Serratia marcescens- An Overview

Since the 1990s, Serratia marcescens, a gram-negative bacillus categorized as an Enterobacteriaceae member, has been known to cause infections acquired in hospitals. Serratia spp. are gram-negative, motile rods without endospores. In nature, S. marcescens is widely distributed.

  • While this organism has been known by several names in the past, including Chromobacterium prodigiosum, it was previously known by the name S. marcescens, which Bizio gave in 1823.
  • Because environmental isolates of S. marcescens typically produce the red pigment prodigiosin, this growth was once frequently mistaken for new blood.
  •  Because of its distinctive red colonies, S. marcescens was once thought to be a benign, non-pathogenic saprophytic water organism frequently used as a biological marker. 
  • Professor Scheurlen of the University of Strasbourg concluded that this organism caused more deaths than many pathogenic bacteria after reviewing a small sample of incidents in 1896. 
  • S. marcescens has now been linked to every imaginable type of infection, including respiratory tract infections, urinary tract infections (UTI), septicemia, meningitis, and wound infections. Its ability to cause infection was once restricted to patients with chronic disabling disorders.

Classification of Serratia marcescens

  • Serratia marcescens belongs to the family Enterobacteriaceae and the genus Serratia.
  •  Within the genus Serratia, there are currently 14 recognized species, eight of which are linked to human infection.
  • The most well-known of the eight species linked to clinical infection are S. marcescens, S. liquefaciens, and S. odorifera.
  • S. marcescens is the most prevalent clinical isolate and significant human pathogen among all Serratia species.
KingdomBacteria
SubkingdomNegibacteria
PhylumProteobacteria
ClassGammaproteobacteria
OrderEnterobacterales
FamilyEnterobacteriaceae
GenusSerratia
SpeciesS. marcescens

Habitat of Serratia marcescens

  • It is a common saprophytic bacterium discovered in food, especially in starchy varieties that offer a favorable growth environment. 
  • This bacteria can be found on plants, insects, vertebral gastrointestinal tracts, and water and soil surfaces.

Serratia marcescens Morphology

  • Microscopically, S. marcescens is a bacillus that measures between 0.5 μm to 0.8 μm in width and 0.9 μm to 2.0 μm in length and has rounded ends. Peritrichous flagella are present, and they are typically moving.
  • Macroscopically, at 24 hours of incubation at 37°C, S. marcescens colonies measure between 1.5 and 2.0 mm in size, are opaque, frequently have a reddish or pink hue due to the production of pigment, and have a distinctive odor (similar to urine) linked to the production of ammonia or trimethylamine. Certain strains result in non-pigmented colonies, which are typically whitish or grayish.
Serratia marcescens
Figure: Serratia marcescens. Image Source: Benutzer:Brudersohn and University of Iowa.

Cultural Characteristics of Serratia marcescens

The ability of S. marcescens to thrive and grow in harsh environments, such as disinfectant antiseptics and double-distilled water, clearly demonstrates its potential to utilize a variety of nutrients. It can grow in temperatures as low as 5°C and as high as 40°C, but it grows best at 37°C. It is well known for the prodigiosin, a red pigment that it produces. It is created at a temperature below 30°C and is composed of three pyrole rings.

1) Serratia marcescens on MacConkey agar

  • On MacConkey agar, convex, effuse, colorless colonies with irregular cremated edges developed, which became pink after 48 hours- a late lactose fermenter.  

2) Serratia marcescens on Blood agar

  • On blood agar, convex, raised, grayish colonies with a narrow zone of hemolysis were seen. 

3) Serratia marcescens on Chocolate agar

  • Large and gray colonies were seen. 

Biochemical Characteristics of Serratia marcescens

The Biochemical characteristics of S. marcescens are tabulated as follows:

Basic Characteristics

S.N.CharacteristicsS. marcescens
1.Gram stainingGram-negative (-ve)
2.CapsuleNon-capsulated
3.ShapeRods
4.CatalasePositive (+)
5.CitratePositive (+)
6.Triple sugar iron(TSI)K/A, no H2S
7.IndoleNegative (-)
8.UreaseNegative (-)
9.OxidaseNegative (-)
10.Nitrate Positive (+)
11.H2SNegative (-)
12.MotilityPositive (+)
13.VP (Voges Proskauer)Negative (-)
14.Spore Negative (-)

Fermentation of

S.N.CharacteristicsS. marcescens
1.GlucosePositive (+)
2.SucrosePositive (+)
3.MannitolPositive (+)
4.FructosePositive (+)
5.DNasePositive (+)
6.GlycerolPositive (+)
7.XyloseNegative (-)
8.LactoseNegative (-)
9.ArabionioseNegative (-)
10.RaffinoseNegative (-)
11.D-dulcitolNegative (-)
12.D-sorbitolPositive (+)

Enzymatic reactions

S.N.CharacteristicsS. marcescens
1.Lysine decarboxylasePositive (+)
2.Ornithine decarboxylase Positive (+)
3.Arginine dehydrolaseNegative (-)
4.LipasePositive (+)
5.GelatinasePositive (+)

Virulence Factors of Serratia marcescens

S. marcescens exhibits various virulence traits, including the production of hemolysin, biofilm, and swarming. Some of these virulence factors give it the ability to suppress the immune response, boost antibiotic resistance, and survive in hostile environments and on surfaces of medical equipment.

