Diseases of the Central Etiologic Agents

Nervous System » Streptococcus pneumoniae

» Heamophilus influenza type
B
» Neisseria meningitidis
» Enterovirus
 Brain & Meninges » HSV
» Meningitis » Mumps virus
» Rabies
» Encephalitis Pathophysiology
» Initially, the infectious agent colonizes or establishes
 Nerve Diseases a localized infection in the host. This may be in the
» Hansen’s form of colonization or infection of the skin,
disease nasopharynx, respiratory tract, gastrointestinal tract,
» Tetanus or genitourinary tract. Most meningeal pathogens are
» Poliomyelitis transmitted through the respiratory route, as
» exemplified by the nasopharyngeal carriage of
Transmissible Spongiform Neisseria meningitidis (meningococcus) and
Encephalopathy nasopharyngeal colonization with S. pneumoniae
(pneumococcus).
» From this site, the organism invades the submucosa
by circumventing host defenses (e.g., physical
barriers, local immunity, phagocytes/macrophages)
and gains access to the CNS by (1) invasion of the
bloodstream (i.e., bacteremia, viremia, fungemia,
parasitemia) and subsequent hematogenous seeding
of the CNS, which is the most common mode of
spread for most agents (e.g., meningococcal,
cryptococcal, syphilitic, and pneumococcal
meningitis); (2) a retrograde neuronal (i.e., olfactory
and peripheral nerves) pathway (e.g., Naegleria
fowleri, Gnathostoma spinigerum); or (3) direct
contiguous spread (i.e., sinusitis, otitis media,
congenital malformations, trauma, direct inoculation
during intracranial manipulation).
Epidemiology
» Most frequent in children less than 5years old with
peak rate in the 6-12months age group.
Incubation Period
» 2-10 days (Meningococcal)
Mode of Transmission
» Person to person thru infected droplets of respiratory
secretion.
» Close contact such as household, day care centers,
nursery schools, military camps.

Signs and Symptoms

» Sudden onset of high fever for 24hours, petechiae,
red macular rashes, nuchal rigidity (stiff neck-pain
w/neck flexion), photophobia.
» Meningeal irritation.
» Kernig sign: In a supine patient, flex the hip to 90°.
While the knee is flexed at 90°, an attempt to further
extend the leg produces pain in the hamstrings and
resistance to further extension.
» Brudzinski sign: Passively flex the neck while the
patient is in a supine position with extremities
extended. This maneuver produces flexion of the
hips in patients with meningeal irritation.

