RT Book, Section
A1 Madoff, Lawrence C.
A2 Jameson, J. Larry
A2 Fauci, Anthony S.
A2 Kasper, Dennis L.
A2 Hauser, Stephen L.
A2 Longo, Dan L.
A2 Loscalzo, Joseph
SR Print(0)
ID 1177742353
T1 Acute Bacterial Arthritis
T2 Harrison's Principles of Internal Medicine, 20e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259644016
LK accesspharmacy.mhmedical.com/content.aspx?aid=1177742353
RD 2024/04/23
AB Bacteria  enter  the  joint  from  the  bloodstream;  from  a  contiguous  site  of  infection  in  bone  or  soft  tissue;  or  by  direct  inoculation  during  surgery,  injection,  animal  or  human  bite,  or  trauma.  In  hematogenous  infection,  bacteria  escape  from  synovial  capillaries,  which  have  no  limiting  basement  membrane,  and  within  hours  provoke  neutrophilic  infiltration  of  the  synovium.  Neutrophils  and  bacteria  enter  the  joint  space;  later,  bacteria  adhere  to  articular  cartilage.  Degradation  of  cartilage  begins  within  48  h  as  a  result  of  increased  intraarticular  pressure,  release  of  proteases  and  cytokines  from  chondrocytes  and  synovial  macrophages,  and  invasion  of  the  cartilage  by  bacteria  and  inflammatory  cells.  Histologic  studies  reveal  bacteria  lining  the  synovium  and  cartilage  as  well  as  abscesses  extending  into  the  synovium,  cartilage,  and—in  severe  cases—subchondral  bone.  Synovial  proliferation  results  in  the  formation  of  a  pannus  over  the  cartilage,  and  thrombosis  of  inflamed  synovial  vessels  develops.  Bacterial  factors  that  appear  important  in  the  pathogenesis  of  infective  arthritis  include  various  surface-associated  adhesins  in  S.  aureus  that  permit  adherence  to  cartilage  and  endotoxins  that  promote  chondrocyte-mediated  breakdown  of  cartilage.