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Klebsiella Pneumoniae: Virulence, Biofilm and Antimicrobial Resistance

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Klebsiella Pneumoniae: Virulence, Biofilm and Antimicrobial Resistance Divya Bharathi PIDJ ESPID REPORTS AND REVIEWS PIDJ-217-384 CONTENTS Klebsiella pneumoniae Vitulence, Biofilm and Resistance in Klebsiella EDITORIAL BOARD Piperaki et al Editor: Delane Shingadia Board Members David Burgner (Melbourne, Cristiana Nascimento-Carvalho George Syrogiannopoulos XXX Australia) (Bahia, Brazil) (Larissa, Greece) Kow-Tong Chen (Tainan,Taiwan) Ville Peltola (Turku, Finland) Tobias Tenenbaum (Mannhein, Germany) Luisa Galli (Florence, Italy) Emmanuel Roilides (Thessaloniki, Marc Tebruegge (Southampton, UK) Steve Graham (Melbourne, Pediatr Infect Dis J Greece) Marceline Tutu van Furth (Amsterdam, Australia) Ira Shah (Mumbai, India) The Netherlands) Lippincott Williams & Wilkins Klebsiella pneumoniae: Virulence, Biofilm and Antimicrobial Hagerstown, MD Resistance Evangelia-Theophano Piperaki, MD, PhD,* George A. Syrogiannopoulos, MD, PhD,† Leonidas S. Tzouvelekis, MD, PhD,* and George L. Daikos, MD, PhD‡ Key Words: Klebsiella pneumoniae, virulence, ingitis in premature neonates and infants as the immune response through cytokine and biofilm, resistance well as serious infections in immunocompro- chemokine production (Fig. 1). Among the mised and malnourished children, whereas effector cells that are recruited first to the in the community, K. pneumoniae is a com- infection site are the neutrophils. Impor- mon cause of urinary tract infections among tant mediators involved in this process are lebsiella pneumoniae is a ubiquitous immunocompetent children. interleukin (IL)-8 and IL-23, which induces K Gram-negative encapsulated bacterium In recent years, most K. pneumoniae production of IL-17 that promotes granu- that resides in the mucosal surfaces of mam- infections are caused by strains termed “clas- lopoietic response.6-7 IL-12 also amplifies the mals and the environment (soil, water, etc.). sic” K. pneumoniae (cKp). These strains expression of IL-17 through production of In humans, K. pneumoniae colonizes the persist in hospital environments and cause interferon-gamma. Other factors participat- gastrointestinal tract and less frequently the infections in debilitated patients. cKp strains ing in the immune response are the produc- 2017 nasopharynx, whence it gains entry to the cir- appear to be distinct from hypervirulent K. tion of IL-1β via activation of the NOD-like culation and other tissues causing infection. pneumoniae (hvKp), a variant that was first receptor pyrin domain containing (NLRP3) In the pre-antibiotic era, K. pneumoniae was described in the Asian Pacific Rim to cause inflammasome pathway and the production an important cause of community-acquired community-acquired, invasive and metastatic of other pro-inflammatory cytokines such as pneumonia, especially in alcoholics and dia- 8 Copyright © 2017 Wolters Kluwer Health, Inc. All rights infections, including liver abscess, endoph- tumor necrosis factor-a (TNF-α) and IL-6. betics. In the antibiotic era, K. pneumoniae thalmitis, meningitis and septic arthritis in The specific factors that K. pneumoniae reserved. became established in hospitals as a leading diabetics and immunocompetent young indi- employs to circumvent the immune defenses are cause of healthcare-associated infections.1 1002 2–5 not fully elucidated. Presently, there are 4 well- In pediatric wards, it causes sepsis and men- viduals. The emergence and spread of new multidrug-resistant (MDR) clones and the characterized virulence factors, namely the fim- international dissemination of hvKp strains briae, the capsule, the lipopolysaccharide (LPS) Accepted for publication May 9, 2017. and siderophores.6,9 K. pneumoniae is equipped 1005 From the *Department of Microbiology, School of have renewed interest in K. pneumoniae. Medicine, National and Kapodistrian University with adhesins, type 1 and type 3 fimbriae, which of Athens, Athens, Greece; †Department of Pedi- facilitate adherence to epithelial and immune 0891-3668 atrics, University of Thessaly, University General VIRULENCE cells as well as to abiotic surfaces (Fig. 1). Based Hospital of Larissa, Larissa, Greece; and ‡First To establish infection, K. pneumoniae Department of Medicine, National and Kapodis- on the composition of capsular polysaccharides trian University of Athens, Laikon General Hospi- must overcome mechanical and chemical (CPs) of K. pneumoniae, 78 distinct capsular 10.1097/INF.0000000000001675 tal, Athens, Greece. barriers and escape host humoral and cellular serotypes (K1 to K78) have been recognized. Of The authors have no funding or conflicts of interest innate defenses. After gaining access to the note, the vast majority of hvKp strains belong to disclose. host, the