  1. Hemolysin production
  • Hemolysin (ShlA), cytotoxic to fibroblasts, epithelial cells, and red blood cells, has been identified as the primary virulence factor for S. marcescens
  • ShIA aids in the production of leukotriene and histamine, which increases vascular permeability and contributes to granulocyte accumulation, edema formation, and other symptoms of bacterial infections.
  • The ShlB gene product controls ShlA export (belonging to the Omp85 subfamily).
  1. Lipopolysaccharides
  • The biological activity of endotoxin is mediated by lipopolysaccharide (LPS), which is found in the outer membrane of gram-negative bacteria. 
  • LPS O-polysaccharides may increase a bacterium’s virulence by allowing it to withstand serum killing. By slowing their penetration and preventing their access to the target site, it defends the cell from toxic agents. 
  • Since this species has more than 24 somatic antigens, the structure of LPS in S. marcescens is variable.
  1. Extracellular products
  • Among enteric bacteria, S. marcescens is exceptional in several ways. It also secretes several proteases, a nuclease, a lipase, extracellular chitinase, and serrawettin, a wetting agent or surfactant that aids in the colonization of surfaces. 
  • S. marcescens produces different types of differentially flagellate cells, and these exhibit various forms of motility depending on whether the growth medium is liquid or solid, in keeping with its diverse habitat. 
  • S. marcescens non-flagellate cells can effectively move across the surface of low-agar media as well.

Pathogenesis of Serratia marcescens

The emerging multidrug-resistant pathogen S. marcescens has the potential to produce a variety of clinical forms. As a significant nosocomial pathogen that primarily affects patients from intensive care units, it has been identified as a critical priority for developing new antibiotics due to its alarming rise in antimicrobial resistance. Different virulence factors that this Enterobacterium possesses enable it to colonize and persist on surfaces, including catheters and medical devices, evade the immune response, and quickly develop antibiotic resistance.

1. Attachment/adherence

  • It has been demonstrated that piliation influences microbial adherence to host epithelial surfaces. S. marcescens has pili, adheres to uroepithelial cells, and causes nosocomial UTI. 
  • There have been proposed to be two classes of adhesins. Mannose-sensitive (MS) pili exhibit mannose-sensitive haemagglutination of guinea pig and chicken erythrocytes, while mannose-resistant (MR) pili agglutinate chicken erythrocytes in the presence of D-mannose. 
  • A human urinary tract isolate of S. marcescens strain US46 appeared to have both Ml2 and MS pili. According to this research, PMNLs are stimulated by MS-piliated bacteria to produce active oxygen radicals, which cause tissue damage in the infected organ.

2. Biofilm formation

  • When bacteria congregate and adhere to a surface, biofilms are created. They can communicate with one another via quorum sensing when they are aggregated together. 
  • A multicellular behavior called biofilm formation enables bacteria to survive in hostile environments and to be resistant to several antimicrobial substances. 
  • The development of biofilms in S. marcescens goes through five stages: initial attachment to a surface, exopolysaccharide production, formation of the biofilm’s initial structure, maturation, and distribution of cells. The development of biofilms aids in the development of chronic infections.

Clinical Manifestations of Serratia marcescens

Serratia marcescens, once considered a benign saprophyte, is now recognized as a significant opportunistic pathogen with a tendency for healthcare-associated infections and antimicrobial resistance. Patients who suffer from debilitating illnesses, those taking broad-spectrum antibiotics, and those receiving intensive care and using devices like tracheostomy tubes or indwelling catheters are most at risk. Contaminated antiseptics and disinfectants have been linked to infections.

1. Respiratory tract infection

  • Up to 80% of postoperative patients who develop S. marcescens bacteremia have S. marcescens isolated from their respiratory tracts, demonstrating the importance of the respiratory tract as a major portal of entry.

2. Urinary tract infection (UTI)

  • Infected catheters generally cause UTIs. Serratia urinary tract infections affect between 30 and 50 percent of patients without any symptoms. Fever, frequent urination, dysuria, pyuria, and pain while urinating are just a few of the symptoms that may appear.

3. Bloodstream infection

  • Fortunately, S. marcescens contamination of donor blood or blood components is a rare side effect of blood transfusion, but it has been documented frequently for decades. 
  • Transfusion-associated complications frequently present as septic or endotoxic shock. 
  • Serratia bacteria can enter the bloodstream and lead to endocarditis, bacteremia, meningitis, osteomyelitis, and arthritis.

4. Wound infection

  • Due to its high mobility, S. marcescens can spread easily from a caregiver’s hands to an exposed catheter or an open wound.

