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Characterizing the Duration of Coxiella Burnetii Shedding and the Genetic Influence Behind a Key Immune Effector Cell.

紀錄類型:	書目-電子資源 : Monograph/item
Title/Author:	Characterizing the Duration of Coxiella Burnetii Shedding and the Genetic Influence Behind a Key Immune Effector Cell./
Author:	Oliveira, Ryan David.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
Description:	79 p.
Notes:	Source: Dissertations Abstracts International, Volume: 83-05, Section: B.
Contained By:	Dissertations Abstracts International83-05B.
Subject:	Veterinary services. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28644507
ISBN:	9798471133617

Characterizing the Duration of Coxiella Burnetii Shedding and the Genetic Influence Behind a Key Immune Effector Cell.
Oliveira, Ryan David.

Characterizing the Duration of Coxiella Burnetii Shedding and the Genetic Influence Behind a Key Immune Effector Cell. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 79 p.

Source: Dissertations Abstracts International, Volume: 83-05, Section: B.

Thesis (Ph.D.)--Washington State University, 2021.

This item must not be sold to any third party vendors.

Coxiella burnetii is a bacterial pathogen distributed around the globe that causes disease in both animals and humans. Humans can develop a syndrome called "Q fever", characterized by a flulike syndrome or pneumonia and hepatitis in the acute phase and by potentially fatal endocarditis or vascular infection in some chronic cases. Sheep and goats infected with C. burnetii can suffer clusters of fetal loss that, via aerosol from birth fluids and the placenta, are a major source of infection for humans. The infectious dose in humans is as low as one bacterium, and the organism is hardy in the environment. On a cellular level, C. burnetii preferentially infects macrophages, a cell type derived in many cases from circulating monocytes, and macrophages are considered important in both the survival and clearance of C. burnetii infection. To better understand and control this transmission cycle, we sought to characterize the infection in sheep both by observing shedding in the natural setting and by conducting a genome-wide association with absolute monocyte counts in sheep blood. In chapter one, we measure prevalence to antibodies against C. burnetii (seroprevalence) and shedding by multiple routes on a large sheep farm that had been associated with a human transmission event of Q fever three decades prior. Our findings demonstrate no detectable levels of C. burnetii by polymerase chain reaction and a seroprevalence similar to that of the average large sheep farm in the United States, challenging a previously held assumption that infection persists indefinitely once established on a premises. Our discussion speculates on reasons shedding may have ceased in the absence of targeted intervention and considers the implications of this finding. In chapter two, we perform a genome-wide association with absolute counts of circulating monocytes in sheep. Several significant sites are discovered, and the regions for which they are predictive includes genes involved in hematopoiesis, macrophage activation, and monocyte differentiation. The results have implications for genetic influences on an important effector cell in C. burnetii infection. Together, these data shed light on both the natural transmission cycle and possible immunologic genes involved in infection.

ISBN: 9798471133617Subjects--Topical Terms:

3433982
Veterinary services.
Subjects--Index Terms:

Coxiella burnetii

Characterizing the Duration of Coxiella Burnetii Shedding and the Genetic Influence Behind a Key Immune Effector Cell.
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520 $a Coxiella burnetii is a bacterial pathogen distributed around the globe that causes disease in both animals and humans. Humans can develop a syndrome called "Q fever", characterized by a flulike syndrome or pneumonia and hepatitis in the acute phase and by potentially fatal endocarditis or vascular infection in some chronic cases. Sheep and goats infected with C. burnetii can suffer clusters of fetal loss that, via aerosol from birth fluids and the placenta, are a major source of infection for humans. The infectious dose in humans is as low as one bacterium, and the organism is hardy in the environment. On a cellular level, C. burnetii preferentially infects macrophages, a cell type derived in many cases from circulating monocytes, and macrophages are considered important in both the survival and clearance of C. burnetii infection. To better understand and control this transmission cycle, we sought to characterize the infection in sheep both by observing shedding in the natural setting and by conducting a genome-wide association with absolute monocyte counts in sheep blood. In chapter one, we measure prevalence to antibodies against C. burnetii (seroprevalence) and shedding by multiple routes on a large sheep farm that had been associated with a human transmission event of Q fever three decades prior. Our findings demonstrate no detectable levels of C. burnetii by polymerase chain reaction and a seroprevalence similar to that of the average large sheep farm in the United States, challenging a previously held assumption that infection persists indefinitely once established on a premises. Our discussion speculates on reasons shedding may have ceased in the absence of targeted intervention and considers the implications of this finding. In chapter two, we perform a genome-wide association with absolute counts of circulating monocytes in sheep. Several significant sites are discovered, and the regions for which they are predictive includes genes involved in hematopoiesis, macrophage activation, and monocyte differentiation. The results have implications for genetic influences on an important effector cell in C. burnetii infection. Together, these data shed light on both the natural transmission cycle and possible immunologic genes involved in infection.
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