Klebsiella pneumoniae in Healthcare Settings
- General Information
- How Klebsiella bacteria are spread
- Preventing Klebsiella from spreading
- Drug-resistant Klebsiella
- Treating Klebsiella infections
- What should patients do if they think they have a Klebsiella–related illness?
- What should patients do if they have been diagnosed with a Klebsiella–related illness?
- How would someone know if their Klebsiella infection is drug-resistant?
- Can a Klebsiella infection spread to the patient’s family members?
- Recommendations and Guidelines
- Infection with Panresistant Klebsiella pneumoniae: A Report of 2 Cases and a Brief Review of the Literature
- Three Klebsiella Bacteria Species Cause Life-Threatening Infections and Share Drug Resistance Genes
- What You Need to Know About a Klebsiella Pneumoniae Infection
Klebsiella pneumoniae in Healthcare Settings
Klebsiella is a type of Gram-negative bacteria that can cause different types of healthcare-associated infections, including pneumonia, bloodstream infections, wound or surgical site infections, and meningitis. Increasingly, Klebsiella bacteria have developed antimicrobial resistance, most recently to the class of antibiotics known as carbapenems. Klebsiella bacteria are normally found in the human intestines (where they do not cause disease). They are also found in human stool (feces). In healthcare settings, Klebsiella infections commonly occur among sick patients who are receiving treatment for other conditions. Patients whose care requires devices like ventilators (breathing machines) or intravenous (vein) catheters, and patients who are taking long courses of certain antibiotics are most at risk for Klebsiella infections. Healthy people usually do not get Klebsiella infections.
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How Klebsiella bacteria are spread
To get a Klebsiella infection, a person must be exposed to the bacteria. For example, Klebsiella must enter the respiratory (breathing) tract to cause pneumoniae, or the blood to cause a bloodstream infection.
In healthcare settings, Klebsiella bacteria can be spread through person-to-person contact (for example, from patient to patient via the contaminated hands of healthcare personnel, or other persons) or, less commonly, by contamination of the environment. The bacteria are not spread through the air.
Patients in healthcare settings also may be exposed to Klebsiella when they are on ventilators (breathing machines), or have intravenous (vein) catheters or wounds (caused by injury or surgery). Unfortunately, these medical tools and conditions may allow Klebsiella to enter the body and cause infection.
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Preventing Klebsiella from spreading
To prevent spreading Klebsiella infections between patients, healthcare personnel must follow specific infection control precautions (see: Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings 2007). These precautions may include strict adherence to hand hygiene and wearing gowns and gloves when they enter rooms where patients with Klebsiella–related illnesses are housed. Healthcare facilities also must follow strict cleaning procedures to prevent the spread of Klebsiella.
To prevent the spread of infections, patients also should clean their hands very often, including:
- Before preparing or eating food
- Before touching their eyes, nose, or mouth
- Before and after changing wound dressings or bandages
- After using the restroom
- After blowing their nose, coughing, or sneezing
- After touching hospital surfaces such as bed rails, bedside tables, doorknobs, remote controls, or the phone
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Some Klebsiella bacteria have become highly resistant to antibiotics. When bacteria such as Klebsiella pneumoniae produce an enzyme known as a carbapenemase (referred to as KPC-producing organisms), then the class of antibiotics called carbapenems will not work to kill the bacteria and treat the infection. Klebsiella species are examples of Enterobacteriaceae, a normal part of the human gut bacteria, that can become carbapenem-resistant.
CRE, which stands for carbapenem-resistant Enterobacteriaceae, are a family of germs that are difficult to treat because they have high levels of resistance to antibiotics. Unfortunately, carbapenem antibiotics often are the last line of defense against Gram-negative infections that are resistant to other antibiotics.
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Treating Klebsiella infections
Klebsiella infections that are not drug-resistant can be treated with antibiotics. Infections caused by KPC-producing bacteria can be difficult to treat because fewer antibiotics are effective against them. In such cases, a microbiology laboratory must run tests to determine which antibiotics will treat the infection.
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See a healthcare provider.
They must follow the treatment regimen prescribed by the healthcare provider. If the healthcare provider prescribes an antibiotic, patients must take it exactly as the healthcare provider instructs. Patients must complete the prescribed course of medication, even if symptoms are gone. If treatment stops too soon, some bacteria may survive and the patient may become re-infected. Patients must wash their hands as often as possible and follow all other hygiene recommendations.
