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HIV and invasive pneumococcal infection
International Journal of Cardiology 198 (2015) 157–158
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
HIV and invasive pneumococcal infection D. Zachariah ⁎, P. Manga Division of Cardiology, Department of Internal Medicine, University of Witwatersrand and Charlotte Maxeke Johannesburg Academic Hospital, 5 Jubilee Rd, Private Bag X39, Parktown, Johannesburg 2193, South Africa
a r t i c l e
i n f o
Article history: Received 24 June 2015 Accepted 27 June 2015 Available online 3 July 2015 Keywords: HIV Pneumococcal disease Austrian syndrome
A 35 year old HIV positive male patient with a history of alcohol abuse was admitted with fever, hypoxemia and confusion. His CD4 lymphocyte cell count was 236 cells/mm3 and he was not on antiretroviral therapy. His clinical evaluation on admission was that of pneumonia with possible meningitis. He had digital clubbing and mild splenomegaly on admission. His chest X-ray confirmed the diagnosis of pneumonia, with bilateral nodular infiltrates. A lumbar puncture confirmed Streptococcus pneumoniae with the following: 280 polymorphonucleocytes/mm3, 10 lymphocytes/mm3 and 5 erythrocytes/mm3, protein of 1.62 g/l and glucose of b0.1 mmol/l. He was treated with high dose intravenous ceftriaxone and dexamethasone. On day 3, his cardiac examination revealed a pan-systolic murmur along the left sternal border and a faint early diastolic murmur over the aortic region. Echocardiography (Figs. 1 & 2) demonstrated a large vegetation of the aortic valve. In addition he had an aortic abscess and a fistula from the aortic root to right ventricle. This was associated with moderate degree of tricuspid regurgitation. Blood cultures grew S. pneumoniae with identical sensitivities to that of the cerebrospinal fluid culture. His sputum, which was only collected post-antibiotic therapy, demonstrated Gram-positive cocci with no further identification. His confusion resolved and his respiratory distress improved on medical therapy. However, he had persistent temperature spikes suggesting ongoing bacteremia and his repeat cerebrospinal fluid remained active. The findings of the repeat lumbar puncture on day 4 were as follows: polymorphonucleocytes 560/mm3, lymphocytes 50/mm3, erythrocytes 60/mm3, protein 1.15 g/l and glucose of 1.8 mmol/l. It was at this point that he was referred for urgent cardiac surgery. ⁎ Corresponding author. E-mail addresses: [email protected] (D. Zachariah), [email protected] (P. Manga).
http://dx.doi.org/10.1016/j.ijcard.2015.06.167 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
Unfortunately, the patient refused any further medical or surgical treatment and despite extensive counseling, refused hospital treatment. Sadly he demised 3 days later. The triad of meningitis, pneumonia and infective endocarditis was first described in 1957 by Robert Austrian and is currently termed the Austrian syndrome [1]. S. pneumoniae is one of the most common Gram-positive pathogenic bacteria in humans. Very rarely (b 3%) does pneumococcal infections cause endocarditis of native heart valves [2]. However, when pneumococcal endocarditis is present, Austrian triad is common among these patients with an incidence as high as 60% [3]. The rarity of this syndrome can be attributed to the current use of effective antibiotics and vaccination. Nevertheless, it still occurs, and when it does, it is associated with a reported mortality as high as 62% without surgery [4]. A review of the literature suggests that it is more frequent in men who abuse alcohol. Other risk factors for invasive pneumococcal infections include human immunodeficiency virus (HIV) infection, splenectomy, connective tissue disease, steroid use, diabetes mellitus and intravenous drug use [5]. With regard to HIV infection, it has been noted that there is a substantial increase in the risk of invasive pneumococcal infection, particularly among patients with low CD4 count less than 200 cells/mm3 [6]. It is unclear whether the use of antiretroviral
Fig. 1. Transesophageal echo picture showing large vegetations of the aortic valve (Tricuspid valve to the left)
158
D. Zachariah, P. Manga / International Journal of Cardiology 198 (2015) 157–158
Fig. 2. Zoomed up picture showing the aorto-right ventricular fistula.
