Pathogenesis

The mode of intracellular replication of chlamydial agents is investigated morphologically and cytochemically with both light and electron microscope. It is established that the small infectious chlamydial cell retains its identity after cellular uptake in a cytoplasmic vesicle derived from the cellular membrane. Inside these vesicles the chlamydial cell is reorganised into a form known as reticulate bodies. These large cells are noninfectious, grow and multiply by binary fission. During a second process of reorganization small dense centered cells assumes infectivity but they do not divide. These small cells are released from the cytoplasm, which are known as inclusions, which are highly resistant to extra cellular environment and have the capacity of infecting the host cells. A well-balanced host-parasite relationship represents the common nature of chlamydial infections. Exceptionally, some animals may experience severe or fetal disease as a result of exposure to chlamydia. The long lasting inapparent or latent state has been reported in several species and in some cases the organisms are excreted but the latently infected animals while in others the organisms are remained in a non-infectious form. Under the conditions of stress, the carrier animals may shed organisms in large numbers and resulted into clinical disease. The intestinal tract is the natural habitat for chlamydiae and fecal shedding is the most important mode of transmission. Chlamydiae multiply within the cells of the reticulo-endothelial system, epithelial cells, synoviocytes and the cells of placenta and fetus. Lesions produced depend upon the virulence of the causative strain. The disease syndromes observed reflects the route of infection and the immune competence of the host animal.