High adherence and biofilm formation were positively correlated with bacterial surface hydrophobicity, type 3 fimbriae expression but not with type 1 pili expression and were not dependent upon the strain's origin. The K. pneumoniae CF3051 reference strain expressing only type 1 fimbriae adhered slightly to glass and polypropylene and did not form biofilm on polystyrene. K. pneumoniae IA565 and CF3097 reference strains producing type 1 and type 3 fimbriae showed efficient adherence to both glass and polypropylene and biofilm formation on polystyrene. Moreover, transformation of the afimbriated, weakly-adherent CF3172 strain with the recombinant pFK10 plasmid carrying the mrk gene cluster resulted in type 3 fimbriae expression, increased surface hydrophobicity, increased adherence to abiotic surfaces and biofilm formation. Thus, type 3 pili constitute the main K. pneumoniae adhesive factor, facilitating adherence and biofilm formation on abiotic surfaces of strains of different origins.

Evaluation of Biofilm Formation Among Klebsiella pneumoniae Isolates and Molecular Characterization by ERIC-PCR

The role of the LPS O side chain in bacterium-cell interactions and cytokine production still remains unclear. However, for mo-DCs exposed to LPS-deficient mutants, in particular the ΔwecA strain, which was barely affected in CPS synthesis, a clear increase in cytokine production was observed. It is therefore likely that the LPS O antigen per se plays a specific role in DC activation.

This observation, combined with the decrease in DC-SIGN previously observed, confirmed that K. pneumoniae CPS can impair the host immune response, probably allowing the bacteria to avoid the host defense and thus to multiply more easily. Yoshida et al. previously found that deletion of CPS increases the levels of TNF-α and IL-6 in bronchoalveolar lavage fluid of mice infected with K. pneumoniae strains, thus allowing a more efficient immune response and a decrease in murine mortality (47).

. Theguideline panel agreed that the use of local antibiograms to in-form antibiotic selection is the preferred approach to initiatingearly appropriate antibiotic coverage while avoiding superfluoustreatment

Clinical Infectious DiseasesIDSAGUIDELINEManagement of Adults With Hospital-acquired andVentilator-associated Pneumonia: 2016 Clinical PracticeGuidelines by the Infectious Diseases Society of Americaand the American Thoracic Society

They are responsible for destructive changes to human lungs inflammation and hemorrhage with cell death, necrosis that sometimes produces a thick, bloody, mucoid sputum .

First, the presence of cell wall receptors enables K. pneumoniae to attach to the host cell, thereby altering the bacterial surface so that phagocytosis by polymorphonuclear leukocytes and macrophages is impaired and invasion of the non-phagocytic host cell is facilitated. Second, invasion of the host cell is also facilitated by the large polysaccharide capsule surrounding the bacterial cell; in addition this capsule acts as a barrier and protects the bacteria from phagocytosis. Third, K. pneumoniae produces an endotoxin that appears to be independent of factors that determine receptors and capsular characteristics.

cell wall receptors, capsular polysaccharide, and endotoxin

Klebsiella Infections Medication

Antibiotics

Infectious Diseases Society of America/AmericanThoracic Society Consensus Guidelines on theManagement of Community-Acquired Pneumoniain Adults

They have no specific growth requirements and grow well on standard laboratory media, but grow best between 35 and 37 °C and at pH 7.2.

Treatment is with 3rd-generation cephalosporins, cefepime, carbapenems, fluoroquinolones, piperacillin/tazobactam, or aminoglycosides.

Symptoms

On an agar medium which included ornithine, raffinose, and Koser citrate, K. pneumoniae strains grew as yellow mucoid colonies at 24 h and there was some increase in colony size at 48 h.

The growth and appearance of these bacteria were not influenced by pH changes over a pH range of 5.2 to 6.4.

In this review, we summarize the current “state of the art” of carbapenem antibiotics and their role in our antimicrobial armamentarium

among Klebsiella pneumoniae isolates ESBL producers increased from 1.5% to 4.0%

Discussion

Those who are living in long-term care facilities or are currently hospitalized and breathing with mechanical ventilators are at even higher risk of developing a lung infection from Klebsiella.

