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[In vitro activity of beta-lactam antibiotics in combination with sulbactam against enterobacteriaceae, Pseudomonas aeruginosa and Acinetobacter. Results of a multicenter study].

The in vitro antimicrobial activity of ticarcillin (TICAR), mezlocillin (MEZLO), piperacillin (PIPER), cefoperazone (CPZ), cefotaxime (CTX) and ceftazidime (CAZ), alone and in combination with 8 micrograms/ml of sulbactam (SULB), was studied by agar dilution against TICAR resistant strains isolated in 8 hospitals over a period of 3 months in 1989 (747 enterobacteria, 110 Ps. aeruginosa and 48 Acinetobacter sp.). SULB did not modify the activity of beta-lactam antibiotics against Ps. aeruginosa. The 6 beta-lactam antibiotics SULB combinations were only active for 27% of Acinetobacter SULB sensitive. SULB restored the activity of: MEZLO, PIPER, CPZ in Enterobacteria producing a penicillinase; PIPER, CTX and CAZ in Enterobacteria producing a broad-spectrum beta-lactamase; MEZLO, PIPER, CTX and CAZ in M. morganii producing a derepressed cephalosporinase.

Acinetobacter↗

Acinetobacter peritonitis in patients receiving continuous ambulatory peritoneal dialysis.

Little is written on peritonitis caused by Acinetobacter species in patients receiving continuous ambulatory peritoneal dialysis (CAPD). A retrospective review of medical records, dialysis unit charts, and microbiology culture logbooks identified 18 such patients treated at our hospital. All cases were community-acquired, and no common epidemiologic link between cases was detected. The most common manifestations were abdominal pain or tenderness (13 patients) and cloudy dialysate (six patients); only two patients had fever. Peritonitis without localized intra-abdominal abscess formation occurred in all instances. Intraperitoneal aminoglycoside therapy for 3 to 14 days (mean 10.7 days) eradicated infection in 14 cases. Two patients were successfully treated with 4 days of intraperitoneal gentamicin followed by 8 days of oral ciprofloxacin; another was cured with 10 days of IV ceftriaxone. Tenckhoff catheter removal was necessary in only one patient. Unlike pseudomonal or fungal peritonitis associated with CAPD, infection due to Acinetobacter species is generally responsive to antimicrobials alone.

Acinetobacter Infections↗

Degradation of labelled lignins and veratrylglycerol-beta-guaiacyl ether by Acinetobacter sp.

Acinetobacter sp. evolved 14CO2 from 14C-(ring)DHP lignin and 14C-teakwood lignin. Veratrylglycerol-beta-guaiacyl ether, a lignin model compound with beta-o-4 linkage was cleaved by Acinetobacter sp. Veratrylglycerol-beta-guaiacyl ether into 2(o-methoxyphenoxy) ethanol and veratrylalcohol 2(o-methoxyphenoxy) ethanol was degraded to guaiacol and then to catechol whereas veratrylalcohol was converted to veratraldehyde, veratric acid, vanillic acid, protocatechuic acid and catechol. Both catechol 1,2-dioxygenase and protocatechuate 3,4-dioxygenase were detected in veratrylglycerol-beta-guaiacyl ether grown cultures.

Acinetobacter↗

[A membrane-bound alanine aminopeptidase from Acinetobacter calcoaceticus. 2. Substrate specificity of the enzyme].

The substrate specificity of the membrane-bound alanine aminopeptidase from Acinetobacter calcoaceticus was investigated with a series of substituted amides of alpha-amino acids. In contrast to mammalian AAP forms, the rate of hydrolysis of the AAP from Acinetobacter calcoaceticus is higher using 4-nitranilide than 2-naphthylamide substrates. The enzyme affinity is very high for alanine substrates and decreases in the series of the amide substituents, from methyl coumarylamides, 4-nitranilides, 4-methoxynaphthylamides to the 2-naphthylamides. The alanine aminopeptidase shows its highest affinity to Ala-MCA (Km = 77 mumol(s)/1).

Acinetobacter↗

Nosocomial infections due to Acinetobacter calcoaceticus.

Fifty four isolates of Acinetobacter calcoaceticus were studied in a period of 6 months. Maximum isolates were from burns cases and environmental sampling from burns ward also grew the same organism, indicating their role as nosocomial pathogen. Acinetobacter may initially be mistaken for Neisseria species. As the organisms show multidrug resistance to commonly used antibiotics their correct identification is important.

Acinetobacter Infections↗

Characterization of a periplasmic insulin-cleaving metalloproteinase from Acinetobacter calcoaceticus.

In Acinetobacter calcoaceticus, a Gram-negative bacterial species, a soluble insulin-degrading proteinase, located in the periplasm as well as in the cytosol, could be established. The periplasmic and cytosolic enzymes agree in their inhibition pattern, pH-optimum and molecular weight. The insulin-degrading enzyme of Acinetobacter calcoaceticus resembles the corresponding proteinases of Escherichia coli. It is a metalloproteinase with a pH-optimum in the neutral range and can be reactivated by divalent ions after EDTA-inhibition, but it is not entirely identical with any of the described proteinases of Escherichia coli in its inhibitory behaviour.

