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1. CNS INFECTIONS
Meningitis
 Inflammation of the brain and spinal cord that may be caused
by either bacterial or viral infection.
 Bacterial meningitis=> Serious infection that is spread by
direct contact with discharge from the respiratory tract of an
infected person.
 Viral meningitis=> Also called aseptic meningitis, is more
common and rarely serious.
It usually presents with flulike symptoms and patients
recover in 1 to 2 weeks
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2. Pathophysiology and Etiology
Common bacteria causing meningitis:
Neisseria meningitidis=> Meningococcal meningitis
Streptococcus pneumoniae => Pneumococcal meningitis
Haemophilus influenzae type b (Hib).
N. meningitides and S. pneumoniae are the major
causes of bacterial meningitis.
Infection generally begins in another area, such as the
URT enters the blood and invades the CNS causing the
meninges to become inflamed and ICP to increase.
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3. Cont’d
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Necrosis of areas in the brain may occur.
Cranial nerve function may be transiently or permanently
affected by meningitis.

4. Cont’d
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5. Signs and Symptoms
The most common symptom of meningitis is
 Headache
 High grade fever and stiff neck
 Photophobia
 Patient with meningococcal meningitis usually presents with
petechiae on the skin and mucous membranes.
 Nuchal rigidity (pain and stiffness when the neck is
moved) is caused by spasm of the extensor muscles of the
neck.
 Positive Kernig’s and Brudzinski’s signs
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6. Cont’d
Kernig’s sign, the examiner flexes the patient’s hip to
90 degrees and tries to extend the patient’s knee and
positive if the patient experiences pain and spasm of the
hamstring.
Brudzinski’s sign is positive when flexion of the
patient’s neck causes the hips and knees to flex
 Nausea and vomiting associated
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7. Cont’d
 Encephalopathy =mental status changes manifested as :
Short attention span, poor memory, disorientation,
difficulty following commands and misinterpret
environmental stimuli
 Late signs of meningitis include lethargy and seizures
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8. Diagnostic Tests
A lumbar puncture
Viral meningitis
 Clear CSF with normal glucose level and normal or
slightly increased protein level.
 No bacteria are seen, but the WBC count is usually
increased.
Bacterial meningitis
 CSF is turbid, or cloudy, because of the massive
number of WBC and lowering glucose level.
 Bacteria are identified by Gram stain and culture
 Elevated protein in CSF.
 MRI or CT scan:- may be done to evaluate for complications
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9. Management
 Meningitis can be fatal if not promptly treated.
 Antibiotics are administered for bacterial meningitis.
 Antipyretics and a cooling blanket may also be used.
Care should be taken to avoid cooling the patient too much
because shivering increases the metabolic demand for
oxygen and glucose.
 A quiet, dark environment lessens the stimulation to a
patient who has a headache or photophobia and
who may be agitated, disoriented, or at risk for seizures
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10. Cont’d
 Analgesics are given to lessen head and neck pain.
 Corticosteroid's and anti-inflammatory
 Antiemetic medications.
 The patient with meningococcal meningitis should be
placed in isolation because this disease can be
transmitted to others.
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11. Cont’d
Nursing Management
 Maintain fluid balance (input and output)
 Maintain body temperature to normal
 Agitated patients, keeping patients from harming
themselves.
 Teach the family about symptoms and treatment
goals for the patient.
 Monitor vital signs
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12. Complications
o Cranial nerve damage may leave the patient
blind or deaf.
o Seizures may continue to occur even after the
acute phase of the illness has passed.
o Cognitive deficits ranging from memory impairment
to profound learning disabilities may occur
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13. Rabies
 Preventable viral disease most often transmitted through the
bite of a rabid animal.
 Rabies virus infects the CNS of mammals, ultimately causing
disease in the brain and death.
Rabies Virus
 Rabies virus belongs to the order Mononegavirales
– Within this group, viruses with a distinct “bullet” shape are classified in
the Rhabdoviridae family, which includes Lyssavirus,
– The genus Lyssavirus includes rabies virus
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14. Cont’d
How is rabies transmitted?
