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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Q fever is a zoonotic infection caused by Coxiella burnetii. The most common clinical manifestation of acute Q fever infection is as an atypical community-acquired pneumonia. The pulmonary findings are accompanied by extrapulmonary findings, most typically an increase in serum transaminases and splenomegaly. Because C. burnetii is difficult to culture, the diagnosis of Q fever is usually made serologically. The diagnosis of acute Q fever atypical community-acquired pneumonia is made by demonstrating a fourfold or greater increase in titer between acute and convalescent specimens or by demonstrating elevated immunoglobulin (IgM) (phase II) titers. Chronic Q fever is manifested as granulomatous hepatitis or more commonly as culture-negative endocarditis (CNE). Chronic Q fever (CNE) is a difficult diagnosis because of difficulty in culturing the organism from the blood and the vegetations with Q fever CNE are small or absent. The diagnosis of chronic Q fever CNE is based on serology. Such patients commonly have highly elevated IgM and IgG titers (phase I/II) titers. Chronic Q fever CNE may involve native or prosthetic heart valves. Q fever prosthetic valve endocarditis is rare compared with native valve Q fever endocarditis. Q fever prosthetic valve endocarditis usually requires valve replacement for cure. We present a case of chronic Q fever bioprosthetic aortic valve endocarditis that was successfully treated with doxycycline monotherapy that did not require aortic valve replacement.
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PMID:Q fever bioprosthetic aortic valve endocarditis (PVE) successfully treated with doxycycline monotherapy. 1837 9

Q fever is a zoonotic disease with a reservoir in mammals, birds, and ticks. Acute cases in human beings can be asymptomatic, or they can present with a flu-like illness, pneumonia, or hepatitis. Approximately 5% of cases progress to chronic Q fever. Endocarditis, the most typical manifestation of chronic Q fever, is usually associated with small vegetations that occur in patients who have had prior valvular damage or who are immunocompromised. We present what we think is the first reported case of superior mesenteric artery embolism from Q fever endocarditis of the aortic valve, in a 39-year-old woman who needed surgical embolectomy and subsequent aortic valve replacement.
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PMID:Q Fever Endocarditis Presenting with Superior Mesenteric Artery Embolism and Renal Infarction. 2704 96

Q fever is a zoonosis caused by the intracellular bacterium Coxiella burnetii. While it is mostly an asymptomatic infection, acute disease can manifest as fever associated with signs of pneumonia or hepatitis. Chronic Q fever develops in 1-5% of infected persons. Patients with a history of cardiac valve surgery, vascular prosthesis or vascular aneurysm, and to a lesser extent patients with pre-existing valvular disease, immune deficiencies, or renal insufficiency, are at highest risk. Most common manifestations are Q fever endocarditis and Q fever vascular infection. We present a case of chronic Q fever, followed by a summary of available literature.
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PMID:A case of recurrent fever in an older man caused by Coxiella burnetii. 2749 24

