Klebsiella pneumoniae

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Klebsiella pneumoniae
"K. pneumonie" on a MacConkey agar plate
K. pneumoniae on a MacConkey agar plate
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Klebsiella
Species:
K. pneumoniae
Binomial name
Klebsiella pneumoniae
(Schroeter 1886) Trevisan 1887
Subspecies

Klebsiella pneumoniae is a

bacterium. It appears as a mucoid lactose fermenter on MacConkey agar
.

Although found in the normal flora of the mouth, skin, and intestines,

nosocomial
infections.

It naturally occurs in the soil, and about 30% of strains can fix nitrogen in anaerobic conditions.[2] As a free-living diazotroph, its nitrogen-fixation system has been much-studied, and is of agricultural interest, as K. pneumoniae has been demonstrated to increase crop yields in agricultural conditions.[3]

It is closely related to

3-hydroxybutyrate
.

History

The genus Klebsiella was named after the German microbiologist Edwin Klebs (1834–1913).[citation needed] It is also known as Friedlander's bacillum in honor of Carl Friedländer, a German pathologist, who proposed that this bacterium was the etiological factor for the pneumonia seen especially in immunocompromised individuals such as people with chronic diseases or alcoholics.

Community-acquired pneumonia caused by Klebsiella pneumoniae may occasionally be called Friedländer's pneumonia.[4]

Epidemiology

Illness most commonly affects middle-aged and older men more often than women with debilitating diseases. This patient population is believed to have impaired respiratory host defenses, including persons with

nosocomial infection
).

In addition to pneumonia, Klebsiella can also cause infections in the

respiratory tract infection, wound infection, osteomyelitis, meningitis, and bacteremia, and sepsis. For patients with an invasive device in their bodies, contamination of the device becomes a risk; neonatal ward devices, respiratory support equipment, and urinary catheters put patients at increased risk. Also, the use of antibiotics can be a factor that increases the risk of nosocomial infection with Klebsiella bacteria. Sepsis
and septic shock can follow entry of the bacteria into the blood.

Research conducted at King's College, London has implicated molecular mimicry between HLA-B27 and two Klebsiella surface molecules as the cause of ankylosing spondylitis.[5]

Klebsiella ranks second to

antibiotic-resistant strains of K. pneumoniae are appearing.[7]

Klebsiella pneumonia

The most common condition caused by Klebsiella bacteria outside the hospital is pneumonia, typically in the form of bronchopneumonia and also bronchitis. These patients have an increased tendency to develop lung abscesses, cavitation, empyema, and pleural adhesions. It has a death rate around 50%, even with antimicrobial therapy.[8]

Pathophysiology

It is typically due to

LBP helps transfer bacteria cell wall elements to the cells.[11][12]

Signs and symptoms

Individuals with Klebsiella pneumoniae tend to cough up a characteristic sputum, as well as having fever, nausea, tachycardia, and vomiting. Klebsiella pneumoniae tends to affect people with underlying conditions, such as alcoholism.[9]

Diagnosis

In terms of the diagnosis of Klebsiella pneumoniae the following can be done to determine if the individual has this infection, with the addition of susceptibility testing to identify drug-resistant organisms:[11][9]

Treatment

Treatment for Klebsiella pneumoniae is by

antibiotic susceptibility testing, the person's health condition, medical history and severity of the disease.[10][13]

Streptomycin(Aminoglycoside)
Cephalosporin (core structure)

Klebsiella possesses

diabetes mellitus (DM); treatment consists of third generation cephalosporins.[medical citation needed
]

Hypervirulent Klebsiella pneumonia

Hypervirulent (hvKp) is a rather recent K pneumoniae variant that is significantly more virulent than classical K. pneumoniae (cKp). While cKp is an opportunistic pathogen responsible for nosocomial infections that usually affect immunocompromised patients, hvKp is clinically more concerning since it also causes disease in healthy individuals and can infect virtually every site of the body. The genetic traits that lead to this pathotype are included in a large virulence plasmid and potentially on additional conjugative elements.[17]

