Version May 2024
INTRODUCTION — Serratia species are gram-negative bacilli of the Enterobacterales order, although they are not a common component of healthy human fecal flora. In the early part of the 20th century, Serratia marcescens was considered a nonpathogenic organism and was used in medical experiments and as a biological warfare test agent [1]. Since the mid-1970s, however, Serratia species have been recognized to cause a full spectrum of human clinical disease. Additionally, Serratia species may harbor multidrug resistance mechanisms that can complicate treatment decisions.
This article will review the microbiology, epidemiology, clinical features, diagnosis, and treatment of infections caused by Serratia species.
Detailed discussion of particular infectious syndromes (eg, complicated urinary tract [UTI] infection or hospital-acquired pneumonia) that Serratia can cause can be found separately in topics dedicated to that syndrome:
●(See "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)
●(See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)
●(See "Conjunctivitis" and "Complications of contact lenses" and "Bacterial endophthalmitis".)
●(See "Health care-associated meningitis and ventriculitis in adults: Clinical features and diagnosis" and "Health care-associated meningitis and ventriculitis in adults: Treatment and prognosis".)
●(See "Complications of abdominal surgical incisions", section on 'Surgical site infection' and "Necrotizing soft tissue infections" and "Septic arthritis in adults" and "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis" and "Overview of the evaluation and management of surgical site infection".)
●(See "Gram-negative bacillary bacteremia in adults".)
●(See "Native valve endocarditis: Epidemiology, risk factors, and microbiology" and "Antimicrobial therapy of left-sided native valve endocarditis".)
MICROBIOLOGY
Nomenclature — The genus Serratia consists of at least 20 species, of which 8 are known to have caused infections in humans (table 1) [2]. S. marcescens is the main human pathogen in the genus. Bartolomeo Bizio, a pharmacist, described an unusual red discoloration of polenta in 1819 in Padua, Italy after a particularly warm and humid summer [1,3]. He was able to cultivate the responsible organism and first named it S. marcescens in 1823 [1,3]. This organism has had a large number of other names in the literature, although only Chromobacterium prodigiosum was used commonly until the 1950s [1].
Characteristics — The genus consists of facultatively anaerobic gram-negative rods (picture 1) in the order Enterobacterales that grow well on most commonly used laboratory media. Many strains of S. marcescens, Serratia plymuthica, and Serratia rubidaea are red-pigmented. However, the red pigment exhibited by S. marcescens is most commonly associated with environmental strains (picture 2). Because of this, the organism was used as a tracer organism in various medical and military experiments in the 1900s before human disease with this pathogen was fully appreciated [1]. Hospital-acquired strains are often not red-pigmented. Such colonies of S. marcescens are generally creamy white to grayish in color and grow well at standard incubator temperatures (35 to 37°C).
Automated bacterial identification systems and matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) will reliably identify the more common Serratia species, including S. marcescens, Serratia liquefaciens, and S. rubidaea. S. marcescens produces the enzymes deoxyribonuclease (DNase), lipase, and gelatinase and is usually a lactose non-fermenter. The other, more uncommon, species may not be as easily identified because many commercial systems may not have evaluated them for inclusion in their databases, although MALDI-TOF technology can reliably identify the uncommon Serratia species. In general, however, the uncommon species, save Serratia fonticola, can at least be identified as belonging to the genus Serratia by DNase and gelatinase production [1]. In some cases, 16S ribosomal ribonucleic acid (rRNA) gene sequencing may be necessary to definitively determine identity, if clinically indicated.
Pathogenesis and virulence factors — S. marcescens and the other Serratia species do not produce many notable virulence factors and are considered opportunistic pathogens, although serious infections may occur in immunocompetent hosts [1]. Serratia species are motile and can adhere to cells via fimbriae. S. marcescens produces different exoproteins and compounds that may contribute to virulence [1,4-7].
EPIDEMIOLOGY
Incidence — The incidence of Serratia infections is estimated to be 10.8 per 100,000 people annually, with a hospital onset rate of 0.4 per 1000 inpatient discharges according to a single Canadian study [8]. In very preterm infants in a multicenter, United States study of 774 hospitals, the incidence of invasive Serratia was higher, around 2.3 Serratia infections per 1000 preterm infants [9].