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How would someone know if their Klebsiella infection is drug-resistant?
The healthcare provider will order laboratory tests to determine if the Klebsiella infection is drug-resistant.
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Can a Klebsiella infection spread to the patient’s family members?
If family members are healthy, they are at very low risk of acquiring a Klebsiella infection. It is still necessary to follow all precautions, particularly hand hygiene. Klebsiella bacteria are spread mostly by person-to-person contact and hand hygiene is the best way to prevent the spread of germs.
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Recommendations and Guidelines
For more information about prevention and treatment of HAIs, see the resources below:
- Siegel JD, Rhinehart E, Jackson M, Chiarello L, and the Healthcare Infection Control Practices Advisory Committee, 2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings
- Guidance for Control of Infections with Carbapenem-Resistant or Carbapenemase-Producing Enterobacteriaceae in Acute Care Facilities MMWR March 20, 2009 / 58(10);256-260
Infection with Panresistant Klebsiella pneumoniae: A Report of 2 Cases and a Brief Review of the Literature
Infections caused by carbapenemase-producing Klebsiella pneumoniae have been reported with increasing frequency, thereby limiting the choice of effective antimicrobial agents available to clinicians. This has prompted the increased use of polymyxins and tigecycline, but resistance to these agents is already emerging. We report 2 cases of infection with panresistant K. pneumoniae.
Nosocomial infections with resistant gram-negative organisms, particularly strains of Klebsiella pneumoniae, have become a significant problem at a time when there is a lack of promising new antimicrobial agents on the horizon . In response to the prevalence of extended-spectrum β-lactamases, carbapenem use increased, and carbapenem resistance soon followed. In 2001, Yigit et al. reported a novel β-lactamase termed “K. pneumoniae carbapenemase” (KPC-1) in North Carolina. Soon after, strains of KPC-producing Klebsiella species were reported in New York City and then upstate New York . We report 2 cases of infection with highly resistant, KPC-producing K. pneumoniae at a tertiary care hospital in New York City. The isolates were resistant to all antibiotic agents tested, including the carbapenems, polymyxin B, and tigecycline. To our knowledge, there have been no previously reported cases of infection due to panresistant K. pneumoniae in the United States.
Case report 1. In July 2007, a 70-year-old woman was admitted to the hospital with a urinary tract infection. She was residing in a nursing home after a recent hospitalization for pneumonia due to KPC-producing K. pneumoniae treated with tigecycline and polymyxin B. An indwelling bladder catheter had been placed at the nursing facility. During admission to the hospital, she reporting having dysuria and suprapubic pain for 2 days. A urinalysis revealed nitrites and a white blood cell count >100 cells per high-power field. Her examination was notable for a temperature of 37.4°C and suprapubic tenderness. A urine culture showed >100,000 colony-forming units (cfu) per mL of a highly resistant, KPC-producing K. pneumoniae strain. The minimum inhibitory concentration (MIC) was 4 µg/mL for tigecycline and 96 µg/mL for polymyxin B. The patient’s catheter was removed, and she began treatment with tigecycline and rifampin. She developed a rash, and the rifampin was discontinued. Her urinalysis results remained unchanged, and her urine culture again showed the presence of >100,000 cfu/mL of K. pneumoniae, which now had an MIC >8 µg/mL for tigecycline. Tigecycline was discontinued after 10 days of treatment, and the patient was discharged to home with persistent dysuria. She subsequently had spontaneous resolution of symptoms, although the last available urine culture specimen, obtained >1 year later, continued to show >100,000 cfu/mL of the panresistant K. pneumoniae.
Case report 2. In March 2008, a 67-year-old man underwent a Whipple procedure at another hospital. Postoperatively, he developed a hepatic abscess. Enterobacter cloacae and K. pneumoniae grew from cultures of samples from the liver abscess. Both organisms were resistant to carbapenem but susceptible to polymyxin B and tigecycline. He was given treatment with tigecycline and empirical treatment with daptomycin and caspofungin. The patient’s postoperative course was prolonged and complicated by multiple organ system dysfunction.
