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Query: UMLS:C0004623 (bacterial infection)
 15,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gross, histologic and ultrastructural changes associated with bacterial infection are described in four porcine valve heterografts that had been in place in patients for 6 days to 28 months. In one patient, culture of the aortic tissue tag included in the heterograft container grew Mycobacterium chelonei; however, examination of the heterograft, recovered at necropsy 6 days after implantation, revealed small colonies of bacteria that differed morphologically from mycobacteria. A second heterograft was the site of staphylococcal infection associated with extensive destruction of collagen in the leaflets. Similar destruction was observed in a third heterograft, which was found to have organisms on ultrastructural study even though bacterial cultures of the valve were negative. The fourth heterograft, from a patient who died of coronary embolism secondary to dislodgment of vegetative material, contained structures resembling lysed bacteria. Observations in these 4 patients and review of published reports of infection involving 43 other patients with porcine valve heterografts indicates that infection in these valves: (1) develops in the fibrin layer that covers the cusps, (2) can involve the collagen in the leaflets, and (3) is uncommonly (three patients) associated with valve ring abscesses.
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PMID:Infection of glutaraldehyde-preserved porcine valve heterografts. 44 72

Auto-antibody to collagen, previously detected in periodontal disease, may represent either a response to local tissue damage or be the manifestation of a disturbance of the host immune response induced by the periodontal flora and its products. In an effort to distinguish between these two hypotheses, this study was undertaken to determine circulating IgG auto-antibody levels in 41 periodontal-disease patients against 12 self-antigens (salmon DS-DNA, calf SS-DNA, human and bovine thyroglobulin, rabbit proteoglycan, horse myoglobin, bovine myosin, actin, fetuin, human transferrin, cytochrome C, and human Type I collagen) and compare them to those in 21 periodontal disease-free subjects. None of the detected IgG auto-antibody levels were significantly different between periodontal disease and control sera (Mann-Whitney U-test, P greater than 0.05) except for human Type I collagen (P less than 0.05). Fifty-six percent of patients and 38% of controls were "broad responders;" i.e., 50% or more of the auto-antibody levels were higher than the median values of the control group; however, these values were not significantly different using the chi-square test. It was concluded that the destruction of connective tissue components is the primary driving force in the induction of the enhanced auto-antibody response found in periodontal disease. This response is apparently secondary to the primary bacterial infection which remains the major etiologic event.
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PMID:Immunity to self-antigens in periodontal disease. 131 26

Mycobacterium avium-Mycobacterium intracellulare (MAI) is an opportunistic intracellular pathogen responsible for the highest incidence of disseminated bacterial infection in patients with AIDS. Treatment of the infection is extremely difficult and has shown limited efficacy. A critical event in the initiation of a variety of bacterial infections involves the adherence of bacteria to host cell surfaces. In the present study, we have shown that MAI organisms bind avidly to extracellular matrix proteins such as laminin, collagen I, and fibronectin in an in vitro attachment assay. Immunoblot analysis of a sonicate of MAI with polyclonal antibodies against different integrin receptors indicated that the sonicate cross-reacts with polyclonal antibodies against a human laminin-binding integrin, alpha 3 beta 1, and a human fibronectin-binding integrin, alpha 5 beta 1, although it is reactive with only the beta 1 subunit in the case of both antisera. Antibodies against the alpha 3 beta 1 and alpha 5 beta 1 integrins specifically inhibited the binding of MAI to laminin, collagen I, and fibronectin by 70 to 97%, depending on the ligand, suggesting that the attachment of MAI to these extracellular matrix proteins may be mediated by a beta 1 integrin. Furthermore, the attachment of MAI to laminin, collagen I, and fibronectin was found to be cation dependent. MAI may use this and other beta 1-containing integrins to adhere and penetrate through basement membrane structures that underlie host cell linings. An understanding of the mechanism of attachment and a definition of the adhesive molecules on the surface of MAI may open up new approaches to the prevention of serious infection caused by this organism.
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PMID:Identification of a beta 1 integrin on Mycobacterium avium-Mycobacterium intracellulare. 137 87

The smear layer was first described as a debris layer which is left on all cavity walls following tooth preparation. It is composed of an outer contiguous layer of amorphous instrumentation matrix which covers all cavity walls, and a deeper zone of matrix plugs which obturate the cut tubules. Recent scanning electron microscopic (SEM) studies have characterized the smear layer as mineralized collagen fibers appearing as globules dispersed within an amorphous cutting matrix. Removal of smear plugs increases the outward hydraulic conductance (Lp) of dentinal fluid flow which may lead to dentinal hyperalgesia, bacterial infection and pulp pathosis if left untreated.
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PMID:[Characterizing the smear layer]. 209 6

The aim of our study was to assess the behaviour of a despecified collagen tissue laid on desepidermized human skin (taking area of skin graft). The collagen tissue was prepared according to Bell's method. The collagen was latticed, contracted by fibroblasts, chemically treated (formaldehyde or glutaraldehyde) to stabilize the fibrils and then despecified by cialit treatment. This tissue laid on superficial, non infected wounds very rapidly took a necrotic appearance and was totally lysed after 10 to 12 days without any modification of the healing course. No bacterial infection was observed. Histological and ultrastructural studies showed desorganization of collagen fibre bundles and tissue invasion by inflammatory cells. Circulating antibodies to collagen were absent at day 30. This model lacks interest as a substitute for superficial tissue replacement, but a healing function could be assigned to its high chemotactic power for polynuclears and macrophages and should allow its use in cases of deep tissue loss.
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PMID:[Behavior on de-epidermized human skin of unspecified reconstituted collagen tissue]. 240 Jan 82

