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Hospital-acquired Pseudomonas aeruginosa endocarditis
~ouwxd of Hospital Infection (1991) 18, 161-163
Letter
to the Editor
Sir,
Hospital-acquired
Pseudomonas
aeruginosa
endocarditis
Pseudomonas aeruginosa is a rare cause of endocarditis. Nevertheless, over the past two decades this organism has emerged as an important pathogen amongst intravenous drug abusers and the number of cases has significantly increased.lm3 We report here an unusual case of hospital-acquired Pseudomonas aeruginosa endocarditis in a non-drug addict hospitalized for viridans streptococcal endocarditis. A 20-year-old non-drug addict male was admitted to another hospital because of prolonged fever. His past medical history included a diagnosis of congenital bicuspid aortic valve. Blood cultures grew viridans streptococci, but vegetations were not seen by echocardiography. Infective endocarditis was diagnosed and the patient was treated with penicillin G, intravenously. Fever disappeared and he was discharged after 3 weeks of antibiotic therapy. Oral penicillin V was recommended for an additional period of 10 days. Four days after discharge, the patient suddenly collapsed at home and was immediately readmitted to the same hospital. The patient was comatose and had a right hemiparesis. A mycotic aneurysm was suspected. One week later he was transferred to our hospital for further investigation and treatment. On admission the patient was afebrile. Both a 4/6 systolic and diastolic murmur were auscultated over the aortic area, a right hemiparesis was evident and bilateral papilloedema was noted at fundoscopy. The rest of the physical examination was unremarkable. Laboratory results were within normal limits. For 4 consecutive days, S/S blood cultures grew Pseudomonas aeruginosa, later identified as serotype 011. A computerized tomography scan of the brain revealed a large left frontoparietal haemorrhage and arteriography showed a large aneurysm of the left middle cerebral artery. Echocardiography demonstrated an enlarged, hypertrophic left ventricle with vegetations seen on the posterior leaflet of the aortic valve. Amikacin and piperacillin were started in doses of 1 g and 24 g daily, respectively, and continued for 6 weeks. Congestive heart failure developed and was successfully treated with furosemide. -4 decision to perform aneurysmectomy was taken because the aneurysm was large and in imminent danger of re-bleeding. The operation was successfully performed 3 weeks after admission. Repeated blood cultures obtained during treatment remained sterile. Three months later aortic valve replacement vvas performed. At surgery, sterile vegetations were found on the aortic valve. The patient recovered, but hemiparesis persisted.
162
Letter
to the Editor
Reviewing the behaviour of P. aeruginosa endocarditis, we found that more than 90% of all reported cases have occurred in intravenous drug abusers.4 Underlying heart disease was found in only 20% of these patients and vegetations affected predominantly the right side of the heart.3 Pseudomonas endocarditis is more frequently biventricular than is bacteraemia from endocarditis caused by other bacteria. ’ Persistent tricuspid valve infection, despite antibiotic therapy is not uncommon’ and this fact may explain the subsequent seeding of the aortic and mitral valves.’ Pseudomonas endocarditis amongst intravenous drug abusers is frequently associated with polymicrobial bacteraemia and, in this setting, P. aeruginosa is the most commonly isolated Gram-negative bacterium.‘p6 Thirty percent of polymicrobial valvular infections are caused by Gram-positive cocci together with Gram-negative bacteria.3 In some of these cases, and as observed in our patient, Gram-negative bacteria are not recovered from blood cultures until 3-21 days after Gram-positive cocci have been isolated.3 Most cases of pseudomonas endocarditis have been described in the Detroit area.’ Although the reasons are not clear, this observation is supported by new clinical, epidemiological and experimental data. Pseudomonas aeruginosa serotype 011 has been isolated from the blood of 9/10 intravenous drug abusers with endocarditis in Detroit,’ and also from both blood and syringes of addicts with endocarditis reported from other areas.7 The same serotype was responsible for a recent outbreak of endocarditis in Chicago where serotype 011 was found to be significantly more common among intravenous drug abusers with endocarditis than among patients with infections other than endocarditis.8 In addition, it has been observed that P. aeruginosa serotype 011 may survive better in the presence of drugs such as pentazocine and tripelennamine,’ a drug combination associated with most cases of pseudomonas endocarditis in Chicago and Detroit. ‘s8 Finally, preliminary observations suggest that serotype 011 adheres more readily to endocardial tissue than other pseudomonas serotypes.’ Pseudomonas aeruginosa in non-addicts is expected to occur as a hospital-acquired infection. Nevertheless, nosocomial endocarditis is uncommonlo’ll and, to our knowledge, only 39 cases of hospital-acquired P. aeruginosa endocarditis have been reported in the English literature.3~4,“~‘2 These patients usually have underlying heart disease or have undergone recent cardiac surgery, particularly valve replacement. Polymicrobial bacteraemia is unusual and endocarditis predominantly involves the left side of the heart.3 Prognosis is bad and the best chance for cure includes early mitral or aortic valve replacement.5~‘2*‘3 Our patient had both an unusual presentation and outcome. A primary source of pseudomonas infection was not found. Valve replacement was required because of severe valvular damage and not for control of infection, which was achieved by medical treatment. Furthermore, the finding of sterile vegetations at surgery may suggest that, occasionally, appropriate
Letter
to the Editor
163
antibiotic therapy alone may also be curative in this difficult-to-treat condition. Finally, this case emphasizes the permanent threat that P. aeruginosa poses to hospitalized patients, including those being treated for more common causes of endocarditis. R. Finkelstein* M. BoulusfM. Markieviczt
Departments of *Internal Medicine, TCardiology and *Infectious Disease Unit Rambarm Medical Center 31096, Haifa, Israel
References I. Reyes MP, Palutke AW, Wylin RF, Lerner AM. Pseudomonas endocarditis in the Detroit Medical Center. 196991972. Medicine 1972: 51: 173-194. 2. Reyes MP, Brown WJ, Lerner AM. Treatment of patients with pseudomonas endocarditis with high dose aminoglycoside and carbenicillin therapy. Medicine 1978; 57: 57-67. 3. Cohen PS, Maguire JH, Weinstein L. Infective endocarditis caused by gram negative bacteria: a review of the literature, 1945-1977. Prog Cardiovasc Dis 1980; 22: 2055242. 4. Pollack M. Pseudomonas aeruginosa. In: Mandell GL, Douglas Jr. RG, Bennett JE (Eds). Principles and Practice of Infectious Diseases. New York: Wiley 1985; 1236-l 2.50. 5. Levine DR, Crane LR, Zervos MJ. Bacteremia in narcotics addicts at the Detroit Medical Center. II. Infectious endocarditis: a prospective comparative study. Rev Znfect Dis 1986; 8: 374-396. 6. Saravolatz LD, Burch KH, Quinn EL, Cox F, Madhaven T, Fisher E. Polymicrobial infective endocarditis: an increasing clinical entity. Am Heart J 1978; 95: 163-168. 7. Rajashekaraiah KR, Rice TW, Kallick CA. Recovery of Pseudomonas aeruginosa from syringes of drug addicts with endocarditis. J Infect Dis 1981; 144: 482. 8. Shekar R, Rice TW, Zierdt CH, Kallick CA. Outbreak of endocarditis caused bv Pseudomonas aeruginosa serotype 011 among pentazocine and tripelennamine abusers in Chicago. J Infect Dis 1985; 151: 203-208. 9. Botsford KB, Weinstein RA, Nathan CR, Kabins CA. Selective survival in pentazocine and tripelennamine of Pseudomonas aeruginosa serotype 011 from drug addicts. J Infect Dis 1985; 151: 209-216. 10. Friedland G, von Reyn F, Levy B, Arbeit R, Dasse P, Crumpacker C. Nosocomial endocarditis. Infect Control 1984; 5: 284-288. 11. Terpenning MS, Buggy BP, Kauffman CA. Hospital-acquired infective endocarditis. Arch Intern Med 1988; 148: 16Olll603. 12. Wieland M, Lederman MM, Kline-King C et al. L,eft sided endocarditis due to Pseudomonas aeruginosa. A report of 10 cases and review of literature. Medicine 1986; 65: 180-189. 13. Reyes MP, Lerner M. Current problems in the treatment of infective endocarditis due to Pseudomonas aeruginosa. Infect Dis 1983; 5: 314321.
