U.S. Food and Drug Administration.ppt

U.S. Food and Drug Administration Notice: Archived Document The content in this document is provided on the FDA’s website for reference purposes only. It was current when produced, but is no longer maintained and may be outdated. Overview of the Infectivity and Epidemiology of Chlamydia trachomatis and Neisseria gonorrhoeae John R Papp, Ph.D. Team Lead, Chlamydia and Gonorrhea Laboratory Laboratory Reference and Research Branch Division of STD Prevention Centers for Disease Control and Prevention The findings and conclusions in this presentation are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention Comparison Chlamydia and Gonorrhea Life Cycles Chlamydia Obligate intracellular pathogens Gonorrhea Fastidious pathogens Both infect columnar epithelial cells Comparison Chlamydia and Gonorrhea Life Cycles Chlamydia ? Life cycle that involves a change in the organism Elementary Body (EB) form that is outside the host cell infects the host cell Reticulate Body (RB) form that is inside the cell replicates to produce more chlamydia Gonorrhea ? Diplococci with adjacent sides flattened Cells divide in 2 planes at right angles Chlamydia Growth Cycle Chlamydia PersistenceIn vitro studies 7000 X 7000 X CONTROL PERSISTENT Large inclusions with enlarged, aberrant RBs RBs do not divide and mature to EBs Different set of proteins measured in persistent state Chlamydia PersistenceIn vitro studies Persistent chlamydia (viable, nonculturable) can be induced by: β-lactam antibiotics (PCN) IFN-gamma Iron / amino acid / nutrient deprivation Natural occurrence with eukaryotic cell differentiation Other organisms (e.g. HSV) Persistent chlamydia is reversible leading to active replication All persistence mechanisms are not the same – there may be different markers for persistence Alteration of Chlamydia Growth in Association with Hormonal Modulation In vitro studies: enhanced inf