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PubMed1995

Pillows, an unexpected source of Acinetobacter.

From 1989 until 1992 an increase in the number of isolations of Acinetobacter was observed in a community hospital in The Netherlands. The organisms were spread throughout the hospital and a common source was suspected. Feather pillows were found to harbour high numbers of acinetobacters. Replacement with synthetic pillows and correction of the laundry procedure resulted in a significant reduction of Acinetobacter isolations. A number of isolates from patients and from pillows were indistinguishable using biotyping, antibiogram typing and cell envelope protein typing. By the use of DNA-DNA hybridization most isolates were identified to A. baumannii and the unnamed closely related genomic species 13. A number of isolates, mostly from pillows, were identified as A. radioresistens. The outcome of cultivation, intervention and typing suggests that the feather pillows played an important role in the outbreak.

Acinetobacter↗
PubMedDate not supplied

Identification and biotyping of clinical isolates of Acinetobacter.

A total of 343 Acinetobacter strains, most isolated from hospital patients, were identified using a 16-test system (acid production from glucose, gelatin hydrolysis and utilization of 14 carbon sources) associated with tests for growth at 37, 41 and 44 degrees C. Of 299 nosocomial isolates, 253 were identified as A. baumannii, 20 as Acinetobacter genospecies 3, 8 as A. haemolyticus, 8 as A. lwoffii, 4 as A. johnsonii and 6 as other (presently) unnamed species. A biotyping system based on the utilization of levulinate, citraconate, L-phenylalanine, phenylacetate, 4-hydroxybenzoate and L-tartrate allowed recognition of 17 biotypes among 247 A. baumannii isolates. This biotyping system should be useful in epidemiological studies of Acinetobacter strains.

Acinetobacter↗
PubMed2005

Activity of meropenem and comparators against Pseudomonas aeruginosa and Acinetobacter spp. isolated in the MYSTIC Program, 2002-2004.

This study examines the susceptibilities of meropenem and other broad-spectrum antimicrobials tested against bacterial isolates collected from hospitalized patients during 2002-2004 from worldwide medical centers participating in the Meropenem Yearly Susceptibility Test Information Collection (MYSTIC) Program. The in vitro activity of meropenem and 5 comparator antimicrobial agents was assessed against Pseudomonas aeruginosa and Acinetobacter spp. Generally, the susceptibility of Australasian and North American isolates was higher than that of the European and South American isolates. The rank order of activity of the antimicrobial agents tested against a worldwide collection of P. aeruginosa was piperacillin/tazobactam (77.7% susceptible) > meropenem (75.4%) > ceftazidime (70.0%) > imipenem (69.7%) > gentamicin (66.1%) > ciprofloxacin (62.0%). Against a worldwide collection of Acinetobacter spp. meropenem (76.1% susceptible) was the most active compound followed by imipenem (74.7%) > gentamicin (51.9%) > ciprofloxacin (40.5%) > piperacillin/tazobactam (39.8%) > ceftazidime (38.1%). The carbapenems appear to be a valuable option for the treatment of serious nosocomial infections caused by P. aeruginosa or Acinetobacter spp. over a broad geographical region.

Acinetobacter↗
PubMed2005

Is IS(ABA-1) customized for Acinetobacter?

An insertion sequence (IS(ABA-1)) was identified in Acinetobacter spp., but not in Enterobacteriacea and Pseudomonas aeruginosa. Numerous copies of the IS were identified in Acinetobacter strains containing the element. In one of the Acinetobacter baumannii strains, IS(ABA-1) was identified adjacent to sulII and transcription of the resistance gene is presumed to be dependent on promoter sequences within the IS. Since the IS is adjacent to ampC and bla(OXA) in this A. baumannii strain, it may be that IS(ABA-1) plays an important role in the expression of antibiotic resistance genes in this genus.

Acinetobacter↗
PubMed2005

Chronic community-acquired Acinetobacter pneumonia that responded slowly to rifampicin in the anti-tuberculous regime.

Acinetobacter baumannii is a well-known cause of hospital-acquired pneumonia. Occasionally, it can present as an acute community-acquired pneumonia with a fulminant course. However, the occurrence of the chronic form of community-acquired Acinetobacter pneumonia is yet to be highlighted. We describe a 62-year-old, HIV negative, non-diabetic male, who was referred for evaluation of consolidation and cavitation in the apicoposterior segment of the left upper lobe for 4 months. For this, he had received anti-tuberculous therapy, which included rifampicin. On investigation, a diagnosis of chronic community-acquired pneumonia due to Acinetobacter baumannii was made. The steady clinico-radiologic improvement observed was attributed to rifampicin in the anti-tuberculous regime. Subsequently, an aspergilloma formed in the cavity.