Letter
to the Editor
Sir,
Hospital-acquired
Pseudomonas
aeruginosa
endocarditis
Pseudomonas aeruginosa is a rare cause of endocarditis. Nevertheless, over the past two decades this organism has emerged as an important pathogen amongst intravenous drug abusers and the number of cases has significantly increased.lm3 We report here an unusual case of hospital-acquired Pseudomonas aeruginosa endocarditis in a non-drug addict hospitalized for viridans streptococcal endocarditis. A 20-year-old non-drug addict male was admitted to another hospital because of prolonged fever. His past medical history included a diagnosis of congenital bicuspid aortic valve. Blood cultures grew viridans streptococci, but vegetations were not seen by echocardiography. Infective endocarditis was diagnosed and the patient was treated with penicillin G, intravenously. Fever disappeared and he was discharged after 3 weeks of antibiotic therapy. Oral penicillin V was recommended for an additional period of 10 days. Four days after discharge, the patient suddenly collapsed at home and was immediately readmitted to the same hospital. The patient was comatose and had a right hemiparesis. A mycotic aneurysm was suspected. One week later he was transferred to our hospital for further investigation and treatment. On admission the patient was afebrile. Both a 4/6 systolic and diastolic murmur were auscultated over the aortic area, a right hemiparesis was evident and bilateral papilloedema was noted at fundoscopy. The rest of the physical examination was unremarkable. Laboratory results were within normal limits. For 4 consecutive days, S/S blood cultures grew Pseudomonas aeruginosa, later identified as serotype 011. A computerized tomography scan of the brain revealed a large left frontoparietal haemorrhage and arteriography showed a large aneurysm of the left middle cerebral artery. Echocardiography demonstrated an enlarged, hypertrophic left ventricle with vegetations seen on the posterior leaflet of the aortic valve. Amikacin and piperacillin were started in doses of 1 g and 24 g daily, respectively, and continued for 6 weeks. Congestive heart failure developed and was successfully treated with furosemide. -4 decision to perform aneurysmectomy was taken because the aneurysm was large and in imminent danger of re-bleeding. The operation was successfully performed 3 weeks after admission. Repeated blood cultures obtained during treatment remained sterile. Three months later aortic valve replacement vvas performed. At surgery, sterile vegetations were found on the aortic valve. The patient recovered, but hemiparesis persisted.
162
Letter
to the Editor
Reviewing the behaviour of P. aeruginosa endocarditis, we found that more than 90% of all reported cases have occurred in intravenous drug abusers.4 Underlying heart disease was found in only 20% of these patients and vegetations affected predominantly the right side of the heart.3 Pseudomonas endocarditis is more frequently biventricular than is bacteraemia from endocarditis caused by other bacteria. ’ Persistent tricuspid valve infection, despite antibiotic therapy is not uncommon’ and this fact may explain the subsequent seeding of the aortic and mitral valves.’ Pseudomonas endocarditis amongst intravenous drug abusers is frequently associated with polymicrobial bacteraemia and, in this setting, P. aeruginosa is the most commonly isolated Gram-negative bacterium.‘p6 Thirty percent of polymicrobial valvular infections are caused by Gram-positive cocci together with Gram-negative bacteria.3 In some of these cases, and as observed in our patient, Gram-negative bacteria are not recovered from blood cultures until 3-21 days after Gram-positive cocci have been isolated.3 Most cases of pseudomonas endocarditis have been described in the Detroit area.’ Although the reasons are not clear, this observation is supported by new clinical, epidemiological and experimental data. Pseudomonas aeruginosa serotype 011 has been isolated from the blood of 9/10 intravenous drug abusers with endocarditis in Detroit,’ and also from both blood and syringes of addicts with endocarditis reported from other areas.7 The same serotype was responsible for a recent outbreak of endocarditis in Chicago where serotype 011 was found to be significantly more common among intravenous drug abusers with endocarditis than among patients with infections other than endocarditis.8 In addition, it has been observed that P. aeruginosa serotype 011 may survive better in the presence of drugs such as pentazocine and tripelennamine,’ a drug combination associated with most cases of pseudomonas endocarditis in Chicago and Detroit. ‘s8 Finally, preliminary observations suggest that serotype 011 adheres more readily to endocardial tissue than other pseudomonas serotypes.’ Pseudomonas aeruginosa in non-addicts is expected to occur as a hospital-acquired infection. Nevertheless, nosocomial endocarditis is uncommonlo’ll and, to our knowledge, only 39 cases of hospital-acquired P. aeruginosa endocarditis have been reported in the English literature.3~4,“~‘2 These patients usually have underlying heart disease or have undergone recent cardiac surgery, particularly valve replacement. Polymicrobial bacteraemia is unusual and endocarditis predominantly involves the left side of the heart.3 Prognosis is bad and the best chance for cure includes early mitral or aortic valve replacement.5~‘2*‘3 Our patient had both an unusual presentation and outcome. A primary source of pseudomonas infection was not found. Valve replacement was required because of severe valvular damage and not for control of infection, which was achieved by medical treatment. Furthermore, the finding of sterile vegetations at surgery may suggest that, occasionally, appropriate
Letter
to the Editor
163
antibiotic therapy alone may also be curative in this difficult-to-treat condition. Finally, this case emphasizes the permanent threat that P. aeruginosa poses to hospitalized patients, including those being treated for more common causes of endocarditis. R. Finkelstein* M. BoulusfM. Markieviczt
Departments of *Internal Medicine, TCardiology and *Infectious Disease Unit Rambarm Medical Center 31096, Haifa, Israel
References I. Reyes MP, Palutke AW, Wylin RF, Lerner AM. Pseudomonas endocarditis in the Detroit Medical Center. 196991972. Medicine 1972: 51: 173-194. 2. Reyes MP, Brown WJ, Lerner AM. Treatment of patients with pseudomonas endocarditis with high dose aminoglycoside and carbenicillin therapy. Medicine 1978; 57: 57-67. 3. Cohen PS, Maguire JH, Weinstein L. Infective endocarditis caused by gram negative bacteria: a review of the literature, 1945-1977. Prog Cardiovasc Dis 1980; 22: 2055242. 4. Pollack M. Pseudomonas aeruginosa. In: Mandell GL, Douglas Jr. RG, Bennett JE (Eds). Principles and Practice of Infectious Diseases. New York: Wiley 1985; 1236-l 2.50. 5. Levine DR, Crane LR, Zervos MJ. Bacteremia in narcotics addicts at the Detroit Medical Center. II. Infectious endocarditis: a prospective comparative study. Rev Znfect Dis 1986; 8: 374-396. 6. Saravolatz LD, Burch KH, Quinn EL, Cox F, Madhaven T, Fisher E. Polymicrobial infective endocarditis: an increasing clinical entity. Am Heart J 1978; 95: 163-168. 7. Rajashekaraiah KR, Rice TW, Kallick CA. Recovery of Pseudomonas aeruginosa from syringes of drug addicts with endocarditis. J Infect Dis 1981; 144: 482. 8. Shekar R, Rice TW, Zierdt CH, Kallick CA. Outbreak of endocarditis caused bv Pseudomonas aeruginosa serotype 011 among pentazocine and tripelennamine abusers in Chicago. J Infect Dis 1985; 151: 203-208. 9. Botsford KB, Weinstein RA, Nathan CR, Kabins CA. Selective survival in pentazocine and tripelennamine of Pseudomonas aeruginosa serotype 011 from drug addicts. J Infect Dis 1985; 151: 209-216. 10. Friedland G, von Reyn F, Levy B, Arbeit R, Dasse P, Crumpacker C. Nosocomial endocarditis. Infect Control 1984; 5: 284-288. 11. Terpenning MS, Buggy BP, Kauffman CA. Hospital-acquired infective endocarditis. Arch Intern Med 1988; 148: 16Olll603. 12. Wieland M, Lederman MM, Kline-King C et al. L,eft sided endocarditis due to Pseudomonas aeruginosa. A report of 10 cases and review of literature. Medicine 1986; 65: 180-189. 13. Reyes MP, Lerner M. Current problems in the treatment of infective endocarditis due to Pseudomonas aeruginosa. Infect Dis 1983; 5: 314321.