Central Nervous System (CNS)

Infections

Prepared by:
John Eric T. Salvador, RN
 Bacterial infections

 Acute bacterial meningitis

 Chronic meningitis
 Tubercular meningitis
 Cryptococcosis
 Fungal meningitis
 Syphilitic meningitis
 Amoebic meningitis
      
Acute Bacterial meningitis
Overview

• The cerebrum, cerebellum, brain stem, spinal cord and their covering
membrane (meninges) constitute The central Nervous System (CNS)

• One specialized defense mechanism of the CNS is the blood-brain barrier

(BBB).

• BBB serve to minimize passage of infectious agents and toxic metabolites

into the cerebrospinal fluid ( CSF) and tissues

• BBB also regulate the rate of transport of plasma proteins, glucose and
electrolytes.

• When CNS infection develops, the BBB poses difficulties in control    
                                                                                        
 CSF Flow

• Within the brain are ventricles, which are

cavities in which CSF is actively produced
• CSF is produced by choroid plexuses, the CSF
fills the lateral ventricles in each half of the
brain
• CSF circulates into the third ventricle, and
then through cerebral aqueduct and to the 4th
ventricles and then to the subarachnoid space
(SAS) over the entire CNS including the
spinal cord
• It is reabsorbed by venous system in the
meninges
Bacterial
meningitis in
patients with
disributed BBB
 Routes of infection
• The disease usually begins as an infection by normal body flora, of:

1. The ear (otitis media) - Haemophilus influenzae

2. The lung (lobar pneumoniae) - Streptococcus pneumoniae

3. The upper respiratory tract (rhinopharyngitis) - Neisseria meningitidis, Haemophilus influenzae,

Streptococcus, Group B

4. The skin and subcutaneous tissue (furunculosis) S. aureus

5. The bone (osteomyelitis) - S. aureus

6. The intestine - E. coli

• This localized infection develops into a bacteremia with a metastatic infection in the leptomeninges
(arachnoid and pia mater),

• Traumatic surgical, or congenital lesions may give direct access

• Males are affected twice as often as females

 Etiology
Neonates (0-2 weeks)
        Escherichia coli
        Streptococcus, Group B
        Staphylococcus aureus
        Listeria monocytogenes
        Streptococcus, Group A

Infants (½ - 3 months)
        Streptococcus, Group B
        Listeria monocytogenes
        Escherichia coli

"Normal" Adults (6-21 years)

 Neisseria meningitidis ( A, B, C, Y, and W-135)       
Streptococcus pneumoniae
 Clinical symptoms
The manifestations of acute bacterial meningitis are
independent of the etiological agent:
They result from:
   

1. Infection, manifestations 2. Increased intracranial pressure,

        a. Chills manifestations of which are:
        b. Fever         a. Headache
        c. Malaise         b. Vomiting
        d. Headache         c. Eye effects
        e. Myalgia         d. Papilledema (late)
        e. Full fontanelle
        f. Enlarged cranium

3. Meningeal irritation
        a. Stiff neck
        b. Spasms of muscles
        c. Nuchal rigidity
        d. Opisthotonos
 4. Hemorrhage
        a. Petechia
        b. Purpura
        c. Ecchymosis

5. Eye effects
        a. Photophobia    
        b. Venous congestion of ocular fundi  
        c. Unequal pupils  
        d. Pupil dilation
       6.Mental status
        e. Sluggish reaction to light
        f. Squint         a. Drowsiness
        g. Diplopia         b. Delirium
        I. Papilledema         c. Coma
 Lab Diagnosis
• Examination CSF is the key to the definitive
diagnosis of acute bacterial meningitis. The CSF
should be examined in every patient in whom the
clinical findings are consistent with even the
possibility of meningitis,
Examine the CSF for:
1. Pressure
2. Clarity
3. Presence of microorganisms
4. Presence of leukocytes
5. Concentration of glucose
6. Concentration of protein
   
 Therapy

1. Correction of fluid and electrolyte deficits.

2. Provision for adequate oxygenation.
3. Monitoring of cardiovascular function:
a. Pulse
b. Arterial blood pressure
c. Central venous pressure
4. Monitoring intracranial pressure - administer
urea or mannitol to reduce cerebral edema.
5. Administration of antibiotics -
 Prevention

Purified polysaccharide vaccines are available

for the prevention of infection by:
• Neisseria meningitidis - each dose of the
multivalent vaccine provides A, C, Y and W-
135 capsular polysaccharides. Effective in
children over 3 months of age.
• Streptococcus pneumoniae, each dose of the
multivalent vaccine provides 23 types of
capsular polysaccharide covering the majority
of strains causing meningitis. Recommended
for children over 2 years of age.
• Streptococcus pneumoniae, each dose of the
multivalent vaccine provides 7 types of
capsular polysaccharide conjugated to a non-
toxic diphtheria toxin. Recommended for
children at 2, 4, 6 and 12 months of age.

