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Biomedical subjects

A J Severijnen

Publications and source records attributed to A J Severijnen.

18 recordsLinked to original sources
PubMed1999

Risk assessment for surgical-site infections in orthopedic patients.

OBJECTIVE: To assess the relative importance of risk factors for surgical-site infections (SSIs) in orthopedic patients and thereby determine which risk factors to monitor in the national surveillance of SSI in The Netherlands. DESIGN: Reanalysis of data on SSI and associated risk factors from two surveillance projects on nosocomial infections, carried out in 1992 and 1993 in The Netherlands: Project Surveillance Nosocomial Infections in the region of Utrecht (PSZU) and the first Project Surveillance Surgical Wound Infections (SWIFT-1). Odds ratios (ORs) were calculated for age, gender, preoperative stay, and the number of operations. In addition, in PSZU, other nosocomial infections, and, in SWIFT-1, prophylactic antibiotics, acute surgery, and wound contamination were studied. PARTICIPANTS: The study was confined to hospitalized orthopedic patients (PSZU, 4,872; SWIFT-1, 6,437). RESULTS: In PSZU, the following ORs were significant in a multivariate model: age 0-44 years, 1.0; 45-64 years, 1.6; 65-74 years, 4.7; and 75-99 years, 6.0. For a preoperative stay over 4 days, the OR was 3.3 (95% confidence interval [CI95], 2.5-4.0), and for multiple surgery, 2.5 (CI95, 1.9-3.0). For females, the OR was 0.8 (not significant). The same model applied to SWIFT-1 gave similar ORs. Adjustment for additional nosocomial infections (PSZU) decreased the ORs for ages over 65 years remarkably. The OR for additional nosocomial infections in patients under 65 years of age was 15.6 (CI95, 4.3-57.4). Adjustment for prophylactic antibiotics, acute surgery, and wound-contamination class (SWIFT-1) did not influence the ORs of the original model, but showed that wound-contamination class was an important risk factor. CONCLUSIONS: Age, additional nosocomial infections, wound-contamination class, preoperative stay, and the number of operations were identified as important risk factors for SSI in Dutch orthopedic patients.

Adolescent↗
PubMed1997

Sentinel system for nosocomial infections in The Netherlands: a pilot study.

OBJECTIVE: To determine the feasibility of standardized surveillance of nosocomial infections (NI) in The Netherlands, using local data on patients with NI collected by infection control practitioners (ICPs) and denominator data on all patients under surveillance obtained from the Dutch National Medical Registry (LMR). DESIGN: A prospective, multicenter study. SETTING: Eight hospitals in the Utrecht region, and the National Institute of Public Health and the Environment. PATIENTS: ICPs traced NI in gynecological and orthopedic patients for 9 to 16 months. Denominator data on all patients under surveillance were obtained from the LMR. RESULTS: Data from 8,922 patients were collected; the ICPs registered 470 patients with 526 NI. Overall, the NI incidence was 5.9 per 100 patients, or 6.3 per 1,000 patient days. Urinary tract infections (UTI) were most frequent (3.3%), followed by surgical-wound infections (SWI; 2.0%) and bloodborne infections (0.12%). The incidence of both SWI and UTI differed markedly between hospitals, only partially on account of differences in patient mix (age, type of operations), antibiotic prophylaxis, and intensity of tracing methods for NI. Delay in the availability of denominator data hampered the timely feedback of incidence figures. CONCLUSIONS: Surveillance of NI in a network of sentinel hospitals offered valuable information on the occurrence of NI and on factors influencing the incidence of NI. It revealed situations in which both NI surveillance and infection control methods in individual hospitals should be improved. Obtaining denominator data on all patients from electronically registered patient discharge data greatly reduces the workload of ICPs and enables surveillance on all types of NI (all body sites and all pathogens). For timely feedback, numerator and denominator data within hospitals must be linked.

Adult↗
PubMed1996

Modeling prevention strategies for gonorrhea and Chlamydia using stochastic network simulations.

