The brain is protected from bacterial invasion from the environment by the skull, the dura, the arachnoid membrane, the pia, and the glia limitans, which is a dense mesh of astrocytic processes on the surface of the brain. Bacterial meningitis is the infection of the arachnoid membrane, subarachnoid space, and cerebrospinal fluid by bacteria. The iinfection may spread to the meninges from an adjacent infected area such as sinusitis, otitis media, and mastoiditis or from the environment through a penetrating injury or congenital defect, such as aa menigomyelocele.
Bacterial toxins cause neuronal apoptosis and cell wall lipopolysaccharide, released from bacteria, damages the blood brain barrier (BBB). A creamy purulent exudate covers the cerebral hemispheres and settles along the base of the brain, around cranial nerves and the openings of the fourth ventricle. Neutrophils in the subarachnoid space infiltrate and damage cranial nerves resulting in cranial nerve deficits, and invade leptomeningeal vessels causing phlebitis and arteritis with thrombosis and ischemic infarction. The glia limitans, a thick tight mesh of astrocytic processes, joined by dense junctions and covered by basement membrane, resists penetration by bacteria and neutrophils. Brain damage in meningitis is caused not only by bacteria but probably more by host responses. This course was produced for the use of students, residents, and staff of NEOMED and affiliated hospitals. Early symptoms of meningitis and septicaemia (the blood poisoning form of the disease) can be like other childhood illnesses, but a baby will usually get ill quickly and get worse fast. What should I do if I am worried about my baby?
If you are seriously worried about someone who is ill, don’t wait for a rash to appear – get medical help.
The darker the skin the harder it is to see a septicaemic rash so check lighter areas like the palms of hands and soles of feet or look inside the eyelids and the roof of the mouth. Remember, a very ill person needs medical help even if there are only a few spots, a rash or no rash at all.
MenB Vaccine Research Appeal We are funding ground breaking research to provide the evidence for an extended MenB vaccination process. A spinal epidural abscess arises when organisms from osteomyelitis or tuberculosis of the vertebral column spread to this space. The subdural space is traversed by bridging arteries and veins but has no vascular network of its own. The subarachnoid space is bounded externally by the arachnoid membrane and internally by the pia, and dips into the brain along blood vessels in the perivascular (Virchow-Robin) spaces.
From there, they get into the blood stream and enter the subarachnoid space through complex interactions with endothelial cells. Increased vascular permeability from BBB damage, in turn, causes cerebral edema, increased intracranial pressure, decreased cerebral perfusion, hypoxia, and neuronal necrosis. The inflamed spinal structures are sensitive to stretch, and pain can be elicited by maneuvers that stretch the spine, such as bending the leg with an outstretched knee (Kernig sign) or bending the neck (Brudzinski sign).
The CSF in meningitis shows hundreds, even thousands of neutrophils and is teeming with organisms. The MRI shows enhancement and high FLAIR signal intensity in the meninges, corresponding to the pathology. Less than 5% of such cases are due to bacterial meningitis and the rest are due to viral (aseptic) meningitis (see viral infections). Undamaged, it provides an effective barrier that prevents the infection from spreading into brain tissue.


