Serratia species are opportunistic gram-negative bacteria classified in the tribe Klebsielleae and the large family Enterobacteriaceae. Serratia are widespread in the environment, but are not a common component of the human fecal flora.[1]

Serratia marcescens is the primary pathogenic species of Serratia.[2] Rare reports have described disease resulting from infection with Serratia plymuthica,[3] Serratia liquefaciens,[4] Serratia rubidaea,[5] Serratia odorifera, and Serratia fonticola.[6]

Some strains of S marcescens are capable of producing a pigment called prodigiosin, which ranges in color from dark red to pale pink, depending on the age of the colonies. The chemical structure of prodigiosin has been unveiled.[7] Serratia are capable of thriving in diverse environments, including water, soil, and the digestive tracts of various animals.[8] S marcescens has a predilection for growth on starchy foodstuffs, where the pigmented colonies are easily mistaken for drops of blood.

In 1819, Bartolomeo Bizio, a pharmacist from Padua, Italy, discovered and named S marcescens when he identified the bacterium as the cause of a miraculous bloody discoloration in a cornmeal mush called polenta. Bizio named Serratia in honor of an Italian physicist named Serrati, who invented the steamboat, and Bizio chose marcescens (from the Latin word for decaying) because the bloody pigment was found to deteriorate quickly.[9]

Since 1906, physicians have used S marcescens as a biological marker for studying the transmission of microorganisms because, until the 1950s, this bacterium was generally considered a harmless saprophyte. Only since the 1960s has S marcescens been recognized as an opportunistic pathogen in humans.[10]

Derivatives of prodigiosin have recently been found to have immunosuppressive properties and antitumor activity in vivo[11, 12] and are also currently being considered as a candidate treatment for Chagas disease.[13]


It appears that at least some Serratia isolates interfere with macrophage function or viability.[14] In the hospital, Serratia species tend to colonize the respiratory and urinary tracts, rather than the gastrointestinal tract, in adults.

Serratia infection is responsible for about 2% of nosocomial infections of the bloodstream, lower respiratory tract, urinary tract, surgical wounds, and skin and soft tissues in adult patients. An outbreak of S marcescens bloodstream infections was identified in patients receiving contaminated bags of parenteral nutrition.[15] Outbreaks of S marcescens meningitis, wound infections, and arthritis have occurred in pediatric wards.

Serratia infection has caused endocarditis and osteomyelitis in people addicted to heroin.

Cases of Serratia arthritis have been reported in outpatients receiving intra-articular injections.

An outbreak of meningitis caused by S marcescens in patients who had undergone spinal anaesthesia for caesarean section has been ascribed to contaminated medications used for this purpose.[16]



United States

Serratia species are responsible for 1.4% of nosocomial bloodstream infections.


The yearly incidence of Serratia bacteremia is 1.03 per 100,000 population, with 47% of episodes having their onset in the community.[17]

The prevalence of Serratia species as a cause of nosocomial infections is diminishing, but these bacteria are still able to cause hospital outbreaks, especially in intensive care units.

In the University Hospital of Heraklion, Crete, 65 (84.4%) of 77 patients with Serratia infection had a S marcescens isolated; the remaining 12 patients had a nonmarcescens Serratia species infection. The most frequently observed infections were respiratory tract infection (32.5%) and keratitis/endophthalmitis (20.8%).[18]



Most (68%) episodes of Serratia bacteremia occur in males.[17]


Outbreaks of Serratia infection occur in neonates and infants. In adults, most Serratia infections are isolated, but occasional nosocomial outbreaks occur.



Pink hypopyon in the absence of hyphema may suggest S marcescens endophthalmitis.[26]

Breast milk can turn pink with Serratia postpartum mastitis.[27, 28]


Laboratory Studies

Imaging Studies


Medical Care

Antibiotic therapy is the primary treatment in most patients with Serratia infection. Home therapy is an option in patients who are clinically stable.

Surgical Care

Purulent collections (abscesses) may require drainage.


Medication Summary

S marcescens is naturally resistant to ampicillin, macrolides, and first-generation cephalosporins. In Taiwan, 92% of the strains are resistant to cefotaxime, but 99% are still susceptible to ceftazidime. Extended spectrum beta-lactamases are produced by most S marcescens strains.[35] International data on antimicrobial susceptibility of Serratia and other nosocomial isolates have been published.[36, 37]

Serratia infections should be treated with an aminoglycoside plus an antipseudomonal beta-lactam, as the single use of a beta-lactam can select for resistant strains. Most strains are susceptible to amikacin, but reports indicate increasing resistance to gentamicin and tobramycin. Quinolones also are highly active against most strains.

Cefepime may be a reasonable option for the treatment of infections with Serratia strains that produce AmpC β-lactamase.[38]

Definitive therapy should be based on the results of susceptibility testing because multiresistant strains are common.

Levofloxacin (Levaquin)

Clinical Context:  For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Cefepime (Maxipime)

Clinical Context:  Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam for IM administration. Poor capacity to cross blood-brain barrier precludes use for treatment of meningitis.

Ertapenem (Invanz)

Clinical Context:  Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by various beta-lactamases including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.

Amikacin (Amikin)

Clinical Context:  Preferred aminoglycoside. Usually synergistic with antipseudomonal beta-lactams. Use both in combination, pending results of susceptibility testing. For gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against Pseudomonas aeruginosa. Irreversibly binds to 30S subunit of bacterial ribosomes. Blocks recognition step in protein synthesis. Causes bacterial growth inhibition.

Aztreonam (Azactam)

Clinical Context:  Usually synergistic with amikacin. Use both in combination, pending results of susceptibility testing. A monobactam that inhibits cell wall synthesis during bacterial growth. Active against gram-negative bacilli.

Meropenem (Merrem IV)

Clinical Context:  Preferred therapy for Serratia meningitis. Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has increased activity against gram-negative bacteria and slightly decreased activity against staphylococci and streptococci compared to imipenem.

Imipenem-cilastatin (Primaxin)

Clinical Context:  Comparable in activity to meropenem.

Ciprofloxacin (Cipro)

Clinical Context:  Greatest anti-P aeruginosa activity among the quinolones. May be particularly useful for isolates resistant to the aminoglycosides.

Class Summary

Empiric antimicrobial therapy should cover all likely pathogens in the context of the clinical setting.

Further Inpatient Care




Basilio J Anía, MD, Associate Professor of Infectious Diseases, Universidad de Las Palmas de Gran Canaria; Consultant in Internal Medicine, Hospital Universitario Dr. Negrín, Spain

Disclosure: Nothing to disclose.

Specialty Editors

Thomas E Herchline, MD, Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Disclosure: Nothing to disclose.


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