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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Up to now no Q fever endocarditis (caused by rickettsia Coxiella burnetii) has been diagnosed in Poland. Potential endocarditis caused by Coxiella burnetii strains can be related to a group of strains present in Poland or sensitivity of Polish Population. The aim of the study was to estimate frequency of Q fever endocarditis is patients of National Institute of Cardiology and to characterize Coxiella burnetii strains and correlation between frequency of Q fever endocarditis and the group of strains. In all patients infective endocarditis and valvular heart disease were diagnosed. In all cases vegetations on TTE or TEE and negative blood cultures were confirmed. No fungal antigens or elevated anti-Candida and anti-Aspergillus antibodies were found. Serological investigations as far as it concerns C. burnetii antibodies were negative in all cases. No Coxiella burnetii infection were found in patients with infective endocarditis and negative blood cultures in the National Institute of Cardiology. However due to high probability of occurrence of such an infection in Poland further investigations in other centers would be useful.
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PMID:[Attempt of estimation of Q fever endocarditis frequency in Poland]. 1176 82

Q fever is a zoonosis caused by Coxiella burnetii. The acute Q fever is usually characterized by a self-limited flu-like syndrome, fever, pneumonia and hepatitis. Symptoms of the chronic Q fever (evolution>3 months) mainly consist of endocarditis with negative culture. Focal neurological symptoms are rarely observed. Neurological symptoms of acute Q fever consist of meningitis or meningo-encephalitis. Neurological symptoms of chronic Q fever are cerebral embolisms from Coxiella burnetii infected heart valves. We herein report two patients with meningoencephalitis revealing acute Q fever.
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PMID:[Meningo encephalitis revealing Q fever: two cases and a review of the literature]. 1193 27

Endocarditis is a rare but severe complication of Q fever, an infectious disease caused by the intracellular pathogen Coxiella burnetii. Heart involvement is the most common clinical presentation of chronic Q fever, and it occurs almost invariably in patients with previous valvular disease or artificial valves, and in the immunocompromised host. The optimal treatment of Q fever endocarditis is still today debated, and recommended duration of treatment varies from one year to one's lifespan. A case of chronic Q fever endocarditis is described in a patient with biological prosthetic aortic valve and aortic homograft, successfully treated with doxycycline and chloroquine for 2 years.
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PMID:Doxycycline and chloroquine as treatment for chronic Q fever endocarditis. 1221 21

Acute Coxiella burnetii infection is most commonly a mild and self-limiting disease with fever, pneumonia and hepatitis. Endocarditis is the most frequent clinical presentation of chronic infection. We report a 2-year-old child with Q fever who presented with acute pericarditis and cardiac tamponade and who developed a chronic hepatic infection.
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PMID:Acute Q fever pericarditis followed by chronic hepatitis in a two-year-old girl. 1223 9

Q fever is a zoonotic disease caused by the bacterium Coxiella burnetii. The most common reservoirs are domesticated ruminants, primarily cattle, sheep, and goats. Humans acquire Q fever typically by inhaling aerosols or contaminated dusts derived from infected animals or animal products. Its highly infectious nature and aerosol route of transmission make C. burnetii a possible agent of bioterrorism. Although up to 60% of initial infections are asymptomatic, acute disease can manifest as a relatively mild, self-limited febrile illness, or more moderately severe disease characterized by hepatitis or pneumonia. It manifests less commonly as myocarditis, pericarditis, and meningoencephalitis. Chronic Q fever occurs in <1% of infected patients, months or years after initial infection. Chronic disease manifests most commonly as a culture-negative endocarditis in patients with valvular heart disease. During 2000-2001, a total of 48 patients who met the case definition of Q fever were reported to CDC. This report describes the case investigations for six of these patients, which indicate that these persons acquired Q fever probably through direct or indirect contact with livestock. To enhance surveillance efforts, health-care providers should report cases of Q fever to state health departments.
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PMID:Q fever--California, Georgia, Pennsylvania, and Tennessee, 2000-2001. 1240 8

Q fever is a zoonosis caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection, and transmission to human beings is mainly accomplished through inhalation of contaminated aerosols. This illness is associated with a wide clinical spectrum, from asymptomatic or mildly symptomatic seroconversion to fatal disease. Q fever in children has been rarely reported. We reviewed published work on this topic. Seroepidemiological studies show that children are frequently exposed to C burnetii. However, children are less frequently symptomatic than adults following infection, and may have milder diseases. Using the standard diagnostic criteria, we identified 46 published paediatric cases only. Self-limited febrile illness and pneumonia were the most common manifestations of acute Q fever. Chronic disease manifested as endocarditis and osteomyelitis. A history of exposure to possible sources of infection with C burnetii in a child with a compatible infectious syndrome should prompt testing for Q fever. Studies are required to determine the spectrum of morbidity associated with Q fever during childhood.
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PMID:Q fever in children. 1240 49

Q fever is a worldwide zoonosis caused by the strictly intracellular bacterium Coxiella burnetii. Among symptomatic patients (one-half of patients remain asymptomatic), acute Q fever most frequently manifests as a self-limited febrile illness, pneumonia, or hepatitis. Endocarditis is the predominant form of chronic Q fever. All the classical techniques of bacteriology may be used for diagnosis of C burnetii infection. Nonetheless, because of the risk of contamination, isolation must be performed in biosafety level 3 laboratories. Moreover, to date no diagnostic tests for detection by polymerase chain reaction or specific antibodies for immunochemistry are available commercially. Hence, Q fever is diagnosed in most cases by serology. The most reliable technique appears to be micro-immunofluorescence, which exhibits both good sensitivity and specificity. A wider use of this serology in cases of blood culture-negative endocarditis, atypical pneumonia, unexplained fever, and hepatitis should lead to an increase of diagnosed cases.
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PMID:Current laboratory diagnosis of Q fever. 1249 Dec 31