Transmitted through direct contact (such as through
broken skin or mucous membranes in the eyes, nose,
or mouth) with saliva or brain/nervous system tissue
from an infected animal.
People usually get rabies from the bite of a rabid
animal.
Possible, but rare for people to get rabies from non-bite
exposures include:
Scratches, abrasions, or open wounds that are exposed to
saliva from a rabid animal.
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15. Cont’d
Rabies virus becomes non-infectious when it dries
out and when it is exposed to sunlight.
If the material containing the virus is dry, the virus
can be considered non-infectious.
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16. Pathophysiology
 Rabies virus is introduced into a muscle through a
bite from another animal, it travels from the site of
the bite to the brain by moving within nerves.
The Person does not appear ill during this time.
A bite by the animal during the incubation period does not
carry a risk of rabies because the virus has not yet made it
to the saliva.
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17. Cont’d
The Infectious Path of the Rabies Virus
1. Person is bitten by a rabid animal.
2. Rabies virus from the infected saliva enters the
wound.
3. Rabies virus travels through the nerves to the spinal
cord and brain.
 This process can last approximately 3 to 12 weeks.
 The Person has no signs of illness during this time.
4. In the brain the virus multiplies rapidly and passes to
the salivary glands.
 The Person begins to show signs of the disease.
5. The infected Person usually dies within 7 days of
becoming sick.
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18. Sign and Symptom
The first symptoms of rabies may be very similar to those of
the flu including
– General weakness or discomfort.
– Fever or headache.
These symptoms may last for days.
There may be also discomfort or a irritation or itching
sensation at the site of the bite progressing within days to
acute symptoms of cerebral dysfunction
 Anxiety
 Confusion and agitation.
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19. Cont’d
As the disease progresses the person may experience:
Delirium
Abnormal behaviour
Hallucinations
Hydrophobia (fear of water) and insomnia.
Acute period of disease typically ends after 2 to 10
days.
Once clinical signs of rabies appear the disease is
nearly always fatal and treatment is typically
supportive.
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20. Diagnosis
 Several tests are necessary to diagnose rabies
ante-mortem (before death) in humans; no
single test is sufficient.
Saliva test by virus isolation or reverse transcription
followed by polymerase chain reaction (RT-PCR).
Serum and spinal fluid are tested for antibodies to rabies
virus.
Skin biopsy specimens are examined for rabies antigen in
the cutaneous nerves at the base of hair follicles.
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21. Management
Extensive wound washing
This first-aid measure includes immediate and thorough
flushing and washing of the wound for a minimum of 15
minutes with soap and water, detergent, povidone iodine or
other substances that remove and kill the rabies virus.
Post-exposure Prophylaxis (PEP)
Dose of human rabies immune globulin (HRIG) and rabies
vaccine given on the day of the rabies exposure and then a
dose of vaccine given again on days 3, 7, and 14.
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22. Exposure risk and indications for PEP
Categories of contact with suspect rabid animal Post-exposure
prophylaxis measures
Category I - touching or feeding animals, animal
licks on intact skin (no exposure)
Washing of exposed skin
surfaces, no PEP
Category II - nibbling of uncovered skin, minor
scratches or abrasions without bleeding (exposure)
Wound washing and
immediate vaccination
Category III - single or multiple transdermal bites
or scratches, contamination of mucous membrane
or broken skin with saliva from animal licks,
exposures due to direct contact with bats (severe
exposure)
Wound washing,
immediate vaccination
and administration of
rabies immunoglobulin
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WHO recommendation for administration of a full PEP
depending on the severity of the contact with the suspected
rabid animal

23. Tetanus (Lockjaw)
 Serious bacterial infection that affects the nervous
system and causes muscles throughout the body to
tighten.
 Also called lockjaw because the infection often
causes muscle contractions in the jaw and neck.
 It can be life-threatening without treatment.
 Approximately 10 - 20 % of tetanus infections are
fatal, according to the CDC
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24. Causes/Etiology
 Bacteria => Clostridium tetani.