Acinetobacter Infections↗
PubMed2005

Prevalence of metallo-beta lactamase (MBL) producing Pseudomonas spp. and Acinetobacter spp. in a tertiary care hospital in India.

OBJECTIVE: Gram-negative bacteria with acquired metallo-beta lactamases production have been increasingly reported in some countries, necessitating their detection. We determined the occurrence of acquired metallo-beta lactamases (MBL) producing bacteria in our teaching hospital. METHOD: The method employed was a rapid technique using a disk of imipenem plus 750 microg of EDTA, on Mueller-Hinton plate which was supplemented with 70 microg/ml of zinc sulfate, to differentiate MBL producing Pseudomonads and Acinetobacter. RESULT: Out of 200 isolates tested, 7.5% of our Pseudomonads and Acinetobacter were shown to be MBL producers. CONCLUSIONS: Though MBL prevalence is still low in our hospital set up, screening for MBL among Pseudomonas and Acinetobacter isolates should be routinely done in laboratory.

Acinetobacter↗
PubMedDate not supplied

An unusual presentation of epidural Acinetobacter infection.

OBJECTIVE: We report a case of spinal-cord compression caused by epidural fat infection with Acinetobacter. The initial magnetic resonance imaging (MRI) scan suggested epidural hematoma or abscess, although both were absent at surgery. CASE REPORT: A 60-year-old man had a thoracic epidural sited at the level of T8/9 for postoperative analgesia after major abdominal surgery. A mixture of bupivacaine 0.1% and fentanyl 2 microg/mL was infused at a rate of 10 mL/h for 48 hours postoperatively. The epidural catheter was then removed, but 24 hours later, the patient still had weakness and numbness in his lower limbs. An MRI scan showed cord compression secondary to a hematoma or abscess from the level of T6 to T11. At laminectomy, no hematoma or abscess was found, but edematous epidural fat was excised. This fat was sent for culture and Acinetobacter was grown. Appropriate antibiotic therapy was given. Over a period of 12 months, the patient has regained near-normal power and sensation. CONCLUSION: Epidural Acinetobacter infection may present atypically without signs of meningism. MRI imaging may be confusing in these infections and lead to incorrect radiological diagnoses. Spinal-cord compression, as a complication of epidural catheter placement, does not have to be caused by hematoma or abscess.

Abdomen↗
PubMed2000

Corneal perforation due to Acinetobacter junii: a case report.

Acinetobacter spp. is emerging as a common cause of nosocomial infections. Community acquired ocular infections due to Acinetobacter are rare. Only one case of perforation of cornea has been reported previously, where old nomenclature was used to describe the causal agent. We report a case of corneal perforation due to Acinetobacter junii for which a therapeutic penetrating keratoplasty was conducted and the patient eventually recovered.

Acinetobacter↗
PubMed2001

Interactions of colistin and rifampin on multidrug-resistant Acinetobacter baumannii.

The increased incidence of nosocomial infections by multidrug-resistant Acinetobacter spp creates demand on the application of some combinations of older antimicrobials on that species. The in vitro activities of colistin and of rifampin and of their interaction were tested on 39 nosocomial isolates of Acinetobacter baumannii. All isolates were resistant to ampicillin/sulbactam, to 3(rd) and 4(th) generation cephalosporins, to amikacin and to ciprofloxacin. MICs were determined by a microdilution technique and interactive studies between 1x or 4x MIC of colistin and rifampin were performed by the time-kill assay. Rifampin was applied at a concentration of 2 microg/mL which is equal to its mean serum level. All isolates were inhibited by colistin and only 15.2% by rifampin. Synergy between 1x MIC of colistin and rifampin was detected in 15.4% of isolates at 6 h of growth and in 51.3% of isolates at 24 h of growth. Synergy between 4x MIC of colistin and rifampin was detected in 15.4% of isolates at 6 h of growth and in 66.7% of isolates at 24 h of growth. It is concluded that colistin is highly active on multidrug-resistant Acinetobacter spp and its activity on A.baumannii is increased in the presence of rifampin, so that their administration might be proposed for nosocomial infections by these isolates.

