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Outbreak of a susceptible strain of Acinetobacter species 13 (sensu Tjernberg and Ursing) in an adult neurosurgical intensive care unit.

Between December 1999 and June 2000, an outbreak caused by Acinetobacter emerged on the neurosurgical intensive care unit of our hospital. It was shown using automated ribotyping using Eco RI and pulsed-field gel electrophoresis that the outbreak was caused by spread of a single strain, which was identified by ribotyping and amplified ribosomal DNA restriction analysis as Acinetobacter DNA group 13TU (sensu Tjernberg and Ursing). The outbreak strain, which showed no antibiotic resistance, was identified in 23 patients, five of whom developed an infection. The organism was also isolated from various environmental sites. Cross-transmission among patients continued despite contact isolation of colonized patients and reinforcement of basic disinfection procedures. Eventually, after implementation of additional stringent measures such as cohorting of positive patients and daily disinfection of the floor, the outbreak was brought under control. This study demonstrates that apart from Acinetobacter baumanii, Acinetobacter 13TU strains, even when they are fully susceptible, may cause outbreaks that are difficult to control. Correct identification to the species level of Acinetobacter by genotypic methods is necessary to get insight in the importance of the different Acinetobacter genomic species in hospital epidemiology.

Acinetobacter↗

Genotypic analysis of Acinetobacter bloodstream infection isolates in a Turkish university hospital.

Acinetobacter baumannii is a significant pathogen of bloodstream infections in hospital patients that frequently causes single clone outbreaks. We aimed to evaluate the genetic relatedness and antimicrobial susceptibility of Acinetobacter spp. bloodstream isolates, in order to obtain insight into their cross-transmission. This prospective study was conducted at the Erciyes University Hospital. During a 1-y period, all patients with nosocomial BSI caused by Acinetobacter spp. were included in the study. All data with regard to the patients, underlying diseases and risk factors for BSI and the severity of disease were collected. Blood culture isolates of Acinetobacter spp. were identified according to their morphology and biochemical reactions. The antimicrobial susceptibility was determined using the Kirby-Bauer disk diffusion test according to the NCCLS; the genetic relatedness of isolates was determined by RAPD-PCR analysis and pulsed-field gel electrophoresis (PFGE). 41 patients acquired a nosocomial bloodstream infection caused by A. baumanii during this period. 88% of these infections (36 of 41) occurred while the patients were treated in the intensive care unit. Nearly 80% of the isolates belonged to 3 genotypes, suggesting cross-transmission in ICU settings where infection control practices are poor. All Acinetobacter isolates were multidrug-resistant and the crude mortality of patients infected with A. baumanii was 80.5%. We concluded that the genetic relatedness of Acinetobacter spp. causing BSI was very high, indicating cross-transmission within the ICU setting. Essential components of an infection control programme to prevent nosocomial transmission of A. baumannii are early detection of colonized patients, followed by strict attention to standard precautions and contact isolation.

APACHE↗

Clinical significance of Acinetobacter species isolated from cerebrospinal fluid.

Medical records of 54 patients whose cerebrospinal fluid (CSF) cultures were positive for Acinetobacter were retrospectively reviewed. In 34 (63.0%) patients, the Acinetobacter isolates were clinically insignificant. In the other 20 (37.0%) patients, presence of the organism was regarded as clinically significant and specific antimicrobial therapy was administered. Patients with clinically significant Acinetobacter in CSF more frequently resided in intensive care units (p = 0.011), had intracerebral hemorrhage (p = 0.012) or previous CNS infection (p = 0.003), had prior antibiotic exposure (p = 0.011), and had undergone neurosurgical procedures (p = 0.003). Their CSF was characteristic of neutrophilic pleocytosis, an elevated protein level, and a low CSF-to-serum glucose ratio. Apart from fever, no significant statistical differences existed in individual clinical symptoms and signs between the 2 groups of patients, while a combination of symptoms efficiently differentiated clinically significant and insignificant Acinetobacter. The finding of multiple CSF specimens positive for Acinetobacter was highly suggestive of an active CNS infection (p<0.001). The high ratio of clinically insignificant Acinetobacter CSF isolates highlights the importance of careful judgment when the organism is cultured from CSF. Antimicrobial therapy must be initiated promptly in patients with identified risk factors, while unnecessary treatment should be avoided in those without them.

