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A cluster of nosocomial cross-infection due to multiple antibiotic-resistant Acinetobacter baumannii: Characterization of the strain and antibiotic susceptibility studies.

A multiple antibiotic-resistant (MAR) strain of Acinetobacter baumannii caused nosocomial cross-infection among 3 patients of a surgical intensive care unit. The isolates were of identical biochemical profile (77776 S-U-) and serotype (serovar 36) and identical in terms of pulsed-field gel electrophoresis macrorestriction (SmaI, ApaI) analysis. This MAR strain was susceptible only to netilmicin, tobramycin, imipenem, meropenem, polymyxin B, and trovafloxacin. The minimal bactericidal concentrations of imipenem and meropenem were markedly higher than the corresponding minimal inhibitory concentrations against this strain. Combined fresh defibrinated human blood (65 vol%) and antimicrobial drug assays yielded the following results: polymyxin was the most rapidly bactericidally effective antibiotic in the presence of blood and in broth. Tobramycin and netilmicin were efficacious in 65 vol% blood. Imipenem was slightly more effective than meropenem in broth, whereas both carbapenems sterilized blood-containing assay tube contents. Trovafloxacin failed to achieve bactericidal activity (to 99.9% kill) in the presence of blood, presumably because this strain was resistant to ciprofloxacin and borderline susceptible to ofloxacin. Trovafloxacin combined with either imipenem or meropenem yielded an indifferent effect. However, the combination of trovafloxacin (2 microg/ml) plus tobramycin (1 microg/ml) achieved sterilization of tube contents in the presence of blood within 4 h after exposure and in broth following extended (overnight) incubation. This MAR strain of A. baumannii was high-level resistant to rifampin; thus the combination of polymyxin B plus rifampin proved indifferent.

Acinetobacter↗
PubMed1989

Susceptibility of Acinetobacter calcoaceticus to antimicrobial drugs, alone and combined, with and without defibrinated human blood.

Twenty-five clinical isolates of Acinetobacter calcoaceticus were examined for susceptibility to 14 antimicrobial drugs. In terms of inhibitory and bactericidal activities, imipenem and polymyxin B were most active, followed by amikacin and ceftazidime. Four isolates were resistant against fluoroquinolones (ciprofloxacin, norfloxacin, ofloxacin). The isolates varied in susceptibility to aztreonam, cefotaxime, cotrimoxazole, gentamicin, mezlocillin, netilmicin and piperacillin. Fresh defibrinated human blood from 3 donors revealed similar killing kinetics against 8 selected isolates. In time-kill curve experiments, human blood enhanced the activity of amikacin more than that of ceftazidime, ciprofloxacin and imipenem against A. calcoaceticus. The combinations of amikacin + imipenem and amikacin + ceftazidime in the presence of human blood were effective against this microorganism. Human blood combined with ciprofloxacin + imipenem was more effective than blood with added ceftazidime + ciprofloxacin.

Acinetobacter↗
PubMed2005

Differential roles of CD14 and toll-like receptors 4 and 2 in murine Acinetobacter pneumonia.

RATIONALE: Acinetobacter baumannii is an opportunistic bacterial pathogen that is increasingly associated with gram-negative nosocomial pneumonia, but the molecular mechanisms that play a role in innate defenses during A. baumannii infection have not been elucidated. OBJECTIVE: To gain first insight into the role of CD14 and Toll-like receptors 4 and 2 in host response to A. baumannii pneumonia. METHODS: Respective gene-deficient mice were intranasally infected with A. baumannii, and bacterial outgrowth, lung inflammation, and pulmonary cytokine/chemokine responses were determined. To study the importance of LPS in the inflammatory response, mice were also challenged with A. baumannii LPS. MEASUREMENTS AND MAIN RESULTS: Bacterial counts were increased in CD14 and Toll-like receptor 4 gene-deficient mice, and only these animals developed bacteremia. The pulmonary cytokine/chemokine response was impaired in Toll-like receptor 4 knockout mice and the onset of lung inflammation was delayed. In contrast, Toll-like receptor 2-deficient animals displayed an earlier cell influx into lungs combined with increased macrophage inflammatory protein-2 and monocyte chemoattractant protein-1 concentrations, which was associated with accelerated elimination of bacteria from the pulmonary compartment. Neither CD14 nor Toll-like receptor 4 gene-deficient mice responded to intranasal administration of LPS, whereas Toll-like receptor 2 knockout mice were indistinguishable from wild-type animals. CONCLUSIONS: Our results suggest that CD14 and Toll-like receptor 4 play a key role in innate sensing of A. baumannii via the LPS moiety, resulting in effective elimination of the bacteria from the lung, whereas Toll-like receptor 2 signaling seems to counteract the robustness of innate responses during acute A. baumannii pneumonia.