Empiric treament of severe nosocomial infections in critically ill patients or in ICU

Effective therapy for severe community acquired K. pneumoniae pneumonia consists of empiric treatment with coverage against Gram negative organisms, aggressive ventilation, and clinical and radiologic surveillance for surgically treatable entities such as pulmonary gangrene, lung abscess and empyema (111, 141, 180). Third generation cephalosporins or quinolones would provide coverage against most community acquired K. pneumoniae. Macrolides (including azithromycin) have no useful activity against K. pneumoniae. The superiority of combinations of third generation cephalosporins and aminoglycosides has been demonstrated in one study (111) but not in others (129, 131). The clinical outcome when chloramphenicol and aminoglycosides are used in combination has been poor (118).

Critically ill patients with nosocomial Klebsiella bacteremia should probably be treated with antibiotics active against ESBL producers until the absence of an ESBL is definitively established.

Selection of antimicrobial therapy for Klebsiella bacteremia should be based on local susceptibility patterns of isolates causing bacteremia. In particular, the likelihood that an isolate may be an ESBL producer is an important consideration.

Figure 1. . Klebsiella pneumoniae antimicrobial drug resistance, United States, 1998–2010. ATM, aztreonam; SXT, trimethoprim/sulfamethoxazole; CAZ, ceftazidime; CIP, ciprofloxacin; TET, tetracycline; TOB, tobramycin; TZP, piperacillin/tazobactam; CPM, cefepime; AMK, amikacin; IPM, imipenem. Ceftriaxone and gentamicin were not included for better data presentation.

Figure 2. . Prevalence of antimicrobial cross-resistance among imipenem-resistant Klebsiella pneumoniae isolates, United States, 2010. TET, tetracycline; AMK, amikacin; GEN, gentamicin; CPM, cefepime; SXT, trimethoprim/sulfamethoxazole; CRO, ceftriaxone; TOB, tobramycin; CIP, ciprofloxacin; TZP, piperacillin/tazobactam; CAZ, ceftazidime; ATM, aztreonam.

8% of Klebsiella spp. isolates were carbapenem resistant in

specific for ferric iron and thus supply iron to the bacterial cells

54Journal of Thi-Qar University No.4 Vol.3 Mar/2008K.pneumoniaehave many virulence factors that make it pathogenicity, these factors are :

Infection with carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae is emerging as an important challenge in health-care settings.[11] One of many CREs is carbapenem-resistant Klebsiella pneumoniae (CRKP). Over the past 10 years, a progressive increase in CRKP has been seen worldwide; however, this new emerging nosocomial pathogen is probably best known for an outbreak in Israel that began around 2006 within the healthcare system there.

Klebsiella pneumoniae is a Gram-negative, nonmotile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium. It appears as a mucoid lactose fermenter on MacConkey agar.

If the specific Klebsiella in a particular patient does not show antibiotic resistance, then the antibiotics used to treat such susceptible isolates include ampicillin/sulbactam, piperacillin/tazobactam, ticarcillin/clavulanate, ceftazidime, cefepime, levofloxacin, norfloxacin, gatifloxacin, moxifloxacin, meropenem, and ertapenem. Some experts recommend the use of meropenem for patients with ESBL-producing Klebsiella. The claim is that meropenem produces the best bacterial clearing.

A number of mechanisms cause carbapenem resistance in the Enterobacteriaceae. These include hyperproduction of ampC beta-lactamase with an outer membrane porin mutation, CTX-M extended-spectrum beta-lactamase with a porin mutation or drug efflux, and carbapenemase production. The most important mechanism of resistance by CRKP is the production of a carbapenemase enzyme, blakpc. The gene that encodes the blakpc enzyme is carried on a mobile piece of genetic material (a transposon; the specific transposon involved is called Tn4401), which increases the risk for dissemination. CRE can be difficult to detect because some strains that harbor blakpc have minimum inhibitory concentrations that are elevated, but still within the susceptible range for carbapenems. Because these strains are susceptible to carbapenems, they are not identified as potential clinical or infection control risks using standard susceptibility testing guidelines. Patients with unrecognized CRKP colonization have been reservoirs for transmission during nosocomial outbreaks. Depending on the type of infection and the mode of infectivity, cells of Klebsiella spp. may adhere and attack upper respiratory tract epithelial cells, cells in gastrointestinal tract, endothelial cells, or uroepithelial cells, followed by colonization of mucosal membranes (phac-aspc.gc.ca).[15]

Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates plasmids as the primary source of the resistance genes.[9] Klebsiella species with the ability to produce extended-spectrum beta-lactamases (ESBL) are resistant to many classes of antibiotics. The most frequent are resistance to aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and trimethoprim/sulfamethoxazole.[10]

are seen mostly in people with a weakened immune system

alcoholism

It naturally occurs in the soil,

Gram-negative, nonmotile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium

As a general rule, Klebsiella infections are seen mostly in people with a weakened immune system. Most often, illness affects middle-aged and older men with debilitating diseases. This patient population is believed to have impaired respiratory host defenses, including persons with diabetes, alcoholism, malignancy, liver disease, chronic obstructive pulmonary diseases, glucocorticoid therapy, renal failure, and certain occupational exposures (such as papermill workers). Many of these infections are obtained when a person is in the hospital for some other reason (a nosocomial infection). Feces are the most significant source of patient infection, followed by contact with contaminated instruments.[citation needed]

ceftazidime (92-95%), ceftriaxone (96-98%), cefotaxime (96%), piperacillin-tazobactam (90-97%), imipeneum (98-100%), gentamicin (95-96%), amikacin (98-99%), triethoprimsulfamethoxazole (SXT) (88-90%).

Selected Virulence Factors

7-14% of pneumonia,

who have diabetes or who suffer from alcoholisms due to a weakened immune system

Capsular Polysaccharide and Lipopolysaccharide O Side Chain

Hospital-acquired infections rely on the urinary tract, lower respirator tract, biliary tract, and surgical wounds to set up colonization

Klebsiella infections are most well-known in hospitals spread through person-to-person contact by contaminated hands of surrounded people in the hospitals, whether it be an employee or a patient. Klebsiella is spread very easily and rapidly, but not through the air. Healthcare settings are most vulnerable to Klebsiella infections due to the nature of procedures that allow easy access of bacteria into the body. Patients who are on ventilators, catheters, or surgery wounds are highly prone to catching this deadly infection

pH range of 5.2 to 6.4

Klebsiellae are lactose-fermenting, urease-positive, and indole-negative organisms,

They have no special culture requirements. Most species can use citrate and glucose as sole carbon sources; thus, they grow well on most ordinary media.

Several virulence factors have been demonstrated to mediate K. pneumoniae infectivity and include, but are most likely not limited to, adherence factors, capsule production, lipopolysaccharide presence, and siderophore activity.

The results of this study indicate that resistance to hLF1-11 and colistin are not strictly associated, and suggest an hLF1-11-induced sensitizing effect of K. pneumoniae to antibiotics, especially to hydrophobic antibiotics, which are normally not effective on Gram-negative bacteria. Altogether, these data indicate that hLF1-11 in combination with antibiotics is a promising candidate to treat infections caused by MDR-K. pneumoniae strains.

When bacteria such as Klebsiella pneumoniae produce an enzyme known as a carbapenemase (referred to as KPC-producing organisms), then the class of antibiotics called carbapenems will not work to kill the bacteria and treat the infection. Klebsiella species are examples of Enterobacteriaceae, a normal part of the human gut bacteria, that can become carbapenem-resistant. CRE, which stands for carbapenem-resistant Enterobacteriaceae, are a family of germs that are difficult to treat because they have high levels of resistance to antibiotics. Unfortunately, carbapenem antibiotics often are the last line of defense against Gram-negative infections that are resistant to other antibiotics.

Klebsiella bacteria have developed antimicrobial resistance, most recently to the class of antibiotics known as carbapenems(https://www.cdc.gov/hai/organisms/cre/index.html).

Drug-resistant Klebsiella

Pathophysiology

Tests for identification of Klebsiella pneumoniae

It is also an opportunistic pathogen for patients with chronic pulmonary disease, enteric pathogenicity, nasal mucosa atrophy, and rhinoscleroma.

Klebsiella pneumoniae is a Gram-negative, non-motile, encapsulated, lactose fermenting, facultative anaerobic, rod shaped bacterium found in the normal flora of the intestines