**7. References**

[1] National Hospital Discharge Survey: survey results and products. Atlanta: Centers for Disease Control and Prevention; 2009 [Accessed July 24, 2009].

http://www.cdc.gov/nchs/nhds/nhds\_products.htm


Staphylococcus Infection Associated with Arthroplasty 481

[23] Kaandorp CJ, van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA. Risk

[26] Jose L. Del Pozo, M.D., Ph.D. and Robin Patel, M.D. Infection Associated with

[30] Marculescu CE, Berbari EF, Cockerill FR III, Osmon DR. Fungi, mycobacteria, zoonotic

[31] Unusual aerobic and anaerobic bacteria associated with prosthetic joint infections. Clin

[32] Berbari EF, Osmon DR, Duffy MC, et al. Outcome of prosthetic joint infection in

[33] Piper KE, Jacobson MJ, Cofield RH, et al. Microbiologic diagnosis of prosthetic shoulder

[34] Marculescu CE, Cantey JR. Polymicrobial prosthetic joint infections: risk factors and outcome. Clin Orthop Relat Res 2008;466:1397–404. [PubMed: 18421538] [35] Berbari EF, Marculescu C, Sia I, et al. Culture-negative prosthetic joint infection. Clin

[36] Peacock S.J. Moore C.E. Justice A. Kantzanou M. Story L. Mackie K. O'Neill G. Day N.P.

[38] Peacock S.J. Day N.P. Thomas M.G. Berendt A.R. Foster T.J. Clinical isolates of

[39] Bocchini C.E. Hulten K.G. Mason E.O. Gonzalez B.E. Hammerman W.A. Kaplan S.L.

osteomyelitis in children. Pediatrics 2006;117:433–440. [PubMed: 16452363] [40] Sdougkos G. Chini V. Papanastasiou D.A. Christodoulou G. Tagaris G.

Orthop Relat Res 2006;451:55–63. Idem. [PubMed: 16906072]

200 episodes. Clin Infect Dis 2006;42:216–23. [PubMed: 16355332]

[27] Bennet G.C. Bennet S.J. Infection of bone and joint. Surgery (Oxford) 2006;24:211–214. [28] Ciampolini J. Harding K.G. Pathophysiology of chronic bacterial osteomyelitis. Why do antibiotics fail so often? Postgrad. Med. J. 2000;76:479–483. [PubMed: 10908375] [29] Trampuz A, Piper KE, Jacobson MJ, et al. Sonication of removed hip and knee

[24] Shirtliff ME, Mader JT. Acute septic arthritis. Clin Microbiol Rev. 2002; 15: 527–44. [25] Udo Geipel. Pathogenic organisms in hip joint infections. International Journal of

Prosthetic Joints. N Engl J Med. 2009 August 20; 361(8): 787–794.

Arthritis Rheum. 1995; 38:1819–25.

Medical Sciences 2009; 6(5):234-240.

2006;451:64–72. [PubMed: 16906078]

Infect Dis 2007;45:1113–9. [PubMed: 17918072]

fibronectin. J. Infect. 2000;41:23–31. [PubMed: 10942636]

2005;246:81–86. [PubMed: 15869965]

17699815]

19261785]

factors for septic arthritis in patients with joint disease. A prospective study.

prostheses for diagnosis of infection. N Engl J Med 2007;357:654–63. [PubMed:

and other organisms in prosthetic joint infection. Clin Orthop Relat Res

patients with rheumatoid arthritis: the impact of medical and surgical therapy in

infection by use of implant sonication. J Clin Microbiol 2009;47:1878–84. [PubMed:

Virulent combinations of adhesin and toxin genes in natural populations of Staphylococcus aureus. Infect. Immun. 2002;70:4987–4996. [PubMed: 12183545] [37] Arciola C.R. Campoccia D. Gamberini S. Baldassarri L. Montanaro L. Prevalence of cna,

fnbA and fnbB adhesin genes among Staphylococcus aureus isolates from orthopedic infections associated to different types of implant. FEMS Microbiol. Lett.

Staphylococcus aureus exhibit diversity in fnb genes and adhesion to human

Panton-Valentine leukocidin genes are associated with enhanced inflammatory response and local disease in acute hematogenous Staphylococcus aureus

Dimitracopoulos G. Spiliopoulou I. Methicillin-resistant Staphylococcus aureus


[6] Levine M. Siegel L.B. A swollen joint: why all the fuss? Am. J. Ther. 2003;10:219–224.