Acinetobacter↗

Antimicrobial resistance of Acinetobacter spp. in Europe.

Bacteria of the genus Acinetobacter are ubiquitous in nature. These organisms were invariably susceptible to many antibiotics in the 1970s. Since that time, acinetobacters have emerged as multiresistant opportunistic nosocomial pathogens. The taxonomy of the genus Acinetobacter underwent extensive revision in the mid-1980s, and at least 32 named and unnamed species have now been described. Of these, Acinetobacter baumannii and the closely related unnamed genomic species 3 and 13 sensu Tjernberg and Ursing (13TU) are the most relevant clinically. Multiresistant strains of these species causing bacteraemia, pneumonia, meningitis, urinary tract infections and surgical wound infections have been isolated from hospitalised patients worldwide. This review provides an overview of the antimicrobial susceptibilities of Acinetobacter spp. in Europe, as well as the main mechanisms of antimicrobial resistance, and summarises the remaining treatment options for multiresistant Acinetobacter infections.

Acinetobacter↗

Spread of novel aminoglycoside resistance gene aac(6')-Iad among Acinetobacter clinical isolates in Japan.

A novel aminoglycoside resistance gene, aac(6')-Iad, encoding aminoglycoside 6'-N-acetyltransferase, was identified in Acinetobacter genospecies 3 strain A-51. The gene encoded a 144-amino-acid protein, which shared modest identity (up to 36.7%) with some of the aminoglycoside 6'-N-acetyltransferases. The results of high-pressure liquid chromatography assays confirmed that the protein is a functional aminoglycoside 6'-N-acetyltransferase. The enzyme conferred resistance to amikacin, tobramycin, sisomicin, and isepamicin but not to gentamicin. The prevalence of this gene among Acinetobacter clinical isolates in Japan was then investigated. Of 264 Acinetobacter sp. strains isolated from geographically diverse areas in Japan in 2002, 16 were not susceptible to amikacin, and aac(6')-Iad was detected in 7. Five of the producers of aminoglycoside 6'-N-acetyltransferase type Iad were identified as Acinetobacter baumannii, and two were identified as Acinetobacter genospecies 3. These results suggest that aac(6')-Iad plays a substantial role in amikacin resistance among Acinetobacter spp. in Japan.

Acetyltransferases↗

O-antigen diversity among Acinetobacter baumannii strains from the Czech Republic and Northwestern Europe, as determined by lipopolysaccharide-specific monoclonal antibodies.

O-antigen-specific monoclonal antibodies (MAbs) are currently being generated to develop an O-serotyping scheme for the genus Acinetobacter and to provide potent tools to study the diversity of O-antigens among Acinetobacter strains. In this report, Acinetobacter baumannii strains from the Czech Republic and from two clonal groups identified in Northwestern Europe (termed clones I and II) were investigated for their reactivity with a panel of O-antigen-specific MAbs generated against Acinetobacter strains from various species. The bacteria were characterized for their ribotype, biotype, and antibiotic susceptibility and the presence of the 8.7-kb plasmid pAN1. By using the combination of these typing profiles, the Czech strains could be classified into four previously defined groups (A. Nemec, L. Janda, O. Melter, and L. Dijkshoorn, J. Med. Microbiol. 48:287-296, 1999): two relatively homogeneous groups of multiresistant strains (termed groups A and B), a heterogeneous group of other multiresistant strains, and a group of susceptible strains. O-antigen reactivity was observed primarily with MAbs generated against Acinetobacter calcoaceticus and Acinetobacter baumannii strains. A comparison of reaction patterns confirmed the previously hypothesized clonal relationship between group A and clone I strains, which are also similar in other properties. The results show that there is limited O-antigen variability among strains with similar geno- and phenotypic characteristics and are suggestive of a high prevalence of certain A. baumannii serotypes in the clinical environment. It is also shown that O-antigen-specific MAbs are useful for the follow-up of strains causing outbreaks in hospitals.

