bacterial meningitis-basic info n research
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Bacterial meningitis remains a disease with associated unacceptable morbidity and
mortality rates despite the availability of effective bactericidal antimicrobial therapy.
Through the use of experimental animal models of infection, a great deal of information
has been gleaned concerning the pathogenic and pathophysiologic mechanisms
operable in bacterial meningitis. Most cases of bacterial meningitis begin with hostacquisition of a new organism by nasopharyngeal colonization followed by systemic
invasion and development of a high-grade bacteremia. Bacterial encapsulation
contributes to this bacteremia by inhibiting neutrophil phagocytosis and resisting classic
complement-mediated bactericidal activity. Central nervous system invasion then
occurs, although the exact site of bacterial traversal into the central nervous system is
unknown. By production and/or release of virulence factors into and stimulation of
formation of inflammatory cytokines within the central nervous system, meningeal
pathogens increase permeability of the blood-brain barrier, thus allowing protein and
neutrophils to move into the subarachnoid space. There is then an intense subarachnoid
space inflammatory response, which leads to many of the pathophysiologic
consequences of bacterial meningitis, including cerebral edema and increased
intracranial pressure. Attenuation of this inflammatory response with adjunctive
dexamethasone therapy is associated with reduced concentrations of tumor necrosis
factor in the cerebrospinal fluid, with diminished cerebrospinal fluid leukocytosis, and
perhaps with improvement of morbidity, as demonstrated in recent clinical trials.
Further information on the pathogenesis and pathophysiology of bacterial meningitis
should lead to the development of more innovative treatment and/or preventive
strategies for this disorder.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=358273
Bacterial surface components, complement, and inflammatory cytokines (eg, tumor necrosis factor, IL-1)
draw neutrophils into the CSF space. The neutrophils release metabolites that damage cell membranes
including those of the vascular endothelium. The result is vasculitis and thrombophlebitis, causing focal
ischemia or infarction, and brain edema. Vasculitis also disrupts the blood-brain barrier, further increasing
brain edema. The purulent exudate in the CSF blocks CSF reabsorption by the arachnoid villi, causing
hydrocephalus. Brain edema and hydrocephalus increase intracranial pressure.
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Systemic complications include hyponatremia due to the syndrome of inappropriate antidiuretic hormone
(SIADH), disseminated intravascular coagulation (DIC), and septic shock. Occasionally, bilateral adrenal
hemorrhagic infarction (Waterhouse-Friderichsen syndrome) results.
http://www.merck.com/mmpe/sec16/ch218/ch218b.html
Three major pathways exist by which an infectious agent (ie, bacteria, virus, fungus, parasite) gains
access to the central nervous system (CNS) and causes disease.
Initially, the infectious agent colonizes or establishes a localized infection in the host. This may be in
the form of colonization or infection of the skin, nasopharynx, respiratory tract, gastrointestinal tract,
or genitourinary tract. Most meningeal pathogens are transmitted through the respiratory route, as
exemplified by the nasopharyngeal carriage ofNeisseria meningitides (meningococcus) and
nasopharyngeal colonization with S pneumoniae(pneumococcus).
From this site, the organism invades the submucosa by circumventing host defenses (eg, physical
barriers, local immunity, phagocytes/macrophages) and gains access to the CNS by (1) invasion of
the bloodstream (ie, bacteremia, viremia, fungemia, parasitemia) and subsequent hematogenous
seeding of the CNS, which is the most common mode of spread for most agents (eg,
meningococcal, cryptococcal, syphilitic, and pneumococcal meningitis); (2) a retrograde neuronal (ie,
olfactory and peripheral nerves) pathway (eg, Naegleria fowleri, Gnathostoma spinigerum); or (3)
direct contiguous spread (ie, sinusitis, otitis media, congenital malformations, trauma, direct
inoculation during intracranial manipulation).
Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular
compartment, presumably by damaging mucosal defenses. Once inside the bloodstream, the
infectious agent must escape immune surveillance (eg, antibodies, complement-mediated bacterial
killing, neutrophil phagocytosis). Subsequently, hematogenous seeding into distant sites occurs,
including the CNS. The specific pathophysiologic mechanisms by which the infectious agents gain
access into the subarachnoid space remain unclear.
