Bacteriuria with Escherichia coli resistant to ciprofloxacin in patients with spinal-cord injury.
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Biomedical subjects
Publications and source records attributed to H N Canawati.
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The activities of trovafloxacin and ciprofloxacin against 38 strains of non-beta-lactamase-producing enterococci, resistant to ampicillin, 34 strains susceptible to ampicillin, and 3 vancomycin-resistant enterococci were studied. Trovafloxacin was more active than ciprofloxacin against all the enterococci studied. The ampicillin-resistant strains were more susceptible than the ampicillin-susceptible strains to both agents. The effect of combining trovafloxacin with gentamicin, ampicillin-sulbactam, novobiocin, rifampin, teicoplanin, and vancomycin was determined for 17 strains by the checkerboard method. An additive effect by inhibition was seen with all antibiotics studied. The results by killing varied with the different agents studied. Gentamicin, ampicillin-sulbactam, and novobiocin produced an additive killing effect with trovafloxacin. Reduced killing was seen when rifampin, vancomycin, or teicoplanin were added to trovafloxacin.
A retrospective review of laboratory records from 1988 to 1996 has shown an increased rate of ciprofloxacin-resistant (cip(r)) Escherichia coli in our rehabilitation center. Resistance increased from 0.6% in 1989 to 5.9% in 1996. Of 7870 E. coli strains isolated during this period, 257 cip(r)-E. coli were recovered from 257 patients. The majority (96%) of these resistant strains were isolated from the urine samples. One hundred and twenty strains of cip(r)-E. coli were also resistant to four other fluoroquinolones. MICs ranging from 64 to 512 micrograms/mL were observed in 75% of the strains and > or = 1028 micrograms/mL in 6.4% of the strains. Resistance to ciprofloxacin was due to possible mutations in topoisomerase gyrA.
Methicillin-resistant Staphylococcus aureus (MRSA) colonization has been a problem in the Rancho Los Amigos Medical Center (RLAMC) since 1978. This study reviews the latest 2 years' use of a protocol to prevent the spread of MRSA while allowing spinal cord injured patients to continue to participate in the rehabilitation program. The protocol included management in a private room, bathing with hexachlorophene, monitoring positive sites and clearing patients after 3 weeks of negative cultures. Clusters of cases were investigated by obtaining nasal cultures from the personnel. Sixty-seven of 584 (11%) SCI patients were colonized from July 1989 to July 1991. The prevalence of MRSA colonization was significantly greater in the pressure ulcer management service (PMS) 49/184 (27%) than in the rehabilitation spinal injury service (SIS) 18/400 (5%). The body sites colonized were wounds (58/67), nares (37/67), throat (30/67), urine (27/67) and perineum (17/67). Oral therapy with combinations of sulfamethoxazole trimethoprim (SXT) or Novobiocin with rifampin together with topical antibiotics (nares and wound sites), used in nine patients with healing wounds or recent flap surgery, resulted in clearing of the colonization in all cases. Identification and treatment of carriers in the personnel and use of preadmission screening cultures for MRSA in patients with pressure ulcers resulted in reduced inpatient admission.
The in vitro activity of cefotaxime (CTX) alone and in combination with its metabolite desacetylcefotaxime (dCTX) was evaluated against 106 isolates of Bacteroides species. and 32 strains of Staphylococcus aureus. All strains were recovered from infected tissues of diabetic patients. Addition of dCTX to the parent compound markedly increased the inhibitory activity against Bacteroides species in general and Bacteroides fragilis and Bacteroides vulgatus in particular. No effect of the combination of both agents on Bacteroides thetaiotaomicron or Bacteroides ovatus was observed; 50% of B. fragilis infections were susceptible to CTX alone and 81% became susceptible to CTX plus dCTX. In addition, a partial synergistic interaction against 20 strains of B. fragilis resulted in a four- to nine-fold reduction in the minimal inhibitory concentration (MIC) after dCTX was added to CTX. Interestingly, 10 of 20 strains that exhibited an MIC of 64-128 micrograms/mL with CTX alone became very susceptible after the combination of parent and metabolite. This favorable positive interaction of both agents was also observed with S. aureus; a two- to four-fold reduction in MIC values was observed when dCTX was added.
Ceftazidime was compared with moxalactam in the treatment of urinary tract infections in patients with spinal cord injury. Patients received ceftazidime or moxalactam, 500 mg twice daily for five days. Urine specimens were collected by urethral catheter. Adequate follow-up was obtained in 26 patients treated with ceftazidime and 13 patients treated with moxalactam. The infecting bacteria were not cultured in significant numbers from the urine of any patients after two to four days of antibiotics, except for 1 patient who had Pseudomonas aeruginosa persisting in the urine while receiving ceftazidime. At five to nine days after completing antibiotic therapy, the cure rate was 42 percent for ceftazidime and 15 percent for moxalactam. The rate of reinfection was significantly lower in the ceftazidime group than the moxalactam group.
