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

The beneficial effects of polynuclear eosinophils (PE) are well known. However, under certain circumstances, PE can be harmful. The heart is a prime target for PE toxicity which is due to release of basic proteins by eosinophils including major basic protein, cationic protein, and peroxidase. The most common manifestation of PE toxicity is chronic parietal endocarditis (CPE) which regroups two entities: Loeffler's fibroplastic endocarditis and Davies' endomyocardial fibrosis. Loeffler's fibroplastic endocarditis occurs mainly in temperate climates. Patients present high, persistent eosinophil levels similar to those observed in essential hypereosinophilic syndrome (EHS) or Chusid syndrome. Davies' endomyocardial fibrosis occurs in tropical countries where eosinophilic helminthiasis are endemic. The incidence of eosinophilic myocarditis (EM) is low but probably underestimated. EM can be observed in any case involving PE and has been described in many cases of drug-induced atopy, in Churg and Strauss syndrome, and in EHS. The most common cause of death is short-term occurrence of cardiogenic shock or dilated hypokinetic cardiomyopathy. Some patients have been successfully treated by early, intensive corticosteroid therapy and/or heart transplantation. The nosological classification of EM and CPE remains controversial. The two disorders may form a continuum with CPE as the second phase. Other authors have suggested that EM and CPE result from the action of PE on two distinct targets, i.e. endothelial cells for EM and myocytes for CPE. In the future, it may be possible to identify subjects with a predisposition to PE-induced heart disease by studying of genes coding for interleukins (IL-5, IL-4, IL-3) and GM-CSF in the 5q31-q33 region of chromosome 5.
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PMID:[The heart and the eosinophil]. 1041 Mar 66

Endocarditis is frequently attributable to oral streptococci, but mechanisms of pathogenesis are not well understood, although monocytes appear to be important. High titers of interleukin-12 (IL-12) are produced by peripheral blood mononuclear cells (PBMC) after engaging Streptococcus mutans, but monocytes in developing endocardial vegetations tend to disappear rather than become macrophages. These data prompted the hypothesis that streptococcus-infected monocytes differentiate into short-lived IL-12-producing dendritic cells (DCs) rather than macrophages. PBMC from healthy subjects were stimulated with six isolates of oral streptococci, three nonstreptococcal oral bacteria, or IL-4 plus granulocyte-macrophage colony-stimulating factor, and the appearance of cells with markers typical of mature DCs (CD83(+), CD86(+), CD11c(+), and CD14(-)) was monitored. Supernatant fluids from the PBMC cultures were harvested and IL-12 p70 levels were determined. S. mutans-stimulated monocytes were analyzed for their ability to elicit allogeneic mixed-lymphocyte reactions. All streptococci examined, except one strain of Streptococcus oralis (35037), rapidly induced up-regulation of CD83 and CD86 and a loss of CD14 in the CD11c(+) monocyte population within 20 h. Induction of IL-12 was CD14 dependent and correlated with streptococcal isolates that promoted the DC phenotype. Major histocompatibility complex (MHC) class II expression was up-regulated by S. mutans, and these cells were short-lived and elicited potent allogeneic mixed-lymphocyte reactions typical of DCs. In summary, monocytes stimulated with endocarditis-associated oral streptococci rapidly exhibited the DC phenotype and functions. These data suggest that the initiation of bacterial endocarditis by oral streptococci may involve monocyte-to-DC differentiation, and this may help explain the low levels of macrophages in the site.
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PMID:Endocarditis-associated oral streptococci promote rapid differentiation of monocytes into mature dendritic cells. 1604 Oct 16

Whipple's disease (WD) is a rare chronic infectious disorder caused by the rod- shaped bacterium Tropheryma whipplei. The disorder is characterized clinically by arthralgia, abdominal pain, diarrhea, malabsorbtion and progressive weight loss. Other important sites of infection include the heart (resulting in the clinical picture of endocarditis and heart failure) and the central nervous system (CNS) (manifestations include confusion, memory loss, focal cranial nerve signs, nystagmus and ophtalmoplegia). The bacterium is presumed to be ubiquitously present. A defect in cellular immune response may predispose patients for an infection with T. whipplei and this might explain the rarity of the disorder despite the ubiquitous bacterial presence. The presumed immunological defect is likely to be quite specific for T. whipplei, since patients are not generally affected by other infections. Decreased production of Interleukin(IL)-12, IL-2 and Interferon (IFN)-g accompanied by an increased secretion of IL-4 are the main features of this defective immunological response. The finding of periodic acid-Schiff (PAS)-positive macrophages in the lamina propria of tissue samples obtained by duodenal biopsy usually establishes the diagnosis. The PAS-positive inclusions represent the remnants of the bacteria. Attempts to isolate the causative agent were unsuccessful for nearby 100 years after the first recognition of the disease. In the year 2000, the bacterium was finally successfully grown on a human fibroblast cell line. Untreated WD patients suffer from a chronic progressive disorder which possibly leads to death. Most patients show a fast clinical improvement to antibiotic therapy, but clinical relapses are described frequently. There is a number of patients, unable to eradicate the bacterium even after several antibiotic treatments and patients with CNS disease, in both of whom alternative therapy strategies are necessary.
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PMID:Current concepts of immunopathogenesis, diagnosis and therapy in Whipple's disease. 1707 38

