[Urinary tract infections. Enterobacteriaceae].
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The study presents a summary of the results regarding the presence of Enterobacteriaceae in domestic animals and birds, endeavouring to explain the origin of the infections. Wild reptiles, amphibians, mammalia, rodents and birds were examined into the demonstration of Enterobacteriaceae, whereby particular attention was paid to the following species: Arizona, Edwardsiella, Citrobacter, Enterobacter, Serratia, Yersinia and Erwinia.
Sera from patients infected with Escherichia coli, Proteus, Klebsiella, and Serratia were studied for precipitins to ultrasonic extracts of these organisms in gel-diffusion plates. Sera from 66 per cent of these patients contained precipitins when initially tested. Twenty-four per cent of sera tested in the first week after onset of infection contained precipitins, but this rose to 78 per cent by the third week. Cross-reactions of sera with Pseudomonas antigens were unusual, but were common with other enterobacterial antigen extracts. However, higher titers were usually present to homologous as compared to heterologus antigens. Sera from seven patients contained precipitins to a common enterobacterial antigen. Precipitins to E. coli, Proteus, Klebsiella, and Serratia were detected in only a small proportion of control sera.
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Immunosuppression increases the risks and severity of infections and is associated with a higher incidence of infection with multidrug-resistant (MDR) pathogens. We evaluated the antimicrobial susceptibility of Enterobacterales and Pseudomonas aeruginosa from patients hospitalized in hospital units where the frequency of immunosuppressed patients is very high. Bacterial isolates were consecutively collected (1/patient) from 75 US medical centres in 2019-2024 and susceptibility tested by broth microdilution. Enterobacterales (n = 2,407) and P. aeruginosa (n = 485) from patients hospitalized in hematology, oncology, and transplant units were evaluated. Carbapenem-resistant Enterobacterales (CRE) were screened for β-lactamases by whole genome sequencing. Enterobacterales were mainly from bloodstream infection (BSI; 53.6%) and urinary tract infection (19.9%) and P. aeruginosa were mainly from BSI (37.9%) and pneumonia (35.0%). Aztreonam-avibactam, ceftazidime-avibactam, and meropenem-vaborbactam were highly active against Enterobacterales (99.9-99.4% susceptible), including MDR isolates (99.6-98.1% susceptible), but only aztreonam-avibactam exhibited good activity against CRE (95.8% susceptible). Ceftolozane-tazobactam showed good activity against Escherichia coli (95.7% S) and Klebsiella pneumoniae (92.8% S), but limited activity against Enterobacter cloacae species complex (75.9% susceptible). All (100.0%) carbapenemase (CBase)-producing CRE isolates were aztreonam-avibactam-susceptible while 77.4% were ceftazidime-avibactam-susceptible and 67.7% were meropenem-vaborbactam-susceptible. The most common CBases were KPC (41.7%), NDM (12.5%), and OXA-48 types (10.4%). Metallo-β-lactamases represented 23.5% of CBases and were identified in 16.7% of CREs. The most active agents against P. aeruginosa were ceftazidime-avibactam (95.7% susceptible), ceftolozane-tazobactam (94.8% susceptible), and tobramycin (91.5% susceptible). Piperacillin-tazobactam and meropenem were active against 81.4% and 82.5% of P. aeruginosa, respectively, and aztreonam-avibactam inhibited 78.6% of P. aeruginosa at ≤8 mg/L.
A solid-phase radioimmunoassay (RIA) procedure was compared with the indirect fluorescent antibody (IFA) test in a serological study of 76 female adults with urinary tract infections. Relative serum antibody activity was determined against patients' homologous infecting enterobacteria by RIA and IFA and against heterologous enterobacterial common antigen (Escherichia coli O14) by RIA. There was marked correlation between results of the IFA and RIA methods using the homologous system; 22 of 51 patients (43%) with pyelonephritis had significantly elevated serum antibody activity by both IFA (titers greater than or equal to 512) and RIA (binding ratio greater than or equal to 2.0) when compared with normal serum controls; three had significant antibody activity detectable by RIA only. Eighteen (72%) of 25 patients with pyelonephritis had RIA binding ratios of greater than or equal to 2.0 against their homologous bacterial isolates and the enterobacterial common antigen; an additional 6 patients had binding ratios of greater than or equal to 2.0 against the antigen only. All 25 patients with cystitis had low serum antibody levels by IFA and RIA when tested against their own isolate as well as enterobacterial common antigen. The RIA procedure was objective, quantitative, and less tedious to perform than IFA.
The ratio of the peak serum concentration after a 500-mg dose of amikacin to the pathogen minimum inhibitory concentration was determined for 95 patients under treatment for serious Gram-negative infections. There were 113 such ratios. The relationship of this inhibitory ratio to the clinical effectiveness and side effects of treatment with this new aminoglycoside was also studied. Mean peak serum concentration of drug was 25.8 microgram/ml, and mean inhibitory ratio was 13.0. Ninety-six per cent of inhibitory ratios were greater than or equal to 1.0. Therapy was rated totally effective in 85% of patients clinically evaluated and partially effective in 3%. Signs of renal or eighth cranial nerve impairment attributable to drug administration were confined to only two patients, and there were no other side effects. The reliability of amikacin therapy appears to be related to dependable serum levels and high inhibitory ratios.
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An eighteen month study of the incidence of nosocomial infections was conducted at a 436 bed general army hospital. The overall rate of nosocomial infection was 1.48 per cent, with a monthly range of 0.42 to 2.30 per cent. Gynecology had the highest rate of 5.8 per cent. Escherichia coli, klebsiella, and Staphylococcus aureus were the major hospital pathogens. No emergence of unusual drug resistance was observed during the course of the study. Further studies should be conducted to establish guidelines of surveillance for nurse-epidemiologists in this type of hospital.