Diagnosis

MENINGITIS
» Inflammation of the meninges
» May be bacterial or viral (aseptic)
» May result from complications of neurosurgery,
trauma, infection or the sinus or ears, or systemic
infections
» Lumbar puncture (high
WBC, high protein, low
glucose, cloudy CSF).
» LP: insertion of a spinal
needle through the L3-L4
interspace into the lumber
subarachnoid space to
obtain CSF; the test is
contraindicated in clients
with increased ICP because
this procedure will cause a
rapid decrease in pressure in
the CSF around the spinal cord, leading to brain
herniation
➢ Preprocedure: obtain informed consent;
have the client empty the bladder
➢ During the procedure: position the client in
a lateral recumbent position and have the
client draw the knees up to the abdomen
and the chin onto the chest; assist with the
collection of specimens (label the
specimens in sequence); maintain strict
asepsis
➢ Postprocedure: monitor V/S
neurological signs that may indicate leakage
of CSF; position the client flat as
prescribed; encourage fluids to replace CSF
obtained from the specimen collection or
from leakage
» G/S of petechial scraping, CSF, blood (Gram
negative diplococci).
Complications
» Deafness, ataxia, seizure, obstructive hydrocephalus,
arthritis, pneumonia, DIC, myocaarditis.
Treatment
» PenG IV
» Chloramphenicol if with allergy to
Pen
» Mannitol (for cerebral edema)
» Dexamethasone (anti-
inflammatory)
Nursing Interventions
» Medications as ordered
» Assess for signs of increasing ICP: widening pulse
pressure, HPN, bradycardia
(Cushing’s Triad)
» Priority: airway, safety
» Strict respiratory precaution
until 1st 24hours of antibiotic
treatment
» Institute seizure precautions
» Keep room dark
» Elevate the HOB 30deg; avoid neck flexion and
extreme hip flexion
» Prevent stimulation and restrict visitors
» Suctioning of secretions; hand washing
RABIES
» Severe viral infection of CNS that is communicated
to humans by the saliva of infected mammals.
» Also Hydrophobia, caused by Rhabdovirus
(neurotropic virus from Genus Lyssavirus).
Pathophysiology
» When the rabies virus enters muscles, it replicates
locally and then is transported through peripheral
sensory nerves to the spinal ganglia, where it
replicates and travels up the spinal cord to the brain.
The virus migrates to the gray matter of the brain and
predominates in the neurons of the limbic system,
midbrain, and hypothalamus. Efferent nerves
transport virus to the acinar glands of the
submaxillary salivary glands, where it achieves high
concentrations.
Epidemiology
» 4.4/100,000 population
» Highest incidence in R IV,V,VII
» Source: saliva of rabid dogs, bats, cats, cattle
Incubation Period
» 5days-6years (average 2-8 weeks); variation in
length of incubation period depend on severity of
bite, site of bite in relation to the richness of nerve
supply and distance from CNS, size of inoculum, age
and immune status of host, protection provided by
and clothing.
Mode of Transmission
» Bites of rabid animals
» Human-to-human transmission has only occurred
with corneal transplants.
» Transmission of virus in saliva through mucous
membranes, open wounds, or scratches is possible
but rarely documented.
Signs and Symptoms
» Rabid dog: withdrawn, dumb, paralytic; furious
stage: bites without provocation.
» In man:
♪ Prodromal: headache; malaise; anorexia; sore
throat; salivation; diaphoresis; tingling sensation;
numbness at site of bite; low grade fever
♪ Excitement/maniacal: hydrophobia;
aerophobia; increased anxiety; cranial affectation
♪ Paralytic stage: die of paralysis or respiratory
arrest
Diagnosis
» History of exposure to saliva of infected animal
» Negri bodies in samples of brain tissue of infected
animal; Fluorescent Rabies Antibody Staining
Treatment
» Symptomatic and supportive
» Wash area of bite with soap and running water.
Nursing Interventions/Considerations
» Strict isolation of aeg throughout the course of
illness; caution against contamination of open wound
or mucous membrane with aeg’s saliva.
» Immunization:
♪ Active
« Purified Verocell Rabies Vaccine (PVRV)
0.5ml/vial
« Purified Duck Embryo Vaccine (PDEV)
1ml/vial
« Purified Chick Embryo Cell Vaccine
(PCECV) 1ml/vial
« May be administered IM/ID
♪ Passive
« Rabies Human Immune Globulin
ENCEPHALITIS
» Acute viral encephalitis (enkephalos + -itis, meaning
brain inflammation) is often an unusual
 manifestation of common viral infections and most ♪ Ridley-Jopling: Depending on the host
commonly affects children and young adults. response to the organism, leprosy can manifest itself
» In general, viral encephalitides can be divided into 4 clinically along a spectrum bounded by the
separate categories based on the cause and tuberculoid (TT) and lepromatous (LL which is the
pathogenesis of the following complications: most severe) forms of the disease. Most patients fall
♪ Acute viral encephalitis; into the intermediate classifications, which include
♪ Postinfectious encephalomyelitis; borderline tuberculoid (BT), midborderline (BB), and
borderline lepromatous (BL).
♪ Slow viral infections of the CNS;
♪ And chronic degenerative diseases of the CNS, ♪ WHO system: classifying leprosy according
which are presumed to be of viral origin. to the number of lesions and the presence of bacilli
on a skin smear.
Etiology « Paucibacillary (PB) leprosy is characterized by
» Person-person spread 5 or fewer lesions with absence of organisms on
♪ Mumps: frequent in unimmunized population smear. Paucibacillary leprosy generally includes
♪ Measles the tuberculoid and borderline lepromatous
♪ Enterovirus group: more serious in neonates categories from the Ridley-Jopling system.
♪ Rubella: uncommon « Multibacillary (MB) leprosy is marked by 6 or
♪ Herpesvirus group: HSV 1&2; VZV; CMV; more lesions with possible visualization of bacilli
EBV on smear. Lepromatous, borderline lepromatous,
» Arthropod-borne and midborderline on the Ridley-Jopling scale are
included in the multibacillary category.
♪ Arbovirus: spread by mosquitoes or ticks;
Japanese encephalitis is the most common Epidemiology
» Spread by mammals » Rarely seen in children below 5years old
♪ Rabies
» Source: infected persons; majority from nasal
secretions of aeg with untreated, multibacillary
forms; little shedding of EA from aeg’s skin occurs.
Pathophysiology
Incubation Period
» The pathophysiology of viral encephalitis varies » 1-5years old
according to the viral family. Viruses enter the CNS
through 2 distinct routes: Period of Communicability
♪ Hematogenous dissemination: most common » As long as there are open lesions
