S. marcescens: Introduction, Classification, Pathogenecityl, Lab Diagnosis

S. marcescens: Introduction, Classification, Pathogenecityl, Lab Diagnosis, Treatment, Prevention and Keynotes

Introduction of S. marcescens

Serratia is a genus of Gram-negative, facultatively anaerobic, rod-shaped lacking spores and capsules bacteria of the family, Enterobacteriaceae. This is a Gram-negative rod/ bacilli that thrive in moist environments. It frequently contaminates solutions and hospital equipment and the human reservoirs are the urinary and respiratory tracts as well as the gastrointestinal tract of children. The genus is named after SerafinoSerrati, an Italian physicist. 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, andBizio chose marcescens (from the Latin word for decaying) because of the bloody pigment was found to deteriorate quickly.

Scientific classification of S. marcescens

Kingdom: Bacteria

Phylum: Proteobacteria

Class: Gamma Proteobacteria

Order: Enterobacteriales

Family: Enterobacteriaceae

Genus: Serratia

Species: S. marcescens

Pathogenicity of Serratia

The mode of transmission organism is usually transmitted from person to person via the hands of health care workers (HCWs) or from environmental reservoirs to patients. The most common species in the genus, S. marcescens, is normally the only pathogen and usually causes nosocomial infections. However, rare strains of S. plymuthica,S. liquefaciens, S. rubidaea, and S. odoriferous have caused diseases through infection. In the hospital, S. 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. Outbreaks of S. marcescens meningitis wound infections, and arthritis has 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. In a population-based study of Serratia bacteremia, the 7-day, and 6-month mortality rates were 5% and 37%, respectively. Meningitis and endocarditis causing by this etiological agent, carry a high mortality rate. S. species cause less than 6% of cases of hospital-acquired bacterial pneumonia. S . marcescens causes 11% of burn-related surgical wound infections.

Laboratory Diagnosis of S. marcescens

Gram Stain: Gram-negative rods without evidence of capsule and spores

Catalase test: Positive

Oxidase test: Negative

Oxidation-Fermentation Test: Facultative Anaerobes

Methyl Red (MR) Test: Negative

Voges-Proskauer (VP ) Test: Positive

Triple sugar iron agar test: Hydrogen sulfide production negative, gas formation (variable), and acid slat with acid butt due to fermenting sucrose

SIM test: Hydrogen sulfide production negative, Indole negative, and motile

Citrate utilization test: Positive

Urease test: Positive

DNase test: Positive

Lipase test: Positive

Gelatinase test: Positive

Growth: It can easily grow on nutrient agar, MacConkey medium, and blood agar. Pigmentation is best expressed on nutrient agar incubating at room temperature.

Molecular Assay:

Small subunit ribosomal RNA (16S rRNA) gene sequence

DNA: DNA hybridization

gyrB-based phylogeny

Treatment of S. marcescens

S. marcescens is intrinsic resistant to ampicillin, macrolides, and first-generation cephalosporins. It is also a common ESBL (Extended-spectrum beta-lactamase) producer and therefore its causing 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; however, reports indicate increasing resistance to gentamicin and tobramycin. Even in Taiwan, 92% of the strains are resistant to third-generation cephalosporin, cefotaxime, yet 99% are still susceptible to ceftazidime.

Epidemiology

The yearly incidence of Serratia bacteremia is 1.03 per 100,000 population, with 47% of episodes having their onset in the community. The prevalence of S. species as a cause of nosocomial infections is diminishing, but these bacteria are still able to cause hospital outbreaks, especially in intensive care units. Outbreaks of Serratia infection occur in neonates and infants. In adults, most Serratia infections are isolated, but occasional nosocomial outbreaks occur.

Keynotes on Serratia

The pigment of Serratia marcescens: Serratia has a good feature forming a pink, red, or magenta, a non-diffusible pigment called prodigiosin. Pigment expresses optimally at room temperature whereas no pigmentation at 37°C. Members of this genus produce characteristic pigment, prodigiosin, and can be distinguished from other members of the Enterobacteriaceae by its unique production of three enzymes-DNase, lipase, and gelatinase.
Derivatives of prodigiosin have recently been found to have immunosuppressive properties and antitumor activity in vivo.
They are responsible for the significant cause of healthcare-associated pulmonary, urinary, and surgical site infections.
Only S. marcescens and S. rubidaea fail to grow at 4 °C.
A Serratia strain with strong biofilm-forming capacity has been conformed by Houdt R V et al.

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