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Antibiotics
Volume 14
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10.3390/antibiotics14030306
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Review

Rare or Unusual Non-Fermenting Gram-Negative Bacteria: Therapeutic Approach and Antibiotic Treatment Options

by
Nicholas Geremia
 1,2,
Andrea Marino
3,*,
Andrea De Vito
4,
Federico Giovagnorio
5,
Stefano Stracquadanio
6,
Agnese Colpani
4,
Stefano Di Bella
7,
Giordano Madeddu
4,
Saverio Giuseppe Parisi
5,
Stefania Stefani
6 and
Giuseppe Nunnari
3
1
Unit of Infectious Diseases, Department of Clinical Medicine, Ospedale “dell’Angelo”, 30174 Venice, Italy
2
Unit of Infectious Diseases, Department of Clinical Medicine, Ospedale Civile “S.S. Giovanni e Paolo”, 30122 Venice, Italy
3
Unit of Infectious Diseases, Department of Clinical and Experimental Medicine, ARNAS Garibaldi Hospital, University of Catania, 95122 Catania, Italy
4
Unit of Infectious Diseases, Department of Medicine, Surgery and Pharmacy, University of Sassari, 07100 Sassari, Italy
5
Department of Molecular Medicine, University of Padua, 35121 Padua, Italy
6
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy
7
Clinical Department of Medical, Surgical and Health Sciences, Trieste University, 34129 Trieste, Italy
*
Author to whom correspondence should be addressed.
Submission received: 26 February 2025 /Revised: 12 March 2025 /Accepted: 14 March 2025 /Published: 16 March 2025

Abstract

:
Non-fermenting Gram-negative bacteria (NFGNB) are a heterogeneous group of opportunistic pathogens increasingly associated with healthcare-associated infections. WhilePseudomonas aeruginosa,Acinetobacter baumannii, andStenotrophomonas maltophilia are well known, rarer species such asBurkholderia cepacia complex,Achromobacter spp.,Chryseobacterium spp.,Elizabethkingia spp.,Ralstonia spp., and others pose emerging therapeutic challenges. Their intrinsic and acquired resistance mechanisms limit effective treatment options, making targeted therapy essential.Objectives: This narrative review summarizes the current understanding of rare and unusual NFGNB, their clinical significance, resistance profiles, and evidence-based therapeutic strategies.Methods: A literature review was conducted using PubMed, Scopus, and Web of Science to identify relevant studies on the epidemiology, antimicrobial resistance, and treatment approaches to rare NFGNB.Results: Rare NFGNB exhibits diverse resistance mechanisms, including β-lactamase production, efflux pumps, and porin modifications. Treatment selection depends on species-specific susceptibility patterns, but some cornerstones can be individuated. Novel β-lactam/β-lactamase inhibitors and combination therapy approaches are being explored for multidrug-resistant isolates. However, clinical data remain limited.Conclusions: The increasing incidence of rare NFGNB requires heightened awareness and a tailored therapeutic approach. Given the paucity of clinical guidelines, antimicrobial stewardship and susceptibility-guided treatment are crucial in optimizing patient outcomes.

    1. Introduction

    Non-fermenting Gram-negative bacteria (NFGNB) are a diverse group of aerobic, non-spore-forming bacilli that do not utilize carbohydrates through fermentation [1]. Commonly found in soil and water, they have emerged as significant opportunistic pathogens, particularly in healthcare settings. The most common NFGNB arePseudomonas aeruginosa,Acinetobacter baumannii, and species of the genusStenotrophomonas [2]. The pathogenicity of NFGNB is often linked to their intrinsic resistance to multiple antibiotics and their capacity to acquire additional resistance mechanisms [3]. This resistance complicates treatment options and poses substantial challenges in clinical management. For instance,P. aeruginosa is known for its antibiotic resistance, making infections difficult to treat [4]. In recent years, infections caused by rare or unusual NFGNB have been increasingly reported, especially among immunocompromised individuals and patients with prolonged hospital stays [5,6,7,8]. These infections are associated with high morbidity and mortality rates, underscoring the need for effective therapeutic strategies [9,10]. Developing new antibiotics and optimizing existing therapeutic approaches are crucial in addressing infections caused by these resistant pathogens [11]. Novel β-lactam/β-lactamase inhibitor (BL/BLI) combinations, such as ceftazidime–avibactam (C/A) and ceftolozane–tazobactam (C/T), have shown promise against certain multidrug-resistant Gram-negative bacteria [12]. Additionally, cefiderocol (FDC), a siderophore cephalosporin, has demonstrated efficacy against a broad spectrum of Gram-negative pathogens, including NFGNB [13,14]. However, most studies focus onP. aeruginosa,A. baumannii, andS. maltophilia; data on rare or unusual NFGNB are limited, making it challenging to develop standardized treatment protocols and fully understand their epidemiology and resistance patterns. Moreover, rare or unusual NFGB comprise a heterogeneous bacteria group with essential differences between different genera and antibiotic spectra activity [15]. This review aims to provide a comprehensive overview of rare or unusual NFGNB, focusing on their taxonomy, microbiological characteristics, and the latest therapeutic approaches, including emerging antibiotic treatment options. Enhancing our understanding of these pathogens and available treatments can improve clinical outcomes and inform future research directions.

    2. Taxonomy and Microbiology

    2.1. General Characteristics and Microbiological Diagnosis

    The heterogeneous group of NFGNB contains aerobic, non-spore-forming bacilli that do not ferment carbohydrates and derive energy by using simple carbohydrates in an oxidative fashion [1,2].
    NFGNB typically grows well on standard culture media, such as blood agar, often appearing without hemolysis [16]. Instead, their growth is enhanced on chocolate agar, particularly with fastidious species likeBurkholderia andStenotrophomonas [17]. Commercial test systems such as API 20NE, Phoenix, MicroScan, and Vitek 2.0 can easily identify NFGNB. However, misidentification is frequent, and the differentiation of species can be particularly challenging. For example, commercial diagnostic tools can confoundBurkholderia spp. withAchromobacter spp. orRalstonia spp. and, in some cases, may require additional testing for correct microbiological identification [18,19]. Moreover, for some species, such asAlcaligenes spp. orAchromobacter spp., biochemical identification at the species level is not possible [18]. For these reasons, new microbiological innovations such as 16S rRNA gene sequencing or matrix-assisted laser desorption/ionization–time of flight (MALDI-TOF) are requested to identify some NFGNB [18].

    2.2. Taxonomy

    NFGNB belong to multiple taxonomic groups, primarily the Pseudomonadota phylum and some from the Bacteroidota phylum [18]. The Bacteroidota phylum consists of three main classes, but the two most clinically relevant are Flavobacteriia and Sphingobacteriia [20]. NFGNB Bacteroidota can have a clinical impact, as shown inFigure 1.
    The Pseudomonadota phylum is divided into Alphaproteobacteria, Betaproteobacteria, and Gammaproteobacteria, with the last two classes having primary clinical importance [18].
    Taxonomic complexity and phenotypic similarity represent the most challenging issues for this bacterial group [18]. The widespread use of ribosomal 16S RNA gene sequence analysis has helped to clarify the taxonomic classification of most of these organisms. It has undergone significant taxonomic revisions, with some new species identifications [19]. Pseudomonadota is represented inFigure 2.

