Mark D. Reisbig
Creighton University
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Featured researches published by Mark D. Reisbig.
Antimicrobial Agents and Chemotherapy | 2002
Ellen Smith Moland; Jennifer A. Black; Jason Ourada; Mark D. Reisbig; Nancy D. Hanson; Kenneth S. Thomson
ABSTRACT Despite the discovery of novel β-lactamases such as extended-spectrum β-lactamases (ESBLs), imported AmpC, and carbapenem-hydrolyzing β-lactamases at least a decade ago, there remains a low level of awareness of their importance and how to detect them. There is a need to increase the levels of awareness of clinical laboratories about the detection of newer β-lactamases. Therefore, a study was conducted in 2000 to investigate the occurrence of these β-lactamases in Klebsiella pneumoniae isolates at 24 U.S. medical centers. To enhance the likelihood of detecting imported AmpC and carbapenem-hydrolyzing β-lactamases, participating laboratories were permitted to include archived strains (1996 to 2000) that were intermediate or resistant to either cefoxitin or imipenem. The β-lactamase production of 408 isolates positive by screening of 1,123 isolates was investigated by ESBL phenotypic confirmation tests; and for AmpC and carbapenem-hydrolyzing β-lactamases, three-dimensional tests, isoelectric focusing, β-lactamase inhibitor studies, spectrophotometric assays, induction assays, and molecular tests were used. ESBL-producing isolates were detected at 18 of the 24 sites (75%), imported AmpC-producing isolates were detected at 10 sites (42%), inducible imported AmpC-producing isolates were detected at 3 sites (12.5%), and a molecular class A carbapenem-hydrolyzing enzyme was detected at 1 site (4%). No class B or D carbapenem-hydrolyzing enzymes were detected. ESBLs and imported AmpC β-lactamases were detected at a significant number of sites, indicating widespread penetration of these enzymes into U.S. medical institutions. Because these enzymes may significantly affect therapeutic outcomes, it is vital that clinical laboratories be aware of them and be able to detect their occurrence.
Journal of Clinical Microbiology | 2003
Johann D. D. Pitout; Mark D. Reisbig; Mike Mulvey; Linda Chui; Marie Louie; Larry Crowe; Deirdre L. Church; Sameer Elsayed; Dan Gregson; Rafiq Ahmed; Peter Tilley; Nancy D. Hanson
ABSTRACT Resistance to the extended-spectrum cephalosporins can occur in Salmonella species via the production of extended-spectrum and AmpC β-lactamases. We describe human infections with Salmonella enterica serotype Newport phage type 14 strains resistant to ceftazidime (CAZ) and cefoxitin (FOX) related to the handling of pet treats containing dried beef. These strains were isolated from five patients in Calgary, Alberta, Canada, during 2002 and were compared to a strain cultured from a commercial pet treat present at the property of one of the patients. The strains were resistant to FOX, CAZ, cefpodoxime, ampicillin, and chloramphenicol; intermediate resistant to ceftriaxone and cefotaxime; and sensitive to the aminoglycosides, ciprofloxacin, cefepime, and imipenem. Isoelectric focusing, multiplex PCR, and sequencing of the amplicons showed that all strains produced the plasmid-encoded AmpC β-lactamase, CMY-2. Restriction analysis of plasmid DNA following transformation demonstrated that blaCMY-2 was encoded on an approximately 140-kb plasmid. Pulsed-field gel electrophoresis showed the human and pet treat Salmonella strains to be highly related. This study is the first to implicate the transfer of multidrug-resistant Salmonella species through the handling of commercial pet treats containing animal products. In addition to documenting the first cases of human infection caused by CMY-2-producing S. enterica serotype Newport strains in Canada, this study illustrates the necessity of rapid and accurate laboratory-based surveillance in the identification of novel types of antimicrobial resistance.
Journal of Clinical Microbiology | 2003
Johann D. D. Pitout; Mark D. Reisbig; E. C. Venter; Deirdre L. Church; Nancy D. Hanson
ABSTRACT Detection of extended-spectrum β-lactamases (ESBLs) in AmpC-producing Enterobacteriaceae is problematic. A modification of the double-disk test (MDDT) has been developed for successful detection of ESBLs in gram-negative bacilli producing well-characterized β-lactamases as well as 212 clinical isolates of Enterobacter cloacae, Enterobacter aerogenes, Serratia marcescens, and Citrobacter freundii. MDDT accurately differentiated between ESBL producers and derepressed chromosomal AmpC mutants. MDDT provides a cost-effective alternative approach for clinical microbiology laboratories for routine susceptibility testing with simultaneous detection of ESBLs in Enterobacteriaceae.
