytogenes are considered to be pathogenic, epidemiological evidence indicates that certain serovar 4b lineages are more likely to cause severe invasive (neuromeningeal, maternal-fetal) listeriosis. Recently described as L. monocytogenes “hypervirulent” clones, no distinctive bacterial trait has been identified so far that could account for the differential pathogenicity of these strains. Here, we discuss some preliminary observations in experimentally infected mice suggesting that serovar 4b hypervirulent strains may have a hitherto unrecognized capacity for prolonged in vivo survival. We propose the hypothesis that protracted survivability in primary infection foci in liver and spleen—the first target organs after intestinal translocation—may cause L. monocytogenes serovar 4b hypervirulent clones to have a higher probability of secondary dissemination to brain and placenta.

Virulence Pattern Analysis of Three Listeria monocytogenes Lineage I Epidemic Strains with Distinct Outbreak Histories

“…This study is thought to create some hypotheses why lineage 1 outbreak clones of serovar 4b might have led to a clinical outcome that was obviously very different from outbreaks of non-serovar 4b isolates. It further provides a hypothesis why some Listeria monocytogenes strains tend to persist in the murine body what was proven for PF49 and P14 [ 16 ].…”

“…In this study, we showed that not only strains of CC1 [ 16 ], but also of CC2 have the potential to survive for extended time periods in the liver, enhancing the possibility for dissemination to the secondary organs. Experiments, e.g., transcriptome analysis of bacteria isolated from organs such as the liver, are needed to determine the molecular mechanism behind the long-term survival of some L. monocytogenes strains in this tissue.…”

“…This unusually long incubation period required for the manifestation of clinical systemic listeriosis implies that L. monocytogenes might persist in host tissues for extended periods without causing overt clinical signs. In a recently published paper, Vazquez-Boland and co-workers stipulated the hypothesis that hypervirulent strains, which survive longer in the liver and the spleen of the host, have a higher probability of secondary dissemination of the brain and the placenta [ 16 ]. Two hypervirulent 4b strains P14 and PF49, both assigned to CC1, were still detectable in the mouse liver three weeks post infection [ 16 ].…”

“…In a recently published paper, Vazquez-Boland and co-workers stipulated the hypothesis that hypervirulent strains, which survive longer in the liver and the spleen of the host, have a higher probability of secondary dissemination of the brain and the placenta [ 16 ]. Two hypervirulent 4b strains P14 and PF49, both assigned to CC1, were still detectable in the mouse liver three weeks post infection [ 16 ]. P14 was isolated from an adult patient with central nervous symptoms in Spain, and PF49 is an epidemic strain from a cheese-associated outbreak in Switzerland [ 17 ].…”

Emergence and global spread of Listeria monocytogenes main clinical clonal complex

“…S7). The finding that SL1 is by far the major sublineage in Lm-CC1 is consistent Lm genomic surveillance era Foodborne origin of listeriosis (Schlech et al, 1983) Lm first genome (Glaser et al, 2001) First networks for Lm molecular surveillance (Swaminathan et al, 2001) Livestock farms as natural Lm reservoirs with its increased virulence and/or transmission [as seen at Lm species level for hypervirulent clones (32)] or may indicate that SL404 and SL150 are restricted to some yet unknown ecological niches. Within SL1, all different GCs were well represented, with strong spatial structure: GC1 is the most prevalent clade in Europe (48%, 593 of 1237), Asia (68%, 17 of 25), and South America (64%, 14 of 22); GC2 is the most prevalent clade in North America (29%, 150 of 512) and Oceania (52%, 84 of 163), while GC3 is the most prevalent clade in Africa (80%, 43 of 54) (Fig.…”