Environmental reservoirs as the primary source of infection — Human infections caused by Serratia species occur worldwide. They are thought to arise from exogenous environmental sources rather than from commensal flora. Since S. marcescens and the other Serratia species are commonly associated with the environment, they are particularly adept at causing nosocomial infections and hospital-associated outbreaks.
The various environmental niches for Serratia species, including S. marcescens, include (table 1):
●Water
●Soil
●Plants
●Animals
●Insects
While environmental Serratia species are sometimes associated with animals and insects, these organisms are not typically transmitted to humans through bites, scratches, or stings. Instead, Serratia species are usually acquired directly from contact with environmental sources. Serratia in the health care environment, specifically, may be related to the ability to form biofilms and resist biocides or disinfectants. Health care exposures may lead to gut colonization prior to invasive infections [10,11]. Serratia can be responsible for bacteremia and endocarditis in persons who inject drugs, likely also related to environmental contamination events [12,13].
Hospital-onset infections — Hospital-onset infections due to Serratia species are most commonly reported in association with outbreaks linked to an environmental or medical exposure, although they also occur outside the outbreak setting. Serratia species are encountered often enough to be included on most annual hospital antibiograms (>30 isolates in a year). Clusters of Serratia infections occurring in the health care setting should be evaluated for a possible common source outbreak.
Outbreaks — Over 200 reported hospital-based outbreaks caused by S. marcescens have been reported in the medical literature since 1950 [1]. Sources of reported outbreaks have included various environmental point sources (eg, tap water [14], disinfectant solutions [15,16], soap [17,18]) and therapeutic agents (eg, blood products [19-21], intravenous solutions [22-26]), as well as carriage and dissemination on health care worker hands [27-29]. Outbreaks have affected pediatric [30] and adult populations, immunocompromised hosts, intensive care units (ICUs) [31,32], and single hospitals as well as institutions across several states.
Some multistate outbreaks of Serratia bloodstream infections have gained national attention in the United States:
●In 2005, an S. marcescens bloodstream infection outbreak was linked to contaminated bags of intravenous magnesium sulfate solution from a nationally distributing compounding pharmacy [23]. In total, the outbreak involved 18 patients in five states over a three-month period. All patient isolates had identical pulse-field gel electrophoresis profiles, as did isolates from unopened bags of magnesium sulfate from the same compounded lot.
●A nine-state outbreak of 162 S. marcescens bloodstream infections from 2007 to 2008 was eventually linked to prefilled heparin and saline syringes from a pharmaceutical manufacturer [24,33]. The US Food and Drug Administration (FDA) investigation concluded that inadequate compliance with regulatory standards was the likely reason for the contaminated products.
Patient risk factors identified in outbreaks due to Serratia have generally been consistent with other hospital-acquired infections and relate to high-risk health care exposures and impaired host immunity (table 2).
Individual infections — Hospital onset infections due to Serratia may also infrequently occur outside of an outbreak scenario. Surveillance reports from European ICUs list Serratia as the primary pathogen in 3.4 percent of bloodstream infections and 5.3 percent of pneumonias [34]. Similarly low percentages are reported in hospitalized patients in North and Latin America: 1.6 percent of bloodstream infections [35] and 2 to 4 percent of pneumonias [36]. A Japanese survey reported 6.8 percent of all urinary tract infections (UTIs) were caused by Serratia species [37].
The presence of an invasive device is an important risk factor for hospital-acquired Serratia infections. However, surveillance data suggest that Serratia is not a predominant device-related infection pathogen in the United States. Although it was previously one of the top 10 pathogens encountered in health care-associated infections, surveillance data from 2015 to 2017 showed that Serratia declined in frequency in the United States and ranked Serratia species below the top 10 for cause of central line-associated bloodstream infections and catheter-associated UTI. For ventilator-associated pneumonia, it was ranked eighth (4.6 percent) among patients in intensive care units and sixth (5.0 percent) among patients in long-term acute care facilities [38]. Serratia was also an infrequent cause of surgical site infections following abdominal (0.4 percent of infections), cardiac (5.5 percent), orthopedic (1.8 percent), and obstetric/gynecologic (1.1 percent) procedures [38]. Serratia is intrinsically resistant to cefazolin, the most commonly used surgical prophylaxis agent. Thus, clusters of Serratia infections occurring in the health care setting should be evaluated for a possible common source outbreak [30]. (See 'Outbreaks' above.)
