Klebsiella Pneumonia

Article Author:
John Ashurst
Article Editor:
Adam Dawson
11/22/2019 9:38:57 AM
PubMed Link:
Klebsiella Pneumonia


In 1882, Carl Friedlander first described Klebsiella pneumoniae as an encapsulated bacillus after isolating the bacterium from the lungs of those who had died from pneumonia. Originally named Friedlander's bacillus, it was not until 1886 when the bacterium garnered the name Klebsiella. Klebsiella pneumoniae is a gram-negative, encapsulated, non-motile bacterium that is found in the environment and has been associated with pneumonia in the alcoholic and diabetic patient population. The bacterium typically colonizes human mucosal surfaces of the oropharynx and gastrointestinal (GI) tract. Once the bacterium enters the body, it can display high degrees of virulence and antibiotic resistance. Today, K. pneumoniae pneumonia is considered the most common cause of hospital-acquired pneumonia in the United States and the organism accounts for 3% to 8% of all nosocomial bacterial infections.[1][2]


Klebsiella pneumoniae is part of the Enterobacteriaceae family and is described as a gram-negative, encapsulate and non-motile bacterium. Virulence of the bacterium is provided by a wide array of factors that can lead to infection and antibiotic resistance. The polysaccharide capsule of the organism is the most important virulence factor and allows the bacteria to evade opsonophagocytosis and serum killing by the host organism. To date, 77 different capsular types have been studied, and those Klebsiella species without a capsule tend to be less virulent. A second virulence factor is lipopolysaccharides that coat the outer surface of a gram-negative bacteria. The sensing of lipopolysaccharides release an inflammatory cascade in the host organism and has been shown to be a major culprit of the sequela in sepsis and septic shock. Another virulence factor, fimbriae, allows the organism to attach itself to host cells. Siderophores are another virulence factor that is needed by the organism to cause infection in hosts. Siderophores acquire iron from the host to allow propagation of the infecting organism.[3][4]

Klebsiella pneumoniae is one of a handful of bacteria that is now experiencing a high rate of antibiotic resistance secondary to alterations in the core genome of the organism. Alexander Fleming first discovered resistance to beta-lactam antibiotics in 1929 in gram-negative organisms. Since that time, K. pneumoniae has been well studied and has been shown to produce a beta-lactamase that causes hydrolysis of the beta-lactam ring in antibiotics. Extended beta-lactamase (ESBL) K. pneumoniae was seen in Europe in 1983 and the United States in 1989. ESBLs can hydrolyze oxyimino cephalosporins rending third-generation cephalosporins ineffective against treatment. Due to this resistance, carbapenems became a treatment option for ESBL. However, of the 9000 infections reported to the Centers for Disease Control and Prevention (CDC) due to carbapenem-resistant Enterobacteriaceae in 2013, approximately 80% were due to K. pneumoniae. Carbapenem resistance has been linked to an up-regulation in efflux pumps, an alteration of the outer membrane, and increases production in ESBL enzymes in the organism.


Humans serve as the primary reservoir for K. pneumoniae. In the general community, 5% to 38% of individuals carry the organism in their stool and 1% to 6% in the nasopharynx. However, higher rates of colonization have been reported in those of Chinese ethnicity and those who experience chronic alcoholism. In hospitalized patients, the carrier rate for K. pneumoniae is much higher than that found in the community. In one-study, carrier rates as high as 77% can be seen in the stool of those hospitalized and is felt to be related to the amount of antibiotics that are being given.[5][6]

Pneumonia caused by K. pneumoniae can be broken down into two categories: community-acquired or hospital-acquired pneumonia.  Although community-acquired pneumonia is a fairly common diagnosis, infection with K. pneumoniae is rather uncommon. In the western culture it is estimated that approximately 3% to 5% of all community-acquired pneumonia is related to an infection caused by K. pneumoniae, but in developing countries such as Africa, it can account for approximately 15% of all cases of pneumonia. Overall, K. pneumoniae accounts for approximately 11.8% of all hospital-acquired pneumonia in the world. In those who develop pneumonia while on a ventilator, between 8% to 12% are caused by K. pneumoniae while only 7% occur in those patients who are not ventilated.