Sixteen clinical isolates of ampicillin-resistant enterococci (ARE) were recovered from the microbiology laboratory of a 450-bed rehabilitation medical center from January 1981 to September 1987. These isolates were detected when a disk diffusion test using 10 micrograms of ampicillin on a blood agar plate revealed no zones of inhibition. Tube macrodilution tests yielded an MIC of greater than or equal to 16 micrograms of ampicillin per ml. None of the isolates were penicillinase producers by the chromogenic cephalosporin disk test. Ten isolates were Enterococcus faecium, four isolates were E. raffinosus, one isolate was E. gallinarum, and one isolate was not identified (lost). There were 6 male and 10 female patients. The sources of isolates were urine (n = 7), wound (n = 5), ascitic fluid (n = 2), blood (n = 2), peritoneal catheter tip (n = 1), Bartholin's cyst abscess (n = 1), rectal swab (n = 2), and pancreatic abscess (n = 1). The organism was isolated from multiple sites in 4 patients, was a pure culture isolate in 5 patients, and was part of a polymicrobial flora in 11 patients. Six patients were diabetic, and four had liver cirrhosis. All but four patients had received at least one antibiotic within 3 weeks of ARE isolation. The MICs (micrograms per milliliter) for 50 and 90% of isolates tested, respectively, were as follows: ampicillin, 64 and 64; penicillin, 128 and greater than 128; vancomycin, 1 and 2; gentamicin, 4 and 16; ciprofloxacin, 1.6 and 3.2; imipenem, 128 and greater than 128; and daptomycin (LY146032), 1.6 and 6.4. ARE may be an emerging pathogen in the hospitalized patient population.
The conventional method of ascitic fluid culture detects bacteria in only 42%-65% of patients who have neutrocytic ascites and suspected spontaneous bacterial peritonitis. In this study ascitic fluid was cultured by the conventional method as well as by a new method consisting of bedside inoculation of blood culture bottles with ascites. The conventional cultures grew bacteria in only 13 (43%) of 30 episodes of neutrocytic ascites, whereas the blood culture bottles grew bacteria in 28 (93%); this difference was significant (p less than 0.0001). The blood culture bottle method also resulted in more rapid detection of bacterial growth. The median concentration of bacteria in infected ascites was one organism per milliliter. Bedside inoculation of blood culture bottles with ascitic fluid is more sensitive than the conventional method in detecting bacterial peritonitis. The insensitivity of the conventional method is probably due to the low concentration of bacteria in infected ascites and the small volume of ascites cultured by this method.
The in vivo and in vitro activity of LY146032 against Streptococcus faecalis GK was examined. The following MICs and MBCs in micrograms per milliliter were obtained: ampicillin, 0.8 and 1.5; vancomycin, 0.8 and 50; gentamicin, 12 and 25; and LY146032, 0.8 and 6. A time-kill-curve study involving approximately 10(6) organisms per ml showed a drop in the number of organisms of almost 2 log10 in the tube containing LY146032 (2 micrograms/ml) plus gentamicin (4 micrograms/ml) compared with bacterial numbers for the control at 4 h of incubation. However, regrowth was observed at 24 and 48 h, and no in vitro synergism was observed with the combination. A sample (1 ml) of overnight growth of this enterococcal strain at a concentration of 10(7) was then injected intravenously into 184 male Wistar rats weighing about 100 g each. After 12 days, 10 rats were sacrificed and the remaining ones were randomized into four treatment groups: (i) untreated control, (ii) LY146032 (3 mg) given subcutaneously, (iii) gentamicin (0.8 mg) given intramuscularly, and (iv) LY146032 plus gentamicin at the same dosages as when the drugs were used singly. The rats received antibiotics for 4 weeks twice daily, and approximately 10 rats in each group were sacrificed for quantitative kidney cultures at 1, 2, 4, and 6 weeks after the start of therapy. At the end of the 4- and 6-week periods, significantly better results were obtained with the combination of LY146032 plus gentamicin than with no treatment or treatment with single antibiotics.
A retrospective analysis of 1578 abdominal paracenteses revealed ten cases of polymicrobial bacterascites, ie, growth of multiple organisms in ascitic fluid with a neutrophil count less than 250 cells/cu mm. Six of the ten paracenteses that documented this condition were traumatic (bloody or producing feculent material). Clinical peritonitis developed in only one patient. No one died as a result of the infection. Polymicrobial bacterascites is rare (0.6% of paracenteses). It is frequently due to a traumatic paracentesis (bowel entry by the paracentesis needle), and is associated with low morbidity.