Preterm infants cared for in neonatal ICUs may be at particular risk for Serratia late-onset bloodstream and central nervous system (CNS) infections. In an observational study from 2018 to 2020 that included >100,000 preterm and low birthweight infants at 774 hospitals in the United States, 279 had Serratia infection [9]. Infants with Serratia infection had higher rates of tracheostomy, gastrostomy, and home oxygen use compared with infants with other infections. Rates of Serratia infection were higher in academic hospitals with large neonatal ICUs that offered complex medical and surgical services.
Community-onset infections — The extent of the role of Serratia species in community-onset infections is not well delineated. In a population-based, laboratory surveillance study in Canada, 65 percent of incident Serratia isolates were associated with community-onset infections [8]. However, this study was not able to distinguish between health care-associated infections that were identified in the community and true community-acquired infections. Nevertheless, community-based environmental reservoirs of Serratia species may play a larger role than previously appreciated, as the literature on Serratia is dominated by reports of outbreaks likely related to a common environmental reservoir and infections following particular environmental exposures [1,14,29,33]. Comparable studies investigating Serratia in patient populations outside health care settings are needed to better define its prevalence.
DISEASE ASSOCIATIONS — Serratia species have been isolated from a variety of clinical specimens (table 1). Serratia species are not, however, the dominant pathogens for any particular clinical syndrome, except for ocular infections. The mechanism of inoculation and the source of the pathogen often remain unknown. Infections due to Serratia species have clinical manifestations similar to infections caused by other bacterial pathogens. Clinical manifestations of particular infectious syndromes (eg, complicated urinary tract infection [UTI] or hospital-acquired pneumonia) are discussed separately in topics dedicated to that syndrome.
S. marcescens is an established human pathogen associated with UTI, pneumonia, and bloodstream infection [35-37,39,40]. Endocarditis caused by Serratia species has been described, especially among persons who inject drugs [41-43].
Skin and soft tissue infections, including various wound infections, surgical site infections [29-31,44-46], and even necrotizing fasciitis [47-49] are infrequently encountered, as well as osteomyelitis and septic arthritis [42].
Central nervous system (CNS) infections due to Serratia are often linked with prior instrumentation such as ventriculoperitoneal shunts and other surgeries, lumbar puncture [50], or spinal injections [51-53]. Meningoencephalitis has been described in neonates [9,54,55].
Serratia species cause a larger proportion of infections of the eye than other infections, and in some studies, they are one of the most commonly isolated pathogens, along with Pseudomonas aeruginosa, among hospital-acquired or contact lens-associated ocular infections [56,57]. These include conjunctivitis, keratoconjunctivitis [58], corneal ulcers, and keratitis [59]. Endophthalmitis caused by Serratia is rare, but long-term outcomes can be severe. In one case series of 10 patients with endophthalmitis caused by S. marcescens, 60 percent experienced complete vision loss [60]. Case series of nosocomial eye infections have been mainly described in neonates and children, post-traumatic ocular infections, and in persons who wear contact lenses [1,59,61].
DIAGNOSTIC EVALUATION — Infection with Serratia species cannot be distinguished from other bacterial pathogens that cause similar infectious syndromes on the basis of signs and symptoms alone. Thus, the diagnosis of Serratia infection is confirmed by identification of the organism on culture of the relevant clinical specimen (eg, blood, sputum, urine, or aspirated body fluid). If endophthalmitis is suspected, vitreous cultures should be collected for diagnosis and susceptibility testing; blood cultures should also be collected to evaluate if the mechanism was hematogenous seeding. Details on diagnosis of particular infectious syndromes (eg, complicated urinary tract [UTI] infection or hospital-acquired pneumonia) are discussed separately in topics dedicated to those syndromes.
Since Serratia species are commonly found in the environment, the clinical presentation should always be taken into account when evaluating recovery of these organisms from clinical specimens in order to distinguish infection from contamination or colonization. For example, pseudo-outbreaks of Serratia due to contaminated specimen tubes during blood culture collection or due to contaminated bronchoscopes have been described [62,63].
