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A retrospective study of the incidence, clinical characteristics, identification, and antimicrobial susceptibility of bacteremic isolates of Acinetobacter ursingii.

Chiu CH, Lee YT, Wang YC, Yin T, Kuo SC, Yang YS, Chen TL, Lin JC, Wang FD, Fung CP - BMC Infect. Dis. (2015)

Bottom Line: The Phoenix system incorrectly identified all 19 isolates.The MALDI-TOF mass spectrometer system correctly identified all 19 isolates.All the A. ursingii isolates were resistant or showed intermediate susceptibility to ceftriaxone and ceftazidime, but were susceptible to levofloxacin and imipenem.

View Article: PubMed Central - PubMed

Affiliation: Division of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. pipi10279@gmail.com.

ABSTRACT

Background: Acinetobacter ursingii bacteremia is rarely reported. We investigated the incidence and clinical features of A. ursingii bacteremia, performance of the identification system, and antimicrobial susceptibility of the isolates. Acinetobacter ursingii bacteremia patients were compared with A. baumannii bacteremia patients.

Methods: In this 9-year retrospective study, A. ursingii was identified using 16S rRNA and 16S-23S rRNA internal transcribed spacer sequence analysis. The performances of the Vitek 2, Phoenix, and matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometer systems for identifying isolates were tested. Pulsed-field gel electrophoresis (PFGE) was used to determine the clonality of the isolates. The minimal inhibitory concentrations of the antimicrobials were determined using the Vitek 2 system.

Results: Nineteen patients were identified. Acinetobacter ursingii was noted in 1.5-5.2 % of all Acinetobacter bacteremia cases. For the PFGE analysis, two isolates had smeared DNA, two had 93 % similarity, and 15 had similarity <80 %. Among 16 patients with complete medical records, 10 (62.5 %) had no identifiable source of A. ursingii bacteremia. Most patients (n = 12) had underlying malignant disease. Patients with A. ursingii bacteremia had lower Acute Physiology and Chronic Health Evaluation II scores than those with A. baumannii bacteremia (median [interquartile range], 17.1 [10.0-24.7] vs. 24.9 [14.6-35.1]). Patients with A. ursingii bacteremia were also less likely admitted to the intensive care unit than patients with A. baumannii bacteremia (18.8 % vs 63.5 %, p value < 0.01). About half of the patients with A. ursingii (50.8 %) and A. baumannii bacteremia (62.5 %) had received inappropriate antimicrobial therapy within 48 h after bacteremia onset. However, patients with A. ursingii bacteremia had significantly lower 14-day (6.25 % vs 29.8 %, p value = 0.04) and 28-day mortality rates (6.25 % vs 37.3 %, p value = 0.02) than patients with A. baumannii bacteremia. Nine isolates (47.4 %) were correctly identified as A. ursingii and the other 10 isolates (52.6 %) were incorrectly identified as A. lwoffii by the Vitek 2 system. The Phoenix system incorrectly identified all 19 isolates. The MALDI-TOF mass spectrometer system correctly identified all 19 isolates. All the A. ursingii isolates were resistant or showed intermediate susceptibility to ceftriaxone and ceftazidime, but were susceptible to levofloxacin and imipenem.

Conclusions: Acinetobacter ursingii is a rare pathogen that mostly caused primary bacteremia in patients with malignancies. Patients with A. ursingii bacteremia had significantly lower disease severity and mortality rates than patients with A. baumannii bacteremia.

No MeSH data available.


Related in: MedlinePlus

The Kaplan-Meier survival curves of patients with bacteremia caused by Acinetobacter ursingii and Acinetobacter baumannii. The 30-day mortality rate of A. ursingii bacteremia was significantly lower than that of A. baumannii bacteremia (p-value = 0.0352)
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Fig2: The Kaplan-Meier survival curves of patients with bacteremia caused by Acinetobacter ursingii and Acinetobacter baumannii. The 30-day mortality rate of A. ursingii bacteremia was significantly lower than that of A. baumannii bacteremia (p-value = 0.0352)

Mentions: About half of the patients with A. ursingii (50.8 %) and A. baumannii bacteremia (62.5 %) had received inappropriate antimicrobial therapy within 48 h of the onset of bacteremia. However, the 14-day (p value = 0.04) and 28-day (p value = 0.02) mortality rates of the A. ursingii group were significantly lower than those of the A. baumannii group. The Kaplan-Meier survival curves also showed that patients with A. ursingii had a higher cumulative survival rate than those with A. baumannii (Fig. 2).Fig. 2


A retrospective study of the incidence, clinical characteristics, identification, and antimicrobial susceptibility of bacteremic isolates of Acinetobacter ursingii.

