A patient develops bacterial meningitis with markedly elevated CSF protein (250 mg/dL), low glucose (25 mg/dL with serum glucose 90 mg/dL), and >1000 PMNs/µL. The low CSF glucose primarily results from:

• A Disrupted GLUT-1 transporter function at the blood-brain barrier reducing glucose influx
• B Increased anaerobic glycolysis by bacteria and activated leukocytes consuming CSF glucose, combined with reduced GLUT-1 transport due to inflammation ✓
• C Elevated CSF lactate competitively inhibiting glucose transport via GLUT-1
• D Hypoglycemia in the serum causing proportionally low CSF glucose

Explanation

Low CSF glucose in meningitis results from a combination: (1) direct consumption by bacteria (enhanced glycolysis) and activated neutrophils and macrophages producing lactate through anaerobic metabolism; (2) inflammatory cytokines impairing GLUT-1 and GLUT-3 transporter function at the blood-brain barrier and choroid plexus. Normal CSF:serum glucose ratio is ≥0.6. Here ratio = 25/90 ≈ 0.28, indicating significant hypoglycorrhachia. Serum glucose at 90 mg/dL is normal, so serum hypoglycemia is not the cause. Lactate does not competitively inhibit GLUT-1 (different transporter/substrate).

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.