Perit Dial Int
27(Supplement_2):
272-280
2007
© 2007 International Society for Peritoneal Dialysis
EVOLUTION OF ANTIBIOTIC RESISTANCE MECHANISMS AND THEIR RELEVANCE TO DIALYSIS-RELATED INFECTIONS
Samson S.Y. Wong,
Pak-Leung Ho and
Kwok-Yung Yuen
Department of Microbiology, Research Centre of Infection and Immunology,
The University of Hong Kong, Hong Kong SAR, PR China
Correspondence to: K.Y. Yuen, Department of Microbiology, The University of
Hong Kong, 4/F University Pathology Building, Queen Mary Hospital, 102
Pokfulam Road, Hong Kong SAR, PR China.
hkumicro{at}hkucc.hku.hk
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ABSTRACT
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As the survival of patients with end-stage renal failure has improved,
their exposure to antibiotics has also increased. Infections, especially
peritoneal dialysis–related peritonitis, are unavoidable because of
lapses in technique and the slow worsening of systemic and peritoneal defense
associated with aging and dialysis. The selective pressure inherent in the use
of antibiotics shapes the pattern of antibiotic resistance in the bacteria
causing peritonitis and extraperitoneal infections, and vice versa.
Renal function–preserving and non-ototoxic regimens that
incorporate double β-lactams (first- and third-generation cephalosporins)
for peritonitis have increased the selective pressure in favor of
methicillin-resistant staphylococci (MRS) and extended-spectrum
β-lactamase (ESBL)–producing Enterobacteriaceae. Attempts to use
the fluoroquinolones as alternatives to β-lactams was met with rocketing
quinolone resistance. The high incidence of MRS led many nephrologists to use
empiric vancomycin—until the début of vancomycin-resistant
enterococci. The recent emergence of heterogeneous and high-level vancomycin
resistance in staphylococci (which are especially prevalent in patients on
dialysis) calls for further prudence in the use of vancomycin.
The coming challenges are ESBL-producing Enterobacteriaceae with
carbapenemase, multi-resistant Pseudomonas, and highly virulent
community-acquired methicillin-resistant Staphylococcus aureus with
Panton–Valentine leukocidin. Antibiotic auditing programs and meticulous
patient training by nurses are the only available defense at the moment. Novel
approaches such as antibiotic-impregnated Tenckhoff catheters, biocompatible
dialysis fluid, and peritoneal immuno-augmentation strategies are eagerly
awaited.
KEY WORDS: Antibiotic resistance; antibiotic control; vancomycin-resistant Staphylococcus aureus; vancomycin-resistant enterococci; extended-spectrum beta-lactamase; carbapenemase; peritonitis.
Antibiotic resistance is a global problem fuelled by widespread use and
abuse of antibiotics in humans and animals alike
(1). The problem of
antibiotic-resistant bacterial infections is especially important in health
care facilities because of the concentration of susceptible patients and high
antibiotic selection pressure. The problem, however, has started to reach into
the community setting, as exemplified by the recent emergence of
community-acquired methicillin-resistant Staphylococcus aureus
(CA-MRSA) in many parts of the world. The present paper discusses the
predisposition to infections in dialysis patients, with a focus on peritoneal
dialysis (PD) peritonitis, followed by a overview of problematic bacterial
pathogens and their relevance to the management of dialysis-related
infections.
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DIALYSIS PATIENTS AND INFECTION
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Infection is the second leading cause of death in dialysis patients, with
an annual percentage mortality secondary to sepsis that is 100 to 300 times
that seen in the general population
(2,3).
Dialysis-related infections (including peritonitis and vascular access
infections) may account for 24% of the infections; the rest are unrelated to
dialysis (4). Staphylococci and
other gram-positive bacteria are the agents most commonly involved in such
infections, accounting for 20% – 40% of the cases of PD–related
peritonitis
(5,6).
In areas with a high incidence of tuberculosis, tuberculous peritonitis
complicating PD is another consideration
(7).