    2.3. Virulence Factors, Role of the Biofilm and General Consideration on Antibiotic Resistance

    Several virulence factors are present in NFGNB. Many species had adhesion structures that are fundamental to initiating that process of colonization and biofilm formation. Typically, NFGNB produce fimbriae (or attachment pili), as well as other surface adhesins, such as nonpilus or afimbrial adhesins [21]. Some bacteria can have flagella that mediate motility in viscous media or over surfaces [2]. In NFGNB, the release of toxic compounds (such as exotoxins) and extracellular enzymes that compromise mucosal integrity can reduce the host’s immune system activity and play a role in the infection progression and potentially lead to systemic dissemination [2,4]. Although lipopolysaccharide (LPS), a fundamental compound of the external membrane of Gram-negatives, can also play an essential role in pathogenetic processes relating to local and systemic inflammation [2,4,22]. Specific accessory structures also contribute to the pathogenesis of NFGNB, such as secretion systems, which are utilized by many bacterial pathogens to transport various protein factors (e.g., adhesins, exotoxins, and exoenzymes) onto the bacterial surface, into the surrounding environment, or directly into host cells, disrupting the normal cellular functions and promoting infection [2]. Biofilm is crucial in NFGNB infections; it can permit survival on surfaces and some medical devices, representing a significant risk factor for hospital-acquired infections [23]. Moreover, biofilm significantly impacts antibiotic therapy effectiveness and can lead to immune escape, having a substantial role in the difficulty of NFGNB eradication [2,4,23].
    Most NFGNB can survive or even replicate under adverse environmental conditions and can commonly be found in water, soil, plants, vegetables, insects, and other sources [24]. Aerobic NFGNB, other than the most widely describedP. aeruginosa andA. baumannii, can be part of the transient physiologic flora and, in many cases, are not pathogenic for humans [18,19]. However, the rise of immunocompromised conditions in modern medicine has played a significant role in the augmented incidence of these rare bacteria [25].
    NFGNB exhibit high intrinsic resistance to major antimicrobial classes, often limiting available treatment options. Both intrinsic and acquired resistance mechanisms have been identified, varying significantly in type and prevalence among different species.
    Antimicrobial therapy should be based on in vitro antimicrobial susceptibility testing (AST) and, whenever possible, the minimum inhibitory concentrations (MICs) of relevant antimicrobials should be determined [19]. However, no specific breakpoints are available due to the lack of standardized susceptibility testing for several antibiotics in this group of microorganisms [26] and the paucity of clinical data. Moreover, many NFGNB have intrinsic resistant patterns that can be particularly challenging in clinical scenarios.Figure 3 shows the intrinsic resistance of the principal species.

    3. Achromobacter

    First recognized in 1923 by the Committee of the Society of American Bacteriologists, 22 species of the genus Achromobacter have been identified so far, and it is continuously evolving; the most common species worldwide isA. xylosoxidans [28,29,30]. The distribution of the other species follows a geographical pattern, withA. dolens andA. insuavis being the most common in Europe [31]. GenusAchromobacter is an obligately aerobic, non-fermentative, oxidase- and catalase-positive, and indole-, urease-, and DNase-negative bacterium [32]. While the identification of the genusAchromobacter has become feasible using MALDI-TOF, allowing us to distinguish it from other non-fermentative bacteria, species identification is still challenging due to the limitations of the MALDI-TOF database and the non-extensive availability of sequencing methods [33].
    Although mainly identified from patients with cystic fibrosis,Achromobacter spp. infection has also been described in subjects with other underlying conditions, including immunocompetent hosts. Reported cases are mostly hospital-acquired and associated with indwelling catheters. Also, nosocomial outbreaks related to contaminated devices have been described [34,35].Achromobacter can cause pneumonia and various other clinical manifestations [36]; case reports and case series have shown a broad clinical spectrum, suggesting thatAchromobacter could affect virtually any organ [34,37,38,39,40].Figure 4 showsA. xylosoxidans growing in a Petri dish.
    Regarding antimicrobial susceptibility,Achromobacter has intrinsic resistance to cephalosporins [except ceftazidime (CAZ)], aztreonam (AZT), ertapenem and aminoglycosides (AMGs); several resistance mechanisms have been described so far.Table 1 synthesizes the principal resistant mechanisms inAchromobacter spp.
    Among the efflux pumps characterized, AxyABM has been demonstrated to play a crucial role in the extrusion of cephalosporin, AZT, and chloramphenicol [41]. However, it cannot be the sole mechanism underlying antibiotic resistance [43]. As for resistance to AMG, the efflux pump AxyXY-OprZ has been described as a significant determinant of high-level resistance. Also, it accounts for resistance to cefepime (FEP), carbapenems, fluoroquinolones (FQs), tetracyclines (TETs), and erythromycin, despite not being the only resistance determinant [44]. Regarding enzymes,Achromobacter spp. constitutively produces OXA-114 β-lactamase, which hydrolyses piperacillin, ticarcillin, benzylpenicillin, and cephalothin; however, the existence of activity against piperacillin, and whether it is affected by tazobactam or not, is not yet clear. The presence of OXA-114 has been proposed as an identification tool for the bacteria. Moreover,Achromobacter spp. can acquire other β-lactamases, including VIM and IMP [45]. The Tripoli metallo-β-lactamase (MBL) was first discovered in a strain ofA. xylosoxidans [46].
    Susceptibility breakpoints are not widely accepted; European Committee on Antimicrobial Susceptibility Testing (EUCAST) breakpoints are only given for trimethoprim–sulfamethoxazole (SXT) [47]. At the same time, cephalosporins, imipenem (IMP), ertapenem, AMG, FQ, and colistin (COL) have intrinsically insufficient activity for breakpoints to be determined [47]. In Clinical and Laboratory Standards Institute (CLSI) recommendations for “Other Non-Enterobacterales”, breakpoints are given for piperacillin, P/T, ticarcillin–clavulanate, CAZ, FEP, cefotaxime or ceftriaxone, cefoperazone, moxalactam, AZT, IMP, MEM, gentamicin (GNT), tobramycin, amikacin (AMK), netilmicin, TET, FQ, SXT, and chloramphenicol [48]. As for other promising antibiotics, a study by Beauruelle et al., reporting the in vitro susceptibility testing of 22 antibiotics onAchromobacter spp. from patients with cystic fibrosis, showed promising results for IMP (70–91% susceptibility) and FDC (91%) [49].
    Despite the increasing data regarding new therapeutic options, the treatment ofAchromobacter spp. remains challenging, especially in patients with high exposure to multiple antibiotics.