Journal of Clinical Microbiology | 2012
Chelsie N. Geyer; Mark D. Reisbig; Nancy D. Hanson
ABSTRACT A multiplex, real-time TaqMan assay was designed to identify clinical isolates carrying plasmid-mediated ampC genes. The specificity and sensitivity of this assay were 100% when testing characterized AmpC/non-AmpC-producing isolates and randomly selected clinical isolates. This is a rapid assay that can be performed in a clinical microbiology laboratory.
Clinical and Translational Science | 2015
R B S Daniel Kirkpatrick; M B S Dan McEntire; J B S Zakary Hambsch; J B S Mitchell Kerfeld; A B S Tyler Smith; Mark D. Reisbig; Charles F. Youngblood; Devendra K. Agrawal
Pain is a hallmark of almost all bodily ailments and can be modulated by agents, including analgesics and anesthetics that suppress pain signals in the central nervous system. Defects in the modulatory systems, including the endogenous pain‐inhibitory pathways, are a major factor in the initiation and chronicity of pain. Thus, pain modulation is particularly applicable to the practice of medicine. This review summarizes the existing literature on pain modulation. Here, we critically reviewed the literature from PubMed on pain modulation published primarily within the past 5 years in high impact journals. Specifically, we have discussed important anatomical landmarks of pain modulation and outlined the endogenous networks and underlying mechanisms of clinically relevant pain modulatory methods. The Gate Control Theory is briefly presented with discussion on the capacity of pain modulation to cause both hyper‐ and hypoalgesia. An emphasis has been given to highlight key areas in pain research that, because of unanswered questions or therapeutic potential, merit additional scientific scrutiny. The information presented in this paper would be helpful in developing novel therapies, metrics, and interventions for improved patient management.
Antimicrobial Agents and Chemotherapy | 2004
Mark D. Reisbig; Nancy D. Hanson
ABSTRACT Little is known about mechanisms involved in high-level expression of plasmid-associated ampC genes. The sequence for blaMIR-1 has been elucidated, and the gene is not inducible. Although the sequence for the promoter (prA) that drives expression of Enterobacter cloacae chromosomal ampC is present upstream of blaMIR-1, high-level expression from blaMIR-1 is directed from a hybrid promoter (prB) located further upstream of prA. The purpose of this study was to determine the influence of each promoter on blaMIR-1 expression and β-lactam resistance. RNA expression by deletion clones with both promoters was measured and compared to that by clones in which −35 and/or −10 elements of prA and/or prB were altered. Primer extension revealed two start sites for blaMIR-1 transcription. Expression of blaMIR-1 in clones with both promoters was 171-fold higher than that in clones carrying only prA. In addition, blaMIR-1 expression from prA increased 11-fold in the presence of the prB −10 element compared to expression driven from prA alone. Ceftazidime and cefotaxime MICs increased 42- and 64-fold, respectively, for the clone expressing blaMIR-1 from both promoters compared to expression from prA alone. The upstream promoter prB of blaMIR-1 is solely responsible for high-level expression required for cefotaxime and ceftazidime resistance. These data suggest that resistance to extended-spectrum cephalosporins mediated by noninducible plasmid-associated ampC genes requires the formation of novel promoter elements that are capable of increasing ampC expression.
