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Haemophilus parainfluenzae mitral prosthetic valve endocarditis in an intravenous drug abuser
Haemophilus parainfluenzae mitral prosthetic valve endocarditis in an intravenous drug abuser David Choi, DO, Marjorie Thermidor, MD, and Burke A. Cunha, MD, Mineola and Stony Brook, New York
Haemophilus species are an infrequent cause of subacute bacterial endocarditis. Of the Haemophilus species causing endocarditis, H. aphrophilus and H. parainfluenzae are more frequent causes of subacute bacterial endocarditis than H. influenzae. H. parainfluenzae requires growth factor V (nicotinamide adenine dinucleotide) and grows very slowly on routine culture media. H. parainfluenzae is a rare cause of “culture negative” endocarditis because it is a slow-growing organism. We present a case of a 42-year-old intravenous drug abuser with H. parainfluenzae mitral prosthetic valve endocarditis. To the best of our knowledge, this is the first case of mitral prosthetic valve endocarditis caused by H. parainfluenzae in an intravenous drug abuser. (Heart Lung® 2005;34:152– 4.)
H
aemophilus parainfluenzae is considered to be a component of the normal flora of the human nasopharynx and may be cultured from the mouth or nasopharynx in 5% to 25% of healthy individuals. Because it is normally found in the oral cavity, dental procedures and nasopharyngeal infections seem to be the main risk factor for developing H. parainfluenzae infection.1-3 The frequency of endocarditis caused by Haemophilus species was estimated to be 0.5% to 1.0%.4 Of the Haemophilus species, H. parainfluenzae has been reported to be more common than H. influenzae. H. parainfluenzaewas found to be the most frequent isolate of Haemophilus species causing endocarditis.1,5,6 Endocarditis caused by H. parainfluenzae and other fastidious organisms may occur with only fever and heart murmur without the other physical findings usually seen with bacterial endocarditis such as Roth spots, Janeway’s lesions, and Osler’s nodes. Valvular heart disease is only found in 48% of cases, and a heart murmur may be the only physical finding suggesting endocarditis. H. parainfluenzae has been implicated as rare causes of epiglottitis, bacteremia, brain abscesses, and meningitis.7,8 Although H. parainfluenzae endoFrom the Infectious Disease Division, Winthrop-University Hospital Mineola, New York, and State University of New York School of Medicine, Stony Brook, New York. Address for reprints: Burke A. Cunha, MD, Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, NY 11501. 0147-9563/$ – see front matter Copyright © 2005 by Mosby, Inc. doi:10.1016/j.hrtlng.2004.07.005
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carditis is a disease of predisposed young adults, it may also affect elderly patients.9 Furthermore, H. parainfluenzae bacteremia has also been associated with infections of myxomas of the mitral valve and pacemaker wires.10,11 “Culture negative endocarditis” may be caused by H. parainfluenzae because it is an aerobic/facultatively anaerobic organism that requires heat-labile factor V (nicotinamide adenine dinucleotide). Growth on standard culture media is slow with colonies appearing usually after 7 days.12 H. parainfluenzae has a propensity to form major arterial embolization.13 This distinctive characteristic occurs in 29% to 85% of patients, and movement of the emboli into the central nervous system is a major cause of morbidity and mortality in patients with H. parainfluenzae endocarditis.14,15
CASE REPORT A 42-year-old man with a medical history significant for endocarditis in 1991, mitral valve replacement and aortic valve replacement in 1991, and CHF for 10 years presented with increased shortness of breath at rest for 3 days, fever, chills, sweats, nausea, vomiting, and diarrhea. The patient had a ventricular tachycardic arrest and was intubated. The patient’s spiked a temperature to 103°F on hospital day 2 with a systolic blood pressure of 90 on pressors. Blood cultures grew gram-negative coccobacilli, and the patient was placed on meropenem 1 g (intravenously) every 8 hours and transferred to Winthrop-University Hospital.