Spores can be found in dust, dirt and animal droppings.
Spores are small reproductive bodies produced by certain
organisms.
Are often resistant to harsh environmental conditions, such as
high heat.
 Person become infected when these spores enter the bloodstream
through a cut or deep wound and bacterial spores then spread to
the CNS and produce a toxin called tetano-spasmin.
Toxin (poison) blocks the nerve signals from spinal cord to
muscles.
This can lead to severe muscle spasms.
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25. Cont’d
 Tetanus infection has been associated with:
Crush injuries
Injuries with dead tissue
Burns
Puncture wounds from piercings, injury (such as
stepping on a nail)
Wounds contaminated with dirt, feces or saliva
 Less commonly, it’s been associated with:
Animal bites
Dental infections
Insect bites
Chronic sores and infections
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26. Clinical manifestation
 Difficulty swallowing
 Spasms and stiffness in various muscles, especially those in
jaw, abdomen, chest, back, and neck.
 Other common tetanus symptoms are:
– Fast heart rate
– Fever
– Sweating
– High blood pressure
 Incubation period —is between 3 and 21 days.
 Symptoms typically appear within 14 days trusted Source of
initial infection.
 Infections that occur faster after exposure are typically more
severe and have a worse prognosis.
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27. Diagnoses
History and physical examination
Sustained spasm of the facial muscles in which the
person appears to be grinning, or painful
muscular contractions.
History of injury or wound
No lab investigation for the tetanus
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28. Management
 Treatment depends on the severity of symptoms.
 Antibiotics such as penicillin to kill the bacteria
 Tetanus anti-toxoid (TAT)=10,000–20,000 IU IM as a single or tetanus
immune globulin (TIG)= 3000–5000 IU of TIG as a single IM to
neutralize the toxins that the bacteria have created in body
 Muscle relaxers to control muscle spasms
 Cleaning the wound to get rid of the source of the bacteria
 Difficulty of swallowing and breathing need a feeding tube or
ventilator
 In some cases, a surgical procedure called debridement is used to remove
dead or infected tissue.
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29. Complications
o Breathing problems due to spasms of the vocal cords
(laryngospasm) and spasms of the muscles that control
breathing
o Pneumonia (an infection of the lungs)
o Brain damage due to lack of oxygen
o Abnormal heart rhythm
o Bone fractures and fractures of the spine due to muscle
spasms and convulsions
o Secondary infections due to prolonged hospital stays
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30. Poliomyelitis
 Is an acute viral infection of the nervous system
caused by poliovirus types 1, 2 and 3.
 It is public health importance lies in the ability of
polioviruses to cause permanent paralysis and
sometimes death.
 It is readily transmitted, causing both endemic and
epidemic disease.
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31. Cont’d
Suggested case definition
Possible: Acute flaccid paralysis(AFP) without other
apparent cause.
Probable: AFP with decreased /absent tendon reflexes,
without other identified cause and with out
sensory or cognitive loss.
Confirmed: Serological evidence or isolation of virus,
together with clinically compatible illness
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32. Cont’d
Transmission
Polio is spread by the faeco–oral route.
Human being is the only reservoir.
Long-term carriage does not occur.
Poor hygiene favours spread
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33. Clinical features
 Most cases of polio are asymptomatic or present with a
sore throat or diarrhoea.
 Paralysis is relatively rare:
The proportion of paralytic cases increases with age from
about 1 in 1000 in infants to 1 in 10 in adults.
 Post-polio syndrome may develop 10–40 years after
recovery from an initial paralytic attack and
Is characterised by further weakening of previously
affected muscles.
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34. Cont’d
 Poliomyelitis should be considered in any patient with AFP
with a history of recent travel to an endemic area.
 Vaccine-associated polio should be considered in a recently
vaccinated individual with AFP (particularly after the first dose)
or in a close contact of a recently vaccinated individual.
 Main differential diagnosis is GBS
 The paralysis in polio is usually asymmetric, whereas in GBS it is
usually symmetrical.
