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INTERNATIONAL JOURNAL OF MEDICAL AND APPLIED SCIENCES E‐ISSN:2320‐3137

51 www.earthjournals.org Volume 3, Issue 3, 2014

Review Article UNDERSTANDING EXTENDED SPECTRUM BETALACTAMASES IN CLINICAL SETTINGS. REVIEW UPDATE

Olowe OA , Adefioye S

Department of Medical Microbiology and Parasitology, College of Health Sciences, Ladoke Akintola University of Technology, Ogbomoso PMB 4400, Osogbo. Osun State. Nigeria

Corresponding Author: Olowe O.A, Department of Medical Microbiology and Parasitology, College of Health Sciences, Ladoke Akintola University of Technology, Ogbomoso PMB 4400, Osogbo. Osun State. Nigeria

ABSTRACT

Extended-spectrum beta-lactamases (ESBL) are β-lactamases capable of conferring bacterial resistance to the penicillins, first, second, and third generation cephalosporins, and aztreonam (but not the cephamycins or carbapenems) and are usually encoded on plasmids which frequently carry genes encoding resistance to other classes of antibiotics were first isolated in mid 1980a, mostly in gram negative bacteria. A considerable geographical spread of the bacteria that produce the extended spectrum β-lactamase is being reported and is becoming a global problem in treating infections with the third generation cephalosporins. That ESBLs are encoded on plasmids and are, therefore, easily transmissible from one organism to another is a therapeutic challenge for physicians as resistance genes for other antimicrobials such as aminoglycosides, and the trimethoprim/sulfamethoxazole are often present on the same plasmid thereby contributing further to the narrowing of the already limited treatment alternatives of choice of antibiotics. The objective of the current review is to provide a better understanding of ESBLs with a focus on their methods of detection, transmission pathways, measures of control and management of infections caused by the bacteria that produce them.

Key words: beta-lactamases, detection, transmission pathways, management, bacteria

INTRODUCTION AND DEFINITION

Antibiotics kill or inhibit the growth of microorganisms, especially bacteria, and are used to treat and prevent infections in man. However, resistance to these antibiotics is becoming more common and the risk to human health posed by ESBL-producing bacteria is of great concern. Penicillins and cephalosporins (the β–lactams) are one of the most commonly used groups of antibiotics in human medicine. The heavy use of these antibiotics is believed to have been a selective force in the emergence of resistance. There is now a growing concern regarding the lack of new antibiotics [1] especially for multidrug-resistant Gram-negative bacteria which produce extended spectrum β-lactamases. Infections caused by the ESBL-producing pathogens are often associated with a high morbidity and mortality and are more difficult to identify by routine laboratory assays, which can lead to a delay in diagnosis and institution of appropriate antimicrobial therapy. Moreover two pointers of ESBLs are eight fold



reduction in MIC and potentiation of the inhibitor zone of third generation cephalosporin in the presence of clavulanic acid.

Extended-spectrum β-lactamases are plasmid-encoded enzymes that inactivate a large number of β-lactam antibiotics, including extended-spectrum and very-broad-spectrum cephalosporins and monobactams. They are also commonly inhibited by β-lactamase inhibitors, such as clavulanic acid, sulbactam, and tazobactam. These enzymes can be carried on bacterial chromosomes (inherent to the organisms) or may be plasmid-mediated with the potential to move from one bacterium to another. The mobility of the enzymes poses a significant clinical impact on the spread and control of infections resulting from the microorganisms that produce them. Infections with ESBL-producing bacteria are especially worrisome due to the following reasons: a.)They are difficult to treat because they carry plasmids that confer resistance to many other antibiotics, b.) Patients may experience a delay in appropriate treatment because the microbes are resistant to first-line antibiotics, c.)Patients may experience significantly longer hospital stays with increased costs and d.) Patients with infections have an increased risk of death. Incidence of these organisms in our routine laboratory is being continuously on the increase throughout the world with limited treatment alternatives. It becomes imperative to know the cause, source and location of these organisms and to formulate treatment policy

ESBLs are primarily produced by the Enterobacteriaceae family of Gram-negative organisms, in particular Klebsiella pneumonia and Escherichia coli. [2] They are also produced by non-fermentative Gram-negative organisms, such as Acinetobacter baumannii and Pseudomonas aeruginosa. [3] According to the Ambler’s method of classification [4], ESBLs belong to the class A group of β-lactamases based on their molecular structures. In furtherance to this, they were classified as belonging to the 2be group of β-lactamases due to their functional characteristics and substrate profiles. [5] The various genotypes of ESBLs are the SHV, TEM, and CTX-M types. [6] Other clinically important types include VEB, PER, BEL-1, BES-1, SFO-1, TLA, and IBC. [3]