• Haemophilus influenzae - each dose of the

monovalent vaccine provides the capsular
polysaccharide from serotype b organisms
conjugated to a protein. Recommended for
children at 2, 4, 6 and 15 months of age.
 Chronic Bacterial Meningitis

Has more insidious onset, with progression of

signs and symptoms over a period of weeks

• Tubercular meningitis
• Syphilitic meningitis
 Clinical Picture

The patient may feel unwell, lose some weight and have no other symptoms
There may be no fever or low fever.

1. Headache - frontal, temporal or retro-orbital. Most common feature and

it becomes progressively more frequent and severe.
2. Mental aberrations (from simple irritability to psychosis)
3. Motor abnormalities (altered reflexes to paralyses)
4. Cranial nerve dysfunctions (aphasia, visual disturbances, hearing loss)
5. Cerebellar signs
6. Evidence of increased intracranial pressure
7. Fever in about 1/3 of patients
 Diagnosis

Best evidence is from CSF.

1. Increased CSF pressure

2. Protein is elevated
3. Glucose is decreased (45% of blood glucose)
4. Leukocytosis (40-400/mm3 - mostly
mononuclear cells)

Radiology 
Prognosis:
Almost always fatal if it goes untreated (90% of
patients die within one year).
 
Treatment:
Antimicrobial therapy
Viral Infection of the CNS

Viral meningitis (Aseptic meningitis)

Viral Encephalitis
 Etiology of primary acute viral infections of CNS
Agent Major age group affected

Enteroviruses Infants, children

Mumps Children
Herps simplex Type-1 and type-2 Adult
Neonates, young adults
Arboviruses Adults
West virus encephalitis
Rabies All ages
Measles Infants, children
Varicella-zoster (HSV-3) Infants and children
Lymphocytic chorimeningitis Adults, children
Epstein-Barr virus (HSV-4) Children, young adults
Other, (HIV) All ages
• Penetration of BBB may be accomplished by means of
virus-laden phagocytes migrating through blood
vessels of the meninges or brain or by passage of
virus particles through the choroid plexus

• There is always some involvement of brain tissue so

the disease is really a meningoencephalitis.

• Generally milder than bacterial or fungal meningitis

and is self limiting.
 
 Clinical picture

The signs and symptoms of viral meningitis are variable. They

may include:
1. Sudden onset
2. Intense frontal or retro-orbital headache
3. Undulating fever that never goes above 40C
4. Skin rash

At the onset of fever or shortly

thereafter there is:
Malaise , drowsiness Nuchal rigidity develops and
Sore throat , myalgia there are almost always
Nausea , vomiting stiffness of the back and
There may also be photophobia , pain on flexion
tinnitus (noise in the ears)
,Vertigo , chest and abdominal pain
 Lab Diagnosis
• CSF is transparent
• May be slightly turbid
• (<500 leukocytes/mm3),monocytes
• glucose is normal
• Protein is elevated.
• Diagnosis requires virus isolation and serological
techniques

Prognosis
• Full recovery with no sequelae
 
Therapy
• Bed rest, analgesic drugs, repletion and conservation of
fluids and electrolytes.
Prognosis
• Full recovery with no sequelae
 
Therapy
• Bed rest, analgesic drugs, repletion and
conservation of fluids and electrolytes.
 Rabies (hydrophobia)

 
Overview:
• Rabies virus is a bullet-shaped, enveloped, single
stranded RNA virus.
• This is primarily a viral infection of non-human
carnivores.
• Transmission to man is rare and is usually effected
through a bite.
• Clinical evidence of involvement of the CNS appears
after an extremely variable period of incubation.  
 Pathogenesis

Inoculation of virus through the epidermis as a

result of an animal bite. Inhalation of heavily
Contaminated material, such as bat dropping
Can also cause infection

Replicates initially in muscle and then enters

The peripheral nervous system
Virus passes along the
Along autonomic nerves
To reach other tissues,
Including the salivary glands
Spread to the CNS gray matter, the Kidneys, and lungs
Pathognomonic lesion the Negri bodies
( eosinophilic cytoplasmic inclusion
Bodies)
 Diagnosis