Acinetobacter Infections↗
PubMed2026

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↗
PubMed2001

Transferable antibiotic resistance in multiresistant nosocomial Acinetobacter baumannii strains from seven clinics in the Slovak and Czech Republics.

Sixty-seven multiresistant nosocomial Acinetobacter baumannii isolates from patients hospitalized mostly in intensive care units of seven clinics in Slovak and Czech Republic were tested to determine their ability to transfer antibiotic resistance. All isolates were resistant to kanamycin, ticarcillin, cephalothin, cefotaxime, ceftazidime, aztreonam and susceptible to carbapenems, sulbactam and ampicillin/sulbactam. Sixty-five out of 67 strains transferred resistance determinants to Escherichia coli K-12 and Proteus mirabilis P-38 recipients. Analysis of selected transconjugants by an indirect selection method showed a more variable pattern of transferred resistance determinants. The clonal spread of strains transferring resistance seems to be an additional risk for occurrence of strains resistant to ceftazidime and aztreonam.

Acinetobacter↗
PubMed2002

In-vitro activity of clinafloxacin compared to ciprofloxacin against Acinetobacter baumannii strains isolated from intensive care unit patients.

The activity of clinafloxacin was compared to that of ciprofloxacin against 154 Acinetobacter baumannii strains isolated from patients treated in Intensive Care Units. Minimum inhibitory concentrations (MICs) were determined by the Epsilometer test method. The majority (87.6%) of the A. baumannii strains tested were resistant to ciprofloxacin (MIC range 0.125->32, MIC50 = >32, MIC90 = >32). On the contrary, only 9.7% of the strains tested were resistant to clinafloxacin (MIC range 0.023->4, MIC50 = 0.75, MIC90 = 2). Due to its superior activity shown against A. baumannii strains, compared to ciprofloxacin, clinafloxacin may be added to the therapeutic armamentarium for hospital-acquired infections caused by A. baumannii in Intensive Care Units.

Acinetobacter Infections↗
PubMed2006

Post-neurosurgical meningitis due to multidrug-resistant Acinetobacter baumanii treated with intrathecal colistin: case report and review of the literature.

Intrathecal colistin (Polymxin E) is becoming an important option for the treatment of post-neurosurgical meningitis caused by multidrug resistant (MDR) Acinetobacter baumannii. We report a case of 28-year-old man who developed meningitis due to MDR A. baumannii associated with an external ventricular drain. The patient was cured using a 4-week course of intrathecal colistin 3.2 mg via external ventricular drain (EVD) daily without any serious side effects.

Acinetobacter Infections↗
PubMed2006

Attributable mortality of Acinetobacter baumannii infections in critically ill patients: a systematic review of matched cohort and case-control studies.

INTRODUCTION: There has been a continuing controversy about whether infection with Acinetobacter baumannii increases morbidity and mortality independently of the effect of other confounding factors. METHODS: We performed a systematic review of matched case-control and cohort studies examining the mortality attributable to infection with or acquisition of A. baumannii (infection or colonization). We included in our review studies that compared mortality and/or morbidity of patients with acquisition of or infection with A. baumannii (cases) with the outcomes of matched patients without A. baumannii isolation from clinical specimens (controls). The relevant studies were identified from searches of the PubMed and the Cochrane Library databases. Two independent reviewers performed the literature search, study selection, and data extraction from nine identified relevant studies. RESULTS: The attributable mortalities, in the hospital and in the intensive care unit, of patients with A. baumannii infection in six matched case-control studies included in our review ranged from 7.8% to 23% and from 10% to 43%, respectively. In addition, a statistically significantly higher mortality was reported for patients with A. baumannii acquisition; that is, colonization or infection (cases) compared with controls without such an acquisition in all four reviewed studies that reported data on this comparison. CONCLUSION: Although definitive statements about the mortality attributable to the acquisition of A. baumannii cannot be made from the available studies because of their methodological heterogeneity, the reviewed data suggest that infection with or acquisition of A. baumannii seems to be associated with increased mortality.