path; e.g. arbovirus
♪ Retrograde neural dissemination: e.g. rabies Mode of Transmission
» Contact (skin-skin; respiratory) with humans with
Signs and Symptoms untreated multibacillary (lepramatous or borderline
» Headache; fever; nuchal types)
rigidity; alterations in
consciousness; behavior Signs and Symptoms
& speech disturbance; » Early manifestations
presence of cold sores, ♪ Color changes in skin which does not disappear
lesions or ulcerations os the even with treatment
oral cavity; signs of ♪ Skin ulcers which does not heal with treatment
increased ICP ♪ Pain and redness of the eyes
♪ Nasal obstruction and nose bleeding
Diagnosis ♪ Muscle weakness and paralysis
» Lumbar puncture; PCR; ♪ Loss of sensation on affected areas
ELISA;CT scan; MRI ♪ Loss of hair growth
♪ Anhydrosis: loss of sweating
Treatment » Late manifestations
» Antiviral agents for viral ♪ Lagophthalmos: inability to close the eyelids
etiology (Acyclovir)
♪ Madarosis: loss or absence of eyebrows
Nursing Interventions ♪ Sinking of bridge of nose
» Supportive ♪ Leonine face
» Assess level of consciousness ♪ Natural amputation – toes, fingers, ears, nose
♪ Contractures: clawing of fingers and toes
» Assess for signs of increased ICP; ♪ Chronic skin ulcers
nuchal rigidity, Kernig’s or ♪ Gynecomastia
Brudzinski’s
» Assist client to turn, cough and deep breathe Diagnosis
frequently
» Elevate HOB 30-45 deg » Lepromine Skin test: determine susceptibility/
resistance
LEPROSY » Skin lesion biopsy
» Also Hansen’s disease; Hansenosis; Lepra Treatment (MDT)
» A chronic disease transmitted from person-person » Paucibacillary
affecting the skin, mucous membranes and nervous
tissue » Dapsone (daily for 6months) + Rifampicin (once a
Etiologic Agent month)
» Multibacillary
» Mycobacterium leprae
Pathophysiology: » Rifampin (monthly) + Dapsone (daily for 6months)
» Leprosy has 2 + Clofazimine (at least 2years)
classification schema:
Nursing Interventions
» Balanced diet, exercise, rest, hygiene
» Meticulous eye care; skin care
» Teach aeg about SE/AE of drugs
» Rifampicin: discoloration of body fluids; rashes;
muscle soreness; anuria (nephrotoxicity);
thrombocytopenia; jaundice (hepatotoxicity)
» Dapsone: causes increase in number of lesions
TETANUS
» An infectious disorder
characterized by increased
muscle tone and spasms
caused by the release of the
neurotoxin tetanospasmin by Clostridium tetani
following inoculation into a human host.
Pathophysiology
» Tetanospasmin, a zinc metalloprotease, is released in
the wound and binds to the peripheral motor neuron
terminal, enters the axon, and, via retrograde
intraneuronal transport, reaches the nerve cell body
in the brainstem and spinal cord. The toxin migrates
across the synapse to presynaptic terminals where it
blocks the release of the inhibitory neurotransmitters
glycine and gamma-aminobutyric acid (GABA) by
cleaving proteins crucial for the proper functioning
of the synaptic vesicle release apparatus. One of
these important proteins is
synaptobrevin. This
diminished inhibition results
in an increase in the resting
firing rate of the motor
neuron, which is responsible for the observed muscle
rigidity.
» The lessened activity of reflexes limits the
polysynaptic spread of impulses (a glycinergic
activity). Agonists and antagonists may be recruited
rather than inhibited, with consequent production of
spasms. Loss of inhibition may also affect
preganglionic sympathetic neurons in the lateral gray
matter of the spinal cord and produce sympathetic
hyperactivity and high levels of circulating
catecholamines. Finally, tetanospasmin can block
neurotransmitter release at the neuromuscular
junction, causing weakness and paralysis.
Epidemiology
» Phil stat: tetanus neonatorum – 0.1/100,000
population
» non-neonatal tetanus – 0.4/100,000 population
» Source: soil, dust
Incubation Period
» 4-21 days
Mode of Transmission
» Spores of bacteria are
usually introduced into an area of injury of wound;
disease develops only after spores are converted to
vegetative forms which produce tetanospasmin under
anoxic condition.
» In neonate, thru
umbilical cord stump
when cut with
contaminated scissors.
Signs and Symptoms
» Trismus: lock jaw
» Risus sardonicus:
sardonic grin
» Opisthotonus: anterior arching of spine
Diagnosis
» Based on clinical manifestations
» Wound culture
Complication
» Pneumonia; atelectasis
Treatment
» Tetanus Immune globulin (TIG) IM: to neutralize
toxin
» Alternative: Tetanus antitoxin (TAT)
» PenG; Metronidazole; Tetracycline
» Diazepam(Valium): control seizure
» Propanolol (Inderal): Beta-adrenergic blocker
Nursing Interventions/Considerations
» Dark room
» Aeg safety
» Maintain F&E, nutrition (NGT)
» Minimal handling
» Seizure precautions
» Oxygenation
» Tracheostomy if prolonged spasms of respiratory
muscles, unable to cough or swallow, laryngeal
obstruction, coma
» Active immunization: as DTP IM
POLIOMYELITIS
» Also infantile paralysis is an enteroviral infection
that can manifest in 4 different forms: inapparent
infection, abortive disease, nonparalytic
poliomyelitis, and paralytic disease.
Etiologic Agent
» Poliovirus
Pathophysiology
» Poliovirus is an RNA virus that is transmitted
through the oral-fecal route or by ingestion of
contaminated water. The viral particles initially
replicate in the nasopharynx and gastrointestinal tract
and then invade lymphoid tissues, with subsequent
hematologic spread. After a period of viremia, the
virus becomes neurotropic and produces destruction
of the motor neurons in the anterior horn and
brainstem. The destruction of motor neurons leads to
the development of flaccid paralysis, which may be
bulbar or spinal in distribution.
Epidemiology
» Polio-endemic countries: India, Pakistan,
Afghanistan, Nigeria, Egypt
» In Phil, the last case occurred in Cebu in 1993
Incubation Period
» 7-14 days; unknown communicability period
Mode of Transmission
» Fecal-oral; oral-oral; ingestion of contaminated water
Signs and Symptoms
» Minor polio
♪ Inapparent/ subclinical
♪ Abortive: recover within 72hours; flu-like,
backache, vomiting
» Major polio
♪ Paralytic: asymmetrical weakness; paresthesia;
urine retention; constipation.
♪ Nonparalytic: slight involvement of CNS;
Poker’s spine or stiffness and rigidity of spine;
spasms of hamstring muscle, with paresis.
♪ Tripod position: extend his arms behind him
for support when upright.
♪ Hoyne’s sign: head falls back when he is in
supine with shoulder elevated.
 ♪ Meningeal irritation: (+) Kernig’s and
Brudzinski’s signs.