MARCH/APRIL 2005
HEART & LUNG
Choi, Thermidor, and Cunha
Medications on admission were warfarin, furosemide, digoxin, carvedilol, and captopril. Social history was significant for a 30-pack per year smoking history, 2 drinks per week of alcohol, former marijuana use, and intravenous drug abuse. Physical examination revealed a slightly malnourished 42-year-old man who was orally intubated at the time of admission and in no apparent distress. The patient was noted to have moderate rhonchi and crackles bilaterally. Cardiac examination was significant for an irregular rate. The abdomen was soft and distended with hypoactive bowel sounds. There was evidence of venous stasis changes on extremities. Admission laboratory values revealed a white blood cell count of 4.4 K/mm3 and a platelet count of 129,000 K/mm3. Serum electrolytes, blood urea nitrogen, and creatinine levels were all within normal limits. Liver function tests revealed a serum glutamic-oxaloacetic transaminase of 28 IU/L, serum glutamic-pyruvic transaminase of 23 IU/L, total protein of 4.8 g/dL, and an albumin level of 2.5 g/dL. The urine contained 2⫹ proteinuria, 64 red blood cells, and trace amounts of leukocyte esterase. The serum amylase level was 35 U/L, and the lipase level was 19 U/L. The coagulation profile, cardiac enzymes, and hepatitis screen were all within normal limits. Blood culture results were positive for gramnegative rods. Chest roentgenogram showed cardiomegaly with plate-like atelectasis remains in the left mid-lung and right base. No effusions or pneumothorax was seen. An electrocardiogram revealed normal sinus rhythm with a left bundle branch block. Data from a Swan-Ganz catheter showed a pulmonary artery pressure of 70/30 mm Hg and a central venous pressure of 14 mm Hg. The cardiac index was 4.4, and the systemic vascular resistance was 550. An ultrasound of the abdomen showed hepatosplenomegaly with ascites secondary to alcoholic liver disease, cholelithiasis, and gallbladder wall thickening. H. parainfluenzae was identified as the blood culture isolate. There was no evidence of oromaxillary infection at the time. On day 6 of admission to Winthrop-University Hospital, the patient was noted to be anemic. Computed tomography of the abdomen was performed and showed a large retroperitoneal bleed with no signs of active bleeding. The patient was transfused and was hemodynamically stable. The patient then underwent a cardiac catheterization, which showed an ejection fraction of 10% to 15%. A transesophageal echocardiogram was performed on day 10 and revealed a dilated left ventricle, systolic function of 10%, dilated left
HEART & LUNG
VOL. 34, NO. 2
H. parainfluenzae PVE in an IV drug abuser
atrium, 9-mm atrial septal defect, dilated and markedly hypokinetic right ventricle, bileaflet aortic valve, and bileaflet mitral valve with a large mobile vegetation. It was decided that the patient would not survive open-heart surgery but was a good candidate for a heart transplant. Repeat blood culture results were negative, and the patient was transferred for cardiac transplant and lost to follow-up.
