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Related Concept Videos

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...
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...
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 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...
Rocky Mountain Spotted Fever01:26

Rocky Mountain Spotted Fever

Rocky Mountain Spotted Fever (RMSF) is a severe tick-borne illness caused by Rickettsia rickettsii, a Gram-negative, coccobacillary bacterium. This pathogen is an obligate intracellular parasite, requiring a host cell for replication. Transmission occurs through the bite of an infected tick. In the United States, the most important vectors are Dermacentor variabilis (American dog tick) and Dermacentor andersoni (Rocky Mountain wood tick), though other tick species may also serve as vectors.
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...

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Related Experiment Video

Updated: Jul 17, 2026

Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery
10:03

Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery

Published on: November 5, 2019

Meningococcal disease associated with an acute post-streptococcal complement deficiency.

Nikolaos Daskas1, Katie Farmer, Richard Coward

  • 1Bristol Royal Hospital for Children, Bristol, UK.

Pediatric Nephrology (Berlin, Germany)
|February 13, 2007
PubMed
Summary

Meningococcal disease typically results from chronic complement deficiencies. This study details a rare case in a child experiencing meningococcal disease due to a temporary complement deficiency linked to post-streptococcal glomerulonephritis.

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Induction of Leptomeningeal Cells Modification Via Intracisternal Injection
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Last Updated: Jul 17, 2026

Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery
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Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery

Published on: November 5, 2019

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection
05:55

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection

Published on: May 7, 2020

Area of Science:

  • Immunology
  • Pediatrics
  • Nephrology

Background:

  • Complement pathway protein deficiencies increase meningococcal disease risk.
  • Deficiencies are usually chronic, stemming from congenital issues or conditions like SLE and MPGN.

Observation:

  • A child presented with meningococcal disease.
  • The child had a transient complement deficiency.

Findings:

  • The transient complement deficiency was caused by post-streptococcal glomerulonephritis (PSGN).
  • This represents a novel cause of complement deficiency leading to meningococcal disease.

Implications:

  • Highlights PSGN as a potential cause of transient complement deficiency.
  • Suggests considering transient complement deficiencies in pediatric meningococcal disease cases.
  • Expands understanding of complement deficiency in infectious disease susceptibility.