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Klebsiella pneumoniae 대표 이미지

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출처: English Wikipedia - Species Pages
Klebsiella pneumoniae is a Gram-negative, nonmotile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium. Although found in the normal flora of the mouth, skin, and intestines,[1] it can cause destructive changes to human lungs if aspirated, specifically to the alveoli resulting in bloody sputum. In the clinical setting, it is the most significant member of the Klebsiella genus of Enterobacteriaceae. K oxytoca and K rhinoscleromatis have also been demonstrated in human clinical specimens. In recent years, klebsiellae have become important pathogens in 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] Members of the Klebsiella genus typically express two types of antigens on their cell surfaces. The first, O antigen, is a component of the lipopolysaccharide (LPS), of which 9 varieties exist. The second is K antigen, a capsular polysaccharide with more than 80 varieties.[4] Both contribute to pathogenicity and form the basis for serogrouping. It is closely related to K. oxytoca from which it is distinguished by being indole-negative and by its ability to grow on both melezitose and 3-hydroxybutyrate. Danish scientist Hans Christian Gram (1853–1938) developed the technique now known as Gram staining in 1884 to discriminate between K. pneumoniae and Streptococcus pneumoniae. The genus Klebsiella was named after the German bacteriologist Edwin Klebs (1834–1913). Also known as Friedlander's Bacillum in honor of Carl Friedlander, a German pathologist, who proposed that this bacteriae was the etiological factor for the pneumonia seen specially in immunocompromised individuals such as sufferers of chronic diseases or alcoholics. K. pneumoniae can cause destructive changes to human lungs via inflammation and hemorrhage with cell death (necrosis) that sometimes produces a thick, bloody, mucoid sputum (currant jelly sputum). These bacteria gain access typically after a person aspirates colonizing oropharyngeal microbes into the lower respiratory tract. As a general rule, Klebsiella infections are seen mostly in people with a weakened immune system. Most often, illness affects middle-aged and older men with debilitating diseases. This patient population is believed to have impaired respiratory host defenses, including persons with diabetes, alcoholism, malignancy, liver disease, chronic obstructive pulmonary diseases (COPD), glucocorticoid therapy, renal failure, and certain occupational exposures (such as paper mill workers). Many of these infections are obtained when a person is in the hospital for some other reason (a nosocomial infection). Feces are the most significant source of patient infection, followed by contact with contaminated instruments. 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 abscess, cavitation, empyema, and pleural adhesions. It has a high death rate of about 50%, even with antimicrobial therapy. The mortality rate can be nearly 100% for people with alcoholism and bacteremia. In addition to pneumonia, Klebsiella can also cause infections in the urinary tract, lower biliary tract, and surgical wound sites. The range of clinical diseases includes pneumonia, thrombophlebitis, urinary tract infection, cholecystitis, diarrhea, upper respiratory tract infection, wound infection, osteomyelitis, meningitis, and bacteremia and septicemia. For patients with an invasive device in their bodies, contamination of the device becomes a risk; for example, 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. Two unusual infections of note from Klebsiella are rhinoscleroma and ozena. Rhinoscleroma is a chronic inflammatory process involving the nasopharynx. Ozena is a chronic atrophic rhinitis that produces necrosis of nasal mucosa and mucopurulent nasal discharge. 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 E. coli for urinary tract infections in older people. It is also an opportunistic pathogen for patients with chronic pulmonary disease, enteric pathogenicity, nasal mucosa atrophy, and rhinoscleroma. New antibiotic-resistant strains of K. pneumoniae are appearing.[6] Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates plasmids as the primary source of the resistance genes.[7] Klebsiella with the ability to produce extended-spectrum beta-lactamases (ESBL) are resistant to many classes of antibiotics. The most frequent resistances include resistance to aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and trimethoprim/sulfamethoxazole.[8] Infection with carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae is emerging as an important challenge in health-care settings.[9] 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.