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Infective Endocarditis Glenda J. Garvey & Harold C. Neu To cite this article: Glenda J. Garvey & Harold C. Neu (1975) Infective Endocarditis, Postgraduate Medicine, 58:3, 107-113, DOI: 10.1080/00325481.1975.11714144 To link to this article:

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co sder • What new populations of patients are at risk for development of endocarditis? • What organisms are increasing in frequency? • What is the recommended prophylactic treatment for patients at risk?

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GLENDA J. GARVEY, MD HAROLD C. NEU, MD College of Physicians and Surgeons Columbia University New York

lnfective Endocarditis New patient populations-drug users and patients who have undergone open heart surgery-have changed the clinical presentation of endocarditis. Chemotherapeutic apptoaches have also changed as different causative bacteria have been found. The primary cause of death is now congestive heart failure, and surgery has assumed new and important roles in therapy.-HCN

two new populations: drug users who administer narcotics intravenously and patients who have undergone open heart surgery, panicularly with prosthetic valve placement. In addition, the percentage of patients over age 50 with endocarditis and no history of rheumatic hean disease has increased significantly in the past 30 or 40 years.3 •4 Among these new groups, the spectrum of organisms has broadened and new presentations and complications of the old disease have appeared, necessitating a reevaluation of standard modes of therapy. Patients With Underlying Valvular Lesions

Distinctions between acute and subacute endocarditis are helpful in understanding the pathogenesis of the disease, but they are less useful in managing the individual case. Therefore, it may be preferable to distinguish profiles of endocarditis not by organisms involved or by the tempo of the infection, but rather by host factors and clinical setting. Although the majority of cases of endocarditis still occur in patients with known valvular disease, recent reviews1 •2 have recognized at least

Vol. 58 • No. 3 • September 1975 • POSTGRADUATE MEDICINE

Organisms involved-Streptococci remain the most frequently identified organisms in endocarditis occurring on previously damaged valves.1 •2 •5 Streptococcus viridans is the most commonly seen streptococcal species, but group D streptococci are increasing in frequency. True enterococcal members of group D streptococci (Strep faecalis, Strep faecium, Strep durans, Strep liquefaciens) have recently been distinguished from nonenterococcal group D streptococci (Strep bovis, Strep equinus) on the basis of biochemical reactions and growth requirements. In the past, those organisms which grew in 6.5% sodium chloride broth were considered to be enterococci. However, with use of the bile esculin test to identify group D streptococci, organisms such as Strep bovis have been included in this group. The distinction is more than a bacteriologie exercise, because group D streptococci


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also cao be divided into two groups on the basis of their sensitivity to penicillin and possibly their differences in virulence. 6 Enterococcal members of group D streptococci cao be inhibited by penicillin, but serum concentrations of 2 to 8 p.g/ml, and occasionally levels of 100 p.g, are required. Enterococcal infection often is difficult to eradicate and complicated by severe valve destruction. Adequate therapy generally requires high dosage of a penicillin in combination with an aminoglycoside (eg, streptomycin, kanamycin, gentamicin). Infection with nonenterococcal group D streptococci probably cao be treated with penicillin alone because these organisms are inhibited by serum levels of 0.015 to 0.12 p.g/ml. Indeed, the clinical course of nonenterococcal group D infection seems to be milder than the course of enterococcal infections and similar to the course of infections caused by Strep viridans. Staphylococci account for 10% to 15% of endocarditis in patients with underlying valvular disease. Staphylococcus aureus is more common than Staph epidermidis. Often the patients are elderly and debilitated, with extracardiac sources of bacterial seeding. The mortality from Staph aureus endocarditis in nonaddicts approaches 80%. Metastatic renal and central nervous system lesions are common. 7 Staph epidermidis has been isolated in elderly patients with underlying valvular disease. The clinical presentation is that of an indolent disease similar in manifestations and prognosis to Strep viridans endocarditis. Gram-negative organisms and fungi are rare causes of endocarditis in patients with underlying valvular disease. Usually, clear predisposing factors are present, such as prolonged intravenous therapy, hyperalimentation, or a long, complicated course after gastrointestinal surgery. Fortunately, pneumococci and gonococci today are rare causes of endocarditis. Pneumococcal endocarditis similar in severity to staphylococcal disease still occurs in elderly alcoholic men. .Clinicat presentation-The diagnosis of bacterial endocarditis is quickly considered in a middle-aged individual who has unexplained fever, a mitral insufficiency murmur, weight loss, splenomegaly, and a few petechial hemorrhages. Today, however, patients often see a physician early in the course of illness, and in the absence of dramatic physical findings the diagnosis may be elusive. Fever is almost always present, and malaise and weight loss are common. However, atypical presentations are being recognized. Patients with no history of fever or anorexia may be admitted to a hospital with apparent acute meningitis, cerebrovascular accident, or symptoms related to other sites of embolization.