Collagen and gelatin containing biomaterials are relatively more susceptible to bacterial infection. Systemic administration or local delivery of antibiotics after implantation does not seem to solve the problem either effectively or easily. Antibiotics may be incorporated in the implant; but many, being water soluble, are quickly absorbed and not effective for adequate time periods. Resorcinol monoacetate (RMA) is a relatively water insoluble antibacterial agent which partially crosslinks collagen and has the potential to be an intrinsic antibiotic in collagenous bioprostheses. This study confirms the efficacy of RMA as a chemical that: (a) mildly crosslinks collagen at pH 3.5-4.5; (b) releases very slowly from the pretreated collagen sponge when washed in aqueous medium; (c) inhibits bacterial growth on the pretreated collagen sponges, at 2% (w/w) concentration, for at least 12 days; (d) remains biocompatible under treated conditions.
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PMID:Collagen based biomaterials: an ideal way of increasing their resistance to infection. 321 16

Vitamin A-deficient rabbits were used to evaluate the role of secondary bacterial infection in the development of keratomalacia and to describe the resultant clinical and morphologic alterations. The conjunctival sacs of vitamin A-deficient rabbits at different stages of corneal involvement were inoculated with Pseudomonas aeruginosa topically. Approximately two weeks after inoculation, corneal ulceration with stromal melting developed in one of three eyes with severe punctate keratitis and in four of seven eyes with xerosis. Ulceration did not develop in any of the eight eyes with early epithelial graying or mild punctate keratitis. Inflammatory cells (primarily polymorphonuclear leukocytes) infiltrated the anterior corneal stroma of infected corneas. Liquefaction of collagen was observed in association with bacteria alone, as well as in association with polymorphonuclear leukocytes. No signs of infection were observed after conjunctival inoculation of Pseudomonas in the eyes of nine control rabbits.
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PMID:Increased susceptibility to infection in experimental xerophthalmia. 679 31

Adult lymphatic filariae (Wuchereria bancrofti, Brugia malayi) can cause blocking of lymphatics producing obliterating endolymphitis lesions. The subsequent extravasation of lymph (or chyle when the obstruction is canal) is at the origin of the formation of lymphedema or elephantiasis, in which the main histological finding is great hypertrophy of collagen elements. This theory involving filaria only is not the full picture, and bacterial infection, mainly by streptococci, is an important factor. The association of filaria with microbes is particularly dangerous because the presence of the latter, or its toxins, causes death of local microfilariae and even adult worms, which are known to be more harmful dead than alive. The progression of the disease, especially in cases with lymphedema, which mainly affects the limbs and the genital organs, depends on three factors: the species of filaria, the degree of transmission, and the receptivity of the patient to the parasite. Large differences are found according to the region involved, and in the same endemic zone, according to the individuals affected. However, they almost always occur progressively in areas where there have been recurrent attacks of acute lymphangitis.
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PMID:[Lymphoedema and elephantiasis due to filariasis. Pathogenesis and clinical aspects (author's transl)]. 700 45

The structural alterations elicited in the rabbit corneal stroma by experimental Serratia marcescens keratitis and by a highly purified serratia protease preparation were compared by gross observation, biochemical analyses, and electron microscopic examination of the affected tissue. Acute inflammation, liquefactive necrosis of the cornea, and descemetocele formation occurred during the development of the infection and after the intracorneal injection of submicrogram amounts of the protease. In vitro incubation of insoluble corneal stromal tissue with the bacterium or with the protease resulted in solubilization of the stromal proteoglycan ground substance; however, specific collagenase activity was not detected. Electron microscopic examination of corneas damaged by the bacterial infection and by the protease revealed loss of ruthenium red staining of the proteoglycan ground substance and dispersal of ultrastructurally normal collagen fibrils. Thus, our findings indicate that the major corneal damage which occurs during serratia keratitis and after the injection of the serratia protease is caused by solubilization and loss of the ground substance of the tissue. In addition, the observation that the major structural alterations observed during serratia keratitis can be reproduced by the bacterial protease supports the idea that the enzyme is involved, at least in part, with the production of severe corneal damage by the bacterium.
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PMID:Characterization of rabbit corneal damage produced by Serratia keratitis and by a serratia protease. 702 49

In order to prevent epidermal down growth when a silicone percutaneous device was implanted, immobilization of collagen was performed onto the surface of a silicone device. The immobilization of collagen was achieved through covalent bonds between the amino groups in the collagen molecules and the carboxyl groups in poly (acrylic acid) chains grafted onto the silicone device surface. When the collagen-immobilized silicone device model was percutaneously implanted in rabbits, no sign of epidermal down growth was observed even 7 weeks after implantation, while the epidermis reached down to the deep part of the dermis as early as 3 weeks after implantation when collagen was not immobilized onto the device model surface. To have tighter fixation of the device models to the surrounding dermal tissue, the silicone device model was covered with a polyethylene sponge having an average interconnecting pore size of 150 microns. Collagen immobilization was also performed onto the sponge surface. Both the collagen-immobilized silicone device models as well as the non-treated models with polyethylene sponge were percutaneously implanted in rabbits and epidermal down growth as well as the occurrence of bacterial infection was examined. Without collagen immobilization onto the sponge surface of the device model, bacterial infection was noticed as early as 2 weeks after the implantation. The number of infected device models increased as the implantation time became longer and bacterial infection was observed in six out of seven device models at the 10th week post implantation. When the sponge surface was immobilized with collagen, bacterial infection was noticed in only one model at the 5th week after implantation. Six out of seven implanted device models with collagen immobilization were free of bacterial infection until the animals were sacrificed 30 weeks after implantation.
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PMID:Surface modification of silicone for percutaneous implantation. 765 31


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