| Serratia marcescens | |
|---|---|
 | |
| Serratia marcescens on an agar plate | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Enterobacterales |
| Family: | Yersiniaceae |
| Genus: | Serratia |
| Species: | S. marcescens |
| Binomial name | |
| Serratia marcescens | |
Serratia marcescens (/səˈreɪʃiəmɑːrˈsɛsɪnz/)[3][failed verification] is a species ofrod-shaped,Gram-negative bacteria in the familyYersiniaceae. It is afacultative anaerobe and an opportunistic pathogen in humans. It was discovered in 1819 byBartolomeo Bizio inPadua, Italy.[4]S. marcescens is commonly involved inhospital-acquired infections (HAIs), also called nosocomial infections, particularlycatheter-associatedbacteremia,urinary tract infections, andwound infections,[5][6] and is responsible for 1.4% of HAI cases in the United States.[7] It is commonly found in therespiratory andurinary tracts of hospitalized adults and in thegastrointestinal systems of children.S. marcescens is a major cause of contact lens associated keratitis.[8][9][10]
Due to its abundant presence in the environment, and its preference for damp conditions,S. marcescens is commonly found growing in bathrooms (especially on tilegrout,shower corners,toilet water lines, and basins), where it manifests as a pink, pink-orange, or orange discoloration and slimy film feeding offphosphorus-containing materials orfatty substances such assoap andshampoo residue.
Once established, complete eradication of the organism is often difficult, but can be accomplished by application of ableach-baseddisinfectant. Rinsing and drying surfaces after use can also prevent the establishment of the bacterium by removing its food source and making the environment less hospitable.
S. marcescens may also be found in environments such as dirt and thesubgingival biofilm of teeth. Due to this, and becauseS. marcescens produces a reddish-orange tripyrrole dye calledprodigiosin, it may causetooth discoloration. Thebiochemical pathway for the production of prodigiosin byS. marcescens has been characterized by analyzing what intermediates become accumulated in specific mutants.[11]
S. marcescens is amotile organism and can grow in temperatures ranging 5–40 °C (41–104 °F) and inpH levels ranging from 5 to 9. It is differentiated from otherGram-negative bacteria by its ability to performcaseinhydrolysis, which allows it to produce extracellularmetalloproteinases which are believed to function in cell-to-extracellular matrix interactions. Since this bacterium is afacultative anaerobe, meaning that it can grow in either the presence ofoxygen (aerobic growth) or in the absence of oxygen (anaerobic growth), it is capable ofnitrate reduction under anoxic conditions. Therefore,nitrate tests are positive since nitrate is generally used as the finalelectron acceptor rather than oxygen.S. marcescens also exhibitstyrosine hydrolysis andcitrate degradation.[12][4] Citrate is used byS. marcescens to producepyruvic acid, thus it can rely on citrate as acarbon source and test positive for citrate utilization.[4] In identifying the organism, one may also perform amethyl red test, which determines if a microorganism performsmixed-acid fermentation.S. marcescens results in a negative test. Another determination ofS. marcescens is its capability to producelactic acid by oxidative and fermentative metabolism. Therefore,S. marcescens is lactic acid O/F+.[13]
| Test | Result[14] |
|---|---|
| Gram stain | − |
| Oxidase | − |
| Indole production | − |
| Methyl red | > 70% − |
| Voges-Proskaeur | + |
| Citrate (Simmons) | + |
| Hydrogen sulfide production | − |
| Urea hydrolysis | > 70% − |
| Phenylalanine deaminase | − |
| Lysine decarboxylase | + |
| Motility | + |
| Gelatin hydrolysis, 22 °C | + |
| Acid from lactose | − |
| Acid from glucose | + |
| Acid from maltose | + |
| Acid from mannitol | + |
| Acid from sucrose | + |
| Nitrate reduction | + (to nitrite) |
| Deoxyribonuclease, 25 °C | + |
| Lipase | + |
| Pigment | some biovars produce red |
| Catalase production (24h) | + |
In humans,S. marcescens can cause anopportunistic infection in several sites,[15] including theurinary tract,respiratory tract, wounds,[7] breasts,[16] and the eye,[17] where it may causeconjunctivitis,keratitis,endophthalmitis, andtear duct infections.[18] It is also a rare cause ofendocarditis andosteomyelitis (particularly in people whouse intravenous drugs recreationally),pneumonia, andmeningitis.[6][7] MostS. marcescens strains are resistant to severalantibiotics because of the presence ofR-factors, which are a type ofplasmid that carry one or more genes that encoderesistance; all are considered intrinsically resistant toampicillin,macrolides, andfirst-generation cephalosporins (such ascephalexin).[6]
Inelkhorn coral,S. marcescens is the cause of the disease known aswhite pox disease.[19] Insilkworms, it can also cause a lethal disease, especially in association with other pathogens.[20]
In research laboratories employingDrosophilafruit flies, infection of them withS. marcescens is common.[citation needed] It manifests as a pink discoloration or plaque in or on larvae, pupae, or the usuallystarch andsugar-based food (especially when improperly prepared).
