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

Serological parameters were compared in 15 cases of Coxiella burnetii infection comprising 5 cases each of primary Q fever, chronic granulomatous hepatitis, and endocarditis. The diagnosis was made on the basis of clinical history and serology and on the isolation of C. burnetii phase I from biopsy specimens of liver and bone marrow from two patients with granulomatous hepatitis and from the aortic valve vegetations of five patients with endocarditis. The temporal sequences of immunoglobulin levels, rheumatoid factor, and specific antibody responses to phase II and phase I antigens of C. burnetii were evaluated as predictive correlates of the three Q fever entities. Serum levels of immunoglobulin classes G, M, and A were variable in all the entities of Q fever. Increased mean levels (in milligrams per deciliter) of immunoglobulin G (IgG) and IgA were noted with chronic disease in the sera of some patients, whereas IgM levels were not significantly different from normal values. Rheumatoid factor was significantly elevated in chronic disease but not in primary Q fever. The temporal sequence of C. burnetii phase II and phase I antibodies were compared by microagglutination, complement fixation, and indirect microimmunofluorescence tests. All of these serological tests were useful in distinguishing primary from chronic disease. Thus, the ratio of anti-phase II to anti-phase I antibodies was greater than 1, greater than or equal to 1, and less than or equal to 1 for primary Q fever, granulomatous hepatitis, and Q fever endocarditis, respectively. Moreover, the high phase-specific IgA antibody titers in the indirect microimmunofluorescence test were diagnostic for endocarditis.
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PMID:Serological evaluation of O fever in humans: enhanced phase I titers of immunoglobulins G and A are diagnostic for Q fever endocarditis. 688 55

Only nine cases of Q fever were recorded in Canada in the 20 years prior to 1978. In the 18 months from August 1979 to January 1981 the disease was diagnosed serologically in six patients from the Maritime provinces. All were epidemiologically unrelated and none had been exposed to animals. Five had pneumonia and one had chronic Q fever with probable prosthetic valve endocarditis. Three of the five pneumonia patients presented with signs and symptoms of an acute lower respiratory tract infection and were indistinguishable clinically from other patients with atypical pneumonias. The other two with pneumonia presented with nonresolving pulmonary infiltrates and complained of decreased energy. Four of the five pneumonia patients responded well to treatment with erythromycin; the fifth required two courses of tetracycline. The patient with chronic Q fever had a large amount of cryoglobulins in his serum and evidence of immune complex disease. These cases indicate that Q fever should be considered as a possible cause of atypical pneumonia in Canada.
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PMID:Q fever in maritime Canada. 707 57

Q fever is endemic throughout much of Australia and is most frequently seen in abattoir workers, farmers and veterinarians. Initially, there is a febrile, influenza-like illness. The infection is usually self-limited within several weeks, but rarely patients may develop infective endocarditis or hepatitis. The diagnosis is usually confirmed by finding risings titres of antibodies specific for C. burneti. The infection is not very responsive to treatment, but if tetracycline is administered early, the duration of fever is shortened.
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PMID:Q fever. 742 57

Eight patients with chronic Q fever endocarditis were treated with tetracycline for up to 40 months. In addition, five of these patients received co-trimoxazole. Six patients had prosthetic valves. Two patients who had Q fever endocarditis on their native valves required valve replacement because of haemodynamic difficulties: in only one did the Q fever endocarditis contribute to the haemodynamic difficulty. One patient died. It is suggested that medical treatment is continued until clinically and haematologically there is no evidence of endocarditis and the Q fever phase 1 antibody titre is less than 200. No recurrence of Q fever endocarditis has been detected in three of our patients who have now stopped treatment.
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PMID:Chronic Q fever endocarditis. 742 49

Q fever is a widespread disease caused by the rickettsia Coxiella burnetii, an obligate intracellular bacteria which man usually acquires through the inhalation of infected dust from subclinically infected animals. Q fever may be acute or chronic. The chronic form mostly presents as endocarditis, which is difficult to diagnose and may ultimately be fatal. Immunocompromised conditions and underlying heart disease are the most important risk factors to consider in cases of Q fever endocarditis. The ultimate diagnosis is based on specific diagnostic tests which include serology, demonstration of C. burnetii in valvular material, isolation of C. burnetii from blood and tissue samples by cell-culture techniques as well as amplification and detection of the bacterial DNA by polymerase chain reaction. Treatment of chronic Q fever endocarditis is complex and requires long-term antibiotic therapy, sometimes associated with heart valve replacement. At the present time neither an optimal antibiotic combination nor the duration of treatment is known and patients with Q fever endocarditis require prolonged follow-up because of the possibility of later relapses.
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PMID:Q fever endocarditis. 924 58