Acinetobacter↗
PubMed1990

Serotyping of clinical isolates of Acinetobacter: serovars of genospecies 3.

A total of 156 clinical isolates of genospecies 3, the second most commonly encountered member of the genus Acinetobacter at our institution, were identified with carbon source utilization tests among 400 Acinetobacter isolates. Checkerboard tube agglutination tests and reciprocal cross-absorption studies with polyclonal rabbit immune sera against heated (100 degrees C, 1 h) cells of serovar candidate strains of genospecies 3 permitted identification of 13 serovars. Minor one-way crossreactions were noted between serovars 10 and 8 and between serovars 2 and 12, respectively. Isolates of serovar 13 cross-reacted extensively one-way with serovar 2 and less so with serovars 4 and 12. Genospecies 3 serovars 3, 7, 8, and 9 cross-reacted with Acinetobacter baumannii serovars 19, 21, 6, and 15, respectively.

Acinetobacter↗
PubMed2026

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↗
PubMed2005

Early prosthetic valve endocarditis due to Acinetobacter baumannii: a case report and brief review of the literature.

Acinetobacter is a highly resistant microorganism, commonly isolated in intensive and post-operative care units. Although rarely reported, it may constitute 1 of the several causes of early prosthetic valve endocarditis. A diffuse, red maculopapular rash may be encountered in patients with Acinetobacter endocarditis. Here we present a case of early prosthetic valve endocarditis due to Acinetobacter baumannii and accompanied by a cutaneous eruption.

Acinetobacter Infections↗
PubMed1998

Appearance of resistance to meropenem during the treatment of a patient with meningitis by Acinetobacter.

A case is reported of a patient who developed Acinetobacter meningitis after an external ventricular drainage system had been fitted for control of intracranial pressure. During the process, nine strains of Acinetobacter isolated from her cerebrospinal fluid were indistinguishable by analysis of total genomic DNA by pulse-field gel electrophoresis. The first eight strains were sensitive to meropenem and imipenem (MICs < 1 g/l). The MIC of the last one, which had been recovered after 32 days during two courses of treatment with meropenem, increased to > 32 g/l for meropenem, while with imipenem the increase was minimal (MIC = 1.5 g/l). The microorganism persisted in the central nervous system despite the administration of different antimicrobials, including intraventricular aminoglycosides and six changes in the external ventricular system. The patient died 68 days after admission to the intensive care unit from bilateral cerebral ischemic lesions, intraventricular hemorrhage and cerebral edema with endocraneal hypertension, the Acinetobacter ventriculitis also contributing to this state.

Acinetobacter↗
PubMed2003

Acinetobacter outbreaks, 1977-2000.

This review of Acinetobacter outbreaks summarizes factors related to the presence and recognition of organism transmission and describes the implementation of control and prevention measures directed at limiting spread. Exogenous transmission of Acinetobacter should be considered when infections are endemic and when case rates increase. Increasing or new antimicrobial resistances in a collection of isolates also suggest transmission, and transmission can be definitively confirmed when isolates are found to be indistinguishable from or related to one another by a discriminatory genotyping test. An investigation for a common source should be conducted. When a common source cannot be found and eliminated, or once an endemically transmitted organism is established, containment or prevention efforts may require aggressive interventions, complex interventions, or both. Colonization at multiple sites, the relative ease of induction of antibiotic resistance in the organism following patient exposure to multiple drugs, and long-term environmental survival provide enhanced opportunities for the transmission of Acinetobacter between and among patients. New approaches and interventional trials are needed to define effective measures for the prevention and control of Acinobacter infections.

Acinetobacter↗
PubMed1992

Community-acquired Acinetobacter pneumonia in the Northern Territory of Australia.

Eleven cases of blood culture-positive, community-acquired pneumonia due to the human commensal Acinetobacter baumannii were studied in Darwin in the Northern Territory of Australia during the 10-year period from March 1981 through February 1991. Demographic risk factors included male gender, age of greater than 45 years, and Aboriginal ethnic background. Multiple clinical risk factors, including cigarette smoking, alcoholism, chronic obstructive airway disease, and diabetes mellitus, were noted in all cases and contributed to the high mortality (64%). In all cases pneumonia was clinically fulminant. A fatal outcome was strongly associated with inappropriate initial antibiotic therapy. All tested isolates of Acinetobacter were sensitive to gentamicin and resistant to cefotaxime. The 34 previously reported cases of community-acquired acinetobacter pneumonia are reviewed, and appropriate therapeutic regimens are identified.

