Meningitis

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MENINGITIS

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MENINGITIS DEFINITION

Meningitis is an inflammation of the membranes (meninges) surrounding your brain and spinal cord.

The swelling associated with meningitis often triggers the “hallmark” signs and symptoms of this condition, including headache, fever and a stiff neck.

Most cases of meningitis in the U.S. are caused by a viral infection, but bacterial and fungal infections also can lead to meningitis. Depending on the cause of the infection, meningitis can get better on its own in a couple of weeks — or it can be a life-threatening emergency requiring urgent antibiotic treatment.

If you suspect that you or someone in your family has meningitis, seek medical care right away. Early treatment of bacterial meningitis can prevent serious complications.

MENINGITIS CAUSES

Meningitis is generally caused by infection of viruses, bacteria, fungi, parasites, and certain organisms. Anatomical defects or weak immune systems may be linked to recurrent bacterial meningitis. In the majority of cases the cause is a virus. However, some non-infectious causes of meningitis also exist.

Bacteria mimic human cells to get in and stay in

A study carried out by researchers at the University of Oxford and Imperial College London, England, showed how bacteria that cause bacterial meningitis mimic human cells in order to evade the body’s innate immune system.

 Viral meningitis

Although viral meningitis is the most common, it is rarely a serious infection. It can be caused by a number of different viruses, such as mosquito-borne viruses. There is no specific treatment for this type of meningitis. In the vast majority of cases the illness resolves itself within a week without any complications.

Bacterial Meningitis

Bacterial meningitis is generally a serious infection. It is caused by three types of bacteria: Haemophilusinfluenzae type b, Neisseria meningitidis, and Streptococcus pneumoniae bacteria. Meningitis caused by Neisseria meningitides is known as meningococcal meningitis, while meningitis caused by Streptococcus pneumoniae is known as pneumococcal meningitis. People become infected when they are in close contact with the discharges from the nose or throat of a person who is infected.

Twenty years ago Hib was the main cause of bacterial meningitis – it is not any more thanks to new vaccines which are routinely administered to children.

The doctor needs to know what type of meningitis has infected the patient. Certain antibiotics can stop some types from infecting others.

Bacterial meningitis in newborns and premature babies

A type of streptococci, called group B streptococci commonly inhabits the vagina and is a common cause of meningitis among premature babies and newborns during the first week of life. Escherichia coli, which inhabit the digestive tract, may also cause meningitis among newborns. Meningitis that occurs during epidemics can affect newborns – Listeria monocytogenes being the most common.

 Bacterial meningitis in children under 5

Children under five years of age in countries that do not offer the vaccine are generally infected by Haemophilusinfluenzae type B.

  Bacterial meningitis in older children

Older children generally have meningitis caused by Neisseria meningitides (meningococcus), and Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) .

Bacterial meningitis in adults

About 80% of all adult meningitis are caused by N. meningitidis and S. pneumoniae. People over 50 years of age have an increased risk of meningitis caused by L. monocytogenes.

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Bacterial meningitis and people with skull damage implanted devices

People who received a recent trauma to the skull are at increased risk of bacteria in their nasal cavity entering the meningeal space. Patients with a cerebral shunt or related device also run a higher risk of infection with staphylococciand pseudomonas through those devices.

Bacterial meningitis and weak immune systems

People with weak immune systems are also at higher risk of infection with staphylococci and pseudomonas.

Bacterial meningitis and ear infections and procedures

Rarely, otitis media, mastoiditis, or some infection to the head or neck area may lead to meningitis. People who have received a cochlear implant run a higher risk of developing pneumococcal meningitis.

A study published in Otolaryngology-Head and Neck Surgery found that children who are stricken with severe hearing loss are five times more likely to contract meningitis.

In countries where tuberculous meningitis is common, there is a higher incidence of meningitis caused byMycobacterium tuberculosis.

 Anatomical defects or disorders of the immune system

Either congenital or acquired anatomical defects may be linked to recurrent bacterial meningitis. An anatomical defect might allow a way to penetrate into the nervous system from the external environment. The most common anatomical defect which leads to meningitis is skull fracture, especially when the fracture occurs at the base of the brain, or extends towards the sinuses and petrous pyramids.

