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A calf was treated for chronic infectious arthritis and osteomyelitis of the carpus and metacarpus by carpal bone excision, debridement, and cancellous bone graft placement in the metacarpal medullary cavity. Following 6 weeks of limb immobilization, carpal-metacarpal arthrodesis was achieved. The heifer is pain free, and has produced 3 calves.
The results from animal studies of bacterial joint infection have demonstrated pathogenic changes in synovium, cartilage, and bone which lead to joint destruction. Mechanisms responsible for the changes in these articular components remain to be more completely defined in order to develop methods to prevent articular destruction. Eradication of the active infectious process with early institution of antibiotics and adequate drainage is required but is not sufficient to prevent chronic destructive processes initiated by the acute bacterial infection. Biochemical effects of changes in the anabolic and catabolic functions of the cells in bone, cartilage, and synovium and the control mechanisms for these functions undoubtedly hold the key to prevention of destruction in infectious arthritis. Much less is understood about the pathogenic changes and mechanisms in infections caused by anaerobic bacteria, mycobacteria, fungi or viruses. Application of advances in immunological, morphological and biochemical techniques to animal models of infectious arthritis provides the opportunity to increase understanding of pathogenic mechanisms and to develop innovative methods of treatment.
In contrast to the outstanding achievements made in therapy for autoimmune arthritides, not least rheumatoid arthritis, the pace of progress in therapy for infectious arthritis remains slow. This has primarily to do with the complex task of, on the one hand, killing the invading microorganisms and, on the other, to down-regulate the exaggerated immune response which participates in the microbial clearance but at the same time contributes to the tissue destruction. The use of experimental models of microbial arthritides has clarified several bacterial virulence factors as well as many haematopoietic cell types and their products that are involved in the pathogenesis of joint infection. Recent studies have documented that T-cell-mediated responses are not only prominent but also decisive with respect to disease sequelae. This chapter also reviews the primarily protective non-antigen-specific immune responsiveness to microbial agents, including the impact of neutrophils, complement system, and nitric oxide. The knowledge gained regarding microbial virulence factors and the host immune responses has prompted researchers to develop new strategies on how to interact in vivo with the infectious process. Some of these approaches are commented upon in this review: e.g. vaccination procedures to prevent septic arthritis and sepsis, as well as therapeutic procedures to minimize joint damage during an ongoing infection.
Propionibacterium acnes, a micro-organism with low pathogenicity, rarely causes arthritis in a joint without a prosthesis. This report deals with two cases of P acnes infectious arthritis probably caused by direct penetration of the micro-organism into the joint space during arthrocentesis, despite the use of strict disinfection procedures. P acnes isolated from synovial fluid cannot be dismissed as a bothersome contaminant without due consideration of the clinical status of the individual patient.
Chemical and cytologic effects and bactericidal activity of gentamicin in septic synovial fluid were evaluated in an experimental model of infectious arthritis in horses. Septic arthritis was induced by inoculation of approximately 7.5 X 10(6) colony-forming units of Escherichia coli into 1 antebrachiocarpal joint in each of 16 clinically normal adult horses. Clinical signs of septic arthritis were evident 24 hours after inoculation. Horses were allotted to 3 groups: group-1 horses (n = 5) each were given 150 mg of gentamicin (50 mg/ml; 3 ml) intra-articularly (IA); group-2 horses (n = 5) each were given 2.2 mg of gentamicin/kg of body weight, IV, every 6 hours; and group-3 horses (n = 6) each were given buffered gentamicin, consisting of 3 mEq of sodium bicarbonate (1 mEq/ml; 3 ml) and 150 mg of gentamicin (50 mg/ml; 3 ml), IA. Synovial fluid specimens were obtained at posttreatment hour (PTH) 0, 0.25, 1, 4, 8, 12, and 24 via an indwelling intra-articular catheter. Synovial fluid pH was evaluated at PTH 0, 0.25, and 24. Microbiologic culture and cytologic examination were performed on synovial fluid specimens obtained at PTH 0 and 24, and gentamicin concentration was measured in all synovial fluid specimens. At PTH 0, E coli was isolated from synovial fluid specimens obtained from all horses. Synovial fluid pH was lower (range, 7.08 to 7.16) and WBC count was higher (range, 88,000 to 227,200 cells/microliters) and predominantly neutrophilic (95 to 99%) at PTH 0 than before inoculation.(ABSTRACT TRUNCATED AT 250 WORDS)
An infection of native joints leads generally to suppurative arthritis, which may be of one joint (monarticular) or several joints (oligoarticular). Bacteria that produce symptoms in multiple joints during bacteraemia, such as Neisseria gonorrhoeae, may also induce inflammation in the neighbouring tendon sheaths. Viral infections frequently involve multiple joints and produce inflammation without suppuration. Chronic granulomatous monarticular arthritis may occur because of infection with either mycobacteria or fungi, which must be differentiated from other causes of chronic monarticular arthritis. A sterile arthritis may occur early in infection (as with hepatitis B), or later (as with a post-infectious arthritis). Any patient presenting with an inflamed joint should have infection as a diagnostic possibility and appropriate cultures must be performed.