Acinetobacter Infections↗
PubMed2025

Genomic and phenotypic insights into ST164 blaNDM-1-positive Acinetobacter baumannii from intestinal colonization in China.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) poses a critical global threat, especially in ICUs. Yet, reports on ST164 CRAB harboring blaNDM-1 remain scarce. This study investigates two clinical CRAB isolates, L4773hy and L4796hy, derived from intestinal colonization in Hangzhou, China, focusing on their phenotypic and genomic characteristics as well as the broader transmission of ST164 A. baumannii. METHODS: Bacterial identification was performed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) mass spectrometry. Antimicrobial susceptibility was assessed via agar and broth microdilution. Whole-genome sequencing employed Illumina NovaSeq 6000 and Oxford Nanopore platforms. Resistance genes, insertion elements, transposons, and integrons were detected using ResFinder, PlasmidFinder, VFDB, ISFinder, pdifFinder, and IntegronFinder. Strains were typed by MLST, and a phylogenetic tree was constructed with kSNP3.0. Genetic environment diagrams were generated using Easyfig 2.2.5. RESULTS: Two blaNDM-1-carrying A. baumannii isolates exhibiting extensive resistance to carbapenems, cephalosporins, and fluoroquinolones. Whole-genome sequencing and genetic environment analysis revealed the presence of a conserved structural sequence (ISAba14-ISAba14-aphA-ISAba125-blaNDM-1-bleMBL) on their chromosomes. Phylogenetic and clonal dissemination analysis showed that ST164 CRAB is primarily distributed in China and exhibits clonal spread. Pathogenicity studies indicated that blaNDM-1-positive ST164 strains have enhanced survival under immune pressure but do not display increased virulence in infection models. CONCLUSION: This study provides the genomic and phenotypic characterization of intestinally colonized ST164 blaNDM-1 positive CRAB in Hangzhou, China. The elucidation of the genetic environment of blaNDM-1 further confirms the clonal dissemination of ST164 isolates, highlighting the importance of enhanced surveillance and infection control measures to mitigate the spread of these multidrug-resistant pathogens.

Acinetobacter baumannii↗
PubMed2003

Rapid imipenem/cilastatin desensitization for multidrug-resistant Acinetobacter pneumonia.

OBJECTIVE: To report a successful case of rapid imipenem desensitization in a critically ill patient with multidrug-resistant Acinetobacter baumannii ventilator-associated pnemonia (VAP). CASE SUMMARY: A 40-year-old white man who had a lengthy stay in the intensive care unit (ICU) following a motorcycle accident developed VAP caused by A. baumannii. treatment with imipenem was necessary due to the bacteria's resistance to all other antibiotics. However, this patient was diagnosed with an allergy to imipenem following exposure earlier in his hospitalization in addition to a positive penicillin skin test. Thus, we attempted rapid desensitization to imipenem using a continuous infusion protocol. The patient was desensitized within 4 hours and was successfully treated for 21 days with a continuous infusion of imipenem combined with daily amikacin. He experienced no adverse reaction during the desensitization process or the remainder of his treatment course. DISCUSSION: The protocol used in this case was modified from a previously reported case, and differed in the speed of desensitization and total daily dose. We assumed that a more gradual escalation of the dose in our modified protocol would prevent the occurrence of adverse events, thereby resulting in more rapid desensitization. Rapid desensitization was necessary in this patient due to the presence of a life-threatening infection. The lower total daily dose of imipenem was in response to impaired renal function. CONCLUSIONS: Therapeutic options for multidrug-resistant pneumonia in the ICU are significantly limited in the presence of imipenem allergy. An option of last resort is to desensitize the patient using a rapid administration protocol. Our modified rapid imipenem desensitization protocol was successful and allowed for effective treatment of life-threatening pneumonia.

