Long-term persistence of Coxiella burnetii after acute primary Q fever

Marmion, B. P.; Storm, P.A.; Ayres, Jon G.; Semendric, Ljiljana; Mathews, Linda; Winslow, William; Turra, Mark; Harris, R. J.

doi:10.1093/qjmed/hci009

Cited by 103 publications

(66 citation statements)

References 38 publications

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“…Although this airborne pathogen can stimulate an efficient immune response that limits bacterial replication, 5 to 10% of hosts fail to completely clear the bacteria (31,32). By mechanisms still not completely understood, C. burnetii can persist as a chronic infection by escaping the microbicidal activities of host cells, such as macrophages.…”

Section: Discussionmentioning

confidence: 99%

Roles of Toll-Like Receptor 2 (TLR2), TLR4, and MyD88 during Pulmonary Coxiella burnetii Infection

et al. 2016

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Coxiella burnetii, the causative agent of Q fever, is an obligate intracellular, primarily pulmonary, bacterial pathogen. Although much is known about adaptive immune responses against this bacterium, our understanding of innate immune responses against C. burnetii is not well defined, particularly within the target tissue for infection, the lung. Previous studies examined the roles of the innate immune system receptors Toll-like receptor 2 (TLR2) and TLR4 in peripheral infection models and described minimal phenotypes in specific gene deletion animals compared to those of their wild-type controls ( Here, we assessed the roles for TLR2, TLR4, and MyD88 in pulmonary C. burnetii infection and compared responses to those that occurred in TLR2-and TLR4-deficient animals following peripheral infection. As observed previously, neither TLR2 nor TLR4 was needed for limiting bacterial growth after peripheral infection. In contrast, TLR2 and, to a lesser extent, TLR4 limited growth (or dissemination) of the bacterium in the lung and spleen after pulmonary infection. TLR2, TLR4, and MyD88 were not required for the general inflammatory response in the lungs after pulmonary infection. However, MyD88 signaling was important for infection-induced morbidity. Finally, TLR2 expression on hematopoietic cells was most important for limiting bacterial growth in the lung. These results expand on our knowledge of the roles for TLR2 and TLR4 in C. burnetii infection and suggest various roles for these receptors that are dictated by the site of infection.

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Section: Discussionmentioning

confidence: 99%

Roles of Toll-Like Receptor 2 (TLR2), TLR4, and MyD88 during Pulmonary Coxiella burnetii Infection

et al. 2016

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“…Our patient's chief complaint suggested chronic renal dysfunction with the development of mild hematuria and proteinuria which are typically associated with an ascending urinary tract infection. Such findings are infrequent but have been reported to be associated with chronic Q fever endocarditis [6,9,19] and rarely due to an acute C. burnetii infection as part of the pathogenesis of glomerular disease [18]. Accordingly, since cardiopulmonary findings were unremarkable in our case, chronic Q fever endocarditis was an unlikely contributing factor, or as the focal source of persisting organisms.…”

Section: Discussionmentioning

confidence: 58%

“…Pneumonia ensues following entry of the pathogen into the lungs and subsequent infection of the alveolar macrophages. Chronic disseminated infections can occur leading to hepatitis and endocarditis, with organisms persisting in cardiac valves which could lead to a life-threatening illness [9]. Many other organs may be involved and other possible, but rare, complications include glomerulonephritis, osteomyelitis, and neurologic abnormalities [2,3,16].…”

Section: Introductionmentioning

confidence: 99%

Serologic detection of a rare case of Q fever in New York City having hepatic and unusual renal complications

Pavia

McCalla

2010

Infection

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“…Although prevalence is controversial, studies have cited that 10%-30% of all patients with acute disease report persistent symptoms (e.g., fatigue, myalgia, night sweats) more than a year after acute infection occurred (10,16). Pregnant women are also at increased risk for severe acute C. burnetii infection because of the bacterium's predilection for the placenta.…”

mentioning

confidence: 99%

Prophylaxis after Exposure toCoxiella burnetii

Moodie¹,

Thompson²,

Meltzer³

et al. 2008

Emerg. Infect. Dis.

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Coxiella burnetii is a category B bioterrorism agent. We numerically evaluated the risks and benefi ts from postexposure prophylaxis (PEP) after an intentional release of C. burnetii to the general population, pregnant women, and other high-risk populations. For each group, we constructed a decision tree to estimate illness and deaths averted by use of PEP/100,000 population. We calculated the threshold points at which the number of PEP-related adverse events was equal to the cases averted. PEP was defi ned as doxycycline (100 mg 2×/day for 5 days), except for pregnant women, where we assumed a PEP of trimethoprimsulfamethoxazole (160 mg/800 mg 2×/day) for the duration of the pregnancy. PEP would begin 8-12 days postexposure. On the basis of upper-bound probability estimates of PEP-related adverse events for doxycycline, we concluded that the risk for Q fever illness outweighs the risk for antimicrobial drug-related adverse events when the probability of C. burnetii exposure is >7% (pregnant women using trimethoprim-sulfamethoxazole = 16%).

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Long-term persistence of Coxiella burnetii after acute primary Q fever

Cited by 103 publications

References 38 publications

Roles of Toll-Like Receptor 2 (TLR2), TLR4, and MyD88 during Pulmonary Coxiella burnetii Infection

Roles of Toll-Like Receptor 2 (TLR2), TLR4, and MyD88 during Pulmonary Coxiella burnetii Infection

Serologic detection of a rare case of Q fever in New York City having hepatic and unusual renal complications

Prophylaxis after Exposure toCoxiella burnetii

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