These newly identified strains were described to overproduce capsule components and siderophores for iron acquisition, among other factors.[18] Although initial studies showed that hvKp is rather susceptible to antibiotic treatment, it has been recently shown that such strains can acquire resistance plasmids and become multiresistant to a variety of antibiotics.[18][19][20]

It originated from Asia, having a high mortality rate among the population. It often spreads to central nervous system and eye causing endophthalmitis, nonhepatic abscesses, pneumonia, necrotizing fasciitis, and meningitis. One visual trait of these strains is hypermucoviscous phenotype and a string test can be used to help the diagnosis.[21] Further examinations and treatments are made on a case-by-case basis, as there are currently no international guidelines.[22]

Transmission

To get a K. pneumoniae infection, a person must be exposed to the

respiratory
tract to cause pneumonia, or the blood to cause a bloodstream infection. In healthcare settings, K. pneumoniae bacteria can be spread through person-to-person contact (for example, contaminated hands of healthcare personnel, or other people via patient to patient) or, less commonly, by contamination of the environment; the role of transmission directly from the environment to patients is
controversial and requires further investigation.[23]
However, the bacteria are not spread through the air. Patients in healthcare settings also may be exposed to K. pneumoniae when they are on
catheters or wounds. These medical tools and conditions may allow K. pneumoniae to enter the body and cause infection.[24]

Resistant strains

Multidrug-resistant Klebsiella pneumoniae

Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates

tetracyclines, chloramphenicol, and trimethoprim/sulfamethoxazole.[26]

NDM carbapenemase[27]

Infection with

carbapenemase-producing Enterobacteriaceae is emerging as an important challenge in health-care settings.[28][29] One of many CREs is carbapenem-resistant Klebsiella pneumoniae (CRKP). Over the past 10 years, a progressive increase in CRKP has been seen worldwide; however, this new emerging nosocomial pathogen is probably best known for an outbreak in Israel that began around 2006 within the healthcare system there.[30] In the US, it was first described in North Carolina in 1996;[31] since then CRKP has been identified in 41 states;[32]
and is routinely detected in certain hospitals in New York and New Jersey. It is now the most common CRE species encountered within the United States.

CRKP is resistant to almost all available antimicrobial agents, and infections with CRKP have caused high rates of morbidity and mortality, in particular among persons with prolonged hospitalization and those critically ill and exposed to invasive devices (e.g., ventilators or central venous catheters). The concern is that carbapenem is often used as a drug of last resort when battling resistant bacterial strains. New slight mutations could result in infections for which healthcare professionals can do very little, if anything, to treat patients with resistant organisms.

A number of mechanisms cause carbapenem resistance in the Enterobacteriaceae. These include hyperproduction of ampC

transposon; the specific transposon involved is called Tn4401), which increases the risk for dissemination. CRE can be difficult to detect because some strains that harbor blakpc have minimum inhibitory concentrations that are elevated, but still within the susceptible range for carbapenems. Because these strains are susceptible to carbapenems, they are not identified as potential clinical or infection control risks using standard susceptibility testing guidelines. Patients with unrecognized CRKP colonization have been reservoirs for transmission during nosocomial outbreaks.[33]

The extent and prevalence of CRKP within the environment is currently unknown. The mortality rate is also unknown, but has been observed to be as high as 44%.[34] The Centers for Disease Control and Prevention released guidance for aggressive infection control to combat CRKP:

