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Bacterial prints in human infectious diseases.

Ample resources have been dedicated to studying bacterial resistance, biofilm formation, and genetic encoding of resistance, metabolism or fitness mutations. However, less is known about bacterial persister cells that display multidrug tolerance, (1) latency (1) or adaptation. (2)

Classically considered to be cellular beings that can survive and multiply without the need of host cells, bacteria have also been shown to display phenotypes leading to internalization into human cells, as is the case with Granulibacter bethesdensis in monocytes and macrophages, (3) Streptococcus pneumoniae in erythrocytes, (4) Staphylococcus aureus in epithelial or endothelial cells, (5,6) or Escherichia coli in urothelial cells. (7) The internalization of bacteria into human cells opens up numerous possibilities for them to evade the immune system and lead to persistence and, potentially, chronic infection, or relapse after an apparently successful antimicrobial therapy.

As the human body is known to be made up of ten times more bacterial cells than human cells (NIH Human Microbiome Project), (8) it becomes crucial to study the pathogenesis of microbial infection, and to identify and define 'sterile' environments in the human body--if any--as well as potential reservoirs for bacterial latency.

Blood cells play a role in clearing bacterial infection, but can also drive bacterial pathogenesis as they travel throughout the body and are ideal transport vehicles for bacteria, providing both nutrients and, at times, protection from the immune system.

To better describe the phases of bacterial infection, the triggers that lead to expression of particular bacterial phenotypes, and to single out a pathway driving chronicisation of bacterial infection, we aim to perform a study of bacterial prints in human infectious diseases, through means of semi-quantitative PCR, microbiologic identification, or microscopy techniques.

Acknowledgement This paper is partially supported by the Sectoral Operational Programme Human Resources Development (SOP HRD), financed from the European Social Fund and by the Romanian Government under the contract number POSDRU/159/1.5/S/137390.

Conflicts of interest None to declare.


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(2.) Hirschhausen N, Block D, Bianconi I, et al. Extended Staphylococcus aureus persistence in cystic fibrosis is associated with bacterial adaptation. Int J Med Microbiol 2013;303:685-92. [CrossRef] [PubMed]

(3.) Chu J, Song HH, Zarember KA, Mills TA, Gallin JI. Persistence of the bacterial pathogen Granulibacter bethesdensis in chronic granulomatous disease monocytes and macrophages lacking a functional NADPH oxidase. J Immunol 2013;191:3297-307. [CrossRef] [PubMed]

(4.) Yamaguchi M, Terao Y, Mori-Yamaguchi Y, et al. Streptococcus pneumoniae invades erythrocytes and utilizes them to evade human innate immunity. PLoS One 2013;8:e77282. [CrossRef] [PubMed] [FullText]

(5.) Sendi P, Proctor RA. Staphylococcus aureus as an intracellular pathogen: the role of small colony variants. Trends Microbiol 2009;17:54-8. [CrossRef] [PubMed]

(6.) Loffler B, Tuchscherr L, Niemann S, Peters G. Staphylococcus aureus persistence in non-professional phagocytes. Int J Med Microbiol 2014;304:170-6. [CrossRef] [PubMed]

(7.) Chen SL, Wu M, Henderson JP, et al. Genomic diversity and fitness of E. coli strains recovered from the intestinal and urinary tracts of women with recurrent urinary tract infection. Sci Transl Med 2013;5:184ra60. [CrossRef] [PubMed] [FullText]

(8.) NIH Human Microbiome Project. Accessed on: July 12, 2014. Available at:

doi: 10.11599/germs.2014.1059

Received: 31 July 2014; accepted: 20 August 2014

Oana Sandulescu, MD, Assistant Lecturer, Department of Infectious Diseases, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; National Institute for Infectious Diseases "Prof. Dr. Matei Bals", No. 1 Dr. Calistrat Grozovici street, Bucharest, 021105, Romania.
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Title Annotation:Expert opinion
Author:Sandulescu, Oana
Date:Sep 1, 2014
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