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Meningococcal meningitis is a bacterial form of meningitis, a serious infection
of the meninges that affects the brain membrane. It can cause severe brain damage
and is fatal in 50% of cases if untreated.
Several different bacteria can cause meningitis. Neisseria meningitidis is the one with
the potential to cause large epidemics. There are 12 serogroups of N.
meningitidis that have been identified, 6 of which (A, B, C, W, X and Y) can cause
epidemics. Geographic distribution and epidemic potential differ according to


The bacteria are transmitted from person-to-person through droplets of

respiratory or throat secretions from carriers. Close and prolonged contact such as
kissing, sneezing or coughing on someone, or living in close quarters (such as a
dormitory, sharing eating or drinking utensils) with an infected person (a carrier)
facilitates the spread of the disease. The average incubation period is 4 days, but
can range between 2 and 10 days.
Neisseria meningitidis only infects humans; there is no animal reservoir. The bacteria
can be carried in the throat and sometimes, for reasons not fully understood, can
overwhelm the body's defenses allowing infection to spread through the bloodstream
to the brain. It is believed that 10% to 20% of the population carriesNeisseria
meningitidis in their throat at any given time. However, the carriage rate may be
higher in epidemic situations.


The most common symptoms are a stiff neck, high fever, sensitivity to light,
confusion, headaches and vomiting. Even when the disease is diagnosed early and
adequate treatment is started, 5% to 10% of patients die, typically within 24 to 48
hours after the onset of symptoms. Bacterial meningitis may result in brain damage,
hearing loss or a learning disability in 10% to 20% of survivors. A less common but
even more severe (often fatal) form of meningococcal disease is meningococcal
septicaemia, which is characterized by a haemorrhagic rash and rapid circulatory


Initial diagnosis of meningococcal meningitis can be made by clinical

examination followed by a lumbar puncture showing a purulent spinal fluid. The
bacteria can sometimes be seen in microscopic examinations of the spinal fluid. The
diagnosis is supported or confirmed by growing the bacteria from specimens of spinal
fluid or blood, by agglutination tests or by polymerase chain reaction (PCR). The
identification of the serogroups and susceptibility testing to antibiotics are important
to define control measures.

Meningococcal disease is potentially fatal and should always be viewed as a

medical emergency. Admission to a hospital or health center is necessary, although
isolation of the patient is not necessary. Appropriate antibiotic treatment must be
started as soon as possible, ideally after the lumbar puncture has been carried out if
such a puncture can be performed immediately. If treatment is started prior to the
lumbar puncture it may be difficult to grow the bacteria from the spinal fluid and
confirm the diagnosis.
A range of antibiotics can treat the infection, including penicillin, ampicillin,
chloramphenicol and ceftriaxone. Under epidemic conditions in Africa in areas with
limited health infrastructure and resources, ceftriaxone is the drug of choice.

There are 3 types of vaccines available.


Polysaccharide vaccines have been available to prevent the disease for over
30 years. Meningococcal polysaccharide vaccines are available in either bivalent
(groups A and C), trivalent (groups A, C and W), or tetravalent (groups A, C, Y and
W) forms to control the disease.


For group B, polysaccharide vaccines cannot be developed, due to antigenic

mimicry with polysaccharide in human neurologic tissues. The first vaccine against
NmB, made from a combination of 4 protein components, was released in 2014.


Since 1999, meningococcal conjugate vaccines against group C have been

available and widely used. Tetravalent A, C, Y and W conjugate vaccines have been
licensed since 2005 for use in children and adults in Canada, the United States of
America, and Europe.
The extended meningitis belt of sub-Saharan Africa, stretching from Senegal in the
west to Ethiopia in the east (26 countries), has the highest rates of the disease. The
26 countries include: Benin, Burkina Faso, Burundi, Cameroon, Central African
Republic, Chad, Cte dIvoire, Democratic Republic of Congo, Eritrea, Ethiopia, The
Gambia, Ghana, Guinea, Guinea Bissau, Kenya, Mali, Mauritania, Niger, Nigeria,
Rwanda, Senegal, South Sudan, Sudan, Tanzania, Togo and Uganda. The risk of
meningococcal meningitis epidemics differs within and among these 26 countries.
In December 2010, a new meningococcal A conjugate vaccine was introduced
nationwide in Burkina Faso, and in selected regions of Mali and Niger (the remaining
regions were covered in 2011), targeting persons 1 to 29 years of age. As of January
2015, 217 million persons have been vaccinated with this new vaccine in 15
countries (Benin, Burkina Faso, Cameroon, Chad, Cte dIvoire, Ethiopia, The
Gambia, Ghana, Mali, Mauritania, Niger, Nigeria, Senegal, Sudan, and Togo).
The MenA conjugate vaccine has several advantages over existing polysaccharide

