Q fever and HIV infection

Raoult, Didier; Lévy, Pierre-Yves; Dupont, Hervé; Chicheportiche, C.; Tamalet, Catherine; Gastaut, Jean‐Albert; Salducci, J

doi:10.1097/00002030-199301000-00012

Cited by 79 publications

(53 citation statements)

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“…(The amount of C. burnetii in the spleen was ϳ10 7 TCID 50 /g; other organs were not examined.) It has been suggested that immunosuppression can amplify the severity of Q fever (1,21,26,27,28). Our findings agree with this theory.…”

Section: Downloaded Fromsupporting

confidence: 91%

“…Immunodeficiency has been indicated as a host factor in chronic Q fever (19,21), and Q fever endocarditis patients have been reported to be in an unbalanced immune state (7,23). Q fever has also been observed in patients with cancer or human immunodeficiency virus infection or undergoing immunosuppressive therapy (13,16,20,21). The SCID mouse has a clear and stable immunodeficient state, so it can be an animal model for the study of Q fever in an immunodeficient host.…”

Section: Discussionmentioning

confidence: 99%

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SCID Mouse Model for Lethal Q Fever

Andoh¹,

Naganawa²,

Hotta³

et al. 2003

Infect Immun

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Q fever, a worldwide zoonosis caused by Coxiella burnetii, has many manifestations in humans. Endocarditis is the most serious complication of Q fever. Animal models are limited to acute pulmonary or hepatic disease and reproductive disorders. An appropriate experimental animal model for Q fever endocarditis does not yet exist. In this study, severe combined immunodeficient (SCID) mice infected with C. burnetii showed persistent clinical symptoms and died, whereas immunocompetent mice similarly infected became asymptomatic and survived. The SCID mice examined in this study had severe chronic lesions in their primary organs: the heart, lung, spleen, liver, and kidney. The heart lesions of the SCID mice were similar to those in humans with chronic Q fever endocarditis: they had focal calcification and expanded macrophages containing C. burnetii. The 50% lethal dose of C. burnetii in SCID mice was at least 10 8 times less than that in immunocompetent mice. The SCID mouse is highly susceptible to C. burnetii, and the immunodeficiency of the host enhances the severity of Q fever. This animal model could provide a new tool for the study of chronic Q fever and Q fever in immunodeficient hosts.

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Section: Downloaded Fromsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

SCID Mouse Model for Lethal Q Fever

Andoh¹,

Naganawa²,

Hotta³

et al. 2003

Infect Immun

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“…Whether the malignancy itself or its treatment predisposes to chronic infection is unknown (21). Additionally, numerous cases of endocarditis have been observed in individuals infected with HIV (22).…”

Section: Discussionmentioning

confidence: 99%

Q fever endocarditis: A case report and review of the literature

Deyell

Chiu²,

Ross

et al. 2006

Canadian Journal of Cardiology

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E ndocarditis is the most common presentation of chronic Q fever, a zoonosis caused by the obligate intracellular bacteria Coxiella burnetii. Commonly believed to be a rare disorder, it has been estimated to account for up to 5% of all endocarditis cases worldwide (1-3). It occurs almost exclusively in patients who have pre-existing valvular disease or who are immunocompromised (4). Unlike typical cases of endocarditis, the clinical presentation of chronic Q fever is often nonspecific. Furthermore, specialized techniques are required for identification of the organism, and echocardiographic evidence of infection is frequently absent (5). Without prompt recognition and appropriate antimicrobial therapy, the course of Q fever endocarditis is severe and potentially fatal. The following case demonstrates many of the clinical features of chronic Q fever and highlights the difficulty of obtaining the diagnosis. CASE PRESENTATIONA 31-year-old Caucasian man presented to a walk-in clinic complaining of progressive, exertional shortness of breath. He had moved to Calgary, Alberta, from Nova Scotia, where he had worked on a dairy farm, two years prior. Due to pre-existing congenital valvular heart disease, he was referred to the Adult Congenital Cardiology Clinic at the University of Calgary (Calgary, Alberta). The patient could barely climb one flight of stairs without significant shortness of breath, and had developed orthopnea and paroxysmal nocturnal dyspnea. He described occasional palpitations, but denied any syncopal episodes, chest discomfort or peripheral edema. There were no symptoms suggestive of systemic infection.Of note, the patient had been diagnosed with congenital aortic stenosis at the age of eight months and underwent open aortic valvulotomy. The patient was found to have a trileaflet valve with significant fusion of the leaflets. Catheterization at the age of 10 years revealed a peak residual gradient of 25 mmHg across the aortic valve with mild aortic insufficiency. Echocardiograms at the ages of 18 and 22 years demonstrated peak gradients of 37 mmHg and 56 mmHg, respectively, moderate aortic insufficiency and preserved left ventricular function. The patient had no cardiology follow-up after the age of 22 years.Physical examination revealed a blood pressure of 110/50 mmHg, a heart rate of 82 beats/min and a normal The case of a 31-year-old man from Alberta diagnosed with Q fever endocarditis is presented. To the authors' knowledge, this is the first case of Q fever endocarditis diagnosed in the province of Alberta. The patient had undergone open valvulotomy for congenital aortic stenosis as an infant. He presented with congestive heart failure secondary to severe aortic regurgitation and underwent mechanical aortic valve replacement. Early failure of the mechanical prosthesis and numerous laboratory abnormalities prompted an investigation for endocarditis, which was initially negative. Markedly positive serology eventually established the diagnosis of chronic Q fever. The patient subsequently underwent...

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“…It generally occurs several months or years after the acute infection in patients with prior valvulopathy [123,169] or who acquired immunosuppression, [124]; however other authors from Spain found that C. burnetii is not more frequent in HIV-infected patients than in other patients [110].…”

Section: In Humansmentioning

confidence: 98%

Is Q Fever an emerging or re-emerging zoonosis?

2005

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-Q fever is a zoonotic disease considered as emerging or re-emerging in many countries. It is caused by Coxiella burnetii, a bacterium developing spore-like forms that are highly resistant to the environment. The most common animal reservoirs are livestock and the main source of infection is by inhalation of contaminated aerosols. Although the culture process for Coxiella is laborious, advances on the knowledge of the life cycle of the bacterium have been made. New tools have been developed to (i) improve the diagnosis of Q fever in humans and animals, and especially animal shedders, (ii) perform epidemiological studies, and (iii) prevent the disease through the use of vaccines. This review summarizes the state of the knowledge on the bacteriology and clinical manifestations of Q fever as well as its diagnosis, epidemiology, treatment and prevention in order to understand what factors are responsible for its emergence or re-emergence. Coxiella burnetii / epidemiology / bacteriology / diagnostic / control

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Q fever and HIV infection

Cited by 79 publications

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SCID Mouse Model for Lethal Q Fever

SCID Mouse Model for Lethal Q Fever

Q fever endocarditis: A case report and review of the literature

Is Q Fever an emerging or re-emerging zoonosis?

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