Automated bacterial identification systems and matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) will reliably identify the more common Serratia species, including S. marcescens, S. liquefaciens, and S. rubidaea. In some cases, 16S ribosomal ribonucleic acid (rRNA) gene sequencing may be necessary to definitively determine identity if clinically indicated, but the species detail is generally not necessary for making treatment decisions.
Antibiotic susceptibility testing guidelines are well established for Serratia species, particularly S. marcescens, and standard sensitivities can be determined using most automated systems [64,65]. Interpretation of susceptibility results, however, requires a nuanced approach due to known mechanisms of antibiotic resistance. (See 'Antimicrobial resistance' below.)
ANTIMICROBIAL RESISTANCE — In addition to intrinsic resistance to various antibiotics, Serratia species can also have broad-spectrum beta-lactam resistance through production of AmpC beta-lactamase, extended-spectrum beta-lactamases (ESBLs), and carbapenemases.
Intrinsic resistance — Serratia species are intrinsically resistant to ampicillin, amoxicillin, ampicillin-sulbactam, amoxicillin-clavulanate, narrow-spectrum cephalosporins (including cefazolin), cephamycins, cefuroxime, macrolides, tetracycline, and nitrofurantoin, fosfomycin, and polymyxins [64-66].
AmpC beta-lactamase — S. marcescens and several other Serratia species encode an inducible, chromosomal AmpC beta-lactamase, although it is typically expressed at low levels [67]. In contrast to other Enterobacterales (eg, Klebsiella aerogenes, Citrobacter freundii, Enterobacter cloacae) that are at moderate to high risk of ampC induction, Serratia is considered to be at lower risk of expressing AmpC (<5 percent of isolates) [68]. At the low levels at which this enzyme is typically expressed, AmpC beta-lactamase mediates resistance to several beta-lactam antibiotics, such as penicillins and first-generation cephalosporins, but resistance to later-generation cephalosporins may not be detected on initial antibiotic susceptibility tests. In the laboratory, the best method to screen for AmpC production is to monitor for cefoxitin or cefotetan resistance since organisms that produce AmpC are intrinsically resistant to cephamycins.
●Inducible AmpC – Exposure to certain beta-lactams can lead to transcriptional induction and transiently increased expression of AmpC beta-lactamase. However, this induction may not be clinically relevant, because most isolates do not have mutations that result in stable expression of high levels of AmpC, and they express only low levels of AmpC when they first encounter antibiotics. For example, imipenem is a potent inducer of AmpC, but induction by imipenem does not result in resistance to imipenem or other carbapenems [69]. Third-generation cephalosporins such as ceftazidime, ceftriaxone, and cefotaxime are weak inducers, and induction may result in a relatively small increase in minimum inhibitory concentration to these agents. If enough AmpC beta-lactamase is produced, this may result in hydrolysis of third-generation cephalosporins, but there is no evidence to suggest this induction is clinically relevant [69].
●Derepressed AmpC and plasmid-mediated AmpC – Derepressed mutants, in contrast to the “induced” example above, are isolates that have pre-existing, constitutive mutations that ensure high levels of AmpC even in the absence of antibiotic pressure. These mutations generally result in higher levels of AmpC than simple induction, and the resistant isolate emerges from mixed populations quickly after exposure to antibiotics. Treatment with third-generation cephalosporins such as ceftazidime or cefotaxime can select for derepressed mutants that cause rapidly emerging resistance and treatment failures. In addition, plasmid-mediated AmpC beta-lactamases that are usually produced at high levels have also been found in some S. marcescens strains.
Both derepressed mutants and plasmid-mediated AmpC producers are resistant to all beta-lactams except carbapenems and perhaps cefepime [67,70]. The cephalosporin plus beta-lactamase inhibitor combination ceftazidime/avibactam has in vitro activity against AmpC-producing organisms including Serratia species; ceftazidime/avibactam maintains in vitro susceptibility even for ceftazidime non-susceptible isolates [71]. However, clinical data on use of these agents for such infections are limited [72].
