Enterobacter

Enterobacter are gram-negative, peritrichous flagellated, motile rod-shaped bacteria that can ferment lactose and utilize citrate as the sole carbon source. Capsule formation is possible but not obligate. Enterobacter spp. is a member of the so-called ESKAPE group(Vale de Macedo GHR et al. 2021), which includes the most important resistant bacterial pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter spp.).

The genus Enterobacter in the order Enterobacterales and the family Enterobacteriaceae is very inhomogeneous. The genus includes 22 species. These species are described in the environment and are classified as opportunistic pathogens in plants, animals and humans. Thus, several species are part of the normal intestinal flora as are other genera of the Entereobactericeae family.

In addition to apathogenic species, there are also potentially pathogenic representatives. The most important human medical representatives are the species of the Enterobacter cloacae complex. This is widespread in nature but can act as a pathogen. Biochemical and molecular studies of E. cloacae have shown their genomic heterogeneity. Currently, the Enterobacter cloacae complex includes 6 species (Mezzatesta ML et al. 2012):

• Enterobacter cloacae strictu sensu
• Enterobacter asburiae
• Enterobacter hormaechei
• Enterobacter kobei
• Enterobacter ludwigii
• Enterobacter nimipressuralis

Enterobacter cloacae and Enterobacter hormaechei are the most commonly isolated species.

Enterobacter are facultative pathogens of bronchitis, cholangitis, urinary tract infections, less frequently of sepsis or, in neonates, meningitis. In Germany, Enterobacter species are responsible for 6.5 % of all nosocomial infections in intensive care units. In the last decades, Enterobacter spp. were mainly perceived as causative agents of nosocomial infections. Evidence to date suggests predominantly endogenous infections with individual strains of the Enterobacter cloacae complex and a route of spread not associated with the hospital. Risk factors for the spread of Enterobacter cloacae complex are:

• Prolonged hospitalization (especially in intensive care units),
• severity of the underlying disease
• Malignancies
• Burn wounds
• Prematurity
• Neonates (Enterobacter are a particular problem in a neonatal intensive care unit)
• Diseases of the gastrointestinal tract
• invasive access/catheters

Germ detection is performed culturally and is unproblematic (Hof et al. 2019). As with all Entererobacteriaceae, the final diagnosis is made via the metabolic activities of the pathogens. Further by MALDI-TOF mass spectrometry.

Preventive measures: Isolation

• Isolation measures of patients with multiresistant gram-negative rods are basically reasonable depending on the inpatient risk areas and are carried out as single room or cohort isolation.
• To prevent the transmission of 3MRGN Enterobacter spp., basic hygiene measures are to be implemented in all hospital areas. Additional measures are not necessary in the endemic situation.
• Isolate patients with colonization or infection by 4MRGN Enterobacter spp. in all hospital areas.

Preventive measures: Screening

• Screen all patients at risk for colonization or infection by 4MRGN Enterobacter spp. and isolate them until results are available. Patients at risk are those with recent contact with the healthcare system in countries with endemic occurrence and patients who have had contact with 4MRGN Enterobacter spp. positive patients, i.e. have been cared for in the same room. In addition, patients with an inpatient hospital stay (> 3 days) in the past 12 months in a region with increased 4MRGN prevalence. All premature and newborn infants receiving intensive care. Screening guidelines are to be defined on the basis of the patient structure and regularly updated on the basis of current information.

In Enterobacter, there is natural resistance to aminopenicillins and older cephalosporins. Multiple resistances are based on R-plasmids. Good results can be achieved with quinolones and aminoglycosides. Sensitivity testing of germ isolates is a mandatory prerequisite for a targeted therapy strategy (Mezzatesta ML et al. 2012).

Previous antibiotic therapy increases the risk for 3MRGN Enterobacter ssp., stays in endemic areas increase the risk for 4MRGN Enterobacter spp.

1. Davin-Regli A et al. (2019) Enterobacter spp.: Update on Taxonomy, Clinical Aspects, and Emerging Antimicrobial Resistance. Clin Microbiol Rev 32:e00002-19.
2. De Oliveira DMP et al (2020) Antimicrobial resistance in ESKAPE pathogens. Clin Microbiol Rev 33:e00181-19.
3. Hof H et al (2019) Enterobacter. In: Hof H, Schlüter D, Dörries R, eds Duale Reihe Medizinische Mikrobiologie. 7th, completely revised and expanded edition. Stuttgart: Thieme p 421
4. KRINKO (2012): Hygiene measures in case of infections or colonization with multiresistant gram-negative rods. Recommendation of the Commission for Hospital Hygiene and Infection Prevention (KRINKO) at the Robert Koch Institute (RKI). Bundesgesundheitsblatt 10: 1311-1354.
5. Loiwal V et al (1999) Enterobacter aerogenes outbreak in a neonatal intensive care unit. Pediatr Int. 41:157-61.
6. Mezzatesta ML et al. (2012) Enterobacter cloacae complex: clinical impact and emerging antibiotic resistance. Future Microbiol 7: 887-902.
7. Vale de Macedo GHR et al. (2021) Interplay between ESKAPE Pathogens and Immunity in Skin Infections: An Overview of the Major Determinants of Virulence and Antibiotic Resistance. Pathogens 10:148.