Acinetobacter↗

The persistence and clonal spread of a single strain of Acinetobacter 13TU in a large Scottish teaching hospital.

This study describes the persistence and spread of a single strain of Acinetobacter 13TU in a large Scottish teaching hospital. Acinetobacter spp. are reported with increasing frequency as a cause of nosocomial infection. The species most implicated in these infections is Acinetobacter baumannii. Following an outbreak of infection with Acinetobacter 13TU within the intensive therapy unit (ITU) of Edinburgh Royal Infirmary (ERI) during 1994-1995, the current epidemiological Acinetobacter situation within the hospital was monitored to determine whether or not control of infection procedures instigated at that time had been successful in controlling the outbreak. Sixty-eight strains of Acinetobacter spp were isolated from clinical specimens received from various wards in the ERI and other associated hospitals over a 7-month period. Each isolate was typed phenotypically by the API20NE system and genotypically by pulsed field gel electrophoresis (PFGE) in order to compare them with the previous outbreak strain. Fifty-three percent of the isolates collected were originally identified as A. junii by API 20 NE, of which 83% (mainly from ITU) were shown to be genotypically related to the previous outbreak strain. Subsequent tDNA fingerprinting of one of the original outbreak strains showed it to be a member of the genospecies 13TU and not A. junii as originally thought.

Acinetobacter↗

Nosocomial infections due to Acinetobacter baumannii in a neurosurgery ICU.

Invasive infections caused by Acinetobacter baumannii in a post-operative neurosurgery ICU were studied. Sixty one patients admitted during a span of 11 months were culture positive for acinetobacter species from blood and/or CSF samples. They were followed up prospectively for evidence of infection and clinical outcome. 40 cases had clinical evidence of infection due to acinetobacter species while in 21 patients, the isolation of the organism was considered a contaminant. Acinetobacter baumannii was the most common organism associated with invasive infections. Respiratory tract was found to be the most common primary source of infection in patients with bacteraemia or meningitis. The age, sex and pre-operative hospital stay were not significantly different in the two groups (p>0.05), while post-operative hospital stay and mortality was significantly higher in patients with invasive infection (p<0.05). Acinetobacter baumannii was isolated from multiple sites (p<0.05) and repeatedly from the same site (p<0.001) in a significantly higher number of patients with invasive infections. Mortality was high in the patients infected with Acinetobacter baumannii. Even amongst the infected group, the patient shaving meningitis showed a higher mortality as compared to the patients having bacteraemia.

Acinetobacter↗

[Pathogenic role of Acinetobacter spp during HIV infection].