History and Physical

The clinical manifestations of pneumonia caused by K. pneumoniae are similar to those seen in community-acquired pneumonia. Patients may present with a cough, fever, pleuritic chest pain and shortness of breath. One stark difference between community-acquired pneumonia caused by Streptococcus pneumoniae and K. pneumoniae is the type of sputum produced. The sputum produced by those with S. pneumoniae is described as “blood tinged” or “rust-colored,” however the sputum produced by those infected by K. pneumoniae is described as “currant jelly.” The reason for this is that K. pneumoniae causes significant inflammation and necrosis of the surrounding tissue.


Laboratory analysis will typically show leukocytosis and is this alone is unable to aid the clinician in diagnosing the organism that caused a patient’s pneumonia. Chest radiograph, however, can aid the physician in narrowing their differential diagnosis to include K. pneumoniae as a cause for the patient’s condition. Pneumonia caused by K. pneumoniae typically causes a lobar infiltrate that is in the posterior aspect of the right upper lung. K. pneumoniae infections rarely cause lung abscesses in those with pneumonia but can commonly be associated with empyema. Another non-specific sign of K. pneumoniae on chest radiograph is the bulging fissure sign. This is related to the large amount of infection and inflammation that the organism can cause. Although these are findings can be used to aid the clinician in narrowing their differential diagnosis, they should not be thought of as indicative of pneumonia caused by K. pneumoniae. In the setting of pneumonia, infection with K. pneumoniae is confirmed by either sputum culture analysis or blood culture analysis.[7][8]

Treatment / Management

Given the low occurrence of K. pneumoniae pulmonary infections in the community, treatment of pneumonia should follow standard guidelines for antibiotic therapy. Once infection with K. pneumoniae is either suspected or confirmed, antibiotic treatment should be tailored to local antibiotic sensitivities. Current regimes for community-acquired K. pneumoniae pneumonia include a 14-day treatment with either a third or fourth generation cephalosporin as monotherapy or a respiratory quinolone as monotherapy or either of the previous regimes in conjunction with an aminoglycoside. If the patient is penicillin allergic, then a course of aztreonam or a respiratory quinolone should be undertaken. For nosocomial infections, a carbapenem can be used as monotherapy until sensitivities are reported.[9][10][11]

When ESBL is diagnosed, carbapenem therapy should be initiated due to its rate of sensitivity across the globe. When CRE is diagnosed, infectious disease consultation should be obtained to guide treatment. Several antibiotic options to treat CRE include antibiotics from the polymyxin class, tigecycline, fosfomycin, aminoglycosides or dual therapy carbapenems. Combination therapy of two or more of the agents as mentioned earlier may decrease mortality as compared to monotherapy alone.

Differential Diagnosis

The differential diagnosis for pneumonia caused by K. pneumoniae should include all organisms that typically cause community-acquired and hospital-acquired pneumonia. Other things to consider include tuberculosis, Aspergillus infection, cancer, and acute respiratory distress syndrome (ARDS).


Pneumonia caused by K. pneumoniae can be complicated by bacteremia, lung abscesses, and the formation of an empyema.

Pearls and Other Issues

  • Klebsiella pneumonia is a gram-negative bacteria that typically cause nosocomial infections and shows a great deal of antibiotic resistance.
  • Radiograph findings should not be used to make a diagnosis of Klebsiella pneumoniae infection definitively. 
  • “Currant jelly” sputum is a hallmark of infection with Klebsiella pneumoniae.
  • K. pneumoniae infections can carry a high degree of antibiotic resistance and lead to a significant amount of patient mortality.

Enhancing Healthcare Team Outcomes

Klebsiella pneumonia is a serious infection, and even with adequate treatment, the mortality rates remain high. This infection is best looked after an interprofessional team that includes an infectious disease expert, pharmacists, nurses, intensivist, dietitian, pulmonologist and respiratory therapist. Nurses who look after these patients should maintain strict infection control protocols to prevent the spread of the organism. Hand washing is crucial for both medical personnel and visitors. Nurses should only ensure that only devices are only used once to minimize transmission from contaminated devices. The pharmacist should ensure that empirical antibiotic prescribing is not carried out, as this only leads to the development of drug resistance. Since many of these patients are frail, a dietary consult should be sought to optimize the calorie intake. Finally, since many of these patients are bedridden, a physical therapy consult should be considered to help with mobility and prevent stiffness of the joints.[6][12] (Level V)


Klebsiella pneumonia usually signals a grim prognosis. Even with optimal therapy, this infection of the lung carries a mortality of 30-50%. The prognosis is usually worse in diabetics, the elderly and those who are immunocompromised. Even those who survive, they often have residual impaired lung function, and recovery can take months. [13][14](Level V)


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