Will you give me more info on meningitis?

Question

I've heard the illness can deafen people and kill, but I wanna know more. So will you give me more information on the disease?

Answer 1

Meningitis is an inflammation of the leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF). It can be useful to divide symptom onset into acute, subacute, and chronic categories. Unlike subacute (1-7 d) or chronic (>7 d) meningitis, which have myriad infectious and noninfectious etiologies, acute meningitis (<24 h) is almost always a bacterial infection caused by one of several organisms. Depending on age and general condition, these gravely ill patients present acutely with signs and symptoms of meningeal inflammation and systemic infection of less than 1 day's duration. Patients may decompensate quickly and require emergency care, including antimicrobial therapy, within 30 minutes of emergency department (ED) presentation.

Not all bacterial meningitis is acute. Approximately 75% of patients with bacterial meningitis present subacutely. These ill patients still require urgent ED diagnosis and care.

The emergence of resistant strains has prompted changes in antibiotic protocols in some countries, including the US. Apart from dexamethasone, neuronal cell protectants still hold only future promise as adjunctive therapy.

The challenges for emergency physicians when treating meningitis are to (1) identify and treat patients with acute bacterial meningitis, (2) assess whether a central nervous system (CNS) infection is present in those with suspected subacute or chronic meningitis, and (3) identify the causative organism. Bacterial meningitis must be excluded. Emergency physicians should be aware that future therapies will be based on improved understanding of the pathogenesis of acute bacterial meningitis and may include caspase inhibitors, antioxidants, poly (ADP-ribose) polymerase inhibitors, inhibitors of lipid peroxidation, and metalloproteinase inhibitors, in addition to antibiotics and steroids.


Pathophysiology: A number of factors influence the development of bacterial meningitis, including virulence of the strain, host defenses, and bacteria-host interactions.

Bacterial seeding usually occurs by hematogenous spread. In those without an identifiable source of infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source. Rarely, infected contiguous structures invade via septic thrombi or osteomyelitic erosion; meningeal seeding also may occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the newborn is transmitted vertically from colonized pathogens in the maternal intestinal or genital tract or horizontally from nursery personnel or caregivers at home.

Once in the CSF, the paucity of antibodies, complement components, and white blood cells (WBCs) allows the bacterial infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in at least 3 critical events: increased permeability of the blood-brain barrier, cerebral edema, and presence of toxic mediators in the CSF. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process and account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose. Exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia).

As intracranial pressure (ICP) continues to rise and brain edema progresses, CNS autoregulatory processes begin to fail. This pivotal event may occur when the transient increase in cerebral blood flow (CBF) reverses and begins to decrease. CBF reduction correlates with the patient's decreasing alertness and changes in mental status.

Without medical intervention, the cycle of decreasing CBF, worsening cerebral edema, and increasing ICP proceeds unchecked. Ongoing endothelial injury may result in vasospasm and thrombosis, further compromising CBF, and may lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CBF, and the patient soon dies from systemic complications or from diffuse CNS ischemic injury.

The pathophysiologies of nonbacterial pathogens are less well understood. Fungal meningitis is thought to unfold in a manner similar to but less acute than bacterial meningitis.
Classic symptoms (not evident in infants or seen often in the elderly) include the following:
Headache
Nuchal rigidity (generally not present in children <1 y or in patients with altered mental status)
Fever and chills
Photophobia
Vomiting
Prodromal upper respiratory infection (URI) symptoms (viral and bacterial)
Seizures (30-40% in children, 20-30% in adults)
Focal neurologic symptoms (including focal seizures)
Altered sensorium (confusion may be sole presenting complaint, especially in elderly)
Symptoms in infants
Fever
Lethargy and/or change in level of alertness
Poor feeding and/or vomiting
Respiratory distress, apnea, cyanosis
Partially treated meningitis: As many as 40% of patients with meningitis were treated previously with oral antibiotics. Seizures may be the sole presenting symptom; fever and changes in level of alertness or mental status occur less commonly than in untreated meningitis.
Low-grade ventriculitis associated with ventriculoperitoneal shunt: Patients may have a less dramatic presentation than those with acute meningitis, with headache, nausea, minimal fever, and malaise.
Fungal meningitis: Headache, low-grade fever, and lethargy are the primary symptoms; the course may be mild with fluctuating symptoms, especially in immunocompromised patients.
Tuberculous meningitis: Fever, weight loss, night sweats, and malaise, with or without headache and meningismus are common symptoms; this infection may follow a protracted course with vague, nonspecific presentation.
Physical: Otherwise healthy patients within age extremes present with clinically obvious acute bacterial meningitis. In contrast, most patients with subacute bacterial meningitis present a diagnostic challenge. Systemic examination occasionally reveals a pulmonary or otitis media co-infection.

