Serratia

RANK: Genus

TAXONOMY: cellular organisms -> Bacteria -> Proteobacteria -> Gammaproteobacteria -> Enterobacteriales -> Enterobacteriaceae -> Serratia

OVERVIEW:

Serratia is a genus of Gram-negative, facultatively anaerobic, rod-shaped bacteria of the Enterobacteriaceae family. 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. odoriferae have caused diseases through infection. Members of this genus produce characteristic red pigment, prodigiosin, and can be distinguished from other members of the Enterobacteriaceae family by their unique production of three enzymes: DNase, lipase, and gelatinase. 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. Outbreaks of S. marcescens meningitis, wound infections, and arthritis have occurred in pediatric wards. Cases of Serratia arthritis have been reported in outpatients receiving intra-articular injections.

This genus contains microbial species that can reside in the human gastrointestinal tract. [PMC 4262072]

Straight rods, 0.5–0.8 × 0.9–2.0 µm in length, with rounded ends. Conform to the general definition of the family Enterobacteriaceae. Gram negative, generally motile, by means of peritrichous flagella. Facultatively anaerobic. Nitrate and chlorate are reduced anaerobically. Growth factors are generally not required. Colonies on nutrient agar are most often opaque, somewhat iridescent, and either white, pink, or red in color. Almost all strains can grow at temperatures between 10 and 36°C, at pH 5–9, and in the presence of 0–4% (w/v) NaCl. The catalase reaction is strongly positive. d-Glucose is fermented through the Embden–Meyerhof pathway. The major glucose entry route involves a phosphoenolpyruvate-dependent phosphotransferase system with both enzyme IIGlc (glucose permease) and enzyme IIMan (mannose permease). Glucose is also oxidized to gluconate in the presence of pyrroloquinoline quinone. Gluconate is oxidized to 2-ketogluconate. Acetoin is produced from pyruvate by all species except S. fonticola. Fructose, d-galactose, maltose, d-mannitol, d-mannose, ribose, and trehalose are fermented and utilized as sole carbon sources. l-fucose is fermented and utilized as sole carbon source by all species except S. fonticola. l-sorbose is not fermented or utilized as sole carbon source. All species but S. fonticola fail to ferment or utilize dulcitol and tagatose. N-acetylglucosamine, d-alanine, l-alanine, citrate, d-galacturonate, d-glucosamine, d-glucuronate, 2-ketogluconate, l-proline, putrescine, l-serine are utilized as sole carbon sources by most strains. Caprate, caproate, caprylate, and tyrosine are utilized as sole carbon sources by all species except S. fonticola. 5-Aminovalerate, butyrate, m-coumarate, ethanolamine and tryptamine are not utilized as sole carbon sources. All species except S. fonticola fail to utilize 3-phenylpropionate. All species except S. entomophila fail to utilize itaconate. Phenylalanine, histidine, and tryptophan deaminases and thiosulfate reductase (H2S from thiosulfate) are not produced. o-Nitrophenyl-β-d-galactopyranoside (ONPG) is hydrolyzed by most strains. Esculin is hydrolyzed by most strains except S. proteamaculans subsp. quinovora. Extracellular enzymes of all species except S. fonticola hydrolyze DNA, lipids (tributyrin, corn oil) and proteins (gelatin, casein), but not starch (in four days), polygalacturonic acid, or pectin. Tween-80 is hydrolyzed by all species except S. odorifera. The organisms occur in the natural environment (soil, water, plant surfaces) or as opportunistic human pathogens.

The mol % G + C of the DNA is: 52–60.

