Clinical S. aureus Isolates Vary in Their Virulence to Promote Adaptation to the Host

Abstract

Staphylococcus aureus colonizes epithelial surfaces, but it can also cause severe infections. The aim of this work was to investigate whether bacterial virulence correlates with defined types of tissue infections. For this, we collected 10–12 clinical S. aureus strains each from nasal colonization, and from patients with endoprosthesis infection, hematogenous osteomyelitis, and sepsis. All strains were characterized by genotypic analysis, and by the expression of virulence factors. The host–pathogen interaction was studied through several functional assays in osteoblast cultures. Additionally, selected strains were tested in a murine sepsis/osteomyelitis model. We did not find characteristic bacterial features for the defined infection types; rather, a wide range in all strain collections regarding cytotoxicity and invasiveness was observed. Interestingly, all strains were able to persist and to form small colony variants (SCVs). However, the low-cytotoxicity strains survived in higher numbers, and were less efficiently cleared by the host than the highly cytotoxic strains. In summary, our results indicate that not only destructive, but also low-cytotoxicity strains are able to induce infections. The low-cytotoxicity strains can successfully survive, and are less efficiently cleared from the host than the highly cytotoxic strains, which represent a source for chronic infections. The understanding of this interplay/evolution between the host and the pathogen during infection, with specific attention towards low-cytotoxicity isolates, will help to optimize treatment strategies for invasive and therapy-refractory infection courses.

Staphylococcus aureus Pneumonia: Preceding Influenza Infection Paves the Way for Low-Virulent Strains

“…However, many alternative adhesins support the internalization process [29] and participate in biofilm formation. For most S. aureus strains obtained from infection and colonization, high invasive capacity in different host cell types was reported [30,31]. In our present study, we even detected a difference between colonizing and pneumonia strains that point to the importance of host cell invasion in lung infection.…”

Silence as a way of niche adaptation: mecC-MRSA with variations in the accessory gene regulator (agr) functionality express kaleidoscopic phenotypes

“…Attenuated virulence favouring host colonization and/or persistence of infection (e.g. small colony variants) is a common concept in bacterial evolution [106][107][108] . The mecC-MRSA lineages CC130, CC49, CC1943 and CC599 were obviously not among those CC's frequently reported for nasal colonization in humans and animals such as CC22 and CC398 [109][110][111][112] .…”

Acapsular Staphylococcus aureus with a non-functional agr regains capsule expression after passage through the bloodstream in a bacteremia mouse model

“…Lack of CP expression benefits the interaction between surface S. aureus adhesins and eukaryotic cell receptors thus promoting internalization of bacteria into the eukaryotic cell milieu 8 . Intracellular location, reduced capacity to cause inflammation 13 , 22 , increased biofilm production and SCV formation 23 may explain why not only S. aureus pulmonary infection of cystic fibrosis patients 24 but also S. aureus osteomyelitis become refractory to antibiotic treatment in spite of appropriate antibiotic treatment. From our bacterial collection we selected non-encapsulated S. aureus isolate HU-14 with a non-functional agr due to an IS 256 insertion in agrC .…”