[9] Blyth M.J. Kincaid R. Craigen M.A. Bennet G.C. The changing epidemiology of acute and

[10] Lazzarini L. Mader J.T. Calhoun J.H. Osteomyelitis in long bones. J. Bone Joint Surg.

[11] Gillespie W.J. Epidemiology in bone and joint infection. Infect. Dis. Clin. North Am.

[12] Jämsen E, Huhtala H, Puolakka T, Moilanen T. Risk factors for infection after knee

[13] Peersman G, Laskin R, Davis J, Peterson M. Infection in total knee replacement: a

[14] Pulido L, Ghanem E, Joshi A, Purtill JJ, Parvizi J. Periprosthetic joint infection: the

[15] Choong PF, Dowsey MM, Carr D, Daffy J, Stanley P. Risk factors associated with acute

[16] Phillips JE, Crane TP, Noy M, Elliott TS, Grimer RJ. The incidence of deep prosthetic

[17] Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and

[18] Murdoch DR, Roberts SA, Fowler VG Jr, et al. Infection of orthopedic prostheses after *Staphylococcus aureus bacteremia*. Clin Infect Dis 2001;32:647–9. [PubMed: 11181131] [19] Berbari EF, Hanssen AD, Duffy MC, et al. Risk factors for prosthetic joint infection: case-control study. Clin Infect Dis 1998;27:1247–54. [PubMed: 9827278] [20] Bongartz T, Halligan CS, Osmon DR, et al. Incidence and risk factors of prosthetic joint

[21] Dowsey MM, Choong PF. Obesity is a major risk factor for prosthetic infection after

[22] Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D. The outcome

regimen. Acta Orthop 2007;78:755– 65. [PubMed: 18236181]

Joint Surg Br 2006;88:943–8. [PubMed: 16799001]

Arthritis Rheum 2008;59:1713–20. [PubMed: 19035425]

children: is there any evidence for how long we should treat? Curr. Opin. Infect.

subacute haematogenous osteomyelitis in children. J. Bone Joint Surg. Br.

arthroplasty: a register-based analysis of 43,149 cases. J Bone Joint Surg Am

retrospective review of 6489 total knee replacements. Clin Orthop Relat Res

incidence, timing, and predisposing factors. Clin Orthop Relat Res 2008;466:1710–5.

hip prosthetic joint infections and outcome of treatment with a rifampin-based

infections in a specialist orthopaedic hospital: a 15-year prospective survey. J Bone

knee arthroplasty in the United States. J Arthroplasty 2008;23:984–91. [PubMed:

infection after total hip or knee replacement in patients with rheumatoid arthritis.

primary hip arthroplasty. Clin Orthop Relat Res 2008;466:153–8. [PubMed:

of bacterial arthritis: a prospective community-based study. Arthritis Rheum. 1997;

[7] Lew D.P. Waldvogel F.A. Osteomyelitis. Lancet 2004;364:369–379. [PubMed: 15276398] [8] Weichert S. Sharland M. Clarke N.M. Faust S.N. Acute haematogenous osteomyelitis in

[PubMed: 12756429]

2009;91:38–47.

[PubMed: 18421542]

18534466]

18196388]

40:884–92.

Dis. 2008;21:258–262. [PubMed: 18448970]

Am. 2004;86-A: 2305–2318. [PubMed: 15466746]

2001;83:99–102. [PubMed: 11245548]

1990;4:361–376. [PubMed: 2212594]

2001;392:15–23. [PubMed: 11716377]


Staphylococcus Infection Associated with Arthroplasty 483

[55] Kahlenberg J.M. Lundberg K.C. Kertesy S.B. Qu Y. Dubyak G.R. Potentiation of

[56] Ting J.P.Y. Willingham S.B. Bergstralh D.T. NLRs at the intersection of cell death and immunity. Nat. Rev. Immunol. 2008;8:372–379. [PubMed: 18362948] [57] Arend W.P. Palmer G. Gabay C. IL-1, IL-18, and IL-33 families of cytokines. Immunol.

[58] Dinarello C.A. Immunological and inflammatory functions of the interleukin-1 family.

[59] Garzoni C. Kelley W.L. Staphylococcus aureus: new evidence for intracellular

[60] Stoodley P. Nistico L. Johnson S. Lasko L.A. Baratz M. Gahlot V. Ehrlich G.D. Kathju S.

[61] Khalil H. Williams R.J. Stenbeck G. Henderson B. Meghji S. Nair S.P. Invasion of bone

[62] Mitchell G. Lamontagne C.A. Brouillette E. Grondin G. Talbot B.G. Grandbois M.

