contagious, spread via tiny drops of fluid from the throat and nose of someone who is infected. The drops may become airborne when the person coughs, laughs, talks, or sneezes. They then can infect others when people breathe them in or touch the drops and then touch their own noses or mouths.
spread between people who are in close contact, such as those who live together or people who are exposed by kissing
N. meningitidis cause epidemics of meningitis. In particular in a crowded day-care situation or a military recruit in a crowded training camp,schools,colleges has fallen ill with meningococcal meningitis
Meningococcus is the bacteria that has caused outbreaks across North America over the last 8 - 10 years including most recently. Understandably the presence of a meningitis epidemic in a community is very scary to parents
Most of the viruses that cause meningitis live in the intestines and tend to be passed on as a result of poor hygiene. Many different viruses can cause viral meningitis, most commonly enteroviruses that normally live harmlessly in people's bowels
L. monocytogenes has been associated with such foods as raw milk, pasteurized fluid milk,cheeses (particularly soft-ripened varieties), ice cream, raw vegetables, fermented raw-meat sausages, raw and cooked poultry, raw meats (of all types), and raw and smoked fish. Its ability to grow at temperatures as low as 0°C permits multiplication in refrigerated foods. In refrigeration temperature such as 4°C the amount of ferric iron promotes the growth of L. monocytogenes.
skull fractures possess abnormal openings to the sinuses, nasal passages, and middle ears. Organisms can pass through openings and cause infection. surgical procedures or who have had foreign bodies surgically placed within their skulls (such as tubes to drain abnormal amounts of accumulated CSF) have an increased risk of meningitis.
also via an uncommon but interesting method called intraneural spread. This involves an organism invading the body at a considerable distance away from the head, spreading along a nerve, and using that nerve as a kind of ladder into the skull, where the organism can multiply and cause meningitis. Herpes simplex virus is known to use this type of spread, as is the rabies virus.
Streptococcus agalactiae (also known as Group B streptococcus) is a beta-hemolytic gram-positive streptococcus.
S. agalactiae is a species of the normal flora of the female urogenital tract and rectum. Its chief clinical importance is that it can be transferred to a neonate passing through the birth canal and can cause serious group B streptococcal infection.
In the western world, S. agalactiae is a major cause of bacterial septicemia of the newborn, which can lead to death or long-term sequelae such as hearing loss. S. agalactiae can also cause neonatal meningitis, which does not present with the hallmark sign of adult meningitis, a stiff neck
rather, it presents with nonspecific symptoms such as fever, vomiting and irritability and can consequently go undiagnosed until it is too late. Somewhat more rarely, S. agalactiae can also cause invasive group B streptococcal disease of the adult in the pregnant, elderly, or immunosuppressed.
The virus or bacteria replicates in the initial organ system (ie, respiratory or gastrointestinal mucosa) and gains access to the bloodstream. Primary viremia or bacteremia introduces the virus or bacteria to the reticuloendothelial organs (liver, spleen, and lymph nodes.)
If the replication persists despite immunologic defenses, secondary bacteremia or viremia occurs, which is thought to be responsible for seeding of the CNS. Rapid viral replication likely plays a major role in overcoming the host defenses.
exudative pus of dead cells ,fluid,fibrin and leucocytes (pus) cause thick whitish grey layer that covers the leptomeninges over the surface of brain and filling sulci and basal cisterns with swollen edematous brain.
damage to neurons can take place if extending to brain cells resulting in their degeneration.
The white appearance of this calf brain is caused by neutrophils within the meninges – a condition known as meningitis. This is usually due to a bacterial infection.
This calf brain shows similar pathology. If a glass slide is pressed to the surface of the brain and stained it would show high numbers of neutrophils.
Bovine This brain shows irregular red spots which are areas of hemorrhage and necrosis caused by the bacteria, Histophilus somni .
if infection becomes localised in brain then can lead to abcess formation especially in case of direct infections.
immune system tries to confine this localised infection therefore may develop fibrous wall around it with perivascular chronic inflamatory cells around it,leading to brain abcess with central suppuration and liqufication due to death of cells .healing may occur with fibrous scar.
With time, a connective tissue capsule is formed by collagen laid down by infiltrating fibroblasts. Often this is more perfectly formed on the outer aspect of the abscess, presumably due to the contribution of the reservoir of potential in the adjacent meninges.
