Klebsiella pneumoniae subsp. pneumoniae

The German microbiologist Carl Friedländer described these bacteria as diplococci, first in 1883 as the causative agent of a rare form of pneumonia(Friedländer pneumonia). The genus Klebsiella is named after Edwin Klebs, a German bacteriologist.

Klebsiella pneumoniae subsp. pneumoniae are gram-negative, predominantly aerobic, facultatively anaerobic, sporeless, immobile rods 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.

The genus Klebsiella in the order Enterobacterales contains several species of human medical importance in the family Enterobatericeae. The species Klebsiella pneumoniae is further subdivided into 3 subspecies. This subdivision is based on features of pathogenesis but not on sufficient distinctness of DNA sequence.

• Klebsiella pneumoniae subsp. ozaenae (Abel 1893); the pathogen is the cause of 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 species live in soil, water and on cereals. Klebsiella pneumoniae is medically relevant as a resident of the gastrointestinal tract. In the intestine, Klebsiella pneumoniae has the ability to survive for a long time without symptoms. The bacterium is transmitted both from person to person, but also through contact with contaminated surfaces. Its resilience, rapid multiplication ability and resistance to antibiotics make Klebsiella pneumoniae a real problem. For example, Klebsiella pneumoniae is resistant to penicillin.

As a pathogen of hospital-acquired infectious diseases, K. pneumoniae, in addition to K. aerogenes, is of particular importance, especially when multi-resistant bacterial strains are involved.

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 marked increase in the virulence of the bacterium.

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 Klebsiaceae (also 4-MRGN) have been repeatedly described.

The detection of germs is generally problem-free and is carried out exclusively by culture. Further differentiation can be made by checking the metabolic performance (so-called coloured series) or by means of the MALDI-TOF method.

Klebsiella pneumoniae and autoimmune diseases: There are studies indicating thatIgA antibodies directed against Klebsiella pneumoniaecross-react with structures of the human cell surface protein HLA-B27. HLA-B27 regulates important functions of the human immune system. Klebsiella pneumoniae is suspected of triggering autoimmune reactions such as ankylosing spondylitis via this mechanism.

Klebsiella pneumoniae is naturally resistant to benzylpenicillin and aminobenzlypenicillins. 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. Relebactam, an intravenously administered inhibitor of class A and C beta-lactamases, is recommended if the germ develops broad resistance.

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).

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