Clubbing, seen now in less than 2% of patients, and splenomegaly, seen in 40%, were once seen in over 80%. Petechiae, splinter hemorrhages, Janeway lesions, and Osler's nodes were previously noted in 50% to 70% of patients but now are noted in 10% to 30%. Laboratory evaluation shows elevated sedimentation rate, anemia, moderately elevated white blood cell count, and microscopie hematuria in the majority of patients. A diffuse increase in serum gamma globulin values and a positive test for rheumatoid factor are seen in about 50% of patients, particularly those with symptoms persisting six weeks or more. 8 The presence of rheumatoid factor reflects, in part, lgM antibody formed to IgG antibody against the infecting organism. Serum complement levels, which may be nonspecifically increased in infection, are markedly decreased in sorne cases, possibly reB.ecting ongoing immune complex formation. Drug Addicts Drug addicts represent the largest population of patients with normal heart valves who are at risk for development of endocarditis.9 Whether the valves in sorne of these patients have been congenitally abnormal or damaged previously is uncertain, but it is weil accepted that most are at !east clinically normal before infection develops, 10 since a murmur is not detected on auscultation at admission in as many as 30%. Although right-sided endocarditis is very unusual in the nonaddict population, over 50% of drug addicts with no known previous heart disease in whom endocarditis develops have involvement of the tricuspid valve alone. 10 Endocarditis limited to the left side of the heart was reported in an early autopsy series9 but is now realized to be less common than right-sided disease. Organisms involved-The organisms isolated in endocarditis in addicts are generally virulent and may play a direct, crucial role in the pathogenesis of infection occurring on previously normal valves. The most common organisms are those normally found on the skin: staphylococci, beta-hemolytic streptococci, enterococci, Gram-negative enteric bacteria such as Pseudomonas aeruginosa 11 and Ps cepacia (from fecal contamination of the skin), and Candida species. Staph attreus accounts for 50% of endocarditis in addicts. lt may infect the right or left heart valves, but when the tricuspid v~lve alone is involved, Staph aureus is nearly always the organism isolated. Gram-negative endocarditis and fungal endocarditis are also seen in addicts. Alterations in immune status (eg, inadequate serum antibody factors and dysfunction of macrophages) may be risk factors.

