Background— The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis that were last published in 1997. Met...

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Prevention of Infective Endocarditis Guidelines From the American Heart Association: A Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group

Background The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis, which were last published in 1997. Methods and Results A writing group appointed by the AHA for their expertise in prevention and treatment of infective endocarditis (IE) with liaison members representing the American Dental Association, the Infectious Diseases Society of America and the American Academy of Pediatrics. The writing group reviewed input from national and international experts on IE. The recommendations in this document reflect analyses of relevant literature regarding procedure-related bacteremia and IE; in vitro susceptibility data of the most common microorganisms, which cause IE; results of prophylactic studies in animal models of experimental endocarditis; and retrospective and prospective studies of prevention of IE. MEDLINE database searches from 1950 through 2006 were done for English language articles using the following search terms: endocarditis, infective endocarditis, prophylaxis, prevention, antibiotic, antimicrobial, pathogens, organisms, dental, gastrointestinal, genitourinary, streptococcus, enterococcus, staphylococcus, respiratory, dental surgery, pathogenesis, vaccine, immunization and bacteremia. The reference lists of the identified articles were also searched. The writing group also searched the AHA online library. The American College of Cardiology/AHA classification of recommendations and levels of evidence for practice guidelines were used. The article subsequently was reviewed by outside experts not affiliated with the writing group and by the AHA Science Advisory and Coordinating Committee. Conclusions The major changes in the updated recommendations include the following. (1) The committee concluded that only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100 percent effective. (2) IE prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE. (3) For patients with these underlying cardiac conditions, prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. (4) Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of IE. (5) Administration of antibiotics solely to prevent endocarditis is not recommended for patients who undergo a genitourinary or gastrointestinal tract procedure. These changes are intended to define more clearly when IE prophylaxis is or is not recommended and to provide more uniform and consistent global recommendations.

Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group.

Sir, Having been involved in trying to arrange a widely, even internationally, afreed schedule of prophylaxis, we read your Editorial and the abstract ofDr Oakley and others2 with considerable interest. We3 have already agreed that amoxycillin may be a good answer to the dental problem but we feel it is still premature to give it unqualified approval as the definitive prophylaxis when given in a single dose before the following points have been elucidated:(1) In the study by Oakley et al., amoxycillin was by no means 100% effective. (2) L forms or persisters were not looked for in blood and have not yet to our knowledge been studied in the laboratory. All penicillins take at least three days to "sterilise" a culture of sensitive bacteria. (3) The rabbit experimental model has not been used to test this regimen. All other regimens have been assessed by this valuable method and incidentally a single dose of benzylpenicillin failed to work in this test.4 McGowan of Glasgow and others are at present setting up a study of amoxycillin and the results are awaited with interest. The suggestion that amoxycillin should be given to all people undergoing dental extraction presents a new departure in medicine. Never before, to our knowledge, has a drug been advised to cover a very common procedure which is predominately carried out in normal people and whose use would be of possible benefit to a tiny minority. Figures for the dangers, the shortfalls, and the cost of this should be available before any general recommendations are made. While some hopeful data exist for amoxycillin, the evidence for a single dose of erythromycin as an alternative appears to have no supporting evidence. If this drug is used, surely it must be given for two to three days. Finally, we know from our own experience that much prejudice and entrenched medical opinion already exist in this difficult field. Any premature new recommendations could lead to the compounding of this situation rather than its improvement. We therefore recommend a pause while the above matters are sorted out, before the suggested changes are generally accepted. We have reviewed the wider problems of prophylaxis elsewhere.3

Prevention of infective endocarditis

After 9–21 days without oral hygiene eleven experimental subjects with previously excellent oral hygiene and healthy gingivae developed heavy accumulations of plaque and generalized mild gingivitis. The individual rate of development of gingivitis was closely correlated with the rate of plaque accumulation. Characteristic bacteriological changes were revealed in the plaque along the gingival margin during this experiment. Initially, i.e. when the teeth were clean and the gingiva healthy, the extremely sparse plaque flora consisted almost exclusively of gram-positive cocci and rods. The first phase of plaque development occurred during the first 2 days without oral hygiene and consisted of a proliferation of the gram-positive cocci and rods and an addition of about 30 per cent gram-negative cocci and rods. During the second phase (after 1–4 days) fusobacteria and filaments appeared and increased until they each made up about seven per cent of the flora. During the third phase (after 4–9 days) the flora was supplemented with spirilla and spirochetes, and at the end of the period without oral hygiene each of these two groups of organisms accounted for about two per cent of the plaque flora. In specific areas the gingival condition was correlated with the composition of the plaque and it was found that mild gingivitis could be diagnosed clinically at approximately the same time as the complex flora was established. However, sub-clinical inflammation started much earlier, probably as a reaction to the first phases of plaque development. When oral hygiene was reinstituted, the plaque in most areas disappeared in 1–2 days and after 7–11 days the Plaque Index for each subject was as low as before the experiment. Correspondingly, after 1–2 days most tooth surfaces only harbored the original sparse flora of gram-positive cocci and rods. The gingival inflammation in an area usually disappeared one day after the plaque had been removed.

Experimental gingivitis in man. II. A longitudinal clinical and bacteriological investigation.

