Sandbox:septic arthritis pathogenesis: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
 
(10 intermediate revisions by the same user not shown)
Line 40: Line 40:
|-
|-
!'''Mechanism of transmission'''
!'''Mechanism of transmission'''
|'''Hematogenous spread:''' Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.<ref name="pmid3288326">Klein RS (1988) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3288326 Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection.] ''Clin Geriatr Med'' 4 (2):375-94. PMID: [https://pubmed.gov/3288326 3288326]</ref> Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.
|                                                                                                                   '''Hematogenous spread:''' Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.<ref name="pmid3288326">Klein RS (1988) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3288326 Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection.] ''Clin Geriatr Med'' 4 (2):375-94. PMID: [https://pubmed.gov/3288326 3288326]</ref> Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.
 
Determinants of hematognous seeding:<ref name="pmid3288326" />  
Determinants of hematognous seeding:<ref name="pmid3288326" />  
* Well vascularized synovium
* Well vascularized synovium
Line 81: Line 80:
!
!
|-
|-
|align=center|Humoral immunity and adaptive immunity also activates by superantigens of pathogens and promote clearance of pathogen by releasing Interferon-gamma, IL-4, IL-10 that reduces the host mortality and joint destruction.
|Humoral immunity and adaptive immunity also activates by superantigens of pathogens and promote clearance of pathogen by releasing Interferon-gamma, IL-4, IL-10 that reduces the host mortality and joint destruction.<ref name="pmid10458752">Hultgren O, Kopf M, Tarkowski A (1999) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10458752 Outcome of Staphylococcus aureus-triggered sepsis and arthritis in IL-4-deficient mice depends on the genetic background of the host.] ''Eur J Immunol'' 29 (8):2400-5. PMID: [https://pubmed.gov/10458752 10458752]</ref><ref name="pmid11145025">Puliti M, von Hunolstein C, Bistoni F, Mosci P, Orefici G, Tissi L (2000) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11145025 Influence of interferon-gamma administration on the severity of experimental group B streptococcal arthritis.] ''Arthritis Rheum'' 43 (12):2678-86. [http://dx.doi.org/10.1002/1529-0131(200012)43:12<2678::AID-ANR7>3.0.CO;2-A DOI:10.1002/1529-0131(200012)43:12<2678::AID-ANR7>3.0.CO;2-A] PMID: [https://pubmed.gov/11145025 11145025]</ref>
!
!
|-
! rowspan="2" |Joint destruction
|As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immunosystem is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction.
|-
|align=center|Potent activation of immune system and release of cytokines and oxygen free radicles<ref name="pmid1111494">Roy S, Bhawan J (1975) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=1111494 Ultrastructure of articular cartilage in pyogenic arthritis.] ''Arch Pathol'' 99 (1):44-7. PMID: [https://pubmed.gov/1111494 1111494]</ref>
'''⬇'''
Activation and release of
Metalloproteinases, Lysosomal enzyames and proteolytic enzymes from lysosomes, neutrophils and other inflammatory cells<ref name="pmid2929280">Riegels-Nielsen P, Frimodt-Møller N, Sørensen M, Jensen JS (1989) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=2929280 Antibiotic treatment insufficient for established septic arthritis. Staphylococcus aureus experiments in rabbits.] ''Acta Orthop Scand'' 60 (1):113-5. PMID: [https://pubmed.gov/2929280 2929280]</ref>
'''⬇'''
Further damage of joint by bacterial toxins<ref name="pmid3654698">Smith RL, Schurman DJ, Kajiyama G, Mell M, Gilkerson E (1987) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3654698 The effect of antibiotics on the destruction of cartilage in experimental infectious arthritis.] ''J Bone Joint Surg Am'' 69 (7):1063-8. PMID: [https://pubmed.gov/3654698 3654698]</ref>
'''⬇'''
Infectious process and inflammatory response lead to joint effusion<ref name="pmid3051098">Mitchell M, Howard B, Haller J, Sartoris DJ, Resnick D (1988) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3051098 Septic arthritis.] ''Radiol Clin North Am'' 26 (6):1295-313. PMID: [https://pubmed.gov/3051098 3051098]</ref><ref name="pmid5297142">Nelson JD, Koontz WC (1966) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=5297142 Septic arthritis in infants and children: a review of 117 cases.] ''Pediatrics'' 38 (6):966-71. PMID: [https://pubmed.gov/5297142 5297142]</ref><ref name="pmid6749955">Knights EM (1982) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=6749955 Infectious arthritis.] ''J Foot Surg'' 21 (3):229-33. PMID: [https://pubmed.gov/6749955 6749955]</ref>
'''⬇'''
Increased intra-articular pressure
'''⬇'''
Mechanical obstruction to the joint blood supply
'''⬇'''
Further destruction of bone and cartilage
|}
|}


