[Infection by glucose-nonfermenting, gram-negative rods--infection by Acinetobacter calcoaceticus].
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Acinetobacter↗
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A novel genus of virulent phage targeting Acinetobacter baumannii: Efficacy and safety in a murine model of pulmonary infection.
Acinetobacter baumannii is a notable opportunistic pathogen responsible for severe hospital-acquired infections, with multidrug-resistant strains posing significant treatment challenges. Phage therapy, which employs bacteriophages as natural bacterial antagonists, has gained renewed attention as a promising solution to combat antibiotic-resistant infections. In this study, we isolated and characterized a novel virulent phage, vB_AbaS_qsb1, which specifically lyses A.baumannii. Phylogenetic and genomic analyses indicate that vB_AbaS_qsb1 is the founding member of a previously unreported genus, which we propose to name Acinibactriovirus, with Acinibactriovirus lysinus as the type species. vB_AbaS_qsb1 demonstrated robust stability across diverse temperature and pH ranges, a short latent period, and no known virulence or antibiotic resistance genes within its 54,713 bp dsDNA genome. Safety assessments showed that high-dose vB_AbaS_qsb1 induced no adverse effects in mice, with histopathology confirming its safety profile. Therapeutic experiments further indicated that vB_AbaS_qsb1 provided at least 50% protection against A.baumannii-induced pneumonia, significantly reducing bacterial loads and inflammation markers, while maintaining high phage titers in lung tissue.This study introduces vB_AbaS_qsb1 as a promising candidate for phage therapy against A.baumannii, offering both innovative insights and a valuable framework for future isolation, genomic characterization, and efficacy evaluation of phages targeting antibiotic-resistant bacteria.
Animals↗
Necrotizing fasciitis associated with Acinetobacter lactucae and Bacillus paramobilis infections in 2 dogs.
Two immunocompetent dogs from separate households were presented to a tertiary referral hospital with soft tissue wounds attributable to severe bacterial infection. A 5-y-old, castrated male Golden Retriever dog (case 1) was presented with extensive hemorrhagic cellulitis of the forelimbs and neck that developed over 48-h and was attributable to Acinetobacter lactucae infection. Additionally, an 8-y-old, spayed female Labrador Retriever-mix dog (case 2) sustained a deep penetrating wound over the left hip that progressed over 24 h to necrotizing fasciitis, from which Bacillus paramobilis was isolated. Histopathologic findings in both cases included severe acute, skeletal muscle necrosis and necrosuppurative myofasciitis, dermatitis, and panniculitis with intralesional rod-shaped bacteria. Whole-genome sequencing and phylogenetic analysis of the bacterial isolates revealed numerous cytolytic toxins and other virulence genes carried by the isolates, expanding the profile of these 2 bacteria. To our knowledge, canine cases of A. lactucae and B. paramobilis associated with necrotizing fasciitis have not been reported previously. In both cases, progression from an inciting incident to septic disease was extremely rapid, occurring within 48 h in case 1 and 24 h in case 2, underscoring the fulminant nature of necrotizing fasciitis.
Animals↗
Outbreak of a multiply resistant Acinetobacter in a surgical intensive care unit: epidemiology and control.
During January, 1976 seven patients in an SICU became colonized or infected with Acinetobacter calcoaceticus (variation, anitratum) at an attack rate of 12.5 per cent. The organism showed a marked reduction in antimicrobial sensitivity from previous experience. Comparison with 34 uninfected control patients indicated that intubation and continuous ventilatory assistance were significantly associated with acquiring the organism (p = 0.0154). Acinetobacter was cultured from nurses' hands, AMBU adaptors, respirator apparatus, respirometers, and unlabeled bottles of saline used for tracheal irrigation. Control measures were designed to interrupt transmission. The investigation identified the nursing techniques and reservoirs that allowed this outbreak to occur, and we emphasize the need for close surveillance of patient care procedures in an intensive care unit.
Acinetobacter↗
[Microbiological analysis of the results of treatment of urinary tract infections with epicillin].
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Acinetobacter Infections↗
Opportunistic infection in children. III. In the normal host.
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Acinetobacter Infections↗
New Delhi metallo-β-lactamase-producing Acinetobacter baumannii in the USA from October, 2013, to March, 2022: a retrospective molecular epidemiological analysis.