Cardiovascular disease is on the rise. In India and other developing countries, rheumatic heart disease (RHD) continues to be a major public health problem and contributes to significant cardiac morbidity and mortality. RHD in the juvenile age group namely juvenile mitral stenosis is a variant which is unique to the Indian subcontinent. Severe valve deformities lead to high morbidity and mortality. Despite various measures no appreciable decline in prevalence of RHD has been documented. At autopsy, mitral valve was most commonly affected either alone or in combination with aortic and tricuspid valves. Both functional and organic involvement of tricuspid valve was documented. It has been convincingly demonstrated that molecular mimicry between Streptococcus pyogenes antigen and human proteins lead to autoimmune reactions both humoral and cell mediated causing RF/RHD. Heart tissues namely the valves, left atrial appendage (LAA) and myocardium reveal variable amounts of infiltration by lymphocytes. Significant endocarditis and valvulitis is observed in these cases. CD4+ T cells are most likely the ultimate effectors of chronic valve lesions in RHD. They can recognize Streptococcal M5 protein peptides and produce various inflammatory cytokines such as TNF-alpha, IFN-gamma, IL-10, IL-4 which could be responsible for progressive fibrotic valvular lesions. Cardiac myosin has been defined as a putative autoantigen recognized by autoantibodies of RF patients. Cross reactivity between cardiac myosin and group A beta hemolytic Streptococcal M protein has been adequately demonstrated. Cardiac myosin has been shown to produce myocarditis in rats and mice. Valvulitis/ endocarditis has been observed in excised LAA, cardiac valves and in hearts at autopsy from cases of RHD. The disease predominantly affects the valvular endocardium culminating in crippling valve deformities. Endocardial infiltrate and their migration into the valve substance has been elegantly demonstrated in rats and mice. Immune responses against cardiac myosin lead to valvular heart disease and infiltration of the heart by Streptococcal M protein reactive T lymphocytes. Mitral valves showed various degrees of calcification. An interesting observation is the nature of calcification in diseased/distorted valves in RHD. Recent studies indicate that calcification is not merely an inactive, "dystrophic" process but involves a regulated inflammatory process associated with expression of osteoblast markers and neoangiogenesis. Increased plasma osteopontin levels correlated with severity of mitral valve calcification. Further evidence of inflammation is supported by high levels of advanced oxidation protein products and high sensitive C-reactive protein in plasma detected in patients with RHD. Presence of inflammatory cells and increased expression of several cytokines in cases of "end stage" RHD reflects a possible subclinical, ongoing insult/injury to some unrecognized antigenic stimulus by beta hemolytic Streptococcal antigens that have sensitized/primed the various target tissues and which further culminate in permanent valve deformities.
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PMID:Pathology and pathogenesis of rheumatic heart disease. 1830 30

Defects in the skin's barrier function are known to make it more likely for skin and soft tissue infection to occur in association with atopic dermatitis. These secondary infections sometimes develop into systemic infections such as bacteremia. Here, we report on our use of anti-IL-4/13 monoclonal antibody (dupilumab) on two cases with atopic dermatitis that was refractory to conventional management techniques and who had a history of serious infection (bacteremia and associated sternal osteomyelitis, infective endocarditis) caused by Staphylococcus aureus. Both cases had underlying congenital heart disease. The dermatological symptoms of both cases showed marked improvement at 16 weeks after the start of dupilumab use. The use of dupilumab on atopic dermatitis may lead to less risk of infection of skin and soft tissues deveroping serious infections due to an underlying congenital disease. When determining the treatment strategy, the cooperation of specialists in a variety of fields as well as the primary care physician was important.
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PMID:[TWO CASES OF USING DUPILUMAB FOR REFRACTORY ATOPIC DERMATITIS WHO HAD HISTORIES OF BACTEREMIA AND UNDERLYING CONGENITAL HEART DISEASE]. 3130 37