Small Animal Clinic, University of Veterinary and Pharmaceutical Sciences, Brno, Czech Republic

Soontornvipart K, Zatloukal J, Kohout P,  Dvorak M. Case study: Clinical and laboratory findings in dogs with septic joint arthritis, Online Journal of Veterinary Research7 : 43-51, 2003. Clinical and laboratory findings were evaluated in 18 dogs with suspected septic arthritis of stifle, elbow, carpal,  hip and/or tarsal joints. In 11 dogs, the arthritis was blood borne, and in 7 occurred after joint surgery or trauma.  All dogs had joint pain and resisted joint movement. Primary bacterial sources were associated with abscesses, bite wounds, enteritis, dermatitis, cystitis and/or endometritis after birth. Sinovial fluid revealed Staphylococcus intermedius, Streptococcus spp, Enterococcus Group 3, Pseudomonas aeruginosa, Coagulative-negative staphylococcus (CNS), and Bacillus spp but only in 8 dogs.  In 16 joints, total nucleated cell count in synovial fluid was 50 x 10⁹/l or more, and  neutrophils varied from 50% to 95%.  Radiography revealed soft tissue swelling or joint effusion (17 joints), subchondral bone destruction (6 joints) and new bone proliferation (11 joints).

KEY-WORDS: Septic Arthritis, Clinical-Laboratory, Dogs

Septic arthritis caused by bacterial infection is rare, but when it does occur, it usually develops rapidly into acute suppurative arthritis. Pain, lameness, and limitation of joint movement occur along with the classic signs of inflammation, swelling, redness, heat, and tenderness. Joint effusion appears early, thus providing an important diagnostic tool. Blood borne suppurative arthritis is unusual in the dog, but when seen, occurs most often in the young or debilitated animal (Schrader, 1982).

The most common entry points are penetrating or surgical wounds. Early diagnosis and treatment prevents the development of septic arthritis. Similarly, injuries treated early by arthrotomy, debridement, and irrigation have a better prognosis than those treated several days later (Piermattei and Flo, 1997). Articular plates have little or no capacity for regenerative healing and there is usually an extension of granulation from one subchondral area to the other across the joint space resulting in ossification/ankylosis.

Organisms reach joint tissue through circulation from a primary septicemia such as bacterial endocarditis, pneumonia, or abscesses (Bennett and Taylor, 1988; Egan et al., 1999). Septic arthritis may develop after arthrocenthesis or injection in patients with rheumatoid arthritis or pre-existing joint diseases (Hultgren et al., 1998; Laho and Kotilaien, 2001; Liu et al., 2001; Mclnnes et al., 1998).

The severity of joint destruction depends on the type of bacteria and the duration of infection. Streptococcus and Staphylococci produce a large number of extracellular and cell-associated molecules such as kinases and peptidoglycans which activate plasminogen to 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.  Prevotella bivia (Laho and Kotilaien, 2001), Morexella kingae (Kingella kingae) (Esteve et al, 2001), Ehrlichiosis (Cowell et al, 1988), Erysipelotrix rhusiopatiae, Yersinia, Chlamydia (May, 1995), Pepto-streptococcus spp., Clostidium spp, Bacteroides spp. and Propionibacterium spp. (Hudgin et al., 1992) have been incriminated in joint infections. However, Staphylococcus aureus, hemolytic Streptococcus, Pseudomonas aeuginosa, and Klebsiella spp. (Abuekteish et al., 1996, Egan et al., 1999, Hultgren et al., 1998) are the most common. Clinical and laboratory findings in dogs (over a 3 year period) with septic arthritis are reported.

Dogs:12 male and 6 female dogs aged 5 weeks to 10 years (7 < 1 year), with 20 suspected septic arthritis joints were treated with Amoxicillin-Clavulanic acid (Synulox®; Augmentin®) (14), Cephalosporin (Cephaclen®) (2), Clindamycin (Antirobe®) (2), Enrofloxacin (Baytril®) (1) and Amikacin (Amikin®) (1 ) for 36 months. Breeds included German Shepherd (2) , Rottweiler (2), Giant Schnauzer (2), Cane Corso (2), Labrador Retriever (2), Brasilian Fila (1), Rhodesian Ridgeback (1), Great Dane (1), Chow Chow (1), Irish Setter (1), Hovawart (1), Bull terrier (1) Great Dane (1) and Bulldog (1).

Clinical examinations: Dogs were examined for septic joint arthritis when presenting temperatures (measured in 16 dogs) greater than 39,2 °C, pain (localized to the joint) made worse by gentle passive motion, swelling of the involved joint, leukocytosis  (>17 x 10⁹ /l) and monoarticular involvement. Lameness was categorized as mild, moderate, and severe. Radiographic examinations were performed in 17 patients on the 19-affected joints. Dogs were again evaluated for arthritis when presenting subchondral bone destruction, new bone proliferation, joint effusion and/or soft tissue swelling around the affected joint.

Sinovial tests: Arthrocentesis was performed aseptically and joint fluid was immediately examined cytologically and microbiologically. The total and differential leukocyte count (taken from 16 dogs) was determined from using the Coulter Counter® (Coulter Electronics Ltd., Harpenden Hearts, England) method. 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 MacConrey agar (CM 7b, Oxoid). All samples were cultured aerobically.