In May 2008, the patient was transferred to our institution. On the day of admission, the patient was febrile, with a temperature of 38.7°C. He arrived sedated and with mechanical ventilation via tracheostomy and an abdominal drain in place. The peripheral white blood cell count was 5.6×103 cells/mm3(neutrophil percentage, 77.1%), and the serum creatinine level was 4.2 mg/dL. Blood cultures of specimens obtained at admission showed no growth. Computed tomography of the abdomen and pelvis showed a large perihepatic abscess and a drain suboptimally positioned. On the basis of the prior culture results, daptomycin and caspofungin were discontinued from the treatment regimen, and polymyxin B was added to tigecycline. The abdominal drain was replaced, and culture specimens were sent to the laboratory.
On hospital day 5, the patient remained febrile and developed hypotension requiring vasopressor support. Cultures of samples from the hepatic abscess showed E. cloacae, K. pneumoniae, and Enterococcus faecium. Both the K. pneumoniae and the E. cloacae isolates were identified as producers of KPC by polymerase chain reaction (PCR) testing. The K. pneumoniae strain was resistant to all antibiotics tested, including tigecycline, and had an elevated MIC for polymyxin B. The E. cloacae strain was similarly resistant, with the exception of an intermediate result for tigecycline (MIC, 4 µg/mL). The patient was taken to the operating room for irrigation and debridement of infected material.
Postoperatively, the patient’s condition continued to deteriorate. Blood cultures of specimens collected on hospital day 8 grew a KPC-producing K. pneumoniae strain resistant to all tested antibiotics except polymyxin B (MIC, 0.75 µg/mL). Daily blood cultures continued to grow K. pneumoniae. On hospital day 12, blood cultures showed a K. pneumoniae strain with a MIC for polymyxin B of 12 µg/mL. Over the next few days, the patient’s condition worsened despite supportive care and continuation of treatment with tigecycline and polymyxin B. He developed worsening sepsis and shock. On hospital day 14, the patient died.
Discussion. Infection with KPC-producing K. pneumoniae has become prevalent in New York City. However, there have been no reports of KPC-producing K. pneumoniae isolates that are also resistant to polymyxin and tigecycline in the United States. There are published reports of highly resistant K. pneumoniae isolates in Greece with decreased susceptibility to the polymyxins, but these isolates were not tested for resistance to tigecycline . We present our experience with these 2 patients to afford a glimpse of a future of potentially untreatable infections and to highlight some unique challenges in dealing with KPC-producing organisms.
We have termed these isolates “panresistant,” but because there is no generally accepted definition for this term, we present the antimicrobial susceptibility data for both isolates in table 1. The isolates were tested using a custom gram-negative card for the automated system Vitek 2 (bioMérieux) that included tigecycline. They were also tested for blaKPCgenes by real-time PCR. Susceptibility to polymyxin B was determined using a commercially available Etest.
Antimicrobial susceptibility patterns for Klebsiella pneumoniae isolates.
Antimicrobial susceptibility patterns for Klebsiella pneumoniae isolates.
Clinicians need accurate susceptibility data to provide effective therapy. However, automated susceptibility systems may be unreliable for detection of carbapenem resistance . A review of several automated systems showed that they incorrectly labeled up to 87% of carbapenemase-producing K. pneumoniae isolates as susceptible to imipenem, as well as reporting varying susceptibilities for the same isolate from day to day . Ertapenem resistance seems to be a marker for carbapenemase production when automated testing methods are used . In our second patient, automated testing reported the MIC for imipenem as ⩽1 µg/mL, but the MIC for ertapenem was elevated. PCR testing was used to confirm the presence of KPC genes. PCR testing for blaKPCgenes can be a useful method of confirming resistance to carbapenem in the United States, where metallo-β-lactamases are not a common mechanism of resistance. If resources are limited, an elevated MIC for ertapenem could be used as a screening method to determine which isolates need further testing . A phenotypic testing method, such as a carbapenem inactivation assay (Hodge test), can also be a reliable method of detecting carbapenemase-producing organisms for laboratories not equipped for PCR . Clinicians must be aware of the testing methods at their institution and their possible limitations.
Currently, the therapeutic options for highly resistant, carbapenemase-producing organisms are limited. Polymyxin B and tigecycline both seem to have reliable efficacy, although this report suggests that resistance to them is emerging.