Apical periodontitis is a sequel to endodontic infection and manifests itself as the host defense response to microbial challenge emanating from the root canal system. It is viewed as a dynamic encounter between microbial factors and host defenses at the interface between infected radicular pulp and periodontal ligament that results in local inflammation, resorption of hard tissues, destruction of other periapical tissues, and eventual formation of various histopathological categories of apical periodontitis, commonly referred to as periapical lesions. The treatment of apical periodontitis, as a disease of root canal infection, consists of eradicating microbes or substantially reducing the microbial load from the root canal and preventing re-infection by orthograde root filling. The treatment has a remarkably high degree of success. Nevertheless, endodontic treatment can fail. Most failures occur when treatment procedures, mostly of a technical nature, have not reached a satisfactory standard for the control and elimination of infection. Even when the highest standards and the most careful procedures are followed, failures still occur. This is because there are root canal regions that cannot be cleaned and obturated with existing equipments, materials, and techniques, and thus, infection can persist. In very rare cases, there are also factors located within the inflamed periapical tissue that can interfere with post-treatment healing of the lesion. The data on the biological causes of endodontic failures are recent and scattered in various journals. This communication is meant to provide a comprehensive overview of the etio-pathogenesis of apical periodontitis and the causes of failed endodontic treatments that can be visualized in radiographs as asymptomatic post-treatment periapical radiolucencies.

Pathogenesis of Apical Periodontitis and the Causes of Endodontic Failures

Preparation and biological activities of endotoxins from oral bacteria.

Knowledge of spirochetal morphology has been gained for the most part by systematic studies of material from infected hosts and in certain instances from pure cultures maintained in the laboratory on artificial culture media. In this regard the hanging drop preparation, the stained smear or section, and dark-field illumination of wet preparations have been used to advantage. The last method has been more universally employed by the exacting investigator to demonstrate the fine structural differences that exist between the various types of spirochetes. The members of the genera Treponema and Borrelia present morphologic and structural features that have been the subject of considerable speculation and controversy for many years. In this laboratory the electron microscope has been used to demostrate some of these controversial structures, and the present paper describes certain results thus far obtained. Eight strains of spirochetes have been used. Two of these were strains of the small oral treponemes identified as FM and MRB; four were strains of Borrelia vincentii, designated as N9, N19, N37, and CON; and two were cultured strains of Treponema pallidum denoted as Nog and Ni (the Noguchi and Nichols strains). The small oral treponemes were morphologically and culturally similar in all details and representative of our collection of this type of spirochete. Under dark-field optical illumination, they showed uniform and closely spaced spirals and had long tapered ends. They were not double contoured. The four strains of B. vincentii were morphologically and culturally similar to one another and were approximately one and one-half times the size of the smaller oral treponemes. By dark-field examination these spirochetes had large, uniform, and widely spaced coils. The extremities were abruptly tapered and the organisms were not double contoured. The strains of T. pallidum were culturally similar to one another; the organisms had uniform and closely spaced spirals and long tapered ends and were not double contoured. In this they resembled the oral treponemes, but were on the average about one and one-half times as long. All spirochetes were grown in a clear liquid medium which is a modification of a "hormone" agar described by Huntoon (1918). This modified broth is essen-

Morphologic Characteristics of Certain Cultured Strains of Oral Spirochetes and Treponema pallidum as Revealed by the Electron Microscope.

Bladen, Howard A. (National Institute of Dental Health, Bethesda, Md.), and Edward G. Hampp. Ultrastructure of Treponema microdentium and Borrelia vincentii. J. Bacteriol. 87:1180–1191.—A small oral Treponema (FM) and Borrelia vincentii (N9) were harvested after 3 to 7 days of incubation and either embedded in Vestopal W or negatively stained with phosphotungstate. The protoplasmic cylinders of both strains were identical except for size, and had a triple-structured cell wall as well as intracellular concentric laminations. Protoplasmic cylinders of both strains were enclosed in a cell envelope which appeared amorphous in negatively stained preparations, but which had a triple-structured wall when viewed in thin sections. The cell envelope of strain FM also acted as an envelope for the terminal filament; no filament envelope was evident in strain N9. Large structures which contained variable numbers of organisms and which were representative of spirochetal granules were observed. Protoplasmic cylinders contained within such granules frequently were devoid of cell envelopes. The axial filament consisted of several individual fibers which usually terminated in small end knobs. Occasionally, a fiber of the axial filament became a fiber of the terminal filament. Fibers of the terminal filament originated in end knobs similar to, but separate from, those to which the axial filament was attached. A periodicity of 60 A was occasionally observed in the terminal filament envelope of strain FM. A microperiodicity of approximately 20 A was also observed. The fibers of the terminal filament of strain N9 were composed of a large number of fibrils approximately 15 A wide. The periodicity and fibrillar structure of the terminal filament is discussed with reference to proposed models of bacterial flagella suggested by X-ray diffraction data.

Ultrastructure of treponema microdentium and borrelia vincentii

Isolation and identification of spirochetes obtained from unexposed canals of pulp-involved teeth

Experimental Infections with Oral Spirochetes

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Edward G. Hampp

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