Asymptomatic Malaria Associated with Protection: Not Causal

Abstract

An otherwise healthy 44-year-old woman (a resident of a mountainous region of Switzerland) presented to the emergency department with acute onset of fever myalgia and disorientation. On physical examination she was in shock without an evident infectious source. Laboratory analyses revealed leukocytosis (WBC count 27000_109 cells/L) and an elevated C-reactive protein level (260 mg/ L). The patient had a history of congenital left ventricular inflow and outflow tract obstruction that was surgically corrected at the age of 15 years. In 1986 and 1996 she had infectious endocarditis of the aortic valve due to Staphylococcus aureus; the aortic valve was replaced by a homograft in 1990. Transesophageal echocardiography showed vegetations on the aortic valve and possibly also on the mitral valve with severe aortic and moderate mitral regurgitation. Therapy with vancomycin gentamicin and rifampicin was initiated. Blood cultures grew methicillin-sensitive S. aureus supporting a diagnosis of S. aureus prosthetic valve endocarditis and treatment was changed to flucloxacillin and rifampicin. The clinical course was complicated by acute renal failure severe thrombopenia and multiple septic emboli (in the brain skin retina and spleen). After 4 weeks of antibiotic therapy the aortic and mitral valves were replaced by mechanical prostheses. Cultures of the aortic valve were sterile but broad-range eubacterial PCR had results positive for Coxiella burnetii. Serologic results confirmed chronic Q-fever (phase 1 IgG titer 1:6400; phase 1 IgA titer 1: 200; phase 2 IgG titer 1:12800; and phase 2 IgA titer 1:400); analysis of stored serum samples from the patient revealed that the infection had been acquired in the previous 12 months. Thus the final diagnosis was chronic Q-fever prosthetic valve endocarditis complicated by acute S. aureus prosthetic valve endocarditis. The postoperative course was uncomplicated. S. aureus prosthetic valve endocarditis was treated for a total of 6 weeks with flucloxacillin and rifampicin. For Q-fever endocarditis therapy with doxycycline and hydroxychloroquine was introduced and will be continued until the phase 1 IgG titer is !1:400 with a minimum treatment duration of 18 months. At the most recent follow-up visit 10 months after the initial presentation the patient was asymptomatic and titers of anti-Coxiella antibodies were decreasing (phase 1 IgG titer 1:3200; phase 1 IgA titer 1:50; phase 2 IgG titer 1: 6400; phase 2 IgA titer 1:100). This case is remarkable for the simultaneous implication of two different bacterial species in the pathogenesis of infective endocarditis with one of the pathogens being discovered incidentally. Reports in the literature on dual-pathogen endocarditis are scarce; 2 cases with concomitant streptococcal and Q-fever endocarditis have been previously described in a large prospective French study [1]. Our patient had underlying cardiac abnormalities predisposing her to C. burnetii endocarditis and resided in an area of Switzerland with a seroprevalence of Coxiella species infection up to 30% [2]. Nevertheless C. burnetii infection was not suspected because all clinical manifestations were compatible with staphylococcal prosthetic valve endocarditis. The diagnosis of Q-fever endocarditis was thus a lucky strike which is disconcerting given the poor prognosis of unrecognized chronic Coxiella infection. In view of our experience we believe that C. burnetii serologic analysis or PCR testing of heart valve tissue are worth performing in all patients with infective endocarditis who have a preexisting valvulopathy and live in a region in which Q-fever is endemic regardless of whether another etiological agent has been identified or not. (full-text)