Acinetobacter Infections↗
PubMed2006

Polymyxin B and doxycycline use in patients with multidrug-resistant Acinetobacter baumannii infections in the intensive care unit.

BACKGROUND: Multidrug-resistant Acinetobacter baumannii (MDR-Ab) has emerged as an increasingly problematic cause of hospital-acquired infections in the intensive care unit (ICU). MDR-Ab is resistant to most standard antimicrobials but often retains susceptibility to polymyxin B and doxycycline. OBJECTIVE: To evaluate the efficacy and toxicity of polymyxin B and doxycycline in the treatment of MDR-Ab infections. METHODS: A retrospective chart review was conducted between March 2002 and May 2005 in patients who received doxycycline or polymyxin B for treatment of MDR-Ab infections in ICUs within Grady Memorial Hospital, Atlanta, GA. RESULTS: Thirty-seven patients with MDR-Ab infections were treated with polymyxin B or doxycycline. Median age was 41 years and median ICU length of stay was 18 days prior to acquisition of MDR-Ab. Clinical cure was observed in 22 of 29 (76%) evaluable patients treated with polymyxin B and 2 of 4 (50%) patients treated with doxycycline. In patients with follow-up cultures, microbiological cure was observed in 17 of 21 (81%) patients treated with polymyxin B and 2 of 3 (67%) patients treated with doxycycline. Nephrotoxicity developed in 21% (7 of 33) of patients who received polymyxin B. Neurotoxicity was observed in 2 (6%) patients who received polymyxin B. No adverse reactions were observed with doxycycline. Overall, crude mortality was 27% (9 of 33) and 75% (3 of 4) among those who received polymyxin B and doxycycline, respectively. Three (9%) deaths were attributed to polymyxin B treatment failure, and no deaths were attributed to doxycycline treatment failure. CONCLUSIONS: Polymyxin B was effectively used to treat a substantial proportion of critically ill patients with MDR-Ab infection and was associated with a similar rate of nephrotoxicity as previously reported. Doxycycline monotherapy was used in a limited number of patients for the treatment of MDR-Ab; further evaluation of its efficacy in larger numbers of patients is warranted.

Acinetobacter Infections↗
PubMed1999

Effect of amikacin on cytotoxic activity and hydrophobicity of Acinetobacter baumannii.

Effect of amikacin at suprainhibitory (2 or 4 x MIC) or supra-subinhibitory concentrations (2 or 4 x MIC + 0.2 x MIC) on bacterial growth, cytotoxicity and cell surface hydrophobicity of three Acinetobacter baumannii strains was studied. Amikacin at suprainhibitory concentrations induced postantibiotic effects (PAEs; suppression of bacterial growth after short time exposure of bacteria to the antibiotic) against all A. baumannii strains. PAEs ranged from 1.2 to 2.9 h (2 x MIC) and 3.5 to 6.3 h (4 x MIC). Supra-subinhibitory concentrations of amikacin (2 x MIC + 0.2 x MIC) manifested a more significant delay of bacterial regrowth (PA SMEs) for two strains (6.6 or 7.5 h) in comparison with PAEs. One strain under these conditions as well as all strains treated with amikacin at 4 x MIC + 0.2 x MIC did not show any regrowth. Amikacin at all concentrations tested significantly reduced cytotoxic activity of A. baumannii evaluated on alveolar epithelial type II cells. Survival of type II cells after application of antibiotic-treated A. baumannii was in the range of 88 to 101% of the control cells. Cell surface hydrophobicity of amikacin-treated bacteria was practically unchanged varying between 94 and 100.9% as compared to the controls.

Acinetobacter↗
PubMed2006

Comparative genomics of multidrug resistance in Acinetobacter baumannii.