Susceptibility testing for tigecycline can be readily done using automated systems, and gram-negative cards containing tigecycline are commercially available. Testing can also be done using Etest, which has been shown to have relatively good agreement with broth microdilution methods and few major errors in results for K. pneumoniae, although some questions have been raised regarding the reliability of the tigecycline Etest for other organisms .
Currently, the Vitek 2 system offers automated testing for polymyxin E (colistin) but not for polymyxin B. However, an Etest is available for polymyxin B. The Clinical and Laboratory Standards Institute (CLSI) provides limited guidance with regard to polymyxin B, leaving individual laboratories to determine appropriate methods and cutoffs. The CLSI document M100-S18 update does note that susceptibility testing for polymyxin B for Enterobacteriaceae and Acinetobacter species should be done by MIC methodologies . These include broth microdilution or Etest. There is published evidence to suggest that disk-diffusion methods are unreliable and should be avoided . CLSI, however, does not provide MIC cutoff values for Enterobacteriaceae. Some authors recommend using ⩾4 µg/mL, which is the CLSI cutoff for Acinetobacter species .
Perhaps the most important challenge in dealing with resistant gram-negative pathogens is the lack of new antibiotic agents. Prudent antimicrobial use becomes increasingly important as we are faced with a shrinking armamentarium of effective drugs. A recent review of polymyxin-resistant pathogens found that the only significant risk factor for polymyxin resistance was previous polymyxin use . Both of our patients developed progressive increases in the MIC for polymyxin B while they were receiving therapy. This is worrisome, because polymyxin use has been steadily increasing in our institution because of the prevalence of carbapenem-resistant gram-negative organisms. In the face of resistance to the polymyxins and tigecycline, we are unaware of any effective alternative therapies for infection caused by carbapenemase-producing Enterobacteriaceae.
It is a rarity for a physician in the developed world to have a patient die of an overwhelming infection for which there are no therapeutic options. These cases were the first instance in our clinical experience in which we had no effective treatment to offer. Trends in urban hospitals are often the harbinger of the future. We share these cases to highlight some troubling issues that soon may be relevant to increasing numbers of physicians and patients across the United States.
Potential conflicts of interest. All authors: no conflicts.
1 Talbot GH , Bradley J , Edwards JEJr, Gilbert D , Scheld M , Bartlett JG . Bad bugs need drugs: an update on the development pipeline from the Antimicrobial Availability Task Force of the Infectious Diseases Society of America, Clin Infect Dis, 2006, vol. 42 (pg. 657-68) 2 NNIS System, National Nosocomial Infections Surveillance (NNIS) System report, data summary from January 1992 through June 2004, issued October 2004, 2004 Atlanta, GA Centers for Disease Control and Prevention, Department of Health and Human Services Available at: http://www.cdc.gov/. Accessed February 2009 3 Yigit H , Queenman AM , Anderson GJ , et al. Novel carbapenem-hydrolyzing β-lactamase, KPC-1, from a carbapenem-resistant strain of Klebsiella pneumoniae , Antimicrob Agents Chemother, 2001, vol. 45 (pg. 1151-61) 4 Bradford PA , Bratu S , Urban C , et al. Emergence of carbapenem-resistant Klebsiella species possessing the class A carbapenem-hydrolyzing KPC-2 and inhibitor-resistant TEM-30 β-lactamases in New York City, Clin Infect Dis, 2004, vol. 39 (pg. 55-60) 5 Bratu S , Landman D , Alam M , Tolentino E , Quale J . Detection of KPC carbapenem-hydrolyzing enzymes in Enterobacter spp. from Brooklyn, New York, Antimicrob Agents Chemother, 2005, vol. 49 (pg. 776-8) 6 Lomaestro B , Tobin E , Shang W , Gootz T . The spread of Klebsiella pneumoniae carbapenemase-producing K. pneumoniae to upstate New York, Clin Infect Dis, 2006, vol. 43 (pg. e26-8) 7 Falagas ME , Bliziotis IA , Kasiakou SK , Samonis G , Athanassopoulou P , Michalopoulos A . Outcome of infections due to pandrug-resistant (PDR) gram-negative bacteria, BMC Infect Dis, 2005, vol. 5 pg. 24 8 Antoniadou A , Kontopidou F , Poulakou G , et al. Colistin-resistant isolates of Klebsiella pneumoniae emerging in intensive care unit patients: first report of a multiclonal cluster, J Antimicrob Chemother, 2007, vol. 59 (pg. 786-90) 9 Falagas ME , Bliziotis IA . Pandrug-resistant gram-negative bacteria: the dawn of the post-antibiotic era?, Int J Antimicrob Agents, 2007, vol. 29 (pg. 630-6) 10 Tenover FC , Kalsi RK , Williams PP , et al. Carbapenem resistance in Klebsiella pneumoniae not detected by automated susceptibility testing, Emerg Infect Dis, 2006, vol. 12 (pg. 1209-13) 11 Anderson KF , Lonsway DR , Rasheed JK , et al. Evaluation of methods to identify the Klebsiella pneumoniae carbapenemase in Enterobacteriaceae, J Clin Microbiol, 2007, vol. 45 (pg. 2723-5) 12 Pillar CM , Draghi DC , Dowzicky MJ , Sahm DF . In vitro activity of tigecycline against gram-positive and gram-negative pathogens as evaluated by broth microdilution and Etest, J Clin Microbiol, 2008, vol. 46 (pg. 2862-7) 13 Clinical and Laboratory Standards Institute Performance standards for antimicrobial susceptibility testing: 18th informational supplement, CLSI document M100-S18, 2008 Wayne, PA Clinical and Laboratory Standards Institute 14 Gales AC , Reis AO , Jones RN . Contemporary assessment of antimicrobial susceptibility testing methods for polymyxin B and colisitin: review of available interpretive criteria and quality control guidelines, J Clin Microbiol, 2001, vol. 39 (pg. 183-90) 15 Matthaiou DK , Michalopoulos A , Rafailidis PI , et al. Risk factors associated with the isolation of colistin-resistant gram-negative bacteria: a matched case control study, Crit Care Med, 2008, vol. 36 (pg. 807-11) © 2009 by the Infectious Diseases Society of America
Aug. 2, 2017
Washington, DC – August 2, 2017—A team of US researchers has discovered that three different species of Klebsiella bacteria can cause life-threatening infections in hospital patients and that all three share genes that confer resistance to the most commonly used antibiotics. The study, published this week in mSphere®, an open-access journal of the American Society for Microbiology, improves physicians’ understanding of Klebsiella infections and could point toward better ways to fight multi-drug resistant strains of these bacteria.
“Since 2001, we’ve seen a global explosion of drug-resistant Klebsiella infections,” says S. Wesley Long, Associate Medical Director of the Diagnostic Microbiology Lab at Houston Methodist Hospital in Texas and lead author of the study. “They are drug-resistant bacteria that are increasingly difficult to treat because they are resistant to many of the available antibiotics.”
Klebsiella are a type of bacteria that cause healthcare-associated infections, which can take the form of pneumonia, sepsis, wound infections and urinary tract infections. Healthcare-associated infections numbered more than 700,000 in the US in 2011 and up to 50 percent of invasive , multidrug-resistant K. pneumoniae infections have been fatal in some studies. In the last two decades, antibiotic-resistant Klebsiella infections have been on the rise around the world.
Long and his team wanted to investigate the nature of Klebsiella infections by studying a large, comprehensive, population-based sample collection. “We need to understand the pathogen on a population level, then we can use the bacterial genomes to predict virulence or antibiotic resistance of the strain, or mortality,” notes Long, a clinical microbiologist.
In a study previously published in mBio®, the researchers sequenced the entire genome of 1,777 Klebsiella from clinical specimens across the greater Houston area. Until now, Klebsiella pneumoniae was thought to be the culprit in most serious Klebsiella infections. However, the research team noticed a group of 28 samples that looked genetically different.
“We built a genetic family tree, essentially, and 28 strains stick off the tree as outliers. These are cousins five times removed and we wondered what are these guys doing at the family reunion?” says Long.
It turned out that, depending on the collection, between 2-12 percent of the samples had been misidentified as Klebsiella pneumoniae, and were in fact two related species, Klebsiella variicola or Klebsiella quasipneumoniae. K. variicola and K. quasipneumoniae had previously been characterized as commensal, nonpathogenic bacteria of the GI tract or agricultural pests, which rarely caused human infections. Long’s team found they were capable of causing invasive and severe infections in patients, with the same rate of mortality as K. pneumoniae.
