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ENCEPHALITIS
ENCEPHALITIS
Endocrine disturbances
• Patient may grow either fat or thin.
• Sexual interest or activity is lost.
Treatment must be symptomatic and
supportive.
Convulsions must be controlled.
Nose and throat secretions should be
sanitarily disposed of.
TSB or alcohol sponges may be given if the
temperature is excessively high.
Unless patient is comatose, oral fluid should
be encouraged.
Oral care should be done strictly.
A mouth gag and protective devices, such as
bedrails, should be available in case
convulsions occur.
Intake and output records should be closely
monitored.
Patients should be observed for neurologic
signs involving speech, swallowing difficulty,
twitching, eye movements, and indications of
paralysis.
The beginning, duration, and frequency of all
convulsions should be carefully observed and
recorded.
CSF analysis
Serologic test- 90% confirmatory, done on
the 7th day of illness
Complement-fixation test
Hemagglutination-inhibition antibody test
ELISA (IgM)
Polymerase chain reaction.
Keep the patient in a quiet, well- ventilated
room.
Stretch linens.
Encourage or perform oral hygiene on the
patient.
Do bed baths if not contraindicated.
Sanitary disposal of nose and throat
secretions.
Oral fluids should be encouraged.
If stupor or coma is present, intravenous
fluids and gavage feeding may be ordered.
Bedrails should be available.
Intake and output records are maintained,
and temperature, pulse, and respiration rates
are taken at four-hour intervals or oftener if
indicated.
Observed for neurologic signs involving
speech, swallowing difficulty, twitching, eye
movements, and indication of paralysis,
Turn the patient to sides at least every 3-4
hours.
Encourage increased oral fluid intake.
Encourage high caloric intake.
Moisten lips with mineral oil.
Render TSB if febrile.
Sleep pattern disturbances
Altered cerebral perfusion
Altered nutrition: Less than body
requirement
Impaired physical mobility
Impaired swallowing
Ineffective airway clearance
Impaired communication
Preventive measures are directed toward the
identification of mosquito vectors.
Prevention and control must be geared
toward the elimination of breeding places,
destruction of larvae, screening of homes,
and use of repellents.
A broad public education program about all
phases of preventive programs is important.
At least four forms of acute encephalitis have
occurred epidemically and sporadically in the
United States: the von Economo, the St.
Louis type, the eastern and western equine
types.
DEFINITION:
Von Economo’s encephalitis is a disease
affecting the central nervous system,
characterized by a variety of symptoms in
different eases, depending upon the site of the
lesions.
“Sleeping sickness “ sometimes applied to this
disease. Synonyms: encephalitis lethargica; the
Vienna type of infectious encephalitis; Type A
encephalitis; epidemic encephalitis
ETIOLOGY:
Neurotropic form of herpes virus.
SOURCES OF INFECTION:
Nasal and oral discharges of infected
individuals or carriers.
PATHOLOGY
The spinal fluid may show a variably
increased cell count, chiefly of the
mononuclear variety; the globulin usually is
increased, and the sugar content may be
increased, and then may be some reduction
of colloidal gold.
The blood shows a leukocytosis.
MODE OF TRANSMISSION:
Direct contact with an infected individual or
carrier, or indirectly by articles freshly soiled
with the discharges from the nose and throat
of infected persons.
SUSCEPTIBILITY
Children and young adults
INCUBATION PERIOD:
Four to twenty –one days
PERIOD OF COMMUNICABILITY:
Probably transmissible during the acute
febrile stage
TREATMENT:
Lumbar puncture is done as a diagnostic and
therapeutic measure.
Treatment is symptomatic.
METHODS OF CONTROL:
Recognition and reporting
Isolation
Quarantine
Immunization
DEFINITION:
St. Louis encephalitis is a
meningoencephalitis caused by a specific
virus and characterized by a varied
symptomatology.
ETIOLOGY
A specific virus has been proved to be the
cause of the St. Louis type.
SOURCES OF INFECTION:
Birds and chickens are a probable source of
infection.
PATHOLOGY:
Vascular congestion of the brain as well as the
spinal cord, engorgement of the blood vessels of
the meninges with diffuse infiltration of
lymphocytes.
Degeneration and necrosis of the gray and white
matter.
MODE OF TRANSMISSION:
Transmitted by the bite of Culex mosquitoes
which have fed on infected fowls and other
birds; mites may serve as vectors.
SUSCEPTIBILITY:
Infants and older age group
INCUBATION PERIOD:
4 to 21 days
CLINICAL MANIFESTATION
Fever
Headache
Drowsiness
Disorientation
Motor disturbances
Meningeal irritation with increase of cells in the
spinal fluid
PERIOD OF CONVALESCENCE:
The course of the disease may be stormy but
recovery usually is rapid.
The temperature returns to normal within 7
to 10 days.
In severe cases, convalescence is prolonged.
COMPLICATIONS AND SEQUELAE:
Sequelae are not common, and when they
do occur, they are less severe than those of
the von Economo type.
Parkinsonism is rare.
DIFFERENTIAL DIAGNOSIS
Complement fixation and neutralization tests
aid in confirming the diagnosis
TREATMENT
The treatment is symptomatic.
METHODS OF CONTROL
Recognition and reporting
Isolation
Immunization
DEFINITION:
Equine encephalomyelitis occurs in the
western and eastern forms.
Both are viral infectious capable of being
transmitted to man.
The western type is a disease primarily of
horses and mules; the eastern type is a
disease primarily of horses, mules and birds.
ETIOLOGY
The virus causing eastern equine
encephalomyelitis is more virulent than the
virus causing the western type of the disease.
SOURCES OF INFECTION
Transmitted by insects, especially several
species of mosquito.
PATHOLOGY
In the western type of the disease the most
marked pathologic changes occur in the brain
and meninges, the spinal cord rarely being
involved.
Foci of degeneration and necrosis are
widespread in the gray matter, and
infiltration of white blood cells is diffuse
In the eastern type, the lesions most
frequently involve the brain stem and basal
ganglia.
Destruction of nerve cells, inflammatory
changes in the small blood vessels and
thrombosis.
INCUBATION PERIOD
The incubation period has not been determined
for eastern encephalomyelitis.
4 to 21 days for the western type of the disease.
CLINICAL MANIFESTATIONS
The western equine type resembles the St. Louis
type clinically.
Eastern type is abrupt onset and more severe
with high fever, vomiting, drowsiness, and
convulsions.
PERIOD OF CONVALESCENCE
Recovery is slow.
The eastern type of the disease is more
severe than the western.
COMPLICATIONS AND SEQUELAE
In the western type sequelae are rare, but
nervous and mental sequelae usually follow
the eastern type.
DIFFERENTIAL DIAGNOSIS
The diagnosis is made by laboratory tests.
TREATMENT
No specific treatment for equine
encephalomyelitis
METHODS OF CONTROL
Recognition and reporting
Isolation
Immunization
Isolation
Comfort of the patient
Care of the mouth
Care of the eyes
Diet
Clinical recording
Disinfection