[10] In the USA, it was first described in North Carolina in 1996;[11] since then CRKP has been identified in 41 states;[12] and is recovered routinely 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 there is very little, if anything, healthcare professionals can do to treat patients with resistant organisms. A number of mechanisms cause carbapenem resistance in Enterobacteriaceae. These include hyperproduction of ampC beta-lactamase with an outer membrane porin mutation, CTX-M extended-spectrum beta-lactamase with a porin mutation or drug efflux, and carbapenemase production. The most important mechanism of resistance by CRKP is the production of a carbapenemase enzyme, blakpc. The gene that encodes the blakpc enzyme is carried on a mobile piece of genetic material (a 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 minimal inhibitory concentrations (MICs) 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. The extent and prevalence of CRKP within the environment is currently unknown. The mortality rate is also unknown, but is suspected to be within a range of 12.5% to 44%.[citation needed] The likelihood of an epidemic or pandemic in the future remains uncertain. The Centers for Disease Control and Prevention released guidance for aggressive infection control to combat CRKP: One specific example of this containment policy could be seen in Israel in 2007.[14] This policy had an intervention period from April, 2007 to May, 2008. A nationwide outbreak of CRE (which peaked in March, 2007 at 55.5 cases per 100,000 patient days) 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. In the United States, the reasons the CDC is recommending the detection of carbapenem resistance or carbapenemase production only for Klebsiella spp. and E. coli are: this facilitates performing the test in the microbiology laboratory without the use of molecular methods, and these organisms represent the majority of CREs encountered in the United States. Effective sterilization and decontamination procedures are important to keep the infection rate of this antibiotic resistant strain, CRKP as low as possible. As with many bacteria, the recommended treatment has changed as the organism has developed resistances. The choice of a specific antimicrobial agent or agents depends on local susceptibility patterns and on the part of the body infected. For patients with severe infections, a prudent approach is the use of an initial short course (48–72 h) of combination therapy, followed by a switch to a specific monotherapy once the susceptibility pattern is known for the specific patient. If the specific Klebsiella in a particular patient does not show antibiotic resistance, then the antibiotics used to treat such susceptible isolates include ampicillin/sulbactam, piperacillin/tazobactam, ticarcillin/clavulanate, ceftazidime, cefepime, levofloxacin, norfloxacin, gatifloxacin, moxifloxacin, meropenem, and ertapenem. Some experts recommend the use of meropenem for patients with ESBL producing Klebsiella. The claim is that meropenem produces the best bacterial clearing. The use of antibiotics is usually not enough. Surgical clearing (frequently done as interventional radiology drainage) is often needed after the patient is started on antimicrobial agents. Multiple drug-resistant K. pneumoniae strains have been killed in vivo by intraperitoneal, intravenous, or intranasal administration of phages in laboratory tests.[15] While this treatment has been available for some time, a greater danger of bacterial resistance exists to phages than to antibiotics.[citation needed] Resistance to phages may cause a bloom in the number of the microbes in environment, as well as among humans (if not obligate pathogenic). This is why phage therapy is used only in conjunction with antibiotics, to supplement their activity instead of replacing it altogether.[16] To prevent spreading Klebsiella infections between patients, healthcare personnel must follow specific infection control precautions.[17] 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:
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출처: 정보없음
Klebsiella pneumoniae는 Enterobacteria에 속하며, 그람음성의 편모가 없는 비운동성으로, 캡슐을 형성하며 유당을 발효하는 통성혐기성의 막대모양 세균이다. 협막을 가지고 점액을 생산하며 탄소원으로 구연산을 이용하고 여러가지 탄수화물에서 산과 가스를 발생시키며 황화수소는 생산하지 않고 메틸레드반응에 음성이며, MacConkey 한천배지에서 점액성의 유당발효 형태를 나타낸다. 자연계에 널리 존재하며, 사람의 호흡기, 장, 비뇨기 등에서 검출되는 급성폐렴의 원인균이다. 입, 피부, 내장 등에서 정상적인 미생물상으로 존재하며 흡입하면 특히 사람과 동물의 폐에서 폐포를 파괴시켜 피가 묻은 가래가 되어 나온다. 임상에서, Enterobacteriaceae의 Klebsiella 속의 가장 심각한 병원균주로서, K. oxytoca와 K. rhinoscleromatis와 함께 인체의 임상검체에서 발견되었다. 폐렴, 심내막염, 복막염, 담낭염, 요로감염증을 일으키며, 유아, 노인, 쇠약자에게는 패혈증을 일으킨다. 자연적으로 토양에 존재하는 균이며 약 30%의 균주가 혐기적 조건에서 질소를 고정 할 수 있다. K. pneumoniae는 농업에서 작물의 수확량을 증가시키는 것으로 알려졌으며, 질소자급영양체로서 질소고정시스템 연구에 이용되어 왔다. Klebsiella 속은 세포표면에 두 가지 형태의 항원이 발현된다. 첫번째 균체 O 항원은 지질다당체 (LPS)의 구성요소이며 9종이 존재하고, 두번째 협막 K 항원은 80개 이상의 종류를 가진 피막다당체로서 둘 모두 병원성에 관련되어 있다. Klebsiella pneumoniae는 indole-negative 및 melezitose에서 성장할 수 있어 K. oxytoca와 유사하지만, 3-하이드록시 부티레이트에서는 서로 달라 구별된다. Klebsiella 속은 독일의 세균학자 Edwin Klebs (1834-1913)의 이름을 따서 명명되었고, 만성질환이나 알코올중독 환자와 같은 면역결핍자에게서 볼 수 있는 폐렴의 원인이 될 수 있다고 주장한 독일 병리학자인 Carl Friedländer의 이름을 따서 Friedlander's 세균으로도 알려져 있다. 일반적으로 Klebsiella 감염은 면역체계가 약화된 사람들에게서 주로 나타난다. 대부분의 경우, 이 질병은 중년 및 고령 남성에게서 발생하며 당뇨병, 알코올 중독, 악성 종양, 간 질환, 만성 폐질환, 신부전 및 호흡기 손상을 일으킨다. 병원내에서의 감염이 많고 대변을 통한 감염이 환자 감염의 가장 중요한 원인이 되고 있으며 오염된 도구와의 접촉에 의해 주로 감염된다. 병원 밖에서 Klebsiella 세균은 기관지 폐렴의 원인이 되며 항균제 치료를 하더라도 사망률은 약 50% 에 이르고, 알코올중독 환자의 사망률은 거의 100% 에 이른다. Klebsiella 균은 여러 항생제에 내성을 갖고 있고, 플라스미드의 내성유전자가 주원인인 것으로 알려져 있으며 거의 모든 종이 베타-락탐 항생제에 내성을 가지고 있다. 저항성은 습한 상태에서는 실온에서 수개월간 생존하나 56~60℃로 가열하면 빠르게 사멸한다.
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