Psittacosis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
The key to understanding the pathogenesis of | The key to understanding the pathogenesis of C. psittaci is that frequent and repeated episodes of reinfection are needed for the development of severe disease.<ref name="pmid3571982">{{cite journal| author=Taylor HR, Johnson SL, Schachter J, Caldwell HD, Prendergast RA| title=Pathogenesis of trachoma: the stimulus for inflammation. | journal=J Immunol | year= 1987 | volume= 138 | issue= 9 | pages= 3023-7 | pmid=3571982 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3571982 }} </ref> Repeated episodes of infection induce a marked and sustained inflammatory response that, with time, leads to scarring and structural damage. A one time exposure to birds is not enough to develop psittacosis. It takes repeated exposure as seen with bird handlers. | ||
Chlamydial persistence usually denominates a state of infection when the pathogen remains viable but non-cultivable, while the host immune system is unable to eliminate it. | Chlamydial persistence usually denominates a state of infection when the pathogen remains viable but non-cultivable, while the host immune system is unable to eliminate it. | ||
Revision as of 14:50, 27 June 2017
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Psittacosis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Psittacosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Psittacosis pathophysiology |
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Risk calculators and risk factors for Psittacosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
The major risk factor for acquiring psittacosis is exposure to birds. Transmission can occur either by inhalation of aerosolized organisms in form of dried feces or respiratory secretions or by direct contact with birds.
Pathophysiology
Transmission
The exact molecular details of bacterial uptake are not well understood. Elementary bodies (EBs) of C. psittaci are thought to infect their target cells in the lung by attachment to the base of cell surface microvilli, where they are actively engulfed by endocytosis or phagocytis. Further studies on the C. psittaci-related species of C. caviae showed that initial attachment is mediated by electrostatic interactions, most likely with glycosaminoglycan (GAG) moieties on the host cell surface. However, the observation that cellular binding of C. psittaci and related chlamydial strains is only partially or not inhibited by heparin strongly suggests that further adherence mechanisms contribute to chlamydial attachment. It was speculated that chlamydial cell contact is a two-step process, i.e. reversible binding followed by irreversible attachment. Although chlamydial entry is extremely efficient, the exact molecular details of bacterial uptake are not well understood. The host protein disulfide isomerase (PDI) has been identified as being essential for both C. psittaci attachment and entry into cells. PDI is highly enriched in the endoplasmic reticulum, but is also found on the cell surface where it catalyzes reduction, oxidation and isomerization of disulfide bonds.
Pathophysiology
Several studies also highlighted the critical importance of host microfilaments, microtubules and microtubule motor proteins (kinesin and dynein) for uptake and intracellular development of C. psittaci and other Chlamydia spp. In all cell types tested, participation of actin and tubulin seems to be necessary for optimal bacterial proliferation. It was also noted that the shutdown of prokaryotic protein synthesis seemed to have no effect on C. psittaci uptake, thus demonstrating that the internalization process does not require protein synthesis on the bacterial side. Once internalized in the early inclusion, the infecting EB transforms into a larger and more conventional bacterial form, the reticulate body (RB). Subsequently, the RB-containing inclusions translocate through a cytoskeleton-dependent mechanism to the perinuclear region, and RBs replicate by binary fission. The mechanisms by which C. psittaci manages its intracellular survival are still under intensive investigation.
Pathogenesis
The key to understanding the pathogenesis of C. psittaci is that frequent and repeated episodes of reinfection are needed for the development of severe disease.[1] Repeated episodes of infection induce a marked and sustained inflammatory response that, with time, leads to scarring and structural damage. A one time exposure to birds is not enough to develop psittacosis. It takes repeated exposure as seen with bird handlers. Chlamydial persistence usually denominates a state of infection when the pathogen remains viable but non-cultivable, while the host immune system is unable to eliminate it.
References
- ↑ Taylor HR, Johnson SL, Schachter J, Caldwell HD, Prendergast RA (1987). "Pathogenesis of trachoma: the stimulus for inflammation". J Immunol. 138 (9): 3023–7. PMID 3571982.