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Bacterial infection joint swelling 1997,how to treat upper respiratory tract infection guidelines,how to treat pseudomonas bacterial infection - New On 2016

The infection of a joint can occur in different ways, (I) via injection or during joint operation through direct colonization, (II) by direct contact with a neighboring infected site, or (III) by haematogenous or lymphogenous seed of the pathogen. If bacteria reach into the joint they can bind to a large number of different binding molecules. A differentiation of arthritis is practicable by examination of typical laboratory medicine and microbiology characteristics in joint fluid. Infection serologyIn reactive arthritis the cultural detection of pathogens is often not possible. The therapeutic approach has to be selected in accordance with the mode of infection (NJI, PJI, RA), the expected or found pathogens, and their resistance.
Acute native joint infectious arthritisEssential for sufficient treatment of acute septic arthritis is the fast and aggressive therapy with the combined application of antimicrobial medication and joint lavage.
Prosthetic Joint InfectionIn the treatment of PJI virtually every conceivable form was tried out, antibiotics alone or in combination with debridement and intraarticular lavage, the ex- and reimplantation of the prosthesis in one or two stages, the arthrodesis or as a last option the amputation. Antibiotic prophylaxisThe perioperative antibiotic prophylaxis is one of the procedures, which clearly demonstrates the reduction of infection rate after joint surgery [22,23]. There are only a few interfaces in medicine of such high importance like the interaction between surgeons, physicians and microbiologists in the preanalytical, analytical and postanalytical phases in the diagnosis and treatment of joint infections.
Herrmann M, Vaudaux PE, Pittet D, Auckenthaler R, Lew PD, Schumacher-Perdreau F, Peters G, Waldvogel FA.
Atkins BL, Athanasou N, Deeks JJ, Crook DW, Simpson H, Peto TE, McLardy-Smith P, Berendt AR.
Correspondence to: Udo Geipel, MD, Institute of Medical Microbiology and Hygiene, University of Saarland Hospital, Kirrberger Strasse, Bldg 43, 66421 Homburg, Germany. The diagnostic path begins with a comprehensive medical examination and PERSONAL HEALTH HISTORY to identify any recent infections, injuries, or surgeries. Surgical debridement (an OPERATION to clean pus and damaged tissue from the infected area) and ANTIBIOTIC MEDICATIONS administered intravenously are the first course of treatment for osteomyelitis. Infections in the bone are particularly hard to treat because the bone’s blood circulation does not deliver antibiotic medications to the bone very effectively. People at particular risk for osteomyelitis are those who have DIABETES or who are on hemodialysis for END-STAGE RENAL DISEASE (ESRD). Another classification of bacterial arthritis distinguishes acute, chronic and reactive forms, which differ in their type of joint infection and their triggering bacteria.
Especially fibrinogen, extracellular matrix proteins and glycosaminoglycans, including fibronectin and laminin, are components of the blood plasma, the bacteria use adhesion to [4,5]. This makes serological analysis to a method principally necessary to detect antibodies against the causing bacteria. It should be remembered that the slowed growth of bacteria in a biofilm on surfaces of joint prosthesis may additionally reinforces antibiotic resistance [18,19].
In all, however, the prolonged antibiotic therapy is a crucial factor.An algorithm has been described, suggesting the surgical management as a function of the time period from surgical intervention till onset of PJI, the type of infection, the implant and soft tissue situation and existing co-morbidities [20].
Typically the infection starts elsewhere in the body and spreads through the BLOOD circulation to the bone, though may originate in the bone as a complication of surgery on the bone (such as open reduction of a FRACTURE or JOINT REPLACEMENT).
X-RAY may show the area of infection, though other imaging procedures such as bone scan or MAGNETIC RESONANCE IMAGING (MRI) often produce more complete information. The infection may cause an ABSCESS (pocket of pus) that in turn causes the death of bone tissue. Chronic osteomyelitis, particularly with abscess, may have a less favorable outcome with extended antibiotic therapy necessary for several months. Trauma to the bone, such as open fracture or surgery, also increases the risk for infection.
Native joint infections of the hip are less common than infections after implantation of prosthetic devices. Reactive arthritis is a postinfectious complication with no need of presence for viable pathogens in the joint. A large number of bacteria specific receptors (adhesins) and adhesion factors have been described. The antibody detection has a great diagnostic value also due to the reduced sensitivity of bacterial culture in joint infections caused by Borrelia or Brucella. Responsible for such an increase against antibacterial substances are changes in cell wall synthesis, which limits the effect of beta-lactam antibiotics and glycopeptides, and the occurrence of bacterial variants with modifications of other metabolic activities, with implications for the action of quinolones, aminoglycosides, and tetracyclines. The most widely used antibiotics in orthopedic surgery are cephalosporins of the first or second generation, like Cefazolin or Cefuroxime. Conclusions must be made for the samples to be investigated, their required numbers and volumes, the sample collection method, time and mode of transport, and the communication of laboratory results.
Bacterial infection causes most osteomyelitis, though other pathogens such as fungi (yeast) may also be responsible. The course of antibiotic treatment may extend six weeks or more, depending on how well the infection responds.