A simulation model was used to study the spread of two sexually transmitted diseases (STDs), namely gonorrhea and genital infection with Chlamydia trachomatis. The model is based on a stochastic pair formation and separation process, which describes the underlying structure of the sexual contact pattern. It is implemented as a Monte Carlo simulation model. Spread of the STDs was modeled in an age-structured heterosexual population with a highly sexually active core group. Contact tracing strategies, screening of various subgroups, and the effect of condom use were compared. The authors conclude that contact tracing is very effective as a prevention strategy, that screening should be targeted to the highly active core group, that age is not sufficient as a determinant for high sexual activity to make screening of certain age groups useful, and, finally, that consistent condom use by a fraction of the population can contribute substantially to the prevention of STDs. All strategies proved more effective for gonorrhea than for Chlamydia prevention, which may explain the relatively high prevalence of Chlamydia found in many heterosexual populations.

Adolescent↗
PubMed1993

Responses of synovial fluid and peripheral blood mononuclear cells to bacterial antigens and autologous antigen presenting cells.

The specificity of T cells in the inflamed joints of patients with rheumatoid arthritis (RA) has been the subject of much study. Bacterial antigens are suspect in the aetiology of rheumatic diseases. The responsiveness of the mononuclear cell fraction of peripheral blood and synovial fluid of patients with RA and of patients with rheumatic diseases other than RA to bacterial antigens such as cell wall fragments of the anaerobic intestinal flora, cell wall fragments of Streptococcus pyogenes, intestinal flora derived peptidoglycan polysaccharide complexes, the 65 kilodalton protein of Mycobacterium tuberculosis, and muramyldipeptide was investigated. No significant difference in response was found to all these bacterial antigens in the synovial fluid of patients with RA compared with the responses in patients with other rheumatic diseases. The highest responsiveness in the synovial fluid of the patients with RA was to the streptococcal cell wall fragments and to the 65 kilodalton protein. Higher responses to several bacterial antigens in the synovial fluid of patients with RA were found compared with peripheral blood from the same patient group. The antigen presenting cell population of the synovial fluid in patients with RA and the patients with other rheumatic diseases was found to be stimulatory for autologous peripheral blood T cells even in the absence of antigen. This suggests an important role for the synovial antigen presenting cell in the aetiology of inflammatory joint diseases.

Adult↗
PubMed1992

Arthritis by autoreactive T cell lines obtained from rats after injection of intestinal bacterial cell wall fragments.

T cell lines (B13, B19) were isolated from the lymph nodes of Lewis rats 12 days after an arthritogenic injection of cell wall fragments of Eubacterium aerofaciens (ECW), a major resident of the human intestinal flora. These cell wall fragments consist of peptidoglycan polysaccharide complexes (PPC). The cell lines that bear the helper phenotype were arthritogenic in knee or ankle joints upon intravenous injection into irradiated Lewis recipients. B13 was, however, not arthritogenic in irradiated F344 recipients that are largely RT1 identical. The arthritis induced in the knee joints of the irradiated Lewis rats was clearly shown by a 99mtechnetium-pertechnetate scanning technique and was confirmed histologically. In vitro the cell lines showed a proliferative response after stimulation with syngeneic spleen cells alone. The proliferation was significantly higher when bacterial PPC, isolated in soluble form from normal feces or ileostomy fluid were added. Recognition by B13 appeared to be MHC class II restricted. These results show that autoreactive T cell lines can be isolated from rats after injection of bacterial cell wall antigens and that these cell lines can be arthritogenic. This suggests a role for autoreactive T cells in the induction of bacterial cell wall arthritis and might give a clue for the arthritogenic properties of the normal human intestinal flora.

Animals↗
PubMed1992

Immunohistology of joint inflammation induced in rats by cell wall fragments of Eubacterium aerofaciens.

