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The first description of Serratia is attributed to Pythagoras in 6th centry B.C., where he reported “bloody” food coloration on food products. Serratia micro-organism was first isolated in 1819 in Italy by Bartolemeo Bizio. The characteristic red pigment produced by Serratia marcescens was first extracted by Dr. Kroft in 1902. Woodward and Clark described the first S. marcescens human infection in a patient with bronchiectasis in 1913.

• The first description of Serratia is attributed to Pythagoras in 6th centry B.C., where he reported “bloody” food coloration on food products. The appearance of bloody food has been reported throughout history as ominous, inspirational, or prophesying.^[1]
• Serratia micro-organism was first isolated in 1819 in Italy by Bartolemeo Bizio. The organism was called Serratia in honor of Serafino Serrati, an Italian Physicist, and marcescens (Latin term for “to decay”) because of the pigment’s rapid decay.^[1][2][3]
• The characteristic red pigment produced by Serratia marcescens was first extracted by Dr. Kroft in 1902. The red pigment was initially referred to as prodigiosin.^[4]
• In 1913, Woodward and Clark described the first S. marcescens human infection in a patient with bronchiectasis.^[5]
• In 1957, the termpseudo-hemoptysis was coined by Robinson and Woolley to describe red sputum that is caused by the Serratia organism, not blood.^[6]

Serratia may be classified according to the Serratia species into the following: S. marcescens (most common), S. fonticola, S. grimesii, S. liquefaciens sensu stricto, S. rubidaea, S. oderifera, S. plymuthica, and S. proteamaculans.

Serratia may be classified according to the Serratia species responsible for the infection into the following:

• S. marcescens (> 90% of all Serratia infections in all age groups)
• S. fonticola
• S. grimesii
• S. liquefaciens sensu stricto
• S. rubidaea
• S. oderifera
• S. plymuthica
• S. proteamaculans

• Note that the S. liquefaciens complex is composed of 3 Serratia strains: S. liquefaciens sensu stricto, S. proteamaculans and S. grimesii.
• Additionally, 4 species of Serratia have been isolated but have not been reported to be clinically relevant. To view the comprehensive list of the 12 Serratia species, click here.

Serratia may be transmitted by either direct contact or by ingestion of contaminated foods. Following transmission, Serratia colonizes and forms pathogenic biofilms. Serratia contains prodigiosin, a pigment that produces the characteristic dark-red or pale pink color. Prodigiosin is thought to contain immunosuppressive and anti-tumor activity. In addition, Serratia contains an LPS-containing outer membrane (endotoxin) and R-factors (responsible for antibiotic resistance). Following colonization, it is thought that Serratia may survive in the human host by altering macrophage function. In humans, Serratia is associated with the development of urinary tract infections, pneumonia, meningitis and cerebral abscess, ocular infections, endocarditis, intra-abdominal infection, osteomyelitis, otitis media, parotitis, and sepsis.

• Serratia is usually transmitted by direct contact, especially in healthcare settings during surgeries, instrumentation, and other procedures.
• Serratia may also be transmitted by ingestion of contaminated foods, especially starchy foods.

• Following transmission, Serratia colonizes and forms pathogenic biofilms. Serratia biofilms may be produces on any surface.
• Serratia contains an outer membrane that contains lipopolysaccharide (LPS). The LPS acts as an endotoxin, whereby when released the LPS over-stimulates the host defenses and cause them to undergo lethal endotoxic shock.
• Serratia strains are usually resistant to several antibiotics because of the presence of R-factors (whose genes code for antibiotic resistance) on plasmids.
• Serratia contains prodigiosin, a pigment that produces the characteristic dark-red or pale pink color. Prodigiosin is thought to contain immunosuppressive and anti-tumor activity, which may be required for the organism’s growth in the human host.^[1][2]

• It is thought that Serratia may survive in the human host by altering macrophage function.^[3]
• The exact mechanism by which Serratia infects the human host is poorly understood.

Serratia is associated with the development of the following diseases:

• Urinary tract infections
• Pneumonia
• Meningitis and cerebral abscesses
• Osteomyelitis
• Ocular infections
• Endocarditis
• Osteomyelitis
• Intra-abdominal infection
• Otitis media
• Parotitis
• Sepsis

Serratia is a short, facultatively anaerobic, Gram-negative, rod-shaped bacteria of the Enterobacteriaceae family. Serratia species are ubiquitous opportunistic pathogens that are frequently present under damp conditions in food, plants, animals, soil, and household items.

