Antibiotic use in animals.
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Biomedical subjects
Publications and source records attributed to M Casewell.
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An evaluation of the training module of an interactive infection control computer-assisted learning (CAL) software program was carried out with ward-based nurses, third-year medical students and infection control personnel. All nursing staff, 87% of the medical students and all infection control staff found the programme easy and enjoyable to use. The module was accessed 3101 times on the hospital network in 18 months with usage settling to between 100-150 times per month. There was a higher level of use by night-duty and weekend staff. Medical students gained as much infection control knowledge from using the CAL package (increase in correct responses from 63.5% to 83.4%;P<0.0001) as they did from a formal lecture (increase in correct responses from 62.1% to 79.5%;P<0.0001). We conclude the training module which is accessible on the hospital wards and across the academic network, is a convenient and effective way for staff and students to gain a basic understanding in evidence-based infection control practices, at locations and times suitable for them.
In order to determine the incidence of infection following sclerotherapy and the role of antimicrobial prophylaxis, a prospective randomized control study was performed comparing i.v. imipenem/cilastatin, with an infusion of dextrose-saline as a control group. One hundred patients with bleeding esophageal varices were included. All episodes of infection were documented during admission to the unit. Ninety-seven patients were evaluable. Post-sclerotherapy bacteremia developed in six (5.6%) of 107 sclerotherapy sessions in the control group and one (1.1%) of the 88 sclerotherapy sessions in the imipenem/cilastatin group (P < or = 0.1, NS): six of these seven post-sclerotherapy bacteremias occurred after emergency sclerotherapy. Infection within 7 days of the procedure was documented after 43 (22.1%) of the 195 sclerotherapy sessions, 18 (20.5%) in the imipenem/cilastatin group and 25 (23.4%) in the control group (P = NS). These infections were significantly more common after emergency sclerotherapy, 40 (34.8%) of 115 sessions, than after elective sclerotherapy, three (3.8%) of 80 sessions (P < or = 0.0001). A short prophylactic antibiotic regime does not reduce the risk of early bacteremia or the frequency of infection after sclerotherapy. The higher risk of infection after emergency sclerotherapy may be therefore related more to the gastrointestinal hemorrhage and its associated effects than to sclerotherapy.
To compare the efficacy of a selective parenteral and enteral antimicrobial regimen in patients with fulminant liver failure, we classified 104 patients on reaching grade II encephalopathy as infected or non-infected. Patients who were infected were randomly assigned to receive IV cefuroxime (group 1) or selective parenteral and enteral antimicrobial regimen (group 2). Noninfected patients were randomly selected to receive either selective parenteral and enteral antimicrobial regimen (group 3) or no initial antimicrobials until clinically indicated (group 4). The four groups were comparable regarding age, sex, cause of disease, coma grade, international normalization ratio, presence of kidney failure and indicators of poor prognosis on admission to the study. Clinical parameters such as white cell count, temperature or changes in the chest radiograph, which were used to stratify patients into those infected or not, were not good predictors of infection because early infection rates were similar in the two groups. Three patients died within 24 hr and were excluded from the analysis. We found 42 microbiologically confirmed infections: group 1, 6 of 21; group 2, 8 of 21; group 3, 9 of 28; and group 4, 19 of 31. A reduction in infection was seen between groups 3 and 4 (p < 0.05). Patients receiving the selective parenteral and enteral antimicrobial regimen (groups 2 and 3) had fewer infections than the control group (group 4) (p < 0.005). Groups receiving early antimicrobial therapy (groups 1, 2 and 3) had a lower incidence of infection compared with group 4 (p < 0.0005). Overall, 55.5% survived, with no significant difference between the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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The true incidence and clinical relevance of fungal infection was ascertained in a prospective study of 50 consecutive patients with acute liver failure. Fungal infection was present in 16 (32%) patients (15 candida, one aspergillus) and in seven was considered the major cause of death. All six untreated died, while five of ten patients treated with anti-fungal therapy survived. The diagnosis was made on positive cultures from at least one significant site or on histological evidence of tissue invasion. All 16 had concomitant bacterial infection and shared features suggestive of a clinical syndrome: deterioration in coma grade after initial improvement; pyrexia unresponsive to antibiotics; established renal failure; and a markedly elevated white cell count. Fungal infection is a common, serious complication of acute liver failure and therapy is indicated for those with positive cultures. A prophylactic trial would be justified in those surviving 5 days, especially, with established renal failure.