DISCUSSION This patient, an intravenous drug abuser (IVDA), had H. parainfluenzae mitral valve prosthetic valve endocarditis (PVE). He had no discernible oral, sinus, or respiratory tract source of H. parainfluenzae. Unlike other cases in the literature, he did not present with peripheral manifestations of endocarditis or large vessel embolization. He had improved clinically on meropenem and had negative blood culture results early after treatment. IVDAs are predisposed to developing tricuspid valve acute bacterial endocarditis, most frequently because of Staphylococcus aureus or Pseudomonas aeruginosa. Aortic valve involvement is the second most likely location for infection in IVDAs with acute bacterial endocarditis. Furthermore, PVE is usually caused by S. epidermidis, that is, coagulase-negative staphylococci or S. aureus caused by methicillin-sensitive strains or methicillin-resistant strains. Almost invariably, cure of PVE requires valve replacement surgery. IVDAs are not particularly predisposed to Haemophilus species as a cause of subacute bacterial endocarditis (SBE) or culture-negative SBE. Haemophilus species are rarely a cause of PVE.16,17 To the best of our knowledge, this is the first case of H. parainfluenzae mitral PVE in an IVDA. Although extremely uncommon, H. parainfluenzae SBE has rarely been cured with antibiotic therapy alone without valve replacement.18-20
REFERENCES 1. Lynn DJ, Kane JG, Parker RH. Haemophilus parainfluenzae and influenza endocarditis: a review of forty cases. Medicine 1977;56:115-28. 2. Dahlgren J, Tally FP, Brothers G, Ruskin J. Haemophilus parainfluenzae—an uncommon cause of septicemia and endocarditis. Scand J Infect Dis 1980;12:85-9. 3. Raucher B, Dobkin J, Mandel L, et al. Occult polymicrobial endocarditis with H. parainfluenzae in intravenous drug abusers. Am J Med 1989;86:169-72. 4. Weinstein L, Rubin RH. Infective endocarditis. Prog Cardiovasc Dis 1973;16:239. 5. Blair DC, Walker W, Soeman T, et al. Bacterial endocarditis due to Haemophilus parainfluenzae. Chest 1977;71:146-9.
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H. parainfluenzae PVE in an IV drug abuser 6. Geraci JE, Wilkowske CJ, Wilson WR, et al. Haemophilus endocarditis: report of fourteen patients. Mayo Clin Proc 1977; 52:209-15. 7. Chow AW, Bushkell LL, Yoshikawa TT, et al. Haemophilus parainfluenzae epiglottitis with meningitis and bacteremia in an adult. Am J Med Sci 1974;267:365-8. 8. Hable KA, Logan GB, Washington JA. Three Haemophilus species. Am J Dis Child 1971;121:35-7. 9. Calio A, Cusumano S, Ullman R, Tjioe D, Cunha B. Haemophilus parainfluenzae endocarditis. Heart Lung 1987;16: 222-3. 10. Ghazi F, Sterba R, Moodie D, Gill C, Ratliff N. Myxoma of the mitral valve associated with Haemophilus parainfluenzae bacteremia. Cleve Clin J Med 1988;55:470-2. 11. Rosenbaum G, Calubiran O, Cunha B. Haemophilus parainfluenzae bacteremia associated with a pacemaker wire localized by gallium scan. Heart Lung 1990;19:271-3. 12. Choo MH, Holmes DR, Gersh BJ, et al. Permanent pacemaker infections: characterization and management. Am J Cardiol 1981;48:559-64. 13. Chunn C, Jones SR, McCutchan JA, et al. Haemophilus parainfluenzae infective endocarditis. Medicine 1977;56:99-113.
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Choi, Thermidor, and Cunha 14. Jemsek JG, Greenberg SB, Gentry LO, et al. Haemophilus parainfluenzae endocarditis: two cases and review of the literature in the past decade. Am J Med 1979;66:51. 15. Ellner JJ, Rosenthal MS, Lerner PI, et al. Infective endocarditis caused by slow-growing, fastidious, gram-negative bacteria. Medicine 1979;58:145. 16. Blair DC, Weiner LB. Prosthetic valve endocarditis due to Haemophilus parainfluenzae biotype II. Am J Dis Child 1979; 133:617-8. 17. Tornos P, Sanz E, Permanyer-Miralda G, et al. Late prosthetic valve endocarditis: immediate and long-term prognosis. Chest 1992;101:37-41. 18. Tornos MP, Almirante B, Pahissa A, et al. Clinical features of endocarditis caused by gram-negative bacilli of HACEK group. Eur Heart J 1990;II:254. 19. Leport C, Vilde JL, Bricaire F, et al. Fifty cases of late prosthetic valve endocarditis: improvement in prognosis over a 15 year period. Br Heart J 1987;58:66-71. 20. Meyer DJ, Gerding DL. Favorable prognosis of patients with prosthetic valve endocarditis caused by gram-negative bacilli of the HACEK group. Am J Med 1988;85:104-7.