Diagnosis
» Throat swab; S/E; lumbar puncture

Treatment
» Non-specific, supportive

Nursing Interventions
» No morphine
» Moist heat application for spasms
» Airway: tracheostomy
» Monitor for respiratory paralysis
» F&E
» Enteric & strict precautions
» Immunization: OPV

Transmissible Spongiform Encephalopathy (TSE)

» Bovine spongiform encephalopathy (BSE), also
known as mad cow disease, and variant Creutzfeldt-
Jakob disease (CJD) are related disorders. They
belong to the family of diseases known as the
transmissible spongiform encephalopathies (TSEs).
TSEs are caused by a transmissible proteinaceous
particle, which is yet to be fully characterized. Other
TSEs include scrapie (a disease of sheep), feline
spongiform encephalopathy, transmissible mink
encephalopathy, and chronic wasting disease of deer
and elk. Human forms include classic CJD, variant
CJD, kuru, Gerstmann-Sträussler-Scheinker disease,
familial fatal insomnia, and sporadic fatal insomnia.
» Human TSEs share the following characteristics:
♪ A prolonged incubation period of several
years.
♪ A progressive debilitating neurologic
syndrome that is invariably fatal.
♪ Pathological changes that are confined to the
CNS and consist of the following 3 classic features:
spongiosis, gliosis, and neuronal loss.
♪ A transmissible agent that does not elicit any
specific immunologic response in the host and is
unusually resistant to conventional inactivation
procedures.
» Epidemiologic, biological, and biochemical data
favor the hypothesis that variant CJD is a BSE
zoonosis, probably arising from a double-species
switch from sheep scrapie to BSE and then from
BSE to human variant CJD
» Like other prion-related diseases, variant CJD is
relentlessly progressive and inevitably leads to death.
» An average incubation period of 11-12 years can be
estimated.
» Early psychiatric features include dysphoria
(sadness), withdrawal, anxiety, irritability, insomnia,
and loss of interest. In a small number of cases, pain,
numbness, or ataxia may be present in the early
stages.