BACKGROUND: Most US carbapenem-resistant Acinetobacter baumannii (CRAB) isolates harbour carbapenem-hydrolysing class D β-lactamases. Other carbapenemases, such as New Delhi metallo-β-lactamase (NDM), are uncommon but emerging. We describe the epidemiology of NDM-producing CRAB reported to the US Centers for Disease Control and Prevention (CDC). METHODS: We defined cases as A baumannii with blaNDM confirmed by molecular testing and isolated from any specimen source from a patient in the USA between Oct 1, 2013, and March 31, 2022, and passively reported to the CDC from regional, state, local public health, and CDC laboratories. Epidemiologically linked cases had epidemiological linkage (eg, overlapping health-care facility stay) with one or more other cases. We assessed case relatedness through analysis of whole-genome sequence data using traditional multilocus sequence typing (MLST; Oxford scheme [sequence typeOX]) and core genome MLST. To understand the potential origins of NDM-CRAB in the USA, we compared sequences of cases to US CRAB without NDM and to NDM-CRAB from non-US locations. FINDINGS: We identified 327 NDM-CRAB cases from 264 patients in 21 US states. Among patients with available epidemiological information, 192 (90%) of 214 had epidemiological linkage to at least one additional case and 13 (7%) of 193 were hospitalised outside the USA 12 months or less before index specimen collection. Five regionally distinct sequence type clusters were identified among the 264 case patients; three (sequence type OX218, sequence type OX281, and sequence type OX1697) were closely related to international NDM-CRAB isolates. INTERPRETATION: We identified regionally distinct NDM-CRAB strains, suggesting localised transmission in the USA. Some NDM-CRAB strains in the USA are closely related to strains identified outside the USA, suggesting that spread followed importation. FUNDING: None.
Acinetobacter baumannii↗
Whole-Genome Analysis Reveals Antimicrobial Resistance and Population Structure of Environmental and Veterinary Acinetobacter baumannii.
Acinetobacter (A.) baumannii is an important multidrug-resistant pathogen increasingly recognized across animal and environmental settings, and carbapenem-resistant A. baumannii (CRAB) is classified as a critical-priority pathogen by the World Health Organization. This study investigated the antimicrobial resistance (AMR) and genomic characteristics of 122 A. baumannii isolates comprising 72 veterinary and 50 environmental isolates collected in Andhra Pradesh, India. Antimicrobial susceptibility testing, whole-genome sequencing (WGS), resistance and virulence gene profiling, multilocus sequence typing (MLST), core-genome analysis, single nucleotide polymorphism (SNP) phylogeny, and pan-genome analysis were performed. Overall, 58.2% of isolates were multidrug-resistant (MDR), and 41.8% were extensively drug-resistant (XDR). Sequence type (ST) 52 predominated among veterinary isolates, whereas ST2 was more frequent among environmental isolates. The presence of carbapenem-resistant isolates along with the ST2 lineage enhances the similarity to clinical A. baumannii. Several intrinsic resistance genes, including blaOXA-23, armA, aph(3″)-Ib, aph(6)-Id, tet(B), mph(E), and msr(E), were more prevalent in the ST2-associated population. Virulence-associated determinants were widely conserved. Core-genome MLST (cgMLST) and core-genome SNP (cgSNP) analyses identified highly related isolates within both lineages, while pairwise SNP differences were 0-7. Pan-genome analysis identified 4204 gene clusters and distinct accessory gene patterns between ST2 and ST52. These findings indicate that resistance gene distribution was closely associated with lineage structure and support integrated genomic surveillance of A. baumannii across animal and environmental reservoirs.
Acinetobacter baumannii↗
Long-term therapy of chronic bacterial prostatitis with trimethoprim-sulfamethoxazole.
Trimethoprim (TMP) meets all of the theoretical requirements of diffusion into, and actual concentration in, human prostatic fluid. When TMP is combined with the sulfonamide sulfamethoxazole (SMX), potentiation of antibacterial activity is achieved and the development of resistant bacterial strains is less likely to occur. In our initial use of TMP-SMX in the treatment of 13 men with chronic bacterial prostatitis due to gram-negative organisms, patients were given two tablets of TMP-SMX twice daily for only 14 days. The results were that two patients (15%) were cured, nine patients (70%) were improved (sterile prostatic fluid during therapy) but eventually relapsed, and two patients (15%) were unchanged by therapy. In our present study 19 patients (31.6%) were totally cured and 9 of 23 (39.1%) gram-negative organisms were permanently cleared from prostatic fluid; 8 of the 9 patients (42.1%) were improved but eventually relapsed with the same organism; 5 of the 19 patients (26.3%) were considered unchanged by therapy.