When such a scenario unfolds, the osteomyelitis becomes chronic and may destroy considerable bone tissue.
Several surgical operations may be necessary to clean the infection site and prevent abscesses from forming.
Prevention is not always possible, though using measures to appropriately care for wounds and respond to early symptoms such as pain can keep the infection contained enough for antibiotic therapy to be effective.
Difficulties in prosthetic joint infections are, (I) a higher age of patients, and, thus an associated presence of other medical risk factors, (II) often long courses of treatment regimes depending on the bacterium and its antibiotic resistance, (III) an increased mortality, and (IV) a high economic burden for removal and reimplantation of an infected prosthetic device. While reactive arthritis often simultaneously affect several joints, the presence of polyarthritic types of non reactive arthritis occur infrequently and then mostly as a result of several bacteriaemic phases.Among joint infections, the hip is the second most frequent localization after the knee joint. The intra- and interspecific variation of the expression of these bacterial pathogenity factors can be correlated with the inherent bacterial virulence [6,7]. Beside the inflammatory parameters, such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and white blood cell count, which are nonspecific and do not provide location-related information, the synovial fluid leukocyte count is a simple, rapid and accurate test. For a medically and economically adequate evaluation in serologic diagnosis the sensitivity and specificity of the various methods must be considered. In principle, the spectrum of available antibiotics is limited by the specific pharmacokinetic requirements in the treatment of joint infections.
For initial therapy in the presence of clustered gram positive cocci in microscopic examination and, therefore, most likely an infection with S. Beneficial characteristics are bactericidal action, effective bone and tissue concentrations, opportunity for oral sequential therapy, and no adverse side effects. The long bones in the leg are the most common locations for osteomyelitis in children; osteomyelitis in adults tends to settle in the hip or pelvis. Blood tests such as complete blood count (CBC) are likely to show elevated white blood cell (WBC) count and other changes in the blood when there is an infection present.
It may be necessary for the orthopedic surgeon to create a surgical wound over the site of the infection to clean it and irrigate the area.
The pathogenic mechanisms responsible for articular infections are well studied only for some bacteria, e.g.
Basically, there are no differences in the bacterial spectrum between hip joint infections and those of other large joints. Staphylococcus aureus has dominance in acute purulent arthritis while coagulase-negative staphylococci can be found mainly in periprosthetic infections and after diagnostic arthroscopies. In this large microbiological and infectiological field a lot of research is done for Staphylococcus aureus.
An overview of the bacteria that most commonly trigger reactive arthritis is listed in Table 3.
Even if these aspects should be included in the selection of the drug of choice, the finding is, however, that (I) for many of these parameters (e.g.
In hospitals with high prevalence of MRSA Vancomycin is also used.Haematogenous infections of the joint prosthesis may be due to transient bacteremia. An initially chosen antimicrobial therapy has to be adapted on the results of diagnostic procedures, the infectious agent detected or most probable, and the planned surgical procedure. Under the HoodBehavior, Neuroscience & Your Brain What Brain Hacks Can Psychologists Teach Us? Hip joint infections, however, are aggravated by the fact that they can exist over a long time with only poor symptoms. Other gram-positive bacteria as causative agents for hip joint infections are streptococci, especially Streptococcus pyogenes, Enterococcus faecalis and Corynebacteria species.A large number of different gram-negative rods act as infectious agents on joints. This is also substantiated by the production of various cytotoxins and the presence of highly effective signaling mechanisms [3].
For gram positive chainlike cocci, thus highly suspicious for a streptococcal infection, penicillin G is empirically given. Thus, antibiotic prophylaxis during dental procedures or genitourinary tract and gastrointestinal tract interventions are useful in order to prevent late-onset prosthetic infection [24].
The bacterial culture in the microbiological laboratory, especially for PJI and other infections probably due to slow-growing bacteria require an extended period of 7 to 14 days. When chronic osteomyelitis accompanies joint replacement, it may be necessary to remove the prosthesis until the infection heals. An increased rate of infection occurs in the pre-damaged joint and is also associated with particular predispositions of the patients (Table 1) [1,2,3]. Another bacterial feature is the formation of a biofilm, a polymeric matrix of saccharides, primarily described in the colonization of foreign material. Thus, joint fluid or intraarticular tissue must be obtained before antibiotic therapy is started. Most of the gram negative rods have their effective therapy initially with a quinolone or a second or third generation cephalosporin.
For infections with staphylococci particularly antibiotic combinations with Rifampicin possesses high cure rates.


