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Identifier

000410850

Title

Μελέτη του εκκριτικού συστήματος του φορέα του πυρετού Q Coxiella burnetii και της απόκρισης του κυττάρου ξενιστή

Alternative Title

Study or the secretion system of the bacterium Coxiella burnetii causing Q fever and the host cells’ response.

Author

Αρβανίτη, Κατερίνα

Thesis advisor

Τσιώτης, Γεώργιος

Reviewer

Αντωνίου, Μαρία
Γανωτάκης, Δημήτριος
Κατερινόπουλος, Χαράλαμπος
Κοκκινίδης, Μιχαήλ
Περγαντής, Σπύρος
Ψαρουλάκη, Άννα

Abstract

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 metabolically inactive form of the bacterium and smaller in size compared to LCVs which are considered the metabolic active form of the pathogen. Based on the structure of the lipopolysaccharide there are two different phases of the bacterium; phase I and phase II. Phase I is present in nature and is highly infectious whereas phase II is created from phase I in culture cells during several passages. After transmission, Coxiella burnetii targets alveolar macrophages and cell infection begins. Type IVb secretion system, is responsible for effector proteins secreted in host cells’ cytoplasm necessary for survival and intracellular replication inside vacuoles named Coxiella containing vacuoles (CCV). As the infection progresses the CCV gets full of bacteria. In the present study, efforts have been made to isolate the core sub complex of the type IVsecretion system but also the three subunits IcmG, IcmK and IcmE separately. Another target was studying the response of the host cell when infected with the pathogen in different time points (1, 3 and 10 days post infection) and if or how the proteome of the host cell is differentiated. Also, the morphology of the eukaryotic cell at the corresponding time points by electron microscopy is observed.

Language

Greek

Subject

Intracellular bacterium

Intracellular replication

Ενδοκυττάριο βακτήριο

Ενδοκυττάριος πολλαπλασιασμός

Πυρετός Q

Issue date

2017-09-15

Collection

School/Department--School of Sciences and Engineering--Department of Chemistry--Doctoral theses