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Query: UMLS:C0014118 (endocarditis)
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Human brucellosis has become a rare disease in Germany since the eradication of bovine and ovine/caprine brucellosis in this country. Therefore, most physicians are unfamiliar with the illnesses clinical presentation, diagnostic tools, and therapeutic strategies. This retrospective study was carried out to evaluate the epidemiological, clinical, and laboratory features of human brucellosis in Germany in the years 2002 and 2003. Thirty-one bacterial isolates from 30 patients sent to the German national reference laboratory were characterized using the genus-specific bcsp31 real-time PCR, the species-specific AMOS-PCR, and standard microbiological methods for the detection and identification of Brucella spp. The medical records of all patients with bacteriologically confirmed brucellosis were evaluated. All 31 isolates proved to be Brucella (30 Brucella melitensis and 1 Brucella suis). Most of the brucellosis patients were infected in endemic countries while visiting friends and relatives during their summer holidays. One case of laboratory-acquired infection was identified. Brucellosis was transmitted mainly by the consumption of contaminated unpasteurized milk or cheese from goats and sheep. The patients presented primarily with flu-like symptoms, i.e. fever, chills, sweating, headaches, arthralgia, and myalgia. In most cases, however, symptoms and signs of focal complications, e.g. spondylitis, endocarditis, and meningoencephalitis, predominated. The rate of complications was much higher than that in endemic countries, presumably as a result of diagnostic delay due to a low index of suspicion. In summary, physicians in nonendemic countries such as Germany must be aware of brucellosis being a possible cause of fever of unknown origin in immigrants and tourists travelling from endemic countries.
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PMID:Human brucellosis in a nonendemic country: a report from Germany, 2002 and 2003. 1595 15

Coxiella burnetii is an obligate intracellular bacterium that causes a worldwide zoonosis, Q fever, and can be misused as a biological warfare agent. Infection in animals (coxiellosis) is mostly persistent. Infection in humans is often asymptomatic, but it can manifest as an acute disease (usually a self-limited flu-like illness, pneumonia, or hepatitis) or as a chronic form (mainly endocarditis, but also hepatitis and chronic fatigue syndrome). C. burnetii infection in pregnant women may result in abortions, premature deliveries, and stillbirths. Infection in nature is maintained and transmitted by ticks as the principal vector and reservoir. Cattle, sheep, and goats are the most important source of human infections. Humans contract C. burnetii infection mostly by aerosol in contact with contaminated environs, wind playing an important factor in spreading the infection. The wide distribution of C. burnetii contributes to a high resistance of its extracellular small cell variant to environmental conditions. Its intracellular large cell variant, adapted to survive under harsh conditions of phagolysosomes, enables long-term survival and persistence of C. burnetii, namely in monocytes/macrophages. Host factors such as underlying disease and cell-mediated immunity play a decisive role in the clinical expression of C. burnetii infection. Complete genome analysis of C. burnetii will certainly contribute to better understanding of the pathogenesis of C. burnetii infection and will improve Q fever diagnosis and immunoprophylaxis.
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PMID:Coxiella burnetii infection. 1648 1

Q fever is a zoonosis with many manifestations. The most common clinical presentation is an influenza-like illness with varying degrees of pneumonia and hepatitis. Although acute disease is usually self-limiting, people do occasionally die from this condition. Endocarditis is the most frequent chronic presentation. Although Q fever is widespread, practitioner awareness and clinical manifestations vary from region to region. Geographically limited studies suggest that chronic fatigue syndrome and cardiovascular disease are long-term sequelae. An effective whole-cell vaccine is licensed in Australia. Live and acellular vaccines have also been studied, but are not currently licensed.
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PMID:Q fever. 1650 66

Human Ehrlichia chaffeensis infections have been reported in North America, Asia and Europe, but only recently have human cases been reported in Brazil. Nine new human cases of E. chaffeensis infection diagnosed on a clinical and serological basis are reported. Serological tests were performed with indoor slides prepared with CDC stock DH-82 cells infected with E. chaffeensis (Arkansas strain). All but two patients were adults. Seven patients were male and two female. The fever duration varied from 4 to 120 days with a median of 6 days. All patients recalled previous tick attack. IgM was detected in four cases. Influenza like syndrome was the most frequent clinical form affecting five patients. Two patients had fever of unknown origin (FUO), one patient had blood culture-negative endocarditis and one had encephalitis. All patients except one recovered. Two patients were correctly treated. One patient with FUO had AIDS and unexplained pancytopenia. The occurrence of human ehrlichiosis by E. chaffeensis remains to be proved in Brazil; the cases reported here highlight the possibility of such disease occurrence in Brazil.
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PMID:More about human monocytotropic ehrlichiosis in Brazil: serological evidence of nine new cases. 1676 8