In a review of the pathogens causing dialysis-related peritonitis in our
hospital during 1995 – 2006 (Yuen KY, unpublished data), we identified
1270 non-duplicate patients (Table
1). Gram-positive bacteria constituted 49.8% of the isolates from
those patients, and gram-negative bacteria, 42.3%. Staphylococci remained the
group of pathogens most commonly involved, with S. aureus accounting
for 40.6% of the staphylococcal species. The second most prevalent group were
the Enterobacteriaceae, followed by environmental gram-negative bacilli such
as Pseudomonas spp., Acinetobacter spp., and
Stenotrophomonas maltophilia. Importantly, 5.7% of the isolates were
fungi, and 2.1%, mycobacteria.
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PROBLEM OF ANTIBIOTIC-RESISTANT BACTERIA IN DIALYSIS PATIENTS
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S. aureus and Coagulase-Negative Staphylococci: The development of
β-lactam resistance among staphylococci is the most vivid example of
bacterial adaptation to antibiotic selection pressure. In many health care
facilities, MRSA has become endemic, and nosocomial outbreaks are frequently
reported. During 2000 – 2004 in our hospital, resistance to methicillin,
erythromycin, and cotrimoxazole were seen in 40.3%, 52.5%, and 33.0% of the
S. aureus isolates respectively (from all sites).
Although fusidic acid is not widely available in some countries (such as
the United States), it remains a valuable agent in the maintenance therapy of
MRSA infections. Its liberal use in the form of topical therapy has resulted
in increasing resistance rates
(8,9).
The resistance rate to fusidic acid among S. aureus from all sites in
our hospital increased to 10.6% in 2004 from 2.6% in 2000.
Today, CA-MRSA is gaining a foothold in many parts of the world. The term
CA-MRSA refers to strains that possess type IV or V staphylococcal cassette
chromosome, a mobile genetic element that carries the mecA gene
encoding penicillin-binding protein 2a, the factor critical to methicillin
resistance. These organisms typically produce Panton–Valentine
leukocidin, an exotoxin that causes the suppurative necrosis typical of this
infection.
Unlike the conventional hospital-acquired MRSA strains, CA-MRSA often
occurs in patients without health care–associated risk factors, and the
associated antibiograms show a greater susceptibility to non-β-lactam
antibiotics (10). The
prevalence of CA-MRSA has reached alarming levels in some centers, with up to
76% of skin and soft-tissue infections seen in the emergency departments being
caused by CA-MRSA (11).
The pressure from increased vancomycin consumption has led to the emergence
of vancomycin resistance in staphylococci and enterococci
(12). Staphylococci with
reduced susceptibility to vancomycin appeared in 1996. These isolates were
called VISA (vancomycin-intermediate S. aureus) or VRSA
(vancomycin-resistant S. aureus) depending on the level of
resistance. Since then, at least 16 cases
(13–26)
of VISA or VRSA infection have occurred
(Table 2). At least 50% of the
patients were suffering from chronic renal failure. Of those, 10 (62.5%) had
received vancomycin before the VISA or VRSA was isolated.
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TABLE 2 Reported Cases of Staphylococcus aureus Infections with Minimum
Inhibitory Concentration (MIC) to Vancomycin of 8 µg/mL or greater
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Earlier strains of VISA were characterized by vancomycin heteroresistance
(that is, only a subpopulation of the bacteria exhibited reduced vancomycin
susceptibility), and the mechanism was mediated by a thickened peptidoglycan
cell wall, thereby hindering the entrance of vancomycin into the cells
(27). When tested by standard
antibiotic susceptibility testing methods, these heteroresistant isolates
showed a minimal inhibitory concentration (MIC) of 2 – 4 µg/mL to
vancomycin, but the resistant subpopulations had a MIC of 8 µg/mL. The
subpopulations (and therefore, heteroresistance) are not readily detectable by
routine laboratory testing techniques.
