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G D Taylor

Publications and source records attributed to G D Taylor.

42 records · Page 3Linked to original sources
PubMedDate not supplied

Trends and sources of nosocomial fungaemia.

Concurrent surveillance of blood culture isolates in a 1000-bed tertiary care hospital over a 7-year period from 1986 to 1993 identified 102 episodes of nosocomial fungaemia, representing 6.6% of all episodes of nosocomial bloodstream infections and 0.49/1000 admissions. No significant change in the frequency, rate, source or microbial aetiology of nosocomial fungaemia occurred over the 7-year period. Candida albicans accounted for 74%, followed by Candida (Torulopsis) glabrata (8%), C. parapsilosis (7%), C. tropicalis (3%), C. lusitaniae (2%), C. krusei, Malassezia furfur Saccharomyces cerevisiae, Hansenula anomala and Cryptococcus albidus (one each). 'Primary' fungaemia, usually attributed to intravascular catheters, was considered to be the source in 65% of cases, with 64% of these patients receiving total parenteral nutrition (TPN). Other important sources of infection included the urinary tract (11%), the gastrointestinal tract (8%) and the respiratory tract (7%). Sixty-four % of patients were in one of the hospital's seven intensive care units (ICUs) when their infection developed, the neonatal ICU and adult medical/surgical ICU each accounting for 21%. Only 7% of cases were associated with neutropenia and another 14% with malignancy or immunosuppression. Death occurred within 7 days of diagnosis of fungaemia in 23 cases. In eight instances, fungaemia was considered the main cause of death. We conclude that in our hospital nosocomial fungaemia is largely caused by C. albicans, occurring in association with intravascular catheter use and TPN in ICU patients. Most cases are not associated with recognized immune defence defects. Fungaemia is associated with a high short-term mortality rate.

Adult↗
PubMedDate not supplied

Bacteremia due to transplantation of contaminated cryopreserved pancreatic islets.

OBJECTIVE: To report two cases of pancreatic islet transplantation-related septicemia, and the results of an investigative protocol to identify potential sources of contamination. DESIGN: Case series. SETTING: University hospital clinical investigational islet transplantation program. RESULTS: The last two of our first seven islet transplantation recipients developed Enterobacter cloacae septicemia within hours of islet infusion. Both had received thawed cryopreserved islet infusions. No source of infection apart from islets could be identified. Pancreas harvesting and islet isolation protocols provided multiple opportunities for contamination. Environmental cultures during a mock islet isolation procedure failed to identify a source of Enterobacter. Previously cryopreserved islet lots were thawed and submitted for culture, 14/47 grew micro-organisms including E. cloacae in four instances. Following revision of protocols for aseptic handling of islets during processing and cryopreservation 55 consecutive pancreata undergoing processing were evaluated; 7 grew micro-organisms on arrival and in 3 cases these persisted through to cryopreservation. CONCLUSION: Two of seven islet transplantation recipients developed septicemia, likely related to infusion of contaminated cryopreserved islets. Using existing technology, for isolating islets from donor pancreata, recipients will remain at risk for this complication. Prevention should entail strict adherence to aseptic technique, and, possibly, use of surveillance microbial cultures during the islet isolation process.

Adult↗
PubMedDate not supplied

Metformin in an HIV-infected patient with protease inhibitor-induced diabetic ketoacidosis.

OBJECTIVE: To describe a case of diabetes mellitus and diabetic ketoacidosis in a patient receiving protease inhibitor therapy and to describe the patient's response to treatment with metformin. CASE SUMMARY: A 49-year-old HIV-positive white man who was receiving indinavir, stavudine, and lamivudine for more than two years presented with shortness of breath and significant weight loss over the previous month. On admission, he had a pH of 7.11 and PaCO2 of 12.9 mm Hg. Laboratory investigations revealed glucose 420 mg/dL, a total carbon dioxide 5 mEq/L, and anion gap of 32. Beta-hydroxybutyrate was 5.9 mmol/L (normal value <0.4 mmol/L). Urine was highly positive for glucose and ketones. The patient was given intravenous fluids and an insulin infusion was started. Five days later, he was discharged on 60 units of insulin per day. Following discharge, efavirenz was substituted for indinavir. Metformin was added and six months following discharge the patient's blood glucose was well controlled with 36 units of insulin per day. DISCUSSION: New-onset diabetes mellitus has been reported in HIV-infected patients receiving protease inhibitors. To date, diabetic ketoacidosis has been an infrequent acute complication. The mechanism by which protease inhibitors cause diabetes is unclear; however, studies have noted insulin resistance and increased proinsulin. Metformin increases the sensitivity of peripheral tissues to insulin and appeared to be useful in this patient. However, further clinical research is needed. CONCLUSIONS: Monitoring glucose concentrations in HIV-positive patients receiving protease inhibitors is important to prevent the development of acute complications, including diabetic ketoacidosis. We recommend that these patients have their fasting serum glucose concentration measured at baseline, with follow-up every three months. The role of metformin and the thiazolidinedione antidiabetic agents in the management of protease inhibitor-induced diabetes requires further study.

Diabetes Mellitus, Type 1↗