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Mixed infections with two or more bacteria or bacteria and fungus, rare in other patients, have been described in addicts. Fungal endocarditis caused by Candida is less common than the literature suggests. Many cases have been caused by long-term use of indwelling polyethylene catheters during treatment of bacterial endocarditis. Clinical presentation-Pulmonary complaints of sudden onset with tachypnea, dyspnea, pleuritic chest pain, and blood-streaked sputum may result from septic pulmonary emboli from an infected tricuspid valve. Such "pneumonia" is common. There may be no diagnostic elues, since clubbing is almost never present and splenomegaly occurs in only 15 % of patients. Murmurs may be absent on initial examination. If the tricuspid valve is involved, there may be a short systolic murmur unaltered by respiration. Right-sided fail;ure is rarely clinically apparent. Ali physical findings may be confined to the lungs. The high incidence of pulmonary involvement and the virulence of the infecting organisms make persistent infection a problem. Nonetheless, addiets with endocarditis-at !east those infected with Staph aureus-have a lower monality rate than nonaddicts, perhaps because the tricuspid valve is more often involved in the addict and insufficiency of this valve is better tolerated than insufficiency of other valves. Also, addicts are usually younger, with previously competent myocardium, and perhaps most important, therapy is initiated early in the disease. Patients Undergoing Cardiac Surgery Patients with patched or sutured congenital hean defects and more significantly those with prosthetic valves are at significant risk for endocarditisP Unfortunately, most of these patients have atypical clinical presentations: high spiking fever and chills, major emboli, or gradually increasing congestive failure. Sorne patients may have no symptoms. Physical examination is often unrevealing. Fever is not universal, and petechiae and splenomegaly are frequently absent. Laboratory findings may be within normallimits. Blood cultures may be negative, panicularly in fungal endocarditis. Fluoroscopy yields indirect evidence for the diagnosis in 10% to 20% of cases by showing rocking or dysfunction of the valve, suggesting disruption of sutures secondary to infection. lt is helpful to consider patients with prosthetic valve infections in two groups: those infected within two months of operation and those who become infected after this period. 13 Barly postoperative infection-Patients with early endocarditis often have had a complicated perioperative course. They may have required prolonged cardiopulmonary bypass, long periods of

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GLENDA J. GARVEY Dr. Garvey is instructor in medicine and member of the division of infectious diseases, College of Physicians and Surgeons, Columbia University, New York.

Dr. Neu is professor of medicine and pharmacology and head of the division of infectious diseases, College of Physicians and Surgeons, Columbia University.

endotracheal intubation, reexploration for bleeding, and long courses of prophylactic antibiotics. The skin- and air-borne organisms associated with early infection are normally of low invasiveness. Staph epidermidis, diphtheroids, and Corynebacterium are the most common. Fungi, such as Candida, Aspergillus, Penicillium, and Paecilomyces, may be involved. At operation, these organisms probably contaminate the surgical field, or during the perioperative period, transient bacteremias may result from use of intravenous and indwelling urinary catheters or nastotracheal tubes. The organisms find ideal conditions for colonization at the fresh operative site at the base of the valve. Fungal endocarditis in sorne cases has been found to be related to inadequate ventilation of the operating rooms. Gram-negative prosthetic valve endocarditis has been reported in the early postoperative period. lt has been suggested that Gram-negative bacteremia often represents seeding from wound infections or from intravenous or bladder catheters rather than true valve infection. 14 At present, however, no satisfactory methods are available to discrimiaate between valvular and nonvalvular infections. Regardless of the organisms isolated, the prognosis for patients in whom endocarditis develops within two months of operation remains extremely grave. Late postoperative infection-Infections occurring more than two months postoperatively are quite similar to classic endocarditis. The spectrum of organisms isolated is similar to that encountered in patients with underlying valvular lesions. Streptococcal species, particularly Strep viridans, are common, as are Staph aureus and Staph epidermidis. Predisposing dental, gastrointestinal, or


genitourinary procedures often are noted in these patients. The prognosis appears to be better for this group than for those with early infection. In one series,13 8 of 19 patients with late infections died, compared with 13 of 19 with early infections. Complications

Cardiac complications of endocarditis include local destruction of the valve, involvement of the

Administration of appropriate

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antibiotics is still considered the initial treatment of choice in almost ali patients with endocarditis.