In order to assess the clinical role of bacterial complications due to Acinetobacter spp. during HIV disease, a retrospective survey of clinical and microbiological data of 2221 HIV-infected patients hospitalised during the past 10 years was carried out, evaluating all episodes of Acinetobacter spp. infection according to several epidemiological, clinical and therapeutic variables. Eleven patients of 2221 (0.5%) suffered from Acinetobacter spp. disease: sepsis in 5 cases, and urinary, respiratory tract disease and bacteremic pneumonia in three, two, and one patient respectively. A. calcoaceticus was responsible in 4 cases, A. lwoffii in three, and Acinetobacter spp. in the 4 remaining cases; 4 patients experienced a polymicrobial infection, and 7 had a prior diagnosis of full-blown AIDS. All patients had a severe HIV-related immunodeficiency (mean CD4+ lymphocyte count 118.2 +/- 45.3 cells/microl). Compared with other localizations, sepsis was related to a lower mean CD4+ cell count (p<.001), and a more frequent occurrence of leucopenia-neutropenia (p<.005). Disease episodes diagnosed after the first 72 hours of hospitalisation (deemed no- socomial in origin), proved more frequent than community-acquired ones (9 cases versus 2), affected predominantly patients with AIDS and neutropenia, and were frequent1y associated with bacteremia (p<.04) The use of broad spectrum antibiotics, corticosteroids and cotrimoxazole, was recognized during the month preceding the diagnosis of Acinetobacter spp. disease, in 6, 4, and 8 cases, respectively. One patient only had an indwelling intravascular catheter, while no recent history of surgery, intensive care, or other invasive procedures was found. At in vitro susceptibility studies, bacterial isolates showed complete resistance to ampicillin and cephalothin, and low sensitivity to second-generation cephalosporins, while a higher susceptibility rate was revealed towards ceftazidime, netilmicin, amikacin, and quinolones, followed by cotrimoxazole and piperacillin. A prompt and appropriate antimicrobial therapy (mostly carried out with cephalosporins and aminoglycosides), led all patients to a clinical and microbiological cure within 6-1.3 days, in the absence of mortality or relapses. As opportunist pathogens with a predominant nosocomial origin, Acinetobacter spp. organisms may be responsible for an appreciable morbidity in patients with HIV disease, especially when additional risk factors (immunodeficiency, underlying diseases, and hospitalisation) are present. Notwithstanding the high drug resistance profile of the majority of isolated organisms, a timely diagnosis and a treatment based on in vitro assays, contribute to avoid recurrences and potentially life-threatening complications.

AIDS-Related Opportunistic Infections↗

[Molecular mechanism of multiple-drug and pan-drug resistance among Acinetobacter species].

OBJECTIVE: To investigate the molecular mechanism of multiple-drug and pan-drug resistance among Acinetobacter species. METHODS: Non-repetitive 90 carbapenem-resistant strains of Acinetobacter species were collected in Beijing, Guangzhou, and Fuzhou 1999-2004. The homology of the isolates was determined by both pulsed field gel electrophoresis and randomly amplified polymorphic DNA typing. Seven representative clones were selected from the 90 strains of Acinetobacter isolated from different hospitals to be used for further study. Analytical isoelectric focusing was used to measure the isoelectric point of the beta-lactamase. Plasmid DNA was extracted and purified Genes of different beta-lactamase, including bla(TEM--), bla(SHV-), bla(PER-), blaI(MP-), bla(VIM-), and bla(OXA-) genes, in these clone strains were amplified and sequenced. PCR was used to analyze the integrons. RESULTS: The P clone strain isolated during an outbreak of pan-drug-resistant Acinetobacter species in Peking Union Medical College Hospital 2004 was not susceptible to most common antimicrobial agents tested. The 7 representative clones produced multiple beta-lactamases: TEM-1, high-level AmpC, SHV-type, OXA-23 carbapenemase and IMP-8 and metalloenzyme respectively. One clone produced PER-1 enzyme. These 7 clone strains were resistant to most beta-lactams (including carbapenems), erythromycin, chloramphenicol, and rifampin. Two clone strains were susceptible to cefoperazone/sulbactam and amikacin while 4 clone strains susceptible to levofloxacin. All of the 7 clones were susceptible to minocycline and colistin. Five different integrons were found, harboring the genes mediating the resistance to aminoglycosides, rifampin, chloramphenicol, and carbapenems (bla(IMP-8)). CONCLUSION: The molecular bases of multiple-drug or pan-drug resistance in Acinetobacter species include production of OXA-23 carbapenemase or IMP type metalloenzyme and integrons with different resistance gene cassettes. Pan-drug-resistant Acinetobacter species are susceptible to old antimicrobials agents, such as colistin and minocycline.

Acinetobacter↗

Clinical and demographic features of infection caused by Acinetobacter species.