Extended-spectrum beta-lactamase (ESBL) — S. marcescens is also known to produce ESBLs, which are plasmid encoded. The prevalence of ESBLs in S. marcescens has not been determined on a large scale in the United States; studies from other countries indicate a large variance in prevalence. As an example, in a study from two hospitals in Poland 19 percent of S. marcescens isolates from 1996 to 2000 were ESBL producers [73]. In contrast, in a separate study from Poland, 70.8 percent of S. marcescens isolates from 2003 to 2004 produced ESBLs [74]. Resistance to third-generation cephalosporins such as ceftazidime or ceftriaxone is the best indication of the presence of an ESBL in a Serratia isolate, although AmpC beta-lactamase expressed at high levels could also mediate resistance to these antibiotics. There are approved ESBL-confirmatory tests for Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, and Proteus mirabilis, but these are not recommended for S. marcescens [75]. (See "Extended-spectrum beta-lactamases".)
Carbapenemase — Some strains of S. marcescens encode chromosomal carbapenemases (the SME family of enzymes) that mediate resistance to penicillins, first-generation cephalosporins, carbapenems (particularly imipenem), and aztreonam [76]. In addition, some S. marcescens strains have been found to harbor plasmid-mediated carbapenemases such as KPC-2, OXA-48, IMP, VIM, and NDM-1, which can strongly hydrolyze carbapenems if produced at high levels [76-79]. (See "Carbapenem-resistant E. coli, K. pneumoniae, and other Enterobacterales (CRE)".)
TREATMENT — Serratia species are generally susceptible to several antibiotic classes: fluoroquinolones, aminoglycosides, trimethoprim-sulfamethoxazole, piperacillin-tazobactam, third- and fourth-generation cephalosporins, aztreonam, and carbapenems [80]. Antibiotic choice depends on the site of infection and the ability of the chosen drug to penetrate into the infected areas, susceptibility testing results, and the likelihood of emerging drug resistance during a treatment course. Institutional antibiogram data should be used to select empiric therapy while awaiting susceptibility information. Typically, either cefepime or piperacillin/tazobactam is used.
Clinical trial data that include patients with Serratia infections in order to evaluate the comparable efficacy of various antibiotic agents are limited. A trial comparing piperacillin-tazobactam with meropenem among 72 patients with bloodstream infection caused by Enterobacterales that produced chromosomal AmpC found no clear difference in overall clinical and microbiologic outcomes; piperacillin-tazobactam resulted in a higher microbiologic failure rate (13 versus 0 percent) but a lower microbiologic relapse rate (0 versus 9 percent, a difference that was not statistically significant) [81]. However, the study size may not have been large enough to detect an overall difference, and there was an imbalance of cointerventions between the two arms that limits interpretation of the findings. Furthermore, only 25 patients with Serratia infection were included, so the trial does not clearly inform optimal antibiotic choice for Serratia. Observational data also suggest no difference in mortality outcomes based on treatment choice, but definitive conclusions are difficult given confounding biases [82-84].
As with any bacterial infection, adequate control of the source of the infection is critical and may include removal of invasive devices and prosthetic material, drainage of abscess, and adequate debridement of infected tissues and bone. Details on other management issues beyond systemic antibiotic choice for particular infectious syndromes (eg, complicated urinary tract infection [UTI], bacteremia, or hospital-acquired pneumonia) are discussed separately in topics dedicated to that syndrome.
Susceptible isolates — In cases of infection caused by isolates that do not have substantial drug resistance, the selection of antibiotics depends on the risk of emergent resistance during treatment, which in turn depends on the site of infection, the initial inoculum, and the presence of retained infected material, as well as the expected duration of therapy and the potential toxicity of treatment.
●Uncomplicated infections/sites with good drug penetration – For uncomplicated infections in sites with good drug penetration, such as UTIs, minor skin and soft tissue infections, and pneumonia, fluoroquinolones, trimethoprim-sulfamethoxazole, piperacillin-tazobactam, third- and fourth-generation cephalosporins, and carbapenems are all appropriate options if the isolate in question is susceptible. Aminoglycosides are generally used as monotherapy only for lower UTIs. (See "Aminoglycosides", section on 'Clinical use'.)
For uncomplicated bacteremia due to Serratia, a reasonable approach is to transition from an intravenous regimen chosen empirically based on the local antibiogram to a highly bioavailable oral agent to which the isolate is susceptible to complete the treatment course. This is discussed in detail elsewhere. (See "Gram-negative bacillary bacteremia in adults", section on 'Duration and route of therapy'.)