• Where there is a history of bite by a known rabid

animal and the bitten person shows typical symptoms
• The manifestations of rabies begins in man anywhere
from 10-240 days after exposure. However, the
incubation period is usually 30-90 days. The length of
this incubation period is a function of:
1. The number of sensory nerves ending in the bitten
area
2. The dose of virus
3. The severity of the bite wounds
4. The distance from the bite wound from the CNS
• Presents as acute fulminate, fatal encephalitis
• Excess motor activity, hallucination
• Muscle spasm, seizures and focal paralysis,
coma
 Lab diagbosis

• CSF shows minimal to no abnormalities

• Lymphocytic pleocytosis (5-30 cell/mm3)
• Detection of rabies antigen by
Immunofluorescent stain of a nape of neck
biopsy
• Virus or antigen detected in brain tissue
• Negri bodies in 80 % of cases
PROGNOSIS:
• Only 4 people have ever recovered from
rabies. CNS sequelae are common.  
TREATMENT:
1. Washing the wound with copious amounts of soap and water.
2. Apply 1% quaternary ammonium compounds after all traces of
soap have been removed.
3. Apply antirabies serum by careful instillation into the wound and
by infiltration around the wound. Administer serum
systemically.
4. Postpone suturing the wound.
5. Institute antitetanus procedures
6. Start administration of vaccine pending autopsy of animal
involved in the bite. Stop treatment if animal is normal.
If rabies symptoms ensue give extensive supportive
care
a. Tracheostomy to prevent hypoxia
 b. Careful tracheal suctioning
 c. Use of supplemental oxygen
d. Control focal seizures with anticonvulsant therapy
 
 Vaccine Available

• Rabies vaccine
• Recombinant vaccine - vaccinia virus with
rabies glycoprotein gene. (1 vaccination)
Fungal infections of the CNS
 Common

Rare
Cryptococcus neoformans
Coccidioides immitis

Uncommon
Pseudoallescheria bodii
Penicillum species
Sporothrix schenkii

Histoplasma capsulatum
Candida species
Aspergillus species
Blastomyces dermatitidis
 Other causes of CNS infections

Parasitic infections

 Trypanosoma
 Acanthamoeba species
 Naegleria fowleri
 Toxoplasama gondii
 Trichinella spiralis
 Taenia solium (cysticercosis)
 Findings of cerebrospinal fluid analysis: Normal versus Infection

clinical situation Leukocytes/mm3 % polymorphonuclears Glucose Protein mg/dl

% of blood

Children &
adults
Normal 0-5 0 ≥ 60 ≤ 30

Viral infection 2-2000 ≤ 50 ≥ 60 30-80

Bacterial infection 5-5000 ≥ 60 ≤ 45 ≥ 60

TB and mycoses 5-2000 ≤ 50 ≤ 45 ≥ 60

Neonates
Normal ( term) 0-32 ≤ 60 ≥ 60 20-170

Normal (preterm) 0-29 ≤ 60 ≥ 60 65-150

 Case presentation # 1
A 3-year-old male with recent history of acute otitis media
presented to the emergency department. Upon examination, he
was febrile to 39.50C and lethargic. No evidence of a rash was
present. His vaccination was history was up to date. Laboratory
studies included a complete blood count, which showed
leukocytosis with a total leukocyte count of 21,000/ml. A lumber
puncture produced cloudy CSF with a cell count of 210
leukocytes/mm3 with 85% neutrophils. The CSF glucose was
decreased, and the CSF protein was elevated. The child received
IV antibiotics, and the CSF sample was sent to the microbiology
Laboratory for CSF Gram stain and culture. CSF smear showed
moderate intracellular Gram-positive cocci in pairs. Subsequent
culture of the CSF grow a mucoid strain of Strep. pneumo
 Case presentation # 2

A 2-years unvaccinated child was seen in the

emergency room with headache and fever.
The spinal fluid was sent to the lab for
culture and sensitivity. The Gram stain
showed many white blood cells and many
Gram-negative rods (small)
 Case presentation # 3
A 52 years-old male arrived at an emergency room in a
disoriented and poorly responsive state with difficult breathing.
The patient’s history included poorly controlled diabetes and
chronic obstructive pulmonary disease secondary to cigarette
smoking. Current medications included steroids his pulmonary
disease. Physical examination showed that the patient was
slightly febrile, lethargic, and in respiratory failure. He showed
deteriorating mental status, and a diagnosis of meningitis was
considered . A lumber tap produced a CSF sample that on direct
smear using calcofluor reagent showed encapsulated budding
yeast. Despite aggressive therapy with amphotericin B and 5-
flucytosine, the patient’s condition failed to improve. The
patient died on the third day of hospitalization.