BACKGROUND: Recently, Acinetobacter emerged as an important pathogen and the prevalence of isolation has increased since the last two decades worldwide. AIMS: To determine Acinetobacter incidence, their clinical demography, antibiotyping and speciation. SETTINGS AND DESIGN: A study of the clinical samples submitted to microbiology laboratory of a teaching hospital over a period of 3 years (December 1994 through November 1997). MATERIALS AND METHODS: Identification, speciation and antibiotyping were performed for the isolates of Acinetobacter recovered from infective samples. Clinical demographic characteristics were studied retrospectively. RESULTS: Total 510 of 5391 (9.6%) of isolates were Acinetobacter, responsible for 71.2% (363 of 510) monomicrobial and 28.8% (147 of 510) polymicrobial infections. The organism was responsible for 156 (30.6%) cases of urinary tract infection and 140 (27.5%) cases of wound infection and was most prevalent in the intensive care unit (30.8%, 140 of 455). The crude mortality rate due to multi-drug resistant Acinetobacter septicemia was 7.9% (36 of 455). The isolates could be classified into 7 species, with A. baumannii being most predominant. No peculiar pattern during antibiotyping was observed, but most of them were multi-drug resistant. CONCLUSION: Multi-drug resistant Acinetobacter nosocomial infection has emerged as an increasing problem in intensive care units of the hospital, responsible for 7.9% deaths. The analysis of risk factors and susceptibility pattern will be useful in understanding epidemiology of this organism in a hospital setup.

Acinetobacter↗

Clinical and microbiological characteristics of bacteremia caused by Acinetobacter lwoffii.

A retrospective study was conducted to analyze the clinical features and pathogenic roles of bacteremia caused by Acinetobacter lwoffii during a 4-year period. Acinetobacter lwoffii (formerly Acinetobacter calcoaceticus var. lwoffii) is recognized as normal flora of the skin, oropharynx and perineum of healthy individuals. There are few reports of Acinetobacter lwoffii bacteremia associated with indwelling catheters in humans, particularly in immunocompromised hosts. The records of 18 patients with Acinetobacter lwoffii bacteremia whose underlying conditions included cancer (11 patients), systemic lupus erythematosus (n=1), chronic obstructive pulmonary disease (n = 2) and other diseases (n = 4), all but one of whom had indwelling catheters during the bacteremic episode, were examined. The clinical syndromes were classified as probable catheter-related bacteremia (n = 14), definite catheter-related bacteremia (n = 2), primary bacteremia (n = 1) or biliary tract infection (n = 1). The infections improved after removal of the catheter and/or appropriate antimicrobial therapy. One death was attributable to the bacteremic event. The results of this study show that indwelling catheter-related Acinetobacter lwoffii bacteremia in immunocompromised hosts appears to be associated with a low risk of mortality.

Acinetobacter Infections↗

Isolation and characterization by conventional methods and genetic transformation of Psychrobacter and Acinetobacter from fresh and spoiled meat, milk and cheese.

Of 126 samples of fresh and spoiled meat and dairy products, 40% were positive for the presence of Moraxella-like bacteria and 64% of Acinetobacter; 279 and 466 strains, respectively, were isolated and a part of these were tested by biochemical methods and DNA transformation assays. In some cases, the Moraxellaceae in the samples examined reached considerable quantitative levels, but their percentage in the microflora was generally low. Moraxella-like bacteria were predominant in fresh meat, Acinetobacter in spoiled meat and milk. Most acinetobacters belonged to biotype lwoffii (sensu lato) and all 90 strains tested were positive for DNA transformation with an auxotrophic Acinetobacter. Moraxella-like bacteria were identified as Psychrobacter immobilis in 96% of 103 transformation assays. Moraxellaceae show lipolytic activity but they are considered of low incidence in food spoilage. Only 3.7% of acinetobacters from dairy sources was able to produce ropy milk. Unlike strains from clinical isolates, psychrobacters and acinetobacters isolated from food often do not grow at 37 degrees C.

Acinetobacter↗

Metallo-beta-lactamase-producing Gram-negative bacilli in Korean Nationwide Surveillance of Antimicrobial Resistance group hospitals in 2003: continued prevalence of VIM-producing Pseudomonas spp. and increase of IMP-producing Acinetobacter spp.