●Severe infections in sequestered sites/infections that warrant long treatment courses – For more severe infections in sequestered sites with impaired drug penetration or high pathogen inoculum and for infections that require long treatment courses, antibiotic selection takes into consideration the potential for emergent AmpC-beta-lactamase-mediated resistance to third-generation cephalosporins that may not be evident during initial susceptibility testing [75]. (See 'AmpC beta-lactamase' above.)
We consider central nervous system (CNS) infections, infections in sequestered sites (eg, endocarditis or osteomyelitis), and cases in which adequate debridement of infected material cannot be performed or infected prosthetic material cannot be removed to be higher-risk situations for emergence of AmpC-mediated resistance. In these situations, we suggest against using third-generation cephalosporins (eg, ceftriaxone or ceftazidime) even if the isolate tests susceptible. This recommendation is based on limited, small studies that report clinical failure in a small proportion of patients [85-89].
For CNS infections, we favor the use of a carbapenem (meropenem) or cefepime. If cefepime is used, high dosing (2 g every 8 hours) or extended infusions should be used to ensure adequate penetration of the infected area. (See "Prolonged infusions of beta-lactam antibiotics".)
For other infections in sequestered sites, transition to oral fluoroquinolones or trimethoprim-sulfamethoxazole is likely appropriate to complete the treatment course, if the isolate is susceptible.
No large studies describe a significant risk of clinical failure with piperacillin-tazobactam therapy for Serratia infections if susceptibility has been proven in vitro [85]. Piperacillin may be less selective for AmpC derepressed mutants than some cephalosporins, and tazobactam has some beta-lactamase inhibitory activity against AmpC. Some microbiology laboratories may suppress reporting of cephalosporin and beta-lactam/beta-lactamase inhibitor susceptibility tests in order to discourage their use for species at risk of AmpC expression.
For suspected endophthalmitis due to Serratia species, ophthalmology consultation is recommended. Intravitreal antibiotic administration is necessary for treatment of endophthalmitis, typically with ceftazidime or an aminoglycoside. Such patients may require vitrectomy if presentation is severe or vitreous cultures do not clear. (See "Bacterial endophthalmitis".)
Topical agents appropriate for less severe ocular infections such as keratitis include fluoroquinolones or aminoglycosides.
Multidrug-resistant isolates — Antibiotic options for multidrug-resistant isolates, either due to high-level expression of AmpC beta-lactamase or an extended-spectrum beta-lactamase (ESBL), are limited, regardless of the site of infection. A carbapenem (imipenem, meropenem, ertapenem) is generally the treatment of choice for most multidrug-resistant isolates.
For isolates that express high levels of AmpC beta-lactamase, the only reliable agents from the beta-lactam class are the carbapenems (see 'AmpC beta-lactamase' above). Data suggest cefepime can potentially be effective, but its role in therapy of infections due to stably derepressed mutants producing AmpC beta-lactamase has not yet been fully defined. In a study of 96 patients with infections due to laboratory-confirmed AmpC beta-lactamase-producing organisms (13 of which were Serratia species), 96 percent of the isolates were susceptible to cefepime [82]. There was no difference in 30-day mortality associated with treatment with cefepime versus meropenem.
Agents from other classes (eg, fluoroquinolones) can still be used despite production of AmpC beta-lactamase if the isolate tests susceptible and the agent is appropriate for the site of infection.
For infections with Serratia species that produce an ESBL, carbapenems remain the drugs of choice. Treatment of infections caused by ESBL-producing organisms is discussed in more detail elsewhere. (See "Extended-spectrum beta-lactamases", section on 'Treatment options'.)
In the case that carbapenems cannot be used for multidrug-resistant Serratia species because of patient intolerance or carbapenem resistance, antibiotic selection should be made in consultation with an expert in treating drug-resistant infections.
There are several agents targeting multidrug-resistant gram-negative organisms, particularly carbapenem-resistant Enterobacteriaceae: ceftazidime-avibactam, meropenem-vaborbactam, imipenem-relebactam, plazomicin, cefiderocol, and eravacycline. Appropriate use of these agents depends on the mechanism of resistance, source of infection, risk of toxicity, and availability of resistance testing. For example, ceftazidime/avibactam is effective against some carbapenemases (KPC) but not others (NDM-1). (See "Combination beta-lactamase inhibitors, carbapenems, and monobactams", section on 'Ceftolozane-tazobactam' and "Combination beta-lactamase inhibitors, carbapenems, and monobactams", section on 'Ceftazidime-avibactam'.)
