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Pulmonic valve endocarditis. (Case Report).


Pulmonic valve endocarditis is an extremely rare infection that shares epidemiologic, clinical, radiologic, microbiologic, and prognostic features with tricuspid valve endocarditis. We report a case of pulmonic valve infection on a structurally normal heart and review the English-language literature on this subject.


Infective endocarditis is a microbial infection of the endothelial surface of the heart and great vessels. The cardiac valves, especially the mitral and aortic valves, are most commonly involved. Right-sided endocarditis is most frequently encountered among intravenous drug abusers and typically involves the tricuspid valve. Pulmonic valve endocarditis is extremely rare, with fewer than 90 cases of pulmonic valve infection being previously reported. (1-14) We present a case of isolated enterococcal pulmonic valve endocarditis affecting a structurally normal heart.


Infective endocarditis involving the pulmonic valve is extremely rare, accounting for only 1.5 to 2.0% of hospital admissions for infective endocarditis. (1) Infection may be isolated to the pulmonic valve alone or may concomitantly affect the mitral or aortic valve. (1-4) Both structurally normal and abnormal heart valves have been associated with pulmonic valve endocarditis. (1-15) The low incidence of infection on the pulmonic valve compared with other cardiac valves may relate to differences in hemodynamic pressures across the valves, oxygen saturation, underlying congenital or acquired valvular abnormalities, and the endothelial lining and relative vascularity of the valves.

A search of the literature from 1960 through 2000 identified only 38 cases (including the present case) of isolated pulmonic valve endocarditis occurring on structurally normal hearts. (1-15) Compared with left-sided heart involvement, pulmonic valve infection tended to affect younger patients, and more than 80% of affected subjects were male. The vast majority of infections were community-acquired. Predisposing factors included intravenous drug abuse (28%), alcoholism (13%), sepsis (7%), central line infection (7%) or other catheter-related infection (5%), gonorrhea (5%), dental extraction (2.6%), bowel surgery (2.6%), liver or renal transplantation (2.6%), and colonic angiodysplasia (2.6%). In 28% of cases, no predisposing factor was identified.

The clinical presentation of pulmonic valve endocarditis is similar to that of tricuspid valve infection. In the cases reviewed, fever, shortness of breath, and pleuritic chest pain predominated, and radiographic and laboratory evidence frequently corroborates the presence of pulmonary embolism. In our patient, it was unclear whether the pulmonary nodules seen on chest film, predominantly lower lobe in location, were due to tuberculosis or septic emboli caused by the pulmonic valve endocarditis (or whether tuberculosis preceded endocarditis). Approximately one-half of patients had pulmonic regurgitant murmur present on cardiovascular examination. Because of the nonspecificity of symptoms and the lack of peripheral stigmas typically associated with left-sided mitral or aortic valve involvement, the diagnosis of pulmonic valve endocarditis may be delayed for up to 6 months. (4)

In the 38 reviewed cases in which no pulmonic valvular abnormality was noted before infection, Staphylococcus aureus was the most common microorganism recovered from blood cultures (44%), followed by streptococci (13%), Streptococcus bovis (5%), gonococcus (5%), pseudomonas (5%), E. coli (5%), Candida albicans (5%), Bacteroides fragilis (2.6%), Haemophilus influenzae (2.6%), and E. faecalis (2.6%). (14) However, no organism was cultured in 10% of the cases. Transthoracic echocardiography was sensitive in detecting pulmonic valve vegetations (29 of 38 cases, or 76%). (2-7,11-15)

Twenty-five patients were treated medically with antibiotics alone (7 patients died), and 13 required surgical intervention and valve replacement. Parenteral antibiotic therapy is generally administered for 4 to 6 weeks. Indications for surgery are the same as those for tricuspid valve infection: persistent bacteremia despite appropriate antimicrobial therapy, locally invasive infection including abscess formation, progressive valve destruction and incompetence, and relapsing infection after completion of a full course of antibiotic therapy. As with other right-sided heart valve infections, the prognosis for pulmonic valve endocarditis is generally better than for mitral or aortic infection. (1)

In our patient with a risk factor of chronic alcohol abuse, pulmonic valve endocarditis was suspected on the basis of radiographic features suggestive of septic pulmonary emboli, supported by transesophageal echocardiography showing a large solitary pulmonic valve vegetation, and confirmed by the microbiologic finding of blood cultures positive for E. faecalis on two occasions, separated temporally by 4 weeks and thus unlikely to represent contamination. These findings satisfied the Duke diagnostic criteria for infective endocarditis. (15)


Pulmonic valve endocarditis is an extremely rare infection that shares epidemiologic, clinical, radiologic, microbiologic, and prognostic features with tricuspid valve endocarditis. We report the first case of pulmonic valve infection caused by enterococci.

Accepted January 15, 2002.


(1.) Ramadan FB, Bcanlands DS, Burwash IG. Isolated pulmonic valve endocarditis in healthy hearts: A case report and review of the literature. Can J Cardiol 2000;16:1282-1288.

(2.) Nakamura K, Satomi G, Sakai T, Ando M, Hashimoto A, Koyanagi H, et al. Clinical and echocardiographic features of pulmonary valve endocarditis. Circulation 1983;67:198-204.

(3.) DePace NL, Iskandrian AS, Morganroth J, Ross J, Mattleman S, Nestico PF. Infective endocarditis involving a presumably normal pulmonic valve. Am J Cardiol 1984:53:385-387.

