Reversible Secondary Carnitine Deficiency Associated With Chronic Achromobacter xylosoxidans Bacteremia Presenting as...

Infectious diseases exert systemic effects beyond localized inflammation, yet selective disruption of host metabolic pathways remains incompletely characterized. Carnitine-dependent fatty-acid transport is essential for mitochondrial energy production, and acquired deficiencies are rarely attributed to infection. Chronic bacteremia has not been clearly linked to functional impairment of this pathway.

A 34-year-old man with no prior metabolic or neuromuscular disease presented with subacute proximal muscle weakness, fasting intolerance, and episodic confusion following several weeks of constitutional symptoms. Evaluation demonstrated hypoketotic hypoglycemia (plasma glucose 46-54 mg/dL with β-hydroxybutyrate <0.3 mmol/L), elevated creatine kinase (peak 2,140 U/L), and reduced plasma free carnitine (12 μmol/L; reference 25-50 μmol/L), indicating impaired mitochondrial fatty-acid transport. Serial blood cultures isolated Achromobacter xylosoxidans, confirming persistent bacteremia. Alternative endocrine, metabolic, and immunologic causes were excluded.

Resolution of metabolic abnormalities following targeted antimicrobial therapy supports an acquired and reversible disruption of fatty-acid transport. Potential mechanisms include inflammation-mediated renal carnitine loss and host-pathogen metabolic competition during prolonged bacteremia.

Chronic Achromobacter xylosoxidans bacteremia may be associated with reversible secondary carnitine deficiency and selective impairment of fatty-acid transport. Plasma free carnitine normalized after antimicrobial therapy and short-term L-carnitine supplementation, with no recurrence during six months of follow-up. Metabolic evaluation should be considered in patients with unexplained hypoketotic hypoglycemia and persistent bloodstream infection.