5. Endocarditis

  • Endocarditis can also very rarely be caused by S. marcescens. It was the most typical cause of Gram-negative endocarditis in intravenous drug addicts during the 1970s.

Lab Diagnosis of Serratia marcescens

1. Morphological and biochemical characteristics

  • Serratia is routinely isolated in the lab from respiratory and urinary sites using selective culture techniques or from the bloodstream and wound sites using blood agar culture. 
  • MacConkey agar, which groups Serratia isolates with the other non-lactose fermenting Enterobacteriaceae, and chromogenic agars, which group them into the broad Klebsiella, Enterobacter, Serratia, and Citrobacter (KESC) grouping, are two examples of common selective agar cultures.
  • At 37°C, it was grown aerobically. Turbidity started to appear on the fifth day, and the inoculum was subcultured on MacConkey and blood agar and incubated aerobically for 24 hours at 37°C. 
  • Then, the colony is observed. Also, different biochemical tests are performed for the differentiation of the species.

2. Automated system/Molecular diagnosis

  • Various methods and platforms are currently available for identifying this organism, including automated tools like Vitek and MicroScan1. 
  • In addition, spectroscopic methods like MALDI-TOF have been developed, and 16S rRNA gene sequencing is used at the molecular level. These two most recent methods enable effective differentiation between Serratia species.

Treatment of Serratia marcescens

  • Due to resistance to numerous antibiotics, including ampicillin and first and second-generation cephalosporins, S. marcescens infections may be challenging to treat. 
  • Although aminoglycosides effectively combat S. marcescens, resistant strains have also recently been discovered. 
  • The length of time the bacteria are exposed to antibiotic concentrations above the MIC is an important parameter when assessing the likely clinical outcome because the killing effect of beta-lactam antibiotics is time-dependent.
  • According to data from a rabbit model, when an aminoglycoside and a beta-lactam antibiotic are combined, the aminoglycoside induces rapid killing and a reduction in the inoculum. In contrast, the beta-lactam antibiotic prevents regrowth in between doses of the aminoglycoside.

Prevention of Serratia marcescens

  • Opportunities for infection control depend not only on the prudent use of antibiotics but also on the implementation of efficient infection control policies in light of the ongoing evidence of S. marcescens healthcare-associated infection.
  • The infection-control team should get involved to stop the spread within the hospital if there is a noticeable increase in the incidence of S. marcescens infections, especially when multi-resistant strains are isolated. 
  • Hand hygiene is crucial in infection control, so whenever S. marcescens is found, all healthcare workers should be reminded of this.
  • It may also be advisable to place patients in specific rooms or units to limit staff contact with non-infected patients while taking isolation precautions into account. 
  • The most effective means of preventing S. marcescens is to wash your hands thoroughly and correctly.

S. marcescens and research on cancer

According to recent research, a new prodigiosin called MAMPDM ((2,2’-[3-methoxyl-1’amyl-5’-methyl-4-(1”-pyrryl))dipyrrylmethene)), which is produced by the Serratia marcescens ost3 strain, may have a significant effect on the treatment of cancer. This red pigment revealed reduced toxicity to non-malignant cells but a selective cytotoxic activity in cancer cell lines. They concluded that Serratia could potentially be used as a source to create an anti-cancer compound in the future.

References 

  1. HEJAZI, A., & FALKINER, F. R. (1997). Serratia marcescens. Journal of Medical Microbiology, 46(11), 903–912. doi:10.1099/00222615-46-11-903
  2. Microbiologist, Freelance clinical. Serratia Marcescens. www.slideshare.net, 1 Mar. 2001, https://www.slideshare.net/doctorrao/serratia-marcescens.
  3. Pathology Outlines – Serratia species. (2022, March 10). www.pathologyoutlines.com. https://www.pathologyoutlines.com/topic/microbiologyserratiaspecies.html
  4. Paul, D., Bhattacharyya, I., Chakraborty, M., Das, P., & Ghosh, S. Das. (2014). A RED ALERT! NOSOCOMIAL INFECTION BY SERRATIA MARCESCENS. Journal of Evolution of Medical and Dental Sciences. https://doi.org/10.14260/jemds/2014/3546
  5. Pinna A, Usai D, Sechi LA, Carta A, Zanetti S. Detection of virulence factors in 
  6. Serratia strains isolated from contact lens-associated corneal ulcers. Acta Ophthalmol. 2011;89:382-7.
  7. Serratia Marcescens – Infectious Disease and Antimicrobial Agents. www.antimicrobe.org,http://www.antimicrobe.org/b26.asp#:~:text=CLINICAL%20MANIFESTATIONS,meningitis%20(72%2C%2074). Accessed 24 Aug. 2022.
  8. Your LH, Ou JT, Leu HS, etal. Extended epidemic of nosocomial urinary tract infections caused by Serratia marcescens. J Clin Microbiol. 2003; 41:4726-32.

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