Once inside the CNS, the infectious agents likely survive because host defenses (eg,
immunoglobulins, neutrophils, complement components) appear to be limited in this body
compartment. The presence and replication of infectious agents remain uncontrolled and incite a
cascade of meningeal inflammation. This process of meningeal inflammation has been an area ofextensive investigation in recent years that has led to a better understanding of meningitis
pathophysiology.
Key advances in the pathophysiology of meningitis include the pivotal role of cytokines (eg, tumor
necrosis factor-alpha [TNF-alpha], interleukin [IL]1), chemokines (IL-8), and other proinflammatory
molecules in the pathogenesis of pleocytosis and neuronal damage during bacterial meningitis.
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Increased CSF concentrations of TNF-alpha, IL-1, IL-6, and IL-8 are characteristic findings in
patients with bacterial meningitis.
The proposed interplay among these mediators of inflammation is as follows:
y The exposure of cells (eg, endothelium, leukocytes, microglia, astrocytes, meningealmacrophages) to bacterial products released during replication and death incites the
synthesis of cytokines and proinflammatory mediators. Recent data indicate that this process
is likely initiated by the ligation of the bacterial components (eg, peptidoglycan,
lipopolysaccharide) to pattern-recognition receptors such as the Toll-like receptors.
y TNF-alpha and IL-1 are the most prominent among the cytokines that mediate this
inflammatory cascade. TNF-alpha 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 molecules 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.
y Many secondary mediators, such as IL-6, IL-8, nitric oxide, prostaglandins (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-alpha and IL-1. Nitric oxide is a free radical molecule that can induce cytotoxicity when
produced in high amounts. PGE2, a product of cyclooxygenase, appears to participate in the
induction of increased blood-brain barrier (BBB) permeability. PAF, with its myriad of 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 inmeningeal inflammation remain unclear and should be investigated further.
y Overall, the net result is vascular endothelial injury and increased BBB permeability leading
to the entry of many blood components into the subarachnoid space. In many patients, this
contributes to vasogenic edema and elevated CSF protein levels. In response to the
cytokines and chemotactic molecules, neutrophils migrate from the bloodstream and
penetrate the damaged BBB, producing the profound neutrophilic pleocytosis characteristic
of bacterial meningitis. The increased CSF viscosity resulting from the influx of plasma
components into the subarachnoid space and diminished venous outflow lead to interstitial
edema, and the products of bacterial degradation, neutrophils, and other cellular activation
lead to cytotoxic edema.
y The ensuing cerebral edema (ie, vasogenic, cytotoxic, 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.
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y The level of cytokines, including IL-6, TNF-alpha, and interferon-gamma, has been found to
be elevated in patients with aseptic meningitis.
Another important component or 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 toobstruction 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 vasogenic edema
(increased BBB permeability) are all thought to play a role in the development of increased ICP.
http://emedicine.medscape.com/article/232915-overview
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BACTERIAL MENINGITIS
Bacterial meningitis is the infection of the arachnoid membrane, subarachnoid space,
and cerebrospinal fluid by bacteria. 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. It extends from the optic chiasm to the cauda equina and
surrounds the brain and spinal cord completely.Meningitis may have a focal origin (sinusitis, mastoiditis, brain abscess, penetrating injury,
congenital defect), but more commonly results from hematogenous dissemination. The most
common organisms of bacterial meningitis in children and adults are Streptococcus
pneumoniae and Neisseria meningitidis. Streptococcus pneumoniae is declining after the
introduction of conjugated vaccines. Hemophilus influenzae, once very common in children, is
now rare thanks to vaccination. In newborns, the most common organisms areEschericia coliand beta hemolytic Streptococcus group B. Babies are frequently infected during passage
through the birth canal.
PATHOGENESIS. The organisms that cause bacterial meningitis colonize the nasopharynx. From
there, they get into the blood stream and enter the subarachnoid space through complex
interactions with endothelial cells. The porous structure of choroid plexus capillaries facilitates
their spillage into the CSF. The CSF is an ideal medium for the spread of bacteria because it
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provides enough nutrients for their multiplication and has few phagocytic cells, and low levels of
antibodies and complement. Initially, bacteria multiply uninhibited and can be identified in
smears, cultures, or by ELISA detection of their antigens before there is any inflammation.