invading organisms are recognized Address for correspondence: George L. Daikos, MD, PhD, to serotypes K1 and K2. The high level of viru- The Pediatric Infectious Disease Journal First Department of Medicine, National and Kapodis- by the immune cells through the pattern lence of hvKp strains is, at least partially, due to trian University of Athens, Laikon General Hospital, recognition receptors and trigger produc- excess production of capsular material (hyper- Athens, Greece. E-mail: [email protected]. tion of various immune mediators. Central mucoviscous phenotype). Although the capsule Copyright © 2017 Wolters Kluwer Health, Inc. All 36 rights reserved. role in the innate immune response plays composition plays an important role in protect- ISSN: 0891-3668/17/3610-1002 the monocyte/macrophage system, which ing K. pneumoniae against the host immune DOI: 10.1097/INF.0000000000001675 has phagocytic capabilities and orchestrates response, it is likely that other factors contribute 10 TheThe ESPIDESPID Reports Reports and and Reviews Reviews of of Pediatric Pediatric Infectious Infectious Disease Diseases Journal series series topics, topics, authors authors and and contents contents are are chosen chosen and and approved approved independently by the Editorial Board of ESPID. October 1002 | www.pidj.com The Pediatric Infectious Disease Journal • Volume 36, Number 10, October 2017 2017 Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. The Pediatric Infectious Disease Journal • Volume 36, Number 10, October 2017 Vitulence, Biofilm and Resistance in Klebsiella FIGURE 1. Schematic presentation of K. pneumoniae virulence factors and of host innate immune response. Capsular polysaccha- rides prevent phagocytosis and block complement-mediated lysis and opsonization. The intact LPS elicits a robust inflammatory response and prevents binding of C1q to bacteria and the subsequent activation of the complement pathway. Certain strains may modify the LPS making it unrecognizable to immune cells, whereas others may use the capsule to prevent LPS detection by toll-like receptor (TLR4) receptors. K. pneumoniae is equipped with types 1 and 3 fimbriae mediating adhesion to biotic and abiotic surfaces facilitating epithelial cell invasion and biofilm formation. It also synthesises siderophores (enterobactin, aero- bactin, yersiniabactin and salmochelin) to acquire iron from the host. The monocyte/macrophage system plays a central role in the innate immune response, through phagocytosis and production of immune mediators such as cytokines and chemokines. Important mediator in this process is IL-23, that induces IL-17 production which along with IL-8 promote neutrophil recruit- ment. IL-17 expression is also amplified by IL-12 through IFN-γ. Other important cytokines are IL-1β, produced via activation of the NOD-like receptor pyrin domain-containing (NLRP3) inflammasome pathway, and other pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-α) and IL-6. Perpendicular line (───│) indicates inhibition. Adapted from Paczosa and Mecsas.6 IFN-γ, interferon-gamma. to virulence as well. Indeed, certain K. pneumo- yersiniabactin are more prevalent in hvKp than are embedded within a self-produced matrix niae strains may modify the LPS to a degree cKp.6,9 Recent data suggest that hvKp strains of extracellular polymeric substance adhere that is not recognized by the host cells and oth- have the ability to produce larger amounts and to each other and/or to a surface.13 Extracel- ers may use capsule to mask LPS from detec- biologically more active iron-acquisition mole- lular polymeric substance is a complex struc- tion by toll-like receptor (TLR4) receptors.10,11 cules than nonvirulent strains, a mechanism that ture comprising polysaccharides, proteins These modifications dampen the inflammatory may contribute to virulence and pathogenesis.12 and DNA. The most clinically significant response and decrease bacterial clearance. Also, Although the clinical manifestations of infec- K. pneumoniae biofilms are those formed the ability of K. pneumoniae to steal iron from tions caused by hvKp strains have been well on the inner surfaces of catheters and other the host is critical for its growth and replication. described, as yet there is no single reliable bio- indwelling devices. K. pneumoniae biofilms Four iron-acquisition molecules (siderophores) logic marker that distinguishes these from other may also contribute to colonization of the have been described in K. pneumoniae: entero- K. pneumoniae strains. gastrointestinal, respiratory and urinary tract bactin, yersiniabactin, salmochelin and aerobac- and the development of invasive infections tin. Enterobactin has the highest affinity for iron, especially in immunocompromised patients. is present in both classical and hypervirulent BIOFILMS Development of K. pneumoniae
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