Metallo-beta-lactamase (MBL)-producing Pseudomonas spp. and Acinetobacter spp. were prevalent in Korean hospitals. In this study, the prevalence and presence of MBL-producing isolates among imipenem-nonsusceptible and imipenem-susceptible isolates, respectively, were screened. The genetic and phenotypic characteristics of MBL-producing isolates were determined. Among imipenem-nonsusceptible isolates, 52 (11.1%) of 467 Pseudomonas spp. were blaVIM-like allele-positive, and 33 (15.1%) of 218 Acinetobacter spp. were either blaVIM- or blaIMP-like allele-positive. One blaVIM-like allele-positive isolate of Acinetobacter spp. was detected among 84 imipenem-susceptible Acinetobacter isolates. The minimum inhibitory concentration for 90% of isolates of imipenem was higher (>128 microg/mL) for Pseudomonas spp. than Acinetobacter spp. (16 microg/mL), although both had blaVIM-like allele. The source of MBL-producing isolates was mostly the sputum and urine of patients in the intensive care unit. Pulsed-field gel electrophoresis analysis suggested the intra- and inter-hospital spread of MBL-producing strains at some hospitals. In conclusion, blaVIM-like allele-positive P. aeruginosa remained highly prevalent, and the proportion of blaIMP-like allele-positive Acinetobacter spp. has increased significantly in most Korean hospitals.

Acinetobacter↗

Comprehensive in vitro evaluation of cefepime combined with aztreonam or ampicillin/sulbactam against multi-drug resistant Pseudomonas aeruginosa and Acinetobacter spp.

Pseudomonas aeruginosa and Acinetobacter spp. are becoming increasingly resistant to antimicrobial agents, and serious infections caused by these organisms often require combination therapy. Interactions of cefepime with either aztreonam (P. aeruginosa; n=46) or ampicillin/sulbactam (Acinetobacter spp.; n=34) were investigated by the chequerboard synergy method against isolates with various resistance phenotypes, including resistance to imipenem (36 P. aeruginosa and 19 Acinetobacter spp.). Synergy or partial synergy interactions occurred with 56.5% of P. aeruginosa and 88.2% of Acinetobacter spp. strains examined. Among the imipenem-resistant strains, synergy or partial synergy interactions were observed in 47.2% of P. aeruginosa and 84.2% of Acinetobacter spp. strains. In addition, the vast majority of impenem-resistant strains showed MIC values within achievable concentrations in plasma for at least one of the antimicrobials evaluated in the combination. The role of combination antimicrobial therapy in the treatment of severe infections caused by multidrug-resistant P. aeruginosa and Acinetobacter spp. should be further evaluated to maximize favourable clinical outcomes.

Acinetobacter↗

Comparison of benzyl alcohol dehydrogenases and benzaldehyde dehydrogenases from the benzyl alcohol and mandelate pathways in Acinetobacter calcoaceticus and from the TOL-plasmid-encoded toluene pathway in Pseudomonas putida. N-terminal amino acid sequences, amino acid compositions and immunological cross-reactions.