==References==
==References==

Latest revision as of 16:06, 16 January 2017

Pathophysiology

Presence of extreme vasularity and absence of limiting of basement membrane, promotes the easy access of infections into the synovial space.[1]

Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[2] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties and contiguous osteomyelitis rupturing into the joint.[3][4]

Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. This kind of spread is more common in children as the small capillaries can cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space.[5][6]

Pathogenesis of septic arthritis depends on multiple factors and it mainly depends on the balance between virulence of the microbial pathogen and the host immune response against the pathogen.

Non-gonococcal arthritis

Staph. aureus is the most common pathogen non gonococcal pathogen that causes septic arthritis. The pathogenesis of septic arthritis by staphylococcus can be a better representation for pathogenesis of most non gonococcal arthritis.

Bacterial colonization and adherence into the synovium

Mechanism of infection transmission

Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[2] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Determinants of hematognous seeding:[2]

  • Well vascularized synovium
  • Absence of limiting basement membrne
  • Recent joint surgery, induces the production of host-derived extracellular matrix proteins( e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection
  • Virulence of microorganism
  • Susceptibility of synovial membrane for microorganism

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[3][4]

Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.

Role of bacterial products in pathogenesis

Non-gonococcal arthritis

Bacterial colonization and adherence into the synovium
⬇
Mechanism of transmission Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[2] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Determinants of hematognous seeding:[2]

  • Well vascularized synovium
  • Absence of limiting basement membrne
  • Recent joint surgery, induces the production of host-derived extracellular matrix proteins( e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection
  • Virulence of microorganism
  • Susceptibility of synovial membrane for microorganism

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[3][4]

Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.

Role of bacterial products in pathogenesis Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process.[7][8] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction.[9]
Escape mechanism developed by pathogen Adherence of pathogen to fibronectin on host tissue with its fibronectin receptors[10]
⬇

Internalization of pathogen by host mechanisms such as pseudopod formation or through receptor-mediated endocytosis via clathrin-coated pits[11]
⬇

After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response[12]

Host immune response Due to rapid proliferation of bacteria predesposes to activation of host acute inflammatory response

⬇

Synovial cells releases host inflammatory cytokines such as IL-1 and IL-6 into the synovium[13]

⬇

Activation of acute phase reactants by Interleukins[14]

⬇

Acute phase reactants bind to pathogen and promote opsonization and phagocytosis and activates complement system[15]

⬇

Phagocytosis of pathogen by macrophages, synovial cells and neutrophils with the release of inflammatory cytokines such as tumor necrosis factor, IL-6 and nitric oxide.[16]

Humoral immunity and adaptive immunity also activates by superantigens of pathogens and promote clearance of pathogen by releasing Interferon-gamma, IL-4, IL-10 that reduces the host mortality and joint destruction.[17][18]
Joint destruction As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immunosystem is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction.
Potent activation of immune system and release of cytokines and oxygen free radicles[19]

⬇

Activation and release of

Metalloproteinases, Lysosomal enzyames and proteolytic enzymes from lysosomes, neutrophils and other inflammatory cells[20]

⬇

Further damage of joint by bacterial toxins[21]

⬇

Infectious process and inflammatory response lead to joint effusion[22][23][24]

