In clinical practice it is the most common species of the genus Serratia to cause human infection and it has been found to cause urinary tract infection, meningitis, pneumonia, infective endocarditis, catheter-associated bloodstream infection, wound infection, and more. Many people in the health professions have likely heard of S. In an effort to call more attention to this important human pathogen and for the sake of sharing some interesting facts, the following is provided. The first description of S.
At that time polenta was an important food of the people, but the cornmeal dish was found to be discolored red during a particularly warm and humid summer. Many strains of S. Through experimentation Bizio was able to cultivate the organism from fresh polenta. He first published his findings anonymously, but later was acknowledged as the author. Figure Figure. Nazzaro G , Veraldi S. Serratia marcescens : an Italian story.
Int J Dermatol. Arcanum: the 19th-century Italian pharmacist pictured here was the first to characterize what are now known to be bacteria of the genus Serratia. Clin Infect Dis. Veraldi S , Nazzaro G. Skin ulcers caused by Serratia marcescens : three cases and a review of the literature. Eur J Dermatol. DOI Google Scholar. Comments character s remaining. Comment submitted successfully, thank you for your feedback.
There was an unexpected error. While S. Results from a recent surveillance programme in the US and Europe, indicate that Serratia spp. Currently Serratia is the seventh most common cause of pneumonia with an incidence of 4. It operates as a true opportunist producing infection whenever it gains access to a suitably compromised host.
Patients most at risk include those with debilitating or immunocompromising disorders, those treated with broad-spectrum antibiotics and patients in ICU who are subjected to invasive instrumentation. The indwelling urinary catheter is a major risk factor for infection.
The risk of a catheterized patient becoming infected with S. The respiratory tract is also recognized as a major portal of entry with S. Not surprisingly, common infections include urinary tract infection in patients with indwelling catheters, respiratory tract infection in intubated patients and bloodstream infection in post-surgical patients, especially in those with intravenous catheters. The organism has also been described as an important cause of ocular infection with high incidence in contact lens-related keratitis 4 , 21 , In the s, S.
The frequency has since subsided, although sporadic cases of Serratia endocarditis still occasionally occur with two of the highest risk groups including intravenous drug users and patients undergoing prosthetic valve surgery. Skin and soft tissue infections are also unusual although rare cases of invasive cellulitis and necrotizing fasciitis have been reported Septic arthritis has also been reported following diagnostic and therapeutic intra-articular injections Over the years, S.
Outbreaks of infection have been traced to medical equipment including nebulisers 87 , bronchoscopes 82 , electrocardiogram leads , laryngoscopes 20 and contaminated solutions such as inhalation medications , prefilled heparin syringes 8 , , saline solutions , parenteral nutrition 3 and antiseptics Many diverse environmental sources such as air conditioning units 82 , urine-collecting basins , bed-pan macerators 42 , liquid soap dispensers and even tap water 46 have also been implicated.
Outside of environmental sources, hospital patients have also been recognized as a reservoir for infection.
The gastrointestinal tract is recognized as the predominant site of colonization for S. Studies have shown, however, that rates of S. Regardless of the source or reservoir, the predominant mode of spread of S. The recovery of epidemic strains of S. Factors such as debilitating clinical condition, lengthy ward-stay and frequent exposure to medical interventions, most likely act by necessitating increased frequency and intensity of direct contact with staff hands In keeping with its role as an agent of opportunistic infection, S.
Whilst almost all isolates produce extracellular products such as DNase, chitinase, lecithinase, lipase, gelatinase and siderophores, it appears that in S. Nevertheless, ongoing studies indicate that S. Almost all isolates of S. This cytotoxin is thought to assist in tissue penetration 43 and may be linked to the expression of an extensive host invasive pathogenic pathway involving bacterial swarming and quorum sensing 58 , If future studies confirm the pathogenic role of biofilm in S.
In the last two decades Enterobacteriaceae have demonstrated an exceptional ability to acquire, transfer, and modify the expression of multiple antimicrobial resistance genes As a typical member of the Enterobacteriaceae family and complementary to its capacity for survival, S.
In addition, clinical isolates display a selective advantage through their readiness to acquire and express many other antimicrobial resistance determinants. In the past, agents such aminoglycosides, fluoroquinolones and third-generation cephalosporins comprised the mainstay of treatment of S. However, many clinical isolates of S.
