Historical Perspectives

Historical perspectives are fraught with interpretation and bias. For this author, particular points of interest include recollections and reminiscence from almost 50 years of medical learning and practice, as an observer to both the science and the management of endocarditis and the personal triumphs and failures in the care of patients with endocarditis. Although these biases will be apparent in this review, my goal is to provide my perspective on what many regard as the most fascinating of infectious diseases.

Several authors attribute the initial description to clinicians and pathologists in the 17th and 18th centuries who described the clinical course and autopsies in patients who in retrospect almost certainly had bacterial endocarditis. This includes Rivierins in 1646, Lancisi in 1707, Glynn in 1749, Morgagni in 1769, and Baillie in 1793 [2]. Baillie clearly differentiated rheumatic endocarditis from what we now know as bacterial endocarditis [3]. Corvisart in 1806 described the "warty" lesions on heart valves and some of these appear, in retrospect, to have been bacterial vegetations [4].

Over the next 75 years, however, rheumatic endocarditis and bacterial endocarditis were not clearly differentiated clinically or pathologically. In1852 Kirkes was the first to describe emboli arising from heart valves in cerebral, renal, splenic and other arteries [5]. Subsequently Virchow and Beckmann each described embolic phenomena and showed that they contained elements which appeared to be bacteria [6,7]. Specifically, Heiberg described chains of cocci in vegetation [8].

In 1859 Quinquaud used the term "chronic" to describe a patient and this allowed subacute bacterial endocarditis to be differentiated from acute [9]. Cayley in 1877 first used the term "infective endocarditis" and this replaced the earlier term "ulcerative endocarditis" [10]. A major advance occurred when Osler in his Gulstonian Lecture in 1885 reported on the clinical course and outcome of 209 cases [11]. He first identified the tendency of bacteria to localize on "diseased valves." He also was the first to mention the importance of bacterial culture.

Meanwhile in Paris, Jaccoud had described endocarditis, and subsequently in France it is often referred to as "Jaccoud's disease" [12]. The long duration of the illness and its subacute presentation was emphasized by both Osler and Jaccoud [11,12].

Numerous other individuals have made important contributions. At the end of the 19th century, the clinical course of endocarditis and its microbial etiology were described fully [11-15]. Thayer and Blumer recovered gono-cocci in the bloodstream of a patient with endocarditis in 1895 and subsequently reviewed a 100 cases of gonococcal endocarditis [13]. Lenhartz introduced material from a vegetative lesion into the urethra of a male patient and produced classical gonococcal urethritis [14]. Schott-

muller isolated the organism which he initially called Streptococcus mitiorseu viridans [15].

The clinical features, including fever and murmur, were well described by Osler in his classic presentations [11,16,17]. The appearance of a new murmur and the clinical features of embolic phenomena were identified as being particularly important for the diagnosis of bacterial endocarditis.

In 1893 Osler saw one of his initial patients and described the "red swollen areas on her fingertips" [16]. Janeway in 1899 described the painless lesions on the palms and soles which now bear his name [18].

Horder carried out classical studies linking ante-mortem blood cultures to post-mortem valve cultures and published these in 1905 [19]. From this time on, positive blood cultures became the sine qua non for diagnosing endocarditis in the vast majority of patients and this remains as important today as it was in 1906.

A paradigm shift in management occurred in 1944 when Loewe and colleagues treated seven consecutive patients successfully with penicillin [20]. Change occurred rapidly with increasing access to penicillin and other antibiotics. By 1947 Seabury reported on the Penicillin Era and showed that it completely changed the practice of infectious diseases and cardiology as it pertained to bacterial endocarditis [21].

These advances were occurring as a part of medical practice as I commenced medical school in 1957. Infectious or bacterial endocarditis was still largely cared for, at least in Canada, by cardiologists, who had a variable interest in microbes and antibiotics. The importance of blood cultures and antimicrobial susceptibility tests including bactericidal tests had been identified. The broad-spectrum bacteriostatic drugs, such as the tetracyclines and chloramphenicol, were shown to be relatively ineffective. The dose of penicillin was gradually increased, initially from 100,000 units a day, which cured only 41% of patients, to 600,000 units a day, which was still associated with a substantial mortality [21,22] At 5 million units daily, the mortality was reduced to 36%. Increasing the dose of penicillin now administered intravenously and in association with streptomycin was quickly recognized as the regimen of choice for penicillin-susceptible streptococci [23].

Anderson and Keefer followed 222 patients who were "responsive to antibiotic therapy" [24]. Of those who responded with negative blood cultures, 21 died within a year—12 from heart failure, 3 from cerebral emboli, and 2 from renal failure. An additional 10% died between one and three years, primarily of heart failure. The risk of reinfection/year was about 2%.

Huge advances have occurred in the diagnosis and management of bacterial endocarditis during the past 40 years and this history is documented within the remaining chapters in this book. The important of enterococcal, staphylo-coccal, and fastidious Gram-negative rod endocarditis have all been recognized, and strategies for early diagnosis and treatment are now routine in most centers. The Duke criteria for diagnosis and its continued modification has made the diagnosis more precise [25]. The diagnosis and management of prosthetic valve infections have also become an important part of the overall management of endocarditis. The appropriate timing for surgical interventions has also become more evidence based.

The role of echocardiography has markedly changed the management of bacterial endocarditis and given us a tool that has enabled more sensitive and specific diagnosis to occur. Today it is difficult to envision management of endocarditis without access to this technology. In particular, transesophageal echocardiography has become routine for excluding this diagnosis in patients with bacteremia, particularly with staphylococci [26].

Recent advances have enabled the diagnosis of very fastidious microorganisms, including Coxiella bruneti, Bartonella sp., and others to now occur with both serologic and cultural tests [27]. Infective endocarditis of unknown etiology is now less common due to continued improvements in microbial diagnosis particularly with the advent of nucleic technologies.

The prevention of endocarditis remains controversial and largely expert consensus-based rather than based on solid scientific evidence. Our current dilemmas in this regard are well reviewed in a subsequent chapter.

Infective endocarditis remains a fascinating illness and continues to intrigue us as clinicians and as individuals attempting to understand the complex biologic processes of host and microbe interactions. Certainly there will be more to learn about this disease. However, we have reached the point in 2006 where we can usually precisely diagnose the infection, localize it to a site on the endocardium, treat it with an established effective regimen, manage complications including surgical interventions with a low mortality, and expect a favorable outcome in over 90% of patients. This is remarkable progress over the past six decades since the advent of penicillin.

Only the future will identify further landmark events that will be highlighted by individuals recording their memories of this disease. In the meantime, as physicians seeing patients with a wide variety of symptoms, we must continue to remember the lessons learned, obtain blood cultures before antimicrobial therapy is instituted and be aware of the many, many presentations of this fascinating illness.

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