Klebsiella

Last updated on: 27.03.2021

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History
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Trevisan 1885; the genus Klebsiella is named after Edwin Klebs, a German bacteriologist.

Definition
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Klebsiella are gram-negative, predominantly aerobic, facultatively anaerobic, sporeless, immobile rods that are surrounded by a mucus capsule (glycocalyx). Typical of Klebsiella is a biofilm that forms on the colonies. Klebsiellae are chemoorganotrophs, i.e. they break down organic substances for energy production. In the oxic environment, they resort to oxidative energy metabolism. They oxidize organic substances to carbon dioxide and water. Under anoxic conditions, they use 2,3-butanediol fermentation for energy production.

Classification
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The genus Klebsiella in the order Enterobacterales contains several species of human medical importance in the family Enterobatericeae:

Klebsiella pneumoniae (the further subdivision of Klebsiella pneumoniae into the three subspecies listed here is based on features of pathogenesis rather than sufficient DNA sequence distinctness).

  • Klebsiella pneumoniae subsp. ozaenae (Abel 1893); the pathogen causes chronic atrophic rhinitis (Ozäna).
  • Klebsiella pneumoniae subsp. pneumoniae (Schroeter 1886)
  • Klebsiella pneumoniae subsp. rhinoscleromatis (Trevisan 1887); the pathogen is the trigger of rhinoscleroma, a granulomatous inflammation of the nasal mucosa.

Klebsiella aerogenes

Klebsiella alba

Klebsiella oxytoca (Flügge 1886)

Klebsiella granulomatosis (primarily described by Aragão & Vianna 1913 as Calymmatobacterium granulomatis, later by Anderson et al. 1944 as Donovania granulomatis; causative agent of granuloma inguinale (Donovanosis). Now placed in the genus as K. granulomatis.

Distinguished from the Klebsiellen are:

  • Raouletella ornithinologica
  • Raouletella terringena
  • Raouletella planticola

Occurrence
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Klebsiella species live in soil, water and on cereals. Of the Klebsiella species, Klebsiella granulomatis as the causative agent of granuloma inguinale, Klebsiella pneumoniae and Klebsiella aerogenes are medically relevant as inhabitants of the gastrointestinal tract. Klebsiella has the ability to survive in the intestine for a long time without symptoms. The bacterium is transmitted both from person to person, but also through contact with contaminated surfaces. Its hardiness, rapid multiplication ability and resistance to antibiotics make Klebsiella pneumoniae a real problem.

Klebsiella granulomatosis is also found in the intestine and can be transmitted by autoinoculation or during sexual intercourse. This STD (sexually transmitted disease-Granulomainguinale) occurs mainly in tropical countries and there among people in poor social conditions, malnutrition and sexual risk behavior.

All Klebsiella species are insensitive (resistant) to penicillin. As pathogens of hospital-acquired infectious diseases, K. pneumoniae, in addition to K. aerogenes, is of particular importance, especially when multi-resistant bacterial strains are involved.

Pathophysiology
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Virulence factors: Klebsiella pneumoniae has several virulence factors:

  • Capsule formation (glycocalyx): the capsule protects against phagocytosis and interferes with the complement system involved in the defense against microorganisms.
  • Adhesins: they allow attachment to host cells. Some adhesins of Klebsiella pneumoniae act simultaneously as hemagglutinins.
  • Fimbriae (pili): formation of type 1 and type 3 fimbriae. Type 1 fimbriae attach to human epithelial cells (e.g. in intestine or urinary tract). Type 3 fimbriae attach to endothelial cells, epithelial cells of the pulmonary alveoli and the urinary tract; furthermore to collagen type V.
  • Lipopolysaccharides (LPS): LPS of the outer membrane act as antigens, the outwardly directed polysaccharide chains are called O-antigens. Klebsiella pneumoniae expresses 9 different O antigens, with O1 being the most abundant. The O antigens also interfere with the complement system response cascade.
  • Bacterial siderophores are also important for pathogenicity. They serve to supply cells with iron ions essential for metabolism by binding Fe3+ ions.
  • Enterobactin: K. pneumoniae produces enterobactin (enterochelin), a toxin whose expression leads to a markedly increased virulence of the bacterium.

Clinical picture
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Klebsiellae are facultative pathogens. About 3-5% of the population are carriers of Klebsiella pneumoniae without becoming ill. However, persons with a weakened immune system (premature babies) may develop severe diseases. Depending on where the bacterium settles, the infections turn out very differently.

Klebsiella pneumoniae and Klebsiella oxytoca can cause pneumonia, lung abscesses, pleurisy, urinary tract infections, cholangitis; cholecystitis; meningitis, osteomyelitis, endocarditis, sepsis, peritonitis, and intra-abdominal abscesses. Nosocomial outbreaks with multidrug-resistant Klebsiella (including 4-MRGN) have been repeatedly described.

Klebsiella pneumoniae subsp. ozaenae is the trigger of chronic atrophic rhinitis(ozaena), Klebsiella pneumoniae subsp. rhinoscleromatis is the trigger of rhinoscleroma, Klebsiella granulomatosis is the trigger of donovanosis (granuloma inguinale).

Diagnostics
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Germ detection is generally straightforward and is performed exclusively by culture (note: Klebsiella granulomatosis cannot be cultured). Further differentiation can be made by checking the metabolic performance(so-called coloured series) or by means of the MALDI-TOF method.

Therapy
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There is a natural resistance benzylpenicillin and aminopenicillins. In addition to these natural resistances, there are other acquired resistances that further complicate treatment. Tigecycline, polymyxins (e.g., colistin), and ceftazidime-avibactam have the highest in vitro activity. In case of broad development of resistance of the germ, Relebactam an intravenously administered inhibitor of class A and C beta-lactamases is recommended.

Note(s)
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Resistance: The increasing resistance of Klebsiella pneumoniae worldwide is mainly induced by plasmid-encoded ESBL and carbapenemases. The highest prevalence is found in Eastern Europe and Asia and among nosocomial isolates. The prevalence of resistance to fluoroquinolones and ESBL strains in Germany is approximately 17%. The resistance rate against meropenem is 1-2 %. Approximately 6 % of all strains show combined resistance to quinolones, 3rd generation cephalosporins and aminoglycosides, in Europe the average is 20.5 % (as of 2020).

Klebsiella's return" was the headline of an article in "Die Zeit" about the return of the bacterium in the premature and newborn ward of Bremen's Klinikum Mitte. Already in 2011, three children died there from the intestinal bacterium. The ward had to close temporarily as a result. Infection of premature babies with Klebsiella is no exception.

Literature
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  1. Russo TA et al (2019) Hypervirulent Klebsiella pneumoniae. Clin Microbiol Rev. 32:e00001-19.
  2. Siu LK et al (2012) Klebsiella pneumoniae liver abscess: a new invasive syndrome. Lancet Infect Dis 12:881-887.
  3. Wyres KL et al (2020) Population genomics of Klebsiella pneumoniae. Nat Rev Microbiol 18: 344-359.
  4. Xu L et al (2017) Systematic review and meta-analysis of mortality ofpatients infected with carbapenem-resistant Klebsiella pneumoniae. Ann Clin Microbiol Antimicrob 16:18. doi: 10.1186/s12941-017-0191-3.
  5. Zhang L et al. (2018) The association of HLA-B27 and Klebsiella pneumoniae in ankylosing spondylitis: A systematic review. Microb Pathog 117:49-54.

Last updated on: 27.03.2021