MARCH/APRIL 2005
HEART & LUNG
Haemophilus species are an infrequent cause of subacute bacterial endocarditis. Of the Haemophilus species causing endocarditis, H. aphrophilus and H. parainfluenzae are more frequent causes of subacute bacterial endocarditis than H. influenzae. H. parainfluenzae requires growth factor V (nicotinamide adenine dinucleotide) and grows very slowly on routine culture media. H. parainfluenzae is a rare cause of “culture negative” endocarditis because it is a slow-growing organism. We present a case of a 42-year-old intravenous drug abuser with H. parainfluenzae mitral prosthetic valve endocarditis. To the best of our knowledge, this is the first case of mitral prosthetic valve endocarditis caused by H. parainfluenzae in an intravenous drug abuser. (Heart Lung® 2005;34:152– 4.)
H
aemophilus parainfluenzae is considered to be a component of the normal flora of the human nasopharynx and may be cultured from the mouth or nasopharynx in 5% to 25% of healthy individuals. Because it is normally found in the oral cavity, dental procedures and nasopharyngeal infections seem to be the main risk factor for developing H. parainfluenzae infection.1-3 The frequency of endocarditis caused by Haemophilus species was estimated to be 0.5% to 1.0%.4 Of the Haemophilus species, H. parainfluenzae has been reported to be more common than H. influenzae. H. parainfluenzaewas found to be the most frequent isolate of Haemophilus species causing endocarditis.1,5,6 Endocarditis caused by H. parainfluenzae and other fastidious organisms may occur with only fever and heart murmur without the other physical findings usually seen with bacterial endocarditis such as Roth spots, Janeway’s lesions, and Osler’s nodes. Valvular heart disease is only found in 48% of cases, and a heart murmur may be the only physical finding suggesting endocarditis. H. parainfluenzae has been implicated as rare causes of epiglottitis, bacteremia, brain abscesses, and meningitis.7,8 Although H. parainfluenzae endoFrom the Infectious Disease Division, Winthrop-University Hospital Mineola, New York, and State University of New York School of Medicine, Stony Brook, New York. Address for reprints: Burke A. Cunha, MD, Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, NY 11501. 0147-9563/$ – see front matter Copyright © 2005 by Mosby, Inc. doi:10.1016/j.hrtlng.2004.07.005
152
www.heartandlung.org
carditis is a disease of predisposed young adults, it may also affect elderly patients.9 Furthermore, H. parainfluenzae bacteremia has also been associated with infections of myxomas of the mitral valve and pacemaker wires.10,11 “Culture negative endocarditis” may be caused by H. parainfluenzae because it is an aerobic/facultatively anaerobic organism that requires heat-labile factor V (nicotinamide adenine dinucleotide). Growth on standard culture media is slow with colonies appearing usually after 7 days.12 H. parainfluenzae has a propensity to form major arterial embolization.13 This distinctive characteristic occurs in 29% to 85% of patients, and movement of the emboli into the central nervous system is a major cause of morbidity and mortality in patients with H. parainfluenzae endocarditis.14,15
CASE REPORT A 42-year-old man with a medical history significant for endocarditis in 1991, mitral valve replacement and aortic valve replacement in 1991, and CHF for 10 years presented with increased shortness of breath at rest for 3 days, fever, chills, sweats, nausea, vomiting, and diarrhea. The patient had a ventricular tachycardic arrest and was intubated. The patient’s spiked a temperature to 103°F on hospital day 2 with a systolic blood pressure of 90 on pressors. Blood cultures grew gram-negative coccobacilli, and the patient was placed on meropenem 1 g (intravenously) every 8 hours and transferred to Winthrop-University Hospital.