Place all patients colonized or infected with carbapenemase-producing Enterobacteriaceae on contact precautions. Acute-care facilities are to establish a protocol, in conjunction with the guidelines of the Clinical and Laboratory Standards Institute, to detect nonsusceptibility and carbapenemase production in Enterobacteriaceae, in particular Klebsiella spp. and Escherichia coli, and immediately alert epidemiology and infection-control staff members if identified. All acute-care facilities are to review microbiology records for the preceding 6–12 months to ensure that there have not been previously unrecognized CRE cases. If they do identify previously unrecognized cases, a point prevalence survey (a single round of active surveillance cultures) in units with patients at high risk (e.g., intensive-care units, units where previous cases have been identified, and units where many patients are exposed to broad-spectrum antimicrobials) is needed to identify any additional patients colonized with carbapenem-resistant or carbapenemase-producing Klebsiella spp. and E. coli. When a case of hospital-associated CRE is identified, facilities should conduct a round of active surveillance testing of patients with epidemiologic links to the CRE case (e.g., those patients in the same unit or patients having been cared for by the same health-care personnel).[35]

In 2019, there were 192,530 global deaths attributed to resistant strains of Klebsiella pneumoniae. [36]

Global deaths (counts) attributable to bacterial antimicrobial resistance by pathogen–drug combination, 2019[36]
3GC 4GC Amino-glycosides Amino-penicillin Anti-pseudomonal BL−BLI Carbapenems Fluoro-quinolones Macrolide MDR & XDR Meticillin Mono INH Mono RIF Penicillin TMP-SMX Vancomycin Total
Acinetobacter baumannii 6,860 3,280 10,400 13,300 811 57,700 40,000 132,351
Citrobacter spp 1,840 1,340 411 2,170 2,300 2,510 10,571
Enterobacter spp 5320 3070 9550 15,300 7,800 4,650 45,690
Enterococcus faecalis 26,800 3,420 30,220
Enterococcus faecium 37,200 14,300 51,500
Other enterococci 12,200 2,200 14,400
Escherichia coli 59,900 11,700 10,500 21,300 29,500 56,000 30,200 219,100
Group A Streptococcus 3,630 3,630
Group B Streptococcus 11,500 13,500 799 25,799
Haemophilus influenzae 2,470 4,290 6,760
Klebsiella pneumoniae 50,100 26,300 7,930 55,700 29,000 23,500 192,530
Morganella spp 168 154 427 749
Mycobacterium tuberculosis 69,810 11,600 3,350 84,760
Proteus spp 4,730 887 1,330 2,970 1,620 11,537
Pseudomonas aeruginosa 10,400 4,370 3,010 10,300 38,100 18,300 84,480
S Paratyphi 4,040 64 4,104
S Typhi 17,200 6,460 23,660
Non-typhoidal Salmonella 5,620 5,620
Serratia spp 1,100 2,610 953 2,450 1,080 8,193
Shigella spp 5,990 5,990
Staphylococcus aureus 2,480 15,900 19,600 121,000 18,700 3,120 180,800
Streptococcus pneumonia 3,330 2,040 41,900 11,200 12,500 12,400 38,700 122,070
Total 140,898 17,074 56,731 16,120 37,800 32,081 242,950 305,737 49,230 76,334 121,000 11,600 3,350 12,199 117,370 23,040 1,264,514

Local outbreaks

Israel 2007-2008. A nationwide outbreak of CRE in Israel peaked in March, 2007 at 55.5 cases per 100,000 patient days and necessitated a nationwide treatment plan. The intervention entailed physical separation of all CRE carriers and appointment of a task force to oversee efficacy of isolation by closely monitoring hospitals and intervening when necessary. After the treatment plan (measured in May, 2008), the number of cases per 100,000 patient days decreased to 11.7. The plan was effective because of strict hospital compliance, wherein each was required to keep detailed documentation of all CRE carriers. In fact, for each increase in compliance by 10%, incidence of cases per 100,000 patient days decreased by 0.6. Therefore, containment on a nationwide scale requires nationwide intervention.[37]

