Klebsiella pneumoniae

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Klebsiella pneumoniae
Klebsiella pneumoniae 01.png
K. pneumoniae on a MacConkey agar plate
Scientific classification
Domain: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Klebsiella
Species: K. pneumoniae
Binomial name
Klebsiella pneumoniae
(Schroeter 1886)
Trevisan 1887

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

Although found in the normal flora of the mouth, skin, and intestines,[1] it can cause destructive changes to human and animal lungs if aspirated (inhaled), specifically to the alveoli (in the lungs) resulting in bloody sputum. In the clinical setting, it is the most significant member of the Klebsiella genus of the Enterobacteriaceae. K. oxytoca and K. rhinoscleromatis have also been demonstrated in human clinical specimens. In recent years, Klebsiella species have become important pathogens in nosocomial infections.

It naturally occurs in the soil, and about 30% of strains can fix nitrogen in anaerobic conditions.[2] As a free-living diazotroph, its nitrogen-fixation system has been much-studied, and is of agricultural interest, as K. pneumoniae has been demonstrated to increase crop yields in agricultural conditions.[3]

Members of the genus Klebsiella typically express two types of antigens on their cell surfaces. The first, O antigen, is a component of the lipopolysaccharide (LPS), of which 9 varieties exist. The second is K antigen, a capsular polysaccharide with more than 80 varieties.[4] Both contribute to pathogenicity and form the basis for serogrouping.

It is closely related to K. oxytoca from which it is distinguished by being indole-negative and by its ability to grow on melezitose but not 3-hydroxybutyrate.


The genus Klebsiella was named after the German bacteriologist Edwin Klebs (1834–1913).[citation needed] Also, it is known as Friedlander's bacillum in honor of Carl Friedländer, a German pathologist, who proposed that this bacterium was the etiological factor for the pneumonia seen especially in immunocompromised individuals such as people with chronic diseases or alcoholics.

Clinical significance[edit]

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]

The most common condition caused by Klebsiella bacteria outside the hospital is pneumonia, typically in the form of bronchopneumonia and also bronchitis. These patients have an increased tendency to develop lung abscess, cavitation, empyema, and pleural adhesions. It has a death rate around 50%, even with antimicrobial therapy.

In addition to pneumonia, Klebsiella can also cause infections in the urinary tract, lower biliary tract, and surgical wound sites. The range of clinical diseases includes pneumonia, thrombophlebitis, urinary tract infection, cholecystitis, diarrhea, upper respiratory tract infection, wound infection, osteomyelitis, meningitis, and bacteremia and septicemia. For patients with an invasive device in their bodies, contamination of the device becomes a risk; for example, neonatal ward devices, respiratory support equipment, and urinary catheters put patients at increased risk. Also, the use of antibiotics can be a factor that increases the risk of nosocomial infection with Klebsiella bacteria. Sepsis and septic shock can follow entry of the bacteria into the blood.

Research conducted at King's College, London has implicated molecular mimicry between HLA-B27 and two Klebsiella surface molecules as the cause of ankylosing spondylitis.[5]

Klebsiella ranks second to E. coli for urinary tract infections in older people.[citation needed] It is also an opportunistic pathogen for patients with chronic pulmonary disease, enteric pathogenicity, nasal mucosa atrophy, and rhinoscleroma.[citation needed] New antibiotic-resistant strains of K. pneumoniae are appearing.[6]

Since the mid-1980s, hypervirulent K. pneumoniae, generally associated with the hypermucoviscosity phenotype, has emerged as a clinically significant pathogen responsible for serious disseminated infections, such as pyogenic liver abscesses, osteomyelitis, and endophthalmitis, in a generally younger and healthier population.[7]



To get a K. pneumoniae infection, a person must be exposed to the bacteria. In other words, K. pneumoniae must enter the respiratory tract to cause pneumoniae, or the blood to cause a bloodstream infection. In healthcare settings, K. pneumoniae bacteria can be spread through person-to-person contact (for example, contaminated hands of healthcare personnel, or other people via patient to patient) or, less commonly, by contamination of the environment; the role of transmission directly from the environment to patients is controversial and requires further investigation.[8] However, the bacteria are not spread through the air. Patients in healthcare settings also may be exposed to K. pneumoniae when they are on ventilators, or have intravenous catheters or wounds. Unfortunately, these medical tools and conditions may allow K. pneumoniae to enter the body and cause infection.[9]

Resistant strains[edit]

Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates plasmids as the primary source of the resistance genes.[10] Klebsiella species with the ability to produce extended-spectrum beta-lactamases (ESBL) are resistant to virtually all beta-lactam antibiotics, except carbapenems. Other frequent resistance targets include aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and trimethoprim/sulfamethoxazole.[11]

Infection with carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae is emerging as an important challenge in health-care settings.[12] 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.[13] In the USA, it was first described in North Carolina in 1996;[14] since then CRKP has been identified in 41 states;[15] and is recovered routinely in certain hospitals in New York and New Jersey. It is now the most common CRE species encountered within the United States.

CRKP is resistant to almost all available antimicrobial agents, and infections with CRKP have caused high rates of morbidity and mortality, in particular among persons with prolonged hospitalization and those critically ill and exposed to invasive devices (e.g., ventilators or central venous catheters). The concern is that carbapenem is often used as a drug of last resort when battling resistant bacterial strains. New slight mutations could result in infections for which healthcare professionals can do very little, if anything, to treat patients with resistant organisms.

