Enterobacter aerogenes

Enterobacter aerogenes

Enterobacter aerogenes

Enterobacter Aerogenes

Enterobacter aerogenes and Enterobacter cloacae are gram-negative bacteria that belong to the family Enterobacteriaceae. They can be both aerobic and anaerobic. Under the microscope, Enterobacter is rod-shaped with rounded ends. Enterobacter aerogenes and Enterobacter cloacae cause wound ( Múñez et al 2012 ), respiratory ( Wang et al 2012 ), and urinary tract infections ( Edlin 2013 ). A drug-resistant strain of Enterobacter aerogenes has emerged ( Karlowsky et al 2013 ). Enterobacter cloacae can also cause ESBL-bacteremia (extended-spectrum β-lactamase producing bacteria) ( Ahmed et al., 2009; Frakking et al 2013 ). There is little research on the use of essential oils on Enterobacter.

Enterobacter Aerogenes

Enterobacter aerogenes, part of the Enterobacteriaceae Family, is a rod-shaped bacteria that causes bacterial infections, and is usually acquired in a hospital or hospital-type atmospheres. It usually causes opportunistic infections, meaning that it will usually only cause a disease in a person or host that has a compromised immune system. Studies are now showing it causing increased alarm in community infections. It rarely is known to cause a disease in someone with a healthy immune system.

Even though they can be extremely sensitive to antibiotics, these bacteria easily become unaffected by typical antibiotics due to their significant ability to become resistant through their adaptive capabilities. These become “drug resistant bacteria” or “superbugs.”

Learn 7 Ways
To Get Rid Of Bacteria
Here

Enterobacter aerogenes are small, white in color, and have flagella surrounding it making it motile. It is Gram-negative and anaerobic. They are seen throughout nature, including fresh water, sewage plants, and vegetables. Although it normally prefers and multiplies quickly in places with a small amount or no oxygen, it can grow and live in oxygen-abundant areas. It is related to Enterobacter Coli and Salmonella. Its preferred temperature for growth is 37 degrees Celsius. In laboratories, it also grows quite quickly in milk nutrients, salts, and dyes.

Surgical procedures, intravenous catheter insertions, and some antibiotic treatments are ways that result in the infection of Enterobacter aerogenes. The gastrointestinal tract is usually where it is found in a human, and it is known to cause respiratory, urinary tract infections, osteomyelitis, and septic arthritis. They also cause burn, wound, and bloodstream infections. It has also been shown to cause meningitis and central nervous system infections.

Epidemiology and Infections

Enterobacter aerogenes is isolated as human clinical specimens from respiratory, urinary, blood, or gastrointestinal tract (Langley et al., 2001). Epidemiology of this species has been particular in Europe: it has regularly been involved in nosocomial infections outbreaks since 1993, particularly in the Western Europe (Georghiou et al., 1995; Grattard et al., 1995; Allerberger et al., 1996; Arpin et al., 1996; Davin-Regli et al., 1996; De Gheldre et al., 1997; Jalaluddin et al., 1998). Until, 2003, E. aerogenes was considered as an important emerging MDR pathogen, particularly in ICUs (Bosi et al., 1999; Chevalier et al., 2008; Figure ​ Figure1 1 ). The situation in 1990s in Europe pointed to the dispersion of an epidemic clone and, since then, it has been extensively detected in European hospitals and health care facilities. The event fitted in with the international spread of the ESBL TEM-24 (blaTEM-24) harbored by an epidemic plasmid (Bosi et al., 1999). The prevalence of Enterobacter sp. infections in clinical wards has also increased due to the introduction of extended-spectrum cephalosporins and carbapenems in the antibiotic therapy (Arpin et al., 1996; Anastay et al., 2013). The consequence of this antibiotherapy is the emergence of “pan-drug E. aerogenes isolates” resistant to last-line antibiotics such as carbapenems and also to colistin, for which no therapeutic option was available (Chevalier et al., 1999; Thiolas et al., 2005; Diene et al., 2013). Interestingly, the role of efflux mechanism in E. aerogenes resistance has been studied within an 8 years of period. This study indicated a noticeable increase of the prevalence of an efflux mechanism, susceptible to pump inhibitor, in clinical isolates collected during this period (Chevalier et al., 2008). After the emergence of ESBL in E. aerogenes and the characterisation of porin mutations in clinical isolates, this role of efflux mechanism highlights a new step in the adaptative evolution in E. aerogenes (Charrel et al., 1996; Malléa et al., 1998; Gayet et al., 2003).