A rare clinical form ofgastroenteritis occurring in early infancy is caused by infection with S. marcescens. Thered color of the diaper can be mistaken forhematuria (blood in the urine), which may cause unnecessary investigations by the physicians.[21]
S. marcescens causescucurbit yellow vine disease, leading to sometimes serious losses in melon fields.[22]
Virulent strains ofS. marcescens can impacthoney bee colonies.[23][24]
Because of its red pigmentation, caused by expression of thedyeprodigiosin,[25] and its ability to grow on bread,S. marcescens has been evoked as a naturalistic explanation ofmedieval accounts of the "miraculous" appearance of blood on theCorporal of Bolsena,[25] though no formal testing of the corporal itself exists to confirm or deny this. The supposed miracle followed a celebration ofMass at Bolsena in 1263, led by aBohemian priest who had doubts concerningtransubstantiation, or the turning of bread and wine into the Body and Blood ofChrist during the Mass. During the mass, theEucharist appeared to bleed and each time the priest wiped away the blood, more would appear.[25] This event is celebrated in a fresco byRaphael calledThe Mass at Bolsena in theApostolic Palace in theVatican City.[26]
S. marcescens growth on bread, calledblood bread,bloody bread, orred bread, is an uncommon but known problem in food manufacturing.[27]
S. marcescens was discovered in 1819 byVenetian pharmacistBartolomeo Bizio, as the cause of an episode of blood-red discoloration ofpolenta in the city ofPadua.[28] Bizio named the organism four years later in honor ofSerafino Serrati, a physicist who developed an earlysteamboat; the epithetmarcescens (Latin for 'decaying') was chosen because of the dyestuff's rapid deterioration–Bizio's observations led him to believe that the organism decayed into amucilage-like substance upon reaching maturity.[29]Serratia was later renamedMonas prodigiosus andBacillus prodigiosus before Bizio's original name was restored in the 1920s.[28]
Until the 1950s,S. marcescens was erroneously believed to be a nonpathogenic "saprophyte",[7] and its reddish coloration was used in school experiments to track infections. During theCold War, it was used as a simulant inbiological warfare testing by theU.S. military,[30] which studied it in field tests as a substitute for thetularemia bacterium, which was being weaponized at the time.
On 26 and 27 September 1950, theU.S. Navy conducted a secret experiment namedOperation Sea-Spray in which balloons filled withS. marcescens were released and burst over urban areas of theSan Francisco Bay Area inCalifornia. Although the Navy later claimed the bacteria were harmless, beginning on 29 September, 11 patients at a local hospital developed very rare, serious urinary tract infections. One of the afflicted patients, Edward J. Nevin, died.[31] Cases ofpneumonia in San Francisco also increased afterS. marcescens was released.[32][33] (That the simulant bacteria caused these infections and death has never been conclusively established.) Nevin's son and grandson lost a lawsuit they brought against the government between 1981 and 1983, on the grounds that the government is immune,[34] and that the chance that the sprayed bacteria caused Nevin's death was minute.[35] The bacterium was also combined withphenol and ananthrax simulant and sprayed across southDorset by US and UK military scientists as part of theDICE trials which ran from 1971 to 1975.[36]
Since 1950,S. marcescens has steadily increased as a cause of human infection, with many strainsresistant to multiple antibiotics.[5] The first indications of problems with theinfluenza vaccine produced byChiron Corporation in 2004 involvedS. marcescens contamination.
