Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with Q fever endocarditis are described. Both patients demonstrated some of the characteristic features of Q fever endocarditis, i.e. the long course of the disease before diagnosis, persistently negative blood cultures, resistance to conventional antibiotic therapy and a dramatic response to tetracycline therapy. Complications included arteriovenous thrombo-embolism and hepatic enlargement, and 1 patient developed an immune complex form of glomerulonephritis. The possibility of Q fever endocarditis should be considered in all patients with infective endocarditis in whom blood cultures are negative and who fail to respond to conventional antibiotic therapy.
 ...
PMID:Q fever endocarditis: a report of 2 cases. 65 35

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
 ...
PMID:Chronic Q fever. 94 Sep 18

Thirteen patients with proven Q fever endocarditis and three additional patients with probable endocarditis are reviewed. The most helpful diagnostic test is the demonstration of a high complement fixing antibody titre to Phase 1 antigen of Coxiella burneti. The macroscopic pathology of the aortic valve is described and includes aneurysmal pockets in the aortic wall and valve annulus which are demonstrable angiographically. Evidence is presented that the infection may be controlled by prolonged tetracycline therapy and that this is accompanied by a falling antibody titre to Phase 1 antigen. Valve replacement is undertaken only for symptomatic and hemodynamic indications. The combined tetracycline therapy and valve replacement have produced a fall in titres with eradication of infection and palliation of the cardiac disability in all patients followed for long periods.
 ...
PMID:Q fever endocarditis in Queensland. 125 90

Q fever is caused by Coxiella burnetii, a strictly intracellular bacterium that lives within the phagolysosome of infected cells. We report here five cases of Q fever in patients with cancer. Three of them had a solid tumor, one had a B cell lymphoma, and one had chronic myeloid leukemia. One patient had acute Q fever, and the four others had chronic Q fever endocarditis. Two patients with endocarditis had no previous history of valvulopathy. C. burnetii was isolated from the valves of two patients. One of the patients with endocarditis died. Patients with cancer who have unexplained fever and live in areas in which C. burnetii is endemic should undergo serological testing for infection with this microorganism.
 ...
PMID:Acute and chronic Q fever in patients with cancer. 157 16

Vaccination with an inactivated, whole cell, Q fever vaccine (Q-vax) induces lasting antibody conversion and a positive delayed-type hypersensitivity (DTH) skin reaction in about 60% of recipients but a long-lasting positive lymphoproliferative or mitogenic response to C. burnetii antigens with peripheral blood mononuclear cells (PBMC) in 85-95% of subjects. Analysis of the lymphoproliferative response to C. burnetii antigens has now been made by fractionation-reconstitution experiments with PBMC from vaccines, from past infections, and from healthy controls. The major contributor to the response in immune subjects proved to be the T lymphocyte. T cells were stimulated by both the phase I and phase II antigens of two prototype strains of C. burnetii and responses were greatly amplified by addition of IL-2. Similar T lymphocyte stimulation profiles were obtained with the 'Priscilla' strain of C. burnetii which represents a different biotype of Coxiella isolated from Q fever endocarditis; Q-vax is therefore likely to protect against endocarditis strains. Fractionation-reconstitution experiments with T and B cells from vaccines and subjects infected in the past, using various antigenic or haptenic fractions from C. burnetii indicate that protein, non-lipopolysaccharide components of the organism are responsible for the mitogenic response of immune T cells. However, the role of the lipopolysaccharide in the protective immunogen has still to be defined.
 ...
PMID:Analysis of the cells involved in the lymphoproliferative response to Coxiella burnetii antigens. 207 May 64

We compared 10 episodes (8 patients) of Q fever endocarditis with 27 episodes (27 patients) of native valve endocarditis. Patients with Q fever endocarditis were more likely to have weight loss (p less than 0.003), experience fatigue (p less than 0.07), have clubbing of the fingers (p less than 0.005), have a diastolic murmur at the time of admission (p less than 0.03), be anemic (p less than 0.05), have a normal white blood cell count (p less than 0.005), and have a higher serum globulin concentration (p less than 0.007). While valve replacement was required for 50% of the episodes in both groups of patients, it was required later--mean 107 days following the onset of treatment--for the Q fever patients than for the native valve patients--mean 27 days. The mortality rates for these two diseases were not significantly different (30% for native endocarditis vs. 12.5% for Q fever endocarditis), but the Q fever patients experienced significantly fewer complications.
 ...
PMID:A comparison of Q fever endocarditis with native valve endocarditis. 237 80