Significant amounts of collagenase and caseinase activity were detected in infected synovial fluid samples. Partial characterisation of the enzymes by gel filtration suggested that synovial fluid from cases of infectious arthritis may contain enzymes from both the synovial cells and neutrophils. This finding was also supported by analysis of sequential synovial fluid samples from 4 infected joints. In 3 joints the concentration of caseinase and in 1 joint collagenase paralleled the decline in total nucleated cell count. However, in 3 joints the concentration of collagenase remained high after the total nucleated cell count had returned to normal, suggesting that this enzyme originated from resident articular cells.
A 63-year-old woman with pancreatic diabetes after a total pancreatectomy and splenectomy developed discitis of the L2/3 intervertebral disk. Rapidly she also developed infectious arthritis of the left knee joint and bacterial meningitis. Aspirate from the left knee contained Enterococcus faecalis. The diagnosis of discitis is generally difficult in the initial period of disease, and patients with diabetes or splenectomy are susceptible to rapid progression of the infection. Early diagnosis of discitis using magnetic resonance imaging of the spine and treatment with antibiotics might have altered her clinical course.
A case of acute hip pain in rheumatoid arthritis is presented, with synovial membrane findings. A patient with classical rheumatoid arthritis suffered three unusual bouts of sudden, severe but transient hip pain. The hips were clinically normal between these episodes. The clinical picture on two of these occasions strongly suggested septic arthritis. Although the synovial fluid was highly inflammatory, cultures were negative. The synovial membrane showed mild lining cell hyperplasia, vascular congestion, and scattered inflammatory cells, predominantly lymphocytes. These findings were not compatible with either pyogenic infection or longstanding rheumatoid arthritis. The clinical and pathological features of acute non-infectious arthritis of the hip appear to delineate a distinct syndrome.
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Septic arthritis results from invasion of the synovium by microorganisms, and most infectious organisms can cause arthritis. In children, septic arthritis is usually associated with systemic infections such as pneumonia or meningitis; in young adults, gonococcal arthritis is the most common cause; and in the aged, septic arthritis is usually superimposed on chronic joint disease. Underlying rheumatoid arthritis is common, and Dr. Knights stresses the importance of recognizing septic arthritis as a complication of rheumatoid arthritis.
'Spontaneous' lymphoblastoid cell lines (LCL) were established from patients with either rheumatoid arthritis (RA) or infectious mononucleosis (IM) or from healthy donors. Differences in Epstein-Barr virus (EBV) strains were determined by measuring the mol. wt. and expression of viral antigens in each of the LCLs. In addition to the previously reported EBV nuclear antigens, the LCLs also contained EBV-induced antigens with mol. wt. of 48K and 58K which were present in all but two of the lines. One of the differences observed between each of the groups of cell lines was their ability to produce viral antigens. Early and late antigens were identified by immunoblotting in most of the RA lines, two of the normal lines but none of the cell lines from patients with IM. Many of the IM cell lines were also found to express multiple EBNA1 antigens. The results demonstrate that a variety of wild-type EBV strains exist. However, the similarities observed in a number of the lines suggest that the diversity of strains may be limited.
