Management of prosthetic joint infection (PJI) remains a therapeutic challenge. We retrospectively studied 69 infected total hip or knee arthroplasties managed between 1980 and 1996 in our institution. Treatment failure, defined as relapse of PJI in the first year following the last antimicrobial treatment, occurred for 14 patients (20.3%). None of the potentially contributive parameters analyzed was significantly predictive of treatment failure. Of the subgroup of 34 patients with PJI who initially underwent debridement with retention of the prosthesis, the 13 (38.2%) who did not require further surgical treatment had symptoms for a significantly shorter duration before debridement (4.85 vs. 54.24 days; P < .0001). Because debridement with retention of the prosthesis rarely enables control of PJI, this therapeutic approach should be considered only when the duration of symptoms is very short.
Antimicrobials have been used successfully for over 6 decades, but genes expressing resistance to them have emerged in strains of bacteria and have disseminated through the global ecosystem to reach infecting microorganisms, produce disease, and seriously interfere with therapy, allowing infections to progress and kill despite antibiotic administration. The upsurge in prevalence of such resistance genes in the bacterial population that colonize and infect humans involves two processes, emergence and dissemination, in both of which there have been contributions from the developing world, where resistance is common and increasing. The emergence of pneumococcal isolates noted in Papua New Guinea and later in South Africa that 1 decade later spread to most of the world and the intercontinental spread between the United States and Venezuela of a new gentamicin resistance gene carried on an epidemic plasmid are examples of the ability of bacteria to travel freely, without regard to borders. Complex societal issues such as the misuse of antibiotics by physicians, pharmacists, and the public; the suboptimal quality of the drugs (emergence); and conditions such as crowding, lack of hygiene, poor or nonexistent hospital infection control practices, or insufficient surveillance (dissemination) play a largely unmeasured role that requires study and solutions. In the meantime, we may intervene to delay the emergence of resistance and to limit its spread by promoting the judicious use of antibiotics both at the local level as well as from multinational organized cooperative efforts. Education and improvement of surveillance and socioeconomic conditions are integral parts of any solution strategy.
Humoral immunity does not play a prominent role during experimental cryptococcosis. However, previous studies have shown that immunoglobulin G (IgG) anti-Cryptococcus neoformans antibodies can mediate cell-dependent yeast killing in vitro. Therefore, the protective effect of a previously described monoclonal IgGl anti-C. neoformans antibody (El) administered intraperitoneally 24 h before intravenous infection with a C.
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