Significance And Scope

Infections involving artificial organs, synthetic vessels, joint replacements, or internal fixation devices usually require reoperation, and may result in amputation, osteomyelitis, or death. Infected cardiac, abdominal, and extremity vascular prostheses result in amputation or death in 25—50% of cases (Dougherty and Simmons, 1982; Gristina and Costerton, 1984; Gristina and Kolkin, 1989; Gristina et al., 1985). Intravenous catheters, periotoneal dialysis, and urologic devices used for more than a few days frequently become infected or cause secondary tissue-sited infections. The aged or immuno-compromised are even more vulnerable to infection. The rate of infection for the total artificial heart approaches 100% when the heart is implanted for more then 90 days (DeVries, 1988; Gristina et aL 1985). The use and development of implanted artificial organs is at a critical pass because of infectious complications.


The relevance of biomaterial and foreign bodies to infection was first suggested by Elek and Conen (1957) in a landmark experiment in 1957 when they reported that a foreign body (a silk suture) decreased the numbers of the infection-producing inoculum from 106 Staphylococcus aureus to 100 organisms. In 1963, after observing the high rate of infection associated with stainless steel implants in orthopedic surgery (10%), Gristina suggested that the internal fixation devices, biomaterials, and dead bone provided a structural framework along which microorganisms (S. aureus and S. albus) colonized and propagated (Gristina and Rovere, 1963). In 1972, Bayston and Penny described the excessive production of an mucoid substance as a possible virulence factor in the colonization of plastic neurosurgical shunts in children by S. epidemtidis (Bayston and Penny, 1972).

Gibbons and van Houte stimulated research in 1975 when they described the attachment and complex interactions of Streptococcus mutans with dental pellicle and plaque (Gibbons and van Houte, 1975).

In 1976, Gristina et al. reported that surface effects and sequestration of ions and substances from metals, polymers, or organic substrata were factors in bacterial colonization of foreign bodies and biomaterials. In this study, some reactive metals inhibited bacterial growth, but growth was abundant adjacent to "inert" substrata such as stainless steel and polymeric sutures. Biomaterials that resisted infection were tolerated by tissues and augmented host defenses were proposed. In 1979 bacterial adhesion and biofilm-mediated polymicrobial infections were demonstrated on tissue and internal fixation devices retrieved from infected surgical wounds (Gristina et al., 1980a, b). The authors hypothesized that microbial adhesion to b i ornate rials and compromised tissues, and production of extracapsular polysaccharides (slime) were the molecular mechanisms tor and explained in part (1) the susceptibility of biomaterial sites to infection (Gristina et al., 1980a, b), (2) resistance to antibiotic treatmem and host defenses, (3) difficulties in identifying the organisms involved, and (4/ the persistence of infection until the prosthesis was removed (Gristina et 4, 1980a, b).

In 1980, Beachey emphasized that bacterial adherence to tissue cells was the primary molecular mechanism for bacterial infection in man and animals, In 1980 and 1981, Gristina et al. (1980a, b), Costerton and Irvin (5981), Peters et al. (1981), and Beachey {1981} reported bacteria) adhesion to metals and polymers as a cause of biomaterial-centered infection.

In 1985, Gristina (Gristina et at., 1985) indicated that compromised rissues and bone were the target substrata for bacterial colonization in osteomyelitis. In 1988, cartilage and collagen were dearly identified as the specific ligands and substrata for bacteria! adhesion in intraarticular sepsis (Voytek et al., 1988 V,

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