Fifty consecutive patients admitted with acute liver failure, minimal grade II encephalopathy, were studied prospectively to determine the incidence, timing and cause of bacterial infection, the relationship to clinical criteria for infection; and the influence of early microbiological diagnosis on clinical outcome. There were 53 proven bacterial infections in 40 patients, whereas in 5 of the remaining 10 patients infection was suspected on clinical grounds in the absence of significant cultures. Seven patients (14%) had more than one bacterial infection, and four patients had simultaneous infections caused by different organisms at each site. Fourteen infections (26.4%) were associated with bacteremia, and in six of these no source was found. Twenty-five infections (47.1%) arose from the respiratory tract, 12 (22.6%) from the urinary tract and 2 (3.7%) from central venous cannulas. Thirty-seven (69.8%) of the 53 infections were due to gram-positive bacteria; Staphylococcus aureus accounted for 19 (35.8%) of all the infections. Thirty patients died (60%), 28 of whom had bacterial infection at some time; in 24 of these the infection was diagnosed less than 24 hr before death. All nine deaths that occurred more than 7 days after admission were directly attributable to microbial infection. Clinical features such as elevated temperature and elevated peripheral white blood cell count were poor indicators of bacterial infection because these were absent in 30.2% of cases. These data show that there is a high incidence of bacterial infection early in the course of acute liver failure and suggest that prophylactic antimicrobial therapy, although unproven, might be justified.
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Out of 184 patients who were infected or colonised with gentamicin-resistant enterobacteria, 17 (9%) harboured more than one strain. Single antibiotic-resistance plasmids were common to more than one of the different organisms isolated from nine patients, strongly suggestive of in-vivo conjugation. An "epidemic" plasmid with a molecular weight of approximately 110 megadaltons was found in 11 distinct strains isolated from four patients. Seven of the organisms harbouring this plasmid were Klebsiella aerogenes. Spread of multiple-resistance plasmids among endemic gentamicin-resistant enterobacteria is not uncommon, and these organisms provide a reservoir of plasmids that may ultimately spread to more pathogenic genera.
The incidence of trimethoprim resistance in enterobacteria causing infection in a London hospital increased from 5.6% in 1970 to 16% in 1979. The proportion of gentamicin-resistant aerobic Gram-negative bacilli had risen to 6.5% by 1979. During a 5-month period in 1977, during which no epidemic was recognized, all isolates resistant to either trimethoprim, gentamicin, tobramycin or amikacin were studied. The proportion of enterobacteria resistant to both trimethoprim and gentamicin (3.8% of the total) was significantly higher than expected assuming no correlation between acquisition of resistance characters. The resistance was transferable in 23% of trimethoprim-resistant and 76% of gentamicin-resistant strains. Trimethoprim resistance was carried by plasmids of seven different incompatibility groups and in at least four instances was part of a transposon. Gentamicin resistance was determined by plasmids of three groups - IncC, IncFII and IncW. Transposition of gentamicin resistance was not shown, though this may have been the means of evolution of the gentamicin R plasmids of InW, which determined aminoglycoside acetyltransferase, AAC(3). Some bacterial strains with their plasmids were endemic. There was evidence for these plasmids (i) acquiring new resistance genes by transposition, (ii) losing resistance genes by deletion and (iii) being transferred between bacterial species in the hospital.
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Food prepared for intensive care patients was frequently contaminated with Klebsiella species. Sixty-eight per cent of nasogastric feeds were contaminated with up to 10(4) klebsiellae per ml. Hospital kitchens were the source of contamination. Three patients ingested klebsiellae and subsequently excreted the same serotype in their faeces. Over a four-week period there was a correlation between kitchen, food, faecal, and clinical serotypes of klebsiellae. Serotypes ingested by intensive care patients occurred more frequently in clinical isolates from intensive care patients than from other hospital patients. Patients often acquired a food strain that had been ingested by another patient on the same ward.
Seventeen per cent of the staff of an intensive care ward were found to have Klebsiella spp contaminating their hands, and these strains could be related to serotypes infecting or colonising patients in the ward on the same day. We identified some simple ward procedures that resulted in contamination of nurses' hands with 100-1000 klebsiellae per hand. Klebsiellae survived on artifically inoculated hands for up to 150 minutes. Handwashing with chlorhexidine hand cleanser reliably gave 98-100% reduction in hand counts, and the introduction of routine handwashing by staff before moving from one patient to the next was associated with a significant and sustained reduction in the number of patients colonised or infected with Klebsiella spp. Staff clothing was occasionally contaminated, but ward air and dust rarely contained klebsiellae.