In early 2008, theU.S. Food and Drug Administration issued a nationwide recall of one lot of Pre-FilledHeparin Lock Flush Solution USP.[37] The heparin IV flushsyringes had been found to be contaminated withS. marcescens, which resulted in patient infections. TheCenters for Disease Control and Prevention confirmed growth ofS. marcescens from several unopened syringes of this product.
S. marcescens has also been linked to 19 cases inAlabama hospitals in 2011, including 10 deaths.[38] All of the patients involved were receivingtotal parenteral nutrition at the time; the two pharmacists responsible for formulating the solution were criminally charged.[39]
Because of its ability to be grown onagar plates into even, well colouredlawns, and the existence of aphage specific toS. marscecens, it has been used to trace water flows inkarst limestone systems. Known quantities of phage are injected into a fixed point in the karst water system and the outflows of interest are monitored by conventional small-volume sampling at fixed time intervals. In the laboratory, the samples are poured onto grownS. marscecens lawns and incubated. Colourless plaques in the lawns indicate the presence of phage. The method was claimed to be sensitive at very high dilutions because of the ability to detect single phage particles.[40][41]
Traditionally, infections byS. marcescens have been treated withcefepime,carbapenems (Siedner et al., 2014; Tamma et al., 2022 as cited in Tavares-Carreon et al., 2023), aminoglycosideamikacin,gentamicin andtobramycin (Bertrand & Dowzicky, 2012; Sader et al., 2014 as cited in Tavares-Carreon et al., 2023). However, recent clinical data has shown declining efficacy for gentamicin and tobramycin, part of a trend towards increasing resistance and a narrowing of treatment options. The development of these resistances to common antibiotics is partially due to adaptive resistance through overexposure and selection of resistant strains, butS. marcescens also has intrinsic resistance from sources such aslipopolysaccharide modifications, which can reduce antibiotic penetration, and adaptive resistance through biofilm production (Tavares-Carreon et al., 2023). Biofilm production increases antibiotic resistance because bacteria at the bottom of the biofilm are less exposed to antibiotics, the bacteria in the biofilm do not grow as quickly, and there are faster rates ofhorizontal gene transfer which allows resistance genes to spread easily within the population. In 2017, the World Health Organization listedSerratia as among the most critical group of bacteria for which new antibiotics are urgently needed due to its resistance to multiple drugs and threat to hospitals, nursing homes, and patients who useventilators and bloodcatheters.[42][43]
S. marcescensskin infections are uncommon, but may be suspected in cases ofcellulitis inimmunocompromised individuals, particularly when conventionalantibiotics are ineffective.[44]S. marcescens is naturally resistant toamoxicillin andamoxicillin/clavulanic acid due to the fact that it produces acephalosporinaseenzyme.[44] It is also resistant to many other antibiotics, includingpenicillin,cephalosporin,tetracycline,macrolide,nitrofurantoin, andcolistin.[45] Broad-spectrum antibiotics such asthird-generation cephalosporins,fluoroquinolones, andimipenem/cilastatin are indicated for treatment ofS. marcescensskin infections.[44]Surgery may also be considered if antibiotics are not rapidly effective.[44][46]
Phloretin may reduce the virulence ofS. marcescens by disruptingquorum sensing and biofilm formation.[47] When treated withchloramphenicol,S. marcescens biofilms demonstrated significant reductions in growth.[43][48] Genetic studies have demonstrated a role for type I pili (fimbriae) inS. marcescens biofilm formation.[46][49]
Red or 'Bloody' bread is the result of growth-pigmented bacteria,Serratia marcescens. However, red bread is not common.
Serratia marcescens is naturally resistant to amoxicillin alone and amoxicillin associated with clavulanic acid. Broad-spectrum antibiotics are indicated to treat S marcescens skin infections, and surgery should be promptly considered in cases of severe skin infections if appropriate antibiotic therapy does not lead to rapid improvement. [...] Although uncommon, an S marcescens skin infection may be suspected in cases of cellulitis in immunocompromised patients, especially when conventional antibiotics are not effective. Serratia marcescens naturally produces a cephalosporinase that confers resistance to amoxicillin and to amoxicillin associated with clavulanic acid. Broad-spectrum antibiotics such as third-generation cephalosporins, fluoroquinolones, or imipenem-cilastatin are indicated in cases of S marcescens skin infections, and surgery should be promptly considered if appropriate antibiotic therapy does not lead to rapid clinical improvement.
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