[63] Mahalingam D. Szegezdi E. Keane M. Jong S. Samali A. TRAIL receptor signalling and

[64] Reott M.A. Ritchie-Miller S.L. Anguita J. Hudson M.C. TRAIL expression is induced in

[65] von Eiff C. Peters G. Becker K. The small colony variant (SCV) concept – the role of

[66] Sendi P. Proctor R.A. Staphylococcus aureus as an intracellular pathogen: the role of small colony variants. Trends Microbiol. 2009;17:54–58. [PubMed: 19162480] [67] von Eiff C. Staphylococcus aureus small colony variants: a challenge to microbiologists and clinicians. Int. J. Antimicrob. Agents 2008;31:507–510. [PubMed: 18180148] [68] Fink B, Makowiak C, Fuerst M, Berger I, Schäfer P, Frommelt L. The value of synovial

[69] Greidanus NV, Masri BA, Garbuz DS, et al. Use of erythrocyte sedimentation rate and

Direct demonstration of viable Staphylococcus aureus biofilms in an infected total joint arthroplasty. A case report. J. Bone Joint Surg. Am. 2008;90:1751–1758.

cells by Staphylococcus epidermidis. Microbes Infect. 2007;9:460–465. [PubMed:

Malouin F. Staphylococcus aureus SigB activity promotes a strong fibronectinbacterium interaction which may sustain host tissue colonization by small-colony variants isolated from cystic fibrosis patients. Mol. Microbiol. 2008;70:1540–1555.

modulation: Are we on the right TRAIL? Cancer Treat. Rev. 2009;35:280–288.

both osteoblasts containing intracellular Staphylococcus aureus and uninfected osteoblasts in infected cultures. FEMS Microbiol. Lett. 2008;278:185–192. [PubMed:

staphylococcal SCVs in persistent infections. Injury 2006;37(Suppl. 2):S26–S33.

biopsy, joint aspiration and C-reactive protein in the diagnosis of late periprosthetic infection of total knee replacements. J Bone Joint Surg Br 2008;90:874–8. [PubMed:

C-reactive protein level to diagnose infection before revision total knee arthroplasty: a prospective evaluation.J Bone Joint Surg Am 2007;89:1409–16.

Annu. Rev. Immunol. 2009;27:519–550. [PubMed: 19302047]

persistence. Trends Microbiol. 2009;17:59–65. [PubMed: 19208480]

16301671]

[PubMed: 18676908]

[PubMed: 19007412]

[PubMed: 19117685]

[PubMed: 16651068]

[PubMed: 17606776]

17331787]

18070069]

18591595]

Rev. 2008;223:20–38. [PubMed: 18613828]

caspase-1 activation by the P2×7 receptor is dependent on TLR signals and requires NF-kappaB-driven protein synthesis. J. Immunol. 2005;175:7611–7622. [PubMed:

producing Panton–Valentine leukocidin as a cause of acute osteomyelitis in children. Clin. Microbiol. Infect. 2007;13:651–654. [PubMed: 17371535]


[42] van de Lest C.H. Vaandrager A.B. Mechanism of cell-mediated mineralization. Curr.

[43] Henriksen K. Neutzsky-Wulff A.V. Bonewald L.F. Karsdal M.A. Local communication

[44] Matsuo K. Irie N. Osteoclast–osteoblast communication. Arch. Biochem. Biophys.

[45] Vaananen H.K. Laitala-Leinonen T. Osteoclast lineage and function. Arch. Biochem.

[46] Everts V. Korper W. Hoeben K.A. Jansen I.D. Bromme D. Cleutjens K.B. Heeneman S.

[47] Boyce B.F. Xing L. Functions of RANKL/RANK/OPG in bone modeling and remodeling. Arch. Biochem. Biophys. 2008;473:139–146. [PubMed: 18395508] [48] Hikita A. Yana I. Wakeyama H. Nakamura M. Kadono Y. Oshima Y. Nakamura K. Seiki

[49] Tsezou A. Poultsides L. Kostopoulou F. Zintzaras E. Satra M. Kitsiou-Tzeli S. Malizos

[50] Jochen Schulze.Thomas Bickert.F. Timo Beil.et al. Interleukin-33 is Expressed in

[51] Garcia-Alvarez F. Navarro-Zorraquino M. Castro A. Grasa J.M. Pastor C. Monzon M.