The pattern of resistance displayed by clinical isolates of S. In the s isolates of S. In the s, however, gentamicin resistance was observed in Serratia. In more recent years, the increased use of other agents such as third-generation cephalosporins and fluoroquinolones has led to a reduction in the use of aminoglycosides. Consequently, the rate of aminoglycoside resistance amongst S. Nevertheless, over the years, clinically significant outbreaks of aminoglycoside-resistant S.
The geographic distribution of different aminoglycoside-modifying enzymes varies considerably depending on regional aminoglycoside usage. AAC 6' -I, which mediates resistance to tobramycin, netilmicin, amikacin and dibekacin, and ANT 2'' -I which confers resistance to gentamicin, tobramycin and dibekacin, are frequently found in the US and the Far East Outside of enzyme inactivation, aminoglycoside resistance may also result from diminished uptake or efflux, which confer low-level resistance to all aminoglycosides.
More recently aminoglycoside resistance has also been attributed to a rare mechanism involving 16S rRNA methylase-mediated ribosomal protection. These enzymes have been shown to mediate high-level resistance to several aminoglycosides, including kanamycin, tobramycin, amikacin, gentamicin, streptomycin and arbekacin 25 , Regardless of the mechanism involved, aminoglycoside resistance is readily detected in S.
In the early s fluoroquinolones were shown to demonstrate considerable activity against S. In the following years, however, the marked increase in the use of fluoroquinolones in hospital patients was reflected by a corresponding increase in the numbers of fluoroquinolone-resistant S.
Reports indicate that over a twelve year period from to , the percentage of fluoroquinolone-resistant S. In more recent years the overall rate of fluoroquinolone resistance has decreased, presumably reflecting increased reliance on beta-lactam therapy.
Nevertheless, as would be expected with an organism with the adaptive capacity of S. As with other members of the Enterobacteriaceae family, fluoroquinolone resistance in S. The main mechanism for resistance involves mutations in the gyrA gene which codes for the A subunit of the target enzyme, DNA gyrase 35 , Similar to the aminoglycosides, fluoroquinolone-resistant S. With the widespread reliance on beta-lactam antibiotics, the frequency of resistance to these common agents has risen steadily among Gram negative bacilli Enterobacteriaceae , have not only evolved to allow for increased production of existing beta-lactamases but also for the production of modified enzymes with extended substrate profiles and decreased susceptibility to beta-lactamase inhibitors 29 , As expected, one of the most striking examples of the potential of Enterobacteriaceae to demonstrate extended beta-lactam resistance is S.
This organism demonstrates most, if not all, common modes of beta-lactam resistance. This resistance is attributed to the presence of a chromosomal AmpC beta-lactamase enzyme. Similar to other Enterobacteriaceae , S. Expression of AmpC is linked to perturbation in cell wall synthesis and the interplay of several gene products associated with cell wall recycling In wild-type isolates uninduced state transcription of the structural ampC beta-lactamase gene is repressed, thus only trace amounts of AmpC beta-lactamase enzyme are produced and resistance is restricted to narrow spectrum beta-lactam agents.
In the presence of beta-lactam agents expression of Amp C is inducible and bacteria produce a transient increase in beta-lactamase production which returns to low-level when the inducer is removed Induction per se is thus not associated with clinically significant resistance. The ampC gene is, however, also capable of undergoing mutation to produce a state of stable derepression or constitutive beta-lactamase over-production These stably-derepressed or hyperproducing mutants segregate spontaneously within the normal inducible population Individual beta-lactam drugs differ in their ability to induce AmpC activity.
Broad-spectrum cephalosporins such as cefotaxime, ceftazidime, ceftriaxone and cefepime are weak inducers of the enzyme and thus remain stable against AmpC-inducible bacteria However, this activity against inducible cells renders the drugs highly selective for the pre-existing resistant derepressed mutants that can survive and overgrow. Consequently, the clinical importance of inducible beta-lactamases and derepressed mutants has increased dramatically since the introduction of third-generation cephalosporins.
Since the selective process occurs within days of treatment with these broad-spectrum agents, it is associated with a high rate of therapeutic failure Once selected, these ampC mutants are stable, can be transferred from patient to patient and may in time, constitute a major proportion of the isolates of that species in a hospital.
Similar to other AmpC-inducible enterobacteria, the selection of derepressed isolates in S. Nevertheless, in contrast to other enterobacteria , where high-frequency selection of AmpC-derepresed mutants results in equally high rates of clinical failure, this has not been the case for S.
