Kaohsiung J Med Sci January 2007 • Vol 23 • No 1 40
Infective endocarditis (IE) is a microbial infection of the endothelial surface of the heart. In addition to the constitutional infection symptoms, which are likely mediated by cytokines, clinical manifestations of IE can be generated by immune complexes deposition or antibody-complement interaction with antigens deposited in tissue. Rheumatologic manifestations of IE, such as Osler’s nodes, have been attributed to local deposition of immune complexes. Although endoph-thalmitis, a severe intraocular infection, is infrequently associated with IE, uveitis, another intraocular inflam-mation, is not. Here, we report an IE case with acute blurred vision caused by uveitis.
C
ASEP
RESENTATIONA 51-year-old man with diabetes, which had been under medical control for more than 6 years, presented with a complaint of intermittent chills and fever for 10 days. The patient had no obvious respiratory tract, gen-itourinary tract, gastrointestinal tract, or skin lesions. Physical examination found a grade III/VI pansystolic murmur over the apex during auscultation. Local heat, erythematous swelling, and tenderness in the right middle proximal interphalanx joint were observed. Subungal hemorrhage in the nail bed of the right thumb appeared later. Transthoracic and transesopha-geal echocardiography revealed vegetation located in the anterior leaflet of the mitral valve and moderate mitral regurgitation (Figure 1). Two separate blood cultures were positive for group B β-streptococcus. Based on Duke criteria, the patient was diagnosed with IE and was treated with parenteral penicillin-G 4 MU every 4 hours for 28 days during hospitalization. Received: April 27, 2006 Accepted: August 16, 2006
Address correspondence and reprint requests to: Dr Tsung-Hsien Lin, Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1stRoad, Kaohsiung 807, Taiwan.
E-mail: [email protected]
I
NFECTIVE
E
NDOCARDITIS WITH
U
VEITIS
:
A R
ARE
C
ASE
R
EPORT
Hsiang-Chun Lee,1Yi-Hon Lai,2Chih-Lee Tsai,1Jeng-Hsien Yen,3,4Tsung-Hsien Lin,1 Wen-Ter Lai,1,4and Sheng-Hsiung Sheu1,4
Divisions of 1Cardiology and 3Rheumatology, Department of Internal Medicine, and 2Department of Ophthalmology, Kaohsiung Medical University Hospital, and 4Department of Internal Medicine,
College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
We report a case of a 51-year-old diabetic male who presented with a complaint of intermittent chills and fever that he had experienced for 10 days. No obvious respiratory tract, genitourinary tract, gastrointestinal tract, or skin lesions were observed. Blood culture data were positive for group B β-streptococcus. Transthoracic and transesophageal echocardiography revealed vege-tation in the anterior leaflet of the mitral valve. The patient was diagnosed with infective endocarditis (IE) and prescribed a parenteral antibiotic. Three days after admission, the patient complained of progressively blurred vision. Slit lamp examination found fine keratic precipitates and aqueous cells in the anterior chambers in both eyes, implying that the patient had uveitis. He was then prescribed a topical steroid for 4 months, and his vision improved gradually. This case is an important reminder that uveitis, not only endophthalmitis, can occur with IE. Treatment for one condition, if misapplied, may worsen the other.
Key Words:endophthalmitis, infective endocarditis, uveitis (Kaohsiung J Med Sci 2007;23:40–4)
Infective endocarditis with uveitis Three days after admission, the patient complained of progressively blurred vision. Slit lamp examination found fine keratic precipitates and aqueous cells in the anterior chambers in both eyes. There was mild edema at the right optic disc; hard exudates and hemorrhage were noted in the macula (Figure 2). Fluorescein angiography demonstrated fluorescence leakage in the right optic disc, and block fluorescence and fluo-rescence leakage on the macula (Figure 3). The patient was diagnosed with uveitis, not endophthalmitis, and prescribed a topical steroid. His vision improved grad-ually. Under a diagnosis of uveitis, an extensive search was made to identify evidence of rheumatologic dis-ease. However, all tests, including HLA-B27, antinu-clear antibody, rheumatoid factor, and VDRL (Venereal
Figure 1. Transesophageal echocardiography shows vegetation located in the anterior leaflet of the mitral valve.