it induces a higher and more sustainable immune response against group A

it reduces the carriage of the bacteria in the throat and thus its transmission;

it is expected to confer long-term protection not only for those who receive the
vaccine, but on family members and others who would otherwise have been

exposed to meningitis;
it is expected to be particularly effective in protecting children under two years
of age, who do not respond to conventional polysaccharide vaccines

II. Nursing Assessment

1. Personal History
My patient Rain Jey Dela Cruz, Male and is 10 days old. He is taken care of by
his parents who are Renalyn Comedia and Jayson Dela Cruz. They live in District 6
Block 67 Lot 14 Pandacaqui, Mexico, Pampanga. His parents are both Filipino and they
are Iglesia Ni Cristo. Rain Jey Dela Cruz was born in January 2, 2015 in Clinic Osme
near their home. He was admitted to Jose B. Lingad Memorial Regional Hospital,
January 3, 2015, 3:06pm due to a complaint of fair jerk and jitters.
2. Family History
Rain Jey Dela Cruz is the only child of Renalyn and Jayson Dela Cruz. They live
in a small house with concrete walls and with good ventilations. The father works as a
construction worker and has enough wages to pay for their daily expenses and bills.
There are no hereditary diseases that can be attributed from her mother side, but her
father had a family health history of Hypertension. Other than the latter, no other
hereditary diseases from both parents are within the patients parents knowledge.
3. History of Past Illness
Prior to His hospitalization, his parents denied in having any record or medical
history of being admitted. They also confirmed that our patient has no allergies to food
and drugs.
4. History of Present Illness

After a being born, Baby Rain Jey was healthy and didnt have any sign of
abnormalities until the midwife gave him a bath the next day. The parents said that it
stopped crying and didnt eat at all. The next day January 3, 2015, 3:06pm, He was
admitted to Jose B. Lingad Memorial Regional Hospital with Positive jerky movement of
extremities, upward rolling of the eyeballs, and poor sucking.

5. Physical Examination
Lymph Nodes

Cephalic edema

Lungs :


Admitting Impression

Left, non-distended
Good tone
T/C Septic Meningitis

After the completion of the case study, the nurse-researcher shall have:
Discussed the statistics and current trends regarding the disease condition;
Assessed the personal history, pertinent family health-illness history and past medical
history in relation to the present disease condition and perform a comprehensive
physical assessment/examination;

Defined Meningitis and relate the modifiable and non- modifiable factors that
contributed to the occurrence of the disease including the signs and symptoms
Provided accurate health education to the patient and the significant others regarding
the disease process and the importance of strict compliance to the treatment regimen;
Formulated conclusions and recommendations based on the case presented.
After the completion of the case study, the patient shall have:
Patients parents would have a better understanding of the disease process;
Complied with the prescribed medical and pharmacologic regimen;
Adhered to the health teachings provided;
Engaged with the interventions that may prevent the occurrence of complications or
further complications;
Displayed improvement of the condition as evidenced by absence of further
complications; and,
Verbalized understanding on the advantages of having regular check-up for the baby
and follow-up of the medical and nursing regimens.

III. Anatomy and Physiology

Blood-Brain Barrier
Since the brain is such a delicate organ, nature has taken extra measures to protect the
brain by creating the blood-brain barrier to limit the diffusion of substances from the
bloodstream into brain tissue selectively.
The blood-brain barrier mainly consists of tight junctions, which seals the endothelial
cells that line the brain capillaries. Astrocytes, a type of neuroglia from the brain, closely

attached to the endothelial cells and release chemicals to regulate the permeabilities of
the tight junctions. The major sites of the blood brain barrier are the arachnoid
membrane, choroid plexus epithelium, and the cerebral microvascular endothelium.
Only a few kinds water-soluble substance can move across the blood-brain barrier, such
as glucose by active transport, urea, creatinine, and ions move across by slow
diffusion. On the other hand, lipid-soluble substances can easily cross the blood-brain
barrier, such as oxygen, carbon dioxide, alcohol, and most anesthetic agents.
When bacteria break through the blood-brain barrier, an infection occurs in the
cerebrospinal fluid.

