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

Rheumatoid factors (RF) occur during the course of various infections such as leprosy, infective endocarditis, tuberculosis, trypanosomiasis, visceral larva migrans, infectious mononucleosis, influenza A, hepatitis A or cytomegalovirus. When first described it seemed logical to assume that host-self-immunization with autologous immune complexes provided the initial stimulus for RF production. Subsequently extensive characterization of bacterial, parasitic and viral Fc receptors has suggested an alternative explanation for rheumatoid factor associated with infections. It seems possible that patients make an initial immune response to infecting agent Fc receptors and that anti-anti-Fc receptors or anti-idiotypes either then directly stimulate rheumatoid factor production or are themselves rheumatoid factors. Such a hypothesis might also be applied to rheumatoid arthritis itself where either infecting agent or autologous cell Fc receptors could be the initial immunizing epitopes involved in rheumatoid factor production.
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PMID:Rheumatoid factors in subacute bacterial endocarditis and other infectious diseases. 307 Jul 27

Leprosy, particularly lepromatous leprosy, is associated with a multitude of (auto) immune aberrations, and its clinical features also have much in common with the collagen diseases. Immunopathological studies of the 2 groups of diseases may thus elucidate the basic mechanisms of both.The reported evidence for a genetically determined hyporeactivity of cell-mediated (CM) immunity in lepromatous subjects is reviewed; most, but not all, of the findings fit such a hypothesis well. The possibility remains that the observed hyporeactivities may be secondary to direct effects of Mycobacterium leprae. Evidence for a general hyperreactivity of the antibody-mediated (AM) immunity in lepromatous leprosy is then reviewed and considered to be fragmentary.The concept and general criteria of autoimmunity are discussed briefly and the high incidence in lepromatous leprosy of various (auto)immune aberrations, resembling those in systemic lupus erythematosus (SLE) and in rheumatoid arthritis is reviewed. Although autoantibodies are not likely to be directly deleterious to the host, immune complexes containing autoantibodies may be pathogenic.Mixed cryoimmunoglobulins, consisting of 2 (IgG-IgM or IgG-IgA) or 3 immunoglobulins, and occasionally also containing measurable amounts of complement components, have recently been encountered in SLE and its variants and also in a number of microbial diseases with autoimmune features (syphilis, streptococcal nephritis and endocarditis, mononucleosis, Mycoplasma pneumoniae pneumonia). They may represent circulating immune complexes, analogous to the IgM (IgA) rheumatoid factors in combination with their IgG reactants. In leprosy also, the existence of pathogenic immune complexes is indirectly suggested by mixed cryoglobulinemia and further by a number of other features reviewed in this article.
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PMID:Immunological aspects of leprosy with special reference to autoimmune diseases. 530 31

A 75 year old man was hospitalized because of rapid deterioration of his general condition, weight loss, night sweat and subfebrile temperature. The patient presented with severely reduced general condition, tachyarrythmia with previously known atrial fibrillation. Laboratory investigations revealed among others a moderately increased CRP-value, normal sedimentation rate and, initially, a normal white cell count. The differential diagnosis included neoplastic and infectious diseases (i.e. endocarditis, tuberculosis), endocrinopathies (i.e. thyreoditis) and general inflammatory or rheumatic diseases. An initially increased CMV-IgM-titer, a rising anti CMV IgG-titer and gradually developing atypical lymphocytosis in particular suggested diagnosis of severe CMV-infection. The diagnosis was confirmed by PCR positive for CMV-DNA in blood. The course of a CMV-primary infection may develop from asymptomatic infection over a mononucleosis-like syndrome to disseminated CMV-infection with multi organ involvement.
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PMID:[75-year-old man with rapid deterioration of his general condition]. 1070 99

A 26-year-old male was treated for acute hepatitis due to Epstein-Barr virus and infectious mononucleosis in our hospital. At 2 weeks after admission, there was relapse with high fever. A blood culture detected methicillin-resistant Staphylococcus aureus. A two-dimensional echocardiogram revealed severe aortic regurgitation and vegetation on the left coronary cusp of the aortic valve. The diagnosis was active infective endocarditis due to methicillin-resistant Staphylococcus aureus in the acute phase of infectious mononucleosis. Following preoperative administration of vancomycin, the aortic valve was replaced with a Carbomedics prosthetic valve. The aortic valve was bicuspid, and the right cusp and non-coronary cusp were conjoined. As the focus of infection was localized to the left coronary cusp, the infected tissue was fully removed with resection of all the cusps. Although fever persisted long after the operation, the blood culture became negative for methicillin-resistant Staphylococcus aureus, and repeated echocardiograms including transesophageal echocardiogram showed no prosthetic valve infection. Vancomycin was administered until the C-reactive protein became negative at 45 days after the operation.
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PMID:Active infective endocarditis due to methicillin-resistant Staphylococcus aureus in the acute phase of infectious mononucleosis. 1207 2

Splenic infarction is a rare feature of infectious mononucleosis (IM) due to Epstein-Barr virus (EBV), limited to three case reports. We report the first case of splenic infarction during acute EBV infection associated with the transient induction of antiphospholipid antibodies. We discuss the role of antiphospholipid antibodies in thrombosis in acute viral infections and postulate other mechanisms of thrombosis. Once other more common causes of splenic infarction, such as endocarditis and lymphoma, have been excluded, the possibility of viral-induced antiphospholipid antibodies should be considered.
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PMID:Splenic infarction due to transient antiphospholipid antibodies induced by acute Epstein-Barr virus infection. 1572 31