Due to the poor encapsulation of the medial aspect of an abscess, which abuts upon or is located within the cerebral white matter, the infection tends to form daughter or satellite abscesses medially which may eventually rupture into the ventricular system
The image above shows a large abscess in the brain. The purulent center is surrounded by a capsule. Often a zone of hyperemia is present adjacent to the wall and there is marked swelling of the adjacent brain tissue
It is produced in the brain by modified ependymal cells in the choroid plexus (approx. 50-70%), and the remainder is formed around blood vessels and along ventricular walls. It circulates from the choroid plexus through the interventricular foramina (foramen of Monro) into the third ventricle, and then through the cerebral aqueduct (aqueduct of Sylvius) into the fourth ventricle, where it exits through two lateral apertures (foramina of Luschka) and one median aperture (foramen of Magendie).
The cerebrospinal fluid is produced at a rate of 500 ml/day. Since the brain can only contain from 135-150 ml, large amounts are drained primarily into the blood through arachnoid granulations in the superior sagittal sinus. Thus the CSF turns over about 3.7 times a day.
ICP monitoring requires admission to the hospital. A small pressure monitor is inserted through the skull into the brain or ventricles to measure the ICP. pressure monitoring (either by lumbar catheter or the intracranial method) can detect an abnormal pattern of pressure waves.
The "gold standard" technique for ICP monitoring is a catheter inserted into the lateral ventricle, usually via a small right frontal burr hole. This can be connected to a standard pressure transducer via a fluid-filled catheter in neurosurgery.
The two principal objections to lumbar puncture in the diagnosis of intracranial hypertension have been the danger of inducing brain-stem compression through tentorial or tonsillar herniation and the contention that spinal fluid pressure is not always an accurate reflection of ICP.
7.Sterilize the field using the sterilizing solution and sponges provided. Clean a 6 inch area around the desired entry site, proceeding outward in concentric circles. Do this 3 separate times. Place sterile drape over the field.
8. Ensure all items in LP tray are ready for use. E.g.. 1% or 2% lidocaine loaded into syringe, collection tubes open, test to see that the stylet slides in/out of LP needle easily, stopcock and manometer for opening pressure measurement ready
9.Local anaesthesia. Using a 25G needle, inject 1% or 2% lidocaine under the skin at the desired entry site. A small bleb under the skin is sufficient. Switch the needle tip to the 22G needle and anaesthetize deeper structures by inserting the needle further, injecting lidocaine while proceeding forward.
10.Insert LP needle. The bevel should be parallel to the spinal column. Always advance the needle with the stylet in place. Aim needle in the midline, slightly cephalad, towards the patient’s umbilicus. Advance needle slowly until it is inserted 2-3 cm, then withdraw the stylet to check for CSF return. Continue to advance the needle, periodically checking for CSF return. Often a "pop'' is appreciated as the needle pierces the dural membrane.
The Xpert EV test, approved for use in March 2007, can rapidly test for enteroviral meningitis. The test uses a reverse-transcription PCR disposable cartridge on which CSF is applied, and enteroviral genetic material is identified if present. Results are ready in 2.5 hours, as opposed to days to weeks in traditional PCR studies.
MRI with contrast is the criterion standard in visualizing intracranial pathology in viral encephalitis HSV-1 commonly affects basal frontal and temporal lobes with a typical picture of diffusely enhancing bilateral lesions.
Additional serum collection 10-21 days later may aid in discerning rising titers in the antibodies against specific viral pathogens; a 4-fold increase in viral antibodies confirms the diagnosis. This is particularly useful for arboviral and LCMV cases, but also is helpful in ruling out toxoplasmosis, leptospirosis, borreliosis, and rickettsial infections. Although some of these studies do not yield an immediate result for clinical decision making, they may be useful for prognostication.
Therapy can be modified as the results of Gram stain, cultures, and PCR testing become available. Patients in unstable condition need critical care unit admission for airway protection, neurologic checks, and prevention of secondary complications.
Cerebral edema does occur in cases of severe encephalitis and may require intracranial pressure control by infusion of mannitol (1 g/kg initial dose followed by 0.25-0.5 g/kg 6 hrly), IV dexamethasone, or intubation and mild hyperventilation, with arterial PCO2 around 28-30 mm Hg