Cerebrospinal Fluid
Cerebrospinal fluid (CSF) is a colorless, transparent liquid that continuously circulates
through the cavities of the brain and spinal cord, and as such, it acts as an internal
circulation system to transport nutrients and wastes between the bloodstream and the
brain and spinal cord. This reducdant circulation protects the brain and spinal cord from
chemical injuries similar to the function of the blood-brain barrier. The CSF also
protects the brain and spinal cord from physical injuries by acting as a shock absorber
between the brain and spinal cord from the skeletal structures (cranium and vertebrae)
CSF is produced in the choroid plexuses, which are networks of capillaries in the
ventricles. The choroid plexuses filter out blood plasma from the bloodstream, which is
the main component of CSF. The choroid plexuses are covered by ependymal cells that
are sealed together with tight junctions. These tight junctions forces the blood plasma
to pass through these ependymal cells, which further filter out the blood plasma,
producing CSF [2].
From the choroid plexuses of each lateral ventricle, CSF flows into the third
ventricle through the interventricular foramina, which are two narrow oval openings.
The choroid plexuses in the third ventricle adds more CSF. Then, CSF flows into
the fourth ventricle throught the cerebral aqueduct. Again, the choroid plexuses in
the fourth ventricle adds more CSF. The fluid then enters the subarachnoid
spacethrough the three openings in the roof of the fourth ventricle. These three
openings are a median aperture and a pair of lateral apertures. Then, CSF
circultates in the central canal of the spinal cord and in the subarachnoid
space around the surface of the brain and spinal cord [2].

The meninges are three connective tissue coverings that encircle the spinal cord and
brain. The spinal meninges surround the spinal cord and are continuous with
the cranial meninges, which encircle the brain [2].
The meninges lined the cranial and vertebral cavities to protect the brain and the spinal
cord, and they are also attached to the cranial bones' inner surfaces, which facilitate the
crainal bones to stabilize the positions of the brain, blood vessels, lymphatic vessels,
and nerves [2].
These three connective tissue coverings are dura mater, which is composed of dense,
irregular connective tissue), arachnoid mater, which is composed of delicate collagen
fibers and some elastic fibers in a spiders web arrangement, and pia mater, which is
a thin transparent connective tissue layer consists of squamous to cuboidal cells within
interlacing bundles of collagen fibers and some fine elastic fibers [2].
The most superficial of the three spinal meninges, the dura mater, forms a sac from the
level of the foramen magnum in the occipital bone, where it is continuous with the dura
mater of the brain, to the second sacral vertebra. The spinal cord is also protected by a
cushion of fat and connective tissue located in the epidural space, a space between
the dura mater and the wall of the vertebral canal [2].
The middle meninx is an avascular covering called the arachnoid mater. It is deep to
the dura mater and is continuous with the arachnoid mater of the brain. Between the
dura mater and the arachnoid mater is a thin subdural space, which contains
interstitial fluid [2].
The innermost meninx is the pia mater, which adheres to the surface of the spinal cord
and brain. Within the pia mater are many blood vessels that supply oxygen and
nutrients to the spinal cord. Between the arachnoid mater and the pia mater is

the subarachnoid space, which contains cerebrospinal fluid that serves as a shock
absorber and suspension system for the spinal cord and brain [2].
All three spinal meninges cover the spinal nerve roots, structures that connect spinal
nerves to the spinal cord, up to the point where they exit the spinal column through the
intervertebral foramina. Triangular-shaped membranous extensions of the pia mater
suspend the spinal cord in the middle of its dural sheath. These extensions,
called denticulate ligaments, are thickenings of the pia mater. They project laterally
and fuse with the arachnoid mater and inner surface of the dura mater between the
anterior and posterior nerve roots of spinal nerves on either side. Extending all along
the length of the spinal cord, the denticulate ligaments protect the spinal cord against
sudden displacement that could result in shock [2].

