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| *Blue inclusions in cytoplasm of Giemsa-stained cels | | *Blue inclusions in cytoplasm of Giemsa-stained cels |
| *Antigen detection kits for diagnosis from swabs | | *Antigen detection kits for diagnosis from swabs |
| + | *Two morphological forms |
| + | **Elementary body, the infective extracellular form, which is small, metabolically inert and osmotically stable; surrounded by cytoplasmic membrane, outer membrane with LPS, but no peptidoglycan |
| + | **Retiuculate body: larger, metabolically active, osmotically fragile |
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| ===Pathogenesis and pathogenicity=== | | ===Pathogenesis and pathogenicity=== |
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− | *Elementary body, the infective form, phagocytosed and internalised into host epithelial cells | + | *Elementary body enters host epithelial cells by receptor-mediated endocytosis |
− | *Transformation into larger reticulate body | + | *Transformation into larger reticulate body within endosome; known as an inclusion |
| *Reticulate body divides by binary fission to form many new chlamydia cells | | *Reticulate body divides by binary fission to form many new chlamydia cells |
− | *Reticulate body has un-crosslinked peptidoglycan, which is cross-linked to form elementary bodies | + | *Reticulate bodies mature and condense to form elementary bodies |
− | *Elementary bodies released from dying host cells to infect other cells | + | *Elementary bodies released from dying host cells after about 72 hours to infect other cells |
− | *Persistent infections | + | *Persistent infections can occur if replication delayed by environmental conditions |
| *Many infections subclinical due to intracellular existence of ''chlamydia'' preventing inflammatory reactions | | *Many infections subclinical due to intracellular existence of ''chlamydia'' preventing inflammatory reactions |
| *Clinical infections occur in non-natural host species | | *Clinical infections occur in non-natural host species |