Nevada 2016. In mid-August 2016, a resident of Washoe County was hospitalized in Reno due to a CRE (specifically Klebsiella pneumoniae) infection. In early September of the same year, she developed septic shock and died. On testing by CDC an isolate from the patient was found to be resistant to all 26 antibiotics available in the US, including drug of last resort colistin.[38] It is believed she may have picked up the microbe while hospitalized in India for two years due to a broken right femur and subsequent femur and hip infections.[39][40][41]

Antimicrobial resistance gene transfer

Klebsiella pneumoniae carries a large number of anti-microbial resistance genes (AMR genes). These genes are transferred via plasmids from and to other human pathogens. One human pathogen that commonly acquires AMR genes from Klebsiella pneumoniae is Salmonella.[citation needed] This could help with treatment of salmonella infections due to having knowledge of possible antibiotic resistance data.[citation needed]

The majority of AMR genes in Klebsiella pneumoniae are plasmid-borne. An example of a niche would be soil, often considered a hotspot for gene transfer.[citation needed]

Horizontal gene transfer of AMR genes by Klebsiella pneumoniae[42]
Total AMR genes per spp Average plasmids
Acinetobacter baumannii 278 1.5
Pseudomonas aeruginosa 263 0
Klebsiella pneumoniae 410 2.5
Enterobacter cloacae 277 2.2
Escherichia coli 204 1

The table shows the number of AMR genes and plasmids (per strain or subspecies) compared to other common bacteria species.[42]

Prevention

To prevent spreading Klebsiella infections between patients, healthcare personnel must follow specific infection-control precautions,[24] which may include strict adherence to hand hygiene (preferably using an alcohol based hand rub (60–90%) or soap and water if hands are visibly soiled. Alcohol based hand rubs are effective against these Gram-negative bacilli)[43] 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.[24]

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[24]

Treatment

K. pneumoniae can be treated with antibiotics if the infections are not

drug-resistant. Infections by K. pneumoniae 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.[24] More specific treatments of Klebsiella pneumonia are given in its section above. For urinary tract infections with multidrug-resistant Klebsiella species, a combination therapy with amikacin and meropenem has been suggested.[44]

Research

Multiple drug-resistant K. pneumoniae strains have been killed in vivo by intraperitoneal, intravenous, or intranasal administration of phages in laboratory tests.[45] Resistance to phages is not likely to be as troublesome as to antibiotics as new infectious phages are likely to be available in environmental reservoirs. Phage therapy can be used in conjunction with antibiotics, to supplement their activity instead of replacing it altogether.[46]

Vaccine development

New data sources outlining the global burden of K. pneumoniae and drug-resistant forms are expected to build momentum into prophylactic vaccine development.[47] The recent 2022 IHME study showed that in 2019 K. pneumoniae was responsible for 790,000 deaths [571,000–1,060,000] in all age groups across 11 infectious syndromes. Importantly, in Sub-saharan Africa K. pneumoniae was responsible for 124,000 [89,000–167,000] neonatal deaths due to bloodstream infections. Based on these and other data, a newly developed prophylactic vaccine would ideally be designed to prevent invasive K. pneumoniae disease in both vulnerable persons but also as a maternal vaccine to prevent neonatal sepsis and global demand assessments have been published.[48] As of June 2023, one single clinical development program for a K. pneumoniae vaccine [Kleb4V/GSK4429016A] was in a Phase 1/2 study in healthy adults aged 18–70 yrs (n=166) [Clinical trials identifier: NCT04959344]. The vaccine is an O-antigen based conjugate where the specific O-antigens in the vaccine remain undisclosed [Michael Kowarik, LimmaTech Biologics, World Vaccine Congress EU, 2022] although only a limited number of O-serotypes can account for a high proportion of clinical isolates.[49] A recent Q1 2024 GSK Corporate R&D pipeline update showed that Kleb4V/GSK4429016A had been removed. The status of the program is now subject to verification.

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External links

Wikispecies has information related to Klebsiella pneumoniae.
Wikimedia Commons has media related to Klebsiella pneumoniae.
Scholia has a topic profile for Klebsiella pneumoniae.
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