The emergence of ESBLs

The emergence of resistance to the β-lactam antibiotics began even before the development of the first β-lactam, penicillin. The first β-lactamase was identified in Escherichia coli prior to the release of penicillin for use in medical practice. [7] TEM-1 was the first plasmid-mediated β-lactamase in the Gram-negative bacteria and was found in the early 1960s in a single strain of E. coli isolated from a blood culture of a patient named Temoniera in Greece. As a result of its being plasmid and transposon mediated, TEM-1 has spread to other species of bacteria of the family Enterobacteriaceae, Pseudomonas aeruginosa, Haemophilus influenzae, and Neisseria gonorrhoeae. Another common plasmid-mediated β-lactamase found in Klebsiella pneumoniae and E. coli is SHV-1 (for sulphydryl variable). [7] Many new β-lactam antibiotics have been developed that were specifically designed to be resistant to the hydrolytic action of β-lactamases. However, with each new class that has been used to treat patients, new β-lactamases emerged that caused resistance to that class of drug. [7] One of these new classes was the oxyimino-cephalosporins, which became widely used for the



treatment of serious infections due to the Gram-negative bacteria in the 1980s. Resistance to these expanded-spectrum β-lactam antibiotics due to the β-lactamases soon emerged quickly. These enzymes were called extended-spectrum β-lactamases (ESBLs) because of their increased spectrum of activity especially against the oxyimino-cephalosporins. The first of these enzymes capable of hydrolyzing the newer β-lactams, SHV-2, was found in a single strain of Klebsiella ozaenae isolated in Germany. [7] Today, over 150 different ESBLs have been described. Figure 1.0 below shows a brief history of the emergence of beta-lactamase resistance in the Gram-negative bacteria over the years.

Fig. 1.0 A brief history of the emergence of beta-lactamases by the Gram-negative bacteria.

Epidemiological and clinical impact of ESBL-producing bacteria

Infection by ESBL-producing organisms is associated with several identifiable risk factors such as hospitalization in an intensive care unit, intra-abdominal sepsis, prior antibiotic therapy, urinary and central venous catheter insertion, mechanical ventilation, surgery and prolonged hospital stay. [8, 9]



Since their first identification at the beginning of the 1980s, ESBL-producing enterobacteriaceae have spread worldwide by nosocomial routes. [10] There is a considerable geographical spread of these β-lactamases and they are becoming a global problem in treating infections with expanded-spectrum β-lactam antibiotics. [9] ESBLs are encoded on plasmids and are therefore easily transmissible from one organism to another. ESBL organisms pose therapeutic challenges for physicians as resistance genes for other antimicrobials such as aminoglycosides, tetracyclines and trimethoprim/sulfamethoxazole are often present on the same plasmid. [11, 12, 13] The incidence of these organisms is continuously increasing throughout the world with limited treatment alternatives. [14] In Europe and the United States, the number of bloodstream infections caused by ESBL-producing strains of the family Enterobacteriaceae is on the increase with the trend having a significant impact on mortality rates and hospital costs. [10] This problem is even more pronounced in developing countries due to poverty and abuse of antibiotic use. In Nigeria, extended spectrum beta- lactamase producing organisms have been isolated with prevalence rates of 25%, 7.5%, 35.3%, 51.3% and 18.3% in South-western Nigeria [15, 16, 17, 18, 19] and in the South- eastern part of the country, prevalence rates of 11.4% and 11.7% were reported in 2009 and 2011 respectively. [20, 21] The CTX-M-15 resistance determinant which has spread globally has also been identified in Nigeria in Klebsiella species and Escherichia coli. [22, 23] Other extended- spectrum β-lactamase resistance genes such as blaVEB, blaOXA and blaCMY, have recently been reported in Nigerian Providencia species strains. [24] Elsewhere in Africa, there has been a report of a high prevalence (70%) of ESBL –producers in Egypt [25] and of CTX-M K. pneumoniae in Kenya [26] and SHV and TEM—types in South Africa. [27] The prevalence of bacteria producing ESBLs varies worldwide, the data from a global surveillance database revealed that the rate of ESBL production was highest among the K. pneumoniae isolates collected in Latin America, followed by Asia/Pacific Rim, Europe, and North America (44.0%, 22.4%, 13.3%, and 7.5%, respectively). [ 28, 2] ESBL Detection

