Related Experiment Video

Updated: Aug 18, 2026

A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side
09:58

A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side

Published on: May 6, 2016

Gentamicin penetration into cerebrospinal fluid in experimental Haemophilus influenzae meningitis

A L Smith1, R S Daum, G R Siber

  • 1Division of Infectious Disease, Children's Hospital and Medical Center, Seattle, Washington 98105.

Antimicrobial Agents and Chemotherapy
|July 1, 1988
PubMed

Insights

Intravenous bolus administration of gentamicin is most effective for achieving therapeutic drug concentrations in cerebrospinal fluid (CSF), especially in meningitis patients. This method maximizes gentamicin penetration into the lumbar CSF.

Area of Science:

  • Pharmacology
  • Infectious Diseases
  • Neuroscience

Background:

  • Meningitis significantly impacts drug distribution in the central nervous system.
  • Understanding gentamicin's cerebrospinal fluid (CSF) penetration is crucial for effective meningitis treatment.

Purpose of the Study:

  • To evaluate the effect of meningitis and different parenteral gentamicin administration methods on CSF drug concentrations.
  • To determine the optimal gentamicin administration route for achieving therapeutic levels in CSF.

Main Methods:

  • Animal models with and without induced meningitis were used.
  • Gentamicin was administered via intramuscular injection, 30-minute intravenous infusion, and intravenous bolus.
  • Drug concentrations in CSF (cisternal, ventricular, lumbar) and serum were measured.

Main Results:

  • Intravenous bolus administration significantly increased gentamicin penetration into CSF in animals with meningitis compared to normal animals.
  • Lumbar CSF achieved the highest gentamicin concentrations following intravenous bolus administration in meningitic animals.
  • Gentamicin's elimination half-life in cisternal CSF was longer than in serum, indicating sustained penetration.

Conclusions:

  • Intravenous bolus administration is the most effective method for maximizing gentamicin penetration into CSF.
  • Maximum gentamicin concentrations in CSF are achieved in the lumbar region following intravenous bolus administration.
  • Meningitis enhances gentamicin's CSF penetration, particularly with intravenous bolus delivery.

More Related Videos

Intracerebroventricular and Intravascular Injection of Viral Particles and Fluorescent Microbeads into the Neonatal Brain05:51

Intracerebroventricular and Intravascular Injection of Viral Particles and Fluorescent Microbeads into the Neonatal Brain

Published on: July 24, 2016

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection05:55

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection

Published on: May 7, 2020

Related Concept Videos

Determination of Multiple Dosing Parameters: Steady-State, Minimum and Maximum Concentrations01:15

Determination of Multiple Dosing Parameters: Steady-State, Minimum and Maximum Concentrations

Gentamicin, an aminoglycoside antibiotic, is commonly administered via intermittent intravenous infusion to treat severe infections. An intermittent one-hour infusion of gentamicin, administered at eight-hour intervals, allows for precise control of plasma drug concentrations, minimizing toxicity while ensuring therapeutic efficacy. Pharmacokinetic principles govern the dynamics of plasma concentrations and can be mathematically described using specific equations.The plasma drug concentration...
Bacterial Meningitis01:24

Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
Cryptococcal Meningitis01:27

Cryptococcal Meningitis

Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...