After a single intraperitoneal injection of cell wall fragments of Eubacterium aerofaciens, a main resident from the human intestinal flora, an acute arthritis develops within 2 days which is followed by a chronic arthritis that lasts at least 90 days. In an earlier report the histological appearance of the joint inflammation during this period has been described. In this study we investigated in more detail the cell types that are involved in the development of arthritis by using cell-type-specific monoclonal antibodies in an immunohistological assay. In the acute phase of arthritis, T-helper cells appeared in the synovial tissue together with ED1-positive (ED1+) and ED3-positive (ED3+) macrophages. After a temporary decline at day 12 all macrophage subsets, as well as T-helper cells, reappeared or increased again at day 33. Later, in the chronic phase (days 47-90), an increased number of ED1-positive (ED1+) cells in the synovial tissue and a decreased number of ED2-positive (ED2+) cells in the synovial lining was the most prominent finding when compared with control rats. These results indicate that, apart from T lymphocytes, macrophages also play an important role in the development and continuation of chronic arthritis in this model.

Acid Phosphatase↗
PubMed1992

Are intestinal bacteria involved in the etiology of rheumatoid arthritis? Review article.

Observations in bowel-related joint diseases give support to this hypothesis. In Crohn's disease and ulcerative colitis, the bowel wall inflammation is complicated in about 20% of the patients by joint inflammation. Bowel infection by Salmonella, Shigella and Yersinia can provoke joint inflammation and supports an etiological link between bowel bacteria and arthritis. The arthropathic properties of the most abundant group of intestinal bacteria, i.e. the obligate anaerobic bacteria, were studied in an animal model. Cell wall fragments (CWF), with peptidoglycan as the major component, from some Eubacterium and Bifidobacterium species induced a severe chronic polyarthritis in Lewis rats after a single intraperitoneal injection. Eubacterium was found in numbers of 10(8)-10(9) per gram in stools of healthy subjects and rheumatoid arthritis (RA) patients. CWF of isolated strains of E. aerofaciens were arthropathic. Soluble peptidoglycan polysaccharide complexes (PG-PS) originating from the obligate anaerobic flora were purified from human intestinal contents. PG-PS from ileostomy fluid that proved to be less processed by intestinal enzymes induced chronic arthritis in rats after a single administration in oil in the base of the tail. It was concluded that the human intestinal bowel contains soluble bacterial cell wall products that are arthropathic in an animal model. Peptidoglycan (PG) or its subunits was reported to be present in mammalian tissues. Immunohistochemical studies from our group showed the presence of intestinal PG-PS in sections of normal rat spleen. Bacterial cell wall or PG-induced joint inflammation in rats is proven to be absolutely dependent on functional T cells. T-cell lines were isolated from the lymph nodes of rats with an E. aerofaciens CWF arthritis. A helper T-cell line B13 was in vivo arthritogenic in knee or ankle joints upon intravenous injection in rats and proliferated in vitro on syngeneic spleen cells alone, but was additionally stimulated by intestinal PG-PS and E. aerofaciens CWF. It was postulated that the arthritogenic T cells that seem to be autoreactive are, in fact, recognizing bacterial PG-PS on antigen-presenting cells (APC). It is generally accepted that RA is a T-cell-dependent process and that therefore the reaction is directed at small peptides bound by the major histocompatibility complex of APC. The only peptides present in arthritis inducing intestinal PG-PS and in CWF are PG peptides interlinking the sugar chains. We feel that the immunoreaction against PG peptides plays a pivotal role in experimental and human arthritis of an unknown etiology.

Amino Acid Sequence↗
PubMed1992

Influence of decontamination on induction of arthritis in Lewis rats by cell wall fragments of Eubacterium aerofaciens. Arthropathic properties of indigenous anaerobic bacteria.