Expert Review of Clinical Pharmacology | 2016
Dan M. McEntire; Daniel R. Kirkpatrick; Nicholas P. Dueck; Mitchell J. Kerfeld; Tyler A. Smith; Taylor J. Nelson; Mark D. Reisbig; Devendra K. Agrawal
ABSTRACT Introduction: Pain represents a necessary physiological function yet remains a significant pathological process in humans across the world. The transduction of a nociceptive stimulus refers to the processes that turn a noxious stimulus into a transmissible neurological signal. This involves a number of ion channels that facilitate the conversion of nociceptive stimulus into and electrical signal. Areas covered: An understanding of nociceptive physiology complements a discussion of analgesic pharmacology. Therefore, the two are presented together. In this review article, a critical evaluation is provided on research findings relating to both the physiology and pharmacology of relevant acid-sensing ion channels (ASICs), transient receptor potential (TRP) cation channels, and voltage-gated sodium (Nav) channels. Expert commentary: Despite significant steps toward identifying new and more effective modalities to treat pain, there remain many avenues of inquiry related to pain transduction. The activity of ASICs in nociception has been demonstrated but the physiology is not fully understood. A number of medications appear to interact with ASICs but no research has demonstrated pain-relieving clinical utility. Direct antagonism of TRPV1 channels is not in practice due to concerning side effects. However, work in this area is ongoing. Additional research in the of TRPA1, TRPV3, and TRPM8 may yield useful results. Local anesthetics are widely used. However, the risk for systemic effects limits the maximal safe dosage. Selective Nav antagonists have been identified that lack systemic effects.
Expert Review of Clinical Pharmacology | 2014
Dan M. McEntire; Daniel R. Kirkpatrick; Mitchell J. Kerfeld; Zakary J. Hambsch; Mark D. Reisbig; Devendra K. Agrawal; Charles F. Youngblood
The perioperative care of obstructive sleep apnea (OSA) patients is currently receiving much attention due to an increased risk for complications. It is established that postoperative changes in sleep architecture occur and this may have pathophysiological implications for OSA patients. Upper airway muscle activity decreases during rapid eye movement sleep (REMS). Severe OSA patients exhibit exaggerated chemoreceptor-driven ventilation during non-rapid eye movement sleep (NREMS), which leads to central and obstructive apnea. This article critically reviewed the literature relevant to preoperative screening for OSA, prevalence of OSA in surgical populations and changes in postoperative sleep architecture relevant to OSA patients. In particular, we addressed three questions in regard to the effects of sedative-hypnotics, anesthetics and analgesics on sleep architecture, the underlying mechanisms and the relevance to OSA. Indeed, these classes of drugs alter sleep architecture, which likely significantly contributes to abnormal postoperative sleep architecture, exacerbation of OSA and postoperative complications.
Clinical and Translational Science | 2015
Zakary J. Hambsch; Mitchell J. Kerfeld; Daniel R. Kirkpatrick; Dan M. McEntire; Mark D. Reisbig; Charles F. Youngblood; Devendra K. Agrawal
Radial artery catheterization has become a preferred route over femoral artery catheterization, in order to monitor the blood pressure of hemodynamically unstable patients or for repeated sampling of arterial blood gases. While the incidence of catheter‐related infection is lower in the radial artery than the femoral artery, infection remains a major issue that requires attention. In this review of the literature, we discuss infectious complications of radial artery catheterization, with a focus on various risk factors and establishing the most common causative agents. We also critically review the role of the innate immune system involving Toll‐like receptors (TLRs) in host‐defense, with the goal of establishing a common pathway used by the innate immune system via TLRs to combat the pathogens that most commonly cause infection in radial artery catheterization. If this pathway can be therapeutically manipulated to preemptively attack pathogenic agents, immunomodulation may be an option in reducing the incidence of infection in this procedure.
Expert Review of Clinical Pharmacology | 2016
Daniel R. Kirkpatrick; Dan M. McEntire; Tyler A. Smith; Nicholas P. Dueck; Mitchell J. Kerfeld; Zakary J. Hambsch; Taylor J. Nelson; Mark D. Reisbig; Devendra K. Agrawal
ABSTRACT Introduction: Mediators in pain transmission are the targets of a multitude of different analgesic pharmaceuticals. This review explores the most significant mediators of pain transmission as well as the pharmaceuticals that act on them. Areas covered: The review explores many of the key mediators of pain transmission. In doing so, this review uncovers important areas for further research. It also highlights agents with potential for producing novel analgesics, probes important interactions between pain transmission pathways that could contribute to synergistic analgesia, and emphasizes transmission factors that participate in transforming acute injury into chronic pain. Expert commentary: This review examines current pain research, particularly in the context of identifying novel analgesics, highlighting interactions between analgesic transmission pathways, and discussing factors that may contribute to the development of chronic pain after an acute injury.