septum, and extension into Valsalva's sinus. This leads to congestive heart failure from incompetent valves or, less frequently, from myocarditis or from damage to the conducting system. The incidenee of congestive heart failure following infective endocarditis is approximately 50%. Central nervous system complications are cornmon 7 but often subtle, with headache or personality change as the only neurologie manifestation. However, meningitis or focal neurologie findings occur in 20% of patients. Cerebrospinal fluid findings may be compatible with aseptic meningitis, ie, pleocytosis with increased monocytes and negative bacterial culture. However, with virulent organisms such as Staph aureus or enterococcus, purulent cerebrospinal fluid may be found. Sudden cerebrovascular accidents with focal neurologie findings are as common as meningitis. Mycotie aneurysms of the cerebral vessels can cause devastating, sudden illness presenting as subarachnoid or intracerebral hemorrhage months to years after an episode of endocarditis.15 The frequency of mycotic aneurysm is difficult to estimate. Renal complications have at least two causes. True embolie phenomena certainly occur and lead to areas of infarction, particularly with staphylococcal endocarditis. There is also evidence for immune complex disease; focal glomerulitis and diffuse glomerulonephritis (acute and chronic) have been described. 16 The latter is characterized by hematuria, deteriorating renal function, low serum complement values, and findings on renal biopsy of IgG and complement deposition along the basement membrane. Unlike loss of renal function due to infarction, renal insufficiency secondary to this immune phenomenon seems at !east


partially reversible with antibiotie treatment of the endocarditis. Diagnosis

Infective endocarditis can be diagnosed when sustained bacteremia is documented in a compatible clinical setting. At !east two venous blood cultures positive for the same organism are necessary. In general, five or six biood cultures are sufficient to guarantee isolation of the organism in at least two. Proper timing of the cultures is a subject of sorne debate. Many investigators believe that since the bacteremia is continuous, blood for culture may be obtained at any time without relation to fever spike or chili. However, others17 recommend. observation of the fever curve for 12 to 24 hours, with blood drawn during the hour before anticipated fever rise, the time when bacteremia is presumed greatest. The incidence of culture-negative endocarditis depends on the techniques and capabilities of the laboratory, the patient population, and the oumber of autopsies performed. About 10% is acceptable. If fungal endocarditis is considered, however, the incidence of negative venous blood cultures may be as high as 50%. Bone marrow and arterial blood cultures, which do not increase the yield of positive cultures in bacterial endocarditis, are being evaluated as aids in diagnosing Candida endocarditis. Serologie techniques for detection of Candida and Aspergillus are also being studied. Agglutinins and precipitins are being tested but at present have not proved helpful in diagnosis. False-positive as weil as falsenegative results complicate interpretation.18 Therapy

Administration of appropriate antibioties is still considered the initial treatment of choiee in almost ali patients with endocarditis. Antibiotics should be selected within the context of each case. When an organism hàs been isolated, minimal inhibitory and bactericidal concentrations of the chosen antibiotic should be determined. Specimens of the patient's serum obtained one to two hours after administration of the antibiotic should be tested for bactericidal level. A ti ter of at least 1:8 is considered satisfactory. lntravenous administration of antibiotie is still the preferred mode of therapy. However, in certain situations (eg, Strep viridans endocarditis in patients with underlying valve disease and Staph aureus endocarditis in addiets) the intramuscular route has given comparable results. Studies have also confirmed that oral therapy may be satisfactory in selected patients with Strep viridans endocarditis if it is combined with intramuscular administration of an aminoglycoside. However, the

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Procedure imposing added risk

Dosage one hour before procedure

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Dosage on day of and two days after procedure Nonallergic


Dental (x-rays, drilling, cleaning, fitting of dental plates)

Procaine penicillin, 1.2 million units lM or Penicillin V, 750 mg orally

Cefazolin, 1gmiM or Erythromycin, 500 mg orally

Penicillin V, 500 mg every 6 hr orally

Erythromycin, 500 mg every 6 hr orally

Genitourinary (cystoscopy, bladder fulguration, prostatectomy, cervical dilation and curettage, vaginal delivery, caesarean section) Gastrointestinal (hemorrhoidectomy, bowel surgery, gallbladder surgery)

Ampicillin, 1.5 gm IV or Amoxicillin, 1 gm orally, plus gentamicin, 60-80 mg lM

Cefazolin, 1 gm lM, plus gentamicin, 60-80 mg lM

Ampicillin, 1.5 gm every 6 hr IV or Amoxicillin, 500 mg every 6 hr orally, plus gentamicin, dose and interval determined by renal function