• Serratia is a ubiquitous opportunistic pathogen that is frequently present under damp conditions in food, plants, animals, soil, and household items (e.g. bathroom tiles).
• Serratia is a short, facultatively anaerobic, Gram-negative, rod-shaped bacteria of the Enterobacteriaceae family.
• It is often associated with hospital-acquired infections.
• Serratia contains enzymes that facilitate its survival under oxygenated conditions against reactive oxygen species. Enzymes include superoxide dismutase, catalase, and peroxidase.
• Serratia has a unique thin cell wall that contains lipopolysaccharides (LPS) that does not resemble the LPS-containing cell walls of other Gram-negative bacteria.
• Out of a total of 12 Serratia species (see Scientific Classification Table), 8 have been reported to be infectious in humans. To view the list of infectiuous Serratia species, click here.
• Serratia is notoriously known for its antimicrobial resistance due to the presence of R-factor and efflux pumps.

• R-factors are genes on plasmids that code for antibiotic resistance and may be transferred from one strain to another.
• Efflux pumps, such as the SdeXY, SdeY, and ABC-type efflux pumps, may eliminate toxins. These pumps may reduce susceptibility to antimicrobial agents, such as erythromycin, tetracycline, norfloxacin, benzalkonium chloride, ethidium bromide, acriflavine, and rhodamine.

Serratia belongs to the following higher order taxa:

• Bacteria (Domain); Proteobacteria (Phylum); Gamma Proteobacteria (Class); Enterobacteriales (Order); Enterobacteriaceae (Family); Serratia (Genus).

The following is the list of Serratia species:

• S. entomophila
• S. ficaria
• S. fonticola
• S. grimesii
• S. liquefaciens
• S. marcescens
• S. odoriferae
• S. plymuthica
• S. proteamaculans
• S. quinivorans
• S. rubidaea
• S. ureilytica

• S. marcescens is a thin, motile (flagellated), non-septated, Gram-negative, facultatively anaerobic rod-shaped bacteria that can grow in temperatures ranging from 5–40 °C and in pH levels ranging from 5 to 9.

• S. marcescens is able to perform casein hydrolysis, which facilitates the production of extracellular metalloproteases thought to function in cell-to-extracellular matrix interactions.
• S. marcescens also exhibits tryptophan– and citrate-degradation. Pyruvic acid, an end-product of tryptophan degradation, and carbon, an end-product of citrate degradation, are then incorporated into metabolic processes.
• S. marcescens produces a reddish-orange (bloody) pigment called prodigiosin. Not all strains, however, are able to produce prodigiosin. It is thought that prodigiosin is an antigen, and during an infection, the production of prodigiosin is limited to avoid the triggering of human immune responses.

• Identification of the organism is commonly done via the following tests:

• Methyl red test, which determines if a microorganism performs mixed-acid fermentation. Typically, S. marcescens results in a negative test due to the production of 2, 3-butanediol and ethanol.
• Voges-Proskauer test, which determines the organism’s ability to convert pyruvatet to acetonin. Typically, S. marcescens results in a positive test.
• Nitrate test, which determines the organism’s ability to produce nitrate products. Typically, S. marcescens results in a positive test.

The following table demonstrates the microbiological characteristics and a comprehensive list of techniques to identify S. marcescens:

Clinically, Serratia may infect multiple organ systems. It may be responsible for urinary tract infection, pneumonia , osteomyelitis, meningitis, cerebral abscess formation, endocarditis, intra-abdominal infections, eye and tear duct infections (conjunctivitis, keratitis, endophthalmitis), otitis media, and rarely parotitis. To learn more about the clinical infection of Serratia, click here.

• 
  Blood agar base plate cultivated colonial growth of Gram-negative, rod-shaped and facultatively anaerobic Serratia marcescens bacteria. From Public Health Image Library (PHIL). ^[2]
• 
  Antibiogram of Serratia marcescens. From WikiMedia.org. ^[3]
• 
  Serratia marcescens on bread. From WikiMedia.org. ^[4]
• 
  Serratia marcescens appears as bloody red spots on culture medium. From WikiMedia.org. ^[5]
• 
  Serratia marcescens appears as bloody red spots on culture medium. From WikiMedia.org. ^[6]
• 
  Serratia marcescens on slates of bread shelves. From WikiMedia.org. ^[6]

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Serratia must be differentiated from other causes of urinary tract infection, pneumonia, endocarditis, meningitis, soft tissue infections, and Skin and soft-tissue infectionswound infections. Differential diagnoses include other infections, such as infections caused by Staphylococcus, Streptococcus, E. coli, Pseudomonas, Haemophilus, tuberculosis, syphilis, and other sexually transmitted infections, as well as other non-infectious systemic diseases, such as tumors, vasculitides, and chemical poisoning.

