Hypothesis-Inflammation Infection- Bacterial, Fungal, Viral, Protozoal Organisms produce toxins or have other chemotactic factors which attract white blood cells such as neutrophils and macrophages. Chemicals produced by infectious organisms or white blood cells are factors that result in the production of pain, fever, and inflammation. Immune-mediated- Host immune system attacks the cells of the synovium/joint components and damage them. These damaged cells and immune cells release cytokines, interleukins, and other factors. These result in signs of inflammation. Trauma- Trauma damages cartilage or parts of the joint capsule. The damaged cells release proteins and chemotactic factors/chemicals. These attract white blood cells to "clean up" the area. These release cytokines that result in signs of inflammation as well. Neoplastic- Neoplasm causes pressure necrosis of joint structures. Dying cells release factors that attract white blood cells which results in inflammation. Inflammation and Actual Mechanisms Infectious- Bacterial products act as chemoattractants. Inflammatory mediators in the plasma in cells are released. Inflammatory mediators damage the cells of the synovial joint. Bacterial endotoxins cause the release of complements, which cause the aggregation of clotting factors, leading to intravascular coagulation. Intravascular coagulation leads to prostaglandin formation, which is involved in production of pain. Infectious causes can include bacteria, viruses, parasites, fungi, rickettsia, mycoplasma, and spirochetes. Immune-mediated- There can be immune-complex deposition in the synovium. In rheumatoid arthritis, there can also be T-Cells, local inflammatory mediators, and cytokines attracted to the joint. The inflammatory response results in the release of lysosomal enzymes which degrades the cartilaginous matrix. Deposition of fibrin impairs nutrient metabolite exchange. Mechanical damage adds to the problem. Trauma- Crushing or penetration damages blood vessels and other cells. The resultant cell contents and blood are chemoattractants for white blood cells. Neoplastic- Mechanism not explicitly found. See above. Degenerative joint disease- Chondrocytes undergo biochemical and metabolic changes. They release IL-1 and TNF-A which stimulate catabolic metalloproteinases and inhibit collagen and proteoglycan synthesis. Also produced are prostaglandins and IL-6 which lead to matrix degradation and inflammation. Based on the history and clinical signs, an immune-mediated disease process is the most likely cause of JocelynŐs lameness. A bacterial infection is also a good possibility, although there is no history of trauma. Rocky Mountain Spotted Fever and Lyme Disease are two possible causes that are transmitted by ticks and not by trauma. Plan Of Action Tests appropriate for clients' monetary situation- Radiographs, CBC If further testing is needed consider- UA, Joint tap and culture, and possibly anti-nuclear antibody or RF test (these will only be used if further rule-outs are needed)