The bacteria causing infective endocarditis have not changed significantly despite the diversity of potential portals of entry. Streptococci (viridans) cause 35 to 45% of cases of endocarditis. Group D streptococci of gastrointestinal origin cause about 20% of cases of endocarditis: Streptococcus bovis is the most commonly isolated species followed by the enterococcus. The beta-haemolytic streptococci of Groups A, B, C and G are rarely isolated. Seventeen to thirty per cent of endocarditis is caused by staphylococci, above all Staphylococcus aureus. These infections are mainly observed in patients with prosthetic valves or intravenous catheters and in intravenous drug addicts. With respect to gram-negative bacilli, enterobacteria are rarely responsible for endocarditis and those of the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, etc.) were isolated in 3% of cases. Q fever and Chlamydia endocarditis are rare, as are fungal infections usually due to Candida. Endocarditis with negative blood cultures is still observed in about 10% of cases.
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PMID:[Bacterial endocarditis: current bacteriological data]. 802 85

Ten male patients with a mean age of 57.5 years (range 27-75 years) underwent homograft aortic valve or root replacement for destructive aortic valve endocarditis. Six patients had native valve endocarditis (one with associated native mitral valve endocarditis) and four had prosthetic valve endocarditis (one with associated prosthetic mitral endocarditis). Causative organisms were Streptococci in six patients, Staphylococci in one, Q fever in one and no organisms were isolated in the remaining two patients. All the patients were operated while on antibiotics (mean lengths of treatment 13 days; range 2-42). The main indication for surgery was cardiogenic shock in five patients, progressive cardiac failure in four patients and uncontrolled sepsis in one patient. Operative procedures involved homograft aortic root replacement with coronary reimplantation (seven patients; associated prosthetic mitral valve replacement in one patient), infracoronary homograft aortic valve replacement (three patients) and a number of other procedures were performed to reconstruct the disrupted cardiac anatomy. Patients were followed up for a mean of 13.2 months (range 2-21). One patient died 4 months postoperatively of an unrelated cause; all the others are asymptomatic with no evidence of recurrent endocarditis. We conclude that homograft aortic valve or root replacement is an effective method of managing destructive aortic valve endocarditis.
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PMID:Homograft aortic valve and root replacement for severe destructive native or prosthetic endocarditis. 803 58

The authors developed monoclonal antibodies to Coxiella burnetti, the agent of Q fever. The selected monoclonal antibody, Cox1D8, did not cross-react with other bacteria and was used for early detection of C burnetti in shell vial cell cultures and for staining C burnetii in paraffin embedded tissues. Formalin or Bouin fixation did not alter the reactivity of the antigen with the antibody. This monoclonal antibody could be useful in the pathologic diagnosis of Q fever hepatitis and endocarditis.
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PMID:Monoclonal antibodies to Coxiella burnetii for antigenic detection in cell cultures and in paraffin-embedded tissues. 813 88

Q fever is caused by a rickettsial microorganism (Coxiella burnetii) harboured in sheep. The highest concentration of organisms are found in birth products. It is a very contagious organism which humans can contract by inhaling aerosolized organisms. Most commonly it leads to an acute 'flu-like illness. Rarely, chronic disease with endocarditis is fatal. Infected patients should be treated with tetracyclines or chloramphenicol. A number of outbreaks have been reported in hospital and research settings. Because of the fear of patients and staff contracting Q fever, Hospital Research Review Boards have increasingly resisted the presence of sheep in medical facilities. The authors have reviewed the circumstances leading to these outbreaks and believe researchers can minimize the risk of Q fever. The most important precautions are to use sheep only from Q fever controlled flocks and, depending on the nature of the research, only male sheep.
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PMID:Minimizing the risk of Q fever in the hospital setting. 816 58

Four mouse monoclonal antibodies reacting with Coxiella burnetti lipopolysaccharide antigens were produced and used in serotyping 17 C. burnetii isolates from acute Q fever and Q fever endocarditis patients in France. Two monoclonal antibodies (1B2 and 3B6) were considered specific for the Priscilla strain, a representative of Q fever endocarditis isolates, and did not react with the Nine Mile strain, which is representative of acute Q fever isolates. Monoclonal antibodies Nos. 1B2 and 3B6 reacted with 75% (3/4) acute Q fever isolates and 85% (11/13) of endocarditis isolates from France. It is reasonable to conclude that Priscilla-like strains cause both acute Q fever and Q fever endocarditis. The hypothesis that Priscilla-like strains only are associated with Q fever endocarditis should be reconsidered.
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PMID:Serotyping Coxiella burnetii isolates from acute and chronic Q fever patients by using monoclonal antibodies. 818 7


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