Polymerase chain reaction and other DNA amplification techniques to identify elusive infections should prove to be an effective tool for the clinical and investigative rheumatologist. The capability to identify and characterize infectious organisms in fluids and tissue will enable early, specific, and potentially curative treatment. Similarly, the capability to exclude infection and differentiate postinfectious diseases will enable other therapies to control the inflammation. Understanding these molecular techniques will most certainly improve clinicians' effectiveness for diagnosis and care.
Disorders of immunoglobulin synthesis are of great interest to rheumatologists. At the diagnostic level, such disorders not uncommonly mimic commoner rheumatic diseases, so it is important that the diagnostic possibility of immunodeficiency be kept in mind. Infections often complicate immunodeficiency and may present in an atypical manner. From the theoretical standpoint, the interactions between infectious agents and patients with impaired immunity suggest ways in which the same or similar agents could be responsible for arthritis of unknown etiology. Furthermore, many immunodeficiency disorders predispose to autoimmunity; establishing the mechanism of this association may offer good insights into the factors that trigger autoimmune disorders in patients with seemingly normal immune competence.
UNLABELLED: In joints with bacterial arthritis, continuing prolonged destruction of cartilage may occur in spite of prompt, effective antibiotic therapy. We measured the extent to which early antibiotic therapy with ceforanide altered the degradation of the cartilage after arthritis due to Staphylococcus aureus had been produced in the knee joint in rabbits. Degradation of the cartilage was quantified by analyses for glycosaminoglycan and collagen. Three weeks after the infection was produced, the cartilage had lost more than half of its glycosaminoglycan whether the antibiotic therapy had been started at one, two, or seven days after infection. Beginning the antibiotic treatment one day after infection reduced over-all loss of collagen by 37 per cent and decreased the area of erosion of the infected articular surfaces. When antibiotic treatment was begun at four, eight, or twelve hours after infection, the loss of glycosaminoglycan averaged 18 per cent. Prophylaxis with antibiotics completely prevented any degradation of the cartilage. CLINICAL RELEVANCE: The findings reported here show how rapidly cartilage loses glycosaminoglycan when it is involved by arthritis caused by staphylococci and how early treatment of the infection reduces the loss of collagen. There is less protection against loss of glycosaminoglycan. The results emphasize the need for early diagnosis and treatment of infectious synovitis and support the rationale for early administration of antibiotics without waiting for identification of the responsible bacteria.
Any patient who presents with an acute monarticular arthritis, especially a new asymmetric effusion with underlying joint disease, should be suspected of having a bacterial process. Because synovial fluid findings (leukocyte counts and glucose) may not be predictive of infection, bacteriologic analysis by smear and culture is necessary in the evaluation of any new synovial effusion. A chronic monarticular process is highly likely to be infectious also, but mycobacterial or fungal etiologies frequently require appropriate culture of synovial tissue in addition to processing fluid. Acute polyarticular syndromes are seen as manifestations of disseminated gonococcal infections (DGI) and certain viral infections in adults. Diagnostic clues include historic and physical findings (exposure history and type of rash). The major pathogen in adults remains Staphylococcus aureus, so initial therapy is directed at this organism unless urinary tract infection is present also. Proper recommended therapy for DGI is ceftriaxone because penicillin-resistant strains are present in many urban centers. Early recognition and treatment of bacterial arthritis may prevent poor outcome, particularly in elderly patients or those with underlying joint diseases. For chronic mycobacterial or fungal infections, surgery may need to be combined with medical management.
In experimentally-induced erysipelas polyarthritis, preexisting cartilage canals in articular cartilage play a crucial role during the very onset of the disease. This observation might have some implications for the pathogenesis of other infectious arthritides in young animals or even rheumatoid arthritis in man.
Five patients with rheumatoid arthritis and no previous hip joint disease developed an acute disabling arthritis in one hip joint. Roentgenograms were negative and synovial fluid from the hip joint was inflammatory, but no crystals were seen and cultures were negative. Four of the five patients responded rapidly to intra-articular corticosteroids, and none of the five has had further hip joint symptoms during a mean follow up period of two years.