Despite the modest elevation in the MIC, treatment failure with vancomycin
can occur. Since 2002, three reports have been published of VRSA that
possesses high-level vancomycin resistance with a MIC ranging from 32 µg/mL
to >256 µg/mL, and these isolates carried the vanA gene, a
major genetic determinant of vancomycin resistance in enterococci
(22–26).
Co-colonization by vancomycin-resistant enterococci (VRE) was also documented
in some of these patients.
The prevalence of β-lactam resistance is more common among
coagulase-negative staphylococci (CoNS) than among S. aureus.
Similarly, glycopeptide resistance appeared earlier in CoNS than in S.
aureus. Moreover, in some studies, the prevalence of glycopeptide
resistance is also higher among the CoNS
(15,28).
In our hospital, 52.7% of the CoNS isolated from PD fluid (1995 – 2006)
were methicillin-resistant, as compared with a 34.2% resistance rate in S.
aureus. Although CoNS are less virulent than S. aureus is, they
remain a major cause of prosthesis-related infections, sometimes exceeding
S. aureus in prevalence.
Enterococcus: Enterococcus casseliflavus and E.
gallinarum are uncommon causes of human infections, and they are
intrinsically resistant to the glycopeptides (vancomycin MIC up to 32
µg/mL). The most common human pathogens, E. faecalis and E.
faecium, may acquire genes resistant to glycopeptides. Dialysis patients
with chronic renal failure are at significant risk for VRE colonization and
infection. Other at-risk populations include cancer patients, transplant
recipients, patients in the intensive care unit, and individuals requiring
prolonged hospitalization and multiple broad-spectrum antibiotics
(29–31).
The nature of antibiotic exposure is one of the determinants of the risk of
VRE acquisition. Agents that exert selective pressure on the emergence of
enterococci (for example, vancomycin, extended-spectrum cephalosporins) and
those causing significant perturbation of the normal anaerobic flora in the
intestine (for example, metronidazole) are associated with higher risks of VRE
colonization
(32,33).
The use of vancomycin in situations for which alternative agents are available
is strongly discouraged.
Enterobacteriaceae: The coliforms are major causes of
dialysis-related peritonitis. Resistance to β-lactam in coliforms is
mediated mainly by β-lactamase production, and two groups of
β-lactamases are particularly important among the Enterobacteriaceae.
Citrobacter, Enterobacter, and Serratia may develop
high-level inducible production of AmpC β-lactamases that imparts
resistance to extended-spectrum cephalosporins. Extended-spectrum
β-lactamase (ESBL) is most prevalent among Escherichia coli and
Klebsiella pneumoniae. Bacteria producing ESBL are resistant to most
β-lactams except the carbapenems. Since the end of the 1990s, the CTX-M
types have emerged as the commonest form of ESBL, causing hospital- and
community-acquired infections globally. Enterobacteriaceae in food animals are
also frequently found to be carrying ESBL
(34).
In a multicenter survey in Hong Kong in 2000, the prevalence of
ESBL-producing E. coli and Klebsiella spp. were 11% and 13%
respectively (35). These
strains are commonly co-resistant to other classes of antibiotics, including
the fluoroquinolones and some aminoglycosides (gentamicin, for example). The
prevalences of ESBL in E. coli and Klebsiella remained in
the range of 15% – 20% and 13% – 14% respectively in our hospital
during 2000 – 2005, and the E. coli isolated from peritoneal
dialysate had resistance rates of 47.1%, 18.4%, 1.5%, 34.6%, 24.3%, and 0.7%
towards cefazolin, cefuroxime, ceftazidime, ciprofloxacin, gentamicin,
amikacin respectively. Those findings necessitated aminoglycosides or
ceftazidime to be combined with cefazolin in the empiric treatment of
dialysis-related peritonitis.
The efficacy of the carbapenems is also being compromised by the appearance
of carbapenem-resistant Enterobacteriaceae. This kind of resistance can occur
through reduced permeability of the outer membrane to carbapenem molecules,
acquisition of metallo-β-lactamase genes, or acquisition of
non-metallocarbapenemase genes
(36). Carbapenem-resistant
Enterobacteriaceae are still uncommon, but they are emerging as pathogens in
some centers
(37–39).
