Microbiology Chapter 26: Infections of the Nervous System – Structure, Function, and Major Pathogens

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This section introduces the historical context of nervous system infections, focusing on Gerhard Henrik Armauer Hansen and his work on leprosy.

Gerhard Henrik Armauer Hansen (1841–1912): Norwegian physician who disproved the hereditary theory of leprosy and identified its bacterial cause (Mycobacterium leprae).
Historical Impact: Leprosy patients were isolated, stigmatized, and subjected to severe social consequences, especially in the U.S. during the early 20th century.
Scientific Milestone: Hansen's 1873 report was the first to link a specific bacterium to a disease, predating Koch's work on tuberculosis.

Infections of the nervous system are particularly severe due to their potential to impair movement, sensation, and cognition.

Poliomyelitis: Can cause paralysis and respiratory failure.
Hansen’s Disease (Leprosy): May result in loss of fingers, toes, or facial deformity.
Social Stigma: Historically, lepers were shunned and symbolically buried before isolation.
Brain/Membrane Infections: Can cause deafness or disability in children.
Antibiotics: Before their development, bacterial CNS infections were often fatal.
Incidence: CNS infections are fortunately uncommon.

Nerve cells (neurons) transmit electrical impulses and are specialized for communication.

Dendrites: Branching projections that receive information.
Cell Body: Contains the nucleus and acts as the command center.
Axon: Long extension that transmits signals to other cells.
Neurotransmitters: Chemicals produced in the cell body, stored in vesicles at the axon end, released to communicate across synapses.
Synapse: The region between two neurons where neurotransmitters are exchanged.
Retrograde Transport: Some viruses can move through the axon toward the cell body via this process.

The nervous system is divided into central and peripheral components, each with distinct roles.

Central Nervous System (CNS): Includes the brain and spinal cord; responsible for processing and integrating information.
Peripheral Nervous System (PNS): Composed of nerves (bundles of axons) that carry sensory and motor information between the CNS and the body.
Motor Neurons: Transmit commands from CNS to muscles and glands.
Sensory Neurons: Carry sensory information to the CNS.
Ganglia: Clusters of neuron cell bodies located outside the CNS.
Encephalitis: Generalized inflammation or infection of the brain.

The CNS is well-protected compared to the PNS, reducing the risk of infection.

Bone Encasing: Skull and vertebral column protect the CNS.
Meninges: Three layers of membranes (dura mater, arachnoid mater, pia mater) cover the brain and spinal cord.
Dura Mater: Tough, fibrous outer layer providing a barrier to infection.
Arachnoid and Pia Mater: Inner membranes separated by the subarachnoid space, which contains cerebrospinal fluid (CSF).
Meningitis: Inflammation of the meninges.
Meningoencephalitis: Inflammation of both the brain and meninges.

CSF is essential for cushioning, supporting, and nourishing the brain and spinal cord.

Production: CSF is produced in the ventricles of the brain and circulates over the CNS.
Function: Cushions the brain, supports neural tissue, and transports nutrients.
Microbiota: The nervous system and CSF are normally sterile; presence of microbes indicates infection.
Diagnosis: Spinal tap or lumbar puncture is used to obtain CSF samples for analysis.
Blood-Brain Barrier: Specialized cells lining CNS capillaries restrict passage of infections and many antibiotics.

Bacterial infections most commonly affect the meninges, causing meningitis, which can progress rapidly and be fatal.

Symptoms: Early symptoms resemble a cold but can escalate quickly to severe illness.
Mortality: Untreated cases can approach 100% fatality; even with treatment, 10–20% fatality and permanent disabilities are possible.
Common Pathogens: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae.

Caused by Streptococcus pneumoniae, this form of meningitis is severe and often leads to neurological damage.

Signs and Symptoms: Sudden severe headache, fever, neck/back pain, nausea, vomiting, deafness, confusion, coma.
Causative Agent: Gram-positive, lancet-shaped coccus; capsule protects against phagocytosis; over 90 serotypes.
Pathogenesis: Encapsulated strains resist phagocytosis, enter bloodstream, bind to meningeal cells, and cause inflammation and swelling.
Epidemiology: Spread by respiratory droplets; case-fatality rate ~20% in adults, higher in elderly.
Treatment: Penicillin (unless resistant); vaccines available for common serotypes; conjugate vaccines for children.

Caused by Neisseria meningitidis, this disease can progress rapidly and is distinguished by purplish skin spots (petechiae).

Signs and Symptoms: Similar to pneumococcal meningitis; petechiae and endotoxic shock are distinguishing features.
Causative Agent: Gram-negative, encapsulated diplococcus; most infections due to serotypes A, B, C, Y, W135.
Pathogenesis: Bacteria attach to mucous membranes, enter bloodstream, release endotoxin causing shock and capillary damage.
Epidemiology: Transmission via respiratory droplets; highest incidence in the "meningitis belt" of Africa.
Treatment: Penicillin or ceftriaxone; vaccines for A, C, Y, W135; prophylactic rifampin for close contacts.

This form of meningitis primarily affects children and is caused by Haemophilus influenzae type b (Hib).

Signs and Symptoms: Progression from mild cold to severe headache, fever, vomiting; infants may show bulging fontanelle.
Causative Agent: Gram-negative, non-motile rod; encapsulated strains a–f cause disease in children, type b (Hib) most serious.
Pathogenesis: Encapsulated bacteria penetrate epithelium, enter bloodstream, resist phagocytosis.
Epidemiology: Healthy adults may carry pathogen; children rarely carry Hib due to immunization; untreated fatality ~90%.
Treatment: Cefotaxime or ceftriaxone; rifampin for close contacts; conjugate Hib vaccine has reduced incidence by >99%.

Newborns are at risk for meningitis caused by several bacteria, often acquired during birth.

Signs and Symptoms: Fever, vomiting, irritability, poor feeding, lethargy, bulging fontanels.
Causative Agents: Streptococcus agalactiae (group B strep), encapsulated E. coli, Listeria monocytogenes.
Pathogenesis: Bacteremia leads to infection of meninges, increased intracranial pressure, possible hydrocephalus and brain abscess.
Epidemiology: Acquired from mother’s genital tract; premature/low birth weight increases risk; death in ~6–20% of cases.
Treatment: IV antibiotics (ampicillin, gentamicin); screening and treating pregnant women for group B strep reduces incidence.