Μελέτη του εκκριτικού συστήματος του φορέα του πυρετού Q Coxiella burnetii και της απόκρισης του κυττάρου ξενιστή
The intracellular pathogen Coxiella burnetii responsible for Q fever is a zoonosis with global distribution (but new Zeeland and Antarctica). C. burnetii is maintained in nature through complex cycles with host organisms (wild and domestic mammals, birds, arthropods even reptiles). Human is an occas...
| Main Authors: | , |
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| Format: | Doctoral or Postdoctoral Thesis |
| Language: | Greek |
| Published: |
University of Crete (UOC)
2017
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| Online Access: | http://hdl.handle.net/10442/hedi/41217 https://doi.org/10.12681/eadd/41217 |
| Summary: | The intracellular pathogen Coxiella burnetii responsible for Q fever is a zoonosis with global distribution (but new Zeeland and Antarctica). C. burnetii is maintained in nature through complex cycles with host organisms (wild and domestic mammals, birds, arthropods even reptiles). Human is an occasional host. Sheep, goats and cattle are the main source of transmission especially during parturition. Infected animals are usually asymptomatic although miscarriages may occur. Bacteria are excreted in the urine, feces and milk but mostly in birth products. Aerosol is the main way of transmission either through excretions of infected animals or via the environment.Two forms of Q fever are reported; acute and chronic form with different symptoms. Common manifestation of acute Q fever is fever with no clear infection (incubation period 2-5 weeks), pneumonia or hepatitis. Acute form of the disease may be asymptomatic. Classic manifestation of Q fever is atypical pneumonia and hepatitis. Hepatitis appears as fever with granulomas development in liver biopsy, viral hepatitis with hepatomegaly but rarely jaundice and hepatitis with no symptoms but fever with increase in serum aminotranserase levels. Due to these heterogeneous symptoms, diagnosis usually delays from 1-14 months. Chronic infection from Coxiella burnetii is the persistent infection for more than 6 months and manifests several months or years after the first infection. Usually (75%), it appears as bacterial endocarditis. Mitral valve and aortic valve are usually affected. Preexisting valve damages, vascular abnormalities (aneurysm, implants) and possible immunosuppression are the main predisposing factors. Moreover, chronic form may appear as aneurysm or implant infection, arthritis, osteomyelitis, chronic hepatitis with fibrosis development, lung fibrosis, lung pseudo-tumor, mixed cryoglobulinemia and chronic fatigue syndrome. Based on structure, the pathogen has two different forms; small cell variants (SCVs) and large cell variants (LCVs). SCVs are the ... |
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