therapy decreases the invasive nature of pneumococcal disease; however, there is one report that suggests that it does not [7]. In pneumococcal endocarditis, the native aortic valve is the most frequent localization of the vegetation [2]. Therapy should be initiated as early as possible for a favorable outcome. Every effort should be made to isolate the etiologic agent and to determine the antibiotic susceptibility. It is important to note that pneumococcal endocarditis caused by penicillin resistant S. pneumoniae isolates is very rare, so prompt commencement of antibiotics is imperative to clinical outcome. Our patient did show initial improvement of his meningeal signs after starting dexamethasone. Dexamethasone has previously been shown to reduce mortality rates in pneumococcal meningitis from 34% to 14% [8]. There is also a report that has shown benefit of steroid use in the Austrian syndrome [9]. Surgical management has a major role in the treatment of pneumococcal endocarditis. There is a significant lowering of mortality from 62% in un-operated patients to 32% in those who undergo surgery [2]. In our case, the cardiac involvement was only recognized on day 3. Austrian reports a delay of 3 to 55 days between admission and diagnosis [1]. In some cases, the endocarditis can appear late, even after initiation of the correct antibiotic therapy and apparent recovery from the pneumonia [10]. In summary, Austrian syndrome is a relatively rare condition that needs a high index of suspicion to be diagnosed. It is associated with a high mortality; hence it should be emphasized that every patient with documented invasive pneumococcal infection, especially those
with HIV, should be screened for cardiac involvement, possibly even warranting echocardiography.
References [1] R. Austrian, Pneumococcal endocarditis, meningitis and rupture of the aortic valve, AMA Ann. Intern. Med. 99 (1957) 539–544. [2] S.I. Aronin, S.K. Mukherjee, J.C. West, et al., Review of pneumococcal endocarditis in adults in the penicillin era, Clin. Infect. Dis. 26 (1998) 165–171. [3] A. Lefort, J.L. Mainardi, Selton-Suty, et al., Streptococcus pneumoniae endocarditis in adults. A multicenter study in France in the era of penicillin resistance (1991–1998). The pneumococcal endocarditis study group, Medicine (Baltimore) 79 (2000) 327–337. [4] C. Velazquez, O. Araji, J.M. Barquero, et al., Austrian syndrome: a clinical rarity, Int. J. Cardiol. 127 (2) (2008) 36–38. [5] S.N. Taylor, C.V. Sanders, Unusual manifestations of invasive pneumococcal infection, Am. J. Med. 107 (1999) 12S–27S. [6] N. French, S.B. Gordon, T. Mwalukomo, et al., A trial of a 7-valent pneumococcal conjugate vaccine in HIV-infected adults, N. Engl. J. Med. 362 (2010) 812. [7] Z.B. Harboe, M.V. Larsen, S. Ladelund, et al., Incidence and risk factors for invasive pneumococcal disease in HIV-infected and non-HIV infected Individuals Before and after the introduction of combined antiretroviral therapy: persisting high risk among HIV-infected injecting drug users, Clin. Infect. Dis. 59 (8) (2014) 1168–1176 (15). [8] J. De Gans, D. Van de Beek, Dexamethasone in adults with bacterial meningitis, N. Engl. J. Med. 347 (2002) 1549–1556. [9] D. du Cheyron, A. Lesage, O. Le Page, et al., Corticosteroids as adjunctive treatment in Austrian syndrome: report of two cases and review of the literature, J. Clin. Pathol. 56 (11) (2003) 879–881. [10] P.J. Munoz, M. Sainzi, M. Rodriguez-creixems, et al., Austrian syndrome caused by highly penicillin-resistant Streptococcus pneumonia, Clin. Infect. Dis. 29 (1999) (000–000).
