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1. MICROBIAL DISEASE OF
THE CENTRAL NERVOUS
SYSTMEM

2. CENTRAL NERVOUSSYSTEM
•The Central Nervous System (CNS) consists of the
brain, which protected by the skull bones, and the
spinal cord, which is protected by the backbone.
•The CNS is covered by three layer of membranes
called meninges: the dura mater, arachnoid mater,
and pia mater. Cerebrospinal fluid (CSF) circulates
between the arachnoid mater and pia mater in the
subarachnoid space.
•Microorganisms can enter the CNS through trauma,
along peripheral nerves, and through the
bloodstream and lymhaticsystem

3. BACTERIAL DISEASES
Bacterial Meningitis
Tetanus
Botulism
Leprosy

4. BACTERIAL MENINGITIS
a. Haemophilusinfluenzae Meningitis
Causative Agent:Haemophilusinflunzae-
an aerobic, gram negative bacteria
that is a common member of the normal throat
microbiota.
Mode of transmission:transmitted from person
to person through respiratory droplet spread. It
may also be rarely acquired through contact with
infected respiratory discharge.

5. Pathophysiology:The bacterial organisms replicate and undergo lysis in the CSF, releasing
endotoxin or cell wall fragment. These substances initiate the release of inflammatory
mediators, which set the stage for a complex but coordinated sequence of events by which
neutrophils binds to cerebral endothelial cells by the release of toxic oxygen products,
permitting fluid to move across the capillary wall
Presenting signs and symptoms: a triad fever, chills, headache, stiff neck, nausea and vomiting.
Eventually meningitis progress to convulsion and coma.
Antimicrobial Treatment:Broad spectrum third generation cephalosporins are usually the first
choice of antibiotics; some experts recommend including vancomycin
Nursing Intervention:
>Rapid IV fluid replacement
>Protect the patient from injury secondary to seizure activity or altered level of consciousness
>Reduce high fever to decrease load of the heart and brain from oxygen demand
> Maintain head or neck in midline position, provide small pillow to support

6. BACTERIAL MENINGITIS
B. Neisseria Meningitis(Meningococcal Meningitis)
Causative Agent:Nesseriameningitides-an aerobic,
gram negative bacterium with a polysaccharide capsule
that is important to its virulence.
Mode of transmission:transmitted from person to
person through droplets of respiratory or throat
secretion from carriers.
Pathophysiology:A bacterium penetrates the blood
brain barrier. Endotoxin binds to plasma endotoxin
binding protein and to the cellular receptor, CD14 and
other cellular receptors triggering an intense
inflammatory response. Activated macrophages produce
a range of proinflammatory cytokines the concentration
of severity of disease.

7. Presenting Signs and Symptoms:stiff neck, high fever, sensitivity to light, confusion,
headache, and vomiting.
Antimicrobial treatment:Range of antibiotics can treat the infection, including
penicillin, ampicillin, and ceftriaxone.
Nursing Interventon:
>Monitor daily body weigh
>Initiate seizure precautions
>Elevate the head of the bed 30 degrees, and avoid neck flexion and extreme hip
flexion
>Rapid IV replacement

8. BACTERIAL MENINGITIS
C. Streptococcus pneumonieMeningitis
Causative Agent:Streptococcus pneumonie-gram positive,
encapsulated diplococcus.
Mode of transmission:transmitted through direct contact
with tiny droplets from an infected person’s mouth, throat or
nose.
Pathophysiology:during the invasive disease, pneumococcal
epithelial adhesion is followed by bloodstream invasion and
activation of the complement and coagulation systems. The
release of inflammatory mediators facilitates pnemococcal
crossing of the blood barrier into the brain, where the
bacteria multiply freely and triggered activation of circulating
antigen presenting cell and resident microglial cell. The
resulting massive inflammation leads to further neutrophil
recruitment and inflammation, resulting in the well-known
features ofbacterial meningitis.