Human infection with the rickettsia Coxiella burnetii presents as an acute flulike primary Q fever, as a subacute granulomatous hepatitis, or, rarely, as chronic endocarditis. We have previously described lymphocyte unresponsiveness to Coxiella antigen in patients with Q fever endocarditis. This unresponsiveness was antigen specific and was mediated in part by adherent suppressor cells. In this report we show that the adherent suppressor cells work via prostaglandin E2 (PGE2)4 production. Addition of the cyclooxygenase inhibitor indomethacin to cultures of PBMC from patients with endocarditis or chronic laboratory exposure resulted in consistent increases in Coxiella-specific lymphocyte proliferation. The degree of increase in proliferation induced by indomethacin correlated strongly with the amount of PGE2 produced in a 4-hr culture stimulated by Coxiella antigen, but it also correlated with the sensitivity to inhibition of mitogenesis by PGE2. The suppressor mechanism was antigen nonspecific, because induction of suppression in vitro by Coxiella antigen also suppressed Candida-induced proliferation when both antigens were present in the same culture. Addition of indomethacin to these antigen cocultures totally reversed the Coxiella-induced suppression, confirming the evidence above that the nonspecific effector mechanism of suppression was prostaglandin (PG)-mediated. Elicitation of suppression, however, was antigen specific and involved a T cell-monocyte suppressor circuit. Supernatants from Coxiella-stimulated immune T cells and from the suppressor subset (OKT8+-enriched) of those T cells, but not unstimulated immune cells, induced augmented PGE2 production by unrelated nonimmune PBMC. We conclude that the lymphocyte unresponsiveness characterizing patients with Q fever endocarditis is modulated in part by an antigen-specific T suppressor cell which secretes a lymphokine to stimulate PGE2 production by adherent cells.
 ...
PMID:Cellular immunity in Q fever: modulation of responsiveness by a suppressor T cell-monocyte circuit. 240 35

We report a case of Coxiella burnetii endocarditis in a 42-year old man presenting with a long-known cardiac murmur and an infectious syndrome of several months duration. The aetiological diagnosis, delayed by the lack of knowledge of a primary Q fever, was established by serology. The infection responded to tetracycline combined with cotrimoxazole, but a valve replacement performed for haemodynamic reasons was followed by serious complications. We remind the readers that Q fever endocarditis must be considered as a possible diagnosis in all cases of endocarditis with negative blood cultures and that specific serological examinations in search of anti-phase I antibodies of the IgA type should be performed as soon as possible, using the indirect immunofluorescence technique. Attention is drawn to the different serological responses of the three clinical types of Q fever infection and to the cellular immunity associated with that disease.
 ...
PMID:[Q fever infectious endocarditis. Apropos of a new case]. 250 89

An acute infectious disease with predominant pulmonary symptoms, Q fever, may become chronic as hepatitis or, more frequently, endocarditis. We report 3 cases of Q fever endocarditis. In 2 of these patients endocarditis developed on cardiac valve prosthesis. The 3 patients have been under doxycycline for more than a year, and their condition is satisfactory. A review of the literature provides additional data on the epidemiological, aetiological, clinical, biological and therapeutic aspects of this rare type of endocarditis. It is recommended to look for chronic Q fever in all cases of endocarditis with negative blood cultures.
 ...
PMID:[Q fever infectious endocarditis. 3 cases]. 295 20

Three patients developed Q fever endocarditis on porcine bioprosthetic valves. They had a subacute or chronic course with nonspecific symptoms, enlargement of the liver and spleen, and cardiac failure due to destruction of the cusps, without disruption of the valve ring. High-phase I-specific IgG and IgA antibody titers against Coxiella burnetii were found. C. burnetii was isolated in each patient by inoculating suspensions of valve tissue into a human fetal diploid fibroblast cell line, which was grown as monolayers on slides contained inside rubber-stoppered tube cultures. Patients were treated successfully with doxycycline, cotrimoxazole, and valve replacement and were followed up for periods of 24 to 42 months; no evidence of deterioration was found. The human fetal diploid cell culture may be an expeditious, easy, and safe method to isolate C. burnetii from cardiac valves. Valve replacement seemed necessary to cure prosthetic-valve endocarditis due to C. burnetii infection. Combined therapy with doxycycline and cotrimoxazole may control the disease and prevent reinfection of the homografts replacing the valves.
 ...
PMID:Q fever endocarditis on porcine bioprosthetic valves. Clinicopathologic features and microbiologic findings in three patients treated with doxycycline, cotrimoxazole, and valve replacement. 325 69


1 2 3 4 5 6 7 8 9 Next >>