Type species: Serratia marcescens


Pathogen
Gut associated
Dysbiosis associated
Catalase producer
Microbial Abundance Data: Serratia
Percent of total population with standard deviation [PMID: 22698087]. Percentages > 1% highlighted.
Buccal
Mucosa
Keratinized
Gingiva
Hard
Palate
Throat
Tonsils
Saliva
Stool
0.000 %
(0.000)
0.000 %
(0.000)
0.000 %
(0.002)
0.001 %
(0.008)
0.000 %
(0.000)
0.001 %
(0.009)
0.000 %
(0.000)
Name
Rank
Client %
Avg %
Avg StdDev
Client StdDev
Serratia
genus
0.000
0.000
DESCENDANTS
INTERACTIONS
METABOLOMICS   
Substrates/ Growth Factors
  • Iron supplements [parent]
  • Acetoin [parent]
  • L-Fucose
  • D-Trehalose

  • Metabolic Endproducts
  • 2,3-Butanediol [parent]
  • Dopamine
  • 5-hydroxytryptamine (5-HT, Serotonin)

  • Growth Inhibited by
  • Pomegranate ellagitannins [parent]

  • Growth Enhanced By
  • Aspartame [parent]

  • Antibiotic Resistance
  • Aminoglycoside (acrb)
  • Glycylcycline (acrb)
  • Macrolide (acrb)
  • Beta lactam (acrb)
  • Acriflavin (acrb)
  • Chloramphenicol (cml_e1)
  • Chloramphenicol (cata1)
  • Paromomycin (aph3ia)
  • Neomycin (aph3ia)
  • Kanamycin (aph3ia)
  • Ribostamycin (aph3ia)
  • Lividomycin (aph3ia)
  • Gentamincin b (aph3ia)
  • Fluoroquinolone (qnrb)
  • Fosmidomycin (rosa)
  • Astromicin (aac3ia)
  • Sisomicin (aac3ia)
  • Gentamicin (aac3ia)
  • Fosmidomycin (rosb)
  • Fosfomycin (fosa)
  • Cephalosproin (bl1_sm)
  • Trimethoprim (dfra12)
  • Spectinomycin (ant3ia)
  • Streptomycin (ant3ia)
  • Tetracycline (tetc)
  • Tobramycin (aac6ib)
  • Netilmicin (aac6ib)
  • Isepamicin (aac6ib)
  • Amikacin (aac6ib)
  • Sisomicin (aac6ib)
  • Dibekacin (aac6ib)
  • Cephamycin (bl2_kpc)
  • Cephalosporin (bl2_kpc)
  • Penicillin (bl2_kpc)
  • Carbapenem (bl2_kpc)
  • Tobramycin (ant2ia)
  • Sisomicin (ant2ia)
  • Kanamycin (ant2ia)
  • Gentamicin (ant2ia)
  • Dibekacin (ant2ia)
  • Bacitracin (baca)
  • Deoxycholate (mdtg)
  • Fosfomycin (mdtg)
  • Cephalosproin (bl2f_sme1)
  • Penicillin (bl2f_sme1)
  • Carbapenem (bl2f_sme1)
  • Trimethoprim (dfra1)
  • Kasugamycin (ksga)
  • Tobramycin (aac3iib)
  • Netilmicin (aac3iib)
  • Sisomicin (aac3iib)
  • Gentamicin (aac3iib)
  • Dibekacin (aac3iib)
  • Tetracycline (tetb)
  • Cephamycin (bl3_vim)
  • Cephalosporin (bl3_vim)
  • Penicillin (bl3_vim)
  • Carbapenem (bl3_vim)
  • Monobactam (bl2be_ctxm)
  • Cephalosporin ii (bl2be_ctxm)
  • Cephalosporin iii (bl2be_ctxm)
  • Penicillin (bl2be_ctxm)
  • Cephalosporin i (bl2be_ctxm)
  • Ceftazidime (bl2be_ctxm)
  • Trimethoprim (dfra17)
  • Cloxacillin (bl2d_oxa1)
  • Penicillin (bl2d_oxa1)
  • Cephalosporin (bl2b_tem)
  • Penicillin (bl2b_tem)
  • Tobramycin (aac6ic)
  • Netilmicin (aac6ic)
  • Isepamicin (aac6ic)
  • Amikacin (aac6ic)
  • Sisomicin (aac6ic)
  • Dibekacin (aac6ic)
  • Cephalosproin (bl3_imp)
  • Cephamycin (bl3_imp)
  • Penicillin (bl3_imp)
  • Carbapenem (bl3_imp)
  • Cephalosporin ii (bl2b_tem1)
  • Penicillin (bl2b_tem1)
  • Cephalosporin i (bl2b_tem1)
  • Chloramphenicol (catb3)