| Klebsiella pneumoniae | |
|---|---|
| K. pneumoniae on a MacConkey agar plate. | |
| Scientific classification | |
| Kingdom: | Bacteria |
| Phylum: | Proteobacteria |
| Class: | Gamma Proteobacteria |
| Order: | Enterobacteriales |
| Family: | Enterobacteriaceae |
| Genus: | Klebsiella |
| Species: | K. pneumoniae |
| Binomial name | |
| Klebsiella pneumoniae (Schroeter 1886) Trevisan 1887 |
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Klebsiella pneumoniae is a Gram-negative, non-motile, encapsulated, lactose fermenting, facultative anaerobic, rod shaped bacterium found in the normal flora of the mouth, skin, and intestines.[1]
It is clinically the most important member of the Klebsiella genus of Enterobacteriaceae.
Seven species of the Klebsiella genus, with demonstrated similarities in DNA homology are known. These are (1) Klebsiella pneumoniae, (2) Klebsiella ozaenae, (3) Klebsiella terrigena, (4) Klebsiella rhinoscleromatis, (5) Klebsiella oxytoca, (6) Klebsiella planticola, and (7) Klebsiella ornithinolytica. Of these, K oxytoca and K rhinoscleromatis have also been demonstrated in human clinical specimens.
In recent years, klebsiellae have become important pathogens in nosocomial infections.
It is closely related to K. oxytoca from which it is distinguished by being indole-negative and by its ability to grow on both melezitose and 3-hydroxybutyrate. 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.
Members of the Klebsiella genus typically express 2 types of antigens on their cell surface. 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.[3] Both contribute to pathogenicity and form the basis for serogrouping.
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The Danish scientist Hans Christian Gram (1853–1938), developed the technique now known as Gram staining in 1884 to discriminate between K. pneumoniae and Streptococcus pneumoniae.
Klebsiella was named after the German bacteriologist Edwin Klebs (1834–1913).
Multiple-resistant Klebsiella pneumoniae have been killed in vivo via intraperitoneal, intravenous or intranasal administration of phages in laboratory tests.[4] While this treatment has been available for some time, a greater danger of bacterial resistance exists to phages than to antibiotics. Resistance to phage may cause a bloom in the number of the microbe in environment as well as among humans (if not obligate pathogenic). This is why phage therapy is only used in conjunction with antibiotics, to supplement their activity instead of replacing it altogether.[5]
K. pneumoniae can cause the disease Klebsiella pneumonia. They cause destructive changes to human lungs inflammation and hemorrhage with cell death (necrosis) that sometimes produces a thick, bloody, mucoid sputum (currant jelly sputum). Typically these bacteria gain access after a person aspirates colonizing oropharyngeal microbes into the lower respiratory tract.
As a general rule, Klebsiella infections are mostly seen 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 (COPD), Glucocorticoid therapy, Renal failure, and certain occupational exposures (such as paper mill workers). Many of these infections are obtained when a person is in the hospital for some other reason (a nosocomial infection).
The most common infection 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 high death rate of about 50% even with antimicrobial therapy. The mortality rate can be nearly 100% for persons with alcoholism and bacteremia.
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 (UTI), cholecystitis, diarrhea, upper respiratory tract infection, wound infection, osteomyelitis, meningitis, and bacteremia and septicemia. If a person has an invasive device in their body then contamination of the device becomes a risk; for example 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.
Two unusual infections of note are from Klebsiella are rhinoscleroma and ozena. Rhinoscleroma is a chronic inflammatory process involving the nasopharynx. Ozena is a chronic atrophic rhinitis that produces necrosis of nasal mucosa and mucopurulent nasal discharge.
Research conducted at King's College, London has implicated molecular mimicry between HLA-B27 and two Klebsiella surface moleculars as the cause of ankylosing spondylitis.[6]
New antibiotic resistant strains of K. pneumoniae are appearing, and it is increasingly found as a nosocomial infection.[7]
Klebsiella ranks second to E. coli for urinary tract infections in older persons. It is also an opportunistic pathogen for patients with chronic pulmonary disease, enteric pathogenicity, nasal mucosa atrophy, and rhinoscleroma. Feces are the most significant source of patient infection, followed by contact with contaminated instruments.
Infection with carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae is emerging as an important challenge in health-care settings. One of many carbapenem-resistant Enterobacteriaceae (CRE) 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.[8] In the USA, it was first described in North Carolina in 1996;[9] since then CRKP has been identified in 24 states 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, particularly among persons with prolonged hospitalization and those who are 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. The worry is that new slight mutations could result in infections for which there is very little, if anything, healthcare professionals can do to treat patients with resistant organisms.
There are a number of mechanisms of Carbapenem Resistance in Enterobacteriaceae. These include (1) Hyperproduction of ampC beta-lactamase with an outer membrane porin mutation (2) CTX-M extended-spectrum beta-lactamase with a porin mutation or drug efflux, and (3) Carbapenemase production. When bacteria such as Klebsiella pneumoniae produce an enzyme known as a carbapenemase, they are referred to as carbapenem-resistant Klebsiella pneumoniae (CRKP).[10]
Put another way, 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 minimal inhibitory concentrations (MICs) 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.
The extent and prevalence of CRKP within the environment is currently unknown. The mortality rate is also unknown but is suspected to be within a range of 12.5% to as high as 44%. The likelihood of an epidemic or pandemic in the future remains uncertain.
The Centers for Disease Control and Prevention (CDC) released guidance for aggressive infection control to combat CRKP.
Place all patients colonized or infected with CRE or 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 (CLSI),[11] to detect nonsusceptibility and carbapenemase production in Enterobacteriaceae, particularly 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 who have been cared for by the same health-care personnel).[12]
The reasons that the CDC is only recommending the detection of carbapenem resistance or carbapenemase production for Klebsiella spp. and E. coli are 1) this facilitates performing the test in the microbiology laboratory without the use of molecular methods and 2) these organisms represent the majority of CRE 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.
As with many bacteria, the recommended treatment has changed as the organism has developed resistances. Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates a plasmid as the source of the resistant genes. Klebsiella with the ability to produce extended-spectrum beta-lactamases ESBL are resistant to many classes of antibiotics. The most frequent resistances include resistance to aminoglycosides, fluoroquinolones, tetracyclines, chloram-phenicol, and sulfamethoxazole-trimethoprim.[13]
The choice of a specific antimicrobial agent or agents depends on local susceptibility patterns and on the part of the body that is 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 mono-therapy once the susceptibility pattern is known for the specific patient.
If the specific Klebsiella in a particular patient does not have antibiotic resistance, then the antibiotics used to treat such susceptible isolates include ampicillin/sulbactam, piperacillin/tazobactam, ticarcillin/clavulanate, ceftazidime, cefepime, levofloxacin, norfloxacin, gaitfloxacin, 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. 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.
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