Acinetobacter baumannii is a species of nonfermentative gram-negative bacteria commonly found in water and soil. This organism was susceptible to most antibiotics in the 1970s. It has now become a major cause of hospital-acquired infections worldwide due to its remarkable propensity to rapidly acquire resistance determinants to a wide range of antibacterial agents. Here we use a comparative genomic approach to identify the complete repertoire of resistance genes exhibited by the multidrug-resistant A. baumannii strain AYE, which is epidemic in France, as well as to investigate the mechanisms of their acquisition by comparison with the fully susceptible A. baumannii strain SDF, which is associated with human body lice. The assembly of the whole shotgun genome sequences of the strains AYE and SDF gave an estimated size of 3.9 and 3.2 Mb, respectively. A. baumannii strain AYE exhibits an 86-kb genomic region termed a resistance island--the largest identified to date--in which 45 resistance genes are clustered. At the homologous location, the SDF strain exhibits a 20 kb-genomic island flanked by transposases but devoid of resistance markers. Such a switching genomic structure might be a hotspot that could explain the rapid acquisition of resistance markers under antimicrobial pressure. Sequence similarity and phylogenetic analyses confirm that most of the resistance genes found in the A. baumannii strain AYE have been recently acquired from bacteria of the genera Pseudomonas, Salmonella, or Escherichia. This study also resulted in the discovery of 19 new putative resistance genes. Whole-genome sequencing appears to be a fast and efficient approach to the exhaustive identification of resistance genes in epidemic infectious agents of clinical significance.

Acinetobacter Infections↗
PubMed2025

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↗
PubMed2006

Fulminant community-acquired Acinetobacter baumannii pneumonia as a distinct clinical syndrome.

STUDY OBJECTIVES: Acinetobacter baumannii (AB) is an important cause of hospital-acquired pneumonia (HAP), and an uncommon but important cause of community-acquired pneumonia (CAP) with high mortality. To better characterize CAP-AB, we compared its clinical features and outcomes with a control group of HAP-AB patients. METHODS: This is a retrospective case-control study comparing CAP-AB and HAP-AB patients, which was performed at United Christian Hospital between July 2000 and December 2003. RESULTS: There were 19 cases of CAP-AB and 74 cases of HAP-AB. When compared with the HAP-AB group, the CAP-AB group had more ever-smokers (84.3% vs 55.4%, respectively; p = 0.031), more COPD patients (63.2% vs 29.7%, respectively; p = 0.014), and fewer median days of hospitalization (HAP-AB group, median, 0 days; CAP-AB group, 0 days [range, 0 to 30 days]; p = 0.049) in the previous year. The CAP-AB group had more patients with positive blood culture findings (31.6% vs 0%, respectively; p < 0.001), a higher frequency of ARDS (84.2% vs 17.6%, respectively; p < 0.001), and disseminated intravascular coagulation (DIC) (57.9% vs 8.1%, respectively; p < 0.001). The median survival time was only 8 days in the CAP-AB group, vs 103 days in the HAP-AB group (p = 0.003). Factors associated with the higher mortality in the CAP-AB group included the presence of AB bacteremia (p = 0.040), platelet count of < 120 x 10(9) cells/L (p = 0.026), pH < 7.35 on presentation (p = 0.047), and the presence of DIC (p = 0.004). CONCLUSIONS: CAP-AB appears to be a unique clinical entity with a high incidence of bacteremia, ARDS, DIC, and death, when compared to HAP-AB. Further studies are needed to investigate the mechanism of the fulminant nature of CAP-AB.

Acinetobacter Infections↗
PubMed2005

Evaluation of adherence, hemagglutination, and presence of genes codifying for virulence factors of Acinetobacter baumannii causing urinary tract infection.

