Burkholderia cepacia, an opportunistic pathogen, is resistant to disinfectants and broad-spectrum antimicrobial agents. This pathogen often causes nosocomial infections in imunocompromised hosts, especially in patients with cystic fibrosis and chronic granulomatous diseases [3, 4]. In addition, patients with cancer or chronic renal disease may also be susceptible to Burkholderia infection [14–16].
In these patients, central venous catheters are the primary source of bacteraemia . Burkholderia bacteremia also noted in patients undergoing haemodialysis . Burkholderia cepacia also causes infective endocarditis and skin and soft tissue pathology. This pathogen rarely causes infective endocarditis; however, there are some reports on the occurrence of this pathology in heroine addicts [4, 10–13] and patients with prosthetic valves and valve replacements [3–5].
In our patients, Burkholderia cepacia had infected mitral valve despite the absence of predisposing factors that would make her susceptible to the infection. This case is different from the previous reports [3–13] in the following issues. First, most of the reported cases of Burholderia cepacia endocarditis involved the prosthetic valve. In contrast, native valve endocarditis was relatively less frequent [3, 4, 7–9]. Burholderia cepacia-induced native valve endocarditis has rarely been reported. As a predisposing condition, most patients with native valve endocarditis had a history of intravenous drug abuse [3, 4, 7–9] and mitral valve endocarditis has mostly been reported in patients having prosthetic valves [3–5]. However, our patient did not exhibit any of the predisposing factors related to this infection described previously.
Second, trimethoprim-sulfamethoxazole is commoly used for the treatment of this infection [4–9]. However, ceftazidime was administered to our patient because of cerebral involvement and risk of trimethoprim-sulfamethoxazole allergy. Brain MRI had revealed cerebral and cerebellar infarctions in our patient. These findings suggest that the emboli had migrated into the cerebral hemispheres and induced an ischemic change of the involved regions. Therefore, an antimicrobial agent, such as ceftazidime, that could penetrate the blood-brain barrier was required in this case.
Antimicrobial resistance of Burkholderia cepacia has posed a great challenge of treating the infection. This pathogen is intrinsically resistant to aminoglycosides and polymyxins. The antimicrobial effective against this pathogen are carbapenem, broad-spectrum beta-lactams (such as, piperacillin-tazobactam and ceftazidime), and trimethoprim-sulfamethoxazole. Therefore, because of such antimicrobial resistance, a combination of drugs and surgical treatment for valvulopathy is required [3–7, 9]. However, we successfully treat the patient without the surgical treatment.
Third, replacement of the prosthetic or native valve has been required in most patients with infective endocarditis [3, 7–9] but we did not need to perform any such surgery in our patient because of the excellent response to antimicrobial therapy. In addition, her valve function was also apparently preserved without surgery. On the bases of her valve function, life expectancy, and the morbidity involved in such surgical treatment, we decided against surgery and we were able to successfully treat the infective endocarditis by antibiotics only.
Fourth, in patients with Burkholderia cepacia endocarditis, the mitral valve is known to be less frequently involved than the tricuspid valve; mitral valve involvement has been reported in only those patients who previously had prosthetic valve replacement or valve repair surgery [3–5], and only 1 study reported aortic valve endocarditis without any predisposing factors .
In summary, we experienced a case of native valve endocarditis with cerebral involvement by Burkholderia cepacia without predisposing factors of Burkholderia infection, successfully managed by antimicrobial treatment only.