Acinetobacter↗

[Evolution of Acinetobacter calcoaceticus in the hospital milieu, from 1971 to 1984].

During the last 10 years the authors have evaluated the increasing part played by Acinetobacter calcoaceticus in nosocomial infections and the increasing resistance of this species to antibiotics. The study involved 850 clinical strains isolated from 1971 to 1984, and 24 antibiotics were tested. A progressive increase in resistance to beta-lactam antibiotics, aminoglycosides and tetracycline was observed, and to date up to 80-90% of the strains are resistant to all but major drugs such as imipenem, ceftazidime, tobramycin and amikacin. A significant difference in susceptibility to the major antibiotics was noticed between Acinetobacter clinical strains isolated before and after 1980. A correlation study between the development of resistant strains and the hospital consumption of antibiotics showed that this was a factor to be taken into account. After the new Bichat Hospital was opened, in 1980, the rate at which var. anitratum strains were isolated rose from 77.5% to 94.5%. The opening of new departments (intensive care units) with a higher risk of infection and a totally different environment probably constitutes the most important factor in this evolution.

Acinetobacter↗

[In vitro study of the pefloxacine-ceftriaxone combination against 18 strains of Acinetobacter].

The bacteriostatic and bactericidal activity of the pefloxacin-ceftriaxone combination was studied in Mueller-Hinton broth against 18 clinical strains of acinetobacter calcoaceticus var. anitratum by the checkerboard technique. The bactericidal activity was tested after 2, 4, 6 and 24 hours contact. MICs were 0.12 to 4 mg/l for pefloxacin and 2 to 64 mg/l for ceftriaxone. The bacteriostatic interaction of the antibiotics was synergistic for 5 strains (FIC index = 0.375 to 0.5) and additive for 13 strains (FIC index = 0.51 to 1). The bactericidal interaction was synergistic for 1 strain after 2 hours, 3 strains after 4 hours, 6 strains after 6 hours, and 12 strains after 24 hours. By the FBC technique at 24 hours, the combination was synergistic for 5 strains (FBC index = 0.375 to 5) and additive for 13 strains (FBC index = 0.51 to 1). No antagonism was detected. The combination is mainly additive but synergism is observed for some strains of acinetobacter. Ceftriaxone prevented the late regrowth noted with pefloxacin.

Acinetobacter↗

[Causes of error in the study of fibrinogen clumping and the diagnosis of Staphylococcus aureus: Micrococci and Acinetobacter].

Rapid presumptive identification of S. aureus, particularly on the agar slant of biphasic blood culture bottles can be performed by modified slide clumping factor tests. We compared two commercial reagents (Staphyslide and Staphaurex) using strains of "Gram-positive cocci arranged in clusters" (S. aureus, S. epidermidis, Micrococcus) or diplococci-like organisms such as Acinetobacter. Micrococcus and Acinetobacter can be responsible for false-positive reactions with sensitized or not sensitized particles. Control reactions with not sensitized particles or autoagglutination tests in water rather than saline must be performed.

Acinetobacter↗

Endemic nosocomial Acinetobacter calcoaceticus bacteremia. Clinical significance, treatment, and prognosis.

The medical records of 27 patients with blood cultures positive for Acinetobacter calcoaceticus over a recent five-year period (0.7% of all positive blood cultures) were reviewed retrospectively to determine the epidemiologic and clinical significance of these isolates. Eighteen isolates represented true bacteremias, 16 of which were hospital acquired. Patients most frequently were located in an intensive care unit or on a surgical ward. A seasonal July-to-September peak incidence was noted. The most common site of primary infection was the respiratory tract. Aminoglycosides, alone or in combination with a second agent, were used to treat all but one infection. Bacteriologic cure was achieved in 15 cases (88%); six patients had polymicrobial sepsis that carried a higher mortality than pure A calcoaceticus bacteremia (50% vs 0%). Acinetobacter, a low-virulence opportunistic pathogen, may be an infrequent but potentially serious endemic agent of nosocomial bacteremia in some institutions. The prognosis of bacteremia, when appropriately treated, appears to be good.

Acinetobacter Infections↗

Enhanced effect of an L-glutamine antagonist, L-(alphaS,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid, by Acinetobacter L-glutaminase-L-asparaginase.

The effect of L-glutamine and L-asparagine depletion by Acinetobacter L-glutaminase-L-asparaginase on the toxicity and antitumor activity of L-(alphaS,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (NSC-163501) was tested in mice. The LD50 of six daily doses of NSC-163501 in BDF1 female mice decreased from 7.5 to 0.3 mg/kg/day by combination treatment with the enzyme. Enzyme therapy also decreased the dose of NSC-163501 needed for maximal prolongation of survival in these mice inoculated with L1210 leukemia. Nevertheless, the combination did not prolong survival in L1210-bearing mice beyond that of higher doses of NSC-163501 alone. In contrast, the combination of enzyme plus NSC-163501 inhibited the growth of established sc implanted Ehrlich ascites carcinoma in ICRf male mice much more than either agent alone. Treatment with Acinetobacter L-glutaminase-L-asparaginase decreased the L-asparagine and L-glutamine levels in acid extracts of the Ehrlich tumor. NSC-163501 did not affect the amide levels or alter the decrease produced by enzyme therapy.

