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Transmissible antibiotic resistance genes in the gram-negative bacteria – what can we do and what should we be doing?
Pathology (2011) 43(S1), pp. S49–S52
Microbiology
MULTIRESISTANT ORGANISMS – MECHANISMS OF RESISTANCE, LABORATORY TESTING, AND EMERGENCE IN DEVELOPING COUNTRIES Jan M. Bell SA Pathology (Women’s and Children’s Hospital), Adelaide, SA, Australia The increasing occurrence of infections with antibiotic-resistant micro-organisms is a significant problem worldwide. Antimicrobial resistance prevalence varies widely between and within countries, and over time. Increasing international trade and travel have also been implemented with spread of resistant micro-organisms from one place to another, such that the resistance is not limited to a problem of any particular nation or region. Antibiotic resistance among Gram-negative micro-organisms, particularly those resistant to carbapenems and extended-spectrum b-lactam antibiotics, are increasingly being seen, not only in hospitals but also in the community. Multidrug-resistant Enterobacteriaceae (mostly Escherichia coli) that produce extendedspectrum-b-lactamases (ESBLs), such as the CTX-M enzymes, have recently emerged as an important cause of UTIs. The rapid spread of carbapenemase-producing Enterobacteriaceae, in particular blaNDM-1 and blaKPC, appears to be a worldwide problem, although the epidemiology varies by continent. Many of these organisms contain multiple-resistance genes, which severely restrict the treatment options available. Most clinical laboratories are familiar with the various diagnostic tests used in the detection of ESBLs. Identifying some of the newer enzymes and especially the metallo-b-lactamases can be both challenging and problematic. Recent changes to interpretative guidelines for the phenotypic detection of both ESBLs and carbapenemases have been made. TRANSMISSIBLE ANTIBIOTIC RESISTANCE GENES IN THE GRAM-NEGATIVE BACTERIA – WHAT CAN WE DO AND WHAT SHOULD WE BE DOING? Jon Iredell1,2, Justin Ellem1, Sally Partridge1,2, Lee Thomas1 1 Centre for Infectious Diseases and Microbiology, Westmead Hospital and 2NHMRC Centre for Research Excellence in Critical Infection/Sydney Emerging Infections Institute, University of Sydney, Sydney, NSW, Australia Among the agents of community-acquired septic shock in countries such as Australia and the US, the major risk of antibiotic failure not easily identified by a simple gene target resides with the Enterobacteriaceae, particularly Escherichia coli and Klebsiella pneumoniae. Streptococcus pneumoniae and Staphylococcus aureus are easily managed with a small handful of markers but the potential causes of b-lactam and aminoglycoside resistance among E. coli and K. pneumoniae are legion. However, the local gene pool may be restricted and a ‘local profile’ may be small enough to use in ‘realtime’ diagnostic and screening tools. Here, we review the experiPrint ISSN 0031-3025/Online ISSN 1465-3931 DOI: 10.1097/01.PAT.0000394563.21002.f0
#
ence with the common phenotypes, the approach to screening, and the major questions we need to resolve before we move these tools into routine practice. The focus in this session is on the markers of b-lactam and aminoglycoside resistance in E. coli and K. pneumoniae, and on the opportunities and pitfalls in the assay systems available to detect them.
DIAGNOSIS OF MALARIA Gillian Rozenberg Department of Haematology, Prince of Wales Hospital, Sydney, NSW, Australia This presentation will cover diagnosis of the five species of human malaria, Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae and Plasmodium knowlesi in the haematology laboratory; thick and thin blood films; parasite density counts and the use of the in vitro immunochromatographic assay for the qualitative detection of circulating Plasmodium antigens in blood.
THE ROLE OF BLOOD GROUPS IN PLASMODIUM FALCIPARUM MALARIA Christine Cserti-Gazdewich Transfusion Medicine and Clinical Hematology, University Health Network and University of Toronto, Canada Plasmodium falciparum remains the deadliest malaria species known to infect humans, with an unprecedented lethality in nonimmune children. This has left the human genome imprinted with the greatest diversity and depth of adaptive mutations attributable to any disease on earth. Most mitigating polymorphisms converge upon the erythrocyte, within and through which malaria’s transformative morbidity is manifested. Plasmodium falciparum is distinctive for the acquired cytoadhesivity of infected erythrocytes (IE), which allows parasites within the red cell mass to avoid splenic clearance via sequestration (IE tethering to microvascular endothelium) and rosetting (IE clumping with uninfected erythrocytes and/or platelets). Intriguingly, many of the host cytoadhesion ligands in this process are blood group antigen systems. Evidence taken from bench to bedside argues for the importance of selected blood groups in the severity of the erythrocytic phase of the disease. These blood group antigen systems, important not as portals of invasion but as cytoadhesive targets exploited by a common receptor expressed on IEs, include the ABO blood group system, CD35 (CR1) in the Knops blood group system, and CD36 (platelet glycoprotein IV). The implications of this knowledge are promising, from the design of novel therapeutic ‘cytoadhesion interruptors’, to transfusion therapy with ‘antigen-negative’ or ‘antigen-competitive’ products.
