Acute Infectious Arthritis

Acute infectious arthritis develops within hours to days. The infection takes place in the joint or periarticular tissues from, is usually bacterial in nature and often affects younger adults with Neisseria gonorrhoeae as the most frequent pathogens. However, there are a number of other bacterial infections that can destroy joint structures quickly. Typical symptoms include a rapid onset of pain, effusion and limitation of active and passive mobility, usually affected in a single joint. The diagnosis is made with cultural examination with synovial fluid. Treatment consists of i.v. Antibiotics and joint drainage to remove the pus.

Acute infectious arthritis can also occur in children, including about 50% are younger than 3 years old. By routinely vaccinating children against Haemophilus influenzae and Streptococcus pneumoniae, the incidence of joint infection in this age group could, however, be significantly reduced.

Acute infectious arthritis develops within hours to days. The infection takes place in the joint or periarticular tissues from, is usually bacterial in nature and often affects younger adults with Neisseria gonorrhoeae as the most frequent pathogens. However, there are a number of other bacterial infections that can destroy joint structures quickly. Typical symptoms include a rapid onset of pain, effusion and limitation of active and passive mobility, usually affected in a single joint. The diagnosis is made with cultural examination with synovial fluid. Treatment consists of i.v. Antibiotics and joint drainage to remove the pus. Acute infectious arthritis can also occur in children, including about 50% are younger than 3 years old. By routinely vaccinating children against Haemophilus influenzae and Streptococcus pneumoniae, the incidence of joint infection in this age group could, however, be significantly reduced. The risk factors are listed in risk factors for infectious arthritis. Substantially increases the risk is with rheumatoid arthritis (RA) and other diseases that cause chronic joint damage in a history of a previous joint infection, with injection of drugs and prosthetic joints (joint prostheses infection) in patients. In RA patients, there is a particular risk for bacterial arthritis (prevalence of 0.3-3.0% annual incidence of 0.5%). When an infectious childhood arthritis no risk factors are mostly to be found. Risk factors for infectious arthritis Older age (50% of adults> 60 years) alcoholism arthrocentesis or joint surgery bacteremia cancer chronic medical illness (eg. As lung or liver disease) Diabetes Hemodialysis hemophilia previous joint infection in prehistory immunodeficiency (incl. HIV) immunosuppressive therapy (incl. Corticosteroids) injecting drugs joint prosthesis RA risk factors for sexually transmitted diseases (eg. As promiscuity, no barriers preventing) sickle cell anemia skin infections SLE The etiology of infectious agent reach the joint in a direct way by the penetration (eg. B. trauma, surgery, joint puncture, bites), expansion of an adjacent infection (z. B. osteomyelitis, Weichteilabszess, infected wound), or by hematogenous spread from a remote infection. The most common pathogens are listed in microorganisms that often cause acute infectious arthritis. In adults, a bacterial etiology most frequently, the classification divides gonococcal and Nichtgonokokken. This distinction is important because gonococcal infections are far less harmful to the joints. In adults, a total of Staphylococcus aureus seems to be the most common cause of infectious arthritis. Methicillin resistance is more common in isolates of S. aureus from community facilities. Neisseria gonorrhoeae is the leading cause undJugendlichen in young adults, N. gonorrhoeae spreads hematogenous infected mucous membranes (cervix, urethra, rectum, pharynx) from. These patients often have a simultaneous genital infection with Chlamydia trachomatis (chlamydia, mycoplasma and ureaplasma mucosal infections). Streptococcus species are also common causes, especially in patients with polyarticular infections. Patients receiving immunosuppressive therapy (eg. As TNF inhibitors, or corticosteroids) can develop septic arthritis by less frequent pathogens (mycobacteria, fungi). Pathophysiology The infectious agent proliferate in synovial fluid and in the synovium. Some bacteria (eg. B. S. aureus) produce virulence factors (adhesins), ie the thus facilitate penetration into the joint and the whereabouts of the infection of the joint tissue. Other bacterial products (eg. B. endotoxins of gram-negative pathogen, cell wall fragments, exotoxins of gram-positive pathogens, immune complexes, which are formed from bacterial antigen and antibodies of the host organism) amplify the inflammatory response. Polymorphonuclear granulocytes migrate into the joint and engulf the infectious agent. The phagocytosis of the bacteria also results in autolysis of granulocytes, with release of lysosomal enzymes in the joint damage the synovium, ligament and cartilage. Granulocytes are thus the most important defense mechanism of the host organism and at the same time the cause of joint destruction. The articular cartilage can be destroyed within hours to days. The inflammatory synovitis may occasionally persist, even if the actual infection was brought to decay by antibiotics. Particularly in cases of gonococcal infection persisting antigen can change cartilage by residual fragments of bacteria and infection and lead to antigenic properties, and it may be – together with the adjuvant effects of persistent bacterial components and immune complexes – develop an immune-mediated, sterile inflammatory synovitis. Microorganisms often an acute infectious arthritis cause patient population microorganism Typical sources adults and adolescents gonococcal (in young adults of reproductive age), other bacteria (Staphylococcus aureus, Streptococcus), Neisseria meningitidis cervical rarely, urethral, ??rectal or pharyngeal infection with bacterial sowing (if gonococci); Newborn bacteremia (with staphylococci and streptococci) Group B streptococci, Escherichia coli (and other gram-negative enteric bacteria), S. aureus maternalfetale transmission; iv Punctures or catheters transmission with bacterial seeding infants (? 3 years) Streptococcus pyogenes, Streptococcus pneumoniae, S. aureus bacteremia (z. B. in otitis media, urinary tract infections, skin infections, meningitis) Children (> 3 years) S. aureus, streptococci, Neisseria gonorrhoeae Pseudomonas aeruginosa, King kingae bacteremia or spread by continuity children with meningitis, bacteremia or palpable purpura N. meningitidis (rare) bacteremia Each age viral pathogens (e.g., parvovirus B19, hepatitis B or hepatitis C virus, rubella virus [active infection and after immunization];. Togaviru s; Chikungunyavirus; varicella; Mumps in adults; adenovirus; Coxsackievirus A9, B2, B3, B4 and B6; . Retroviruses including HIV, Epstein-Barr virus) viremia or immune complex deposition patients (with possible tick bite Borrelia burgdorferi causes Lyme disease) bacteremia patients with bite wounds (human, dog or cat, rat) often polymicrobial Human Eike Ella corrodens, group B streptococci , S. aureus, oral anaerobes (e.g., Fusobacterium sp, Peptostreptococci, Bacteroides sp…) dog or cat: S. aureus, Pasteurella multocida, Pseudomonas sp, Moraxella sp, Haemophilus sp… Rat: S. aureus, Streptobacillus moniliformis, Spirillum minus direct penetration into the joint (mostly small finger joints) Elderly patients with severe joint trauma or serious illnesses (. Eg immunosuppression, hemodialysis, SLE, RA, diabetes, cancer) staphylococci (especially wherein RA), gram negative bacteria (eg. B., Enterobacter, P. aeruginosa, Serratia marcescens), Salmonella sp. (Va * in SLE) skin infections patients with polyarticular infections patients with joint injury acnes ((by trauma, arthrocentesis or arthrotomy), infection by continuity, diabetes or cancer Streptococci Anaerobic z. B. Propionibacterium, Peptostreptococcus magnus, Fusobacterium sp., Clostridium sp, Bacteroides sp)..; often as a mixed infection with facultative or aerobic bacteria such as S. aureus, Staphylococcus epidermidis, E. (Coli pharyngitis, cellulitis, infections in the gastrointestinal tract and genital tract abdomen, groin, odontogenic infections, sinusitis, Extremitätenischämien, decubitus HIV-infected patients S. aureus, streptococci, Salmonella sp., Mycobacteria skin, mucous membranes, catheters, injection