When bacteria die, lipids and oligosaccharides, including endotoxin, are released from their walls.
Some of these components cause vascular injury and shock. Symptoms of sepsis may develop
and even death from gram-negative shock may occur before any inflammation appears. Bacterial
cell wall components also induce meningeal macrophages, astrocytes, and microglial cells to
produce interleukin-1 (IL-1), tumor necrosis factor(TNF-), and other inflammatory mediators.
These cytokines attract circulating granulocytes and monocytes into the CSF. As they lyse,
granulocytes and monocytes release powerful lysosomal enzymes and free radicals, which
destroy neural tissue and damage blood vessels. Polyunsaturated fatty acids released from the
membranes of dying neutrophils also cause increased vascular permeability. The results of
vascular injury are increased permeability (cerebral edema) and vasculitis (ischemia).
The results of inflammation are tissue and vascular injury (vasculitis) and increased
intracranial pressure. Brain tissue, cranial nerve, and vascular injury is caused by lysosomal
enzymes and free radicals released by granulocytes and monocytes. Increased intracranialpressure is caused by increased vascular permeability and leakage of proteins in the
interstitial space (cerebral edema) and CSF. Vasculitis causes infarcts and increased intracranial
pressure causes or aggravates hypoxic-ischemic encephalopathy (HIE).
CLINICAL FINDINGS. The initial symptoms of meningitis are fever,severe headache,
and stiff neck. 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 or
bending the neck. As the disease progresses, confusion, coma, and seizures develop. These
complications are due to HIE, increased intracranial pressure, and a toxic metabolic
encephalopathy. HIE is due to shock. The toxic metabolic encephalopathy is probably caused
by unknown diffusible substances (perhaps cytokines) that have a neurotoxic action.
DIAGNOSIS AND PATHOLOGY. The cornerstone in the diagnosis of bacterial meningitis is CSF
examination. The CSF in meningitis shows hundreds, even thousands of neutrophils and is
teeming with organisms. CSF protein is elevated and glucose is low(because it is consumed
by inflammatory cells).
Bacteria in the CSF Inflammatory cells in thesubarachnoid space
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This purulent exudate covers the
cerebral hemispheres and settles
along the base of the brain, around
cranial nerves and the openings of
the fourth ventricle. TheMRI shows
enhancement and high FLAIR signal
intensity in the meninges,
corresponding to the pathology.
A child presenting with fever,
headache, and CSF pleocytosis is a
diagnostic dilemma. Less than 5% of such cases are due to bacterial meningitis and the rest are
due to viral (aseptic) meningitis (see viral infections). Yet, to play it safe, physicians admit such
patients to hospital and treat them with antibiotics. Unnecessary hospitalizations can be avoided
if a standard set of criteria are taken into account. These are: CSF positive Gram stain, CSF
absolute neutrophil count (ANC) >100 cells/L, CSF protein >80 mg/dL, peripheral blood ANC
>10,000, and a history of preceding seizure. The presence of these findings strongly favors
bacterial meningitis. Alternatively, viral PCR of CSF, which has a turnaround time of a few hours,
can confirm aseptic meningitis.
The late complications of meningitis
include cranial nerve deficits and
ischemic infarction. 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. This
causeshydrocephalus. These
complications take time to develop and
may appear after the inflammation hassubsided.
They may be prevented by prompt treatment. The effects of HIE and
cerebral infarction are especially devastating in newborn babies in whom
the brain can literally melt away.
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. Undamaged, it provides an effective barrier
that prevents the infection from spreading into brain tissue. Thus, brain
abscess as a complication of meningitis is rare.
Brain damage in meningitis is caused not only by bacteria but probably
more by host responses. These responses have a protective purpose (toeliminate bacteria) but are excessive and indiscriminate and set in motion
destructive cascades that damage everything in their way, mostly host tissues. Modulating these
reactions, in addition to killing bacteria, can reduce the morbidity and mortality of meningitis.
