Septic Arthritis in Dogs: A Retrospective Study

Soontornvipar t K. , P. Kohout , P. Proks: Septic Arthritis in Dogs: A Retrospective Study of 20 Cases (2000-2002). Acta Vet. Brno 2003, 72: 405-413. Septic arthritis might be difficult to diagnose due to nonspecific clinical signs and radiological findings in early stage of the disease. An early diagnosis is important for achieving favorable prognosis. Diagnosis of septic arthritis was confirmed by physical and orthopedic examinations, evaluation of radiographs and synovial fluid analysis including leukocyte and neutrophil counts, cytological examination and bacterial culture. Sensitivity and specificity of these diagnostic methods were retrospectively evaluated from clinical records of 18 dogs with 20 septic joints treated in the Department of Surgery and Orthopaedics in Small Animal Clinic at University of Veterinary and Pharmaceutical Sciences Brno from January 2000 till the end of 2002. Our patients affected by septic arthritis belonged to medium to large breed dogs. Infection of 13 septic joints in 11 patients was spread by hematogenous route, whereas the other 7 joints (in 7 patients) were infected during surgical procedure or after joint injury. Recurrence of hematogenous joint infection was found in 2 patients. In all the patients, exercise intolerance and painful reaction in affected joint were detected. Cultures of synovial fluid samples were positive in only 8 cases. Staphylococcus intermedius, Streptococcus spp., Enterococcus Group 3, Pseudomonas aeruginosa, coagulase-negative staphylococcus and Bacillus spp. were isolated. Radiographic findings included joint effusion, osteoarticular destruction and new bone proliferation and these were not specific for septic arthritis. We found that diagnostic methods used in this study showed high sensitivity but low specificity. Complex diagnostic approach including physical, orthopaedic and radiographic examinations, and synovial fluid evaluation should be performed to achieve correct diagnosis and effective treatment. Joint infection, radiography, synovial fluid, diagnosis, treatment Inflammatory joint diseases caused by infection or immunological factors are not rare in small animal practice but they occur infrequently. Generally, the septic arthritis caused by bacterial infection is very rare (Schrader 1982). Bacterial infections of joints usually begin suddenly and develop rapidly into an acute suppurative arthritis. Pain, lameness, and limitation of joint motion occur along with the classic signs of inflammation, swelling, redness, heat, and tenderness. Joint effusion is present early, thus providing a very important diagnostic tool. Suppurative arthritis due to hematogenous spread is unusual in the dog and, when seen, is most often in the young or debilitated animal. The severity of joint destruction depends on the type of bacteria and the duration of infection. Each type of bacteria can cause arthritis in a different way. Streptococci and staphylococci produce a large number of extracellular and cell-associated molecules such as kinases and peptidoglycans. They activate plasminogen and result in plasmin, which removes chondroprotein from cartilage matrix (Liu et al. 2001). Corynebacterium pyogenes infection causes severe pannus formation (granulation) over cartilaginous surfaces, whereas Clostridium species can elaborate collagenase. Although many pathogens have been incriminated in joint infections such as Prevotella bivia (Laho and Koti laien 2001), Moraxella kingae (Kingella kingae) (Esteve et al 2001), ehrlichiosis (Cowell et al 1988), Erysipelothrix rhusiopathiae, Yersinia, Chlamydia (May 1995), Peptostreptococcus spp., Clostridium spp., Bacteroides spp. and Propionibacterium spp. (Hudgin et al. 1992) were reported, the ones that most commonly attack these tissues are Staphylococcus aureus, hemolytic Streptococcus, Pseudomonas aeruginosa, and Klebsiella spp. (Abuekteish et al. 1996; Egan et al. 1999; Hultgren et al. 1998). The infecting organism reaches the joint tissue (by hematogenous spread) as a result of a primary septicemia from a bacterial endocarditis, pneumonia, or abscess in another part of the body (Bennett and Taylor 1988; Egan et al. 1999). Furthermore, septic arthritis may develop after arthrocenthesis or injection especially in the patient with rheumatoid arthritis or with preexisting joint diseases (Hultgren et al. 1998; Laho and Koti laien 2001; Liu et al. 2001; Mclnnes et al. 1998). The most common entry is a surgical wound (during surgical procedure) or a direct penetrating wound (e.g. bite wounds). It was reported that males are almost two and half times more often victims of aggression than females and that the highest incidence of bite wounds was in oneand two-year-old animals (Baranyiová