9. Presenting Signs and Symptoms:Fever, drowsiness, impaired consciousness, severe headache,
vomiting, stiff neck and pain moving the neck
Antimicrobial Treatment:Dexamethasone has been shown to be beneficial as adjunct therapy
in the treatment of pneumococcal meningitis if administered 15 to 20 minutes before the first
dose of antibiotic and every 6 hours for the next 4 days.researchsuggest that dexamethasone
improves the outcome in adults and does not increase the risk for gastrointestinal bleeding.
Nursing Intervention:
>Ensuring close neurologic monitoring
>Encourage patient to stay hydrated either orally or peripherally
>Protect the patient from injury secondary to seizure activity or altered level of consciousness
>Assisting getting rest in a quiet, darkened room
>Monitoring daily body weight; serum electrolytes; and urine volume, specific gravity and
osmolality; especially if syndrome of inappropriate antidiuretic hormone is suspected.

10. TETANUS
Causative Agent: Clostridumtetani
obligately anaerobic, endospore forming,
gram positive rod.
It is especially common in soil
contaminated with animal fecal waste.
advance case of tetanus
Mode of transmission: spores get into the
body through broken skin, usually through
injuries fromcontaminated objects. Certain
breaks in the skin are more likely to get
infected with tetanus bacteria.

11. Pathophysiology:when tetanus toxin is taken up into nerve terminals of lower motor neurons,
the nerve cells that activate voluntary muscle. Tetanustoxin is a zinc metalloproteinase that
target protein that is necessary for the release of neurotransmitter from nerve endings through
fusion of synaptic vesicles with the neuronal plasma membrane. The initial symptoms of local
tetanus infection may therefore flaccid paralysis, caused by interference with vesicular release
of acetylcholine at the neuromuscular junction, as occur in butulinumtoxin. However, unlike
botulinum toxin, tetanus toxin undergoes extensive retrograde transport in axons of lower
motor neurons and thus reaches the spinal cord or brainstem. Here the toxin is transported
across synapses and taken up by nerve endings ihibitioryGABA ergicand gylnergicneurons that
control the activity of the lower neurons. Once inside inhibitory nerve terminals, tetanus toxn
cleaves VAMP, thereby inhibiting the release GABA and glycine. The result is a partial, functional
denervation of the lower motor neurons which lead to their hyperactivity and to increased
muscle activity and in the form of rigidity and spasms.
Presenting Signs and Symptoms: Spasms and stiffness in your jaw muscles, stiffness in the neck
muscles, difficulty swallowing, Fever, Elevating Blood pPressureand rapid heart rate.

12. Antimicrobial Treatment: Administer Human TIG 500 units by intramuscular injection or intravenously as
soon as possible; in addition administer age appropriate TT-containing vaccine, 0.5 cc by intramuscular
injection. Metronidoleis preferred, penicillin G, tertracyclines, macrolides, clindamycin, cephalosporins
and chloramphenicol are also effective;
Nursing Intervention:
>Protect the client from injury
>Monitor for signs and symptoms of arrhythmias
>Prevent client from having spasms by:
-controlling the environment
-avoiding stress, pain, coughing or flatus to ccurin patient
-avoid touching, turning and jarring the bed of the client
>Maintain adequate airway and ventillation

13. LEPROSY
Causative Agent:Mycobacterium leprae
the first bacterium to be identified as
causing disease in humans.
Mode of Transmission: spread person to
person by nasal secretions or droplets.
They speculate that infected droplets
reach other peoples' nasal passages and
begin the infection there.