Signs of meningeal irritation
Nuchal rigidity or discomfort on neck flexion
Kernig sign: Passive knee extension in supine patient elicits neck pain and hamstring resistance.
Brudzinski sign: Passive neck or single hip flexion is accompanied by involuntary flexion of both hips.
Papilledema is present in only one third of meningitis patients with increased ICP; it takes at least several hours to develop.
Focal neurologic signs
Isolated cranial nerve abnormalities (principally III, IV, VI, VII) in 10-20% of patients
Associated with a dramatic increase in complications from lumbar puncture (LP) and portends a worse outcome
Systemic findings
Extracranial infection (eg, sinusitis, otitis media, mastoiditis, pneumonia, urinary tract infection) may be noted.
Arthritis is seen with N meningitidis, less commonly with other bacteria.
Nonblanching petechiae and cutaneous hemorrhages are seen classically with N meningitidis; however, these also can occur with other bacterial and viral infections.
Endotoxic shock with vascular collapse is characteristic of severe N meningitidis infection.
Altered mental status, from irritability to somnolence, delirium, and coma
Infants
Bulging fontanelle (if euvolemic)
Paradoxic irritability (ie, quiet when stationary, cries when held)
High-pitched cry
Hypotonia
Examine skin over entire spine for dimples, sinuses, nevi, or tufts of hair, which may indicate a congenital anomaly communicating with the subarachnoid space.
Causes: Meningitis is caused by the following pathogens in each age group:

Neonates - Group B or D streptococci, nongroup B streptococci, Escherichia coli, and L monocytogenes
Infants and children - H influenzae (48%), S pneumoniae (13%), and N meningitidis
Adults - S pneumoniae, (30-50%), H influenzae (1-3%), N meningitidis (10-35%), gram-negative bacilli (1-10%), staphylococci (5-15%), streptococci (5%), and Listeria species (5%)
Risk factors
Aged 60 years or older
Aged 5 years or younger, especially children with diabetes mellitus, renal or adrenal insufficiency, hypoparathyroidism, or cystic fibrosis
Immunosuppressed patients are at increased risk of opportunistic infections and acute bacterial meningitis. Immunosuppressed patients may not show dramatic signs of fever or meningeal inflammation.
Crowding (eg, military recruits and college dorm residents) increases risk of outbreaks of meningococcal meningitis.
Splenectomy and sickle cell disease increase the risk of meningitis secondary to encapsulated organisms.
Alcoholism and cirrhosis: Multiple etiologies of fever and seizures in these patients make meningitis challenging to diagnose.
Diabetes
Recent exposure to others with meningitis, with or without prophylaxis
Contiguous infection (eg, sinusitis)
Dural defect (eg, traumatic, surgical, congenital)

Thalassemia major
Intravenous (IV) drug abuse
Bacterial endocarditis
Ventriculoperitoneal shunt
Malignancy (increased risk of Listeria species infection)
Some cranial congenital deformities

Answer 2

really depends on the meningitis, my daughter had it about two months ago and my cousin had a different type a few years ago, my daughter recovered and is recovering a lot quicker then my cousin did!

My cousin is in his mid thirties and had a real hard time to get better, he still is not 100%. It honestly takes years and a lot of patience.

Good luck if you know someone with it.

Answer 3

You can find all the information about Meningitis on these sites :-
http://www.meningitis.org/
http://www.nlm.nih.gov/medlineplus/meningitis.html
http://www.musa.org/
http://www.nmaus.org/
For more you can search the web for Meningitis or Google it !
Best of Luck !
Take care and God Bless !

Answer 4

Here's all the info you need...http://en.wikipedia.org/wiki/Meningitis

Answer 5

meningitisis an inflammation of the meninges which are the membranes surrounding the brain and spine. can be viral or bacteria. different treatment for each. different severity and prognosis.

Answer 6

Try this website......