    4. Alcaligenes

    Alcaligenes is a genus of Gram-negative, aerobic, non-fermenter, oxidase-positive, catalase-positive, motile rod-shaped bacteria belonging to the family Alcaligenaceae. These bacteria are widely distributed in environmental reservoirs such as soil, water, and organic matter and can colonize the human gastrointestinal tract. Among its species,Alcaligenes faecalis is the most clinically relevant, primarily causing opportunistic infections in immunocompromised individuals or patients with underlying health conditions [50]. Although considered a relatively rare pathogen,A. faecalis has gained prominence due to its association with healthcare-associated infections and the emergence of significant antimicrobial resistance mechanisms. Its ability to survive in aqueous environments makes it a potential contaminant in hospital settings, particularly in devices such as respirators, hemodialysis systems, and intravenous catheters [51].
    A six-year retrospective study in Taiwan reported 61 cases ofA. faecalis infections between 2014 and 2019, with cystitis being the most frequently observed condition (41%), followed by diabetic foot ulcers (14.8%), pneumonia (13.1%), and bloodstream infections (BSIs) (4.9%) [51]. These infections were frequently polymicrobial, withA. faecalis isolated alongside other pathogens, such asProteus vulgaris,Enterococcus spp., andP. aeruginosa. The majority of infections occurred in elderly patients with comorbidities, particularly those with a history of intravenous antibiotic exposure within three months of diagnosis.A. faecalis has also been isolated from surgical wounds, prosthetic devices, and respiratory secretions, reinforcing its role as a significant opportunistic pathogen [52]. Moreover, geographic variability in its prevalence and clinical impact indicates that local environmental factors and healthcare practices influence its epidemiology. While typically opportunistic,A. faecalis can occasionally act as a primary pathogen in severe cases, such as endocarditis, meningitis, or septicemia [50].
    A key challenge in managingA. faecalis infections lies in its ability to resist multiple classes of antibiotics. Several mechanisms contribute to its multidrug-resistant (MDR) phenotype. Producing β-lactamase enzymes, including carbapenemases, allows the bacterium to hydrolyze and inactivate β-lactam antibiotics, such as penicillins, cephalosporins, and carbapenems. Specific genes such asblaOXA-10 andblaPER-1 have been identified inA. faecalis strains, encoding β-lactamases with activity against a broad spectrum of β-lactams [53].
    Efflux pumps further complicate treatment by actively expelling antibiotics, reducing their intracellular concentrations and effectiveness. The AcrAB-TolC efflux system, encoded by theacrAB genes, is a well-characterized multidrug efflux pump in Gram-negative bacteria, includingA. faecalis. This system is critical in resistance to FQs, such as ciprofloxacin (CPX) and levofloxacin (LVX) [51]. Resistance to FQs is also mediated by mutations in thegyrA andparC genes, which encode the subunits of DNA gyrase and topoisomerase IV, respectively [23,51].
    Another major contributor to resistance is its ability to form biofilms on medical devices and host tissues. Biofilms act as protective barriers, reducing the penetration of antibiotics and shielding bacteria from host immune responses. This biofilm-associated resistance is particularly problematic in infections involving prosthetic devices, catheters, and other medical implants [54]. In recent years, the emergence of extensively drug-resistant (XDR) strains ofA. faecalis has shown resistance to almost all available antibiotics. In the 2019 study, susceptibility testing revealed that the best sensitivity rate was 66.7% for IMP, MEM, and CAZ, while CPX and P/T demonstrated sensitivity rates below 50% [51].
    TreatingA. faecalis infections requires a carefully tailored approach based on AST, as empirical antibiotic therapy is often ineffective due to the organism’s resistance profile. However, it is essential to remember that no specific breakpoints are available for EUCAST. In general, carbapenems, such as IMP and MEM, remain the first-line agents for treating serious infections caused byA. faecalis. However, the increasing prevalence of carbapenem-resistant strains has limited their utility. In cases involving XDRA. faecalis, tigecycline (TG) has emerged as a viable option, even demonstrating efficacy against strains resistant to carbapenems and other classes of antibiotics [51]. GNT and AMK may also be effective, mainly when combined with β-lactams, though their nephrotoxicity and ototoxicity require careful monitoring, especially in elderly patients. FQs, such as LVX, have been used for less severe infections, but their efficacy is increasingly undermined by resistance [53].
    For biofilm-associated infections, adjunctive therapies targeting biofilm disruption are gaining attention. These include enzymatic agents that degrade the biofilm matrix and novel anti-biofilm compounds that enhance antibiotic penetration [54]. Emerging therapies, such as bacteriophages and antimicrobial peptides, are being explored for their potential to combat MDR and XDR pathogens, includingA. faecalis. These approaches offer promise, particularly for infections refractory to conventional treatments.
    Developing new antibiotic combinations, such as C/A, meropenem–vaborbactam (M/V), and FDC, represents another promising avenue [13,55,56]. While their efficacy againstA. faecalis has not been extensively studied, these agents offer hope due to their activity against other resistant Gram-negative pathogens [13].

    5. Burkholderia

    Initially,Burkholderia species were classified under the Pseudomonadaceae family. In the early 1990s, they were included in the Burkholderiaceae family asB. cepacia [57,58]. The genus is divided into two large groups:B. cepacia complex (Bcc) andB. pseudomallei complex (Bpc) [59]. The two groups do not comprise all the species.
    In the Bcc group, different species are included. These bacteria cause infections in humans, especially in immunocompromised and cystic fibrosis patients and in immunocompetent individuals [60,61]. The modifications occurring in the lung during this pathology are favorable for colonization by various pathogens, including Bcc, which is the most threatening for cystic fibrosis patients [62,63]. The most virulent species of the complex areB. cenocepacia andB. multivorans [59,64,65].B. cenocepacia, due to its aggressive behavior and persistence in the lung airways, is considered a relative contraindication for lung transplants [66]. Despite the adequate treatment of the infections, the disease often results in chronic illness [66]. In some cases, Bcc species can develop the “cepacia” syndrome, characterized by necrotizing pneumonia and BSIs, usually affecting immunocompetent individuals [67,68]. Pathogens in the Bcc express many antibiotic-resistant mechanisms, it difficult to treat them treat correctly [59,69]. Also, the determination of antimicrobial susceptibility is a matter of debate. The CLSI offers the cut-off values of the main antibiotics employed in Bcc treatment. At the same time, the EUCAST has not set any cut-off values for any antibiotic under either method due to the few studies available and the absence of correlation between MICs obtained in vitro and the clinical result in vivo [70]. Moreover, Bcc expresses numerous intrinsic resistance patterns, such as resistance to aminopenicillin (excluded for piperacillin and P/T), cephalosporins (excluded CAZ and FEP), AZT ertapenem, CPX, chloramphenicol, AMGs, trimethoprim, Fosfomycin, and COL [27]. This complex situation is a threat to physicians in terms of the choice of the correct treatment. In vitro data and previous studies show that SXT, CAZ, MEM, and doripenem are the most effective antibiotics [48,71,72]. Minocycline (MIN) and doxycycline (DOXI) are considered good oral alternatives [73], but the choice is only supported by in vitro susceptibility. The new BL/BLI, including C/A and M/V, could be an alternative option, overwhelming the production of β-lactamases conferred by thepenA gene. Still, they succumb to efflux pump activity [74]. Eravacycline, a novel antibiotic of the TET family with broad-spectrum activity, is reported to have some activity againstB. cenocepacia, but with MIC50/90 values of 8/32 g/L, which are relatively moderate/high [75]. The available studies suggest the use of combinations based on CAZ, MEM, doripenem, C/A, C/T, and FQs, coupled with FDC, for their in vitro activities [57,59,64,69,76,77]. In a summary of multinational surveillance studies, 94 Bpc species were collected and tested for FDC, with MIC90 values ranging from 0.03 to 1 g/L, suggesting good activity against Bpc pathogens [78]. Another study evaluated the susceptibility of FDC of the various non-fermenter species, including 7 isolates of Bpc with all strains inhibited by FDC with MIC < 25 g/L [79]. Delafloxacin (DELA), a fourth-generation quinolone, has been evaluated in vitro against Bcc pathogens. In detail, 57 isolates of Bcc were tested: MIC50 values were 0.25 g/L forB. cepacia andB. multivorans and 2 g/L forB. cenocepacia. The authors concluded by showing the potential activity of DELA [80]. Other therapeutic strategies include a combination of inhalation drugs with intravenous administration, in particular, inhaled tobramycin with FDC [64] or prolonged ATZ [81,82]. However, results are scarce. Furthermore, new therapies, such as bacteriophages [83] and large-molecule polycationic glycopolymers, are under evaluation for clinical practice, with the latter restoring antibiotic activity [84]. Finally, new compounds based on auranofin analogs have shown promising results in eradicating persistent infection, thus enabling newer treatment options, alone or combined with antibiotics [85].
    The Bpc group includesB. mallei (the causative agent of glanders) [86],B. pseudomallei (the causative agent of Melioidosis) [87],B. humpydoensis, andB. thailandensis [59,88].B. mallei andB. pseudomallei are considered biological weapons [86]. Although both infections can lead to severe disease with high mortality rates if not promptly treated,B. pseudomallei is far more common in humans thanB. mallei and expresses more sophisticated mechanisms of antimicrobial resistance [59,88,89,90].B. pseudomallei is considered a tropical pathogen. It is usually encountered in Thailand, but is likely to be widespread in Southeast Asia, the Indian subcontinent, Sri Lanka, China, and Papua Nuova Guinea [91,92,93]. Clinical manifestations ofB. pseudomallei are varied, ranging from cutaneous disease to sepsis syndrome with necrotizing pneumonia [89]. Also, the disease can be divided into four types: (i) an acute type, (ii) a subacute type, (iii) a chronic type, and (iv)a latent or asymptomatic type [89,94]. In the acute type, there are two stages of therapy: the intensive phase and the eradication phase [89,94]. Notably, although the Bpc pathogens share a lot of genetic homologies,B. pseudomallei has more complex gene expression thanB. mallei andB. thailandensis, ultimately leading to much more pronounced antimicrobial resistance [59,95].B. pseudomallei is intrinsically resistant to anti-bactericidal penicillins [except for amoxicillin–clavulanic acid (A/C)], first-, second-, and third-generation cephalosporins (except for CAZ), AMGs, and rifamycins [91,94,96,97]. For Bpc, EUCAST has different interpretation breakpoints for the principal antibiotic used in case of infections (i.e., amoxicillin–clavulanic acid, CAZ, IMP, MEM, DOXI, TET and SXT) [47]. The intensive phase is based on intravenous treatment with CAZ, MEM, or IMP [89,90,94,98,99], with a minimum duration of therapy of 2 weeks. This lasts up to 4–6 weeks if metastatic infection coexists [94,100]. The previously cited antibiotics can be coupled with SXT if deep-seated infections exist. The eradication phase begins when the patient is hemodynamically stable, the C-reactive protein (CRP) levels have fallen, and any abscesses or deep-seated infections have significantly improved or been resolved [90,94,99]. This phase lasts 3 to 6 months and consists of SXT, alone or combined with DOXI or A/C [89,94]. Treatment forB. mallei is similar to that forB. pseudomallei, consisting of intravenous therapy with CAZ, MEM, or IMP [99,101] and oral SXT, A/C, or DOXI [99,101,102]. Among new antimicrobial therapies, Burnard et al. tested 246B. mallei clinical isolates for FDC, showing MICs ranging from 0.03 to 16 g/L [103]. Tackling the antimicrobial resistance patterns of Bpc, new therapeutic strategies have been studied. Antibiotic treatments with C/T, finafloxacin, rifampicin, auranofin, doripenem, ertapenem, TG, moxifloxacin (MOXI), and MMV688271 (a new antifungal agent) have been tested forB. pseudomallei, showing in vitro susceptibility [104]. Alongside these drugs, potentiation compounds have been evaluated, like silver nanoparticles (AgNPs) and NanoClusters [104]. Also, the use of antibody therapy, antimicrobial peptides, and phage therapy has been proposed [104]. ForB. mallei, antibiotic potentiation, with a whole-killed vaccine coupled with MOXI, SXT, or azithromycin, has been suggested for treatment [104]. Resistant mechanisms are shown inTable 2.
    B. gladioli are commonly found in water and soil and can serve as nosocomial pathogens. While infections are rare, occasional outbreaks have been documented, and the development of multidrug resistance remains a potential issue [19].B. gladioli has been documented as a cause of disease in patients with cystic fibrosis, chronic granulomatous disease and other immunocompromising conditions [19,110]. No specific breakpoints are available, and this could represent particular challenges due to its potential for multidrug resistance. AST should be guided by susceptibility testing. Standard treatment options include SXT, MEM, IMP, and FQ. In severe cases, combination therapy may be necessary, and surgical intervention might be required for localized infections such as abscesses. For patients with cystic fibrosis or other immunocompromising conditions, prolonged treatment and careful monitoring are essential to prevent recurrence [111].