 There is always residual paralysis in polio, whereas patients with
GBS usually recover completely.
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35. Diagnoses
Stool culture to identify polio virus.
Poliovirus can be recovered from faeces for up to 6 weeks
and in nasopharyngeal secretions for up to 1 week from
onset of paralysis.
At least two stool samples, 24 hours apart, should be
obtained within 7 days of the onset of paralysis.
Serological or by CSF examination
N:B:-All cases of AFP should be investigated to
exclude polio.
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36. Management
 Isolate the patient
 Fever, headache, back, and neck and muscle pain are relieved
by using pain relievers and muscle relaxant medications.
 Usually NSAIDs like Ibuprofen, Diclofenac and Acetaminofen are
preferred.
 Artificial ventilator for respiratory muscle paralysis
 Antibiotics for prevention of UTI, Pneumonia
 Bethanechol or urinary catheter for urine retention
 Positioning
 Physiotherapy
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37. Response to a case or cluster
 Immediate notification, by telephone to the CDC and to the regional
and national epidemiologist.
 Request urgent stool virology.
 Treat a single case of indigenous wild polio as a national public
health emergency.
 If confirmed, mass vaccination with OPV would be required,
possibly at the national or subnational level.
 In the event of an outbreak, involve international agencies such as
WHO.
 For an imported case, notify WHO or relevant national surveillance
unit.
 For vaccine-associated cases, no specific action is required, although
it may be an opportunity to review vaccine coverage locally
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38. ANTHRAX
 Caused by the spore-forming bacterium Bacillus anthracis.
 Is found worldwide in soil.
 Animals become infected through grazing in contaminated
areas.
 Under natural conditions, humans contract the disease after
close contact with infected animals or contaminated animal
products such as hides, wool or meat.
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39. Classification and Epidemiology
Has three clinical forms in humans:
 Inhalational
 Cutaneous and
 Gastrointestinal.
Cutaneous anthrax
Is the most likely way to develop anthrax.
Results from inoculation of spores subcutaneously through
a cut or abrasion.
Gastrointestinal and oro-pharyngeal anthrax
Occur in rural parts of the world where anthrax is endemic.
Result from ingestion of meat contaminated with spores.
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40. Cont’d
Cutaneous Anthrax
– Primary lesion appears as a nondescript, painless, pruritic papule,
usually on an exposed area such as the face, head, neck, or upper
extremity.
– Papule enlarges and develops a central vesicle or bulla with
surrounding brawny, non-pitting edema.
– Central vesicle enlarges and ulcerates over 1 to 2 days, becoming
hemorrhagic, depressed, and necrotic and leading to a central black
eschar.
– Satellite vesicles may be present.
– The eschar dries and falls off over the next 1 to 2 weeks.
– Tender regional lymphadenopathy, fever, chills, and fatigue may
occur.
– Systemic disease has been reported to have a mortality of 20% if
untreated.
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41. Cont’d
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42. Cont’d
INHALATIONAL ANTHRAX
Clinical presentation and diagnosis.
C/M develop rapidly after germination of anthrax spores.
Incubation period = 1 to 6 days but may be prolonged by
antibiotic administration.
Described as a two-stage disease.
Initial stage
Nonspecific, flulike illness lasting from several hours to a
few days.
Early clinical presentation includes: some combination of
fever, myalgia, headache, cough, mild chest discomfort,
weakness, abdominal pain, and chest pain.
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43. Cont’d
Profound malaise, fever, and drenching sweats are prominent
symptoms, and nausea and vomiting are frequent.
Classically, the initial stage is followed 1 to 3 days later,
sometimes after brief improvement, by the rapidly
progressive second stage
Second stage
Characterized by fever, dyspnea, diaphoresis, cyanosis, and
shock.
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44. Diagnosis
 There is no rapid screening test to diagnose inhalational
anthrax in its early stages.
 Chest x-ray or CT scan, or both, and
 Culture and smear of peripheral blood.