of drugs, lying vascular catheter z weakened. as for hemodialysis, apheresis or parenteral nutrition) gram-negative bacteria, S. aureus, streptococcus bacteremia can * inflammation be such that a lower threshold for aspiration and culture is needed; serious circumstances (eg. as immunosuppression, hemodialysis, SLE, RA, diabetes, cancer) may increase the risk for unusual infections (eg. as fungal, mycobacterial) increase. Symptoms and discomfort within a few hours to days, patients develop moderate to severe joint pain, warmth, tenderness, swelling, limited active and passive mobility and sometimes redness. Systemic symptoms are very pronounced or lacking. Infants and children can by limited spontaneous movements of a limb (pseudoparalysis), touch sensitivity, impaired food intake and a high, moderate or no fever is striking. Gonoccocal The gonoccocal can cause a distinctive dermatitis-polyarthritis-tenosynovitis syndrome. Classic manifestations include fever (for 5-7 days), multiforme lesions (petechiae, papules, pustules, hemorrhagic vesicles or bullae, necrotic lesions) on the mucous membranes and on the skin of the fuselage, hands or the lower extremities and migratory arthralgia, arthritis and tenosynovitis, which opens into a persistent arthritis in one or more joints. Most common of which are the small joints of the fingers, wrists, elbows, knees and ankles, rarely affected the joints of the axial skeleton. The symptoms of the original mucosal infection (z. B. urethritis, cervicitis) can fehlen.Nichtgonokokkenarthritis Nichtgonokokkenarthritiden cause progressive moderate to strongest joints, which are reinforced by motion and palpation. Septic joints are often swollen, reddened and overheated. In 50% of patients the fever is missing entirely or is not very pronounced; only 20% suffer from chills. Virulent microorganisms (eg., S. aureus, Pseudomonas aeruginosa) cause a more fulminant arthritis usually while less virulent microorganisms cause (eg. As coagulase-negative staphylococci, Propionibacterium acnes) to a less fulminant arthritis. In 80% of adult patients, the bacterial Nichtgonokokkenarthritis monoartikuläres shows a pattern of involvement, usually in one of the larger peripheral joints (knee, hip, shoulder, hand, ankle joint, or elbow). In children even ? 90% run monoarticular, most commonly the knee (39%), hip (26%) and ankle (13%) affected. A polyarticular infection is more common in patients receiving immunosuppression, concomitant chronic arthritis (z. B. RA, osteoarthritis) or have a streptococcal infection. In patients receiving the drugs by injection, and those with underlying vascular catheters is an infestation of the axial joints (sternoclavicular, kostochondral, hips, shoulders, vertebral body, symphysis pubis, sacroiliac joints) often. H. influenza can be a dermatitis-arthritis syndrome similar to gonococcal arthritis hervorrufen.Infektiöse by bite wounds Infection through bites by humans, dogs or cats developed generally within 48 hours. Rat bites call systemic symptoms such as fever, rash and joint pain or arthritis genuine regional adenopathy within 2-10 days hervor.Virale infectious arthritis Viral infectious arthritis usually causes symptoms that are similar to the bacterial Nichtgonokokkenarthritis, but more often than polyarticular with bacterial Muster.Borrelia burgdorferi -Arthritis patients with arthritis by B. burgdorferi often have other symptoms of Lyme disease (Lyme disease: symptoms and complaints) or have only an acute mono or oligoarthritis on. A polyartikuläres RA-like syndrome is quite uncommon and usually of a different diagnosis. Diagnostic arthrocentesis with examination of the synovial fluid and culture blood culture Occasionally imaging Usually blood count and BSG (or CRP) is a suspicion of infectious arthritis, patients with acute monoarthritis and patients with other symptom combinations that (for certain infectious arthritis syndromes z. B. migratory polyarthritis, tenosynovitis, typical skin symptoms of disseminated gonococcal infection, erythema migrans and other typical for Lyme disease findings – Lyme disease: symptoms and complaints). Even mild monoarticular joint symptoms should in patients receiving immunosuppressive