    6. Elizabethkingia

    The bacteria belonging to theElizabethkingia genus are aerobic, non-fermenting, non-motile, catalase-positive, oxidase-positive, indole-positive, and Gram-negative bacilli belonging to the family Flavobacteriaceae. They were first described by Centers for Disease Control and Prevention (CDC) microbiologist Elizabeth O. King in 1959 [112,113]. The genus was initially classified as Flavobacterium. It was then reclassified as Chryseobacterium in 1994, and received its current taxonomic designation in 2005 [114]. It has an environmental distribution (e.g., water, soil), but can also colonize hospital settings [113].
    In recent years, there has been an increase in reported outbreaks ofElizabethkingia infections, likely due to improved identification methods (e.g., MALDI-TOF) and a rise in the number of immunocompromised individuals. Countries reporting numerous cases include Saudi Arabia and India; a link may exist between warmer climates and mosquitos [115,116].
    Infections caused byElizabethkingia spp. have been reported worldwide, with documented outbreaks in North America, Europe, Asia, and Africa. The outbreaks often occur in hospital settings, especially in intensive care units (ICUs) and neonatal wards. Currently, this genus is known to comprise eight species, which includeE. meningoseptica,E. anophelis, E. miricola,E. bruuniana,E. ursingii,E. argenteiflava,E. umeracha, andE. occulta [114,117,118]. However,E. meningoseptica,E. anophelis, andE. miricola are the most common species. Historically,E. meningoseptica was the most commonly isolated species in the genus. However,E. anopheles has emerged as the predominant pathogen, accounting for 59–99% of clinical isolates, whileE. meningoseptica constitutes only about 1–21% (Lin et al., 2019). This apparent shift may be due to improved identification techniques, which mainly use MALDI-TOF [113].
    Elizabethkingia can cause various infections, including meningitis, bloodstream infections (BSIs), pneumonia, urinary tract infections (UTIs), and skin and soft tissue infections (ABSSIs). Infections are particularly problematic in newborns and immunocompromised patients, and are recognized in particular for causing neonatal sepsis and meningitis, particularly in premature infants [114]. A large case series in children, reported in a review by Dziuban et al., demonstrated that 73.9% of cases presented with meningitis, 23.7% with sepsis, 6.7% with pneumonia, and 2.5% with gastroenteritis/diarrhea [114].Elizabethkingia infections are implicated in outbreaks of severe infections in about one-third of cases, with mortality rates between 24% and 60% [113,114,119,120,121]. Typically, these outbreaks are linked to many sources, including contaminated saline solutions, respiratory equipment, and skin drains [122].Figure 5 showsE. anophelis growing in the Petri dish.
    Elizabethkingia spp. is known for its resistance to many commonly used antibiotics, making the treatment of infections difficult. It constitutively produces β-lactamases and is naturally resistant to most β-lactam drugs, including carbapenems and AZT, except for piperacillin and P/T. Three β-lactamases were identified inElizabethkingia: one D-class serine (CME) and two wide-spectrum MBLs with carbapenemase activity, namely, BlaB, and GOB [123]. No breakpoints are available for EUCAST, and for this reason most studies use breakpoints, which are interpreted according to CLSI guidelines. These showed that the most effective agents for in vitro susceptibility were MIN (100%), LVX (65–80%), and SXT (63–90%). Sensitivity to carbapenems was less than 2% and sensitivity to cephalosporins and AMG was also low [123,124]. Additionally, other researchers reported high sensitivity to rifampin (94%) [125]. Both in vitro and in vivo data on FDC forElizabethkingia infections are scant; however, a case series of 22 CPX-non-susceptible strains tested for FDC revealed high MICs (>32 mg/L) [126]. Notably,Elizabethkingia can produce biofilms, with over one-third of strains being strong biofilm formers [125]. This is especially significant when the respiratory tract is affected, such as ventilator-associated pneumonia in patients with bronchiectasis [127].