[52] Lacey D.C. Simmons P.J. Graves S.E. Hamilton J.A. Proinflammatory cytokines inhibit

inflammation. Osteoarthritis Cartilage 2008;17:735–742. [PubMed: 19136283] [53] Lau Y.S. Wang W. Sabokbar A. Simpson H. Nair S. Henderson B. Berendt A. Athanasou

[54] Creagh E.M. O'Neill L.A. TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-

children. Clin. Microbiol. Infect. 2007;13:651–654. [PubMed: 17371535] [41] Cassat J.E. Dunman P.M. McAleese F. Murphy E. Projan S.J. Smeltzer M.S. Comparative

2005;187:576–592. [PubMed: 15629929]

2008;473:201–209. [PubMed: 18406338]

2008;15:1888–1890. [PubMed: 18971305]

Precursor Cells. Journal of Bone and Mineral Research.

Injury 2006;37(Suppl. 2):S41–S48. [PubMed: 16651071]

Biophys. 2008;473:132–138. [PubMed: 18424258]

Opin. Orthop. 2007;18:434–443.

19345750]

16939398]

[PubMed: 17018528]

658. [PubMed: 19123052]

16807108]

producing Panton–Valentine leukocidin as a cause of acute osteomyelitis in

genomics of Staphylococcus aureus musculoskeletal isolates. J. Bacteriol.

on and within bone controls bone remodeling. Bone 2009;44:1026–1033. [PubMed:

Peters C. Reinheckel T. Saftig P. Beertsen W. Osteoclastic bone degradation and the role of different cysteine proteinases and matrix metalloproteinases: differences between calvaria and long bone. J. Bone Miner. Res. 2006;21:1399–1408. [PubMed:

M. Tanaka S. Negative regulation of osteoclastogenesis by ectodomain shedding of receptor activator of NfkappaB ligand. J. Biol. Chem. 2006;281:36846–36855.

K.N. Influence of interleukin 1alpha (IL-1alpha), IL-4, and IL-6 polymorphisms on genetic susceptibility to chronic osteomyelitis. Clin. Vaccine Immunol.

Differentiated Osteoblasts and Blocks Osteoclast Formation from Bone Marrow

Martinez A. Garcia-Alvarez I. Castillo J. Lozano R. Effect of age on cytokine response in an experimental model of osteomyelitis. Biogerontology 2009;10:649–

osteogenic differentiation from stem cells: implications for bone repair during

N.A. Staphylococcus aureus capsular material promotes osteoclast formation.

operate in innate immunity. Trends Immunol. 2006;27:352–357. [PubMed:


**22** 

*Cameroun* 

**Arthroplasty in HIV/SCD Carriers** 

*University Hospitals of Yaoundé* 

J. Bahebeck, D. Handy Eone, B. Ngo Nonga and T. Kingue Njie

Due to the growing of HIV pandemic in the world and especially in Africa during the last two decades, it has become more and more frequent to find HIV infected patients with an absolute indication of arthroplasty. In fact, the indication of arthroplasty in these patients may be a very challenging issue. Even though all of these patients are not immune depressed, due to the known natural history of HIV carriage, the risk of future immune depression remain and logically the risk of immediate, early, or late infection of arthroplastic implants and subsequent loosening or worse, generalized infection. The literature on this question remains very scarce ; the first section of this chapter will present a classification of HIV carriers elected to Arthroplasty, describe protective measures for each class of patients, and present immediate , short and mid term expected results, based an a systematic analysis, and Authors own experience. The second section will be focused on arthroplasty in sickle cell disease (SCD) carriers, as these types of patients usually demand arthroplasty at the end stage of secondary vascular necrosis, the most frequent adult joint complication of their genetic condition. Lastly, as Very few, if any, is known in case where both conditions (HIV & SCD) are combined in the same patient demanding arthroplasty, a

**1. Introduction** 

short section will be proposed.

Introduction

Section A Summary

Section A: Arthroplasty in HIV carriers

Work up and classification of HIV carriers elected for arthroplasty

Prophylactic antibiotic therapy in HIV carriers undergoing arthroplasty

Due to the spreading of HIV worldwide during the latest decades, it had become more and more frequent in the orthopaedic practice, to indicate an arthroplasty, especially of the hip, in patients living with HIV. This virus has been incriminated by many authors as a possible causal agent in the case of bone's aseptic necrosis. The profiles of the HIV infected patients are variable: some are previous known carriers, other are discovered at the time of the preoperative workup. The duration of the preoperative antiretroviral treatment vary also from one patient to another. Anyhow, the main question for the orthopedic surgeon is to find out what is the level of the immune system of a person living with HIV and who is a candidate for an arthroplasty? In another words, what is the infection risk of the implant,

Antiretroviral therapy in HIV carriers demanding arthroplasty

General principles & practices of antiretroviral therapy

Pathogenesis of HIV infection

