Patients admitted to intensive care units are extremely susceptible to infection due to hospital acquired pathogens. One of the most important reasons for the occurrence of infection is attributable to the fact that these patients are exposed to several prosthetic devices for diagnostic or therapeutic procedures. From this point of view the problem of prostheses-associated infection is presently of major concern in hospital acquired infection since the number of artificial polymers implanted in the human body is rapidly increasing in many medical fields. Several types of plastic and metal prostheses are utilized for medical purposes and they greatly differ in tissue compatibility. Only recently some information has been obtained about their susceptibility to bacterial adhesion and colonization. The thermodynamic approach considers hydrophobicity, or surface free energy, as the major factor in facilitating bacterial attachment, but probably this approach is inherently too simplistic and does not consider important factors such as conditioning films bathing the surface of the polymer. Moreover, in this model bacteria are considered as individual cells, but the available body of evidence indicates that cells form aggregates embedded in a matrix sticking to the surface. This sessile mode of growth, as opposed to that of free living cells (planktonic) has profound effect on growth, shape, metabolism of attached bacteria influencing sensitivity to antibiotic, disinfectants and to cellular and humoral host defenses. Adherent bacteria cannot be easily ingested by polymorphonuclear neutrophils (PMNs) which are rendered ineffective by aspecific activation upon contact with several polymers. All these factors contribute to make these infections chronic and cryptic by posing difficult diagnostic and therapeutical problems.
A clinical and microbiological study was carried out to assess the therapeutic efficacy of two different antibiotics, lincomycin and amoxicillin, in the treatment of patients suffering from odontogenic abscesses. Microbiological analyses revealed that the majority of infections were supported by mixed aerobic and anaerobic bacterial flora. The assessment of clinical parameters clearly showed that patients receiving pharmacological treatment with lincomycin achieved a more rapid and efficacious recovery from disease in comparison to patients treated with amoxicillin.
The stability of F'lac, pW101 and pHSG298 in Escherichia coli K12 exposed to subinhibitory concentrations of beta-lactam antibiotics, amikacin and tetracycline was studied. High molecular weight low copy plasmids (F'lac and pW101) were eliminated from bacteria treated with PBP-3 binding molecules, while a low molecular weight high copy extrachromosomal element (pHSG298) was not. None of the carbapenem antibiotics, mecillinam, amikacin or tetracycline promoted high rate plasmid loss from their hosts. Under the same conditions, plasmid-mediated ampicillin-resistance due to beta-lactamase production was also lost from F'lacTn1-carrying bacteria. In contrast, the high copy R6K plasmid was stably inherited in their hosts with the exception of those organisms treated with cefixime. When the same experiments were performed with a Klebsiella pneumoniae strain induced to form filaments by azithromycin at sub-MICs, F'lacTn1 and pW101 loss was detected, while pHSG298 was stably inherited. These results confirm previous observations that plasmid stability is correlated with cell shape and that recovery is more easily achieved when bacteria undergo an unbalanced division resulting in cell filamentation.
