Klebsiella pneumoniae

Klebsiella pneumoniae is a rod-shaped bacterium that is Gram-negative, non-motile, and encapsulated. It ferments lactose, grows without oxygen, and appears as a mucoid colony on MacConkey agar. Though it normally lives harmlessly in the mouth, skin, and intestines, it can cause serious damage if aspirated into the lungs, destroying alveoli and producing a bloody, jelly-like sputum that may be brownish or yellow. Among the Klebsiella genus in the Enterobacteriaceae family, it is the most important in hospitals, where it has become a major cause of infections acquired during care. Other species, K. oxytoca and K. rhinoscleromatis, have also been found in human samples.

In nature, K. pneumoniae lives in soil. About 30% of strains can fix nitrogen in low-oxygen conditions, making them free-living diazotrophs. This nitrogen-fixation system has been studied extensively and is useful in agriculture, as the bacterium has been shown to boost crop yields. It is closely related to K. oxytoca but can be told apart because it does not produce indole and can grow on melezitose, not 3-hydroxybutyrate.

The genus was named after German microbiologist Edwin Klebs. The bacterium is also called Friedlander’s bacillus after Carl Friedländer, a German pathologist who identified it as the cause of pneumonia in people with weakened immune systems, such as those with chronic diseases or alcoholism. Pneumonia from this bacterium caught outside the hospital is sometimes called Friedländer’s pneumonia.

Outside hospitals, K. pneumoniae most often causes pneumonia, usually bronchopneumonia or bronchitis. These patients are more likely to develop lung abscesses, cavities, empyema, and pleural adhesions. Antibiotic resistance is highest in Asia. A 2016 study in Turkey found that bloodstream infections from Klebsiella have a death rate around 50%, even with treatment.

The infection typically follows aspiration, and alcoholism is a risk factor. It also commonly causes hospital-acquired urinary tract infections and affects people with COPD. In the body, the neutrophil myeloperoxidase system fights the bacteria, and oxidative inactivation of elastase plays a role. Lipopolysaccharide-binding protein helps transfer bacterial cell wall components to cells.

People with K. pneumoniae pneumonia often cough up “currant jelly” sputum and may have fever, nausea, fast heart rate, and vomiting. The infection tends to strike those with underlying conditions like alcoholism.

Diagnosis can involve blood culture, complete blood count, sputum culture, chest X-ray, and CT scan. Susceptibility testing is used to find drug-resistant strains.

Treatment relies on antibiotics such as aminoglycosides, piperacillin/tazobactam, and cephalosporins, chosen based on susceptibility testing, the patient’s health, medical history, and disease severity. The bacterium produces beta-lactamase, making it resistant to ampicillin. Many strains have acquired extended-spectrum beta-lactamase, adding resistance to carbenicillin, amoxicillin, and ceftazidime. They remain susceptible to aminoglycosides and some cephalosporins, and clavulanic acid can partly inhibit the beta-lactamase. In intensive care units, multidrug-resistant infections have led to the return of colistin, but colistin-resistant strains have appeared. In 2009, strains carrying the New Delhi metallo-beta-lactamase (NDM-1) gene, which resists the carbapenem antibiotics, were found in India and Pakistan. In Taiwan, some cases cause liver abscesses in people with diabetes, treated with third-generation cephalosporins.

A newer, more dangerous variant called hypervirulent K. pneumoniae (hvKp) has emerged. Unlike classical K. pneumoniae (cKp), which mostly infects immunocompromised patients in hospitals, hvKp can sicken healthy people and attack nearly any body site. Its genetic traits come from a large virulence plasmid and possibly other mobile elements. These strains overproduce capsule components and siderophores for iron uptake. While early studies found hvKp sensitive to antibiotics, it has since acquired resistance plasmids, becoming multidrug-resistant. Originating in Asia, it has a high death rate. It often spreads to the central nervous system and eye, causing endophthalmitis, nonhepatic abscesses, pneumonia, necrotizing fasciitis, and meningitis. A visible clue is a hypermucoviscous appearance, and a string test can help diagnose it. Because no international guidelines exist, treatment is decided case by case. HvKp can also live in the gastrointestinal tract of healthy people, helping it spread in communities.