Cefazolin, 1 gm every 8 hr lM, plus gentamicin, dose and interval determined by renal function

general recommendation is thar oral therapy be reserved for only those patients who cannot tolerate parenteral therapy because of the unpredictability of gastrointestinal absorption. Oral therapy should be administered only in the hospital. In vitro and in vivo studies show that a combination of penicillin and streptomycin kills Strep viridans most rapidly. However, clinically excellent results have been reported using penicillin alone. Accepted dose regimens of penicillin range from 6 to 24 million units/day. Procaine penicillin (1.2 million units every six hours intramuscularly) or penicillin V ( 1.2 gm every six hours orally) with streptomycin (500 mg every 12 hours intramuscularly) has been used. For patients who caonot tolerate penicillin, cephalothin (2 gm every four hours) or vancomycin (500 mg every six hours) alone or with streptomycin has proved satisfactory. Optimum length of therapy is not known, but three to four weeks is generally recommended. If streptomycin is used, therapy may be discontinued after rwo weeks. Because of the organisms' sensitivity to penicillin, nonenterococcal group D streptococcal endocarditis may be treated like Strep viridans endocarditis. Enterococcal endocarditis requires more rigorous therapy. The intravenous route must be used, and treatment of choice is a penicillin (24 million units/day) or ampicillin (12 gm/day) in combinarion with an aminoglycoside. Streptomycin may be used if synergy is demonstrated; otherwise gentamicin is preferred. Therapy with both anti-

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biotics is continued for six weeks. Penicillin alone is not considered acceptable therapy. In patients who cannot receive penicillin, vancomycin (500 mg every six hours intravenously) alone or with an aminoglycoside is the alternative therapy, since cephalosporins are unsatisfactbry for enterococcal endocardi ti s. Most staphylococci must be assumed to be penicillin-resistant until careful sensitivity testing is performed. Therefore, one of the penicillinaseresistant penicillins, such as methicillin, nafcillin, or oxacillin, should be used in doses of 12 gm/ day (2 gm every four hours) for six weeks. Cephalothin, cefazolin, or vancomycin may be used in penicillin-allergic patients. Intravenous therapy is preferred, but if it is not possible, intramuscular treatment with cefazolin ( 1 gm every six hours) has given satisfactory results in selected patients. The Gram-negative organisms and fungi pose difficult treatmenr problems. Careful identification and determination of serum bactericidal levels to check reporred disk sensitivities are vital to adequate treatment of endocarditis caused by these organisms. Ps aeruginosa should be treated with carbenicillin (30 gm/day) and gentamicin (4.5 to 6 mg/kg/day). Ps cepacia will respond to oral trimethoprim-sulfamethoxazole alone or in combination with polymyxin. Other organisms should be treated with the appropriate bactericidal agents as determined by careful evaluation. At present, amphotericin B, alone or in combination with 5-fluorocytosine, is the only therapy


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available for patients with fungal endocarditis. In patients with underlying valvular disease in whom no organism can be identifi.ed, a full course of therapy for enterococcal endocarditis is recommended. Why Patients Die With Endocarditis In the preantibiotic era, active infection was the major cause of death from endocarditis in patients with underlying valvular disease. Today it is unusual for such patients to die of infection, because the organisms are sensitive to antibiotics of low toxicity. Addicts and patients with prosthetic valves still die of infection, however. Often the infection is unsuspected and untreated, or particularly with fungi, blood cultures may be persistently negative, making selection of appropriate therapy difficult. ln addicts, the organism may be resistant to available antibiotics or sensitive only to prohibitively toxic drugs. In patients with prosthetic valves, the presence of the prosthesis may prevent eradication of the organisms. Although death from active infection still does occur, congestive heart failure now is the leading cause of death during treatment and follow-up. Cardiac failure in two thirds of those who die is secondary to perforated, insufficient valves. Patients with aortic valve infection are particularly at risk for heart failure and death during therapy. ln patients with prosthetic valve infection, vegetations may erode sutures, or large vegetations (particularly in fungal infections) may fi.ll the cage and paralyze bali motion. Embolization remains a major cause of death from endocarditis. Emboli may lead to infarction in any organ system or to formation of mycotic aneurysm. Emboli to the coronary vessels may precipitate acute myocardial infarction and death. In addicts with infection of the right side of the heart, multiple septic emboli may establish satellite foci of infection in the lung, leading to death from intractable infection or pulmonary hypertension or both. Embolie phenomena during adequate therapy and up to one year after treatment have been reported.