Acinetobacter baumannii is a strictly aerobic bacterium which causes severe infections, however its pathogenic characteristics are not well defined. Thirteen A. baumannii strains isolated from urine of hospitalized and nonhospitalized patients with different ages were investigated for the presence of virulence factors. The isolates belonged to biotypes 2, 6, and 9 and were sensitive to imipenem. The majority of them showed resistance to amikacin, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, norfloxacin, and trimethoprim-sulfamethoxazole. None of A. baumannii strains presented genes codifying for 17 different virulence factors previously described in uropathogenic Escherichia coli, when tested by polymerase chain reaction (PCR). Nine isolates agglutinated human group AB erythrocytes, in presence of mannose, but none of them agglutinated group O erythrocytes. Adherence to polystyrene was observed in 7 isolates, and this result did not correlate with that obtained in hemagglutination assay. All the isolates were able to grow in iron-limiting conditions, showing that A. baumannii produces some type of siderophore. However, the genes iutA and fyuA, from iron uptake system of E. coli and Yersinia sp., respectively, were not present in the isolates, suggesting the presence of a different type of siderophore. The fimbriae of A. baumannii strains that mediates the adherence are possibly mannose-resistant, even though the mechanism of adherence to human epithelial cells still remains to be elucidated.

Acinetobacter Infections↗
PubMed2005

An outbreak of Acinetobacter baumannii septicemia in a neonatal intensive care unit of a university hospital in Brazil.

We studied an outbreak of two multi-drug resistant clones of Acinetobacter baumannii in the Neonatal Intensive Care Unit of the Uberlândia Federal University Hospital in Minas Gerais state, Brazil, and we analyzed the contribution of cross-transmission in the rise in infection rates. Eleven neonates who developed multi-drug resistant A. baumannii nosocomial infection were matched to 22 neonates who were admitted to the same unit and did not develop an infection during the outbreak period, in order to identify risk factors for infection. Three out of the 11 neonates died. Epidemiological investigation included molecular typing, using pulsed field gel electrophoresis. Prior to the outbreak, from December 2001 to March 2002, no case of infection by this microorganism was diagnosed. Environmental and healthcare worker hand cultures were negative. Nine isolates had similar pulsed field gel electrophoresis patterns and two had another clone. The first clone was brought into the unit by an infected patient who was transferred from another hospital without a history of antibiotic use. The second clone did have its origin clearly defined. Both infected groups led us to conclude that several factors contributed to infection with A. baumannii. These factors were: exposure to antibiotics and invasive devices, birth weight < 1500 g, age < or = 7 days and duration of hospitalization > or = 7 days. Based on logistic regression, infected neonates were more exposed to carbapenem and mechanical ventilation than the control group. Cross transmission between infants contributed to the rise in the rates of multi-drug resistant A. baumannii infection.

Acinetobacter Infections↗
PubMed1999

Evaluation of Acinetobacter baumannii infection and colonization, and antimicrobial treatment patterns in an urban teaching hospital.

In 1990 there was a sudden increase in the incidence of colonization and infection due to Acinetobacter baumannii (AB) in our intensive care units (ICUs). The isolates were multiply resistant to beta-lactam and aminoglycoside antibiotics, but remained susceptible to imipenem, amikacin, and ampicillin-sulbactam. We examined the frequency of infection and colonization with AB and the effects of increased imipenem and amikacin therapy on Pseudomonas aeruginosa. We also used disease-matched controls to determine the clinical and financial impacts of treating colonization. All patients with at least one AB isolate from January-December 1992 were identified retrospectively and classified as infected or colonized based on published Centers for Disease Control criteria; the control group was selected from a computerized medical records data base matching primary diagnostic codes (102 patients both groups). The 102 patients yielded 140 isolates, 124 resistant AB and 16 sensitive AB. Thirty three patients were infected, 69 colonized. Mortality correlated with APACHE II scores. Patients acquired the organism approximately 2 weeks after admission; they had a mean ICU stay of 27.35 days, compared with 5.53 days for controls. Patients with positive AB cultures required significantly more use of ventilators than those with negative AB cultures. They also had significantly longer hospital stay, more bed transfers, greater duration and number of antibiotics, and higher hospital and pharmacy charges. Unnecessary treatment for colonization with either imipenem or amikacin resulted in a substantial decrease of P. aeruginosa susceptibility to each agent. The financial impact of treating colonization was significant and is a potential area for cost avoidance. Our results emphasize the need to extubate and move patients to non-ICU beds as soon as possible to decrease the risk of nosocomial infection. It also highlights the need to avoid treating colonization, thus avoiding unnecessary antibiotic therapy.

Acinetobacter↗