therapy (eg. Corticosteroids, TNF inhibitors) with risk factors (eg. As RA), joint prosthesis, or extra-articular infection with a tendency to dissemination in joints (eg. As genital gonococcal infection, suggestive of this diagnosis pneumonia, bacteremia, any anaerobic infection). Tips and risks should be provided, arthrocentesis and culture of synovial fluid to rule out a joint infection in patients with joint effusion and findings that are consistent with a bacterial infectious arthritis, even if a known joint disease (eg. As RA) as a likely reason appears. General Arthritis The investigation of Gelenkpunktats is the most important diagnostic measure. The fluid is examined macroscopically, determination of leukocytes (with distinction), Gram stain, aerobic and anaerobic culture and search for crystals are the other important measures. A foul-smelling aspirate suggests an anaerobic infection. The infectious synovial contains> 20,000 / ul (sometimes> 100,000 / ul) leukocytes thereof> 95% granulocytes. The WBC count tends to be higher than in infectious gonoccocal in bacterial Nichgonokokkenarthritis. The leukocyte count is lower at a early treated or anbehandelten infection. By Gram stain, microorganisms can be detected in only 50-75% of the joints with acute bacterial arthritis, most commonly staph. With a positive result of the Gram stain is suspected, but not until the cultures provide the definitive proof. Are crystals prove so does not close the one of coexistent infection. Sometimes can not distinguish between an infectious and other arthritis using the synovial fluid. In such a case, and if the clinic does not help, a bacterial arthritis should be assumed until the contrary such. As is proved by cultures. Blood tests, such as blood cultures, blood count and BSG (or CRP) are usually carried out with. However, normal findings in these studies do not rule out an infection. Similarly, white blood cell count, ESR or CRP may be elevated in both non-infectious inflammation of the joints (including gout) as well as infectious arthritis. The uric acid serum levels should not be used to diagnose or exclude a gout as the cause of arthritis, since the mirror may be normal or even decreased. X-rays of the affected joint, the diagnosis does not prove it, but they can rule out other causes contemplated (eg. As fractures). In the early bacterial arthritis radiographically only soft tissue swelling and signs of effusion can be seen. Without treatment, however, the first destructive changes such as joint space (corresponding to a cartilage destruction) and erosions or foci of subchondral osteomyelitis are seen after 10-14 days. Is an air Sickle seen in the joint, this indicates an infection with Escherichia coli or anaerobes. An MRI is to think when the joint inspection and puncture is difficult to access (eg. As axial joints). By MRI or ultrasound, the location of the effusion or abscess can be made exactly visible, the effusion it one puncture and drainage for diagnostic and therapeutic purposes more accessible. The MRI can also make early an associated osteomyelitis visible. A technetium scintigraphy may give false negative results in infectious arthritis. Since there is a accumulation by increased blood flow in the inflamed synovial membrane and bone in metabolically active, it provides the other hand, even with a non-infectious arthritis, as in gout positive results. Nuclear Medicine and MRI do not distinguish between infection and crystal-induced arthritis. MRI of the wrist gonoccocal © Springer Science + Business Media var model = {thumbnailUrl: ‘/-/media/manual/professional/images/153_gonococcal_arthritis_slide_2_springer_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media / ? manual / professional / images / 153_gonococcal_arthritis_slide_2_springer_high_de.jpg lang = en & thn = 0 ‘, title:’ MRT a gonoccocal in the wrist ‘, description:’ u003Ca id = “v37892876 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eDas T1-weighted MRI with gadolinium and coronary fat suppression of a wrist with septic gonoccocal shows diffuse synovial enrichment and erosions. u003c / p u003e u003c / div u003e ‘credits’ © Springer Science + Business Media’

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