ABSTRACT
OBJECTIVE: To determine the impact of a campus-community pharmacy partnership to foster awareness and use of National Library of Medicine (NLM) databases, including MedlinePlus, among minority populations. DESIGN: Uncontrolled study with pretest and posttest. SETTING: Two community pharmacies and Bethel World Ministry in the Washington, D.C., metropolitan area. PARTICIPANTS: 8 student pharmacists and pharmacy residents and 92 patients. INTERVENTION: Training of patients by student pharmacists and pharmacy residents in the use of NLM databases during prescription-fill wait time. MAIN OUTCOME MEASURES: Pre- and post-survey responses and telephone followup designed to assess familiarity with NLM databases, including MedlinePlus. RESULTS: Overall, the familiarity of the participants with MedlinePlus and NLM databases increased fivefold before versus after training. The 1-week follow-up confirmed this trend. However, no statistically significant differences in responses (pre-and posttest/follow-up) to the surveys were observed in regard to specific questions on daily and future use of the NLM databases available on the Internet. CONCLUSION: Awareness and use of MedlinePlus by study participants increased.
Subject(s)
MedlinePlus , Minority Groups/education , National Library of Medicine (U.S.) , Patient Education as Topic , Adolescent , Adult , Awareness , Community Pharmacy Services , Data Collection , Female , Humans , Male , Pharmacists , Schools, Pharmacy , United StatesABSTRACT
OBJECTIVES: To determine if differences in drug-related Staphylococcus aureus killing, associated in vivo with neutropenia, is neutrophil-related in vitro, and the mechanisms of this interaction. METHODS: To evaluate the influence of living neutrophils on drug-S. aureus interactions, cell wall enzymes, the PBPs, were isolated and their binding to five (beta lactam and other) antibiotics was evaluated following incubation (or not) with neutrophils. S. aureus killing by the test drugs was assayed in growth media of sterile filtered abscess fluid, either neutropenic infected or normal infected. At MBCs for the test isolate, each drug or saline control was incubated with S. aureus 10(6)and dilution-plated. RESULTS: Neutrophil incubation with S. aureus eliminated the S. aureus PBP-2 band in all Western blots irrespective of the drug used to tag the PBPs. Time-kill of S. aureus grown in neutropenic or normal abscess fluid showed greater kill by all drugs in neutropenic abscess fluid (p=0.029 6h incubation). Killing difference between the media correlates with drug PBP-2 activity. CONCLUSIONS: Drug activity against S. aureus in vitro is changed by neutrophil incubation. The neutrophil-induced loss of S. aureus PBP-2 drug binding suggests novel host-bacterial interaction that may impinge on drug treatment of S. aureus infections.
Subject(s)
Anti-Bacterial Agents/pharmacology , Neutrophils/physiology , Staphylococcal Infections/drug therapy , Staphylococcal Infections/microbiology , Staphylococcus aureus/drug effects , Staphylococcus aureus/physiology , Abscess/drug therapy , Abscess/microbiology , Animals , Cells, Cultured , Microbial Sensitivity Tests , Penicillin-Binding Proteins/metabolism , Rats , Staphylococcus aureus/enzymologyABSTRACT
Mycobacterial infection occurs frequently in patients that receive protease inhibitors, which are drugs used to treat AIDS, but are known for metabolic effects. Proteases of microbial antigens have been recognized as important regulators of host inflammation and cellular response. To evaluate protease inhibitor effect on a mycobacterial infection, a pilot animal model was established. Mycobacterium bovis (bacillus Calmette-Guerin, or BCG) infection was compared in rats that received ritonavir and those that did not. Tissues and serum from one drug-treated and one control were analyzed weekly. Fewer acid-fast bacilli (AFBs) were consistently found in the drug-treated group by 3 separate measures: culture of tissue homogenates on solid media, tissue granuloma counts on organ sections, and staining of tissues for AFBs. Possible mechanisms of the observed relative resistance to BCG infection in ritonavir-treated rats were explored, by evaluating M. bovis cell wall lipids and proteins and by measuring infection-related cytokines in treated and control animals.