Although the cause (or causes) of rheumatoid arthritis is unknown, many workers have suggested that microorganisms play a part. The intestinal flora in particular has been related to the development of joint inflammation. It has been shown previously that cell wall fragments of several anaerobic Gram positive intestinal bacteria of human origin are arthritogenic after a single intraperitoneal injection in Lewis rats. The part played by indigenous microflora in this model has now been studied by decontaminating Lewis rats before the injection of Eubacterium aerofaciens cell wall fragments. The pattern and severity of arthritis appeared to be comparable in decontaminated and control rats. The second goal of this work was to isolate arthritogenic bacteria from the autochthonous intestinal flora of rats. Only a limited number of bacteria showing a resemblance to arthritogenic strains from human intestinal flora (i.e. E aerofaciens and Bifidobacterium adolescentis) could be isolated. These strains did not induce chronic arthritis after intraperitoneal injection. This may explain why spontaneous arthritis did not develop in Lewis rats.

Animals↗
PubMed1991

Histology of joint inflammation induced in rats by cell wall fragments of the anaerobic intestinal bacterium Eubacterium aerofaciens.

To study the arthropathic properties of human intestinal bacteria, cell wall fragments (CWF) of the anaerobic bowel bacterium Eubacterium aerofaciens were injected intraperitoneally (i.p.) in arthritis-susceptible Lewis rats. Rat paw joints were subsequently studied for histopathological changes. A persisting synovitis accompanied by marginal erosions of cartilage and bone and a marked periosteal apposition of new bone tissue were the main features of the polyarthritis induced. These results are discussed in relation to streptococcal cell wall induced arthritis and compared with histopathological findings in rheumatoid arthritis (RA) in man.

Animals↗
PubMed1990

Intestinal flora of patients with rheumatoid arthritis: induction of chronic arthritis in rats by cell wall fragments from isolated Eubacterium aerofaciens strains.

The composition of the obligate anaerobic intestinal flora of patients with rheumatoid arthritis (RA) differed from that of healthy subjects (HS). Total numbers of aerobes as well as anaerobic coccoid rods were found elevated when compared with HS. Eubacterium species were found in all stool samples of both groups; Bifidobacterium species were present in seven (RA) and eight (HS) out of 10 subjects. From the flora of two RA patients and two HS Eubacterium species were isolated and identified. Cell wall fragments from four E. aerofaciens strains (two from RA, two from HS) were tested for arthritis induction in rats. All four strains induced chronic arthritis which was histologically confirmed. We concluded that in the normal intestinal flora of RA patients Eubacterium species are present in high numbers (i.e. greater than 10(9)/g faeces); cell walls from isolated E. aerofaciens strains had arthropathic properties.

Animals↗
PubMed1990

Flare-up reaction of streptococcal cell wall induced arthritis in Lewis and F344 rats: the role of T lymphocytes.

One i.p. injection of a sterile suspension of streptococcal cell walls (SCW) induces chronic erosive polyarthritis in susceptible Lewis rats, but not in resistant F344 or nude Lewis rats. Because continuous exacerbations may be one possible mechanism underlying chronic disease, we studied the mechanism of these flare-up reactions in Lewis and F344 rats. Injection of SCW into the right knee joint of rats induced a transient monoarthritis in both strains. Reactivation of the subsided arthritis by i.v. administration of the same antigen could be evoked only in the Lewis rat. Even repeated i.v. challenges with SCW failed to induce a flare-up reaction in the F344 rat, while the Lewis rat went through an exacerbation after every challenge. Removal of T lymphocytes by monoclonal antibodies before induction of an exacerbation rendered Lewis rats refractory to flare-up reactions, thus indicating the T cell-dependence of this reaction. Furthermore, when cell walls from heterologous bacteria were tested for their capacity to induce exacerbations of SCW-induced monoarthritis and to induce proliferation of SCW-specific T lymphocytes in vitro, a strong correlation between both features was found, again pointing to a role for SCW-specific T cells in exacerbations. Together, these data support our hypothesis that chronic arthritis is the result from repeated reactivations of a waning arthritis which are dependent on antigen-specific T lymphocytes.

Animals↗
PubMed1990

Chronic arthritis induced in rats by cell wall fragments of Eubacterium species from the human intestinal flora.

