Hypothesis 2
Group 11-Final Case

Although not a common finding in small animals, a bacterial infection within the stifle joint could explain the clinical signs of this dog.  This patient fits the typical signalment of septic arthritis in that she is a middle-aged Labrador retriever.  There are four major means of infection: hematogenous,  extension of osteomyelitis, trauma, and iatrogenic.  

There is no history that would support a hypothesis of iatrogenic introduction of bacteria to the joint, so this can be discarded.  Hematogenous spread of bacteria is a possibility, but you would expect to see some other signs of systemic or local infection from which the bacteria could disseminate.  There is no history of fever, gastrointestinal disease, pneumonia, dental problems, or other sources of infection.  While this method of infection is more likely than iatrogenic, it is unlikely.  This leaves extension of osteomyelitis or traumatic introduction of bacteria into the joint.  From the history, trauma seems most likely.  Acute osteomyelitis is generally from infection of a fracture site or dead bone fragment, the presence, of which, is unlikely from the history.  Bonnie goes on hikes in the woods, plays fetch with her owner, and has a propensity to chase other dogs and cats.  These activities provide ample opportunity for her to impale herself on a stick or thorn, or receive a bite wound in the area of her stifle.  Whatever the case, the mechanism of infection and development of clinical signs are similar.

Any wound or trauma can damage tissue that can be infiltrated by bacteria, which can begin to proliferate or move to nearby soft tissues or joints.  In order for a joint to become infected, the bacteria must be of sufficient virulence and number to bind to the synovium and begin to proliferate.  In joints, the synovial capillary tufts favor entrapment of bacteria and localize them to the synovial lining of the joint.  Once the bacteria begin to multiply, the immune system is stimulated and a series of events begins within the joint.  

The bacteria set off a cascade of events that lead to the clinical signs of heat, pain, swelling, redness, and loss of normal function: the immune response. The immune system releases chemical mediators like histamine that cause vasodilation (redness and heat) and vascular permeability .  Serous exudate rich in protein seeps out of the leaky capillaries (swelling).  The histamine and other chemotactic factors attract phagocytes such as neutrophils and later monocytes to the area of inflammation (further swelling) to engulf and lyse the bacteria, and then clean up the waste.  The chemical mediators also irritate nerve endings in the joint capsule (pain and loss of function).  Lysosomal enzymes from leukocytes can begin to digest the debris with in the joint.  However, these enzymes are not specific.  Once released, they will begin to digest whatever material with which they come into contact.  This includes cartilage and ligaments within the joint.  With aggressive inflammation, joint effusion and possible instability can develop as in this case.