Journal of Cardiology Cases 13 (2016) 153–154
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Case Report
Infective endocarditis in a patient with atopic dermatitis Milton James Micallef (MBBS, BA (Hons), BSc)*, Avisham Ramphul (BMed, BChD) Armidale Rural Referral Hospital, Armidale, NSW, Australia
A R T I C L E I N F O
A B S T R A C T
Article history: Received 6 August 2015 Received in revised form 24 December 2015 Accepted 18 January 2016
We present the case of a 39-year-old plumber who was diagnosed with infective endocarditis due to Staphylococcus aureus. The route of entry was attributed to the patient scratching pruritic lesions of his poorly controlled atopic dermatitis (eczema). We recommend that medical practitioners of patients with poorly controlled atopic dermatitis should pay particular attention to, and take measures to mitigate against, this risk. Crown Copyright ß 2016 Published by Elsevier Ltd on behalf of Japanese College of Cardiology. All rights reserved.
Keywords: Endocarditis Atopic dermatitis Staphylococcus aureus
Introduction Staphylococcus aureus is the causative organism in approximately half of all cases of infective endocarditis [1], and it is well known as a commensal organism of the skin. There are only few cases reported associating exacerbations of atopic dermatitis (eczema) with infective endocarditis [2–5]. Here we present a case where the sole predisposing factor to the development of the endocardial infection was a flare of atopic dermatitis, with the aim of highlighting this risk factor in at-risk individuals, and the need to consider strategies to reduce the risk of significant morbidity arising from a manageable condition. Case report We present the case of a 39-year-old plumber who presented to the hospital with a two-day history of nausea, vomiting, diarrhea, fever, and exertional dyspnea. He had an uncomplicated medical history consisting of atopic dermatitis (eczema) and a generalized anxiety disorder (on escitalopram), and was otherwise fit and well. He denied any recent contact with raw sewage, had never smoked nor used any intravenous drugs, and had not undergone any recent dental procedure. At presentation, he was pyrexic (40.2 8C), plethoric, tachycardic (100 bpm), normotensive, and saturating normally. Blood cultures
* Corresponding author at: Armidale Rural Referral Hospital, Rusden Street, Armidale, NSW 2350, Australia. Tel.: +61 2 4921 3000; fax: +61 2 6776 4704. E-mail address:
[email protected] (M.J. Micallef).
were taken. Provisionally he was diagnosed with a viral gastroenteritis, and admitted to the ward without receiving any antibiotics. By the following morning, 2 of 4 blood culture bottles had positive reports of Gram-positive cocci, later identified as methicillin-sensitive S. aureus (MSSA). Upon review, the patient was obtunded, lying immobile and supine, with photophobia, neck stiffness, and a positive Kernig sign. There were no focal neurological signs, nor papilledema on direct ophthalmoscopy. On auscultation of the precordium, there was a grade 3 pansystolic murmur in the region of the apex, with no palpable thrill. There were no cutaneous stigmata of embolic disease; however, there were multiple eczematous lesions on the face, trunk, and limbs. His skin was dry and there were areas of lichenification which were worse on the knees and elbows. He regularly applied moisturizer and 1% hydrocortisone acetate cream. Exacerbations of his dermatitis were managed with 2.5% hydrocortisone acetate prescribed by his general practitioner. He recalled suffering from atopic dermatitis since childhood but had noticed more frequent exacerbations over the preceding two years. He could not identify any exacerbating factors. Two of his siblings as well as his two children had atopic dermatitis. He had never been seen by a dermatologist. Further blood cultures were collected, and the patient was administered empirical doses of gentamicin, benzylpenicillin, and vancomycin. Subsequent to susceptibility testing and on infectious diseases specialist advice, the regimen was changed to flucloxacillin 2 g 6-hourly, and subsequently increased to 4-hourly. Lumbar puncture was performed to exclude bacterial meningitis. There were no red cells, no white cells, normal glucose, mildly raised protein (0.57 g/L), no growth on aerobic and anaerobic
http://dx.doi.org/10.1016/j.jccase.2016.01.006 1878-5409/Crown Copyright ß 2016 Published by Elsevier Ltd on behalf of Japanese College of Cardiology. All rights reserved.
M.J. Micallef, A. Ramphul / Journal of Cardiology Cases 13 (2016) 153–154
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Fig. 1.