of the prosthesis. Surgery during the initial course of antibiotic therapy is now being considered for persistent infection, intractable heart failure, and embolization. Despite effective antibiotics, persistent or relapsing infection does occur, particularly in patients with prosthetic valve endocarditis. Sorne of these patients may be cured by antibiotic therapy alone, buf many will require surgical excision of the infec*d prosthesis. ln one series, 60% of patients tre,ated with antibiotics alone died, while 45% of patients treated with antibiotics and surgery died. Surgery for infection has usually been reserved for cases in which relapse occurs after an 8- to 12-week initial course of antibiotics. Addicts with endocarditis due to relatively resistant organisms may also be candidates for earlier surgical intervention. Total tricuspid valvulectomy without valve replacement has had favorable results in selected patients with persistent right-sided endocarditis or embolization from tricuspid vegetation or both. There are no universally accepted recommendations regarding surgery for fungal endocarditis. Our experience suggests that early excision of the involved valve-if possible within days of the diagnosis-may eradicate the infection before the fungus has deeply invaded the heart tissue. Surgery may also markedly decrease the fungal inoculum, thereby improving the chance of cure within the limits imposed by the toxic antifungal agents. Recent studies20 also demonstrate that surgical intervention may be lifesaving when congestive heart failure occurs during treatlllent. At present, a major indication for surgery is the abrupt occurrence of intractable congestive failure unresponsive to a full cardiotonic regimen. Embolization is being evaluated as an indication for surgical intervention. Two or more clinically apparent major emboli are indications for surgery at sorne centers. However, a single embolus may cause sudden death or leave the patient with profound neurologie deficit. If those patients at risk for major emboli could be identified, early replacement of their valves might be considered.

The Role of Surgery Drainage of skin abscesses or full exCISIOn of thrombosed suppurative veins to prevent recurrent infection are weil accepted surgical procedures. In patients with persistent heart failure, valve replacement has been performed months after a full course of antibiotic therapy. Surgeons have been reluctant to attempt valve replacement during antibiotic therapy, but recent studies19 have shown that valve replacement early in the course of treatment, even within 24 hours, is feasible and rarely leads to infection or disruption

Prevention Too little is known to define a completely successful approach to prevention of endocarditis. Patients at risk must be identifi.ed and educated. Present recommendations for valve protection during dental, gastrointestinal, and genitourinary procedures probably are not adequate to provide insurance against infection. 21 Table 1 lists current recommendations for prophylactic treatment of patients with underlying valvular heart disease of any etiology, prosthetic valves, or corrected congenital heart defects.


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Patients receiving antibiotics may have the oral pharynx recolonized with relatively resistant organisms. Sorne patients receiving oral penicillin prophylaxis for acute rheumatic fever have mouth flora relatively resistant ro penicillin and should receive an increased dose of penicillin for valve protection if dental work is performed. Patients being treated with penicillin for endocarditis have been shown ro have penicillin-resistant streptococci and staphylococci in their mouths. Thus, when dental work is done, these patients should receive oxacillin coverage for valve protection, in addition ro daily penicillin therapy for endocarditis.