Acinetobacter Infections↗
Bronchopneumonia and endocarditis: caused by Acinetobacter anitratum (Herellea vaginicola).
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Acinetobacter Infections↗
Community-acquired Acinetobacter calcoaceticus var anitratus pneumonia.
Two patients had community-acquired Acinetobacter calcoaceticus var anitratus pneumonia. Both patients were alcoholic and one was cirrhotic. One patient died and the other received two weeks of gentamicin therapy and survived. Misinterpretation of the sputum Gram stain delayed diagnosis and institution of proper therapy in both cases. In addition to organisms sensitive to penicillins such as Neisseria or Haemophilus, Acinetobacter must be considered in the differential diagnosis of community-acquired Gram-negative coccobacillary pneumonia.
Acinetobacter↗
Antibiotic-resistant Acinetobacter baumannii can be killed by a combination of bacteriophages and complement.
Infections caused by multidrug-resistant Acinetobacter baumannii are an emerging global health threat. Although phages have shown promising results in treating bacterial infections, the mechanisms of the combined effect of phages and innate immunity on clearing A. baumannii remain unclear. Here, we report a synergistic effect of the complement system and phages on clearing multidrug-resistant A. baumannii. We show that A. baumannii rapidly adapts and becomes resistant to phage or serum complement by modifying the expression of capsule and lipooligosaccharides, which can be regulated through reversible transposon mutagenesis in the K locus. Compared to the encapsulated phenotype, the non-encapsulated, phage-resistant A. baumannii showed a higher level of membrane attack complex deposition and were susceptible to killing by complement. In contrast, the encapsulated phenotype escaped the complement system by shedding the membrane attack complex to the environment. Thus, while the complement system targets the non-encapsulated phenotype, the phage infects and eliminates the encapsulated subpopulation. These results suggest means of combatting antibiotic-resistant A. baumannii by a simultaneous treatment with phages and complement, a combination which can be supplemented further with antibacterial antibodies.
Acinetobacter baumannii↗
A regulator of amino acid catabolism controls Acinetobacter baumannii gut colonization.
Asymptomatic gut colonization increases the risk of clinical infection and transmission by the multidrug-resistant pathogen Acinetobacter baumannii. Ornithine utilization was shown to be critical for A. baumannii competition with the resident microbiota to persist in gut colonization, but the regulatory mechanisms and cues are unknown. Here, we identify a transcriptional regulator, AstR, that specifically activates the expression of the A. baumannii ornithine utilization operon astNOP. Phylogenetic analysis suggests that AstR was co-opted from the Acinetobacter arginine utilization ast(G)CADBE locus and is specialized to regulate ornithine utilization in A. baumannii. Reporter assays showed that astN promoter expression was activated by ornithine but inhibited by glutamate and other preferred amino acids. astN promoter expression was similarly activated by incubation with fecal samples from conventional mice but not germ-free mice, suggesting AstR-dependent activation of the astN promoter responds to intermicrobial competition for amino acids. Finally, AstR was required for A. baumannii to colonize the gut in a mouse model. Together, these results suggest that pathogenic Acinetobacter species evolved AstR to regulate ornithine catabolism, which is required to compete with the microbiota during gut colonization.
Animals↗
Growth inhibition of Acinetobacter by 5-chloro-indole-3-acetic acid.
The Acinetobacter calcoaceticus-baumannii complex includes high-priority, multidrug-resistant pathogens for which novel antibiotics are urgently needed. Many bacterial strains from this complex harbor a so-called iac gene cluster that codes for the catabolism of indole-3-acetic acid (IAA). Here, we demonstrate that possession and expression of iac genes represent an Achilles' heel for Acinetobacter species, which can be exploited to suppress bacterial growth by treatment with IAA and its analog 5-chloro-IAA.IMPORTANCEAcinetobacter baumannii is a deadly bacterial pathogen and one of the leading causes of hospital-acquired infections worldwide. It is also known for its resistance to many antibiotics currently available. In this study, we show that Acinetobacter bacteria choke on a mixture of IAA and 5-chloro-IAA, offering a path to the discovery and development of a novel drug treatment.
Indoleacetic Acids↗
Mechanisms of cefiderocol resistance in carbapenem-resistant Acinetobacter baumannii: a Swiss 2023-2025 collection.