Answer 7

Meningitis is inflammation of the membranes (meninges) covering the brain and the spinal cord. Although the most common causes are infection (bacterial, viral, fungal or parasitic), chemical agents and even tumor cells may cause meningitis. Meningitis can produce a wide range of symptoms including fever, headache or confusion and in extreme cases, deafness, brain damage, stroke, seizures or even death. Encephalitis and brain abscess can complicate infective meningitis.

Symptoms
The classical symptoms of meningitis are headache, neck stiffness and photophobia (intolerance of bright light); the trio is called meningism. Fever and chills are often present, along with myalgia. An altered state of consciousness or other neurological deficits may be present depending on the severity of the disease. In meningococcal meningitis or septicaemia, a petechial rash may appear. A lumbar puncture to obtain cerebrospinal fluid (CSF) is usually indicated to determine the cause and direct appropriate treatment.

Convulsions and hydrocephalus are known complications of meningitis.


Diagnosis
Most important in the diagnosis of meningitis is examination of the cerebrospinal fluid. A lumbar puncture should be performed promptly whenever the diagnosis of meningitis is suspected. The opening pressure is recorded and the cerebrospinal fluid sample is taken for microscopic examination (complete blood count with differential), chemical analysis (glucose and protein) and microbiology (gram staining and bacterial cultures).

In patients with focal neurological deficits or signs of increased intracranial pressure, a CT scan of the head should be obtained to help determine if there is a raised intracranial pressure that might cause a serious or fatal brain herniation during lumbar puncture. In the absence of these signs, a CT scan is unnecessary and should not delay lumbar puncture and initiation of antibiotic therapy.


Pathophysiology
Meningitis and encephalitis are usually caused by viruses or bacteria. Most often, the body’s immune system is able to contain and defeat an infection. But if the infection passes into the blood stream and then into the cerebrospinal fluid that surrounds the brain and spinal cord, it can affect the nerves and travel to the brain and/or surrounding membranes, causing inflammation. This swelling can harm or destroy nerve cells and cause bleeding in the brain.


Pathology

Interior view of a brain with meningitis caused by Haemophilus influenzae. Source: CDCPurulent (suppurative) leptomeningitis is a diffuse purulent inflammation. The leptomeninges (arachnoid and pia matter) contain purulent exudate (pus): leukocytes (neutrophils), fibrin, germs, proteins, necrotic debris. Blood vessels in the subarachnoidian space and those intracerebral are congested and neutrophil margination is present[1].

Causes

Infectious
G020: Viruses are the most common cause of meningitis.
G00-G01: Major bacteria that cause Bacterial meningitis are Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (pneumococcus) and Haemophilus influenzae. Less-common bacterial causes include Listeria monocytogenes, Lyme disease (Borrelia burgdorferi), Staphylococcus and Escherichia coli. In developing countries, Mycobacterium tuberculosis is a common cause of bacterial meningitis. Streptococcus agalactiae is an important cause of neonatal meningitis associated with a high mortality rate.
G021:In immunocompromised patients, fungal meningitis may occur, typically caused by Cryptococcus neoformans.
There is a geographic variation in the incidence of the bacteria, e.g. in rural Thailand the most common cause is S. suis.

Non-infectious
Non-infectious causes include:

Tumors
Leukemia
Lymphoma
Brain tumors
Cerebral metastasis
Sarcoidosis
Drugs
Intrathecal drugs
Methotrexate
Lead poisoning

Treatment
Bacterial Meningitis has a high mortality rate if it goes untreated and is thus a severe medical emergency. All suspected cases, however mild, need emergency medical attention. Early treatment of bacterial meningitis is important to its outcome. Strong doses of general antibiotics may be prescribed first, followed by intravenous antibiotics in more severe cases. Broad spectrum antibiotics should be started even before the culture results are available, on the presumption that all cases are bacterial in nature, until otherwise proven. If lumbar puncture can not be performed because of raised intracranial pressure (likely due to edema or concomitant brain abscess), a broad spectrum intravenous antibiotic should be started immediately (this is often a third generation cephalosporin or, in less affluent countries, chloramphenicol). When cerebrospinal fluid gram stain, or blood or CSF culture and sensitivity results, are available and confirm the bacterial nature of the infection, then the empiric treatment can be refined by switching to more specific antibiotics. Appropriate antibiotic treatment for most types of meningitis can reduce the risk of dying from the disease to below 15 percent.