Recurrent septic joint arthritis was diagnosed over a 3 year period in 18 dogs (20 joints). In all cases septic arthritis was monoarticular. Affected were 8 stifle, 5 elbow, 4 carpal, 2 hip and 1 tarsal joint(s). Seven pups had hematogenous septic arthritis and 1 may have contracted the condition after surgery. Four joints were associated with previous arthrotomy, 1 with arthroscopy and 1 with joint trauma. Hematogenous infection was diagnosed in thirteen joints. Bacterial sources were abscesses (2 joints), bite wounds (2 joints), enteritis (1 joint), dermatitis and cystitis (1 joint) and endometritis after birth (1 joint) but primary bacterial sources were not identified in 6 joints. In one dog, arthritis may have been induced hematogenously and/or by direct infection through joint surgery.

Joint pain was present in all patients and swelling with local temperature rises occurred in all except 2 hip joints. Severe, moderate, and mild lameness occurred in 3, 8 and 9 dogs, respectively . Acute lameness (< 1 week) was detected in 10 and chronic lameness (> 1 month) in 5 dogs.  Rectal temperatures increased above 39.2 °C in 9 dogs, and leucocytosis (>17 x 10⁹ /l) was detected in 5 dogs.

Radiographic soft tissue swelling or joint effusion (17 joints) appeared in all dogs with subchondral bone destruction in 6 joints and new bone proliferation in 11. The subchondral bone destruction was associated with chronic lameness.

Arthrocentesis was performed in all joints but in 2 there was only enough fluid for cytology. In 18 synovial fluid samples, total nucleated cell counts from synovial fluid was evaluated and its average was 83,8 x 10⁹ /l with a range of 15.1 to 223.7 x 10⁹ /l). In 16 septic joints, total nucleated cell count in synovial fluid was higher than 50 x 10⁹ /l.  The proportion of neutrophil in synovial fluid was varied from 50% to 95%. However, in 15 samples, the proportion of neutrophil was > 90%.

Bacteria (cocci) were detected in four samples. Bacterial culture results from synovial fluid were positive in 8 samples. In one dog, positive cultivation was obtained from the private practice 2 days before admission to our clinic. Type of bacteria, route of infection and suspected primary source of bacteria were presented in Table 1.

Probability of positive cultivation was not related to any clinical, paraclinical and laboratory signs of septic arthritis. In vitro cultivation was associated with bacteria in synovial fluid and direct route of joint infection (Fisher´s test; p=0.15).

Antibiotic treatments with Amoxicillin-Clavulanic acid (Synulox®; Augmentin®) in 14 dogs, Cephalosporin (Cephaclen®) in 2, Clindamycin (Antirobe®) in 2, Enrofloxacin (Baytril®) in 1, and Amikacin (Amikin®) in 1, resolved the condition. In 2 dogs, arthritis recurred in different joints at 3 weeks and 2 years (after treatment) but resolved after a repeat treatment. In one dog, recurrent septic arthritis associated with coexistent systemic lupus erythematosus (SLE) in a different joint was resolved with azathioprim (Imuran®) and corticosteroid.

Affected dogs were medium to large breeds, 70% of cases were blood borne 30% by infection after joint surgery or direct trauma. Risk of infection by the hematogenous route is high in puppies; in the present study, 87.5% of puppies (<1 year), became infected through blood. These findings confirm those reported previously (Bittegeko et al, 1993).

In the present study, all the dogs presented non-specific joint effusion with  mild to severe osteoarthritis; not a definitive diagnosis. In fact, bone proliferation is not commonly found in septic arthritis; however, it can be found in dogs with pre-existing hip dysplasia, cruciate ligament rupture, fragmentation of the coronoideus process and un-united anconeal process. Subchondral bone destruction was detected only in 6 joints with chronic lameness. In human patients, radiography and scintigraphy are used to localize inflammatory foci (Corsten and Van der Meer, 1999; Perez, 1999). Arthritis often appears clinically before radiographic change is presented. Therefore radiographs and MRI do not  assist in the diagnosis (Strouse et al., 1999). In fact, bacterial arthritis may be confused with other arthritides (Owen and Ackerman, 1978) due to their similar radiographic abnormalities. However, plain X-rays may be useful to detect associated conditions and to study progression.

In the present work 78% of dogs had a leukocyte count greater than 50,000 cell/microliter and the percentage of sinovial fluid neutrophils varied from 50% to more than 95% in all patients, suggesting bacterial infection in joints (Dubost et al., 2000). In septic arthritis, about 50% of patients have fever with acute lameness and always have leukocytosis.  Joint fluid appears with polymorphonuclear leukocytes from 40,000/mm3 to 50,000/mm3 in early infection, rising rapidly to 100,000/mm3 or higher depending on the type of organism and the duration and severity of the infection. Sinovial fluid glucose is usually reduced (in contrast to blood glucose) due to the inceased metabolism of polymorphonuclear leukocytes (Dubost et al., 2000).

Staphylococci, Streptococci and Pseudomonas isolated in the present study have been reported in sinovia of persons and small animals (Abuekteish et al, 1996, Egan et al, 1999, Knight et al, 1996, Dubost et al, 2000; Ryan et al, 1997)  However, the cultures reported herein were lower than previously found (Egan et al, 1999; Boon, 1997; Fink and Nelson, 1986; Ryan et al, 1997; Boon, 1997; Barton et al, 1987; Fink and Nelson, 1986;Goldenberg and Cohen, 1976; Welkon et al, 1986). Purulent exudates exert an inhibitory effect upon bacterial growth, which may explain the overall low sensitivity of synovial fluid cultures in the dogs.

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