MARCH/APRIL 2005
HEART & LUNG
Choi, Thermidor, and Cunha
Medications on admission were warfarin, furosemide, digoxin, carvedilol, and captopril. Social history was significant for a 30-pack per year smoking history, 2 drinks per week of alcohol, former marijuana use, and intravenous drug abuse. Physical examination revealed a slightly malnourished 42-year-old man who was orally intubated at the time of admission and in no apparent distress. The patient was noted to have moderate rhonchi and crackles bilaterally. Cardiac examination was significant for an irregular rate. The abdomen was soft and distended with hypoactive bowel sounds. There was evidence of venous stasis changes on extremities. Admission laboratory values revealed a white blood cell count of 4.4 K/mm3 and a platelet count of 129,000 K/mm3. Serum electrolytes, blood urea nitrogen, and creatinine levels were all within normal limits. Liver function tests revealed a serum glutamic-oxaloacetic transaminase of 28 IU/L, serum glutamic-pyruvic transaminase of 23 IU/L, total protein of 4.8 g/dL, and an albumin level of 2.5 g/dL. The urine contained 2⫹ proteinuria, 64 red blood cells, and trace amounts of leukocyte esterase. The serum amylase level was 35 U/L, and the lipase level was 19 U/L. The coagulation profile, cardiac enzymes, and hepatitis screen were all within normal limits. Blood culture results were positive for gramnegative rods. Chest roentgenogram showed cardiomegaly with plate-like atelectasis remains in the left mid-lung and right base. No effusions or pneumothorax was seen. An electrocardiogram revealed normal sinus rhythm with a left bundle branch block. Data from a Swan-Ganz catheter showed a pulmonary artery pressure of 70/30 mm Hg and a central venous pressure of 14 mm Hg. The cardiac index was 4.4, and the systemic vascular resistance was 550. An ultrasound of the abdomen showed hepatosplenomegaly with ascites secondary to alcoholic liver disease, cholelithiasis, and gallbladder wall thickening. H. parainfluenzae was identified as the blood culture isolate. There was no evidence of oromaxillary infection at the time. On day 6 of admission to Winthrop-University Hospital, the patient was noted to be anemic. Computed tomography of the abdomen was performed and showed a large retroperitoneal bleed with no signs of active bleeding. The patient was transfused and was hemodynamically stable. The patient then underwent a cardiac catheterization, which showed an ejection fraction of 10% to 15%. A transesophageal echocardiogram was performed on day 10 and revealed a dilated left ventricle, systolic function of 10%, dilated left
HEART & LUNG
VOL. 34, NO. 2
H. parainfluenzae PVE in an IV drug abuser
atrium, 9-mm atrial septal defect, dilated and markedly hypokinetic right ventricle, bileaflet aortic valve, and bileaflet mitral valve with a large mobile vegetation. It was decided that the patient would not survive open-heart surgery but was a good candidate for a heart transplant. Repeat blood culture results were negative, and the patient was transferred for cardiac transplant and lost to follow-up.
DISCUSSION This patient, an intravenous drug abuser (IVDA), had H. parainfluenzae mitral valve prosthetic valve endocarditis (PVE). He had no discernible oral, sinus, or respiratory tract source of H. parainfluenzae. Unlike other cases in the literature, he did not present with peripheral manifestations of endocarditis or large vessel embolization. He had improved clinically on meropenem and had negative blood culture results early after treatment. IVDAs are predisposed to developing tricuspid valve acute bacterial endocarditis, most frequently because of Staphylococcus aureus or Pseudomonas aeruginosa. Aortic valve involvement is the second most likely location for infection in IVDAs with acute bacterial endocarditis. Furthermore, PVE is usually caused by S. epidermidis, that is, coagulase-negative staphylococci or S. aureus caused by methicillin-sensitive strains or methicillin-resistant strains. Almost invariably, cure of PVE requires valve replacement surgery. IVDAs are not particularly predisposed to Haemophilus species as a cause of subacute bacterial endocarditis (SBE) or culture-negative SBE. Haemophilus species are rarely a cause of PVE.16,17 To the best of our knowledge, this is the first case of H. parainfluenzae mitral PVE in an IVDA. Although extremely uncommon, H. parainfluenzae SBE has rarely been cured with antibiotic therapy alone without valve replacement.18-20
REFERENCES 1. Lynn DJ, Kane JG, Parker RH. Haemophilus parainfluenzae and influenza endocarditis: a review of forty cases. Medicine 1977;56:115-28. 2. Dahlgren J, Tally FP, Brothers G, Ruskin J. Haemophilus parainfluenzae—an uncommon cause of septicemia and endocarditis. Scand J Infect Dis 1980;12:85-9. 3. Raucher B, Dobkin J, Mandel L, et al. Occult polymicrobial endocarditis with H. parainfluenzae in intravenous drug abusers. Am J Med 1989;86:169-72. 4. Weinstein L, Rubin RH. Infective endocarditis. Prog Cardiovasc Dis 1973;16:239. 5. Blair DC, Walker W, Soeman T, et al. Bacterial endocarditis due to Haemophilus parainfluenzae. Chest 1977;71:146-9.