To investigate arthritis-inducing properties of Eubacterium species, which are major residents of the human intestinal flora, cell wall fragments (CWF) of several Eubacterium strains were prepared and tested in an animal model. After a single intraperitoneal injection in the rat, CWF of E. aerofaciens, E. contortum, and E. lentum induced a chronic polyarthritis. E. limosum and E. tortuosum CWF induced an acute self-limiting joint inflammation, whereas E. rectale CWF failed to do so. The rhamnose contents of the isolated CWF were not related to their arthritis-inducing properties. Paradoxically, the sensitivity of CWF to lysozyme digestion, which is regarded as a parameter for the clearance of CWF in tissues, appeared to be positively correlated with the ability of Eubacterium CWF to induce chronic joint inflammation. Our findings show the diversity in arthritis-inducing properties among different species of the anaerobic genus Eubacterium and underline the importance of the anaerobic intestinal flora in the induction of joint inflammation.

Animals↗
PubMed1989

Cell wall fragments from major residents of the human intestinal flora induce chronic arthritis in rats.

To investigate the involvement of human intestinal flora in joint inflammation, cell wall fragments of 9 anaerobic gram positive bacteria of the human fecal flora were prepared and tested for arthropathic properties in the rat. A single intraperitoneal injection of cell wall fragments from Eubacterium aerofaciens or Bifidobacterium species induced persistent chronic arthritis, in contrast to those from Eubacterium rectale, Clostridium species and Lactobacillus leichmanii. The results show that cell wall fragments of major residents from the human fecal flora can induce chronic arthritis in the rat and support the hypothesis that normal human intestinal flora plays a role in the induction of arthritis in man.

Animals↗
PubMed1988

Induction of chronic arthritis in rats by cell wall fragments of anaerobic coccoid rods isolated from the faecal flora of patients with Crohn's disease.

Crohn's disease and ulcerative colitis are accompanied by seronegative arthritis in about one fifth of the cases. In the present study, cell wall fragments from major residents such as Eubacterium, Coprococcus and Peptostreptococcus species, isolated from the faecal flora of patients with Crohn's disease, were tested for properties to induce chronic arthritis in Lewis rats. Cell wall fragments from Eubacterium contortum strains Me44 and Me47 were found to induce chronic arthritis; Peptostreptococcus productus strain C 18 cell wall fragments induced acute self-limiting arthritis. Coprococcus comes strain Me46 cell walls, on the other hand, were found to be lethal to the majority of rats inoculated, whereas those which survived did not develop acute or chronic arthritis. The results indicate that intraperitoneal injection of a single dose of cell wall fragments from bacteria that are major residents of the human anaerobic faecal flora can induce chronic inflammatory joint disease in the rat.

Animals↗
PubMed1988

Streptococcal cell wall-induced arthritis and flare-up reaction in mice induced by homologous or heterologous cell walls.

Intra-articular injection of cell walls from the gram-positive bacterium Streptococcus pyogenes induces an arthritis in both streptococcal cell wall (SCW)-primed and naive mice. This joint inflammation subsides after 2 weeks but it could be reactivated by systemic injection of SCW in a dose-dependent way. The primary arthritis as well as the flare-up reaction were more vehement in immunized than naive mice. Pretreatment with antilymphocyte serum of nonimmunized arthritic mice before systemic challenge completely inhibits the flare-up reaction, suggesting the involvement of lymphocytes in the reactivation. Dose-response studies showed that intravenous challenge with SCW amounts too small to induce a primary arthritis were able to reactivate a chronic arthritis, implying that an inflamed joint is in a hyperreactive state, probably due to locally retained lymphocytes. Arthritis as a result of injection with SCW can be reactivated by fragments of a nonrelated, gram negative endogenous bacterium, Escherichia coli. The latter finding might be of importance for the understanding of the pathogenesis of chronic arthritis: once an arthritis is induced by one bacterium, other (unrelated) bacteria, probably derived from an endogenous source, may be able to reactivate the inflammatory process, thus contributing to chronicity.

Animals↗