An external file that holds a picture, illustration, etc.
Object name is fmicb-06-00392-g001.jpg

Schematic illustration of the timing of Enterobacter species during the emergence of resistance outbreaks in France hospitals (Arpin et al., 1996; Bornet et al., 2000; Chevalier et al., 2008; Lavigne et al., 2012; Mezzatesta et al., 2012; Anastay et al., 2013; Robert et al., 2014). ESBLs, extended-spectrum β-lactamases.

Since 2010, E. aerogenes in France is the fifth highest Enterobacteriaceae and the seventh highest Gram-negative Bacillus responsible for notorious nosocomial infections (Carbonne et al., 2013; Figure ​ Figure2 2 ). Despite its intrinsic resistance to ampicillin and constant expression of ESBL that is associated with other resistance mechanisms contributing to MDR phenotype, its prevalence has significantly dropped (reduction factor of 20) in France (Anastay et al., 2013; Jarlier and INVS, 2014). Its position was displaced in the context of hospital acquired infections, because of the dramatic rise of the E. coli pandemic clone O25:H4-ST131 along with K. pneumoniae and E. cloacae, ESBL, and/or carbapenemase producing strains. Although, E. aerogenes causes septic shock more readily in patients thus leading to a higher mortality rate (Song et al., 2010; Lavigne et al., 2012), E. cloacae is now the most frequently observed clinical isolate among Enterobacter sp. It can be associated with the dissemination of actual epidemic plasmids bearing most prevalent resistant genes and expressing new β-lactamases or carbapenemases (Figure ​ Figure2 2 ).

An external file that holds a picture, illustration, etc.
Object name is fmicb-06-00392-g002.jpg

Distribution of the main species of Enterobacteriaceae-ESBL (n for 10,000 patient days): evolution 2002–2013 from the French national coordination of MDRB surveillance (Carbonne et al., 2013; Jarlier and INVS, 2014). ENT AER, Enterobacter aerogenes; ENT CLO, E. cloacae; ESC COL, E. coli; KLE PNE, Klebsiella pneumoniae; TOT ENB, Total Enterobacteriaceae; ESBLs, extended-spectrum β-lactamases.

Enterobacter cloacae is ubiquitous in terrestrial and aquatic environments (water, sewage, soil, and food). The species occurs as commensal microflora in the intestinal tracts of humans and animals and is also pathogens in plants and insects. This diversity of habitats is mirrored by the genetic variety of E. cloacae (Mezzatesta et al., 2012). Recently, MLST and PFGE epidemiological methods data revealed world circulation of several epidemic clonal complexes (Izdebski et al., 2014).

It is also a well-known nosocomial pathogen contributing to bacteremia, endocarditis, septic arthritis, osteomyelitis, and skin/soft tissue infections, and lower respiratory tract- urinary tract and intra-abdominal infections (Fata et al., 1996). E. cloacae tends to contaminate various medical, intravenous, and other hospital devices (Dugleux et al., 1991). Nosocomial outbreaks have also been associated with the colonization of certain surgical equipment and operative cleaning solutions (Wang et al., 2000). Since a decade, E. cloacae has been repeatedly reported as a nosocomial pathogen in neonatal units and several outbreaks of infection have been reported (Fernandez-Baca et al., 2001; Pestourie et al., 2014). Today, variability among strains are less frequent and outbreaks due to clonal E. cloacae hyper-producing AmpC β-lactamase and ESBL carrier isolates are described from neonate specimens, adults urines/feces samples or from environmental samples (Pestourie et al., 2014).