We report here a persistent form of Coxiella burnetii infection. There have been no prospective surveys of chronic C. burnetii infection reported in Japan. Until recently, it was not possible to distinguish between previous and current infection with serological tests for antibody to C. burnetii. The nested PCR method, however, allows us to appreciate the current infection by detecting C. burnetii DNA with high sensitivity. Inoculation method using an A/J mouse was performed to confirm the viability of C. burnetii. To obtain an approximation of the prevalence of C. burnetii infection in the general population, we evaluated a random sample of patients with symptoms of continuous low-grade fever for one month or more. Analysis of 54 subjects with protracted debility and fatigue symptoms identified 13 subjects as carriers of C. burnetii (24.1%). There were no significant differences in age, C-reactive protein levels (0.69 +/- 1.19 mg/dl), white blood cell counts (6,089 +/- 2,189/microliter), eosinophil (3.4 +/- 3.6%) between the patients with C. burnetii infection and infection-free subjects. All thirteen patients had experienced protracted low-grade fever (up to 37.5 degrees C) for four months to seven years (30.5 +/- 27.7 months). Transthoracic echocardiography showed no evidence of endocarditis, or echosonography revealed no abnormal findings in the liver or kidneys. Although domestic animals constitute an important reservoir of C. burnetii, only two of the positive subjects had direct contact with them and none of the positive subjects were occupationally exposed to farm animals or common sources of infection. None had a history of hospitalizations for pneumonia or hepatic disease. Interestingly, five of the thirteen patients had a history of consulting a psychiatrist, and furthermore, one had a history of several admissions in a psychiatric hospital due to chronic fatigue symptoms. Ten of the patients had a high IgE titer (> 295 IU/ml), which shows a higher prevalence than in patients without C. burnetii (76.9%: 22.0%, P = 0.001). Four of them had markedly elevated IgE levels, in excess of 2,000 IU/ml. The mean value of IgE was higher in the patients with C. burnetii infection than in infection-free subjects (1,388 +/- 1,706: 533 +/- 913 IU/ml, p < 0.045). Two subjects were rheumatoid factor positive and another three had autoimmune thyroiditis. Twelve of the 13 subjects provided written informed consent for treatment with minocycline (200 mg/day). One month later, all subject became asymptomatic and apyretic (37.1 +/- 0.43 degrees C to 36.7 +/- 0.56 degrees C; p < 0.025), and nested PCR did not identify C. burnetii DNA in serum samples. It should be noted that persistent symptoms including low-grade fever were observed for two weeks after the start of medication. Furthermore, three patients had persistent symptoms, and DNA detection by the nested PCR method became positive in all three patients within a few months.
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PMID:[Prevalence and clinical characterization of Coxiella burnetii infection in patients with protracted low-grade fever]. 1250 73

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines. Their amounts were higher in patients with hepatitis than in patients with fever or pneumonia. In patients with valvulopathy, who exhibited the highest risk of chronic evolution, the amounts of TNF and IL-10 were higher than in patients without valvulopathy. TNF production was specifically enhanced in patients who developed Q fever endocarditis. These results show that acute Q fever is associated with cytokine overproduction. Persistent TNF amounts were associated with the occurrence of endocarditis in patients with valvulopathy, and that may be a marker of chronic evolution of Q fever.
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PMID:Dysregulation of cytokines in acute Q fever: role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever. 1266 Sep 42

Coxiella burnetii (C.b.) is a strictly intracellular, Gram-negative bacterium. It causes Q fever in humans and animals worldwide. The animal Q fever is sometimes designated "coxiellosis". This infection has many different reservoirs including arthropods, birds and mammals. Domestic animals and pets, are the most frequent source of human infections. Q fever may appear basically in two forms, acute and chronic (persistent). The latter form of Q fever in animals is characteristic by shedding C.b. into the environment during parturition or abortion. Human Q fever results usually from inhalation of contaminated aerosols originating mostly from tissue and body fluids of infected animals. Q fever may appear in humans either in an acute form accompanied mainly by fever (pneumonia, flu-like disease, hepatitis) or in a chronic form (mainly endocarditis). Diagnosis of Q fever is based on isolation of the agent in cell culture, its direct detection, namely by PCR, and serology. Detection of high phase II antibodies titers 1-3 weeks after the onset of symptoms and identification of IgM antibodies are indicative to acute infection. High phase I IgG antibody titers >800 as revealed by microimmunofluorescence offer evidence of chronic C.b. infection. For acute Q fever, a two-weeks-treatment with doxycycline is recommended as the first-line therapy. In the case of Q fever endocarditis a long-term combined antibiotic therapy is necessary to prevent relapses. Application of Q fever vaccines containing or prepared from phase I C.b. corpuscles should be considered at least for professionally exposed groups of the population. Infections caused by C.b. are spread worldwide and may pose serious and often underestimated health problems in human but also in veterinary medicine. Though during the last decades substantial progress in investigation of C.b. has been achieved and many data concerning this pathogen has been accumulated, some questions, namely those related to the pathogenesis of the disease, remain open.
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PMID:Q fever--still a query and underestimated infectious disease. 1269 56


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