Acinetobacter↗
PubMed1992

Infective endocarditis of a native valve due to Acinetobacter: case report and review.

A case of community-acquired infective endocarditis of a native valve that was caused by Acinetobacter calcoaceticus subspecies anitratus is presented. The previously reported cases are reviewed, and therapy for this disorder is discussed. The presence of a transient maculopapular rash involving the palms and soles but sparing the face is suggested as a possible early clinical clue to the diagnosis. Native valve endocarditis caused by Acinetobacter species is an acute, aggressive illness that is more likely to be fatal than the prosthetic valve form; of the previously described patients, five of 15 with native valve endocarditis and one of six with prosthetic valve endocarditis died. In the appropriate clinical setting, we recommend therapy with an antimicrobial agent known to be active against Acinetobacter organisms when blood cultures are reported to yield oxidase-negative, gram-negative coccobacilli until the final identification of the microorganism is known.

Acinetobacter Infections↗
PubMed1994

Bacteremia with Acinetobacter species: risk factors and prognosis in different clinical settings.

Acinetobacter species are widespread environmental gram-negative coccobacilli that are associated with nosocomial infections; these bacteria are considered to be of relatively low virulence and rarely cause invasive disease. Fifty-two cases of bacteremic episodes due to Acinetobacter species were reviewed, and risk factors and outcomes of these cases were examined. It was noted that these cases belonged to a few clinical groups with markedly different outcomes. Eighteen patients had malignancies (predominantly hematologic), and bacteremia often developed after respiratory infection. Nine patients suffered traumatic injuries and developed bacteremia with Acinetobacter species after endotracheal intubation in the intensive care unit and respiratory colonization. Four burn patients, three of whom had burns covering > or = 50% of their body surface areas, had burn infections prior to bacteremia. While many patients had central venous catheters, in only four cases were the catheters clearly infected prior to the positive blood culture. Prior use of antibiotics was widespread in all groups of patients, and isolates showed high levels of antimicrobial resistance, particularly to beta-lactam agents. The outcome of infection correlated more closely with the type of underlying illness than with other factors such as biovar, polymicrobial bacteremia, or appropriate therapy. Patients with malignancies and burn patients fared poorly (10 of 18 and 2 of 4 patients, respectively, died), while trauma patients and patients with other illnesses did well.

Acinetobacter↗
PubMed2002

Antibiotic resistance among clinical isolates of Acinetobacter in the UK, and in vitro evaluation of tigecycline (GAR-936).

A survey was conducted of the antimicrobial susceptibilities of 595 Acinetobacter spp. isolated from routine clinical specimens in 54 sentinel laboratories throughout the UK during 2000. Isolates of the Acinetobacter baumannii complex (genomic groups 2, 3 and 13TU; n = 443) were distinguished from other genomic groups (n = 152) by PCR fingerprinting of tDNA spacer regions. MICs of amikacin, cefotaxime, ceftazidime, ciprofloxacin, colistin, gentamicin, imipenem, meropenem, minocycline, piperacillin, piperacillin/tazobactam, rifampicin, sulbactam and tetracycline were determined on IsoSensitest agar and interpreted, wherever possible, using BSAC breakpoints. Tigecycline (GAR-936), a new glycylcycline, was also tested. Resistance to cephalosporins, aminoglycosides and ciprofloxacin was widespread, but carbapenems, colistin, sulbactam, minocycline and tigecycline were each active against >80% of the isolates. Isolates of A. baumannii were more often resistant to cefotaxime, ceftazidime, piperacillin, piperacillin/tazobactam, ciprofloxacin, gentamicin and tetracyclines than those belonging to other genomic groups, but were less often resistant to colistin; no significant differences between genomic groups were noted in the susceptibilities to amikacin, carbapenems, rifampicin or sulbactam. The relative activities of the tetracyclines were minocycline > tigecycline > tetracycline. Thirteen carbapenem-resistant isolates (MICs > or =8 mg/L; 2.2%) were received from six centres; four centres sent single isolates; one sent three and one sent six. An allele of bla(IMP) was detected in one of these isolates, but the other 12 isolates either had carbapenemase-independent resistance, or undetectable carbapenemase activity combined with other resistance mechanisms. In conclusion, carbapenems, colistin and minocycline retained greatest activity against the Acinetobacter isolates collected. Tigecycline was less active than minocycline, but both agents overcame most tetracycline resistance.

Acinetobacter↗