⬇

Increased intra-articular pressure

⬇

Mechanical obstruction to the joint blood supply

⬇

Further destruction of bone and cartilage

References

  1. ↑ Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Klein RS (1988) Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection. Clin Geriatr Med 4 (2):375-94. PMID: 3288326
  3. ↑ 3.0 3.1 3.2 Atcheson SG, Ward JR (1978) Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway. Arthritis Rheum 21 (8):968-71. PMID: 737020
  4. ↑ 4.0 4.1 4.2 Gray RG, Tenenbaum J, Gottlieb NL (1981) Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum 10 (4):231-54. PMID: 6787706
  5. ↑ Barton LL, Dunkle LM, Habib FH (1987) Septic arthritis in childhood. A 13-year review. Am J Dis Child 141 (8):898-900. PMID: 3498362
  6. ↑ Buckholz JM (1987) The surgical management of osteomyelitis: with special reference to a surgical classification. J Foot Surg 26 (1 Suppl):S17-24. PMID: 3559051
  7. ↑ Herrmann M, Vaudaux PE, Pittet D, Auckenthaler R, Lew PD, Schumacher-Perdreau F et al. (1988) Fibronectin, fibrinogen, and laminin act as mediators of adherence of clinical staphylococcal isolates to foreign material. J Infect Dis 158 (4):693-701. PMID: 3171224
  8. ↑ Rydén C, Tung HS, Nikolaev V, Engström A, Oldberg A (1997) Staphylococcus aureus causing osteomyelitis binds to a nonapeptide sequence in bone sialoprotein. Biochem J 327 ( Pt 3) ():825-9. PMID: 9581562
  9. ↑ Yacoub A, Lindahl P, Rubin K, Wendel M, Heinegård D, Rydén C (1994) Purification of a bone sialoprotein-binding protein from Staphylococcus aureus. Eur J Biochem 222 (3):919-25. PMID: 8026501
  10. ↑ Lammers A, Nuijten PJ, Smith HE (1999) The fibronectin binding proteins of Staphylococcus aureus are required for adhesion to and invasion of bovine mammary gland cells. FEMS Microbiol Lett 180 (1):103-9. PMID: 10547450
  11. ↑ Essawi T, Na'was T, Hawwari A, Wadi S, Doudin A, Fattom AI (1998) Molecular, antibiogram and serological typing of Staphylococcus aureus isolates recovered from Al-Makased Hospital in East Jerusalem. Trop Med Int Health 3 (7):576-83. PMID: 9705193
  12. ↑ Ram S, Mackinnon FG, Gulati S, McQuillen DP, Vogel U, Frosch M et al. (1999) The contrasting mechanisms of serum resistance of Neisseria gonorrhoeae and group B Neisseria meningitidis. Mol Immunol 36 (13-14):915-28. PMID: 10698346
  13. ↑ Koch B, Lemmermeier P, Gause A, v Wilmowsky H, Heisel J, Pfreundschuh M (1996) Demonstration of interleukin-1beta and interleukin-6 in cells of synovial fluids by flow cytometry. Eur J Med Res 1 (5):244-8. PMID: 9374445
  14. ↑ Osiri M, Ruxrungtham K, Nookhai S, Ohmoto Y, Deesomchok U (1998) IL-1beta, IL-6 and TNF-alpha in synovial fluid of patients with non-gonococcal septic arthritis. Asian Pac J Allergy Immunol 16 (4):155-60. PMID: 10219896
  15. ↑ Verdrengh M, Tarkowski A (1998) Granulocyte-macrophage colony-stimulating factor in Staphylococcus aureus-induced arthritis. Infect Immun 66 (2):853-5. PMID: 9453655
  16. ↑ Sakiniene E, Bremell T, Tarkowski A (1997) Inhibition of nitric oxide synthase (NOS) aggravates Staphylococcus aureus septicaemia and septic arthritis. Clin Exp Immunol 110 (3):370-7. PMID: 9409638
  17. ↑ Hultgren O, Kopf M, Tarkowski A (1999) Outcome of Staphylococcus aureus-triggered sepsis and arthritis in IL-4-deficient mice depends on the genetic background of the host. Eur J Immunol 29 (8):2400-5. PMID: 10458752
  18. ↑ Puliti M, von Hunolstein C, Bistoni F, Mosci P, Orefici G, Tissi L (2000) Influence of interferon-gamma administration on the severity of experimental group B streptococcal arthritis. Arthritis Rheum 43 (12):2678-86. <2678::AID-ANR7>3.0.CO;2-A DOI:10.1002/1529-0131(200012)43:12<2678::AID-ANR7>3.0.CO;2-A PMID: 11145025
  19. ↑ Roy S, Bhawan J (1975) Ultrastructure of articular cartilage in pyogenic arthritis. Arch Pathol 99 (1):44-7. PMID: 1111494
  20. ↑ Riegels-Nielsen P, Frimodt-Møller N, Sørensen M, Jensen JS (1989) Antibiotic treatment insufficient for established septic arthritis. Staphylococcus aureus experiments in rabbits. Acta Orthop Scand 60 (1):113-5. PMID: 2929280
  21. ↑ Smith RL, Schurman DJ, Kajiyama G, Mell M, Gilkerson E (1987) The effect of antibiotics on the destruction of cartilage in experimental infectious arthritis. J Bone Joint Surg Am 69 (7):1063-8. PMID: 3654698
  22. ↑ Mitchell M, Howard B, Haller J, Sartoris DJ, Resnick D (1988) Septic arthritis. Radiol Clin North Am 26 (6):1295-313. PMID: 3051098
  23. ↑ Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
  24. ↑ Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955
Retrieved from "https://www.wikidoc.org/index.php?title=Sandbox:septic_arthritis_pathogenesis&oldid=1283432"