BRAIN ABSCESS
Brain abscess is a newly formed cavity in brain tissue, filled with pus. The bacteria that cause
brain abscess spread from adjacent air sinuses or the middle ear, or via the blood stream from
Meningitis-purulent exudate Meningitis-purulent exudate
Postmeningitic
hydrocephalus
Vascular narrowing after
meningitis
Severe brain atrophypost neonatal
meningitis
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the lungs (bronchiectasis, lung abscess), or from the heart (bacterial endocarditis). The location
of the abscess corresponds to its source. Frontal sinusitis causes frontal lobe abscess, and
mastoiditis temporal lobe abscess. Hematogenous abscesses are often multiple.
Abscess, early phaseTemporal lobe abscess
Multiple absceses post
meningitis
The bacterial flora of brain abscess depends on the source of the infection. In the case of
sinusitis and otitis, it is usually mixed, including anaerobes. Bacteremia alone does not cause
brain abscess. Some tissue damage, probably a small ischemic lesion, is required to start the
process. Bacteria in the blood seed this necrotic nidus and spread around it causing brain
necrosis and acute inflammation (cerebritis). The necrotic center cavitates while, at theperiphery, a vascular zone of brain tissue with macrophages, mononuclear cells, and reactive
astrocytes contains the infection. 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.
Increased vascular permeability in the inflamed tissue causescerebral
edema. 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). Systemic antibiotics are effective in the phase of cerebritis.
Once a capsule develops, it is a barrier to antibiotics. Thus, the treatment of
chronic abscess requires drainage or surgical excision in addition to systemic
antibiotics.Brain abscess causes loss of neurological function due to destruction of brain
tissue. More important, it causes increased intracranial pressure. Its mass
effect is due to the collection of pus and to cerebral edema around the abscess. Since the
infection is contained within brain tissue, the CSF usually shows only a few mononuclear cells
with normal protein and glucose.
http://www.neuropathologyweb.org/chapter5/chapter5aSuppurative.html
Bacterial Meningitis
y Bacterial meningitis is a serious infection of the fluid in the spinal cord and the
fluid that surrounds the brain.
Brain abscess
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y Bacterial meningitis is most commonly caused by one of three types of
bacteria: Haemophilus influenzae type b, Neisseria meningitidis,
and Streptococcus pneumoniae bacteria.
y The bacteria are spread by direct close contact with the discharges from the nose
or throat of an infected person.
y Bacterial meningitis can be treated with antibiotics.
y Prevention depends on use of vaccines, rapid diagnosis, and prompt treatment of
close personal contacts.
What is bacterial meningitis?
Meningitis is an infection of the fluid in the spinal cord and the fluid that surrounds the
brain. Meningitis is usually caused by an infection with a virus or a bacterium. Knowing
whether meningitis is caused by a virus or a bacterium is important because ofdifferences in the seriousness of the illness and the treatment needed.
VIRAL MENINGITIS is usually relatively mild. It clears up within a week or two
without specific treatment. Viral meningitis is also called aseptic meningitis.
BACTERIAL MENINGITIS is much more serious. It can cause severe disease that can
result in brain damage and even death.
What bacteria cause bacterial meningitis?
Bacterial meningitis is most commonly caused by one of three types of
bacteria:Haemophilus influenzae type b (Hib),Neisseria meningitidis, and Streptococcus
pneumoniae.
Before the 1990s, Hib was the leading cause of bacterial meningitis, but new vaccines
being given to children as part of their routine immunizations have reduced the
occurrence of serious Hib disease. Today,Neisseria meningitidis and Streptococcus
pneumoniae are the leading causes of bacterial meningitis. Meningitis caused
byNeisseria meningitidis is also called MENINGOCOCCAL MENINGITIS. Meningitis
caused by Streptococcus pneumoniae is called PNEUMOCOCCAL MENINGITIS.
It is important to know which type of bacteria is causing the bacterial meningitis because
antibiotics can prevent some types from spreading and infecting other people.
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Where is bacterial meningitis found?
Bacterial meningitis is found worldwide. The bacteria often live harmlessly in a person's
mouth and throat. In rare instances, however, they can break through the body's immune
defenses and travel to the fluid surrounding the brain and spinal cord. There they begin to
multiply quickly. Soon, the thin membrane that covers the brain and spinal cord(meninges) becomes swollen and inflamed, leading to the classic symptoms of
meningitis.