B A
Figure 2.(A) Mild edematous changes in the optic disc and (B) hemorrhage as well as hard exudates on the macula in the right fundus.
A B
Figure 3.Fluorescein angiography shows (A) fluorescence leakage in the right optic disc and (B) fluorescence block as well as fluorescence leakage at the macula.
Disease Research Laboratory), were negative. The patient was referred to a rheumatologist, who also excluded the possibility of rheumatologic disease. Following discharge, the patient underwent ophthal-mologic clinical follow-up. Cells in the bilateral vitre-ous body had been observed for 2 additional months after completing 28 days of parenteral penicillin-G therapy. The patient was treated with a topical steroid and subconjunctival steroid injections for 4 months. He was followed up for 3 years. Moderate mitral regur-gitation remained unchanged. However, the patient experienced no significant sequelae as a result of uveitis. His visual acuity was normal in both eyes.
D
ISCUSSIONThe patient was first clinically diagnosed with endo-carditis based on Duke criteria. He met two major and one minor criteria: echocardiography disclosing vegetation attached to the mitral valve; positive blood culture with a pathogen that is a member of group B β-hemolytic streptococcus; and subungal hemorrhage [1].
Group B streptococcus (S. agalactiae) is a rare cause of IE. Adults with chronic immunosuppressive condi-tions, such as alcoholism, diabetes mellitus, neoplasias, and HIV-infection, are at an increased risk for group B streptococcus endocarditis. Group B streptococcus endocarditis is typically characterized by acute onset, large vegetations, rapid valvular destruction, and fre-quent complications. Its clinical course is more aggres-sive than endocarditis caused by other streptococcus species [2].
Rheumatologic manifestations are known to com-plicate IE. A retrospective study demonstrated that peripheral arthritis was clinically evident in 15% of IE patients without history of intravenous drug use [3]. Poststreptococcal reactive arthritis, with a latency ranging from 4 days to 6 weeks [4], has been reported and may be present in the form of oligoarthritis or polyarthritis, although the pathogens identified in those case reports were all group A β-streptococci. Since group B β-streptococci has not been reported in any cases of poststreptococcal reactive arthritis [5], this patient’s arthritis at the right middle interphalanx joint was considered a rheumatologic manifestation cited as occurring with IE rather than reactive arthritis.
Ophthalmologic involvement in IE cases is uncom-mon. Hematogenous dissemination of a pathogen into the intraocular space can generate endophthalmitis, 70% of which is caused by Gram-negative microbes [6]. In a study of endogenous endophthalmitis, group B streptococcus was found in 7% of cases; the main source of infection was IE [7]. Patients with group B endogenous endophthalmitis typically experience a dramatic vision loss. A reverse relative afferent pap-illary defect and cream-like hypopyon are usually present [8]. Antibiotic therapy with good intraocular penetration should be initiated immediately, as delayed treatment can compromise visual prognosis; vision loss rate reportedly reaches 37.5% [6]. Uveitis, how-ever, is a non-infectious inflammatory disease that can easily be mistaken as endophthalmitis. In an epi-demiologic study of 2,943 autopsies, 98% of posterior uveitis in patients with systemic diseases was non-granulomatous inflammation [9]. Poststreptococcal uveitis has been infrequently reported in cases with poststreptococcal syndrome, which includes acute rheumatic fever, poststreptococcal reactive arthritis, and acute glomerulonephritis [10,11]; the pathogen involved in poststreptococcal syndrome is group A streptococcus. In cases of streptococcal infection, uveitis is considered to be an immunologic response to exoge-nous and endogeexoge-nous antigens. Drop in visual acuity in uveitis is related to inflammatory changes and onset of disease complications and/or treatment, includ-ing cataracts, glaucoma, and cystic macular edema. Retinal vasculitis manifests as inflammatory infil-trates along the retinal vessels with vascular leakage or occlusion that can be highlighted by fundus fluo-rescein angiography. Medical therapy includes topical, locally injected, and systemically administered anti-inflammatory treatments [12]. Based on this patient’s clinical manifestations, a diagnosis of uveitis was made and the patient’s uveitis was cured by topical steroid.