As a result of their clinical importance, clinical diagnostic laboratories should be able to recognize ESBL producers. Numerous laboratory detection strategies have been developed for ESBLs. According to the Clinical and Laboratory Standards Institute (CLSI) criteria, enterobacterial resistance to ceftriaxone, cefotaxime, ceftazidime, cefepime, and aztreonam is defined by MICs > 16 µg/ml. [29, 30] However, since several ESBL producers have MIC values for extended-spectrum cephalosporins and aztreonam below the standard breakpoints for resistance (e.g., between 2 and 8 µg/ml), the real prevalence of these organisms may be unappreciated. [30] Since the inaccurate identification of ESBL producers bears important clinical implications for antibiotic therapy and infection control measures, specific reporting guidelines have been issued. [29, 30] For all confirmed ESBL producers, the general consensus directs that they should be reported as resistant to all penicillins, cephalosporins (except for cephamycins: cefoxitin and cefotetan), and aztreonam irrespective of routine in vitro antimicrobial susceptibility results. [29, 30] This list does not include the cephamycins (cefotetan and cefoxitin), which should be reported according to their routine test results. [31] Isolates exhibiting an MIC ≥ 2 µg/ml should be confirmed phenotypically using ceftazidime



plus ceftazidime/clavulanic acid or cefotaxime plus cefotaxime/clavulanic acid comparative testing. A 3-step two-fold concentration decrease in an MIC for either antimicrobial agent tested in combination with clavulanic and versus its MIC when tested alone should be considered an ESBL producer. [32] For laboratories that use the disc diffusion method, isolates exhibiting zone diameters less than or equal to 22 mm for ceftazidime and 27 mm for cefotaxime should be confirmed phenotypically. A greater than 5 mm increase in zone diameter for either antimicrobial agent tested in combination with clavulanic acid versus its zone when tested alone should be considered an ESBL producer. [32]

Semi-automated systems (Phoenix, VITEK 2 and Microscan) are widely used for species identification and susceptibility testing by clinical laboratories to decrease the in-laboratory turnaround time and to improve cost-effectiveness. [33] However, each system has inherent strengths as well as recognized limitations. Specific media that are selective for ESBL producers can also be used especially for the identification of faecal carriage. Examples of such media are ChromID ESBL, bioMerieux, Brilliance ESBL agar, Oxoid and CHROMagar CTX. The colorimetric test (Cica βTest, marketed by MastGroup) can also be used for ESBL detection in the laboratory. Other methods that can be used for the in vitro detection of ESBLs in bacteria are cephalosporin/clavulanate combination disks on Iso-Sensitest agar, disk replacement test and the three dimensional test. The principle behind all ESBL detection methods is that the activity of extended-spectrum cephalosporins against ESBL-producing bacteria is enhanced by the presence of clavulanic acid. The appropriate strains for quality control of ESBL detection tests are: K. pneumoniae ATCC 700603 (SHV-18 ESBL), Escherichia coli CCUG62975 (CTX-M-1 group ESBL and acquired CMY AmpC) and E. coli ATCC 25922 (ESBL-negative)

Failures to rapidly and reliably identify ESBL-producing isolates may delay the institution of appropriate infection control measures and further contribute to their uncontrolled distribution. The problem arises from the observation that the enzymes vary in their substrate affinities and in their catalytic efficiencies, and also because β-lactams differ in their penetration rates into bacterial cells. [33] Recognition of ESBL-producers is, therefore, of major clinical concern as inappropriate treatment of invasive infections with cephalosporins can lead to therapeutic failures and adverse clinical outcome. [34]

The final identification is performed by molecular characterization of the genes conferring resistance. Molecular identification of ESBL genes is performed by screening assays using polymerase chain reaction (PCR) or micro-array and subsequent sequence analysis. Lists of primers for the most important β-lactamases in Enterobacteriaceae have been published. [35] Several commercial micro-arrays have been developed for rapid and specific detection of β-lactamase genes. [36] Identification of the subtype of the ESBL genes detected by PCR or micro-array is normally conducted by sequence analysis of PCR fragments. Plasmid isolation and electrophoresis in agarose gels provides information on the number and mass/size of plasmids present in one isolate. Transfer of plasmids to well-characterized recipients by conjugation or electroporation facilitates the typing of individual plasmids. Categorization of plasmids into incompatibility groups can be performed by PCR-based replicon typing method, targeting the major plasmid families of Enterobacteriaceae. [37] Novel plasmid



families can be recognized by complete DNA sequencing and also by using the relaxase gene as a phylogenetic marker. [38] Further characterization of plasmids belonging to groups I, F, N, HI2, and HI can be performed by plasmid multilocus sequence typing (MLST) [39](http://pubmlst.org/plasmid/).

The purpose of molecular typing is to determine the genetic relatedness of isolates to allow for source tracking/attribution. The discriminatory power varies among methods and influences the conclusions that can be drawn from the results. The choice of method is determined by the goal of the work. Pulsed-field gel electrophoresis or multiple loci variable number of tandem repeats analysis is often used to identify clonal clusters of isolates that are related to a certain “outbreak” in a restricted time frame. MLST is often the method used to identify the relatedness of isolates of the same species from different backgrounds (e.g, animal vs human).