How do people get bacterial meningitis?
The bacteria are spread by direct close contact with the discharges from the nose or throat
of an infected person. Fortunately, none of the bacteria that cause meningitis are very
contagious, and they are not spread by casual contact or by simply breathing the airwhere a person with meningitis has been.
What are the signs and symptoms of bacterial meningitis?
In persons over age 2, common symptoms are high fever, headache, and stiff neck. These
symptoms can develop over several hours, or they may take 1 to 2 days. Other symptoms
can include nausea, vomiting, sensitivity to light, confusion, and sleepiness. In advanced
disease, bruises develop under the skin and spread quickly.
In newborns and infants, the typical symptoms of fever, headache, and neck stiffness may
be hard to detect. Other signs in babies might be inactivity, irritability, vomiting, and
poor feeding.
As the disease progresses, patients of any age can have seizures.
Who is at risk for bacterial meningitis?
Anyone can get bacterial meningitis, but it is most common in infants and children.
People who have had close or prolonged contact with a patient with meningitis caused by
Neisseria meningitidis or Hib can also be at increased risk. This includes people in the
same household or day-care center, or anyone with direct contact with discharges from a
meningitis patient's mouth or nose.
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How is bacterial meningitis diagnosed?
The diagnosis is usually made by growing bacteria from a sample of spinal fluid. The
spinal fluid is obtained by a spinal tap. A doctor inserts a needle into the lower back and
removes some fluid from the spinal canal. Identification of the type of bacteria
responsible for the meningitis is important for the selection of correct antibiotictreatment.
What complications can result from bacterial meningitis?
Advanced bacterial meningitis can lead to brain damage, coma, and death. Survivors can
suffer long-term complications, including hearing loss, mental retardation, paralysis, and
seizures.
What is the treatment for bacterial meningitis?
Early diagnosis and treatment are very important. If symptoms occur, the patient should
see a doctor right away. Bacterial meningitis can be treated with a number of effective
antibiotics. It is important, however, that treatment be started early.
How common is bacterial meningitis?
In the United States, bacterial meningitis is relatively rare and usually occurs in isolatedcases. Clusters of more than a few cases are uncommon.
In parts of Africa, widespread epidemics of meningococcal meningitis occur regularly. In
1996, the biggest wave of meningococcal meningitis outbreaks ever recorded hit West
Africa. An estimated 250,000 cases and 25,000 deaths in Niger, Nigeria, Burkina Faso,
Chad, Mali, and other countries paralyzed medical care systems and exhausted vaccine
supplies.
Is bacterial meningitis an emerging infectious disease?
With the decline in Hib disease, cases of bacterial meningitis have decreased since 1986.
Meningococcal meningitis is a continuing threat in day-care centers and schools. Healthy
children and young adults are susceptible, and death can occur within a few hours of
onset.
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How can bacterial meningitis be prevented?
y Vaccines -- There are vaccines against Hib, some strains of Neisseria meningitidis,
and many types ofStreptococcus pneumoniae.
The vaccines against Hib are very safe and highly effective. By age 6 months of
age, every infant should receive at least three doses of an Hib vaccine. A fourth
dose (booster) should be given to children between 12 and 18 months of age.
The vaccine againstNeisseria meningitidis (meningococcal vaccine) is not
routinely used in civilians in the United States and is relatively ineffective in
children under age 2 years. The vaccine is sometimes used to control outbreaks of
some types of meningococcal meningitis in the United States. New meningococcal
vaccines are under development.
The vaccine against Streptococcal pneumoniae (pneumococcal vaccine) is not
effective in persons under age 2 years but is recommended for all persons over age
65 and younger persons with certain medical problems. New pneumococcal
vaccines are under development.
http://www.dhpe.org/infect/Bacmeningitis.html
First of all and primarily, you need to know the general inflammatory response because it iswhat occurs whenever there is any invasion by bacteria, virus or some foreign body or
substance. That is basic to ALL body invasions:
http://allnurses.com/forums/f50/histamine-effect-244836.html . When you see "itis" at the
end of a medical disease, immediately start thinking about the inflammatory response--
period, end of story.