14. Pathophysiology:microorganism that has a predilection for the skin and nerves. M. leprae
primarily infects Schwann cells in the peripheral nerves leading to nerve damage and the
development of disabilities. Despite reduced prevalence of M. lepraeinfection in the endemic
countries following implementation of multidrug therapy (MDT) program by WHO to treat
leprosy, new case detection rates are still high-indicating active transmission. The susceptibility
to the mycobacteria and the clinical course of the disease are attributed to the host immune
response, which heralds the review of immunopathology of this complex disease.
Presenting Sign and Symptoms: Early symptoms begin in cooler areas of the
body and include loss of sensation. Signs of leprosy are painless ulcers,
skin lesions of hypopigmented macules (flat, pale areas of skin)
, and eye damage (dryness, reduced blinking).
Antimicrobial Treatment:The first-line drugs are dapsone, rifampin, and clofazimine. ... Second-
line agents include minocycline, ofloxacin, and clarithromycin, which can be used to treat a
single skin lesion or to treat patients with dapsone allergy.

15. Nursing Intervention
>Diagnose the impaired tissue integrity and monitor the characteristics of the lesion
such as size, color, odor and drainage.
>Clean the wounds with saline or nontoxic substances as indicated.
>Apply sterile bandage to cover the wounds and maintain aseptic technique
>Examine the wound damage daily during each dressing changes.
⦁Routinely monitor temperature and color of skin.

16. VIRALDISEASES
Poliomyelitis
Rabies
Arboviral Encephalitis

17. POLIOMYELITIS
Causative Agent:human
enterovirus and member of the
family ofPicornaviridae.
Mode of transmission:Polio
viruses are spread predominantly
by the fecal–oral route.

18. Pathophysiology:The virus enters via the fecal-oral or respiratory route, then enters the
lymphoid tissues of the GI tract. A primary (minor) viremia follows with spread of virus to the
reticuloendothelial system. Infection may be contained at this point, or the virus may further
multiply and cause several days of secondary viremia, culminating in the development of
symptoms and antibodies.
Inparalytic infections,poliovirus enters the CNS—whether via secondary viremia or via
migration up peripheral nerves is unclear. Significant damage occurs in only the spinal cord and
brain, particularly in the nerves controlling motor and autonomic function. Inflammation
compounds the damage produced by primary viral invasion. Factors predisposing to serious
neurologic damage include Increasing age (throughout life),Recent tonsillectomy or
intramuscular injection, pregnancy, impairment of B-cell function, and physical exertion
concurrent with onset of the CNS phase.
PRESENTING SIGN AND SYMPTOMS:which can last up to 10 days, include fever, sore throat,
headache, vomiting, fatigue, back pain or stiffness, neck pain, stiffness in the arms or legs,
muscle weakness or tenderness

19. ANTIMICROBIAL TREATMENTS: No drug can kill the virus once an infection has begun. Treatment is
directed at controlling the symptoms of the disease. People with minor poliomyelitis are treated
with bed rest and over-the-counter medicines to control fever and muscle aches.
People with major poliomyelitis may require additional treatments, including Physical therapy,
Measures to prevent urinary tract infections, Mechanical breathing support
NURSING INTERVETION:
>Maintain a patentairway, and keep a tracheotomy tray at the patient’s bed side.
>Encourage a return to mild activity as soon as possible.
>Prevent fecal impaction by giving enough fluids to ensure an adequate daily urine output of low
specific gravity.
>Provide good skin care, re-position the patient often, and keepbed linensdry.
>Toalleviatediscomforts, use foam rubber pads and sandbags or light splints as ordered.
>Wash hands thoroughly after contact with the patient or any of his secretions and excretions.

20. RABIES
Causative Agent:Rabies virus, a member of
genus lyssavirus having a characteristic of bullet
shape. Lyssavirus are single stranded RNA viruses
with no proofreading capability and mutant
strains develop rapidly.
Mode of Transmission:The most
commonmodeofrabiesvirustransmissionis
through the bite and virus-containing saliva of an
infected host. Thoughtransmissionhas been
rarely documented via other routes such as
contamination of mucous membranes (i.e., eyes,
nose, mouth), aerosoltransmission, and corneal
and organ transplantations.