[1] Netter, F. H. (2006). Atlas of Human Anatomy (4th ed.). Philadelphia: Saunders Elsevier.
[2] Simk, M., Fiedeler, U., Gazs, A., & Nentwich, M. (2010, December). Can nanoparticles
end up in the brain? NanoTrust Dossiers(014en).
[3] Tortora, G. J., & Derrickson, B. (2009). Principles of Anatomy and Physiology (12th ed.).
Danver, United States of America: John Wiley & Sons, Inc.

IV. Patient and His Illness

a. Pathophysiology
Various bacteria including the major meningeal pathogens (e.g., S. pneumoniae)
undergo autolysis under harsh conditions such as exposure to antimicrobial agents
and/or growth to stationary phase. Autolysis consists of self-digestion of the cell wall by
peptidoglycan hydrolyases termed autolysins. At least 3 autolysins are recognized in
pneumococci, but the major autolysin is the N-acetyl-muramoyl-l-alanine amidase (LytA)
Activation of LytA and autolysis result in the release in subcapsular bacterial
components including peptidoglycan, lipoteichoic acid, bacterial DNA, and pneumolysin
Mechanisms of immune activationVarious cell wall products of meningeal pathogens are
well-known inducers of the inflammatory host response. The inflammatory response in
the subarachnoid space characteristic of acute purulent meningitis can be reproduced
by the intracisternal challenge with whole heat-killed unencapsulated pneumococci,
their isolated cell walls, lipoteichoic acid, or peptidoglycan, but not by the injection of
heat-killed encapsulated strains or isolated capsular polysaccharide. Exact mechanisms
of immune activation by pneumococcal cell wall products remain poorly understood, but
recent in vitro studies suggest that the first step in immune activation is binding of
peptidoglycan and/or lipoteichoic acid to the pattern recognition receptor membrane
CD14 (mCD14). mCD14 is not a transmembrane molecule and thus by itself cannot
transmit the activating signal into the cell
A second step in immune activation is necessary and this potentially occurs through the
toll-like receptor-2 (TLR-2). Coexpression of CD14 and TLR-2 in Chinese hamster ovary
fibroblasts confers responsiveness to pneumococcal peptidoglycan and heat-killed S.
pneumoniae as evidenced by inducible translocation of the nuclear transcription factor
NF-B. These studies also suggest that pneumococci stimulate both a TLR-2
dependent and a TLR-2independent pathway; however, in a model of pneumococcal
meningitis, TLR-2deficient mice responded to live pathogens virtually to the same
extent as wild type mice (Koedel et al., unpublished data). Leukocyte infiltration into the
subarachnoid space and brain mRNA expression of proinflammatory cytokines and

chemokines did not differ between TLR-2deficient and wild type mice inoculated with
live pneumococci. It appears that mechanisms other than binding of pneumococcal cell
wall products to TLR-2 play a central role in the induction of the host immune response
during pneumococcal meningitis. It appears that both TLR-2dependent and
independent (pneumolysin) pathways are sufficient to cause inflammation in the
absence of the other, but in vivo both are likely activated
TLR-2independent immune activation may be mediated at least in part by the
pneumococcal toxin pneumolysin. Pneumolysin stimulates the production of
inflammatory mediators in vitro including tumor necrosis factor (TNF)-, interleukin (IL)1, and IL-6. Pneumolysin is also an inducer and/or activator of enzymes such as
phospholipase A2, COX-2, and inducible NITRIC OXIDE synthase (iNOS). However, in a
rabbit meningitis model, a pneumolysin-deficient pneumococcal strain resulted in an
inflammatory response similar to that induced by injection of the wild type strain,
suggesting that pneumolysin is not essential for the induction of meningeal inflammation
Another potential trigger of immune activation during acute meningitis is bacterial DNA
released during bacterial autolysis. Bacterial DNA has substantial immune stimulatory
effects on B, NK, and dendritic cells and on monocytes and macrophages. The activity
of bacterial DNA is mediated by unmethylated CpG motifs, in particular base contexts.
In fact, when mice or rats are injected intracisternally with bacterial DNA or
unmethylated CpG oligonucleotides, meningitis developed within 12 h. Bacterial DNA
appears to initiate CNS inflammation by stimulation of macrophages and
proinflammatory products such as TNF-. TLR-9 is absolutely required for cellular
responses to CpG DNA, and TLR-9deficient mice show no response to CpG DNA
(inflammatory cytokine production from macrophages, maturation of dendritic cells, or
proliferation of splenocytes) . TLR-9deficient mice are also completely resistant to the
lethal effects of CpG DNA without production of serum proinflammatory cytokines. Thus,
the role of the CpG DNATLR-9 pathway for immune activation in acute bacterial
meningitis deserves further evaluation. In summary, subcapsular bacterial components
act as inducers of the host inflammatory response in acute bacterial meningitis, but the