Monitoring — Patients with Serratia infections should be monitored for clinical response during treatment. For cases in which the patient is not clinically improving on cephalosporin therapy or in which cultures are repeatedly positive, susceptibility testing should be repeated and therapy adjusted accordingly. Emergence of AmpC-derepressed mutants may be seen in as early as three to four days [75]. (See 'AmpC beta-lactamase' above.)
Duration of therapy — Duration of therapy depends on the site of infection and the patient's clinical response. Infection with Serratia species does not warrant a longer course of therapy than generally indicated for the type of infection. Duration of therapy for particular infectious syndromes (eg, complicated UTI or hospital-acquired pneumonia) is discussed separately in topics dedicated to that syndrome.
SUMMARY AND RECOMMENDATIONS
●Microbiology – Serratia marcescens is the main human pathogen in the genus, which consists of facultatively anaerobic gram-negative rods in the order Enterobacterales that grow well on most commonly used laboratory media. (See 'Microbiology' above.)
●Epidemiology – S. marcescens and the other species are widely present in the environment and thus are associated in particular with hospital-onset infections and hospital-associated outbreaks. Clusters of infections due to Serratia that occur in hospitalized patients should trigger evaluation for a potential common source outbreak. (See 'Epidemiology' above and 'Hospital-onset infections' above.)
●Spectrum of Serratia infections – Serratia species can cause a wide spectrum of human infections that involve the urinary tract, bloodstream, skin and soft tissue, bone, respiratory tract, central nervous system (CNS), and eye. However, infections due to Serratia species are relatively infrequent compared to other pathogens for these syndromes, except for eye infections. (See 'Disease associations' above.)
●Antimicrobial resistance patterns – Serratia species are intrinsically resistant to ampicillin, amoxicillin, ampicillin-sulbactam, amoxicillin-clavulanate, narrow-spectrum cephalosporins, cephamycins, cefuroxime, macrolides, tetracyclines, fosfomycin, nitrofurantoin, and the polymyxins. Additionally, Serratia species have the potential to harbor multidrug resistance mechanisms (such as AmpC or extended-spectrum beta-lactamases and carbapenemases) and to develop resistance to broad-spectrum beta-lactams during therapy. (See 'Antimicrobial resistance' above.)
●Antimicrobial selection
•Uncomplicated infections – For uncomplicated infections in sites with good drug penetration, such as urinary tract infections (UTIs), minor skin and soft tissue infections, uncomplicated bacteremia, and pneumonia, fluoroquinolones, trimethoprim-sulfamethoxazole, piperacillin-tazobactam, third- and fourth-generation cephalosporins, and carbapenems are all appropriate options for treatment if the isolate in question is susceptible. Aminoglycosides are generally used as monotherapy only for lower UTIs. (See 'Susceptible isolates' above.)
•Severe or complicated infections – The risk of emergence of AmpC-mediated resistance during therapy is likely higher with CNS infections, infections in sequestered sites that require prolonged antibiotic therapy, and cases in which infected material cannot be removed or adequately debrided. For patients with such infections, we suggest not using a third-generation cephalosporin (eg, ceftriaxone or ceftazidime) even if the isolate tests susceptible (Grade 2C). Instead, for CNS infections, we favor the use of a carbapenem (meropenem) or cefepime. For other infections in sequestered sites, fluoroquinolones and trimethoprim-sulfamethoxazole are likely appropriate. (See 'Susceptible isolates' above.)
High-level expression of AmpC beta-lactamase or an extended-spectrum beta-lactamase further limits treatment options, generally the carbapenem class is the primary option. However, cefepime and agents outside the beta-lactam class may still be effective in isolates that produce AmpC if testing demonstrated susceptibility to those agents. (See 'Multidrug-resistant isolates' above.)
●Antimicrobial duration and adjustment – Duration of therapy depends on the site of infection and the patient's clinical response. Culture and susceptibility testing should be repeated and therapy adjusted accordingly for patients who do not clinically improve on cephalosporin therapy because of the potential to select for AmpC beta-lactamase-producing isolates. (See 'Monitoring' above and 'Duration of therapy' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