Q or "query" fever is a zoonosis caused by the organism Coxiella burnetii. Cattle, sheep and goats are the most common reservoirs of this organism. The placenta of infected animals contains high numbers (up to 10(9)/g) of C. burnetii. Aerosols occur at the time of parturition and man becomes infected following inhalation of the microorganism. The spectrum of illness in man is wide and consists of acute and chronic forms. Acute Q fever is most often a self-limited flu-like illness but may include pneumonia, hepatitis, or meningoencephalitis. Chronic Q fever almost always means endocarditis and rarely osteomyelitis. Chronic Q fever is not known to occur in animals other than man. An increased abortion and stillbirth rate are seen in infected domestic ungulates.Four provinces (Nova Scotia, New Brunswick, Ontario and Alberta) reported cases of Q fever in 1989.A vaccine for Q fever has recently been licensed in Australia.
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PMID:Q fever - a review. 1742 43

Coxiella burnetii, the causative agent of Q fever, is a Gram negative coccobacillus. It resides and replicates in the host s monocytes and macrophages. The developmental cycle of C. burnetii includes macrocellular and microcellular forms and the formation of spore-like bodies. It undergoes a phase variation of outer cell surface antigens from virulent phase I to avirulent phase II after passaging in the yolk sac of embryonated chicken eggs or in cell cultures. C. burnetii belongs to the most resistant bacteria. The main reservoirs of C. burnetii are cattle, sheep and goats. Human Q fever usually results from inhalation of contaminated aerosols. Acute infection mostly takes the course of a flu-like disease, atypical pneumonia or hepatitis, the chronic form resembles endocarditis. Laboratory examinations are based on the presence of antibodies. The drugs of choice are broad-spectrum antibiotics.
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PMID:[Q fever]. 1770 1

We report about a 42-year-old farmer with leucocytosis, elevation of transaminases and liver cirrhosis as an underlying condition. The diagnosis of Q fever hepatitis was made through liver biopsy and serology. Under therapy with doxycycline, transaminases initially increased again; after switching to ciprofloxacin, the patient could be discharged 3 weeks after admission. Q fever is caused by Coxiella burnetii. The most frequent acute manifestation is a self-limiting flu-like illness. Chronic Q fever mostly presents as endocarditis. The diagnosis is made through histology ("doughnut" granulomas), PCR, serology (acute: anti-phase II antibodies, chronic: anti-phase I antibodies) and culture. Standard therapy is doxycycline.
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PMID:[A 42-year-old farmer with nonspecific leucocytosis and elevated transaminases. Acute septic reaction in Coxiella burnetii infection]. 1830 71

Q fever is a common zoonosis with almost a worldwide distribution caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection and transmission to humans is usually via inhalation of contaminated aerosols. Infection in humans is often asymptomatic, but it can manifest as an acute disease (usually a self-limited flu-like illness, pneumonia or hepatitis) or as a chronic form (mainly endocarditis, but also hepatitis and chronic-fatigue syndrome). In Tunisia, although prevalence of anti-Coxiella burnetii was high among blood donors, Q fever was rarely reported and frequently miss diagnosed by physicians. This study is a review of epidemiological and clinical particularities of Q fever in Tunisia.
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PMID:[Q Fever in Tunisia]. 1855 22

Q fever is a zoonotic infection caused by Coxiella burnetii. Two forms of the disease have been described: an acute form with pneumonia, hepatitis or a flu-like syndrome; and a chronic form in which endocarditis is the most frequent clinical expression. We report a 77 year old male with fever and an erythematous nodule on the right leg. Biopsy revealed a granulomatous lobular panniculitis with some granulomas rimmed by an eosinophilic material, giving a "doughnut" or "fibrin-ring" appearance. Q fever serological studies were positive. Cutaneous signs, among them panniculitis, are probably underestimated during the acute phase of the disease, and recognizing different granulomatous patterns may contribute to the diagnosis.
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PMID:Histopathology of a granulomatous lobular panniculitis in acute Q fever: a case report. 1975 Dec 28

Q fever is a zoonotic disease of worldwide significance caused by the obligate intracellular bacterium Coxiella burnetii. Humans with Q fever may experience an acute flu-like illness and pneumonia and/or chronic hepatitis or endocarditis. Various markers demonstrate significant phylogenetic separation between and clustering among isolates from acute and chronic human disease. The clinical and pathological responses to infection with phase I C. burnetii isolates from the following four genomic groups were evaluated in immunocompetent and immunocompromised mice and in guinea pig infection models: group I (Nine Mile, African, and Ohio), group IV (Priscilla and P), group V (G and S), and group VI (Dugway). Isolates from all of the groups produced disease in the SCID mouse model, and genogroup-consistent trends were noted in cytokine production in response to infection in the immunocompetent-mouse model. Guinea pigs developed severe acute disease when aerosol challenged with group I isolates, mild to moderate acute disease in response to group V isolates, and no acute disease when infected with group IV and VI isolates. C. burnetii isolates have a range of disease potentials; isolates within the same genomic group cause similar pathological responses, and there is a clear distinction in strain virulence between these genomic groups.
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PMID:Coxiella burnetii isolates cause genogroup-specific virulence in mouse and guinea pig models of acute Q fever. 1978 60


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