(4.) Cassling RS, Rogler WC, MeManus BM. Isolated pulmonic valve infective endocarditis: A diagnostically elusive entity. Am Heart J 1985; 109:558-567.

(5.) Cherukuri AK, Maloney M, O'Briain DS, Weir DG. Isolated pulmonary valve endocarditis: A rare or an underdiagnosed disease? Jr J Med Sci 1994;163:494-495.

(6.) Soding PF, Klinck JR. Kong A, Farrington M. Infective endocarditis of the pulmonary valve following pulmonary artery catheterisation. Intensive Care Med 1994;20:222-224.

(7.) Cremieux AC, Witchitz S, Malergue MC, Wolff M, Vittecocq D, Vilde JL, et al. Clinical and echocardiographic observations in pulmonary valve endocarditis. Am J Cardiol 1985;56:610-613

(8.) Winslow T, Foster E, Adams JR. Schiller NB. Pulmonary valve endocarditis: Improved diagnosis with biplane transesophageal echocardiography. J Am Soc Echocardiogr 1992;5:206-210.

(9.) Murray NH, Cheesman MG, Millar-Craig M. Echocardiographic demonstration of Escherichia coli endocarditis restricted to the pulmonary valve. Br Heart J 1988;60:452-454.

(10.) Fourestie V. Benvenuti C, LeJonc JL, LeMaire F, Benhaiem-Sigaux N. Fatal acute circulatory failure in pulmonary valve endocarditis. Am J Cardiol 1986:57:895 (letter).

(11.) Berger M, Wilkes HS, Gallerstein PE, Berdoff RL, Goldberg E. M-mode and two-dimensional echocardiographic findings in pulmonic valve endocarditis. Am Heart J 1984;107:391-393.

(12.) Johnson DH, Rosenthal A, Nadas AS. A forty-year review of bacterial endocarditis in infancy and childhood. Circulation 1975:51:581-588.

(13.) Roberts WC, Buchbinder NA. Right-sided valvular infective endocarditis: A clinicopathologic study of twelve necropsy patients. Am J med 1972;53:7-19.

(14.) Hall B, Dowling HF. Negative blood cultures in bacterial endocarditis: A decade's experience. Med Clin North Am 1966:50:159-170.

(15.) Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: Utilization of specific echocardiographic findings--Duke Endocarditis Service. Am J Med 1994;96:200-209.


* Isolated pulmonic valve endocarditis is a rare infection, and its occurrence on a structurally normal heart is extremely rare.

* Pulmonic valve endocarditis shares epidemiologic, clinical, radiographic, microbiologic, and prognostic features with tricuspid valve endocarditis.

* Most cases of pulmonic valve endocarditis are community-acquired, with illicit drug use being a major risk factor and Staphylococcus aureus being the most common causative organism.

* Surgical intervention may sometimes be necessary for successful management of pulmonic valve endocarditis.

Case Report

A 53-year-old former alcoholic and ex-smoker came to the hospital with a 2-month history of intermittent fever, cough, and weight loss. The cough was initially dry but later became productive of greenish sputum. There was no history of exposure to tuberculosis. Apart from pallor, findings on physical examination were unremarkable. Initial laboratory workup revealed a hypochromic, microcytic anemia, and the patient had colonoscopy, which showed only mild right-sided angiodysplasia and internal hemorrhoids. One blood culture drawn the day after colonoscopy during a fever spike grew Entero coccus faecalis. An x-ray of the chest showed bilateral lower-lung field consolidation and multiple discrete nodular densities (Fig. 1). Diagnostic bronchoscopy revealed no significant abnormality. Treatmeat with oral clarithromycin was empirically begun, and the patient was discharged. His symptoms failed to improve, however, and 1 month later, he returned with persistent high-grade fever and cough, bilateral pleuritic chest pain, and a 7-kg weight loss. Physical examination at this time found him to be chronically ill appearing and pale, with a body temperature of 38.5[degrees]C (101.3[degrees]F). Cardiovascular examination was unremarkable, and respiratory examination revealed only a few coarse crepitations bilaterally at the lung bases. The complete blood count showed a white blood cell count of 8,200/[mm.sup.3] with a normal differential, and a single blood culture drawn at admission again grew E. faecalis. Transthoracic echocardiography showed no cardiac abnormality; however, because the isolation of enterococci from two previous blood cultures raised the suspicion of infective endocarditis, transesophageal echocardiography was performed, which revealed a large, solitary, sessile vegetation on the pulm onic valve (Fig. 2). Treatment with intravenous ampicillin and gentamicin was started, but streptomycin was substituted because enterococcal isolate was resistant to gentamicin (minimum inhibitory concentration, 64 mg/ml). During the second week of therapy, culture of a respiratory specimen from the previously performed bronchoscopy revealed growth of Myco bacterium tuberculosis, and four-drug antituberculous therapy was initiated. Ampicillin and streptomycin were continued for 4 weeks. At the time of this writing, the patient continues to receive antituberculous therapy and is doing well. Tracing of household contacts revealed no additional cases of active tuberculosis.

From the Department of Medicine, Aga Khan University Medical College, Karachi, Pakistan.

Reprint requests to Muhammad Tariq, MBBS, MRCP (UK), Section of General Medicine, Department of Medicine, Aga Khan University, P.O. Box 3500, Stadium Road, Karachi 74800, Pakistan. Email:

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Article Details
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Author:Islam, Najmul
Publication:Southern Medical Journal
Geographic Code:1USA
Date:Jun 1, 2003
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