The fluoroquinolones and aminoglycosides are alternatives for the treatment
of resistant gram-negative infections. Fluoroquinolone resistance appears
readily with increased use of those agents. It is commonly mediated by
mutations in the target proteins DNA gyrase and topoisomerase IV (gyrA,
gyrB, parC, parE genes), and is sometimes attributable to increased
expression of multidrug efflux pumps or decreased uptake as a result of porin
reduction
(40,41).
Resistance to aminoglycosides is most commonly mediated by enzymatic
deactivation of the compound by a multitude of aminoglycoside-modifying
enzymes. Other possible mechanisms are target-site alteration and reduced
uptake by the bacterial cell
(42). The fact that many of
these antibiotic resistance genes are carried on mobile genetic elements such
as plasmids and integrons means that horizontal gene transfer can readily
occur. Outbreaks in health care settings have been the result
(43–45).
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ENVIRONMENTAL GRAM-NEGATIVE BACILLI (NON-FERMENTERS)
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The three main pathogens in the non-fermenter category are
Pseudomonas spp. (especially P. aeruginosa),
Acinetobacter baumannii, and Stenotrophomonas maltophilia.
As compared with other bacteria, these species exhibit a relatively high level
of antibiotic and biocide resistance. In addition to the presence of
underlying diseases and prolonged hospitalization, the most important risk
factor for the emergence of multi-resistant P. aeruginosa and A.
baumannii is prior use of broad-spectrum antibiotics, especially
carbapenems, fluoroquinolones, and third-generation cephalosporins
(46).
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THERAPEUTIC STRATEGIES
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The empiric antibiotic regimen for dialysis-related peritonitis should have
adequate coverage against the pathogens that most commonly cause peritonitis,
taking into account the prevalences and patterns of resistance of pathogens at
that institution, and the patient's previous culture results. Current
guidelines recommend the use of a first-generation cephalosporin (for example,
cefazolin) against gram-positive bacteria, with the potential for using
vancomycin in patients with severe allergy to β-lactams
(47). An anti-pseudomonal
agent should be included for gram-negative coverage, which generally involves
the use of a third- or fourth-generation cephalosporin (for example,
ceftazidime or cefepime) or an aminoglycoside (for example, gentamicin or
amikacin). A combination of two cephalosporins should be used only when the
patient's urine output is more than 100 mL daily
(48). Short courses of
intraperitoneal aminoglycosides do not affect residual renal function in
dialysis patients
(47,49).
Alternative regimens include intraperitoneal imipenem/cilastatin and oral
fluoroquinolones. Imipenem/cilastatin should be reserved for situations in
which ESBL-producing Enterobacteriaceae infections are highly prevalent or the
patient has a history of recurrent infections of this kind. Although oral
fluoroquinolones produce high drug concentrations in the peritoneal dialysate,
their use is limited by the fact that resistance among gram-positive and
gram-negative bacteria alike are alarmingly high in many centers.
Known-pathogen therapy against multiresistant pathogens is problematic, and
few clinical trials of new antibiotics or alternative agents are currently
underway. Intraperitoneal vancomycin may still be used for VISA infection
unless the MIC level is high, as in the case of vanA-positive VRSA
isolates. An alternative agent should be added intraperitoneally or
systematically for VISA or VRSA infection as guided by susceptibility test
results. Options include linezolid, quinupristin/dalfopristin, tigecycline,
daptomycin, fusidic acid, rifampicin, doxycycline, and cotrimoxazole. The
latter four agents should be given in combination with other antibiotics to
reduce the development of resistance.
Options for VRE are limited. Ampicillin should obviously be used if the
strain is susceptible. Other possibilities include linezolid,
quinupristin/dalfopristin (but not for E. faecalis), and tigecycline.
The carbapenems remain the drug of choice for ESBL-producing
Enterobacteriaceae, and aminoglycosides such as amikacin are also useful if
the strains are susceptible. Systemic or intraperitoneal polymyxins can be
used against multiresistant coliforms and non-fermenters
(50–53).