21. Presenting Sign and Symptoms:Paresthesia, pain, or intense itching at the inoculation site is
pathognomonic forrabiesand occurs in 50% of cases during this phase; this may be the
individual's onlypresenting sign.Symptomsmay include the following: Malaise.
Antimicrobial Treatment: Rabiesshots include: A fast-acting shot (rabiesimmune globulin) to
prevent the virus from infecting you. Part of this injection is given near the area where the
animal bit you if possible, as soon as possible after the bite.
Nursing Intervention:
>Isolate the patient
>Give emotional and spiritual support
>Darken the room and prove a quiet environment
>Patient should not be bathed and there should not be any running water in the room or within
the hearing distance of the patient.
>If IV fluid has to be given it should be wrapped and needle should be securely anchored in the
vein to avoid dislodging in times of restlessness

22. ARBOVIRAL ENCEPHALITIS
Causative Agent : Arthropod-borne viruses
(arboviruses) are of paramount concern as a group
of pathogens at the forefront of emerging and re-
emerging diseases. Here, we
discussarbovirusesfrom diverse families
(Flaviviruses, Alphaviruses, and the Bunyaviridae)
that arecausative agentsofencephalitisin humans
Mode of Transmission:Arboviral encephalitis:
Inflammation of the brain (encephalitis) caused by
infectionwith anarbovirus, a virustransmittedby a
mosquito, tick or another arthropod.Infectionof
vertebrates, including humans, occurs when an
infected arthropod feasts upon them for a blood
meal.

23. Pathophysiology:Arthropod-borne viruses (arboviruses) are of paramount concern as a group of pathogens
at the forefront of emerging and re-emerging diseases. Although some arboviral infections are asymptomatic
or present with a mild influenza-like illness, many are important human and veterinary pathogens causing
serious illness ranging from rash and arthritis to encephalitis and hemorrhagic fever. Here, we discuss
arboviruses from diverse families (Flaviviruses, Alphaviruses, and theBunyaviridae) that are causative agents
of encephalitis in humans. An understanding of the natural history of these infections as well as shared
mechanisms of neuroinvasionand neurovirulence is critical to control the spread of these viruses and for the
development of effective vaccines and treatment modalities.
Presenting Sign and Symptoms:Headache, Feeling unwell, Drowsiness,Fever, Vomiting, Stiff neck, Muscle
soreness or trembling, Confusion, Convulsions, Sensitivity to light, Extreme weakness
Antimicrobial Treatment: There are no specific medications or therapies to rid your body of an arbovirus.
Treatment involves careful monitoring and symptom relief. Get plenty of rest and drink lots of fluids to
avoiddehydration. If your fever rises or your symptoms get worse, seek medical attention. Depending on
which vimonitoryour blood pressure, heart rate, temperature, and respiration
Nursing Intervention
>Pain Management: Alleviation of pain or a reduction in pain to a level of comfort that is acceptable to the
patient
>AnalgesicAdministration: Use of pharmacologic agents to reduce or eliminate pain

24. >Environmental Management: Comfort: Manipulation of the patient’s surroundings for promotion of
optimal comfort
>Anxiety Reduction: Minimizingapprehension, dread, foreboding, or uneasiness related to an
unidentified source or anticipated danger
>Provision of a modified environment for the patient who is experiencing a chronic confusionalstate
>Calming Technique: Reducing anxiety in patient experiencing acute distress
>Delusion Management: Promoting the comfort, safety, and reality orientation of a patient experiencing
false, fixed beliefs that have little or no basis in realityEnvironmentalManagement: Safety: Manipulation
of the patient’s surroundings for therapeutic benefi
>Temperature Regulation: Attaining and/or maintaining body temperature within a normal range
>Fever Treatment: Management of a patient with hyperpyrexia caused by nonenvironmental factors
>Nutrition Management: Assisting with or providing a balanced dietary intake of foods and fluid
>Weight Gain Assistance: Facilitating gain of body weight
>Eating Disorders Management: Prevention and treatment of severe diet restrictions and over exercising
or binging and purging of foods and fluids