    7. Moraxella

    Moraxella is a genus of Gram-negative, aerobic, oxidase-positive bacteria, withM. catarrhalis being the most clinically significant species [128].M. catarrhalis commonly colonizes the human upper respiratory tract and is associated with various infections [129,130]; commonly, it causes otitis media and sinusitis, especially in children, and lower respiratory tract infections, especially in people with chronic obstructive pulmonary disease [131,132,133]. Invasive infections are less common but cases have been reported of BSIs, endocarditis, septic arthritis, and meningitis, especially in immunocompromised patients [134]. Other less common species areM. lacunata,M. osloensis,M. nonliquefaciens, andM. bovis [134]. These species rarely cause infection in immunocompetent individuals.M. osloensis, typically a commensal organism, has been associated with BSIs and septic arthritis in immunocompetent individuals [135]. Similarly,M. lacunata,M. nonliquefaciens, andM. bovis are generally considered part of the normal human flora but can occasionally cause infections, particularly in individuals with cancer or compromised immune systems [136,137,138,139].
    M. catarrhalis is also known for producing β-lactamase enzymes, contributing to its antibiotic resistance profile. In particular, studies have reported that β-lactamase production rates inM. catarrhalis isolates range from 80% to 99% [140,141,142]. These enzymes, primarily BRO-1 and BRO-2, hydrolyze the β-lactam ring of susceptible antibiotics, rendering them ineffective. BRO-1 is more prevalent and typically associated with higher MICs for penicillin varieties compared to BRO-2 [143]. These enzymes are synthesized in the cytoplasm and transported to the periplasmic space via the twin-arginine translocation (Tat) pathway [144]. However, β-lactamase inhibitors such as clavulanic acid can inactivate these β-lactamases [145,146]. Additionally,M. catarrhalis releases outer membrane vesicles containing β-lactamases, which can inactivate β-lactam antibiotics in the extracellular environment, potentially protecting neighboring bacteria and complicating polymicrobial infections [147,148]. The high prevalence of β-lactamase production inM. catarrhalis necessitates careful selection of antibiotic therapy. Despite that, A/C remains the treatment of choice, as other molecules can be associated with other resistant mechanisms. Also, resistance to SXT, macrolides, and TET has been reported, underscoring the importance of local susceptibility patterns in guiding effective treatment [149,150,151,152]. Fortunately, the interpretation of AST is permitted by the presence of breakpoints for EUCAST and CLSI [47,48].Figure 6 shows evidence ofM. catarrhalis colonies on TSA.
    Regarding new antibiotic treatments, limited data are available on the efficacy of agents such as FDC, M/V, C/A and C/T againstM. catarrhalis. These antibiotics have shown promise against various MDR Gram-negative bacteria; however, their specific activity againstM. catarrhalis has not been studied extensively.

    8. Other Rare Non-Fermenting Gram-Negative Bacteria

    Many other NFGNB have a clinical impact on human infections [15], further complicating treatment decisions due to the lack of specific breakpoints and standardized therapeutic approaches.
    Ochrobactrum spp. are non-enteric, Gram-negative organisms closely phylogenetically related to the genusBrucella. The taxonomic classification is still problematic forOchrobactrum spp., with publication by bacterial taxonomists who includedOchrobactrum within the genusBrucella [153]. Even though they are considered pathogens with low virulence, clinical reports have increasingly been described in the literature [154,155]. Most cases were related to hospital-acquired infections, immunocompromised hosts, or patients with tumors [155,156]. Species isolates from human samples areO. anthropic,O. intermedium,O. oryzae,O. pseudogrignonense,O. pseudintermedium, andO. tritici [155]. Treatment is often complex due to the emerging problem of antibiotic resistance. In particular, many strains show resistance to penicillins, cephalosporins and, in some cases, carbapenems [157]. Resistance to β-lactam antibiotics is associated with a chromosomal gene (blaoch) similar to the Ambler-class C β-lactamase gene. This gene encodes an AmpC-like enzyme called OCH [158]. Leading carbapenem resistance, a plasmid-borneblaoxa-181 gene has been found in someO. intermedium strains [159]. Although this genus could show resistant mechanisms,Ochrobactrum maintains susceptibility to CPX and SXT, suggesting that the combination of these two drugs may be helpful for the empirical treatment ofOchrobactrum infections [157]. Moreover, in most cases described in the literature, AMG, FQ, carbapenem, and SXT were used alone or as a part of the combination treatment [155].
    Bergeyella spp. are uncommonly identified as a cause of human disease, often presenting as ABSSIs, BSIs, and infective endocarditis [160].B. zoohelcum is the principal human pathogen, and it has been isolated from wound infections following animal bites but also in severe human infections, such as BSIs, endocarditis, and meningitis [160,161].Bergeyella is usually susceptible to most antimicrobial agents, such as β-lactams and FQs. Successful treatment with ampicillin–sulbactam, A/C, cefazolin with GNT, cefuroxime, and CPX has been reported [160,162,163].
    Weeksella virosa is rarely and uncommonly implicated in infections in humans. It is clinically associated with BSIs, peritonitis, pneumonia, and UTIs in immunocompromised patients and, in many cases, related to nosocomial infections [164,165]. Typical empirical treatment should include piperacillin, AZT, or carbapenems; instead, SXT, CPX and AMG should not be used unless AST is available [164,166].
    Chryseobacterium spp. are ubiquitous in soil and water and have also been recovered from foods and the hospital environment [167].C. indologenes is the variant most frequently isolated from human specimens [168]. Most reported cases are nosocomial, and are often associated with immunosuppression or indwelling catheters.Chryseobacterium spp. has been reported in the cases of BSIs, peritonitis, pneumonia, empyema, pyelonephritis, cystitis, meningitis, and central venous catheter (CVC)-related infections [169].C. indologenes is intrinsically resistant to penicillin (excluding piperacillin and P/T), AZT, third-generation cephalosporins (excluding FEP), carbapenem, and AMG [27]. Moreover, it is uniformly resistant to erythromycin, clindamycin, vancomycin, and teicoplanin [15]. The most potent agents reported againstChryseobacterium spp. are quinolones (garenoxacin, gatifloxacin, and LVX, each with 98.0% susceptibility), SXT (>95% susceptibility), and rifampin (85.7% susceptibility) [170].
    The family Comamonadaceae includes the generaComamonas,Delftia andAcidovorax.Comamonas includesC. aquatica,C. kerstersii,C. terrigena, andC. testosteronei. The genusDelftia consists ofD. acidovorans, formerly designatedC. acidovorans. Finally,Acidovorax includesA. facilis,A. delafieldii, andA. temperans [15]. Rare cases of CVC-related BSIs (C. testosteroni,D. acidovorans,Acidovorax spp.), meningitis (C. testosteroni), endocarditis (C. testosteroni,D. acidovorans), conjunctivitis (C. testosteroni), and otitis media (D. acidovorans) have been reported [15]. The antibiotic treatment ofComamonas infections can be particularly challenging. Most clinical isolates ofComamonas are susceptible to various antibiotics, including P/T, cephalosporins, carbapenems, FQ, SXT, and AMG antibiotics [171]. However, in several cases,C. testosteroni was reportedly resistant to CPX, GNT, and CAZ [172]. Resistance to β-lactams class antimicrobials can occur due to the presence of several genes encoding Class A β-lactamases, oxacillinases (i.e.,blaOXA-1), and carbapenemases (i.e.,blaIMP-8 andblaGES-5) [171].D. acidovorans usually show susceptibility to CPX (90.7%), CAZ (94.4%), P/T (94.0%) and carbapenems (MEM susceptibility 94.6%, IMP susceptibility 94.2%) [173,174]. AMG should not be used because of the high risk of resistance [173].Acidovorax infections are so rare that no general treatment recommendations can be made; in some cases, patients are treated with FQ or P/T [175].
    The genusOligella includesO. urethralis (derived fromM. urethralis and CDC group M-4) andO. ureolytica (derived from CDC group IVe). Both species have been implicated in BSIs, arthritis, and genitourinary infections [19,176].O. urethralis is intrinsically susceptible to penicillins, cephalosporins, and carbapenems. In contrast,O. ureolytica can display decreased susceptibility to ampicillin or amoxicillin, suggesting chromosomal encoding of the penicillinase gene. FQ, AMG, and SXT show inconsistent activity in vitro againstO. ureolytica [176].
    Pandoraea spp. are usually isolated from soil, water, plants, fruits and vegetables. The most frequent infections are pneumonia (in many cases related to cystic fibrosis) and BSIs. Upper respiratory infections, osteomyelitis, pancreatitis, and endocarditis are rare [177].Pandoraea spp. is considered an MDR pathogen, and most species resist β-lactams and AMG [177]. A possible explanation for MDR is the germ’s production of certain enzymes, carbapenemases (i.e., OXA-62), and efflux pumps [178]. In cases of systemic infection, aggressive antimicrobial treatment is mandatory to reduce the risk of fatal outcomes. It could include carbapenems, especially IMP, or cephalosporins with SXT, followed by AMG and FQ [177].
    The genusPsyrobacter is an extremely rare human pathogen. Some cases are reported in meningitis, wound infections, and BSIs [179].
    The genusRalstonia is emerging as an opportunistic human nosocomial pathogen in immunocompromised patients, especially in persons with cystic fibrosis [180]. This genus comprises three species of human interest:R. insidiosa,R. mannitolilytica, andR. pickettii [180].Ralstonia spp. are generally MDR [181]. SXT and FQ antibiotics are considered the best treatment options [180,181]. However, TG also shows good in vitro activity againstRalstonia isolates [180]. Different resistant mechanisms were associated with this bacteria, including efflux pumps and β-lactamases (OXA-22-like and OXA-60-like subfamily) [180].
    Rhizobium spp. are phytopathogenic organisms in water, soil, and environmental plants. They are rarely associated with human infections. However, some cases are associated withR. radiobacter infections [182,183].Rhizobium spp. are generally susceptible to cephalosporins (second- and third-generation), ticarcillin, IMP, TET, COL, SXT, and FQs [19].
    Shewanella spp. is a genus of NFGNB that is rarely an opportunistic human pathogen [184]. A variety of factors can influence the infection. Firstly,Shewanella spp. are distributed in water environments. Recreational or occupational exposure, seafood ingestion, puncture wounds caused by marine organisms, or the direct exposure of a wound to aquatic environments can increase the risk of infection [185]. Secondly,Shewanella can be found in patients with immunocompromised states, including malignancies, severe heart failure, hepato-renal failure, and neutropenia [185]. SeveralShewanella spp. have recently emerged as worldwide pathogens, includingS. algae, S. putrefaciens, andS. xiamenensis [186,187,188].Shewanella spp. are generally resistant to penicillins but susceptible to third-generation cephalosporins, IMP, CPX, AMGs, SXT, and TETs [19].
    Bacteria belonging to theSphingobacterium are ubiquitous but rarely involved in human infections [189]. The few reported diseases resulting fromSphingobacterium usually occurred in severely comorbid patients and immunocompromised hosts [190].
    Sphingobacterium spp. in vitro are usually intrinsically resistant to many commonly used antibiotics and can grow in antiseptics and disinfectants [191].S. multivorum can produce extended-spectrum β-lactamase (ESBL) and MBL, resulting in resistance to penicillins, cephalosporins and carbapenems [192]. In addition,Sphingobacterium spp. show resistance to AMG and polymyxin B and are susceptible to FQ, TET, and SXT [190].
    InTable 3, we summarize the possible therapeutic options for different NFGNB.