1. N-Terminal sequences were determined for benzyl alcohol dehydrogenase, benzaldehyde dehydrogenase I and benzaldehyde dehydrogenase II from Acinetobacter calcoaceticus N.C.I.B. 8250, benzyl alcohol dehydrogenase and benzaldehyde dehydrogenase encoded by the TOL plasmid pWW53 in Pseudomonas putida MT53 and yeast K(+)-activated aldehyde dehydrogenase. Comprehensive details of the sequence determinations have been deposited as Supplementary Publication SUP 50161 (5 pages) at the British Library Document Supply Centre, Boston Spa. Wetherby. West Yorkshire LS23 7BQ, U.K., from whom copies can be obtained on the terms indicated in Biochem. J. (1991) 273. 5. The extent of sequence similarity suggests that the benzyl alcohol dehydrogenases are related to each other and also to established members of the family of long-chain Zn2(+)-dependent alcohol dehydrogenases. Benzaldehyde dehydrogenase II from Acinetobacter appears to be related to the Pseudomonas TOL-plasmid-encoded benzaldehyde dehydrogenase. The yeast K(+)-activated aldehyde dehydrogenase has similarity of sequence with the mammalian liver cytoplasmic class of aldehyde dehydrogenases but not with any of the Acinetobacter or Pseudomonas enzymes. 2. Antisera were raised in rabbits against the three Acinetobacter enzymes and both of the Pseudomonas enzymes, and the extents of the cross-reactions were determined by immunoprecipitation assays with native antigens and by immunoblotting with SDS-denatured antigens. Cross-reactions were detected between the alcohol dehydrogenases and also among the aldehyde dehydrogenases. This confirms the interpretation of the N-terminal sequence comparisons and also indicates that benzaldehyde dehydrogenase I from Acinetobacter may be related to the other two benzaldehyde dehydrogenases. 3. The amino acid compositions of the Acinetobacter and the Pseudomonas enzymes were determined and the numbers of amino acid residues per subunit were calculated to be: benzyl alcohol dehydrogenase and TOL-plasmid-encoded benzyl alcohol dehydrogenase, 381; benzaldehyde dehydrogenase I and benzaldehyde dehydrogenase II, 525; TOL-plasmid-encoded benzaldehyde dehydrogenase, 538.

Acinetobacter↗

Acinetobacter calcoaceticus septicemia in patients with cancer.

At our institution, 95 cases of Acinetobacter septicemia occurred over a ten-year period (1973 to 1982) in patients being treated for cancer. In 24 patients the infection was polymicrobial, while Acinetobacter ssp was the only offending pathogen in 71 patients. In 76 patients (80%), the infection was related to an indwelling central venous catheter (CVC). A sharp increase in the frequency of Acinetobacter septicemia was noticed in the years 1981 and 1982 and coincided with a marked increase in the number of indwelling CVCs in use. Acute leukemia and breast cancer were the malignancies most commonly associated with Acinetobacter septicemia. The isolates of Acinetobacter calcoaceticus from the patients in this study were highly susceptible to the aminoglycosides and moderately susceptible to trimethoprim-sulfamethoxazole (TMP-SMX), carbenicillin, and tetracycline. Seventy-nine patients recovered from their infection with removal of the CVC and antimicrobial chemotherapy. Acinetobacter sp was the cause of death in none of the 16 patients who died. A calcoaceticus is an important nosocomial pathogen causing infections predominantly in immune compromised patients and frequently associated with indwelling catheters.

Acinetobacter Infections↗

The thin pili of Acinetobacter sp. strain BD413 mediate adhesion to biotic and abiotic surfaces.

Two structurally different appendages, thin and thick pili, are found in members of the genus Acinetobacter. The presence of pilus structures correlates with different phenotypes, such as adherence to surfaces, a trait not only observed in pathogenic Acinetobacter species, as well as motility. However, their distinct individual roles were unknown. To characterize the role of different pili in the physiology of Acinetobacter, we isolated the thin pili from the cell surface of Acinetobacter sp. strain BD413 (recently recognized as representative of Acinetobacter baylyi), a soil bacterium that rapidly takes up naked DNA from its environment. Electron microscopy revealed that the pilus has an external diameter of 2 to 3 nm for single filaments. The filaments are packed into right-handed bundles. The major protein constituting the pilus was purified, and the encoding gene, acuA, was cloned. AcuA was found to be weakly related to the structural subunit of F17 pili of Escherichia coli. Analyses of the acuA flanking DNA region led to the identification of three closely associated genes, acuD, acuC, and acuG, whose deduced proteins are similar to chaperone, usher, and adhesin of F17-related pili, respectively. Transcriptional analyses revealed that acuA expression is maximal in the late-stationary-growth phase. Mutation of acuA led to a loss of thin pili and concomitantly loss of adhesion to polystyrene and erythrocytes but not loss of competence. Therefore, thin pili of Acinetobacter sp. strain BD413 are suggested to be assembled by the chaperone/usher pathway and are involved in adherence to biotic and abiotic surfaces.

Acinetobacter↗