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==Pathophysiology== ===Entry into host=== ''Rickettsia rickettsii'' can be transmitted to human hosts through the bite of an infected tick. As with other bacterium transmitted via ticks, the process generally requires a period of attachment of 4 to 6 hours. However, in some cases a ''Rickettsia rickettsii'' infection has been contracted by contact with tick tissues or fluids.<ref>{{cite journal|last1=Dantas-Torres|first1=Filipe|title=Rocky Mountain spotted fever|journal=The Lancet Infectious Diseases|volume=7|issue=11|pages=724β732|doi=10.1016/s1473-3099(07)70261-x|year=2007|pmc=1607456|pmid=698647|url=http://archives.lib.state.ma.us/2452/238632|type=Submitted manuscript|hdl=2452/113243}}</ref> Then, the bacteria induce their internalization into host cells via a receptor-mediated invasion mechanism.{{citation needed|date=June 2021}} Researchers believe that this mechanism is similar to that of ''[[Rickettsia conorii]]''. This species of ''Rickettsia'' uses an abundant cell surface protein called OmpB to attach to a host cell membrane protein called Ku70. It has previously been reported that Ku70 migrates to the host cell surface in the presence of "Rickettsia".<ref name="Martinez (9)">{{cite journal|last1=Chan|first1=Yvonne|last2=Cardwell|first2=Marissa|last3=Hermanas|first3=Timothy|last4=Uchiyama|first4=Tsuneo|last5=Martinez|first5=Juan|title=Rickettsial Outer-Membrane Protein B (rOmpB) Mediates Bacterial Invasion through Ku70 in an Actin, c-Cbl, Clathrin and Caveolin 2-Dependent Manner|journal=Cellular Microbiology|date=April 2009|volume=11|issue=4|pages=629β644|doi=10.1111/j.1462-5822.2008.01279.x|pmid=19134120|pmc=2773465}}</ref> Then, Ku70 is ubiquitinated by c-Cbl, an E3 [[ubiquitin ligase]]. This triggers a cascade of signal transduction events resulting in the recruitment of [[Arp2/3]] complex. [[CDC42]], protein tyrosine kinase, phosphoinositide 3-kinase, and Src-family kinases then activate Arp2/3. This causes the alteration of local host cytoskeletal actin at the entry site as part of a zipper mechanism.<ref name="Walker (11)">{{cite journal|last1=Walker|first1=David|title=Rickettsiae and Rickettsial Infections: The Current State of Knowledge|journal=Clinical Infectious Diseases|date=2007|volume=45|doi=10.1086/518145|pages=S39βS44|pmid=17582568|doi-access=free}}</ref> Then, the bacteria is phagocytosized by the host cell and enveloped by a [[phagosome]].<ref name="Martinez (9)" /> Studies have suggested that rOmpB is involved in this process of adhesion and invasion. Both rOmpA and rOmpB are members of a family of surface cell antigens (Sca) which are autotransporter proteins; they act as ligands for the Omp proteins and are found throughout the ''rickettsiae''.<ref>{{cite journal|last1=Noriea|first1=Nicholas|last2=Clark|first2=Tina|last3=Hackstadt|first3=Ted|title=Targeted Knockout of the Rickettsia rickettsii OmpA Surface Antigen Does Not Diminish Virulence in a Mammalian Model System|journal=Journal of Molecular Biology|volume=6|issue=2|doi=10.1128/mBio.00323-15|pages=e00323β15|pmid=25827414|pmc=4453529|year=2015}}</ref> ===Exit from host cell=== The cytosol of the host cell contains nutrients, [[adenosine triphosphate]], amino acids, and nucleotides which are used by the bacteria for growth. For this reason, as well as to avoid phagolysosomal fusion and death, rickettsiae must escape from the [[phagosome]]. To escape from the phagosome, the bacteria secrete phospholipase D and hemolysin C. This causes disruption of the phagosomal membrane and allows the bacteria to escape. Following generation time in the cytoplasm of the host cells, the bacteria utilizes [[actin]] based [[motility]] to move through the cytosol.<ref name="Martinez (9)" /> RickA, expressed on the rickettsial surface, activates Arp2/3 and causes actin polymerization. The rickettsiae use the actin to propel themselves throughout the cytosol to the surface of the host cell. This causes the host cell membrane to protrude outward and invaginate the membrane of an adjacent cell.<ref name="Walker (11)" /> The bacteria are then taken up by the neighboring cell in a double membrane vacuole that the bacteria can subsequently lyse, enabling spread from cell to cell without exposure to the extracellular environment.{{citation needed|date=January 2023}} ===Consequences of infection=== ''Rickettsia rickettsii'' initially infect blood vessel endothelial cells, but eventually migrate to vital organs such as the brain, skin, and the heart via the blood stream. Bacterial replication in host cells causes endothelial cell proliferation and inflammation, resulting in mononuclear cell infiltration into blood vessels and subsequent red blood cell leakage into surrounding tissues. The characteristic rash observed in Rocky Mountain spotted fever is the direct result of this localized replication of rickettsia in blood vessel endothelial cells.<ref name=Koy2018 />
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