To the Editor: Acetobacter indonesiensis, first described in 2000 (1), belongs to the group of acetic acid bacteria (AAB), which includes the genera Acetobacter, Gluconobacter, Asaia, Granulibacter, and others in the family Acetobacteriaceae. AAB are of great industrial interest for use in vinegar fermentation processes because they oxidize alcohols or sugars incompletely, which leads to acetic acid accumulation (2). AAB are widespread in nature and can be isolated from various sources, including vinegar, alcoholic beverages, tropical fruits, and flowers (1,2). AAB have rarely been associated with human disease. We describe a case of A. indonesiensis bacteremia in a child in Germany.

A 9-year-old girl with late-infantile metachromatic leukodystrophy was admitted to Marienhospital Herne, Herne, Germany, on February 9, 2015, for elective fundoplication. Because of her advanced neurologic disability, she required extensive nursing care and had several invasive medical devices, including a port catheter (detailed patient data in Technical Appendix). Soon after her admission, fever developed, and C-reactive protein levels increased (Technical Appendix Table 1). Physical examination and further diagnostic investigations (e.g., chest radiograph) revealed no focus of infection. Because she had experienced recurrent pneumonia and candidemia (the latter led to port catheter exchange 1 month previously), antimicrobial drug treatment with piperacillin/tazobactam and caspofungin was administered.

One blood culture, drawn from the port catheter on day 3 of the hospital stay, yielded slowly growing multidrug-resistant bacteria (agar diffusion indicated zones of inhibition only for imipenem, meropenem, fosfomycin, and tigecycline). By partial sequencing of the 16S rRNA gene, we identified the isolate as A. indonesiensis. Details of microbiological analyses, colony morphologic features, 16S rDNA-based phylogenetic analysis, and antimicrobial drug susceptibility testing results are given in the online Technical Appendix.

Because the patient clinically responded to piperacillin/tazobactam and caspofungin treatment, therapy was continued for 15 days, although piperacillin/tazobactam showed no in vitro activity against the A. indonesiensis isolate. Despite the patient’s improved condition, 1 control blood culture drawn from the port on hospital day 10, while she was receiving antimicrobial treatment, yielded A. indonesiensis, although another blood culture drawn peripherally on hospital day 14 yielded no growth. Port catheter exchange was advised but was not performed, according to the parents’ wishes.

The first report of human infection with AAB can be traced to 2004, when peritonitis, associated with Asaia bogorensis, was reported in a peritoneal dialysis patient (3). Further reports include a description of Granulibacter bethesdensis as a cause of lymphadenitis in patients with chronic granulomatous disease (4), isolation of Gluconobacter spp. from a culture of blood from an intravenous drug user and of Gluconobacter spp. and Asaia spp. from sputum samples of cystic fibrosis patients (5), a case of A. bogorensis bacteremia in an intravenous drug user (6), and central venous catheter–associated cases of Asaia lannaensis bacteremia in a child with cancer who had received a bone marrow transplant (7) and in children who had idiopathic dilated cardiomyopathy (8).

Regarding Acetobacter spp., only 2 reports on human infection have been published: A. cibinongensis bacteremia in a patient receiving chronic hemodialysis with signs of an infected arteriovenous fistula and suspected intravenous drug abuse (9) and A. indonesiensis pneumonia in a cystic fibrosis patient who was receiving immunosuppressive treatment because of a recent lung transplant (10). Similar to the case we report, species identification in those cases was achieved only with the help of sequencing methods in both cases. In the A. indonesiensis pneumonia case, results of antimicrobial drug susceptibility testing found that the bacteria showed multidrug resistance, as in the case we report, but susceptibility to aminoglycosides.

Of note, the aforementioned AAB infections all occurred in chronically ill patients or intravenous drug users. Similarly, children with metachromatic leukodystrophy are prone to healthcare- and device-associated infections involving opportunistic pathogens, and frequent use of broad-spectrum antibiotics may predispose the children for infection with multidrug-resistant bacteria. In the case we report, frequent accessing of the port, including for parenteral nutrition, may have further promoted microbial colonization.

Because a focus of infection was not apparent and because A. indonesiensis grew in 2 blood cultures independently drawn from the port but not in the blood culture obtained from peripheral venipuncture, we assume the patient’s port catheter harbored the infectious agent. The fact that several previously reported AAB infections were catheter-associated may further support our suspicion. However, we could not confirm this assumption because the port was not removed and cultured.

The patient clinically responded to piperacillin/tazobactam and caspofungin treatment, despite a lack of in vitro activity against the A. indonesiensis isolate. Although this response might be explained by the presence of a second pathogen (which was not cultured but covered by the given antimicrobial agents), the control blood culture drawn from the port still yielded A. indonesiensis and at least argues for persistent colonization of the port. Because of pathogen persistence in blood culture and limited therapeutic options owing to the multidrug-resistance of the isolate, we believe the port should have been removed in this case.

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