et al. 2003). A penetrating joint wound has the potential to be a permanently disabling injury. Early and effective treatment may be relatively simple, but if septic arthritis develops, effective treatment is difficult. Early diagnosis and treatment are of utmost importance. Nevertheless, when there has been a delay in instituting the proper treatment, the presenting problem may be septic arthritis. Successful results are dependent upon early diagnosis and proper treatment. Penetrating joint injuries treated early by arthrotomy, dèbridement, and irrigation have a better prognosis than those treated several days later since sepsis and potential irreparable damage may be avoided (Piermattei and Flo 1997). Today, because of the development of specific antibiotic agents and the early aggressive treatment, the complete course of suppurative arthritis is seen less often. It is imperative that the clinician can make an early and accurate diagnosis so that the infection may be treated aggressively and cured before irreversible joint damage takes place (Sakiniene and Coll ins 2002). This is fortunate because the articular plate has little or no capacity for regenerative healing. With the loss of articular plates, there is usually an extension of granulation from one subchondral area to the other across the joint space. As the granulation ages, it forms collagen scar tissue, and a fibrous ankylosis is the result. The collagen often calcifies as it condenses, followed usually by ossification/ankylosis. In short, if the joint infection progresses to destruction of the articular plate, joint destruction and patient crippling will be the result. The purpose of our study is to present the clinical and laboratory findings associated with septic arthritis in small animal practice and to determine sensitivities of clinical, paraclinical and laboratory signs of septic arthritis. 406 Table 1 Bacterial culture from synovial fluid Type of bacteria Route of infection Suspected primary source Staphylococcus spp. Direct route Infection after arthrotomy: UAP Streptococcus spp. Direct route Infection after arthrotomy: CCL Pseudomonas aeruginosa Direct route Infection after arthrotomy: CCL Bacillus spp. Direct route Trauma after kicking of horse Pseudomonas aeruginosa Hematogenous route Endocarditis Streptococcus spp. Hematogenous route Not detected Enterococcus Hematogenous route Enteritis Staphylococcus coagulase negative Hematogenous route Cystitis Corynebacterium striatum * Hematogenous route Septicemia, abscess after vaccination * cultivation positive from sample obtained in private practice two days earlier Materials and Methods Clinical records of 18 dogs with 20 suspected septic joints, treated at the Department of Surgery and Orthopaedics in Small Animal Clinic, University of Veterinary and Pharmaceutical Sciences Brno, during a threeyear period (from January 2000 till the end of December 2002) were reviewed and evaluated. Clinical signs were diagnosed and evaluated when the patients were presented with the following clinical conditions: fever (> 39.2 °C), pain (localized to the joint) made worse by gentle, passive motion, swelling of the involved joint, leukocytosis (> 17 × 109.l-1), monoarticular involvement. Lameness was categorized into 3 degrees of severity (mild, moderate, and severe lameness) according to veterinarian’s justification. Based on duration of gait abnormality, the lameness was classified as acute (< 1 week duration) or chronic (> 1 month). Radiographic examinations were performed in 17 patients on the 19affected joints. In 3 patients, the clinical signs were sufficient to diagnose, so the radiographic examination was not performed. Radiographic changes were interpreted and evaluated by the veterinary radiologist. Radiographic findings were observed as the following changes: subchondral bone destruction, new bone proliferation, joint effusion/soft tissue swelling around the affected joint. Arthrocentesis was performed aseptically and joint fluid was immediately examined cytologically and microbiologically. The total leukocyte count was determined using the Coulter Counter® (Coulter Electronics Ltd., Harpenden Hearts, England). Synovial fluid was smeared onto the slide and then stained with May-Grünwald and Giemsa-Romanowsky for the differential leukocyte counts. The proportion of neutrophils and other white blood cells were recorded. Synovial fluid was inoculated onto Amies transport medium (CM 425, Oxoid) or Cary-Blair medium (CM 519, Oxoid). Bacterial culture was performed by inoculation of the sample onto Blood agar base (CM 854, Oxoid) and MacConkey agar (CM 7b, Oxoid). All samples were cultured aerobically. All dogs were treated with antibiotics. The follow up and the outcome of treatment were observed and recorded.