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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. I agree to Shutterstock's Website Terms, Privacy Policy, Licensing Terms and to receive emails that I can opt out of at any time. The four key organs that make up the lymphoid system with bone marrow (upper left), lymph nodes (upper right), spleen (lower right) and thymus (lower left). Parasitic encephalitis of the brain showing normal healthy brain on the left and infected brain with massive influx of inflammatory cells on the right. Myositis - Inflammation of the skeletal muscle with influx of large numbers of inflammatory cells, death (necrosis) of muscle fibers and hemorrhage. Normal healthy brain (top) and brain with metastatic lymphoma (bottom) with tumor cells invading and replacing healthy brain tissue. Microscopic view of brain to show acute encephalitis (inflammation) on the right and normal healthy brain on the left. All plans come as a Standard license, and can be upgraded to an Enhanced license at any time. When checked, Shutterstock's safe search screens restricted content and excludes it from your search results. Lightboxes allow you to categorize groups of photos and send them to your friends or colleagues. PsychologyPsychologySee all Driven to Distraction: Analyzing the Psyche of Risky Drivers High Pain Tolerance?
Researchers from the University of Zurich and the University Hospital Zurich reveal possible new treatment methods for a rare, usually fatal brain disease. Humans carry a multitude of viruses and bacteria in their gut, on their skin and in other organs. Two studies conducted by an international team of researchers from the University of Zurich, the University Hospital Zurich, the National Institutes of Health in the USA, San Raffaele Hospital in Milan, the University of Tubingen, and the UZH spin-off Neurimmune now reveal that the antibodies in PML patients often fail to recognize the JC virus they are infected with.
In multiple sclerosis (MS) patients, for instance, the treatment with a particular antibody, Tysabri, prevents immune cells from reaching the brain – but at the same time, also inhibits the brain’s immunosurveillance. The researchers now reveal potential ways to vaccinate against PML preventatively or, if the brain has already been infected, treat it with virus-specific human antibodies.
Infection (light zone) in the brain of multiple sclerosis patients suffering from progressive multifocal leukoencephalopathy (PML). Neuroscience NewsNeuroscience News posts news from various labs, universities, hospitals and news departments around the world. News about information technology, artificial intelligence, robotics, astronomy, space exploration, neuroscience, nanotechnology, aging, stem cells, quantum computing etc.
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). Inflammation of the bronchi (right) with the airway filled with thick mucus, inflammatory cells and debris (sputum).
Everyone who signs up gets full access to our entire library, including our curated collections. Our Standard license allows you to use images for anything, except large print runs over 500,000+ or for merchandising. Once you have downloaded your image, you have life-long rights to use it under the terms of the license purchased. If JC viruses enter the brain during the treatment, they go undetected, which can cause PML, the most significant side effect of the highly effective TysabriTM. By vaccinating mice and a PML patient with the virus’ coating protein, the international groups were able to demonstrate that the antibody response was so strong that the patient was soon able to eliminate the JC virus. 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.
If at any time you're unsatisfied with your experience with us, you can cancel your subscription. Once the immune system is compromised, however, such as in patients with tumors, leukemia, AIDS, autoimmune diseases and certain immunosuppressive treatments, the JC virus is able to alter its genetic information and infect the brain,” explains Roland Martin, professor of neurology at the University of Zurich. The so-called active vaccination method was developed at the University of Zurich and the University Hospital Zurich, and has already been used successfully on two more patients.
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.

The JC-virus-specific antibodies that are of interest for the treatment of the existing brain infection were developed by the group at the University of Zurich and the University Hospital Zurich together with colleagues from the University of Tubingen and the biotechnology company Neurimmune in Schlieren.
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. This pathogen was first isolated from the brain of a patient who was suffering from a rare brain disease known as progressive multifocal leukoencephalopathy (PML). Only if the immune system function is completely restored can the JC virus be removed from the brain.
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 virus, which more than 60 percent of the global population are infected with, normally resides in the kidneys and certain other organs.
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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