59% of recurrent meningitis cases are due to anatomical defects, while 36% are due to weakened immune systems.

 

MENINGITIS PATHOPHYSIOLOGY

Most cases of meningitis are caused by an infectious agent that has colonized or established a localized infection elsewhere in the host. Potential sites of colonization or infection include the skin, the nasopharynx, the respiratory tract, the gastrointestinal (GI) tract, and the genitourinary tract. The organism invades the submucosa at these sites by circumventing host defenses (eg, physical barriers, local immunity, and phagocytes or macrophages).

An infectious agent (ie, a bacterium, virus, fungus, or parasite) can gain access to the CNS and cause meningeal disease via any of the 3 following major pathways:

  • Invasion of the bloodstream (ie, bacteremia, viremia, fungemia, or parasitemia) and subsequent hematogenous seeding of the CNS
  • A retrograde neuronal (eg, olfactory and peripheral nerves) pathway (eg,NAEGLERIA FOWLERI or GNATHOSTOMA SPINIGERUM)
  • Direct contiguous spread (eg, sinusitis, otitis media, congenital malformations, trauma, or direct inoculation during intracranial manipulation)

Invasion of the bloodstream and subsequent seeding is the most common mode of spread for most agents. This pathway is characteristic of meningococcal, cryptococcal, syphilitic, and pneumococcal meningitis.

Rarely, meningitis arises from invasion via septic thrombi or osteomyelitic erosion from infected contiguous structures. Meningeal seeding may also occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the newborn may be transmitted vertically, involving pathogens that have colonized the maternal intestinal or genital tract, or horizontally, from nursery personnel or caregivers at home.

Local extension from contiguous extracerebral infection (eg, otitis media, mastoiditis, or sinusitis) is a common cause. Possible pathways for the migration of pathogens from the middle ear to the meninges include the following:

  • The bloodstream
  • Preformed tissue planes (eg, posterior fossa)
  • Temporal bone fractures
  • The oval or round window membranes of the labyrinths

The brain is naturally protected from the body’s immune system by the barrier that the meninges create between the bloodstream and the brain. Normally, this protection is an advantage because the barrier prevents the immune system from attacking the brain. However, in meningitis, the blood-brain barrier can become disrupted; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread.

When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, WBCs, and other infection-fighting particles to enter the meninges and brain. This process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection.

Depending on the severity of bacterial meningitis, the inflammatory process may remain confined to the subarachnoid space. In less severe forms, the pial barrier is not penetrated, and the underlying parenchyma remains intact. However, in more severe forms of bacterial meningitis, the pial barrier is breached, and the underlying parenchyma is invaded by the inflammatory process. Thus, bacterial meningitis may lead to widespread cortical destruction, particularly when left untreated.

Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis. These processes account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose in patients with this disease.

Exudates extend throughout the CSF, particularly to the basal cisterns, resulting in the following:

  • Damage to cranial nerves (eg, cranial nerve VIII, with resultant hearing loss)
  • Obliteration of CSF pathways (causing obstructive hydrocephalus)
  • Induction of vasculitis and thrombophlebitis (causing local brain ischemia)

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INTRACRANIAL PRESSURE AND CEREBRAL FLUID

One complication of meningitis is the development of increased intracranial pressure (ICP). The pathophysiology of this complication is complex and may involve many proinflammatory molecules as well as mechanical elements. Interstitial edema (secondary to obstruction of CSF flow, as in hydrocephalus), cytotoxic edema (swelling of cellular elements of the brain through the release of toxic factors from the bacteria and neutrophils), and vasogenicedema (increased blood brain barrier permeability) are all thought to play a role.

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

CEREBRAL EDEMA

The increased CSF viscosity resulting from the influx of plasma components into the subarachnoid space and diminished venous outflow lead to interstitial edema. The accumulation of the products of bacterial degradation, neutrophils, and other cellular activation leads to cytotoxic edema.

The ensuing cerebral edema (ie, vasogenic, cytotoxic, and interstitial) significantly contributes to intracranial hypertension and a consequent decrease in cerebral blood flow. Anaerobic metabolism ensues, which contributes to increased lactate concentration and hypoglycorrhachia. In addition, hypoglycorrhachia results from decreased glucose transport into the spinal fluid compartment. Eventually, if this uncontrolled process is not modulated by effective treatment, transient neuronal dysfunction or permanent neuronal injury results.