Coxiella burnetii is the causative agent of Q fever, a zoonotic infection. The bacteria is a gram-negative, pleomorphic, coccobacilli and capable to survive and proliferate within the host cell's phagolysosome. There are two morphological cell types of C.burnetii including small and large cell variants. C.burnetii is divided into phase I and phase II serologically variants according to LPS structure in the cell wall. Phase I is the natural phase found in infected animals or humans and is highly infectious. Phase II is not very infectious and could be obtained only in laboratories after serial passages in cell cultures or embryonated egg cultures. Q fever can be asymptomatic (in 50% of the cases), acute or chronic. Major presentations of acute Q fever are flu-like illness, pneumonia, and hepatitis, whereas the chronic form presents mainly as infective endocarditis. The aim of this study was to obtain C.burnetii phase II variant from C.burnetii phase I variant by a phase change study. In this study, C.burnetii was isolated by cell culture method from the heart valve tissue of a Q fever endocarditis case. C.burnetii phase I antigen for the indirect fluorescent antibody test (IFAT) was prepared from the isolated strain. For the isolation and identification of C.burnetii, heart valve tissue of the patient was homogenized and DNA was extracted by tissue extraction kit. C.burnetii DNA in the valve tissue was determined by real-time PCR (Rt-PCR). This C.burnetii DNA positive specimen was inoculated into Vero cells by shell vial centrifugation method. The scraped Vero cells were fixed on the slides after one week of incubation and IFAT was performed using C.burnetii phase I IgG positive sera, bacteria that were grown in and surrounding the Vero cells stained apple green were determined microscopically. Infected cells were disrupted by freeze and thaw method to obtain bacterial suspension. The DNA obtained from the bacterial suspension was again found to be positive for C.burnetii by Rt-PCR. Isolation sample was found to be positive in PCR at an earlier cycle compared to heart tissue sample, thus the bacterial growth was also confirmed with PCR. 16S ribosomal RNA gene of our isolate was amplified by PCR using 27F and 1492 primers and then sequenced. The DNA sequences were compared with reference DNA sequences of GeneBank; and the nucleotide sequence of the 16S ribosomal RNA gene of our isolate was found to be 99% similar to C.burnetii strain ATCC VR-615 an accession number NR104916. Serial cell culture passages of the isolated strain were performed to obtain C.burnetii phase II variant from C.burnetii phase I variant. After each passage, presence of phase change was investigated by IFAT using C.burnetii phase I and phase II IgG positive sera. At the end of 17 cell culture passages, phase change could not be observed. C.burnetii phase I IFAT antigen was prepared from the obtained bacterial suspension. In this study, we presented the isolation and identification of C.burnetii by cell culture, molecular and serological methods from the heart valve of a patient with endocarditis for the first time in our country.
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PMID:[First Isolation of Coxiella burnetii in Turkey from a Patient with Endocarditis; Antigen Production and Phase Change Study]. 3141 29

Introduction: Coxiella burnetii infection is still challenging physicians, mainly because no international coordination has been stated to standardize the therapeutic strategy and improve the clinical outcomes.Areas covered: Based on the recent knowledge on Q fever, we review here the clinical practices from Q fever diagnosis to therapy. We searched PubMed and Google Scholar to perform the qualitative synthesis.Expert opinion: Four major critical points are highlighted in this review. The first point is that Q fever diagnosis has been reviewed in the light of the new diagnosis tools, including molecular biology, transthoracic echocardiography, and 18F-FDG-PET/CT-scan imaging. Q fever diagnosis results from the presence of a microbiological criterion in addition to a lesional criterion. Second, the identification of the anticardiolipin antibodies as a novel biological predictive marker for acute Q fever complications (hemophagocytic syndrome, acute Q fever endocarditis, alithiasic cholecystitis, hepatitis, and meningitis). Third, the observation of a coincidence between Q fever and non-Hodgkin lymphoma that has made persistent C. burnetii infection a risk of non-Hodgkin lymphoma. Finally, we expose here the close follow-up we proposed from the French National Reference Center for patients with Q fever infection to detect relapse and complications.
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PMID:New insights in Coxiella burnetii infection: diagnosis and therapeutic update. 3178 15

Q fever is a zoonotic disease that is caused by Coxiella burnetii, a gram-negative coccobacillary bacterium. Human infection primarily occurs following the inhalation of aerosols containing C. burnetii. The infection can either present in an acute or chronic form. The three main presentations are flu-like syndrome, atypical pneumonia, and hepatitis. Chronic Q fever mainly affects the heart where the disease manifests as endocarditis. In this case report, the patient was born at term with congenital heart defects, namely double outlet right ventricle (DORV), ventricular septal defects (VSD), and coarctation of the aorta. He underwent coarctation repair and pulmonary artery binding. At the age of three years, he presented with palpitation, sudden high-grade fever, myalgia, and dyspnea. Endocarditis was suspected due to a history of a surgical repair of congenital heart defects. Blood cultures were negative, however, a diagnosis of Q fever endocarditis was confirmed based on serologic titers. Q fever endocarditis is a challenging diagnosis since the echocardiography findings are often nonspecific. Moreover, Q fever can present as negative-culture endocarditis with low sensitivity of blood and tissue polymerase chain reaction (PCR) for C. burnetii. Hence, the modified Duke criteria has considered phase 1 immunoglobulin G (IgG) titers of 1:800 or more as diagnostic for infective endocarditis. Although uncommon, physicians should maintain a high index of suspicion for Q fever endocarditis, especially among patients with pre-existing structural heart disease and associated symptoms and risk factors such as animal exposure.
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PMID:Q Fever Endocarditis in a Saudi Child: A Case Report and Literature Review. 3193 13


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