In terms of immunogenetic factors, HLA-B27 is commonly identified in patients with acute uveitis irrespective of presence of underlying ankylosing spondylosis [13]. No evidence existed of underlying rheumatologic disease in this patient, and his HLA-B27 test was negative. The uveitis in this case of IE was probably associated with streptococcus-associated immune complex. The pathogenesis of uveitis in group B streptococcus bacteremia warrants further study.
Infective endocarditis with uveitis To our knowledge, this patient is the first reported
case of IE associated with uveitis.
Infectious endocarditis can be complicated with vas-cular embolism, immunologic phenomena, and rheu-matic manifestations. Ophthalmologic involvement is rare in patients with IE. This case is an important reminder that accurate diagnosis and differentiation between endophthalmitis and uveitis are crucial as the strategies for treating these two diseases are dif-ferent. This patient’s uveitis was treated successfully by local steroid use. This is the first reported case of IE complicated by uveitis.
R
EFERENCES1. Bernard DP. Diagnosis of infective endocarditis. BMJ 2002;325:845–6.
2. Rollan MJ, San Roman JA, Vilacosta I, et al. Clinical profile of Streptococcus agalactiae native valve endocardi-tis. Am Heart J 2003;146:1095–8.
3. Gonzalez JC, Gonzalez GM. Rheumatic manifestations of infective endocarditis in non-addicts: a 12-year study.
Medicine 2001;80:9–19.
4. Aviles RJ, Ramakrishna G, Mohr DN, et al. Poststrepto-coccal reactive arthritis in adults: a case series. Mayo
Clin Proc 2000;75:144–7.
5. Kobayashi S, Tamura N, Ikeda M, et al. Uveitis in adult patients with poststreptococcal reactive arthritis: the first two cases reported associated with uveitis. Clin
Rheumotal 2002;21:533–5.
6. Arcieri ES, Jorge EF, Rocha FJ. Bilateral endogenous endophthalmitis associated with infective endocardi-tis: case report. Braz J Infect Dis 2001;5:356–9.
7. Chihara S, Siccion E. Group B streptococcus endocardi-tis with endophthalmiendocardi-tis. Mayo Clin Proc 2005;80:74. 8. Lee SY, Chee SP. Group B streptococcus endogenous
endophthalmitis—case report and review of literature.
Ophthalmology 2002;109:1879–86.
9. Hofmann HM, Giarelli L. Posterior uveitis in systemic diseases. A pathologic and epidemiologic study. Klin
Monatsbl Augenheilkd 1986;189:173–5.
10. Knox CM, Wong IG, Love P. Chronic uveitis following a streptococcal illness. Can J Ophthalmol 1999;34:99–100. 11. Leiba H, Barash J, Pollack A. Poststreptococcal uveitis.
Am J Ophthalmol 1998;126:317–8.
12. Smith JR. Management of uveitis. Clin Exp Med 2004; 3:21–9.
13. Careless DJ, Chiu B, Rabinovitch T, et al. Immunogenetic and microbial factors in acute anterior uveitis. J Rheumatol 1997;24:102–8.
!"VR==Q==OT= !"VR==U==NS= !"#$%&' !"!#$ %&'()*+ UMT !"#$NMM
!"#$%&'#$=
!
N= = O= = N= = PIQ= = N= = NIQ= = NIQ !"!#$ %= =N !"#= =O= =P !"# Q !"!= !"# !"#=RN= !"#!$%&'()*+,-./01#234567 !"#$%&'()&'*+&,-./01234#5= Öêçìé= _= J ëíêÉéíçÅçÅÅìë= !"#$%&'()*+,-"./012 345678 !"#$%&'()*+,-./0123456789:;-<=>?@A !"#$%&'()*+,-./0123456789:&;+<=>?@ !"#$%&'#()*+,-./"'0123456789:;<=>? !"#$%&'()*+, !"#$%&!'(& E !=OMMTXOPWQMQF