host receptor systems and downstream elements of signal transduction are still largely
Intracellular signal transduction pathwaysFor meningeal pathogens, the major
inflammatory stimuli are lipopolysaccharide (LPS) and peptidoglycan for gram-negative
and gram-positive organisms, respectively. These inflammatory stimuli activate I-B
kinase NF-B pathways and 3 mitogen-activated protein kinase (MAPK) pathways:
extracellular signal-regulated kinases (ERK) 1 and 2, c-Jun N-terminal kinase (JNK),
and p38. As a result of activation of these signaling pathways, a variety of transcription
factors are activated: NF-B (p50/p65) and activator protein-1 (cFos/cJun), which
coordinate the induction of many genes encoding a variety of inflammatory mediators
Soluble peptidoglycan strongly activates ERK-1 and -2 in the mouse macrophage cell
line RAW264-7 and moderately activates JNK, while weak activation of p38 MAPK is
observed. In contrast, LPS strongly activates all of these kinases, suggesting a similar
but not identical activation of signal transduction pathways by these major inflammatory
mediators of meningeal pathogens
Pneumococcal cell wall components release inflammatory mediators by mouse
microglia, which is dependent on both p38 and ERK-2/ERK-1 MAPK activities. These
same MAPKs are also activated when rat or human astrocytes are stimulated with
various pneumococcal cell wall fragments. In addition, pneumococci activate NF-B in
undifferentiated human and mature murine monocytes. Although the signaling pathways
involved in immune inactivation only recently became a major focus of research activity,
a rat model of pneumococcal meningitis showed a marked increase in NF-B activity.
Pharmacologic inhibition of NF-B led to a significant reduction of host inflammatory
responses as evidenced by lower CSF leukocyte and IL-6 concentrations . It appears
that NF-B is a central transcriptional activator of many genes that encode proteins,
host factors, or both involved in the pathophysiology of pneumococcal meningitis,
including cytokines, chemokines, and adhesion molecules

Proinflammatory cytokinesMultiple cytokines play an important regulatory role in the

control of inflammation. TNF-, IL-1, and IL-6 are major early response cytokines that
trigger, often in synergy, a cascade of inflammatory mediators, including other
cytokines, arachidonic acid metabolites, chemokines, and reactive nitrogen and oxygen
intermediates. Multiple cell types within the CNS including cerebromicrovascular
endothelial cells, astrocytes, and microglia produce all 3 cytokines. Increased
concentrations of these cytokines have been detected in CSF samples from patients
with acute bacterial meningitis and concentrations of IL-1, but not IL-6 and TNF-, are
associated with significantly worse disease outcome or disease severity
Brain mRNA and protein expression of IL-1, IL-6, and TNF- are markedly upregulated in rodents during the acute stage of experimental pneumococcal meningitis.
Recent studies with genetically engineered mice provide further insight into the role of
acute phase cytokines in the pathophysiology of pneumococcal meningitis. For
example, brain bacterial titers were not affected by either TNF- or TNF receptor
deficiency in murine models of CNS infection. Furthermore, leukocyte recruitment into
the subarachnoid space was not affected by TNF deficiency. In contrast, mice with
targeted disruption of TNF receptors p55 and p75 had decreased meningeal
inflammation. It appears that other TNF receptor ligands (e.g., lymphotoxin-) must
contribute to the induction and/or maintenance of the inflammatory response during
pneumococcal meningitis. Intracisternal inoculation of pneumococci caused a three-fold
increase in CSF leukocyte concentrations in IL-6deficient mice when compared with
wild type controls. Increased CSF pleocytosis is thought to result from higher brain
expression of the potent neutrophil chemoattractant macrophage inflammatory protein
(MIP)-2. These observations are similar to those in animal models of endotoxin-induced
lung injury and endotoxemia, where IL-6 appears to control the extent of the
inflammatory response by down-regulating the expression of chemokines and/or
proinflammatory cytokines