Chiu CH, Lee YT, Wang YC, Yin T, Kuo SC, Yang YS, Chen TL, Lin JC, Wang FD, Fung CP - BMC Infect. Dis. (2015)

The Kaplan-Meier survival curves of patients with bacteremia caused by Acinetobacter ursingii and Acinetobacter baumannii. The 30-day mortality rate of A. ursingii bacteremia was significantly lower than that of A. baumannii bacteremia (p-value = 0.0352)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4590261&req=5

Fig2: The Kaplan-Meier survival curves of patients with bacteremia caused by Acinetobacter ursingii and Acinetobacter baumannii. The 30-day mortality rate of A. ursingii bacteremia was significantly lower than that of A. baumannii bacteremia (p-value = 0.0352)
Mentions: About half of the patients with A. ursingii (50.8 %) and A. baumannii bacteremia (62.5 %) had received inappropriate antimicrobial therapy within 48 h of the onset of bacteremia. However, the 14-day (p value = 0.04) and 28-day (p value = 0.02) mortality rates of the A. ursingii group were significantly lower than those of the A. baumannii group. The Kaplan-Meier survival curves also showed that patients with A. ursingii had a higher cumulative survival rate than those with A. baumannii (Fig. 2).Fig. 2

Bottom Line: The Phoenix system incorrectly identified all 19 isolates.The MALDI-TOF mass spectrometer system correctly identified all 19 isolates.All the A. ursingii isolates were resistant or showed intermediate susceptibility to ceftriaxone and ceftazidime, but were susceptible to levofloxacin and imipenem.

View Article: PubMed Central - PubMed

Affiliation: Division of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. pipi10279@gmail.com.

ABSTRACT

Background: Acinetobacter ursingii bacteremia is rarely reported. We investigated the incidence and clinical features of A. ursingii bacteremia, performance of the identification system, and antimicrobial susceptibility of the isolates. Acinetobacter ursingii bacteremia patients were compared with A. baumannii bacteremia patients.

Methods: In this 9-year retrospective study, A. ursingii was identified using 16S rRNA and 16S-23S rRNA internal transcribed spacer sequence analysis. The performances of the Vitek 2, Phoenix, and matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometer systems for identifying isolates were tested. Pulsed-field gel electrophoresis (PFGE) was used to determine the clonality of the isolates. The minimal inhibitory concentrations of the antimicrobials were determined using the Vitek 2 system.

Results: Nineteen patients were identified. Acinetobacter ursingii was noted in 1.5-5.2 % of all Acinetobacter bacteremia cases. For the PFGE analysis, two isolates had smeared DNA, two had 93 % similarity, and 15 had similarity <80 %. Among 16 patients with complete medical records, 10 (62.5 %) had no identifiable source of A. ursingii bacteremia. Most patients (n = 12) had underlying malignant disease. Patients with A. ursingii bacteremia had lower Acute Physiology and Chronic Health Evaluation II scores than those with A. baumannii bacteremia (median [interquartile range], 17.1 [10.0-24.7] vs. 24.9 [14.6-35.1]). Patients with A. ursingii bacteremia were also less likely admitted to the intensive care unit than patients with A. baumannii bacteremia (18.8 % vs 63.5 %, p value < 0.01). About half of the patients with A. ursingii (50.8 %) and A. baumannii bacteremia (62.5 %) had received inappropriate antimicrobial therapy within 48 h after bacteremia onset. However, patients with A. ursingii bacteremia had significantly lower 14-day (6.25 % vs 29.8 %, p value = 0.04) and 28-day mortality rates (6.25 % vs 37.3 %, p value = 0.02) than patients with A. baumannii bacteremia. Nine isolates (47.4 %) were correctly identified as A. ursingii and the other 10 isolates (52.6 %) were incorrectly identified as A. lwoffii by the Vitek 2 system. The Phoenix system incorrectly identified all 19 isolates. The MALDI-TOF mass spectrometer system correctly identified all 19 isolates. All the A. ursingii isolates were resistant or showed intermediate susceptibility to ceftriaxone and ceftazidime, but were susceptible to levofloxacin and imipenem.

Conclusions: Acinetobacter ursingii is a rare pathogen that mostly caused primary bacteremia in patients with malignancies. Patients with A. ursingii bacteremia had significantly lower disease severity and mortality rates than patients with A. baumannii bacteremia.

No MeSH data available.


Related in: MedlinePlus