Corticosteroids such as prednisone may be ordered to relieve brain pressure and swelling and to prevent hearing loss that is common in patients with Haemophilus influenza meningitis. Pain medicine and sedatives may be given to make patients more comfortable.

Unlike bacteria, viruses cannot be killed by antibiotics. Patients with mild viral meningitis may be allowed to stay at home, while those who have a more serious infection may be hospitalized for supportive care. Patients with mild cases, which often cause only flu-like symptoms, may be treated with fluids, bed rest (preferably in a quiet, dark room), and analgesics for pain and fever. The physician may prescribe anticonvulsants such as dilantin or phenytoin to prevent seizures and corticosteroids to reduce brain inflammation. If inflammation is severe, pain medicine and sedatives may be prescribed to make the patient more comfortable.

Infection of the meninges usually originates through spread from infection of the neighbouring structures (which include the sinuses and mastoid cells of the ear). These should be investigated when diagnosis of meningitis is confirmed or suspected. Infected sinuses may need to be drained.

If the patient is commonly in contact with many others (for example at school or in army barracks), people in the surroundings (and usually family members) may be started on prophylactic treatment; this is generally done with the antibiotic rifampicin, which is otherwise mainly used in tuberculosis. Alternative drugs used for prophylaxis include ciprofloxacin and ceftriaxone. Ceftriaxone is the preferred agent for prophylaxis in pregnant women. If there is a risk of neonatal meningitis caused by Streptococcus agalactiae (Group B Streptococcus), then ampicillin, penicillin G, or clindamycin may be used during childbirth.

Vaccination
Vaccinations against Haemophilus influenzae (Hib) have decreased early childhood meningitis significantly.

Vaccines against type A and C Neisseria meningitidis, the kind that causes most disease in preschool children and teenagers in the United States, have also been around for a while. Type A is also prevalent in sub-Sahara Africa and W135 outbreaks have affected those on the Hajj pilgrimage to Mecca.

A vaccine called MeNZB for a specific strain of type B Neisseria meningitidis prevalent in New Zealand has completed trials and is being given to everyone in the country under the age of 20. There is also a vaccine, MenBVac, for the specific strain of type B meningoccocal disease prevalent in Norway, and another specific vaccine for the strain prevalent in Cuba.


Epidemiology

Western World
20,000 to 25,000 cases of bacterial meningitis are seen in the United States every year. In developing countries, the incidence is probably higher. Mostly adults are infected, where it can be community acquired or nosocomial. Vaccination against Haemophilus influenzae has reduced the incidence in children.

Meningitis may occur in outbreaks in communities who have close contact with each other, such as in dorms or military establishments. In the large majority of such outbreaks, neisseria meningitidis is the etiologic agent.

The African Meningitis Belt
The "Meningitis Belt" is an area in sub-Saharan Africa which stretches from Senegal in the west to Ethiopia in the east in which large epidemics of meningococcal meningitis occur. It contains an estimated total population of 300 million people. The largest epidemic outbreak was in 1996, when over 250,000 cases occurred and 25,000 people died as a consequence of the disease.

History
The symptoms of meningitis were recorded in the Middle Ages along with those of tuberculosis and the Black Plague, but it was first accurately identified by the Swiss Vieusseux (a scientific-literary association,) during an outbreak in Geneva, Switzerland in 1805. In the 19th Century meningitis was a scourge of the Japanese Imperial family, playing the largest role in the horrendous pre-maturity death rate the family endured. In the mid-1800s, only the Emperor Komei and two of his siblings reached maturity out of fifteen total children surviving birth. Komei's son, the Emperor Meiji, was one of two survivors out of Komei's six children, including an elder brother of Meiji who would have taken the throne had he lived to maturity. Five of Meiji's fifteen children survived, including only his third son, the Taisho Emperor, who was feeble-minded, perhaps as a result of having contracted meningitis himself. By Emperor Hirohito's generation the family was receiving modern medical attention. As the focal point of tradition in Japan, during the Tokugawa Shogunate the family was denied modern "Dutch" medical treatment then in use among the upper caste; despite extensive modernization during the Meiji Restoration the Emperor insisted on traditional medical care for his children. The inbreeding produced among the very few families considered worthy of marriage into the imperial line, most of whom were descendents from that same line and therefore none too distant cousins of one another, also played an important role.