@entity5259 is among the microorganisms most often isolated from cases of food spoilage and causes @entity344 as well as nongastrointestinal infections elicited by the emetic toxin @entity43704 , enterotoxins, and a panel of tissue-destructive virulence factors. This opportunistic pathogen is increasingly associated with rapidly fatal @entity14235 and immunocompromised individuals. Fatality results from either the misdiagnosis of @entity5259 as a contaminant of the clinical specimen or from failure of antibiotic therapy. Here we report for the first time that exposure to @entity5292 antibiotics induces a phenotype switching of emetic @entity5259 subpopulations to a slow-growing small colony variant ( @entity6723 ) state. Along with altered antibiotic resistance, SCVs showed distinct phenotypic and metabolic properties, bearing the risk of antibiotic treatment failure and of clinical misdiagnosis by standard identification tests used in routine diagnostic. The @entity6723 subpopulation is characterized by enhanced production of the toxin @entity43704 , but it does not secrete tissue-destructive and immune system-affecting enzymes such as @entity8705 . SCVs showed significantly prolonged persistence and decreased virulence in the Galleria mellonella model for @entity2348 , indicating diversification concerning their ecological lifestyle. Importantly, diversification into coexisting wild-type and @entity6723 subpopulations also emerged during @entity4509 pressure during in vivo infection experiments. IMPORTANCE: This study shows for the first time that pathogenic spore-forming @entity5259 strains are able to switch to a so far unreported slow-growing lifestyle, which differs substantially in terms of developmental, phenotypic, metabolic, and virulence traits from the wild-type populations. This underpins the necessity of molecular-based differential diagnostics and a well-chosen therapeutic treatment strategy in clinical environments to combat @entity5259 in a tailored manner. The reported induction of @entity6723 in an endospore-forming @entity1 pathogen requires further research to broaden our understanding of a yet unexplored antibiotic resistance mechanism in sporulating bacteria. Our work also raises a general question about the ecological meaning of @entity6723 subpopulation emergence and importance of @entity6723 in sporeformer populations as an alternative route, next to sporulation, to cope with stresses encountered in natural niches, such as soil or host interfaces.

The Endospore-Forming Pathogen XXXX Exploits a Small Colony Variant-Based Diversification Strategy in Response to @entity5292 Exposure.

@entity1 :: ('9606', 'Species') :: ['human'] @entity6723 :: ('227859', 'Species') :: ['SCV'] @entity2348 :: ('MESH:D001424', 'Disease') :: ['bacterial infections'] @entity14235 :: ('MESH:D016870', 'Disease') :: ['clinical infections especially linked to neonates'] @entity344 :: ('MESH:D005767', 'Disease') :: ['gastrointestinal diseases'] @entity5292 :: ('D000617', 'Chemical') :: ['aminoglycoside'] @entity8705 :: ('MESH:D052536', 'Disease') :: ['sphingomyelinase and phospholipase'] @entity4509 :: ('MESH:D000583', 'Chemical') :: ['amikacin'] @entity5259 :: ('1396', 'Species') :: ['Bacillus cereus', 'B.  cereus'] @entity43704 :: ('MESH:C089294', 'Chemical') :: ['cereulide']
@entity5259 :: (1396,Species) :: ['Bacillus cereus']