Figure 1
Mechanisms of brain damage in experimental pneumococcal meningitis. NF-B, a
transcriptional activator of many genes involved in the pathogenesis of bacterial
meningitis, encodes host factors including proinflammatory cytokines, chemokines (e.g.,
interleukin [IL]-8), and adhesion molecules. The proinflammatory cytokines IL-1
and tumor necrosis factor (TNF)- are synthesized as inactive precursors that are
processed to mature active forms by proteases (casbase 1 [Casp1], also known as IL-

1converting enzyme, and TNF-converting enzyme [TACE]). IL-1 and TNF- are
potent activators of NF-B. This process may lead to the uncontrolled expression of
proinflammatory mediators and the increased expression of adhesion molecules both
on the endothelium (e.g., intercellular adhesion molecule [ICAM]-1) and on neutrophils,
leading to subsequent massive influx of leukocytes into the subarachnoid space. Once
present, activated leukocytes release a complex variety of potentially cytotoxic agents
including oxidants and proteolytic enzymes (e.g., matrix metalloproteinases [MMP]),
which may contribute to tissue destruction. Also, peroxynitrite may cause brain damage
via a variety of independent mechanisms. The best studied are attack of
polyunsaturated fatty acids, leading to lipid peroxidation, and an alternative pathway
that involves oxidant-induced DNA strand breakage and subsequent poly (ADP ribose)
polymerase (PARP) activation, which initiates an energy-consuming intracellular cycle
that ultimately results in cellular energy depletion and cell death. Both mechanisms
likely contribute to cell injury during pneumococcal meningitis. ECM, extracellular
matrix; MIP, macrophage inflammatory protein

Figure 2
Vicious cycle of pathophysiologic alterations leading to neuronal injury during bacterial
meningitis. BBB, blood-brain barrier; CBV, cerebral blood volume

V. Medical Management
This Chapter is a summary of the management of care rendered to the patient, which
was presented through a table.
Pulse Rate

12, 2015

13, 2015









Clinical Chemistry Result Form

Hematology Result Form

ABO Blood
RH Typing
WBC Count




N10 x 12
hours at
8-9gtts/ hr





120mg with
10cc D5W in

















Liquid Diet

VI. Conclusion

With early diagnosis and treatment, term infants are not likely to experience long-term
health problems associated with neonatal sepsis; however, if early signs or risk factors
are missed, mortality increases. Residual neurologic damage occurs in 15-30% of
neonates with septic meningitis.
Mortality from neonatal sepsis may be as high as 50% for infants who are not treated.
Infection is a major cause of fatality during the first month of life, contributing to 13-15%
of all neonatal deaths. Low birth weight and gram-negative infection are associated with
adverse outcomes Neonatal meningitis occurs in 2-4 cases per 10,000 live births and
contributes significantly to mortality from neonatal sepsis; it is responsible for 4% of all
neonatal deaths.
In preterm infants who have had sepsis, impaired neurodevelopment is a
concern. Proinflammatory molecules may negatively affect brain development in this
patient population. In a large study of about 6000 premature infants who weighed less
than 1000 g at birth, preterm infants with sepsis who did not have meningitis had higher
rates of cognitive deficits, cerebral palsy, and other neurodevelopmental disabilities than
infants who did not have sepsis.

Infants with meningitis may acquire hydrocephalus or periventricular leukomalacia. They

may also have complications associated with the use of aminoglycosides, such as
hearing loss or nephrotoxicity.
That is why regular checkup and proper diet during pregnancy is a very important
aspect for the babys outcome to be able to prevent any abnormalities at birth. Baby
Rain Jeys parents should have a strict compliance to the medical treatment, health
teachings and medical check up every now and then is advised. They should always
keep their eyes and focus on the baby to help fasten the recovery.


Balibago, Angeles City
College of Nursing

In partial fulfillment of the Requirements in



Submitted to
Mrs. Mary Anne S. De Dios

Submitted by
Molina, Ruth Anne C.

February 4, 2014