These responses have a protective purpose (to eliminate bacteria) but are excessive and indiscriminate and set in motion destructive cascades that damage everything in their way, mostly host tissues.
The bacteria that cause brain abscess spread from adjacent air sinuses or the middle ear, or via the blood stream from the lungs (bronchiectasis, lung abscess), or from the heart (bacterial endocarditis). Hypervascularity and vascular leakage account for the "ring enhancing" pattern after contrast injection, which gives abscess its characteristic radiological image (necrotic tumors may have a similar appearance).
Meningitis vaccines give excellent protection but can't prevent all forms of meningitis and septicaemia. Look out for tiny red or brown pin-prick marks which can change into larger red or purple blotches and blood blisters. Bacteria can penetrate into the brain from the environment if there is a break in the continuity of these protective layers. It extends from the optic chiasm to the cauda equina and surrounds the brain and spinal cord completely. The most common organisms of bacterial meningitis in children and adults are Streptococcus pneumoniae and Neisseria meningitidis.
The porous structure of choroid plexus capillaries facilitates their spillage into the CSF. Cells of the innate immune system of the brain, located in the BBB, choroid plexus, and ependyma, detect bacteria and secrete cytokines, chemokines, and complement, which attract circulating neutrophils into the CSF. Yet, to play it safe, physicians admit such patients to hospital and treat them with antibiotics.
The thick fibrinopurulent exudate in the subarachnoid space organizes into fibrous tissue that blocks the exits of the fourth ventricle and impairs CSF circulation around the cerebral convexities. Modulating these reactions, in addition to killing bacteria, can reduce the morbidity and mortality of meningitis. Patients with brain abscess present most frequently with headache and may also have symptoms of infection, focal neurological deficits due to destruction of brain tissue, and seizures. Such a discontinuity may be due to congenital defects (encephalocele, meningomyelocele) or may be caused by trauma or a shunt. However, a cranial epidural abscess may develop when bacteria colonize a traumatic epidural hematoma, or when infection from air sinuses extends in the plane between the dura and bone.
The CSF is an ideal medium for the spread of bacteria because it provides enough nutrients for their multiplication and has few phagocytic cells, and low levels of antibodies and complement. Neutrophils have powerful lysosomal enzymes and free radicals, which they use to kill bacteria, but have a short life span. These complications are due to HIE, increased intracranial pressure, and a toxic metabolic encephalopathy. Unnecessary hospitalizations can be avoided if a standard set of criteria are taken into account. Bacteria can also spread to the brain from infected adjacent air sinuses, the middle ear and the mastoids. Initially, bacteria multiply uninhibited and can be identified in smears, cultures, or by ELISA detection of their antigens before there is any inflammation. These complications take time to develop and may appear after the inflammation has subsided. They can reach the brain either directly through the bone, especially in areas where the bone plate is thin, or through veins (diploic veins, dural venous sinuses, intracerebral veins).


If they are large enough, they compress the brain and spinal cord, resulting in loss of function and increased intracranial pressure.
In newborns, the most common organisms are beta hemolytic Streptococcus group B (Streptococcus agalactiae) and Eschericia coli. The toxic metabolic encephalopathy is probably caused by unknown diffusible substances (perhaps cytokines) that have a neurotoxic action. Bacteria in the blood seed this necrotic nidus and spread around it causing brain necrosis and acute inflammation (cerebritis). Since the infection is contained within brain tissue, the CSF usually shows only a few mononuclear cells with normal protein and glucose.
The various protective layers may also help contain infections within certain spaces or planes. In babies, group B sreptococcal infection is frequently acquired during passage through the birth canal but meningitis may also develop a few days or weeks after birth. In infants, meningitis may present with nonspecific signs such as a depressed state, apneic spells, changes in heart rate, and atypical seizures. Alternatively, viral PCR of CSF, which has a turnaround time of a few hours, can confirm aseptic meningitis.
The effects of HIE and cerebral infarction are especially devastating in newborn babies in whom the brain can literally melt away. CSF cultures are positive in a minority of cases, however lumbar puncture should be avoided because of the risk of herniations.
This damage is followed by formation, in the subdural space, of a vascularized inflamed connective tissue and then a fibrous scar.
Nosocomial sources of meningitis include craniotomy, internal and external ventricular shunts, penetrating cranial fractures, closed head injuries with CSF-leaking basilar skull fractures, external lumbar catheters, and rarely lumbar puncture. So, brain damage in bacterial meningitis is caused in part by the direct action of bacteria and in part by the antibacterial inflammatory response.
The necrotic center cavitates while, at the periphery, a vascular zone of brain tissue with macrophages, mononuclear cells, and reactive astrocytes contains the infection. Histologically, acute subdural empyema shows a layer of neutrophils overlying the arachnoid membrane. The brain has elaborate mechanisms for controlling inflammation but, in some cases, unbalanced defense reactions can cause severe injury. In 4-5 weeks, collagen (derived from vascular cells) is laid down in this reactive zone forming a thick capsule that walls off the infection.
The inflammatory cells may infiltrate the arachnoid membrane and extend into the subarachnoid space.
Thus, the treatment of chronic abscess requires drainage or surgical excision in addition to systemic antibiotics.



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