Routes of spread and classification
Pathogens invade the structures of the central nervous system through several pathways. The hematogenous route is the most common, but the infection can also spread by contact (e.g., from the middle ear or paranasal sinuses), as well as lymphogenously or along nerve trunks (perineurally).
The diseases are classified according to several criteria:
- By etiology: bacterial, viral, fungal, parasitic, and prion infections.
- By localization: meningitis (meninges), encephalitis (brain), myelitis (spinal cord), and their combinations (meningoencephalitis, encephalomyelitis, meningomyelitis). Intracranial abscesses and granulomas are classified separately.
- By clinical course: ranging from fulminant to chronic.
Purulent CNS infections
These occur when tissues are damaged by pyogenic bacteria (staphylococci, streptococci, etc.). The primary mechanism is contact spread of the pathogen or the formation of bacterial emboli. Common ENT pathologies—such as otitis media, tonsillitis, rhinosinusitis, as well as pneumonia—frequently serve as the source of infection.
Suppuration is less commonly triggered by traumatic brain injury, cranial osteomyelitis, or infective endocarditis.
Morphological picture of lesions
CNS infections rarely present with isolated changes of a single type. A combination of pathological processes is usually observed, creating a variegated microscopic picture.
Three predominant types of changes are distinguished:
- Inflammation: exudative (with pus formation, as in staphylococcal meningitis) or productive.
- Tissue damage: neuronal dystrophy and necrosis.
- Demyelination: destruction of the myelin sheaths of nerve fibers.
For example, in purulent meningitis, the pia mater is infiltrated with a yellow-greenish exudate. The process begins locally at the site of infection entry and then spreads to the basal or convex (convexital) surface of the brain.
Features of brain abscesses
Abscesses—localized collections of pus—frequently form following traumatic brain injuries (in the white matter) or as a result of infected intracerebral hematomas.
They frequently develop around foreign bodies:
- Primary: bullets, metal fragments.
- Secondary: bone fragments, hair, tissue debris.
The morphology of an abscess depends on the pathogen. Staphylococcal lesions tend to encapsulate, forming a clear boundary. Streptococci, by contrast, typically provoke a diffuse, widespread purulent inflammation that extends to the meninges (meningitis) or brain ventricles (periventricular encephalitis).
Briefly: answers to topical questions
Which microorganisms are the main causative agents of purulent CNS infections?
The main causative agents of purulent central nervous system infections are various bacteria, the composition of which depends on the age and immune status of the patients. In the perinatal period, the primary pathogens are Streptococcus agalactiae, Escherichia coli, and Listeria monocytogenes. In older children and adults, Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b play the leading role. In individuals over 60 years of age, Streptococcus agalactiae and Streptococcus pneumoniae are more common. In addition, purulent meningitis can be caused by staphylococci, group A streptococci, Klebsiella, and Proteus.
What types of viral encephalitis are distinguished by etiology?
Based on etiology, viral encephalitis can be associated with herpes viruses, enteroviruses, arboviruses, rhabdoviruses, and other viruses. Slow viral CNS infections include: measles virus, causing subacute sclerosing panencephalitis; rubella virus, causing progressive congenital rubella and progressive rubella panencephalitis; tick-borne encephalitis virus, causing the progressive form of tick-borne encephalitis; herpes simplex virus, causing subacute herpetic encephalitis; HIV; HTLV-1 and HTLV-2; and JC polyomavirus, causing progressive multifocal leukoencephalopathy.
What is the macroscopic appearance of the meninges and the brain in purulent meningitis?
The macroscopic picture in purulent meningitis is characterized by pronounced changes in the meninges and brain parenchyma. The pia mater is markedly hyperemic and covered with a continuous layer of yellowish purulent masses or an accumulation of yellow-greenish exudate. The exudate may initially be localized to a specific area and then spread over vast regions of the basal and convexital surfaces of the brain. Meanwhile, the volume and mass of the brain are increased due to edema, the gyri are flattened, and the brain tissue becomes soft and soggy.
What complications and causes of death are characteristic of purulent meningitis?
Purulent meningitis is characterized by severe complications, including elevated intracranial pressure, hydrocephalus, epileptic seizures, arterial and venous thromboses, subdural effusion, sensorineural hearing loss, and hemorrhagic brain infarction secondary to venous thrombosis. The leading life-threatening complication is cerebral edema and swelling. In early stages, death occurs due to progressive edema resulting from dislocation and herniation of the cerebellar tonsils into the foramen magnum with compression of the medulla oblongata, leading to respiratory and cardiac arrest. At later periods, a fatal outcome is possible due to meningoencephalitis or purulent ependymitis.
Class and exam questions
What is the difference between meningitis and encephalitis?
Meningitis is inflammation of the meninges alone. Encephalitis is damage to the brain parenchyma itself. When both are inflamed, the diagnosis is "meningoencephalitis".
What serves as a frequent source of purulent CNS infection?
The infection typically enters by contact from nearby foci of purulent inflammation: in otitis media, sinusitis, or tonsillitis. Bacteria can also be seeded via pneumonia or infective endocarditis.
What is the difference between the effects of staphylococci and streptococci on the brain?
Staphylococci typically cause the formation of abscesses that eventually encapsulate. Streptococcal flora tend to cause a diffuse purulent inflammation that spreads along the meninges and ventricles.
What else to study on this topic
- Etiology and pathogenesis of ischemic strokes
- Stages of microscopic changes in cerebral infarction
- Mechanisms of intracerebral hemorrhage formation
- Types of cerebral vascular aneurysms
- Complications and outcomes of acute cerebrovascular accidents
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