Necrotizing infection of the scrotum (Fournier gangrene) rapidly spreads to adjacent skin with fever and toxemia and is life-threatening. Subcutaneous gas and a foul-smelling wet discharge from the skin are usually present. The infection is not cured with antibiotic therapy alone and requires immediate extensive debridement of all necrotic tissue. Repeated debridement each several days under general anesthesia is necessary until healthy granulation is present in the wound. Reconstruction with skin flaps or skin grafts shortens hospitalization and prevents the dense scar tissue and immobility of the tests that can occur with spontaneous epithelization.
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From Aug. 1, 1974, to July 31, 1975, inclusive, 19-1% of Pseudomonas aeruginosa and 50-0% of Serratia marcescens isolates from a general hospital were gentamicin resistant as determined by standardised disc testing; 80% of 118 different clinical isolates showed minimum inhibitory concentrations larger than or equal to 16 mug/ml of gentamicin in agar-dilution testing. All gentamicin-resistant S. marcescens and 79% of Ps. aeruginosa isolates were susceptible to amikacin, while tobramycin and sisomicin were shown to have little advantage over gentamicin. A wide variety of immunotypes was found for Ps. aeruginosa, but only two predominant types were found for S. marcescens. Most isolates originated from the urinary tract, but nine which came from urine or wounds were also isolated from blood. Resistant strains seemed to be as virulent as sensitive strains. A common source was not found. Clinical improvement was noted in 13 of 17 patients treated with amikacin. The high frequency of gentamicin resistance is a continuing problem in this hospital and soon may be in others.
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Am J Clin Pathol 63:438-445, 1975. The effects of procedural variations on the activities of gentamicin, tobramycin, sisomicin, kanamycin, and amikacin in vitro were evaluated using 134 clinical isolates. In broth dilution studies, a change in assay medium from brain-heart infusion broth to Mueller-Hinton broth resulted in significant changes in minimal inhibitory concentrations in 36% (242 of 670) of assays. A change in the bacterial population size utilized in broth dilution studies resulted in significant changes in minimal inhibitory concentrations in 34% (155 of 456) of assays. These variations in activities appeared to depend more on the organism tested than on the particular aminoglycoside used; with strains of Staphylococcus aureus, Proteus, and Providenica being most affected. For all five aminoglycosides, minimal inhibitory concentrations determined by broth dilution, regardless of medium, showed poor correlation with zone sizes obtained by the Bauer-Kirby technic. These results suggest that unless some standard assay procedure for activity of aminoglycosides is adopted, meaningful comparison of results within and among laboratories will not be possible.
Little is know about the clinical significance of isolating Citrobacter in the clinical laboratory. During a one-year period, 116 Citrobacter isolates were obtained from 77 patients with 83 suspected infectious episodes. The majority of the suspected infectious episodes involved the urinary tract (45%) or respiratory tract (41%). Citrobacter diversus was associated with 42% of the episodes, Citrobacter freundii with 29%, and Citrobacter species with 29%. In 42% of the suspected infectious episodes, the presence of Citrobacter was considered clinically significant; in the others, the significance of the Citrobacter isolates was indeterminate or considered to be commensal. Two thirds of the significant infections were hospital-acquired. Most patients (73%) from whom Citrobacter was cultured had underlying diseases or factors predisposing to infection. These data suggest that Citrobacter is a cause of significant opportunistic nosocomial infection in the hospital.
The efficacy and safety of amikacin were evaluated in 42 patients with infections presumed to be due to gram-negative rods. The dosage of 7.5 mg of amikacin/kg every 12 hr was administered intramuscularly to 32 patients and intravenously to seven patients; three patients with renal impairment were given a modified regimen. The duration of treatment was three to 51 days (mean, 9.6 days). Of 19 patients with acute pyelonephritis, five had positive blood culture results. Ten patients had chronic urinary infection, and isolates of Pseudomonas aeruginosa from four of these patients acquired resistance to amikacin during therapy. Of seven patients with gram-negative bacteremia from sources other than the urinary tract, four showed satisfactory and three had less than optimal responses to therapy with amikacin. Two patients with chronic osteomyelitis or soft tissue infection improved but subsequently relapsed. Two patients with acute febrile illness, in whom the etiologic agent was unidentified, recovered. Serial audiograms revealed no change in 26 of 27 patients; one had a significant deterioration in hearing. A transient rise in the level of serum creatinine was noted in three patients. Serial tests of liver function revealed no abnormalities.
Trends in relative susceptibility of clinical isolates, mostly from newborns with nosocomial infections, to the aminoglycosides in use in a hospital for children are described and related to practical therapeutic aspects. Currently, amikacin is the most effective of the available antibiotics against many gram-negative bacterial species, and its administration appears to be as complicated as that of other aminoglycosides. With 5 mug/ml taken as the cut-off point for susceptibility in vitro, 90% of 211 clinical isolates (Pseudomonas aeruginosa, Escherichia coli, Klebsiella, Serratia, and other species) could be considered sensitive to amikacin; the respective figures for sensitivity to sisomicin, gentamicin, and tobramycin were 80.5%, 66%, and 70%. Cross-resistance of microorganisms to amikacin and gentamicin, sisomicin, or tobramycin has not been demonstrated. Treatment with amikacin was successful in 13 of 15 children (premature and normal newborns with primarily septicemia); death of two patients was attributable to the underlying disease. For neonatal infections we recommend 12 mg of amikacin/kg per day; determination of the minimal inhibitory concentration for the causative pathogen and monitoring of serum concentrations are desirable.
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