 Pleural fluid and cerebrospinal fluid, as well as
 Biopsy specimens taken from the pleura and
lung, are also potentially useful for culture and other testing
when disease is present in these sites,
Sputum culture and Gram stain are unlikely to be useful.
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45. THERAPEUTIC INTERVENTION.
• Early IV antibiotic treatment may improve survival in
inhalational anthrax.
• Aggressive supportive care including:
 Attention to fluid, electrolyte, and acid-base disturbances
 Drainage of pleural effusions, also play an important role in
treatment.
• At present, intravenous ciprofloxacin or doxycycline plus
one or two additional antimicrobials are recommended.
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46. INFECTION CONTROL
Person-to-person transmission of anthrax is not
known to occur.
Patients may be hospitalized in a standard hospital
room with standard barrier isolation precautions.
No treatment is necessary for contacts of cases.
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47. TOXOPLASMOSIS
 Caused by Toxoplasma gondii
– Protozoan parasite that causes a spectrum of disease from
asymptomatic lymphadenopathy to congenital mental retardation,
chorio-retinitis and encephalitis in the immuno-compromised.
Epidemiology
o Human exposure to toxoplasmosis is worldwide and common.
o 20%-40% of healthy adults in developed countries are seropositive.
o It is more common in Mediterranean countries than in Northern
Europe.
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48. Clinical features
 Acute infection is usually asymptomatic, but may produce a
mononucleosis-like illness.
 Congenital infection may occur following acute infection
during pregnancy.
 Congenital toxoplasmosis is characterised by foetal hepato-
splenomegaly, chorioretinitis and mental retardation.
 In the immuno-compromised, cerebral reactivation of
toxoplasmosis may occur, with presentation as encephalitis.
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49. Laboratory confirmation
 Acute toxoplasmosis may be diagnosed serologically.
– Specific IgM antibodies appear during the first 2 weeks, peak
within 4–8 weeks, and then typically become undetectable within
several months.
– IgG antibodies rise more slowly, peak in 1–2 months, and may
remain high for years.
– Congenital infection requires the demonstration of IgM in neonatal
blood; evidence of acute infection during pregnancy indicates the
need for foetal blood sampling at 18 weeks and cord blood at
delivery
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50. Cont’d
• Serology is not useful for diagnosis of toxoplasmosis
in patients with AIDS.
• Cerebral toxoplasmosis is usually diagnosed on the
basis of clinical features, a positive agglutination test
and CT/MRI scan appearance.
• Specific diagnosis in patients with AIDS and CNS
symptoms requires a brain biopsy.
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51. Transmission
The cat is the definitive host and transmits the
infection through faecal shedding of oocysts.
Children may come into contact with oocysts
from pets, soil or sandpits.
Adults are usually infected by ingestion of
undercooked meat.
Congenital infection usually occurs following
primary infection in a pregnant woman.
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52. Pathogenesis
– The incubation period is 10–25 days. There is
no person-to-person spread.
Prevention
 Pregnant women in particular should avoid raw or undercooked
meat.
 Contact with soil or food possibly contaminated with cat faeces
should be avoided.
 Chemoprophylaxis has been recommended for AIDS patients
with positive IgG serology once CD4 cells are low.
 Protect sandpits and play areas from cats.
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53. Reference
 Linda s. Williams, paula d. Hopper (2007) Understanding
medical surgical 3rd Edition
 Suzanne C. O’Connell Smeltzer, & Brenda G. Bare. (2010).
Brunner and Suddarth’s Text Book of Medical-Surgical Nursing.
12th Edition.
 Lewis,M.S.,Heitkemper,M.M.,and Dirksen, S.(2000). Medical
Surgical Nursing :Assessment And Management Of Clinical
Problems .5th Ed.
 Kasper L, Braunwald el al.(2015). Harrison’s princeples of
internal medicine,19th Edition.
 Mulugeta Alemayehu, CDC lecture note for nursing student,
Hawasa university
 Jeremy.H, Norman .B et al.(2005). Communicable Disease
Control Handbook ,2nd editon
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