have been phagocytized, where the phagocyte eventually migrates to the lymph node, where chronic infection occurs. Furthermore, the surface lipid is cytotoxic and can cause death to macrophages. In a prospective study involving 12 Boer goats, inoculation with mycolic acid compared to control animals provided statistically significant evidence of pathological changes in the lung compared to a control group. Groups inoculated with mycolic acid or C. pseudotuberculosis were evaluated through histopathology compared to a control. Both groups showed haemorrhage, congestion, oedema, inflammation, and necrosis. Organs affected by these degenerative changes included the lung, heart, kidney, and spleen, though severity varied within organs and within mycolic-only and C. pseudotuberculosis-infected groups. The importance of this virulence factor has also been highlighted where mice that have been injected with mycolic acid were shown to produce a chronic abscessation that increased with higher doses. Differences in strain genomics Four different strains of C. pseudotuberculosis are recognized: Cp1002, CpC231, Cp119, and CpFRC41. Comparing genes within these strains, the largest genome was found to be 2377 genes, of which 1851 genes were shared among all four strains. In a CpFRC41 strain isolated from a girl, a gene was found to encode for superoxide dismutase among other specific virulence factors. Superoxide dismutase is involved in evading the immune system by deactivating reactive chemicals secreted by the body that would otherwise kill the bacterial cell. When comparing strains Cp1002 and CpC231 in the sixth pathogenictiy island (PiCp6), Cp1002 contained the gene pipA1, where CpC231 contained pipB. This island (6) codes for proline iminopeptidase, which is involved with removal of proline from proteins. Of great importance, only a small portion of the documented virulence factors have been listed here. Through genomic evaluation, many more possible virulence factors have been found. Treatment Antimicrobial Therapy Treatment of C. pseudotuberculosis in infected animals has been proven difficult, primarily due to the nature of the lesions and the facultative intracellular nature of the organism. Strains of C. pseudotuberculosis have shown to be susceptible to numerous antimicrobial therapies in vitro, including ampicillin, gentamicin, tetracycline, lincomycin, chloramphenicol, and others. Treatment within live animals (in vivo) is thought to be limited due to the firm capsule and thick, caseous nature of the abscess lesions, which make them a difficult target for antimicrobial therapy. Most strains of C. pseudotuberculosis have been shown to be intrinsically resistant to streptomycin, with varying resistance to penicillin and neomycin depending on