Enterobacter cloacae has an intrinsic resistance to ampicillin, amoxicillin, first-generation cephalosporins, and cefoxitin owing to the production of constitutive AmpC β-lactamase. It exhibits a high frequency of enzymatic resistance to broad-spectrum cephalosporins. Resistance of Enterobacter sp. to third-generation cephalosporins is most typically caused by overproduction of AmpC β-lactamases, and thus treatment with third-generation cephalosporins may select for AmpC-overproducing mutants. AmpC overproduction is due to the derepression of a chromosomal gene or by the acquisition of a transferable ampC gene from plasmids or other mobile elements. The AmpC plasmid-mediated resistance is distinguished from chromosomal enzyme production because they are not inducible. However they represent a problem due to its increasing prevalence among clinical isolates. The enzyme confers a resistance to third-generation cephalosporins and ureido- and carboxy-penicillins and is not inhibited by common inhibitors of β-lactamases. Fourth-generation cephalosporins retain reasonable activity against derepressed strains, but if strains are also ESBL producers, they become resistant to this antibiotic class. The prevalence of ESBL and CTX-M producers represented approximatively 5% of the isolates in the recent studies and ESBLs are most often plasmid-mediated. These characteristics, associated with the frequent endogenous intestinal carriage of E. cloacae, may result in abnormally high levels in the bowels of hospitalized patients, especially those who have received cephalosporins (Potron et al., 2013).

Résistance

Les infections à Enterobacter sont généralement causées par des bactéries courantes dans le tube digestif humain. Aux États-Unis, les infections causées par ce genre le placent au huitième rang des agents pathogènes les plus courants dans les infections nosocomiales.

Ces organismes sont multi-résistants, ce qui indique qu'ils ne sont pas sensibles aux traitements jugés utiles pour lutter contre les infections qu'ils produisent.

On sait que E. aerogenes emploie au moins trois mécanismes de résistance; enzymes inactivantes, altération des cibles pharmacologiques et altération de la capacité des médicaments à pénétrer et / ou à s'accumuler dans leurs cellules.

De plus, étant une bactérie à Gram négatif, il est hautement antibiotique et produisant β-lactamase, ce qui implique une grande résistance à divers antibiotiques tels que les antibiotiques β-lactames, l'ampicilline, l'amoxicilline, l'acide clavulanique, la céphalothine et la céfoxitine, en produisant l'enzyme β-lactamases.

주요 특징

문 및 발견

Enterobacter aerogenes는 인간 위장의 미생물 및 다른 동물의 일부입니다. 토양, 수역 및 유제품에서도 발견됩니다..

그것은 Kruse에 의해 1896 년에 기술되었고, Enterobacteriaceae의 가족에 속하며 그 분류 학적 분류는 지난 세기의 70 년대 이후 오늘까지 논의 주제가되어왔다.

의료 이익

이 종은 사람의 임상 샘플, 호흡기, 비뇨기, 혈액 및 위장관에서 분리되어 있기 때문에 의학 분야에서 특히 중요합니다..

1993 년부터 유럽에서 역학적 인 발병이보고되었으며 2003 년까지 다중 병원성 병원균, 특히 중환자 실 (intensive care units)으로 간주되었다..

벨기에에서이 종은 감염된 환자의 사망률이 높습니다.

전송

E. aerogenes가 발견되는 다른 서식지 때문에 감염은 여러 가지 방법으로 얻을 수 있습니다.

일반적으로 감염은 다음에서 발생합니다.

  • 환자 자신의 식물상.
  • 의료 종사자의 손을 통해 의료 기기 (카테터 또는 인젝터)를 환자에게 삽입하는 동안.
  • 오염 된 장비가 환자 및 장기 이식에 도입되는 수술 절차에서 박테리아의 송신기가 기증자 인 경우.

대부분의 원내 감염은 관련된 환자의 이전 식민지에서 내생 적으로 발생하는 것으로 보입니다. 면역 억제 상태에있는 사람, 어린이 및 노인들은이 감염에 더 취약합니다..

Leave a Reply