CYTOKINES AND SECONDARY MEDIATORS IN BACTERIAL MENINGITIS

Key advances in understanding the pathophysiology of meningitis include insight into the pivotal roles of cytokines (eg, tumor necrosis factor alpha [TNF-α] and interleukin [IL]-1), chemokines (IL-8), and other proinflammatory molecules in the pathogenesis of pleocytosis and neuronal damage during occurrences of bacterial meningitis.

Increased CSF concentrations of TNF-α, IL-1, IL-6, and IL-8 are characteristic findings in patients with bacterial meningitis. Cytokine levels, including those of IL-6, TNF-α, and interferon gamma, have been found to be elevated in patients with aseptic meningitis.

The proposed events involving these inflammation mediators in bacterial meningitis begin with the exposure of cells (eg, endothelial cells, leukocytes, microglia, astrocytes, and meningeal macrophages) to bacterial products released during replication and death; this exposure incites the synthesis of cytokines and proinflammatory mediators. This process is likely initiated by the ligation of the bacterial components (eg, peptidoglycan and lipopolysaccharide) to pattern-recognition receptors, such as the Toll-like receptors (TLRs).

TNF-α and IL-1 are most prominent among the cytokines that mediate this inflammatory cascade. TNF-α is a glycoprotein derived from activated monocyte-macrophages, lymphocytes, astrocytes, and microglial cells.

IL-1, previously known as endogenous pyrogen, is also produced primarily by activated mononuclear phagocytes and is responsible for the induction of fever during bacterial infections. Both IL-1 and TNF-α have been detected in the CSF of individuals with bacterial meningitis. In experimental models of meningitis, they appear early during the course of disease and have been detected within 30-45 minutes of intracisternal endotoxin inoculation.

Many secondary mediators, such as IL-6, IL-8, nitric oxide, prostaglandins (eg, prostaglandin E2 [PGE2]), and platelet activation factor (PAF), are presumed to amplify this inflammatory event, either synergistically or independently. IL-6 induces acute-phase reactants in response to bacterial infection. The chemokine IL-8 mediates neutrophil chemoattractant responses induced by TNF-α and IL-1.

Nitric oxide is a free radical molecule that can induce cytotoxicity when produced in high amounts. PGE2, a product of cyclooxygenase (COX), appears to participate in the induction of increased blood-brain barrier permeability. PAF, with its myriad biologic activities, is believed to mediate the formation of thrombi and the activation of clotting factors within the vasculature. However, the precise roles of all these secondary mediators in meningeal inflammation remain unclear.

The net result of the above processes is vascular endothelial injury and increased blood-brain barrier permeability, leading to the entry of many blood components into the subarachnoid space. In many cases, this contributes to vasogenicedema and elevated CSF protein levels. In response to the cytokines and chemotactic molecules, neutrophils migrate from the bloodstream and penetrate the damaged blood-brain barrier, producing the profound neutrophilicpleocytosis characteristic of bacterial meningitis.

GENETIC PREDISPOSITION TO INFLAMMATORY RESPONSE

The inflammatory response and the release of proinflammatory mediators are critical to the recruitment of excess neutrophils to the subarachnoid space. These activated neutrophils release cytotoxic agents, including oxidants and metalloproteins that cause collateral damage to brain tissue.

Pattern recognition receptors, of which TLR A4 (TLRA4) is the best studied, lead to increase in the myeloid differentiation 88 (MyD88)-dependent pathway and excess production of proinflammatory mediators. At present, dexamethasone is used to decrease the effects of cellular toxicity by neutrophils after they are present. Researchers are actively seeking ways of inhibiting TLRA4 and other proinflammatory recognition receptors through genetically engineered suppressors.[4]

BACTERIAL SEEDING

Bacterial seeding of the meninges usually occurs through hematogenous spread. In patients without an identifiable source of infection, local tissue and bloodstream invasion by bacteria that have colonized the nasopharynx may be a common source. Many meningitis-causing bacteria are carried in the nose and throat, often asymptomatically. Most meningeal pathogens are transmitted through the respiratory route, including NEISSERIA MENINGITIDIS (meningococcus) and S PNEUMONIAE (pneumococcus).

Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment, presumably by damaging mucosal defenses. Once in the bloodstream, the infectious agent must escape immune surveillance (eg, antibodies, complement-mediated bacterial killing, and neutrophil phagocytosis).

Subsequently, hematogenous seeding into distant sites, including the CNS, occurs. The specific pathophysiologic mechanisms by which the infectious agents gain access to the subarachnoid space remain unclear. Once inside the CNS, the infectious agents likely survive because host defenses (eg, immunoglobulins, neutrophils, and complement components) appear to be limited in this body compartment. The presence and replication of infectious agents remain uncontrolled and incite the cascade of meningeal inflammation described above.

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MENINGITIS SYMPTOMS

It’s easy to mistake the early signs and symptoms of meningitis for the flu (influenza). Meningitis signs and symptoms may develop over several hours or over one or two days.

The signs and symptoms that may occur in anyone older than age of 2 include:

  • Sudden high fever
  • Severe headache that isn’t easily confused with other types of headache
  • Stiff neck
  • Vomiting or nausea with headache
  • Confusion or difficulty concentrating
  • Seizures
  • Sleepiness or difficulty waking up
  • Sensitivity to light
  • Lack of interest in drinking and eating
  • Skin rash in some cases, such as in meningococcal meningitis

SIGNS IN NEWBORNS

Newborns and infants may not have the classic signs and symptoms of headache and stiff neck. Instead, signs of meningitis in this age group may include:

  • High fever
  • Constant crying
  • Excessive sleepiness or irritability
  • Inactivity or sluggishness
  • Poor feeding
  • A bulge in the soft spot on top of a baby’s head (fontanel)
  • Stiffness in a baby’s body and neck

Infants with meningitis may be difficult to comfort, and may even cry harder when picked up.

MENINGITIS DIAGNOSIS

A procedure called a lumbar puncture, or spinal tap, will help determine whether someone has meningitis. During the procedure, an area of the lower back is injected with an anesthetic, and a needle is slipped between two bones in the spine to obtain a small sample of spinal fluid. The fluid is normally clear, so if it appears cloudy and contains white blood cells, you may have meningitis.

 

Lab analysis will help determine which specific type of meningitis you have — bacterial, viral, or fungal. Samples of blood, urine, and secretions from your nose or ears may also be taken. Because the disease can progress very rapidly, treatment will begin immediately — even before the results of the tests are known.

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MENINGITIS TREATMENT

The treatment depends on the type of meningitis you or your child has.

BACTERIAL MENINGITIS

Acute bacterial meningitis requires prompt treatment with intravenous antibiotics and, more recently, cortisone medications, to ensure recovery and reduce the risk of complications, such as brain swelling and seizures. The antibiotic or combination of antibiotics that your doctor may choose depends on the type of bacteria causing the infection. Your doctor may recommend a broad-spectrum antibiotic until he or she can determine the exact cause of the meningitis.

Infected sinuses or mastoids — the bones behind the outer ear that connect to the middle ear — may need to be drained.

VIRAL MENINGITIS

Antibiotics can’t cure viral meningitis, and most cases improve on their own in several weeks. Treatment of mild cases of viral meningitis usually includes:

  • Bed rest
  • Plenty of fluids
  • Over-the-counter pain medications to help reduce fever and relieve body aches

If the cause of your meningitis is a herpes virus, an antiviral medication is available.

OTHER TYPES OF MENINGITIS

If the cause of your meningitis is unclear, your doctor may start antiviral and antibiotic treatment while a cause is being determined.

Fungal meningitis is treated with antifungal medications. However, these medications can have serious side effects, so treatment may be deferred until a laboratory can confirm that the cause is fungal. Chronic meningitis is treated based on the underlying cause, which is often fungal.

Noninfectious meningitis due to allergic reaction or autoimmune disease may be treated with cortisone medications. In some cases, no treatment may be required, because the condition can resolve on its own. Cancer-related meningitis requires therapy for the individual cancer.

 

By Medifit Education

www.themedifit.in