Transmission and spread of ESBL producing organisms

ESBL-producing organisms are frequently being transmitted from a common source. Examples of such sources are ultrasonography coupling gel, bronchoscopes, blood pressure cuffs and glass thermometers (used in axillary measurement of temperature). [34] ESBL-producing organisms have also been isolated from patients' soap, sink basins, babies' baths and bed linings. The carriage of ESBL producers on the hands of health care workers has also been well documented by various researchers as a very important means of spread of these microbes in the hospitals. Individuals whose gastrointestinal tracts are colonized with ESBL producers are a very good reservoir for the transmission of these organisms both in the community and in the hospitals. Cockroaches have also been implicated as possible vectors of infection [34] as published by Cotton et al. [40] where an ESBL-producing Klebsiella pneumoniae isolated from cockroaches was indistinguishable from that of infected patients.

Measures of control of infections caused by ESBL producing bacteria

The spread of bacteria from patient to patient must be prevented through good hand hygiene of healthcare professionals and cleaning of medical equipment and the environment [34] Screening is advocated in patients being admitted or transferred from other institutions, including nursing and residential homes. [41] Surveillance of infected and high risk patients is used to either monitor an outbreak or, preferably, prevent one. Patients who are infected with such infections should be nursed in a single room, or cohorting may be necessary if such isolation facilities are limited. [41] Antimicrobial stewardship is of paramount importance, especially in this era of increasingly resistant organisms, coupled with a lack of antimicrobial options. Selection pressure must be avoided by judicious and prudent use of antibiotics. Certain medical procedures that can increase the risk of infection by promoting translocation of these organisms from colonising areas should be avoided. Gastrointestinal surgery, intubation, and urinary catheterization are all associated with this occurrence [42,41] In an outbreak situation, it is important to establish whether the infection is caused by the same clone (oligoclonal) or by multiple clones (polyclonal) of the aetiologic agent. [34] Alternative medicines against bacterial infections that render bacteria harmless instead of killing them



would be a solution to antibiotic resistance. [42] Thorough investigation and termination of infected sources must also be done to avoid re-occurrence of infection outbreaks.

Treatment of infections caused by ESBL producers

The management and treatment of infections caused by ESBL-producing bacteria can be challenging and bothersome. The reason for this is that ESBL-producing bacteria are often multi-resistant to various antibiotics. Antibiotics that are regularly used for the empirical therapy of serious infections, especially the third-generation cephalosporins (e.g. cefotaxime and ceftriaxone) are often not effective against the ESBL-producing organisms. The type of ESBL enzyme produced and the site and severity of infection are important considerations in determining antimicrobial therapy. [44] It is therefore necessary to conduct active surveillance for ESBL-producing organisms in order to describe fully the local epidemiology of a given institution and/or referring centers. β-Lactam/β-lactamase inhibitor combinations are usually active against organisms possessing a single ESBL. [34] The production of multiple ESBLs by many bacteria has however decreased the effectiveness of these drug combinations. Another problem being encountered with the therapy of ESBL infections is that even if an agent is selected that has activity against the bacteria in vitro, clinical efficacy in patients is not always guaranteed. Cephamycins are stable to the hydrolytic effects of ESBLs, unfortunately ESBL-producing organisms may lose their outer membrane proteins leading to their resistance to these drugs. [34]

Currently, the carbapenems (imipenem and meropenem) are the only class of antimicrobials that have consistently been effective against ESBL-producing bacteria. Carbapenems remain stable in the presence of ESBL enzymes and their small compact size allows for easy passage through porins into Gram-negative bacilli. [34] Thus, carbapenems are often the preferred antimicrobial agents for the treatment of serious infections caused by ESBL-producing organisms.

CONCLUSIONS

Infections with ESBL-producing bacteria are increasing significantly while their treatment options are continually decreasing due to a mounting up of selective pressures on the available antibiotics used against such infections. Laboratory diagnosis of infections through screening and confirmation by prescribed standards must be carried out to ensure judicious use of antibiotics. For enhanced therapeutic management of bacterial infections, there is need to encourage routine continual monitoring and evaluation of antibiotic treatment regimen and choice of drugs. Finally an understanding of resistance pattern synonymous to bacterial strains and location will help to guide the appropriate and judicious antibiotic use. There is possibility that the restricted use can lead to the withdrawal of selective pressure and resistant bacteria will no longer have survival advantage in such environment. Furthermore the spread of ESBL infections must be avoided through proper hand and environmental hygiene. Surveillance studies must also be conducted constantly in every community and hospital setting to guide against infection outbreaks. Urgent work is required to develop quicker, cost-



effective and reliable diagnostic tools as well as new effective therapies for the treatment of these infections.

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