Serratia infection pathophysiology: Difference between revisions

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{{CMG}}
{{CMG}}
==Overview==
==Overview==
''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 infection]]s, [[pneumonia]], [[meningitis]] and [[cerebral abscess]], [[Eye disease|ocular infection]]s, [[endocarditis]], [[osteomyelitis]], [[otitis media]], [[parotitis]], and [[sepsis]].
''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 infection]]s, [[pneumonia]], [[meningitis]] and [[cerebral abscess]], [[Eye disease|ocular infection]]s, [[endocarditis]], [[intra-abdominal infection]], [[osteomyelitis]], [[otitis media]], [[parotitis]], and [[sepsis]].


==Pathophysiology==
==Pathophysiology==
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*[[Endocarditis]]
*[[Endocarditis]]
*[[Osteomyelitis]]
*[[Osteomyelitis]]
*[[Intra-abdominal infection]]
*[[Otitis media]]
*[[Otitis media]]
*[[Parotitis]]
*[[Parotitis]]

Latest revision as of 21:45, 6 February 2016

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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.

Pathophysiology

Transmission

  • 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.

Pathogenesis

Colonization and Formation of Biofilms

  • 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]

Interference with Macrophage Function

  • 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.

Associated Diseases

Serratia is associated with the development of the following diseases:

References

  1. Pérez-Tomás R, Viñas M (2010). "New insights on the antitumoral properties of prodiginines". Curr Med Chem. 17 (21): 2222–31. PMID 20459382.
  2. Chang CC, Chen WC, Ho TF, Wu HS, Wei YH (2011). "Development of natural anti-tumor drugs by microorganisms". J Biosci Bioeng. 111 (5): 501–11. doi:10.1016/j.jbiosc.2010.12.026. PMID 21277252.
  3. Remuzgo-Martínez S, Aranzamendi-Zaldunbide M, Pilares-Ortega L, Icardo JM, Acosta F, Martínez-Martínez L; et al. (2013). "Interaction of macrophages with a cytotoxic Serratia liquefaciens human isolate". Microbes Infect. 15 (6–7): 480–90. doi:10.1016/j.micinf.2013.03.004. PMID 23524146.