{"title":"Cardiovascular Infections","authors":"R. Wani, Satya Das","doi":"10.1093/oso/9780198801740.003.0037","DOIUrl":null,"url":null,"abstract":"Infective endocarditis (IE) is inflammation of the endothelial lining of the heart valves due to infective causes. IE is a rare condition with an incidence rate of three to nine cases per 100,000 population with a male to female ratio of 2:1. The rate is higher in people with unrepaired cyanotic congenital heart disease, prosthetic heart valves and previous endocarditis. Other risk factors for IE include: rheumatic fever (now accounts for < 10% of IE cases in developed countries), degenerative conditions of heart valves, intravenous drug abuse, diabetes, and HIV infection. One third of the cases are now healthcare associated infection (HCAI), particularly with haemodialysis, cardiac surgery, implantable cardiac devices, intravascular lines, and urinary catheters. In the past decade Staphylococcus aureus has replaced viridans streptococci as the leading cause of IE, the rate of enterococcal (mostly E. faecalis) and Bartonella IE has increased, while that of culture negative endocarditis has decreased. Untreated IE is a uniformly fatal condition, but the mortality rate can be reduced to 5–40% with appropriate treatment. There are two important prerequisite steps to the development of IE: 1. A damaged endothelium due to high pressure gradient and turbulent blood flow around a heart valve or septal defect. Fibrin and platelet deposition occur on the roughened endothelium forming a non-infective thrombus or vegetation. 2. Bacteraemia due to endocarditis-prone organisms resulting from trauma to mucous membranes (e.g. oral cavity, urinary, and gastrointestinal tract) or other colonized tissue or foreign body, which is not cleared by host defence mechanisms. Micro-organisms then attach to the damaged endothelium through a specific ligand-receptor interaction (hence the predilection for certain organisms to cause endocarditis, e.g. viridans streptococci from the mouth), colonize the thrombus, and grow and multiply within it to give rise to a mature/infective vegetation, which is the pathological hallmark of IE. Virulent organisms, classically S. aureus, can apparently infect a healthy endocardium. Damage to the endothelium results in valvular incompetence/regurgitation and symptoms and signs of heart failure and when severe, it is a potentially fatal condition that requires urgent valve surgery, even if the infection has fully responded to antimicrobial therapy.","PeriodicalId":274779,"journal":{"name":"Tutorial Topics in Infection for the Combined Infection Training Programme","volume":"16 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2019-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tutorial Topics in Infection for the Combined Infection Training Programme","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/oso/9780198801740.003.0037","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9
Abstract
Infective endocarditis (IE) is inflammation of the endothelial lining of the heart valves due to infective causes. IE is a rare condition with an incidence rate of three to nine cases per 100,000 population with a male to female ratio of 2:1. The rate is higher in people with unrepaired cyanotic congenital heart disease, prosthetic heart valves and previous endocarditis. Other risk factors for IE include: rheumatic fever (now accounts for < 10% of IE cases in developed countries), degenerative conditions of heart valves, intravenous drug abuse, diabetes, and HIV infection. One third of the cases are now healthcare associated infection (HCAI), particularly with haemodialysis, cardiac surgery, implantable cardiac devices, intravascular lines, and urinary catheters. In the past decade Staphylococcus aureus has replaced viridans streptococci as the leading cause of IE, the rate of enterococcal (mostly E. faecalis) and Bartonella IE has increased, while that of culture negative endocarditis has decreased. Untreated IE is a uniformly fatal condition, but the mortality rate can be reduced to 5–40% with appropriate treatment. There are two important prerequisite steps to the development of IE: 1. A damaged endothelium due to high pressure gradient and turbulent blood flow around a heart valve or septal defect. Fibrin and platelet deposition occur on the roughened endothelium forming a non-infective thrombus or vegetation. 2. Bacteraemia due to endocarditis-prone organisms resulting from trauma to mucous membranes (e.g. oral cavity, urinary, and gastrointestinal tract) or other colonized tissue or foreign body, which is not cleared by host defence mechanisms. Micro-organisms then attach to the damaged endothelium through a specific ligand-receptor interaction (hence the predilection for certain organisms to cause endocarditis, e.g. viridans streptococci from the mouth), colonize the thrombus, and grow and multiply within it to give rise to a mature/infective vegetation, which is the pathological hallmark of IE. Virulent organisms, classically S. aureus, can apparently infect a healthy endocardium. Damage to the endothelium results in valvular incompetence/regurgitation and symptoms and signs of heart failure and when severe, it is a potentially fatal condition that requires urgent valve surgery, even if the infection has fully responded to antimicrobial therapy.