OBJECTIVES: The numbers of infections caused by carbapenem-resistant Acinetobacter baumannii (CRAB) are increasing globally and present a significant burden on healthcare systems. This study describes the CRAB isolates received at the Swiss National Reference Centre for Emerging Antibiotic Resistance (NARA) over a 3-year period, from January 2022 to December 2025, and aimed to characterize the prevalence and mechanisms of FDC resistance. METHODS: Two-hundred and thirty-four non-duplicate CRAB isolates were submitted to NARA over the study period from hospitals and laboratories across Switzerland. Susceptibility testing was performed by disk diffusion and broth microdilution, according to EUCAST methodology. Whole-genome sequencing was performed on 11 isolates. ADC alleles were cloned into vector pVRL1 and transformed into Escherichia coli Top10. RESULTS: All isolates exhibited resistance to the carbapenems, and most were resistant to cephalosporins. Most isolates harboured an acquired class D carbapenemase, most frequently OXA-23 (181/234; 77.4%). One quarter of isolates were resistant to cefiderocol (FDC), exhibiting MICs ranging from 4->32 mg/L. Whole genome sequencing analyses, performed on 11 FDC-resistant isolates, identified that FDC resistance was due a combination of mechanisms including NDM and PER-production, mutations within the iron transporters, piuA and pirA, and the overexpression of ADC variants. CONCLUSIONS: This study showed that OXA-23 was the dominant mechanism of carbapenem-resistance in CRAB in Switzerland. Almost one quarter of CRAB isolates were resistant to "last resort" antimicrobial, FDC. The mechanisms of FDC resistance identified in this study emphasise that resistance to this antimicrobial is often complex and multifactorial, requiring high-resolution methods, including WGS, to identify.
Acinetobacter baumannii↗
Characterization of blaOXA-542-mediated carbapenem resistance in Acinetobacter baumannii.
BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) causes multiple anatomical site infections, representing a significant public health threat. AIM: This study reports the isolation and characterization of a carbapenem-resistant A. baumannii harbouring blaOXA-542, followed by a comprehensive investigation of its antimicrobial resistance mechanisms and genomic characteristics. METHODS: Firstly, antimicrobial susceptibility testing was performed using the broth microdilution method. Subsequently, whole-genome sequencing was employed to identify and characterize the resistance and virulence determinants. The functional validation of resistance mechanisms was performed by gene knockdown and construction of expression vectors. The fitness cost of β-lactamase expression was identified by a bacterial growth kinetic test. Molecular docking was utilized to predict potential binding sites of β-lactamase and carbapenems. Finally, the genetic characteristics of the isolates were analysed through comparative genomics analyses and phylogenetic tree construction. RESULTS AND CONCLUSIONS: The results demonstrated that blaOXA-542 confers resistance to carbapenem and penicillin in A. baumannii and Escherichia coli while exhibiting no significant impact on cephalosporins. The ability of blaOXA-542 to hydrolyze meropenem was further confirmed by modified carbapenem inactivation assay (mCIM). Expression of blaOXA-542 in E. coli BL21 showed no significant growth rate alteration. Comparative analysis of the blaOXA-542 genetic environment revealed a close association with Acinetobacter pitti. This study reports the emergence of blaOXA-542-mediated carbapenem and penicillin resistance in a novel A. baumannii lineage (ST2795Pas/ST3464Oxf), highlighting the urgent need for rational antibiotic use against specific pathogens.
Acinetobacter baumannii↗
Deciphering the genomic landscape of novel Acinetobacter non-baumannii lineages causing neonatal septicemia: carbapenem resistance and virulence.