    9. Discussion

    Rare or unusual NFGNB are emerging as increasingly important pathogens in community and healthcare settings, particularly among immunocompromised individuals and patients with underlying conditions. Despite their diverse taxonomy, these organisms share a common challenge: their intrinsic and acquired resistance mechanisms, which limit effective antibiotic options and complicate treatment strategies. The epidemiology of these rare NFGNB varies significantly, with some species likeBurkholderia andAchromobacter being more frequently associated with chronic infections, such as in cystic fibrosis patients [43,109]. In contrast, others, likeElizabethkingia andMoraxella, are more often linked to opportunistic infections in critically ill individuals [127,140]. Their ability to persist in hospital environments and form biofilms further contributes to outbreaks and increased morbidity.
    Antibiotic resistance among these pathogens is a significant concern. Many exhibit resistance to β-lactams, AMG, and FQ due to various mechanisms, including efflux pumps, β-lactamase production, and target site modifications [142]. Treatment options are often limited and require tailored approaches based on susceptibility testing. Novel BL/BLI combinations or FDC have shown promise in select cases. Combination therapy may be necessary in severe infections, especially in multidrug-resistant strains. Given the limited clinical data and the absence of standardized treatment guidelines for many of these organisms, further research is needed to establish optimal therapeutic regimens. Developing new antimicrobial agents, improved stewardship, and rapid diagnostic techniques will be critical in managing infections caused by these rare but increasingly relevant pathogens.

    10. Materials and Methods

    A comprehensive literature search was conducted to identify relevant studies concerning NFGNB infections, particularly on rare bacteria. The search strategy was implemented using online databases [PubMed (USA)/MEDLINE (USA)/Google Scholar (Google, Mountain View, CA, USA) ] and books written by experts in microbiology and infectious diseases. The search was not restricted by language, region, study type, or publication date and covered articles up to the cutoff date of January 2025. Conference abstracts or unpublished studies are also included. The following keywords and MeSH were used: “Achromobacter AND human infections”, “Achromobacter AND treatment”, “Achromobacter AND resistance mechanism”, “Alcaligenes AND human infections”, “Alcaligenes AND treatment”, “Alcaligenes AND resistance mechanism”, “Burkholderia AND human infections”, “Burkholderia AND treatment”, “Burkholderia AND resistance mechanism”, “Elizabethkingia AND human infections”, “Elizabethkingia AND treatment”, “Elizabethkingia AND resistance mechanism”, “Moraxella AND human infections”, “Moraxella AND treatment”, “Moraxella AND resistance mechanism”, “Ochrobactrum AND human infections”, “Ochrobactrum AND treatment”, “Ochrobactrum AND resistance mechanism”, “Bergeyella AND human infections”, “Bergeyella AND treatment”, “Bergeyella AND resistance mechanism”, “Weeksella AND human infections”, “Weeksella AND treatment”, “Weeksella AND resistance mechanism”, “Chryseobacterium AND human infections”, “Chryseobacterium AND treatment”, “Chryseobacterium AND resistance mechanism”, “Comamonas AND human infections”, “Comamonas AND treatment”, “Comamonas AND resistance mechanism”, “Delftia AND human infections”, “Delftia AND treatment”, “Delftia AND resistance mechanism”, “Acidovorax AND human infections”, “Acidovorax AND treatment”, “Acidovorax AND resistance mechanism”, “Oligella AND human infections”, “Oligella AND treatment”, “Oligella AND resistance mechanism”, “Pandoraea AND human infections”, “Pandoraea AND treatment”, “Pandoraea AND resistance mechanism”, “Psyrobacter AND human infections”, “Psyrobacter AND treatment”, “Psyrobacter AND resistance mechanism”, “Ralstonia AND human infections”, “Ralstonia AND treatment”, “Ralstonia AND resistance mechanism”, “Rhizobium AND human infections”, “Rhizobium AND treatment”, “Rhizobium AND resistance mechanism”, “Shewanella AND human infections”, “Shewanella AND treatment”, “Shewanella AND resistance mechanism”, “Sphingobacterium AND human infections”, “Sphingobacterium AND treatment”, “Sphingobacterium AND resistance mechanism”, “Rare Non-fermenting Gram-negative AND human infections”, “Non-fermenter bacteria AND human infections”, “Unusual AND Non-fermenting Gram-negative”, “Rare AND Non-fermenting Gram-negative”, “Unusual AND Non-fermenter bacteria”, “Rare AND Non-fermenter bacteria”. We screened the articles by title, abstract and full text. After an initial screening of titles and abstracts of the published articles, the reviewers evaluated the full articles to assess the eligibility for each study’s inclusion in this narrative review. A study was included to determine if it was likely to provide valid and valuable information according to their view’s objective.