2011 Royal College of Pathologists of Australasia
Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.
Microbiology
MULTIRESISTANT ORGANISMS – MECHANISMS OF RESISTANCE, LABORATORY TESTING, AND EMERGENCE IN DEVELOPING COUNTRIES Jan M. Bell SA Pathology (Women’s and Children’s Hospital), Adelaide, SA, Australia The increasing occurrence of infections with antibiotic-resistant micro-organisms is a significant problem worldwide. Antimicrobial resistance prevalence varies widely between and within countries, and over time. Increasing international trade and travel have also been implemented with spread of resistant micro-organisms from one place to another, such that the resistance is not limited to a problem of any particular nation or region. Antibiotic resistance among Gram-negative micro-organisms, particularly those resistant to carbapenems and extended-spectrum b-lactam antibiotics, are increasingly being seen, not only in hospitals but also in the community. Multidrug-resistant Enterobacteriaceae (mostly Escherichia coli) that produce extendedspectrum-b-lactamases (ESBLs), such as the CTX-M enzymes, have recently emerged as an important cause of UTIs. The rapid spread of carbapenemase-producing Enterobacteriaceae, in particular blaNDM-1 and blaKPC, appears to be a worldwide problem, although the epidemiology varies by continent. Many of these organisms contain multiple-resistance genes, which severely restrict the treatment options available. Most clinical laboratories are familiar with the various diagnostic tests used in the detection of ESBLs. Identifying some of the newer enzymes and especially the metallo-b-lactamases can be both challenging and problematic. Recent changes to interpretative guidelines for the phenotypic detection of both ESBLs and carbapenemases have been made. TRANSMISSIBLE ANTIBIOTIC RESISTANCE GENES IN THE GRAM-NEGATIVE BACTERIA – WHAT CAN WE DO AND WHAT SHOULD WE BE DOING? Jon Iredell1,2, Justin Ellem1, Sally Partridge1,2, Lee Thomas1 1 Centre for Infectious Diseases and Microbiology, Westmead Hospital and 2NHMRC Centre for Research Excellence in Critical Infection/Sydney Emerging Infections Institute, University of Sydney, Sydney, NSW, Australia Among the agents of community-acquired septic shock in countries such as Australia and the US, the major risk of antibiotic failure not easily identified by a simple gene target resides with the Enterobacteriaceae, particularly Escherichia coli and Klebsiella pneumoniae. Streptococcus pneumoniae and Staphylococcus aureus are easily managed with a small handful of markers but the potential causes of b-lactam and aminoglycoside resistance among E. coli and K. pneumoniae are legion. However, the local gene pool may be restricted and a ‘local profile’ may be small enough to use in ‘realtime’ diagnostic and screening tools. Here, we review the experiPrint ISSN 0031-3025/Online ISSN 1465-3931 DOI: 10.1097/01.PAT.0000394563.21002.f0
#
ence with the common phenotypes, the approach to screening, and the major questions we need to resolve before we move these tools into routine practice. The focus in this session is on the markers of b-lactam and aminoglycoside resistance in E. coli and K. pneumoniae, and on the opportunities and pitfalls in the assay systems available to detect them.
DIAGNOSIS OF MALARIA Gillian Rozenberg Department of Haematology, Prince of Wales Hospital, Sydney, NSW, Australia This presentation will cover diagnosis of the five species of human malaria, Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae and Plasmodium knowlesi in the haematology laboratory; thick and thin blood films; parasite density counts and the use of the in vitro immunochromatographic assay for the qualitative detection of circulating Plasmodium antigens in blood.
THE ROLE OF BLOOD GROUPS IN PLASMODIUM FALCIPARUM MALARIA Christine Cserti-Gazdewich Transfusion Medicine and Clinical Hematology, University Health Network and University of Toronto, Canada Plasmodium falciparum remains the deadliest malaria species known to infect humans, with an unprecedented lethality in nonimmune children. This has left the human genome imprinted with the greatest diversity and depth of adaptive mutations attributable to any disease on earth. Most mitigating polymorphisms converge upon the erythrocyte, within and through which malaria’s transformative morbidity is manifested. Plasmodium falciparum is distinctive for the acquired cytoadhesivity of infected erythrocytes (IE), which allows parasites within the red cell mass to avoid splenic clearance via sequestration (IE tethering to microvascular endothelium) and rosetting (IE clumping with uninfected erythrocytes and/or platelets). Intriguingly, many of the host cytoadhesion ligands in this process are blood group antigen systems. Evidence taken from bench to bedside argues for the importance of selected blood groups in the severity of the erythrocytic phase of the disease. These blood group antigen systems, important not as portals of invasion but as cytoadhesive targets exploited by a common receptor expressed on IEs, include the ABO blood group system, CD35 (CR1) in the Knops blood group system, and CD36 (platelet glycoprotein IV). The implications of this knowledge are promising, from the design of novel therapeutic ‘cytoadhesion interruptors’, to transfusion therapy with ‘antigen-negative’ or ‘antigen-competitive’ products.
2011 Royal College of Pathologists of Australasia
Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.