Male patients with spinal cord injury and urinary tract infection with Pseudomonas aeruginosa were treated with cefsulodin (1.0 or 1.5 Gm) every six hours or an aminoglycoside (amikacin 5 mg/Kg or tobramycin 1 mg/Kg) every eight hours for seven days. The study was discontinued after treating 6 patients with aminoglycosides because of the poor results with these antibiotics. At five to nine days after completing treatment P. aeruginosa was eliminated from the urine of 12 to 15 patients (80%) treated with cefsulodin and 3 of 6 patients (50%) treated with an aminoglycoside. When examined at four to six weeks 5 of 15 (33%) of the cefsulodin group had persistent infection or relapse, while 5 of 6 (83%) infections treated with an aminoglycoside either persisted or relapsed. Cefsulodin was discontinued in 1 patient, known to be allergic to penicillin, because of hypersensitivity resulting in periorbital edema and rash. No other serious side effects were noted with cefsulodin or the aminoglycosides. These results indicate that cefsulodin is an effective antibiotic in the treatment of urinary tract infection with P. aeruginosa in patients with neurogenic bladder resulting from spinal cord injury and confirmed previous observations of a poor response of Pseudomonas urinary tract infection to aminoglycosides in this group of patients.
The quantitative microbiology of 25 pressure sores in different stages of healing was examined in 25 patients with spinal cord injury. When grossly necrotic tissue was present (stage 1), 5.8 isolates per patient with a density of 6.4 log10/g was recovered, with comparable findings for aerobes and anaerobes. In the absence of necrotic tissue but with the presence of undermining (stage 2), 1.5 aerobic and 0.2 anaerobic isolates were recovered per patient with a mean density of 2.7 and 0.1 log10/g of tissue for aerobic and anaerobic isolates, respectively. The lesions were almost sterile in patients with no necrotic tissue and no undermining (stage 3). Foul smell was always associated with the presence of anaerobes in deep tissue cultures, however, six patients with nonfoul-smelling lesions yielded anaerobes. A 75% quantitative concordance was seen between swab and biopsy culture results. The quantitative concordance between peripheral and central biopsy culture results was 63%, showing variability in results from different sampling areas. No relationship was observed between the density of microorganisms and the eventual outcome of the myocutaneous flap procedure.
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Bone biopsies were performed in spinal cord injured patients with pressure ulcers in whom osteomyelitis was suspected. Roentogenograms and bone and gallium scans were also evaluated to determine their usefulness in diagnosing osteomyelitis. Infected bone underlying pressure ulcers revealed only mild focal inflammatory changes which did not correlate well with x-ray and nuclear scan abnormalities. Negative scans, however, essentially ruled out osteomyelitis. There was no clear association of delayed healing or recurrence of pressure sore with osteomyelitis. Antibiotic therapy of greater than three weeks' duration did not significantly affect the outcome of the disease.
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Twenty-nine isolates of anaerobic bacteria from foot infections in diabetic patients were tested, using the agar dilution method, for in vitro susceptibility to nine antimicrobial agents. Imipenem and metronidazole showed excellent activity; clindamycin and chloramphenicol were next in terms of efficacy. Cefoxitin and moxalactam demonstrated good activity, although three isolates of the Bacteroides fragilis group were resistant to moxalactam. Penicillin G, cefotaxime, and cefoperazone showed poor activity against the B fragilis group but were quite active against other anaerobes. Among the newer beta-lactam antibiotics studied, imipenem, cefoxitin and, to a lesser extent, moxalactam appear promising for clinical use as anti-anaerobic antibiotics in the treatment of foot infections in diabetic patients.
A number of indirect methods have been developed to determine the site of urinary tract infection, including the measurement of LDH in urine [1]. Although LDH has been thought to be from the kidneys, it has also been noted that leukocytes could contribute LDH isoenzymes 4 and 5 [2]. Seventeen patients with injured spinal cords and significant bacteriuria were included in this study. Urine specimens obtained by urethral catheter were cultured, and PMNLs identified with Sternheimer-Malbin stain were counted in a hemacytometer. A positive test for antibody-coated bacteria and the lack of patient response to five to 10 days of antibiotic therapy were used as an indication of upper urinary tract infection. Levels of LDH isoenzymes 4 and 5 (cathodal) correlated with the number of PMNLs in the urine (r = 0.63, P less than 0.01). There was no correlation of PMNLs with LDH isoenzymes 1 and 2 (r = 0.18). In addition, there was no correlation of LDH isoenzymes 4 and 5 with the level of urinary tract infection. These results suggest that the PMNLs in the urine are the source of the LDH isoenzymes 4 and 5.
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