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.[16]

The extent and prevalence of CRKP within the environment is currently unknown. The mortality rate is also unknown, but has been observed to be as high as 44%.[17] The Centers for Disease Control and Prevention released guidance for aggressive infection control to combat CRKP:

Place all patients colonized or infected with carbapenemase-producing Enterobacteriaceae on contact precautions. Acute-care facilities are to establish a protocol, in conjunction with the guidelines of the Clinical and Laboratory Standards Institute, to detect nonsusceptibility and carbapenemase production in Enterobacteriaceae, in particular Klebsiella spp. and Escherichia coli, and immediately alert epidemiology and infection-control staff members if identified. All acute-care facilities are to review microbiology records for the preceding 6–12 months to ensure that there have not been previously unrecognized CRE cases. If they do identify previously unrecognized cases, a point prevalence survey (a single round of active surveillance cultures) in units with patients at high risk (e.g., intensive-care units, units where previous cases have been identified, and units where many patients are exposed to broad-spectrum antimicrobials) is needed to identify any additional patients colonized with carbapenem-resistant or carbapenemase-producing Klebsiella spp. and E. coli. When a case of hospital-associated CRE is identified, facilities should conduct a round of active surveillance testing of patients with epidemiologic links to the CRE case (e.g., those patients in the same unit or patients having been cared for by the same health-care personnel).[18]

One specific example of this containment policy could be seen in Israel in 2007.[19] This policy had an intervention period from April, 2007, to May, 2008. A nationwide outbreak of CRE (which peaked in March, 2007 at 55.5 cases per 100,000 patient days) necessitated a nationwide treatment plan. The intervention entailed physical separation of all CRE carriers and appointment of a task force to oversee efficacy of isolation by closely monitoring hospitals and intervening when necessary. After the treatment plan (measured in May, 2008), the number of cases per 100,000 patient days decreased to 11.7. The plan was effective because of strict hospital compliance, wherein each was required to keep detailed documentation of all CRE carriers. In fact, for each increase in compliance by 10%, incidence of cases per 100,000 patient days decreased by 0.6. Therefore, containment on a nationwide scale requires nationwide intervention.

In the United States, the reasons the CDC is recommending the detection of carbapenem resistance or carbapenemase production only for Klebsiella spp. and E. coli are: this facilitates performing the test in the microbiology laboratory without the use of molecular methods, and these organisms represent the majority of CREs encountered in the United States. Effective sterilization and decontamination procedures are important to keep the infection rate of this antibiotic-resistant strain, CRKP, as low as possible.

In mid-August 2016, a resident of Washoe County was hospitalized in Reno due to a CRE (specifically Klebsiella pneumoniae) infection. In early September of the same year, she developed septic shock and died. On testing by CDC an isolate from the patient was found to be resistant to all 26 antibiotics available in the US, including drug of last resort colistin.[20] It is believed she may have picked up the microbe while hospitalized in India for two years due to a broken right femur and subsequent femur and hip infections.[21][22][23][24][25]

Prevent from spreading[edit]

To prevent spreading Klebsiella infections between patients, healthcare personnel must follow specific infection-control precautions,[9] which may include strict adherence to hand hygiene (preferably using an alcohol based hand rub (60-90%) or soap and water if hands are visibly soiled. Alcohol based hand rubs are effective against these Gram-negative bacilli)[26] and wearing gowns and gloves when they enter rooms where patients with Klebsiella–related illnesses are housed. Healthcare facilities also must follow strict cleaning procedures to prevent the spread of Klebsiella.[9]

To prevent the spread of infections, patients also should clean their hands very often, including:

  • Before preparing or eating food
  • Before touching their eyes, nose, or mouth
  • Before and after changing wound dressings or bandages
  • After using the restroom
  • After blowing their nose, coughing, or sneezing
  • After touching hospital surfaces such as bed rails, bedside tables, doorknobs, remote controls, or the phone[9]


K. pneumoniae can be treated with antibiotics if the infections are not drug-resistant. Infections by K. pneumoniae can be difficult to treat because fewer antibiotics are effective against them. In such cases, a microbiology laboratory must run tests to determine which antibiotics will treat the infection.[9]

As with many bacteria, the recommended treatment has changed as the organism has developed resistances. The choice of a specific antimicrobial agent or agents depends on local susceptibility patterns and on the part of the body infected. For patients with severe infections, a prudent approach is the use of an initial short course (48–72 h) of combination therapy, followed by a switch to a specific monotherapy once the susceptibility pattern is known for the specific patient.

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, ertapenem and ciprofloxacin. Some experts recommend the use of meropenem for patients with ESBL-producing Klebsiella. The claim is that meropenem produces the best bacterial clearing.

The use of antibiotics is usually not enough. Surgical clearing (frequently done as interventional radiology drainage) is often needed after the patient is started on antimicrobial agents.


Multiple drug-resistant K. pneumoniae strains have been killed in vivo by intraperitoneal, intravenous, or intranasal administration of phages in laboratory tests.[27] Resistance to phages is not likely to be as troublesome as to antibiotics as new infectious phages are likely to be available in environmental reservoirs. Phage therapy can be used in conjunction with antibiotics, to supplement their activity instead of replacing it altogether.[28]


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