Still image from the patient’s trans-thoracic demonstrating mitral valve vegetation.
echocardiogram
culture, and negative polymerase chain reaction for Neisseria meningitidis, Herpes simplex, and Streptococcus pneumoniae. Transthoracic echocardiogram (Fig. 1) demonstrated a small vegetation on the posterior leaflet of the mitral valve, which had prolapsed, with moderate associated mitral regurgitation. Subsequent trans-esophageal echocardiogram confirmed this and also revealed a widely patent foramen ovale. The patient was diagnosed with MSSA mitral valve endocarditis (Duke criteria diagnostic with 2 major, 1 minor). All presenting symptoms and signs had subsided within 48 h of initiating therapy, and within 72 h blood cultures became negative. The conclusion was drawn that the point of entry of MSSA was any one of the patient’s eczematous lesions which he had admitted to scratching to the point of hemorrhage. The patient was prescribed a 6-week course of flucloxacillin 12 g continuous infusion daily. Following completion of antibiotic therapy, the patient underwent elective mitral valve repair and closure of the patent foramen ovale. Discussion Atopic dermatitis is often complicated by infections of bacterial, viral, or fungal origin. This can be attributed to defective epithelial barriers, decreased antimicrobial peptides, and immunological deficiencies. Colonization of S. aureus is commonly observed in skin lesions in patients with atopic dermatitis. Continual scratching due to pruritus can lead to breakdown in skin surface integrity, and may result in a bacteremia. While many organisms can cause infective endocarditis, S. aureus is responsible for approximately 50% of cases; it is commonly the causative organism in patients with skin abscesses and indwelling intravenous lines [1]. Streptococcus viridans is the second most commonly identified organism.
While most cases of congenital heart disease and infective endocarditis do not seem to be preceded by any significant event, cardiovascular surgery (28%), respiratory tract infections (20%), dental procedures (16%), and infections of other systems including the skin (9%) have been identified as possible causes in those cases where a predisposing factor was identified [1,3]. Given the high prevalence of atopic dermatitis, it is surprising that a review of the literature revealed few reported cases of patients with atopic dermatitis and infective endocarditis. Onoda et al. reported two cases where acute aortic and/or mitral valve endocarditis was complicated by recurrent cutaneous infections caused by severe atopic dermatitis [2]. Grabczynska and Cerio described a case of a 24-year-old diagnosed with infective endocarditis following a refractory exacerbation of eczema just prior to presentation, treated with oral prednisolone 30 mg; though in his case there were recurrent episodes of endocarditis and a complex congenital heart disease [3]. Buckley reported a case of a child undergoing a course of acupuncture for atopic dermatitis, the needles of which were inserted through inflamed skin around the knees, with the result of a septic arthritis and S. aureus-related endocarditis [4]. Pike and Warner reported a case of bacterial endocarditis in a child with severe atopic dermatitis, recurrent staphylococcal skin infections, and an immunodeficiency [5]. While there is no absolute evidence to define our case as a complication of atopic dermatitis, the seriousness of the infection as well as the paucity of information in the literature warrants clinical vigilance. The patient reported pruritus around his eczematous lesions and admitted to continual scratching prior to presentation, to the point of bleeding, and he had a proven staphylococcal bacteremia with no alternative and more likely cause identified. Prevention of complications of atopic dermatitis is critical in order to avoid potential life-threatening infections such as infective endocarditis. We therefore recommend active management of eczematous lesions, routine use of emollients, patient education, judicious use of systemic immunosuppressants, and that specialist dermatology input be sought in cases where poor control is encountered. Hand and nail hygiene should be encouraged, and the role of antiseptic body washes (e.g. triclosan) should be investigated as a potential for prophylaxis. Conflict of interest None declared. References [1] Atkinson JB, Robinowitz M, McAllister HA, Forman MB, Virmani R. Cardiac infections in the immunocompromised host. Cardiol Clin 1984;2:671–85. [2] Onoda K, Mizutan H, Komada T, Kanemitsu S, Shimono T, Shimpo H, Yada I. Atopic dermatitis as a risk factor for acute native valve endocarditis. J Heart Valve Dis 2000;9:469–71. [3] Grabczynska SA, Cerio R. Infective endocarditis associated with atopic eczema. Br J Dermatol 1999;140:1193–4. [4] Buckley DA. Staphylococcus aureus endocarditis as a complication of acupuncture for eczema. Br J Dermatol 2011;164:1393–408. [5] Pike AG, Warner JO. Atopic dermatitis complicated by acute bacterial endocarditis. Acta Paediatr Scand 1989;78:463–4.