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
HIV and invasive pneumococcal infection D. Zachariah ⁎, P. Manga Division of Cardiology, Department of Internal Medicine, University of Witwatersrand and Charlotte Maxeke Johannesburg Academic Hospital, 5 Jubilee Rd, Private Bag X39, Parktown, Johannesburg 2193, South Africa
a r t i c l e
i n f o
Article history: Received 24 June 2015 Accepted 27 June 2015 Available online 3 July 2015 Keywords: HIV Pneumococcal disease Austrian syndrome
A 35 year old HIV positive male patient with a history of alcohol abuse was admitted with fever, hypoxemia and confusion. His CD4 lymphocyte cell count was 236 cells/mm3 and he was not on antiretroviral therapy. His clinical evaluation on admission was that of pneumonia with possible meningitis. He had digital clubbing and mild splenomegaly on admission. His chest X-ray confirmed the diagnosis of pneumonia, with bilateral nodular infiltrates. A lumbar puncture confirmed Streptococcus pneumoniae with the following: 280 polymorphonucleocytes/mm3, 10 lymphocytes/mm3 and 5 erythrocytes/mm3, protein of 1.62 g/l and glucose of b0.1 mmol/l. He was treated with high dose intravenous ceftriaxone and dexamethasone. On day 3, his cardiac examination revealed a pan-systolic murmur along the left sternal border and a faint early diastolic murmur over the aortic region. Echocardiography (Figs. 1 & 2) demonstrated a large vegetation of the aortic valve. In addition he had an aortic abscess and a fistula from the aortic root to right ventricle. This was associated with moderate degree of tricuspid regurgitation. Blood cultures grew S. pneumoniae with identical sensitivities to that of the cerebrospinal fluid culture. His sputum, which was only collected post-antibiotic therapy, demonstrated Gram-positive cocci with no further identification. His confusion resolved and his respiratory distress improved on medical therapy. However, he had persistent temperature spikes suggesting ongoing bacteremia and his repeat cerebrospinal fluid remained active. The findings of the repeat lumbar puncture on day 4 were as follows: polymorphonucleocytes 560/mm3, lymphocytes 50/mm3, erythrocytes 60/mm3, protein 1.15 g/l and glucose of 1.8 mmol/l. It was at this point that he was referred for urgent cardiac surgery. ⁎ Corresponding author. E-mail addresses: [email protected] (D. Zachariah), [email protected] (P. Manga).
http://dx.doi.org/10.1016/j.ijcard.2015.06.167 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
Unfortunately, the patient refused any further medical or surgical treatment and despite extensive counseling, refused hospital treatment. Sadly he demised 3 days later. The triad of meningitis, pneumonia and infective endocarditis was first described in 1957 by Robert Austrian and is currently termed the Austrian syndrome [1]. S. pneumoniae is one of the most common Gram-positive pathogenic bacteria in humans. Very rarely (b 3%) does pneumococcal infections cause endocarditis of native heart valves [2]. However, when pneumococcal endocarditis is present, Austrian triad is common among these patients with an incidence as high as 60% [3]. The rarity of this syndrome can be attributed to the current use of effective antibiotics and vaccination. Nevertheless, it still occurs, and when it does, it is associated with a reported mortality as high as 62% without surgery [4]. A review of the literature suggests that it is more frequent in men who abuse alcohol. Other risk factors for invasive pneumococcal infections include human immunodeficiency virus (HIV) infection, splenectomy, connective tissue disease, steroid use, diabetes mellitus and intravenous drug use [5]. With regard to HIV infection, it has been noted that there is a substantial increase in the risk of invasive pneumococcal infection, particularly among patients with low CD4 count less than 200 cells/mm3 [6]. It is unclear whether the use of antiretroviral
Fig. 1. Transesophageal echo picture showing large vegetations of the aortic valve (Tricuspid valve to the left)
158
D. Zachariah, P. Manga / International Journal of Cardiology 198 (2015) 157–158
Fig. 2. Zoomed up picture showing the aorto-right ventricular fistula.