    11. Conclusions

    Rare NFGNB pose an increasing challenge, particularly in immunocompromised patients and critically ill settings. Their intrinsic and acquired resistance limits treatment options, making susceptibility-guided therapy essential. In many cases, treatments are not guided by solid evidence-based literature. Enhancing diagnostic strategies, developing new antibiotics, and implementing research programs on this rare pathogenic entity will be crucial to optimizing infection management and combating resistance spread.

    Author Contributions

    Conceptualization, A.M., N.G. and A.D.V.; methodology, N.G.; validation, all authors; formal analysis, N.G. and F.G.; investigation, all authors; data curation, A.M., N.G., A.D.V., S.S. (Stefano Stracquadanio), F.G., A.C. and S.D.B.; writing—original draft preparation, all authors; writing—review and editing, N.G.; visualization, N.G. and S.S. (Stefano Stracquadanio); supervision, G.M., S.D.B., S.S. (Stefania Stefani), S.G.P. and G.N. All authors have read and agreed to the published version of the manuscript.

    Funding

    This research received no external funding.

    Institutional Review Board Statement

    Not applicable.

    Informed Consent Statement

    Not applicable.

    Data Availability Statement

    Not applicable.

    Conflicts of Interest

    The authors declare no conflicts of interest.

    Abbreviations

    The following abbreviations are used in this manuscript:
    ABSSIacute bacterial skin and skin structure infection
    A/Camoxicillin–clavulanic acid
    AMGaminoglycoside
    AMKamikacin
    ASTantimicrobial susceptibility testing
    AZTaztreonam
    BccB. cepacia complex
    BL/BLIβ-lactam/β-lactamase inhibitor
    BpcB. pseudomallei complex
    BSIbloodstream infection
    CAZceftazidime
    CDCCenters for Disease Control and Prevention
    C/Aceftazidime–avibactam
    CLSIClinical and Laboratory Standards Institute
    CRPC-reactive protein
    C/Tceftolozane–tazobactam
    DELAdelafloxacin
    DOXIdoxycycline
    ESBLextended-spectrum β-lactamase
    EUCASTEuropean Committee on Antimicrobial Susceptibility Testing
    FEPcefepime
    FDCcefiderocol
    FQfluoroquinolone
    GNTgentamicin
    ICUintensive care unit
    IMPimipenem
    LPSlipopolysaccharide
    MALDI-TOFmatrix-assisted laser desorption/ionization time of flight
    MBLmetallo-β-lactamase
    MDRmultidrug-resistant
    MEMmeropenem
    M/Vmeropenem–vaborbactam
    MICminimum inhibitory concentration
    MINMinocycline
    MOXIMoxifloxacin
    NFGNBnon-fermenting Gram-negative bacteria
    OXAoxacillinase
    PCRpolymerase chain reaction
    P/Tpiperacillin–tazobactam
    TETtetracycline
    TGtigecycline
    UTIurinary tract infection
    XDRextensively drug-resistant