Studies investigating S. Currently there is no standardized laboratory method for AmpC detection Cefoxtin resistance can used as a marker for AmpC production, however, this test is non-specific as several class A beta-lactamases and some carbapenemases can mediate this resistance. A three dimensional cefoxitin disc diffusion test can be used for AmpC detection, but this method is laborious for routine use and results are inoculum-dependent Despite the absence of a simple, reliable detection method, the level of resistance associated with constitutive AmpC over-production, even in S.
Moreover, since AmpC expression is chromosomally-mediated, all isolates of S. Hence, it is generally agreed that identification of this organism is sufficient to alert the clinician that the isolate has the potential to develop AmpC-mediated cephalosporin resistance Outside of the expression of chromosomal AmpCbeta-lactamase, S.
In common with all Enterobacteriaceae, S. However, in addition to these narrow-spectrum enzymes, S. ESBLs are derived from mutation of classical plasmid-encoded beta-lactamases, which extend the hydrolytic spectrum of the enzymes to include broad-spectrum agents such as cefotaxime, ceftazidime and cefepime Unlike AmpC production where high levels of beta lactamase correlate with in vitro demonstration of resistance, ESBLs tend to demonstrate lower beta-lactam hydrolytic efficiency.
Since ESBL-mediated resistance is not readily detected, clinical laboratories are required to adopt specialized screening methods Early inhibitor-based detection methods using the clavulanic-double disc synergy test, where the clavulanic inhibitor was used to potentiate the activity of the indicator drug against an ESBL-producing isolate by enhancing the zone of inhibition, have been found to be unreliable Current ESBL detection methods rely on standardized susceptibility testing using a range of indicator cephalosporins.
In isolates with evidence of reduced susceptibility, ESBL production is then confirmed using combination tests where cephalosporin susceptibility is repeated, in the presence and absence of clavulanic acid ESBL inhibitor Nevertheless, the application of these combination susceptibility methods remains limited in isolates such as S. Broad spectrum carbapenem beta-lactam antibiotics, such as imipenem and meropenem, resist inactivation by chromosomal AmpC and plasmid-mediated ESBL beta-lactamases.
In general, both these carbapenems have MIC90 values for S. Nevertheless, in keeping with the alarming spread of carbapenem resistance amongst Enterobacteriaceae, a small number of S. SME-1, a class A chromosomal beta-lactamase with activity against narrow spectrum cephalosporins, carbapenems and monobactams, was first described in a clinical isolate of S.
In these sporadic infections, isolates were recovered from different regions in the US, suggesting that convergent evolution of these enzymes may have occurred following selection with increased clinical use of imipenem 22 , The increased use of carbapenems has also been associated with the acquisition of plasmid-mediated carbapenemases in S.
Class B plasmid-encoded metallo-carbapenemases first appeared in S. These IMP carbapenemases, mediate high-level cross-resistance to cephalosporins and carbapenems but, to date, have only been implicated in infrequent outbreaks of S. A further plasmid-mediated carbapenemase, GES-1, has also been described in an isolated outbreak of S. This cleaning process should be followed by intensive disinfection procedures using a chlorinated product like bleach to ensure the organism's control.
When the surface of the toilet bowl begins to develop a film of pink slime, it's time to repeat the cleaning process followed by a thorough disinfection of the area. However, it is important to note the cleaning the services are flushing the bowl using chlorinated products will never eliminate the presence of Serratia marcescens completely.
However, taking the appropriate steps listed above can control and manage the bacteria. The deadly bacterium is inherently resistant to most common narrow-spectrum penicillin medications.
This includes amoxicillin, ampicillin, ampicillin-sulbactam, amoxicillin-clavulanate and numerous cephalosporins. Because of that, over the last four decades, the bacterium has become a severe health care-associated pathogen that revealed its multiple antimicrobial resistant properties.
That said, many hospitals never experience problems associated with Serratia marcescens when identified, take appropriate measures to readily treat those affected. However, other hospital settings are highly susceptible to cross infections due to a lack of following disinfecting procedures in the healthcare population.
Research shows that infection outbreaks usually coincide with the breakdown of hospital procedures to control infections. It is in the settings at the pathogen continues to thrive in the hospital causing it to become highly resistant to any treatment. Due to the high susceptibility of some hospital environments failure to control Serratia marcescens infections, certain preventative measures can be highly effective.
This includes isolating multi-resistant strains of the bacteria, implementing strict and hygiene policies and identifying and isolating the organism through a microbiology laboratory analysis before choosing the appropriate therapy to control the infection throughout the hospital population.
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