“Not only are these cousins of K. pneumoniae causing similar infections, but they are also sharing these powerful drug resistance genes,” says Long. The sequencing of all bacterial genetic material present showed that all three Klebsiella species were sharing drug-resistance genes amongst themselves—including at least two genes that code for powerful enzymes that disable a broad spectrum of penicillin-like antibiotics.
Long says that these findings will not likely change the way Klebsiella infections are treated. “But in the race of trying to understand pathogens and find new antibiotics, or therapies outside the box of traditional antibiotics, this expands our knowledge of what pathogenic Klebsiella look like.” Other genetic traits that the three Klebsiella species share might be exploited as an Achilles’ heel weakness and attacked by new, targeted therapies. Long also says the work stresses the importance of doing large, comprehensive, population-based studies that take a close genetic look at patient samples: “If you are not looking, you don’t know what you’re missing.”
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What You Need to Know About a Klebsiella Pneumoniae Infection
Because K. pneumoniae can infect different parts of the body, it can cause different types of infections.
Each infection has different symptoms.
K. pneumoniae often causes bacterial pneumonia, or infection of the lungs. It happens when the bacteria enter your respiratory tract.
Community-acquired pneumonia occurs if you get infected in a community setting, like a mall or subway. Hospital-acquired pneumonia occurs if you get infected at a hospital or nursing home.
In Western countries, K. pneumoniae causes about 3 to 5 percent of community-acquired pneumonia. It’s also responsible for 11.8 percent of hospital-acquired pneumonia worldwide.
Symptoms of pneumonia include:
- yellow or bloody mucus
- shortness of breath
- chest pain
Urinary tract infection
If K. pneumoniae gets in your urinary tract, it can cause a urinary tract infection (UTI). Your urinary tract includes your urethra, bladder, ureters, and kidneys.
Klebsiella UTIs occur when the bacteria enters the urinary tract. It can also happen after using a urinary catheter for a long time.
Typically, K. pneumoniae cause UTIs in older women.
UTIs don’t always cause symptoms. If you do have symptoms, you might experience:
- frequent urge to urinate
- pain and burning when urinating
- bloody or cloudy urine
- strong-smelling urine
- passing small amounts of urine
- pain in the back or pelvic area
- discomfort in the lower abdomen
If you have a UTI in your kidneys, you might have:
- pain in the upper back and side
Skin or soft tissue infection
If K. pneumoniae enters through a break in your skin, it can infect your skin or soft tissue. Usually, this happens with wounds caused by injury or surgery.
K. pneumoniae wound infections include:
- necrotizing fasciitis
Depending on the type of infection, you might experience:
- flu-like symptoms
In rare cases, K. pneumoniae can cause bacterial meningitis, or inflammation of the membranes that cover the brain and spinal cord. It happens when bacteria infect the fluid around the brain and spinal cord.
Most cases of K. pneumoniae meningitis happen in hospital settings.
Generally, meningitis causes a sudden onset of:
- high fever
- stiff neck
Other symptoms may include:
- sensitivity to light (photophobia)
If K. pneumoniae is in the blood, it can spread to the eye and cause endophthalmitis. This is an infection that causes inflammation in the white of your eye.
Symptoms may include:
- eye pain
- white or yellow discharge
- white cloudiness on the cornea
- blurred vision
Pyogenic liver abscess
Often, K. pneumoniae infects the liver. This can cause a pyogenic liver abscess, or a pus-filled lesion.
K. pneumoniae liver abscesses commonly affect people with diabetes or who have been taking antibiotics for a long time.
Common symptoms include:
- pain in the right upper abdomen
If K. pneumoniae enters your blood, it can cause bacteremia, or the presence of bacteria in blood.
In primary bacteremia, K. pneumoniae directly infects your bloodstream. In secondary bacteremia, K. pneumoniae spreads to your blood from an infection somewhere else in your body.
One study estimates about 50 percent of Klebsiella blood infections originate from Klebsiella infection in the lungs.
Symptoms usually develop suddenly. This might include:
Bacteremia needs to be treated immediately. If left untreated, bacteremia can become life threatening and turn into sepsis.
Bacteremia is a medical emergency. Go to the nearest emergency room or call 911 or your local emergency services if you suspect you might have it. Your prognosis is better if you’re treated early. It will also lower your risk of life-threatening complications.