therapy decreases the invasive nature of pneumococcal disease; however, there is one report that suggests that it does not [7]. In pneumococcal endocarditis, the native aortic valve is the most frequent localization of the vegetation [2]. Therapy should be initiated as early as possible for a favorable outcome. Every effort should be made to isolate the etiologic agent and to determine the antibiotic susceptibility. It is important to note that pneumococcal endocarditis caused by penicillin resistant S. pneumoniae isolates is very rare, so prompt commencement of antibiotics is imperative to clinical outcome. Our patient did show initial improvement of his meningeal signs after starting dexamethasone. Dexamethasone has previously been shown to reduce mortality rates in pneumococcal meningitis from 34% to 14% [8]. There is also a report that has shown benefit of steroid use in the Austrian syndrome [9]. Surgical management has a major role in the treatment of pneumococcal endocarditis. There is a significant lowering of mortality from 62% in un-operated patients to 32% in those who undergo surgery [2]. In our case, the cardiac involvement was only recognized on day 3. Austrian reports a delay of 3 to 55 days between admission and diagnosis [1]. In some cases, the endocarditis can appear late, even after initiation of the correct antibiotic therapy and apparent recovery from the pneumonia [10]. In summary, Austrian syndrome is a relatively rare condition that needs a high index of suspicion to be diagnosed. It is associated with a high mortality; hence it should be emphasized that every patient with documented invasive pneumococcal infection, especially those
with HIV, should be screened for cardiac involvement, possibly even warranting echocardiography.
References [1] R. Austrian, Pneumococcal endocarditis, meningitis and rupture of the aortic valve, AMA Ann. Intern. Med. 99 (1957) 539–544. [2] S.I. Aronin, S.K. Mukherjee, J.C. West, et al., Review of pneumococcal endocarditis in adults in the penicillin era, Clin. Infect. Dis. 26 (1998) 165–171. [3] A. Lefort, J.L. Mainardi, Selton-Suty, et al., Streptococcus pneumoniae endocarditis in adults. A multicenter study in France in the era of penicillin resistance (1991–1998). The pneumococcal endocarditis study group, Medicine (Baltimore) 79 (2000) 327–337. [4] C. Velazquez, O. Araji, J.M. Barquero, et al., Austrian syndrome: a clinical rarity, Int. J. Cardiol. 127 (2) (2008) 36–38. [5] S.N. Taylor, C.V. Sanders, Unusual manifestations of invasive pneumococcal infection, Am. J. Med. 107 (1999) 12S–27S. [6] N. French, S.B. Gordon, T. Mwalukomo, et al., A trial of a 7-valent pneumococcal conjugate vaccine in HIV-infected adults, N. Engl. J. Med. 362 (2010) 812. [7] Z.B. Harboe, M.V. Larsen, S. Ladelund, et al., Incidence and risk factors for invasive pneumococcal disease in HIV-infected and non-HIV infected Individuals Before and after the introduction of combined antiretroviral therapy: persisting high risk among HIV-infected injecting drug users, Clin. Infect. Dis. 59 (8) (2014) 1168–1176 (15). [8] J. De Gans, D. Van de Beek, Dexamethasone in adults with bacterial meningitis, N. Engl. J. Med. 347 (2002) 1549–1556. [9] D. du Cheyron, A. Lesage, O. Le Page, et al., Corticosteroids as adjunctive treatment in Austrian syndrome: report of two cases and review of the literature, J. Clin. Pathol. 56 (11) (2003) 879–881. [10] P.J. Munoz, M. Sainzi, M. Rodriguez-creixems, et al., Austrian syndrome caused by highly penicillin-resistant Streptococcus pneumonia, Clin. Infect. Dis. 29 (1999) (000–000).