Summary Older patients with underlying valvular disease, drug addicts, and patients who have had surgery

for repair of congenital heart disease or replacement of a valve are the major groups at risk for infective endocarditis. New profiles of this disease have been delineated, but much of the pathophysiology of the classic as weil as the newer forms of endocarditis remains unclear. Greater understanding of host defense factors is needed before a fully satisfacrory approach ro diagnosis, therapy, and prevention can be defined. Address reprint requests to Harold C. Neu, MD, Department of Medicine, College of Physicians and Surgeons, Columbia University, 630 W !68th St, New York, NY 10032. For ReadySource on infection control, sec page 225. Summary self-test on infection control begins on page 217.

REFERENCES 1. Cherubin CE, Neu HC: Infective endocarditis at the Presbyterian Hospital in New York City from 1938-1967. Am J Med 51:83, 1971 2. Fin land M, Barnes MW: Changing etiology of bacterial endocarditis in the antibacterial era. Ann lntern Med 7.2:341, 1970 3. Burnside JW, Desanctis RW: Bacterial endocarditis on calcification of the mitral anulus fibrosus. Ann lntern Med 76:615, 1972 4. Angrist A, Oka M: Pathogenesis of bacterial endocarditis. JAMA 183:249, 1973 5. Lerner PI, Weinstein L: Infective endocarditis in the antibiotic era. N Engl J Med 27 4:199, 259, 388, 1966 6. Hoppes WL, Lerner PI: Nonenterococcal grou p-D streptococcal endocarditis caused by Streptococcus bovis. Ann lntern Med 81:588, 1974 7 Ziment 1: Nervous system complications in bacterial endocarditis. Am J Med 47:593, 1969 8. Williams RC Jr, Kunkel HG: Rheumatoid factors and their disappearance following therapy in patients with subacute bacterial endocarditis. Arthritis Rheum 5:126, 1972 9. Cherubin CE, Baden M, Kavaler F, et al: Infective endocarditis in narcotic addicts. Ann Intern Med 69:1091, 1968 10. Conway N: Endocarditis in heroin addicts. Br Heart J 31:543, 1969 11. Reyes MP, Palutke WA, Wylin RF, et al: Pseudomonas endocarditis in the Detroit Medical Cen· ter. Medicine 52:173, 1973

12. Hariston P, Lee WH: Management of infected prosthetic heart valves. Am Thorac Surg 9:229, 1970 13. Dismukes WE, Karchmer AW, Buckley MJ, et al: Prosthetic valve endocarditis. Circulation 48:365, 1973 14. Sande MA, Johnson WD, Hook EW, et al: Sustained bacteremia in patients with prosthetic valves. N Engl J Med 286:1067, 1970 15. Morgan WL, Bland EF: Bacterial endocarditis in the antibiotic era with special reference to the later complications. Circulation 19:753, 1959 16. Gutman RA, Striker GE, Gilliland BC, et al: The immune complex glomerulonephritis of bacterial endocarditis. Medicine 51:1, 1972 17. Weinstein L, Rubin RH: Infective endocarditis1973. Prog Cardiovasc Dis 16:239, 1973 18. Seelig MS, Speth CP, Kozinn PJ, et al: Candida endocarditis after cardiac surgery. J Thorac Cardiovasc Surg 65: 58.), 197 3 19. Manhas DR, Mohri H, Hesse! EA: Experience with surgical management of primary infective endocarditis: A collected review of 139 patients. Am Heart J 84:738, 1972 20. Griflin FM Je, Jones G, Cobbs CC: Aortic insufliciency in bacterial endocarditis. Ann lntern Med 76:23, 1972 21. Du rack DT, Petersdorf RG: Chemotherapy of experimental streptococcal endocarditis. 1. Comparison of commonly recommended prophylactic regimens. J Clin lnvest 52:592, 1973

~_1o_n______________~~-a_ns_w~e Patients most otten die from endocarditis today because of a. Embolization b. Failure to diagnose c. Congestive heart failure d. lnability to eradicate the organism

Vol. 58 • No. 3 • September 1975 • POSTGRADUATE MEDICINE



Infective endocarditis.

Postgraduate Medicine ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: Infective Endocarditis Glen...
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