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    Figure 1. Bacteroidota taxonomical classification of the principal human pathogens.
    Figure 1. Bacteroidota taxonomical classification of the principal human pathogens.
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    Antibiotics 14 00306 g002aAntibiotics 14 00306 g002b
    Figure 2. Pseudomonadota taxonomical classification of the principal human pathogens.
    Figure 2. Pseudomonadota taxonomical classification of the principal human pathogens.
    Antibiotics 14 00306 g002aAntibiotics 14 00306 g002b
    Antibiotics 14 00306 g003
    Figure 3. Intrinsic resistance/expected resistant phenotypes in non-fermenter bacteria. R = resistant [27].
    Figure 3. Intrinsic resistance/expected resistant phenotypes in non-fermenter bacteria. R = resistant [27].
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    Antibiotics 14 00306 g004
    Figure 4.Achromobacter xylosoxidans colonies on tryptic soy agar (TSA) with a pale pink to whitish coloration. The colonies are moderately sized, circular, and have a smooth, glistening surface with no evident hemolysis halo.
    Figure 4.Achromobacter xylosoxidans colonies on tryptic soy agar (TSA) with a pale pink to whitish coloration. The colonies are moderately sized, circular, and have a smooth, glistening surface with no evident hemolysis halo.
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    Antibiotics 14 00306 g005
    Figure 5.Elizabethkingia anophelis colonies on TSA appear large, mucoid, and translucent, with an irregular and wavy growth pattern. They have a glistening, moist texture without visible hemolysis.
    Figure 5.Elizabethkingia anophelis colonies on TSA appear large, mucoid, and translucent, with an irregular and wavy growth pattern. They have a glistening, moist texture without visible hemolysis.
    Antibiotics 14 00306 g005
    Antibiotics 14 00306 g006
    Figure 6.Moraxella catarrhalis colonies on TSA appear pale and whitish. The colonies are medium-sized, irregular, and slightly rough in texture, with a matte or granular surface and without visible hemolysis.
    Figure 6.Moraxella catarrhalis colonies on TSA appear pale and whitish. The colonies are medium-sized, irregular, and slightly rough in texture, with a matte or granular surface and without visible hemolysis.
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    Table 1.Achromobacter spp. common resistant mechanisms.
    Table 1.Achromobacter spp. common resistant mechanisms.
    Type of Resistant MechanismAntibiotics AffectedReference
    Multidrug Efflux Pumps[32,41]
    AxyABMCephalosporins (except cefuroxime and FEP), AZT and chloramphenicol
    AxyXY-OprZAMG, TET, TG, FQ, FEP, carbapenems
    β-Lactamases[32]
    OXA-114-likePiperacillin, ticarcillin, benzylpenicillin, cephalothin
    ESBL and AmpCAll β-lactams except carbapenems
    Metallo-β-lactamasesAll β-lactams except AZT
    Other mechanisms[32,42]
    aac(6′)Ib-cr, qnrA, oqxA, oqxBFQ, AMG
    gyrA,ParCFQ
    Biofilmβ-lactams and AMG
    AMG = aminoglicoside, AZT = aztreonam, FEP = cefepime, FQ = fluoroquinolone, TET = tetracycline, TG = tigecycline.
    Table 2.Burkholderia spp. common resistant mechanisms.
    Table 2.Burkholderia spp. common resistant mechanisms.
    Type of Resistant MechanismAntibiotics AffectedReference
    Class A β-lactamases (genepenA,penB andpenR)Mutations lead to CAZ resistance, IMP, A/C[59]
    The efflux pump system of the resistance nodulation cell divisionIntrinsic resistance to penicillin, first and second-generation cephalosporins, gentamycin, tobramycin, streptomycin, polymyxin[91,96,105]
    Reduced outer membrane permeability/modified LPS structurePolymixin[59]
    Alteration in drug targetsMutations affecting topoisomerases type II enzymes, DNA gyrase, and topoisomerases type IV leads to FQ resistance.
    Mutations in the dihydrofolate reductase led to SXT resistance    		[59,106,107]
    BiofilmUnlike planktonic organisms,B. pseudomallei biofilm production is associated with resistance to multiple antimicrobials, including CAZ, IMP, SXT[108,109]
    A/C = amoxicillin–clavulanic acid, CAZ = ceftazidime, DNA = deoxyribonucleic acid, FQ = fluoroquinolone, IMP = imipenem, LPS = lipopolysaccharide, SXT = trimethoprim–sulfamethoxazole.
    Table 3. Empirical antibiotic treatment suggested for NFGNB infections.
    Table 3. Empirical antibiotic treatment suggested for NFGNB infections.
    MicroorganismMild to Moderate DiseaseSever Disease *References
    Achromobacter
    xylosoxidans    		No prior antibiotic exposure
    • Ceftazidime
    • Trimethoprim/sulfamethoxazole
    • Ciprofloxacin
    Prior antibiotic exposure
    • Meropenem or imipenem cilas-tatin
    • Cefiderocol
    • Eravacycline
    		No prior antibiotic exposure
    • Ceftazidime + trimethoprim/sulfamethoxazole
    • Meropenem or Imipenem cilastatin + Trimethoprim/sulfamethoxazole
    Prior antibiotic exposure
    • Cefiderocol + trimethoprim/sulfamethoxazole
    You can consider also ciprofloxacin as a part of the treatment    		[32,49]
    Alcaligenes
    faecalis
    • Meropenem or imipenem cilastatin
    • Tigecycline
    • Fluoroquinolone
    		No prior antibiotic exposure
    • Meropenem or imipenem cilastatin
    prior antibiotic exposure
    • Meropenem or imipenem cilastatin + tigecycline
    • Meropenem or imipenem cilastatin + Aminoglycoside
    • Meropenem or imipenem cilastatina + Fluoroquinolones
    		[51,53]
    Burkholderia
    cepacia
    complex
    • Trimethoprim/sulfamethoxazole
    • Fluoroquinolone
    • Ceftazidime
    • Minocycline or doxycycline
    		No prior antibiotic exposure
    • Trimethoprim/sulfamethoxazole
    • Ceftazidime
    Prior antibiotic exposure
    • Ceftazidime + trimethoprim/sulfamethoxazole
    • Meropenem or doripenem + trimethoprim/sulfamethoxazole
    Alternatives
    • Cefiderocol (need prior testing) + one or more antibiotics previously cited
    • Ceftazidime/avibactam (need prior testing) ± one or more antibiotics previously cited
    • Meropenem/vaborbactam (need prior testing) ± one or more antibiotics previously cited
    		[48,71,72,73,74,75]
    Burkholderia pseudomallei
    complex    		IV initial therapy
    • Ceftazidime
    • Meropenem
    Eradication therapy
    • Trimethoprim/sulfamethoxazole
    		[89,94]
    Burkholderia
    gladioli
    • Trimethoprim/sulfamethoxazole
    • Meropenem or imipenem cilastatin
    • Fluoroquinolone
    		No prior antibiotic exposure
    • Trimethoprim/sulfamethoxazole + fluoroquinolone
    Prior antibiotic exposure
    • Meropenem or imipenem cilastatin + trimethoprim/sulfamethoxazole
    • Meropenem or imipenem cilastatin + fluoroquinolone
    		[111]
    Elizabethkingia
    meningoseptica
    • Minocycline
    • Levofloxacin
    • Trimethoprim/sulfamethoxazole
    		No prior antibiotic exposure
    • Minocycline + Levofloxaicin
    • Minocycline + trimethoprim/sulfamethoxazole
    • Trimethoprim/sulfamethoxazole + Levofloxacin
    Prior antibiotic exposure
    • Same combinations, eventually with rifampin or cefiderocol
    		[124,125,126]
    Moraxella
    catharallis
    • Amoxicillin/clavulanic acid alternatives:
    • Azitromycin
    • Trimethoprim/sulfamethoxazole
    		[149,150,151,152]
    Ochrobactrum spp.
    • Ciprofloxacina + trimethoprim/sulfamethoxazole
    		[155,157]
    Bergeyella spp.
    • Ampicillina/sulbactam or Amoxicillina/clavulanic acid
    • Cefazolin + gentamycin
    • Cefuroxime
    • Ciprofloxacin
    		[160,162,163]
    Weeksella virosa
    • Piperacillin
    • Aztreonam
    • Carbapenem
    		[164,166]
    Chryseobacterium spp.
    • Levofloxacin
    • Trimethoprim/sulfamethoxazole
    Eventually, consider rifampin as a part of the treatment    		[170]
    Comamonas spp.
    • Piperacillin/tazobactam
    • Carbapenems
    • Trimethoprim/sulfamethoxazole
    Consider combination therapy based on the risk of resistant strains    		[171]
    Delftia
    acidovorans
    • Ceftazidime
    • Piperacillin/tazobactam
    • Meropenem or imipenem cilastatin
    • Ciprofloxacin
    		[173,174]
    Acidovorax spp.
    • Piperacillin/tazobactam
    • Fluoroquinolones
    		[175]
    Oligella spp.
    • Cephalosporins
    • Carbapenems
    		[176]
    Pandoraea spp.
    • Imipenem cilastatin + trimethoprim/sulfamethoxazole
    		[177]
    Ralstonia spp.
    • Fluoroquinolone + trimethoprim/sulfamethoxazole
    Eventually, consider tigecycline as a part of the treatment    		[180,181]
    Rhizobium spp.
    • Cefalosporins
    • Ticarcillin
    • Imipenem cilastatin
    • Tetracyclines
    • Colistin
    • Fluoroquinolones
    • Trimethoprim/sulfamethoxazole
    Consider combination therapy based on the risk of resistant strain    		[19]
    Shewanella spp.
    • Cefalosporins
    • Imipenem cilastatin
    • Tetracyclines
    • Aminoglycosides
    • Fluoroquinolone
    • Trimethoprim/sulfamethoxazole
    Consider combination therapy based on the risk of resistant strain    		[19]
    Sphingobacterium spp.
    • Fluoroquinolones
    • Tetracyclines
    • Trimethoprim/sulfamethoxazole
    • Consider combination therapy based or the risk of resistant strain
    		[190,192]
    * The literature does not provide studies with sufficient scientific robustness to recommend monotherapy, even in cases of antibiotic susceptibility, for severe infections. Combination therapy is suggested to overcome pathogen resistance. Moreover, true clinical breakpoints are currently lacking for the majority of the antibiotics tested; therefore, in vitro susceptibility data may not have a reliable clinical correlation.
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    © 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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    MDPI and ACS Style

    Geremia, N.; Marino, A.; De Vito, A.; Giovagnorio, F.; Stracquadanio, S.; Colpani, A.; Di Bella, S.; Madeddu, G.; Parisi, S.G.; Stefani, S.; et al. Rare or Unusual Non-Fermenting Gram-Negative Bacteria: Therapeutic Approach and Antibiotic Treatment Options.Antibiotics2025,14, 306. https://doi.org/10.3390/antibiotics14030306

    AMA Style

    Geremia N, Marino A, De Vito A, Giovagnorio F, Stracquadanio S, Colpani A, Di Bella S, Madeddu G, Parisi SG, Stefani S, et al. Rare or Unusual Non-Fermenting Gram-Negative Bacteria: Therapeutic Approach and Antibiotic Treatment Options.Antibiotics. 2025; 14(3):306. https://doi.org/10.3390/antibiotics14030306

    Chicago/Turabian Style

    Geremia, Nicholas, Andrea Marino, Andrea De Vito, Federico Giovagnorio, Stefano Stracquadanio, Agnese Colpani, Stefano Di Bella, Giordano Madeddu, Saverio Giuseppe Parisi, Stefania Stefani, and et al. 2025. "Rare or Unusual Non-Fermenting Gram-Negative Bacteria: Therapeutic Approach and Antibiotic Treatment Options"Antibiotics 14, no. 3: 306. https://doi.org/10.3390/antibiotics14030306

    APA Style

    Geremia, N., Marino, A., De Vito, A., Giovagnorio, F., Stracquadanio, S., Colpani, A., Di Bella, S., Madeddu, G., Parisi, S. G., Stefani, S., & Nunnari, G. (2025). Rare or Unusual Non-Fermenting Gram-Negative Bacteria: Therapeutic Approach and Antibiotic Treatment Options.Antibiotics,14(3), 306. https://doi.org/10.3390/antibiotics14030306

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