Salmonella enterica, Shigella species, and Yersinia species are classically described as pathogens for purulent and reactive forms of arthritis. Swabs, also from intraoperative sites should not be sent into the laboratory due to the small quantity of carried material. Finally it should be noted that the occurrences of postoperative joint infections should be combined with investigations regarding their epidemiological value (e.g. Also swabs or tissue from superficial wounds or fistula often show the growth of skin flora and not the relevant bacteria. Cefazolin, Cefuroxime), possibly in combination with an anti-staphylococcal penicillin (e.g.
Also in this constellation Rifampicin plays in staphylococcal infections a prominent role [21].
On the other hand the implanted foreign material causes in addition to the severe joint disease present an additional reduction in local resistance, which facilitates haematogenous infections.
It was also shown that bacteria inside the biofilm have an increased resistance to the local host defenses and to antibiotics [8].
The prosthetic materials are also additional binding sites for various bacteria, and act as a starting point for prosthetic infections. In otherwise healthy people it is associated with iatrogenic modes of infection during diagnostic procedures. Additionally, through the conversion into so-called small colony variants (Figure 2) additional modifications of bacterial cells develop [9], while significantly reducing treatment efficiency and triggering chronic processes. Extending this repertoire with newer antibiotics, especially Linezolid, Daptomycin and Tigecyclin were introduced for PJI therapy.
Thus, in addition to the local conditions, the bacterial properties and their specific pathogenity have to be considered for understanding the whole mechanism of infection. Campylobacter species, however, are classic agents of reactive arthritis, as well as the obligate intracellular bacteria Chlamydia trachomatis, Mycoplasma pneumoniae, and Ureaplasma urealyticum. The formation of an inflammatory response, with the local generation of cytokines and reactive bacterial and host specific metabolic products leads to a joint injury, not seldom to irreversible destruction. Especially in PJI an operational approach is useful to obtain and examine several materials. A valid rating for the newest (lipo)glycopeptides Oritavancin, Dalbavancin, Telavancin, and for the cephalosporins Ceftobiprol and Ceftarolin in treatment of methicillin-resistant staphylococci is currently not possible. Basically, a too late or not sufficiently cured joint infection can cause trophic and functional limitations or can even be the starting point of a progressive infection spreading in continuity, lymphogenic or haematogenic. Thus, effective therapy strategies must combine calculated antibiotic regimes with local surgical interventions.Joint replacement surgery increases the risk of infections due to intraoperative bacterial wound contamination, leading to an early onset of the typical symptoms.
Although molecular techniques have a high value as a diagnostic procedure, only bacterial cultures can complete the diagnostic testing by antibiograms. In general, the detection and treatment of acute infectious arthritis is an acute emerging situation, in which a delay may progress to further septic inflammation [2]. Less commonly identified organisms for joint infections often accompanied with osteitis or osteomyelitis are Brucella species and Mycobacterium tuberculosis.
The material of the joint prosthesis is also covered by host proteins such as fibrinogen and fibronectin, which in turn facilitates bacterial colonization, leading to a delayed type of PJI. Anaerobes, such as Bacteroides fragilis, are rarely found and are usually part of a polymicrobial infection.
The foreign material allows not only a surface colonization; it is also responsible for a reduction of the local defense mechanisms.
Slow-growing bacteria as a pathogen in question, the presence of bacteria modificated by antibiotic pretreatment, SCV or biofilm production need an extended culture period [16]. Both, joint defect formation and chronification, if NJI, are not treated quickly and efficiently, and increasing mortality, high economic burden for removal of infected joint prosthesis and implant renewing [17] always require the increased effort in sampling and microbiological analysis. The immunological mechanism of the frequent association with HLA-B27 is not yet fully understood.
Using immunological and molecular biological procedures bacterial antigens can be detected in synovial fluid and synovial membrane [11]. Although in some studies viable bacteria could be detected [12], in an overview of research results it can be concluded that bacterial antigenetic material or antigen-antibody complexes are haematogenous deposited in the joint. This triggers a local inflammatory immune reaction, even without local bacterial proliferation [3,13].



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23.04.2014, author: admin


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