Serratia urinary tract infection (UTI) must be differentiated from other causes of abdominal discomfort, dysuria, hematuria, pyuria, and/or polyuria, such as:

• Other causes of UTI

• E. coli
• Enterobacter spp.
• Enterococcus spp.
• Haemophilus spp.
• Klebsiella spp.
• Mycoplasma spp.
• Proteus spp.
• Providencia spp.
• Pseudomonas spp.
• Staphylococcus spp.
• Ureaplasma spp.
• Tuberculous infection of the urinary tract
• Sexually transmitted infections (e.g. N. gonorrhea or Chlamydia)
• Parasitic infections (e.g. threadworms)
• Viruses (e.g. HSV)

• Pyelonephritis (acute or chronic)
• Appendicitis
• Benign prostatic hypertrophy
• Prostatitis
• Chronic pelvic pain
• Urinary tract obstruction
• Vesicoureteral reflux
• Polycystic kidney disease
• Metal toxicity
• Sarcoidosis
• Genitourinary malignancy (e.g. bladder cancer)
• Renal transplant rejection
• Interstitial cystitis
• Atrophic vaginitis
• Vulvovaginitis
• Urethritis
• Behcet disease
• Epididymitis
• Pregnancy
• Colovesical fistula
• Diverticulitis
• Glomerulonephritis
• Nephrolithiasis
• Trauma
• Endometritis
• Pelvic inflammatory disease
• Ureterocele

Serratia pneumonia must be differentiated from other causes of fever, chest pain, productive cough, dyspnea, and blood per sputum, such as:

• Other infectious causes of pneumonia:

• Streptococcus spp.
• Staphylococcus spp.
• Anaerobes
• Chlamydia spp.
• E. coli
• Haemophilus spp.
• Acinetobacter spp.
• Legionella spp.
• Tuberculosis or non-tuberculous Mycobacterium spp. (e.g. MAC)
• Mycoplasma spp.
• Moraxella spp.
• Pseudomonas spp.
• Fungal infections (e.g. Candida, Aspergillus)
• Pneumocystis pneumoniae infection
• Viral pneumonia (e.g. influenza, parainfluenza, VZV, HSV, RSV, CMV, adenovirus, metapneumovirus, coronavirus, measles)
• Atypical infections (Q-fever, tularemia, psittacosis)

• Bronchiolitis
• Epiglottitis
• Asthma
• Interstitial lung disease
• Respiratory distress syndrome
• Atelectasis
• Bronchiectasis
• Bronchitis
• COPD exacerbation
• Foreign body aspiration
• Lung abscess
• Respiratory failure
• Pulmonary embolism
• Chemical pneumonitis
• Sepsis
• Sarcoidosis
• Heart failure
• Pulmonary of thoracic malignancy

Serratia intra-abdominal infection must be differentiated from other causes of abdominal pain and fever, such as:

• Other intra-abdominal infections

• E. coli
• Streptococcus spp.
• Lactobacillus spp.
• Enterococci
• Yersinia spp.
• Klebsiella spp.
• Campylobacter spp.
• Acinetobacter spp.
• Clostridium spp.
• Proteus spp.
• Pseudomonas spp.
• Anaerobes
• Fungal infections (e.g. candidiasis, histoplasmosis, cryptococcosis, coccidiodomycosis)
• Parasitic infections (e.g. amoebiasis, giardiasis, Cryptosporidium)

• Peritonitis
• Familial Mediterranean fever
• Inflammatory bowel disease
• Celiac disease
• Meckel’s diverticulum
• Myocardial infarction
• Abdominal tumor
• Hepatitis and liver disease
• Perforated viscus
• Peritoneal cyst
• Pyelonephritis
• Splenosis
• Vasculitis (E.g. Henoch-Schonlein purpura, systemic lupus erythematosus, polyarteritis nodosa)
• Appendicitis
• Ischemic colitis
• Portal vein thrombosis or mesenteric vein thrombosis
• Abdominal abscess
• Abdominal obstruction
• Volvulus
• Intussusception
• Ileus
• Pancreatitis, pancreatic pseudocyst, pancreatic abscess, or pancreatic cancer
• Cholecystitis or cholangitis
• Diverticulitis
• Pelvic inflammatory disease
• Pregnancy
• Endometritis
• Sarcoidosis