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PREVENTIVE STRATEGIES
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The risk factors associated with colonization or infection by resistant
bacteria follow a similar pattern. Colonization and infection tend to be more
common among patients requiring prolonged hospitalization, those with
significant underlying diseases and indwelling devices, and in particular,
those exposed to multiple broad-spectrum antibiotics. The antibiotics in
question vary with the bacteria. For gram-positive bacteria, exposure to
vancomycin is the main risk factor. For the Enterobacteriaceae and
non-fermenters, third-generation cephalosporins, carbapenems, and
fluoroquinolones are commonly implicated.
Primary prevention for the emergence of resistant bacteria is impossible,
given that many patients with chronic comorbidities require frequent
hospitalizations, indwelling devices, and antibiotic use. Judicious use of
antibiotics is the clearly the prerequisite and should focus on the
extended-spectrum cephalosporins, carbapenems, and glycopeptides
(54). An antibiotic
stewardship program should be part of every hospital's antibiotic policy.
Rational choice of antibiotics (for example, a shift from extended-spectrum
cephalosporins to ureidopenicillins) and compliance from clinicians can make
substantial contributions to reducing the prevalence of resistant bacteria
(55–57).
Although data are still lacking, controlling the use of vancomycin is
likely to be beneficial in curtailing the emergence of VISA and VRSA. At our
centre, CoNS and S. aureus with reduced susceptibility to
glycopeptides were reported in 1999. After that, a program was implemented to
audit the use of glycopeptides, and we failed to find any similar strains
during the following 7 years (Figure
1). Basic infection control measures are crucial to preventing
spread and outbreaks of multiresistant bacteria
(58–60).
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Figure 1 — Monthly usage of glycopeptides in Queen Mary Hospital, 1995 –
1998, and prevalence of bacteremic staphylococci heteroresistant to
vancomycin. [Data from (15)
and (55)]
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Nephrologists and dedicated dialysis nurses must educate dialysis patients
on the importance of hand hygiene and disinfection techniques when performing
CAPD. Food hygiene is often neglected by these patients, and the importance of
that measure is reflected in the occasional cases of peritonitis caused by
enteric pathogens such as Salmonella, Campylobacter, Aeromonas, and
Plesiomonas. Specific measures to prevent dialysis-related
peritonitis are still investigational. Exit-site care with povidone iodine has
not been universally effective in reducing the incidence of peritonitis
(61,62).
Other potential strategies include PD catheters impregnated with
antimicrobials [chlorhexidine, silver sulfadiazine, and triclosan
(63)] and development of new
PD fluids that will preserve peritoneal leukocyte functions through pH values
that are more physiologic and reduced levels of glucose degradation products
(64).
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EMERGING THREATS AND CONCLUSIONS
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The four most pressing threats from resistant bacterial pathogens are
community- and hospital-acquired MRSA, VRE, ESBL-producing and
carbapenem-resistant Enterobacteriaceae, and multiresistant P.
aeruginosa and A. baumannii. Globally, CA-MRSA is already
assuming epidemic proportions, and VRE is endemic in many Western countries.
The ESBL-producing Enterobacteriaceae have also been described in the
community (65), and it is
likely only a matter of time before carbapenem-resistant Enterobacteriaceae,
Pseudomonas, or Acinetobacter start to emerge outside health
care settings. Establishment of these pathogens in the community setting will
drive a vicious cycle toward the wider use of antibiotics.
It is against this backdrop that preventive measures against the emergence
of bacterial resistance should be strongly advocated. Despite the fact that
emergence of resistance is unavoidable, minimizing the selection pressure
through judicious use of antibiotics has repeatedly been shown to be effective
against a number of resistant bacteria. In the absence of an unlimited supply
of new antibiotics, this strategy appears to be the most rational to employ
against this inevitable problem.
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TOP
ABSTRACT
DIALYSIS PATIENTS AND INFECTION
