Phenotypic and molecular characterization of hyperpigmented group B Streptococci.

Lupo, Agnese; Ruppen, Corinne; Hemphill, Andrew; Spellerberg, Barbara; Sendi, Parham (2014). Phenotypic and molecular characterization of hyperpigmented group B Streptococci. International journal of medical microbiology IJMM, 304(5-6), pp. 717-724. Elsevier 10.1016/j.ijmm.2014.05.003

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Group B Streptococcus (GBS) causes invasive infections in neonates, older adults and patients with comorbidities. β-hemolysin/cytolysin is an important GBS virulence factor. It is encoded by the cyl operon and confers GBS hemolytic activity. Isolates displaying hyperpigmentation are typically hyperhemolytic. Comparison of clonally identical isolates displaying different levels of pigmentation has shown transcriptional dysregulation due to mutations in components of the control of the virulence S/R (CovS/R) regulatory system. In addition, hyperpigmented isolates show decreased CAMP factor and decreased capsule thickness. In analogy to findings in group A Streptococcus, a pivotal role of CovS/R has been proposed in the host-pathogen interaction of invasive GBS infection. However, corresponding investigations on multiple clinical GBS isolates have not been performed. We prospectively collected hyperpigmented isolates found in a diagnostic laboratory and performed phenotypic, molecular and transcriptional analyses. In the period from 2008 to 2012, we found 10 isolates obtained from 10 patients. The isolates reflected both invasive pathogens and colonizers. In three cases, clonally identical but phenotypically different variants were also found. Hence, the analyses included 13 isolates. No capsular serotype was found to be significantly more frequent. Bacterial pigments were analyzed via spectrophotometry and for their hemolytic activity. Data obtained for typical absorbance spectra peaks correlated significantly with hemolytic activity. Molecular analysis of the cyl operon showed that it was conserved in all isolates. The covR sequence displayed mutations in five isolates; in one isolate, the CovR binding site to cylX was abrogated. Our results on clinical isolates support previous findings on CovR-deficient isogenic mutants, but suggest that - at least in some clinical isolates - for β-hemolysin/cytolysin and CAMP factor production, other molecular pathways may be involved.

Item Type:

Journal Article (Original Article)

Division/Institute:

05 Veterinary Medicine > Research Foci > Host-Pathogen Interaction
04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Infectiology
04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases
05 Veterinary Medicine > Department of Infectious Diseases and Pathobiology (DIP)

UniBE Contributor:

Lupo, Agnese; Ruppen, Corinne and Sendi, Parham

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

1438-4221

Publisher:

Elsevier

Language:

English

Submitter:

Annelies Luginbühl

Date Deposited:

13 Oct 2014 15:39

Last Modified:

17 Aug 2018 11:53

Publisher DOI:

10.1016/j.ijmm.2014.05.003

PubMed ID:

24933304

Uncontrolled Keywords:

Group B streptococci, Streptococcus agalactiae, Granadaene pigment, cyl operon, covS/R, β-Hemolysin

BORIS DOI:

10.7892/boris.53859

URI:

https://boris.unibe.ch/id/eprint/53859

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