Acinetobacter↗

Equine myositis and septicemia caused by Acinetobacter calcoaceticus infection.

Myositis and septicemia caused by Acinetobacter calcoaceticus were diagnosed in a mare. The infection was characterized clinically by ventral swelling and edema, diarrhea, listlessness, and rectal temperature of 39.4 C. The mare was treated symptomatically for 2 days but died on the 3rd day. Conditions seen at necropsy were myositis, enteritis, typhlitis, colitis, and hepatitis. Lymph nodes were moderately enlarged throughout the body. Gross lesions in musculature were edema, scarring, petechiae, and an occasional exxhymosis. The enteritis was catarrhal, with excessive mucus and moderate hyperemia. The typhlitis and colitis were hemorrhagic. The swollen liver had a diffuse mottled pale and red pattern. Microscopic lesions in skeletal muscle consisted of petechiation, necrosis, scarring, and edema. Cardiac muscle was also scarred and necrotic, but edema was not prominent. Periacinal necrosis was found in the liver. Acinetobacter calcoaceticus was isolated from myocardium and liver.

Acinetobacter Infections↗

[Apalcillin: in vitro activity compared with that of carbenicillin, ticarcillin, mezlocillin, piperacillin against Enterobacteriaceae and Acinetobacter].

The in vitro activity of apalcillin was compared with that of carbenicillin, ticarcillin, mezlocillin and piperacillin against clinical isolates of Enterobacteriaceae and Acinetobacter. 1 168 strains were tested by a routine disk diffusion method. They were grouped into different patterns of resistance by results to ampicillin, carbenicillin and cephalotin. The MICs were determined for 300 of these strains. Apalcillin, mezlocillin and piperacillin are active against most strains of E. coli, P. mirabilis, Klebsiella and C. diversus resistant to carbenicillin and ticarcillin. Apalcillin is the most active penicillin against Acinetobacter; it is almost as active as piperacillin, the best drug against Enterobacteriaceae.

Acinetobacter↗

Taxonomic implications of quantitative transformation in Acinetobacter calcoaceticus.

Quantitative transformation of streptomycin resistance marker was carried out with strains of Acinetobacter calcoaceticus. Standard recipient strain was the competent BD4-Ss. Transformation proceeded in a liquid system with a concentration of 20 micrograms/ml of streptomycin resistant DNA (Sr-DNA) from BD4, 17 reference strains of Acinetobacter, and 42 recent clinical isolates of the acid forming variant (anitratus) and 12 of the non-acid forming variant (lwoffi) as donors of Sr-DNA. The exposure time was 20 min before interruption with DNase and quantitated plating. Among the strains examined were differentiated 16 biotypes as based on oxidative acid production from glucose and lactose, haemolysis, urease, gelatinase, and growth with citrate as the sole carbon source. Autologous transformation gave a transformation of 2.94 (+/- 0.66)% of the recipient cells (quantitated by colony forming units). Sr-DNA from 50 of 63 strains were able to transform BD4-Ss. The transformation ratio was 0.06-6.4% of autologous BD4 transformation. Two further recent clinical isolates were weakly transformation competent. Competence was only found in autologous transformation. The major portion (50/63) of the strains belong to the BD4 genotype of A. calcoaceticus, but the taxonomic position of the 13 non-donors in respect to BD4 could not be evaluated by transformation because of lack of a competent recipient. The strains transforming BD4 belonged to both the glucose acidifyers and the non-acidifyers without genetic distinction. The results are consistent with recognition of both as belonging to the same species, but with their recognition as species variants: A calcoaceticus var, anitratum and A. calcoaceticus var. lwoffi.

Acinetobacter↗

[Acinetobacter isolates from environmental sampling in hospitals (author's transl)].

By environmental culturing Acinetobacter could be isolated from human sources and wet sites as well as from air and dry surfaces. In variety "anitratus" strains from patients and hospital personal resistance against antibiotics and metal salts was more dominant than in other strains. Acinetobacter strains were more tolerant of dryness than E. coli but less than Micrococcus luteus. By repeated contacts Acinetobacteres could be recovered from contaminated surfaces of polyvinyl chloride in significantly higher numbers than from paving tile.

Acinetobacter↗

Hydrocephalus and cerebral palsy due to Acinetobacter meningitis in neonate.

Earlier reports on acinetobacter infections in neonates described the infections as essentially opportunistic and indolent. We described here a case of acinetobacter infection in a neonate, which ran a relentless course and resulted in hydrocephalus and cerebral palsy. The difficulty encountered in establishing a bacteriological diagnosis in the absence of a qualified microbiologist is stressed.

Acinetobacter Infections↗