The cardinal signs and symptoms of inflammation are redness, heat, swelling and pain and
these are due to the pathophysiology of the inflammatory response. They are because (1)
redness due to the dilation of the blood vessels, (2) heat also due to the vasodilation and
increased blood flow, (3) edema due to intravascular fluids leaking into the surroundingtissues from the increased permeability of the blood vessels, and (4) pain due to the pain
receptors being stimulated by the swollen tissue and pH changes from all these chemicals
excreted during the inflammatory response. It is easy to see these symptoms when the
inflammation is, let's say, in a boo boo on the surface of the skin--you see the reddened
skin, can feel the heat if you touch it, notice the swollen bump and see the draining pus.
When it is occurring inside the body in tissues like the meninges you can't "see" these
things happening with your own eyes, but take my word for it--it is going on! We have to
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look for other assessment data as evidence of it.
Now, with meningitis, the infection is either introduced directly through a fracture of the
sinuses or skin contamination if there is a myelomeningocele. The inflammation response
kicks right in.
However, meningitis is often a complication of some other bacterial infection in the body,
often in the paranasal sinuses due to sinusitis, the mastoid due to otitis media or even the
lungs (pneumonia). How? The blood stream. Let's go back to the pathophysiology of the
inflammatory response. Keep in mind that with any infection inflammation ALWAYS occurs;
it is the general response to any bacterial invasion AND it results in vascular permeability.
Think of vascular permeability as a free ticket and open doors in the cell walls, an invitation,
for any bacteria to hop aboard the River Blood running nearby and take a ride. If they step
off at the meninges, hello bacterial meningitis.
Now, you are saying that you are having a hard time relating the signs and symptoms withthe pathophysiology of meningitis. This is the list of symptoms that I come up with for
bacterial meningitis. If I'm missing one that you found, please post it. Every single one of
them in some way traces its way back to one of the 4 cardinal signs of inflammation. Keep
in mind that the brain is encased in the skull and the spinal cord in the spinal canal so that
swelling causes serious problems for them because the tissues have no room to expand, so
swollen brain and spinal cord cells get crushed, irritated, start to elicit funky manifestations
and if the swelling isn't stopped, they will start permanently dying.
y headache, often worsens with movement (cardinal sign of Inflammation: Pain)y Fever (cardinal sign of Inflammation: Heat--invading bacteria cause the body to
reset it's thermostat to a higher level)y nausea/vomiting (the effect of the toxic substances spewed into the body by the
invading bacteria)y weakness (weakness of the muscles secondary to irritation of the nerve cells that
control them)y photophobia [sensitivity to light] (cardinal sign of Inflammation: Edema--the edema
irritates the nerve cells of the optic nerve which produces the visual changes)y confusion, delirium (cardinal sign of Inflammation: Edema)y seizures (cardinal sign of Inflammation: Edema--the edema irritates the nerve cells
of the brain which produces the seizure)y meningismus [the general term for irritation of the brain and spinal cord]y rigors [sudden chills followed by profuse heat and sweating] (cardinal sign of
Inflammation: Heat--invading bacteria cause the body to reset it's thermostat to ahigher level)
y profuse sweating (cardinal sign of Inflammation: Heat--invading bacteria cause thebody to reset it's thermostat to a higher level)
y Kernig's sign [reflex contraction and pain in the hamstring muscles when the leg isflexed and then extended] (a symptom of meningeal tissue irritation due to edema)
y Brudzinski's sign [neck pain and resistance to flexing the head and neck forwardtoward the sternum of the chest] (a symptom of meningeal tissue irritation due toedema)
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y declining level of consciousness (cardinal sign of inflammation: Edema)y cranial nerve palsies (cardinal sign of Inflammation: Edema--the edema irritates the
nerve cells of the spinal cord which results in the palsies)y symptoms of increased intracranial pressure (cardinal sign of Inflammation: Edema)
http://allnurses.com/nursing-student-assistance/relating-pathophysiology-signs-301632.html
http://en.wikipedia.org/wiki/Intracranial_pressure