Multi-drug-resistant Enterococcus spp. as a cause of non-responsive septic synovitis in three horses

Abstract

CASE HISTORY: Three Thoroughbred horses, a 6-week-old filly (Case 1), a 15-year-old broodmare (Case 2) and a yearling filly (Case 3), sustained synovial sepsis secondary to trauma.

CLINICAL FINDINGS: Case 1 presented with a heel bulb laceration communicating with the distal interphalangeal joint. Arthroscopic lavage was performed and treatment commenced using systemic and local broad spectrum antimicrobial drugs. A pure growth of multi-drug-resistant (MDR) Enterococcus gallinarum was cultured from samples of synovium and joint fluid. Antimicrobial treatment was changed according to the susceptibility results. Response to treatment was poor and despite repeat arthroscopic lavage and intra-osseous regional perfusion of antimicrobials the filly was subject to euthanasia 24 days after the initial injury. Post-mortem examination confirmed septic synovitis, cartilage degeneration and osteomyelitis.

Case 2 sustained a full thickness wound to the carpus which was sharply debrided and closed. The wound dehisced with effusion within the tendon sheath. Drainage was established and treatment included systemic broad spectrum antimicrobials, topical lavage with povodine-iodine and manuka honey infusion. A mixed infection including MDR Enterococcus faecalis was cultured from the synovial fluid. Antebrachiocarpal joint effusion developed 21 days after initial injury and joint sepsis was confirmed. Arthroscopic lavage and tendon sheath debridement were performed, followed by treatment with systemic and local antimicrobials. The mare improved and was discharged. Three months later lameness recurred and corticosteroids were administered intra-articularly. The mare became non-weight bearing lame and was subject to euthanasia. Post-mortem examination confirmed joint sepsis of the antebrachiocarpal and intercarpal joint.

Case 3 presented with a complete articular open fracture of the tibial crest. Under general anaesthesia the fracture was stabilised and the wounds debrided and closed. Systemic broad-spectrum antimicrobials were administered. Six days later the wound dehisced and a bone fragment was removed. Three weeks post-surgery the wound deteriorated with a purulent discharge. Culture of the discharge revealed a mixed bacterial infection, including a MDR Enterococcus faecalis. Femoropatellar joint involvement was confirmed, and treatment included joint lavage, local and systemic antibiosis, and manuka honey instilled into the wound. The filly initially improved, and then deteriorated such that euthanasia was performed.

DIAGNOSIS: All three cases had synovial sepsis with MDR Enterococcus spp.

CLINICAL RELEVANCE: Increased awareness of MDR pathogens in equine wound infections is essential. Prompt diagnostic testing, appropriate therapy, infection control strategies and on-going monitoring and management are vital to limit the clinical impact of these organisms.     

Antigenic stability of fimbriae of Bacteroides nodosus

Successful vaccination of sheep against footrot and attempts to eradicate the disease depend on there being a limit to the antigenic diversity of the causative bacterium, Bacteroides nodosus. Fimbrial antigenic variation was therefore investigated in vivo, both under conditions of chronic infection and under the pressure of a vaccine-induced immune response, to ascertain whether this represented an obstacle to such goals. Material was available from 5 experiments and although B. nodosus appeared to have undergone changes in its fimbrial antigens in one of these, the possibility that superinfection was responsible for the variation detected could not be ruled out because all sheep in this case were maintained at pasture. Overall, the results provided no evidence of fimbrial antigenic shift in B. nodosus in vivo and in conclusion, the survival of the organism in the sheep's foot, both in long-term natural infection and following vaccination, must therefore be related to factors other than the ability to undergo antigenic variation in order to evade the host's immune response.