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H. parainfluenzae PVE in an IV drug abuser 6. Geraci JE, Wilkowske CJ, Wilson WR, et al. Haemophilus endocarditis: report of fourteen patients. Mayo Clin Proc 1977; 52:209-15. 7. Chow AW, Bushkell LL, Yoshikawa TT, et al. Haemophilus parainfluenzae epiglottitis with meningitis and bacteremia in an adult. Am J Med Sci 1974;267:365-8. 8. Hable KA, Logan GB, Washington JA. Three Haemophilus species. Am J Dis Child 1971;121:35-7. 9. Calio A, Cusumano S, Ullman R, Tjioe D, Cunha B. Haemophilus parainfluenzae endocarditis. Heart Lung 1987;16: 222-3. 10. Ghazi F, Sterba R, Moodie D, Gill C, Ratliff N. Myxoma of the mitral valve associated with Haemophilus parainfluenzae bacteremia. Cleve Clin J Med 1988;55:470-2. 11. Rosenbaum G, Calubiran O, Cunha B. Haemophilus parainfluenzae bacteremia associated with a pacemaker wire localized by gallium scan. Heart Lung 1990;19:271-3. 12. Choo MH, Holmes DR, Gersh BJ, et al. Permanent pacemaker infections: characterization and management. Am J Cardiol 1981;48:559-64. 13. Chunn C, Jones SR, McCutchan JA, et al. Haemophilus parainfluenzae infective endocarditis. Medicine 1977;56:99-113.
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www.heartandlung.org
Choi, Thermidor, and Cunha 14. Jemsek JG, Greenberg SB, Gentry LO, et al. Haemophilus parainfluenzae endocarditis: two cases and review of the literature in the past decade. Am J Med 1979;66:51. 15. Ellner JJ, Rosenthal MS, Lerner PI, et al. Infective endocarditis caused by slow-growing, fastidious, gram-negative bacteria. Medicine 1979;58:145. 16. Blair DC, Weiner LB. Prosthetic valve endocarditis due to Haemophilus parainfluenzae biotype II. Am J Dis Child 1979; 133:617-8. 17. Tornos P, Sanz E, Permanyer-Miralda G, et al. Late prosthetic valve endocarditis: immediate and long-term prognosis. Chest 1992;101:37-41. 18. Tornos MP, Almirante B, Pahissa A, et al. Clinical features of endocarditis caused by gram-negative bacilli of HACEK group. Eur Heart J 1990;II:254. 19. Leport C, Vilde JL, Bricaire F, et al. Fifty cases of late prosthetic valve endocarditis: improvement in prognosis over a 15 year period. Br Heart J 1987;58:66-71. 20. Meyer DJ, Gerding DL. Favorable prognosis of patients with prosthetic valve endocarditis caused by gram-negative bacilli of the HACEK group. Am J Med 1988;85:104-7.
MARCH/APRIL 2005
HEART & LUNG