Diagnosis Case 3

	The diagnosis for this case is septic arthritis due to trauma.  The mother probably 
did step on the foal causing the introduction of Klebsiella pneumoniae into the joint.

Pathogenesis
	In order to get septic arthritis there must be introduction of bacteria into the joint.  
The inoculation of the synovial membrane or synovial fluid with bacteria will cause an 
inflammatory reaction.  The bacteria were probably introduced through trauma.  Horses 
are particularly susceptible to joint infection because of the minimal soft tissue covering 
over the joints.  This lack of soft tissue covering provides little protection of the joint.  
Although traumatic septic arthritis usually occurs in older animals, the trauma of the 
mother stepping on the foal leads us to believe that the infection was due to trauma.
	The foal probably did not get the joint infection from the hematogenous route (i.e. 
through the umbilicus) because the patient is afebrile, the leukogram is normal and only 
one joint is infected.
	The clinical signs also point to arthritis with the toe-touching lameness.  The 
physical findings did not say if there was heat, but there is pain and swelling associated 
with the joint.
	Joint infections start with the introduction of bacteria into the joint capsule.  The 
synovial capillary tufts are an ideal place for bacterial colonization.  Once the bacteria 
have colonized the joint, they stimulate a cascade of events beginning with damage to the 
chondrocyte or cartilage matrix.  The damage to the cartilage matrix is started with the 
inflammation of the joint and the release of enzymes and inflammatory mediators that 
cause the destruction of the articular cartilage.  The loss of glycosaminoglycans and 
proteoglycans from the matrix ultimately causes the breakdown of proteoglycan and 
collagen.  Free fragments are released into the synovial fluid.  The synovial macrophages 
are released to remove debris.  The inflammatory process causes the synovial membrane 
to thicken.  The subsynovial layer thickens due to increased activity of fibroblasts and 
fibroplasia.  The synovial vasculature becomes more permeable in response to the 
inflammation and as a result, more fluid accumulates in the joint.
	The inflammatory products released during the inflammation of the joint cause 
the serious damage to the joint.  Cytokines such as interleukin-1 decrease the ability of 
chondrocytes to produce normal proteoglycans and cartilage.  The destruction of the 
cartilage matrix is the final result of the inflammatory process.
	Damage to the collagen fibrils results in decreased strength and inability to 
constrain the proteoglycan molecules.  The normal relationship between collagen and 
proteoglycan molecules is lost and the hydrophilic proteoglycans swell.  The 
proteoglycan swelling causes the swelling of the whole cartilage.  The joint cannot 
withstand normal forces of movement and fissures and clefts will develop within the 
articular cartilage.
	The process can go further and damage the subchondral bone, but this did not 
occur in the foal.  The inflammation, pain, swelling, and joint disease were all enough to 
make the foal lame and painful in the joint.