Serratia marcescens

Serratia marcescens is a species of Gram-negative, rod-shaped bacterium in the family Enterobacteriaceae. A human pathogen, S. marcescens is involved in nosocomial infections, particularly catheter-associated bacteremia, urinary tract infections and wound infections,^[1][2] and is responsible for 1.4% of nosocomial bacteremia cases in the United States.^[3] It is commonly found in the respiratory and urinary tracts of hospitalized adults and in the gastrointestinal system of children.

Due to its ubiquitous presence in the environment, and its preference for damp conditions, S. marcescens is commonly found growing in bathrooms (especially on tile grout, shower corners, toilet water line, and basin), where it manifests as a pink discoloration and slimy film feeding off phosphorus-containing materials or fatty substances such as soap and shampoo residue.

Once established, complete eradication of the organism is often difficult, but can be accomplished by application of a bleach-based disinfectant. 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, supposedly "sterile" places, and the subgingival biofilm of teeth. Due to this, and the fact that S. marcescens produces a reddish-orange tripyrrole pigment called prodigiosin, S. marcescens may cause extrinsic staining of the teeth. The biochemical pathway illustrating the production of prodigiosin by S. marcescens is unknown except for the final two steps. In these steps, a monopyrrole (MAD) and a bipyrrole (MBC) undergo a condensation reaction by way of a condensing enzyme to ultimately form prodigiosin.

Contents 1 Identification 2 Pathogenesis 3 History 4 References 5 External links

Identification

S. marcescens is a motile organism and can grow in temperatures ranging from 5–40°C and in pH levels ranging from 5 to 9. It is differentiated from other Gram-negative bacteria by its ability to perform casein hydrolysis, which allows it to produce extracellular metalloproteinases which are believed to function in cell-to-extracellular matrix interactions. S. marcescens also exhibits tryptophan and citrate degradation. One of the end products of tryptophan degradation is pyruvic acid, which is then incorporated into different metabolic processes of S. marcescens. A final product of citrate degradation is carbon. Thus, S. marcescens can rely on citrate as a carbon source. In identifying the organism, one may also perform a methyl red test, which determines if a microorganism performs mixed-acid fermentation. S. marcescens results in a negative test. Another determination of S. marcescens is its capability to produce lactic acid via oxidative and fermentative metabolism. Therefore, it is said that S. marcescens is lactic acid O/F+.^[4]

Test	Result
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)	+

^[5]

Pathogenesis

S. marcescens can cause infection in several sites, including the urinary tract, respiratory tract, wounds,^[3] and the eye, where it may cause conjunctivitis, keratitis, endophthalmitis, and tear duct infections.^[6] It is also a rare cause of endocarditis and osteomyelitis (particularly in people who use intravenous drugs recreationally), pneumonia, and meningitis.^[2][3] Most S. marcescens strains are resistant to several antibiotics because of the presence of R-factors, which are a type of plasmid that carry one or more genes that encode resistance; all are considered intrinsically resistant to ampicillin, macrolides, and first-generation cephalosporins (such as cephalexin).^[2]

In elkhorn coral, S. marcescens is the cause of the disease known as white pox disease.^[7] In silkworms, it sometimes occurs as a secondary pathogen in viral flacherie disease.

Also in Drosophila research laboratories, infection with S. marcescens is common. It manifests itself as a pink discolouration or plaque in or on larvae, pupae, or the usually starch and sugar-based food (especially when improperly prepared).

History

Serratia marcescens was discovered in 1819 by Venetian pharmacist Bartolomeo Bizio, as the cause of an episode of blood-red discoloration of polenta in the city of Padua.^[8] Bizio named the organism four years later in honor of Serafino Serrati, a physicist who developed an early steamboat; the epithet marcescens (Latin for "decaying") was chosen because of the pigment's rapid deterioration (Bizio's observations led him to believe that the organism decayed into a mucilage-like substance upon reaching maturity).^[9] Serratia was later renamed Monas prodigiosus and Bacillus prodigiosus before Bizio's original name was restored in the 1920s.^[8]

Until the 1950s, S. marcescens was erroneously believed to be a nonpathogenic "saprophyte",^[3] and its reddish coloration was used in school experiments to track infections. It has also been used as a simulant in biological warfare tests by the United States Military.^[10][11] On September 26 and 27, 1950, the United States Navy conducted a secret experiment named "Operation Sea-Spray" in which some S. marcescens was released by bursting balloons of it over urban areas of the San Francisco Bay Area in California. Although the Navy later claimed the bacteria were harmless, beginning on September 29, 11 patients at a local hospital developed very rare, serious urinary tract infections, and one of these individuals, Edward J. Nevin, died. Cases of pneumonia in San Francisco also increased after S. marcescens was released.^[12],[13]

Since 1950, S. marcescens has steadily increased as a cause of human infection, with many strains resistant to multiple antibiotics.^[1] The first indications of problems with the influenza vaccine produced by Chiron Corporation in 2004 involved S. marcescens contamination.

Because of its red pigmentation, caused by expression of the pigment prodigiosin,^[14] and its ability to grow on bread, S. marcescens has been evoked as a naturalistic explanation of medieval accounts of the "miraculous" appearance of blood on the Eucharist that led to Pope Urban IV instituting the Feast of Corpus Christi in 1264. This followed celebration of a mass at Bolsena in 1263, led by a Bohemian priest who had doubts concerning transubstantiation, or the turning of bread and wine into the Body and Blood of Christ during the Mass. During the Mass, the Eucharist appeared to bleed and each time the priest wiped away the blood, more would appear. While Serratia possibly could generate a single appearance of red pigment, it is unclear how it could have generated more pigment after each wiping, leaving this proposed explanation open to doubt. This event is celebrated in a fresco in the Apostolic Palace in the Vatican City, painted by Raphael.^[15]

In early 2008, the U.S. Food and Drug Administration (FDA) issued a nationwide recall of one lot of Pre-Filled Heparin Lock Flush Solution USP.^[16] The heparin IV flush syringes had been found to be contaminated with Serratia marcescens, which resulted in patient infections. The Centers for Disease Control (CDC) confirmed growth of S. marcescens from several unopened syringes of this product.

Serratia marcescens has also been linked to 19 cases in Alabama hospitals in 2011, including ten deaths.^[17] All of the patients involved were receiving total parenteral nutrition at the time, and this is being investigated as a possible source of the outbreak.^[18]

References

External links

• med/2103 at eMedicine