25. FUNGAL DISEASES
Cryptococcus Meningitis

26. CRYPTOCOCCUS NEOFORMANS MENINGITIS
Causative Agent:Cryptococcosisis the
infection caused by the
telemorphicfungicalledCryptococcus.
They form spherical cells, resembling
yeasts, reproduce by duding, and
produce extremely heavy polysaccharide
capsules.
Mode of transmission:aerosolization
and inhalation, in which the infectious
yeast particles become airborne and
then are inhaled by the host and
penetrate in to small airways

27. Pathophysiology:Cryptococcosisis acquired by inhalation and thus typically affects the lungs.
Many patients present with asymptomatic, self-limited primary lung lesions. In
immunocompetent patients, the isolated pulmonary lesions usually heal spontaneously without
disseminating, even without antifungal therapy. After inhalation,Cryptococcusmay
disseminate, frequently to the brain and meninges, typically manifesting as microscopic
multifocal intracerebral lesions. Meningeal granulomas and larger focal brain lesions may be
evident. Although pulmonary involvement is rarely dangerous,cryptococcal meningitisis life
threatening and requires aggressive therapy.
Presenting Signs and symptoms: abdominal pain and swelling; nausea; loss of appetite;
unintentional weight loss; weakness/fatigue; confusion; headache; fever; sweating; swollen
glands; blurred vision; bleeding into the skin/rash; bruising; nerve pain/numbness/tingling;
chest pain, tenderness of the sternum, and bone pain .
Antimicrobial Treatment:Suramin,pentamidine

28. PRIONSDISEASES
Creutzfeldt-Jakob Disease

29. CREUTZFELDT-JAKOB DISEASE
Causative Agent:It belongs to a group of diseases
called Transmissible Spongiform Encephalopathies
(TSEs) that affect humans and other animals. TSEs
are thought to be caused by the buildup of an
abnormal, transmissible protein called 'prion' in the
brain.
Mode of transmission:Familial CJD is caused by an
inherited abnormal gene.IatrogenicCJD is
transmitted during medical or surgical procedures,
e.g. human tissue/organ transplant.VariantCJD
(vCJD) is linked to the consumption of food products
from cattle infected with a type of TSE called Bovine
Spongiform Encephalopathy (BSE, commonly known
as 'Mad Cow Disease'). There were also overseas
vCJDcases associated with blood transfusion.

30. Pathophysiology:the prion crosses the blood brain barrier and deposited
in brain tissue and causes degeneration of the brain tissue. Cell death
occurs and spongyformchanges are produced in the brain.
Presenting Signs and Symptoms:Creutzfeldt-Jakob disease is marked by
rapid mental deterioration, usually within a few months. Initial signs and
symptoms typically include: Personality changes, Anxiety,Depression,
Memory loss, Impaired thinking, Blurred vision or blindness, Insomnia,
Difficulty speaking, Difficulty swallowing, Sudden, jerky movements

31. ANTIMICROBIAL TREATMENT:Currently, there is no cure for Creutzfeldt-Jakob disease (CJD). Researchers
have tested many drugs, including acyclovir, amantidine, antibiotics, antiviral agents, interferon and
steroids. Treatment is aimed at alleviating symptoms and making the patient as comfortable as possible.
Drugs can help relieve pain if it occurs. The drugs clonazepam and sodium valproate may help relieve
myoclonus or irregular, jerking movements.
NURSING INTERVENTION:
>Minimize touching, turning and movement
>Promote a calm, quiet approach and create a quiet environment >Relax the muscles using
benzodiazepines.
>Careful planning to reduce the need for touching the person
>Controlling environmental activity and noise.
>Provide or encourage to use of sortlighting.
>Encourage verbalization of feelings
>Perform daily activities optimally
>Encourage the family to monitor the daily activities.