Serratia meningitis / cerebral abscess must be differentiated from other causes of headache, fever, and altered mental status, such as:

• Encephalitis
• Delirium tremens
• Brain tumor
• Subarachnoid hemorrhage
• Ischemic stroke
• Kawasaki disease
• Measles
• Monkeypox
• Rubella
• Coxsackievirus infection
• Syphilis
• Molluscum contagiosum
• Infectious mononucleosis
• Toxic erythema
• Rat-bite fever
• Parvovirus B19 infection
• Scarlet fever
• Leptospirosis
• Subdural empyema
• Febrile seizure
• Herpes simplex infection
• VZV infection
• Listeriosis
• E. coli infection
• Streptococcal infection
• Tick-borne disease

Serratia endocarditis must be differentiated from other causes of fever, petechiae, and abnormal heart murmurs, such as:

• Other causes of infectious endocarditis

• Staphylococcus spp.
• Enterococcus
• Gram-negative bacilli
• Pseudomonas
• S. bovis
• HACEK organisms
• Chlamydia spp.
• Coxiella burnetii
• Bartonella
• Tropheryma whipplei
• Citrobacter koseri
• Neisseria bacilliformis

• Lyme disease
• Lymphoma
• Pulmonary embolism
• Drug fever
• Cotton fever
• Tuberculosis
• Candidiasis
• Aspergillosis
• Histoplasmosis
• Coccidiodomycosis
• Blastomycosis
• Sarcoidosis
• Sepsis

The annual incidence of Serratia infection is approximately 1 per 100,000 individuals. Serratia may infect individuals of all age groups, but infections in infants and young children are more common. Males are slightly more predisposed to the development of Serratia infections with a male to female ratio of 1.3 to 1.

• The annual incidence of Serratia infection is approximately 1 per 100,000 individuals.^[1]
• Approximately half of all Serratia infections are community-acquired.
• Less than 2% of all hospital-acquired infections are caused by Serratia.^[1]

• Serratia may infect individuals of all age groups.
• Serratia commonly infects infants and young children.

• Males are slightly more predisposed to the development of Serratia infections.
• The male to female ratio for Serratia infection is approximately 1.3 to 1.^[1]

Common risk factors for the development of Serratia infection include recent surgery (head, abdominal, ocular, genitourinary, or cardiac valve replacement), recent instrumentation, recent procedures (bronchoscopy, urinary catheterization), mechanical ventilation, recent trauma or burn, blood transfusions, diabetes mellitus, use of contact lenses, and IV drug use.^{[1][2][3][4][5][6]}

Risk factors for the development of Serratia infection include:^{[1][2][3][4][5][6]}

• Parenteral feeding
• Mechanical ventilation
• Bronchoscopy
• Head trauma
• Recent head, abdominal, ocular, or genitourinary surgery
• Surgical scar
• Recent burn
• Recent cellulitis, phlebitis, or other skin infection
• Cardiac valve replacement
• Blood transfusions
• Catheter placement
• Diabetes mellitus
• Urinary tract obstruction
• IV Drug use
• Use of contact lenses

Screening for Serratia infection among asymptomatic individuals is not recommended.

Screening for Serratia infection among asymptomatic individuals is not recommended.

Following transmission, approximately 30% to 50% of individuals do not develop any clinical manifestations. The incubation period of Serratia is not known, but is thought to range from several days to several weeks. Clinical manifestations of Serratia depend on the location of the colonization (e.g. respiratory tract, urinary tract, meninges, heart valves). Complications and prognosis are dependent to the site of Serratia infection.

• Following transmission, approximately 30% to 50% of individuals do not develop any clinical manifestations.
• The incubation period of Serratia is not known, but is thought to range from several days to several weeks.
• Clinical manifestations of Serratia depend on the location of the colonization (e.g. respiratory tract, urinary tract, meninges, heart valves)
• Clinical manifestations are usually non-specific and include fever and typical signs and symptoms of the clinical disease.
• If left untreated, patients with Serratia infection typically progress and develop complications.

Complications of Serratia infection depend on the clinical syndrome. Complications may include complications of the following disease:

• Complications of urinary tract infection
• Complications of pneumonia
• Complications of meningitis
• Complications of endocarditis
• Complications of skin infection

• With prompt and adequate treatment, patients with Serratia recover without any long-term sequelae.
• Prognosis of Serratia infection is generally good in urinary tract infections, pneumonia, and local wound infections.
• The prognosis is poorer when Serratia causes meningitis or endocarditis, given the prognosis of the clinical syndromes themselves.