BACKGROUND: Acinetobacter non-baumannii (Anb) species are reported worldwide to cause infections in both adults and neonates, although less frequently than Acinetobacter baumannii. However, limited information is available on their genomic diversity, resistance mechanisms, and virulence potential. This study investigates novel Anb isolates causing neonatal septicemia in India to characterize their resistance and pathogenic traits. METHODS: Anb isolates from neonatal blood cultures (2007-2025) were identified by VITEK2 Compact system, MALDI-TOF MS, and Whole-genome sequencing (WGS). Antimicrobial susceptibility was tested by VITEK2. Genomic analysis included MLST, resistome, virulome, plasmid typing, integrons, and core-genome phylogeny analysis. In vitro and in vivo studies assessed pathogenic potential of Anb species. RESULTS: Anb infections were low (11%) among the neonates during the study period. WGS revealed 11 novel Sequence Types (STs) which include A. indicus, A. variabilis, A. schindleri, and A. bereziniae. Six out of these eleven Anbs harbored carbapenemases such as bla NDM-1 and/or bla OXA-58-like genes (bla OXA-58, bla OXA-420). bla NDM-1 was acquired via Tn125 transposon. ISAba125 was located upstream of bla NDM-1, and a conserved structure extending to IS91 family transposase was detected in bla NDM-1-harboring genomes. bla OXA-58-like genes were found to be associated with ISAba3. Most carbapenemases were likely located on chromosome. Class 1 integrons carrying multiple antimicrobial resistance genes (ARGs) and diverse plasmid replicase families were detected in Anbs. Core genome phylogeny showed that the study Anbs were not closely related to the global Anbs. In vitro virulence-associated assays (biofilm formation, surface motility, adherence/invasion, apoptosis) and in vivo lethality in murine infection model showed reduced pathogenicity, reinforcing earlier observations that Anb species are generally less virulent than A. baumannii. Several virulence factors (VFs) were detected; however, no clear correlation was observed between virulence genes, in vitro pathogenicity, and in vivo lethality. CONCLUSION: These results indicate the multifactorial nature of Anb pathogenicity and the current limitations of knowledge of its VFs. However, the presence of numerous VFs suggests a capacity to cause disease, particularly in vulnerable host populations such as neonates. Furthermore, the presence of multiple ARGs indicates a strong potential for persistence and dissemination in hospital environments with high antibiotic pressure. Overall, these findings underscore the importance of continued AMR surveillance, genome characterization and further investigations into Anb pathogenicity.
Acinetobacter non-baumannii↗
Difficult-to-treat resistant Gram-negative bacteria and genomic resemblances between colonization and infection among patients in an intensive care unit of a tertiary care hospital in Bangladesh.
Colonization with difficult-to-treat-resistant Gram-negative bacteria (DTR-GNB) increases the risk of subsequent infections with limited treatment options. This study aimed to assess the burden of DTR-GNB colonization in ICU patients, explore its association with clinical outcomes, and examine genomic similarities. This secondary analysis included patients enrolled within 24 h of ICU admission between July 2023 and January 2024. Rectal swabs were collected at enrollment, on days 3, 7, and weekly during ICU stay to detect colonization. Bacterial isolates grown on selective chromogenic agar media were identified and tested for antimicrobial susceptibility using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and automated broth microdilution, respectively. Blood, urine, and/or tracheal aspirate cultures were performed if clinically suspected sepsis. Whole-genome sequencing (WGS) was performed on paired colonization and infection isolates, and genomic relatedness was assessed using FastANI, core-genome single-nucleotide polymorphism (SNP) analysis, and phylogenetic reconstruction. Among 373 patients, 181 (48.5%) were colonized with DTR-GNB; 76 (20.4%) at enrollment, and 105 (53.0%) acquired during hospital stay. Among 52 (13.9%) patients evaluated for suspected infection, 30 (57.7%) had positive cultures, predominantly Acinetobacter baumannii (n = 15) and Klebsiella pneumoniae (n = 11) of DTR-phenotypes. Compared to non-colonized patients, patients colonized with DTR-GNB had higher risks of infections (risk ratio [RR]: 2.18, 95% CI: 1.27-3.76) and longer ICU stays (median 7 vs 2 days, P < 0.001). DTR-GNB-infected patients had a higher risk of death (RR: 1.57, 95% CI: 1.34-1.84) compared to patients without DTR-GNB infection. WGS revealed that 13 of 14 paired colonization-infection isolates were conspecific, with three pairs being highly clonal; whereas the remaining pairs showed greater genomic divergence, consistent with the SNP and phylogenetic analyses. While common, more than half acquired DTR-GNB colonization from the ICU. Its association with subsequent infection and prolonged ICU stays underscores the need for enhanced infection prevention and control measures to mitigate nosocomial transmission and improve patient outcomes.IMPORTANCEThis study underscores the growing threat posed by difficult-to-treat resistant Gram-negative bacteria (DTR-GNB) in intensive care units. Nearly half of critically ill patients were colonized, with a considerable proportion acquiring these multidrug-resistant organisms during their ICU stay. Colonization with these pathogens substantially increased the risk of subsequent infections, even by the same colonizing strain, prolonged ICU stays, and likely worsened clinical outcomes due to the unavailability of susceptible antibiotics. Alarmingly, more than 90% of patients infected with DTR-GNB expired in the hospital. These findings highlight the urgent need for robust infection prevention and control strategies to curb nosocomial transmission and mitigate the impact of DTR-GNB on vulnerable patient populations. Addressing this emerging resistance phenotype is critical to improving patient safety and reducing the burden on healthcare systems.
Humans↗