Infectious Pathologies of the CNS Flashcards
what is the significance of infectious CNS disorders
rare
major cause of morbidity and mortality
how do infectious CNS disorders occur
when pathogens invade the CNS/PNS via various modes of transmission and get past protective barriers
what type of germs present a challenge in prevention and treatment
drug-resistant germs
how are bacteria and viruses removed in the CNS
via reticuloendothelial system in the blood brain and blood cerebrospinal fluid barriers
glial cells go to work once an infectious pathogen in identified
immune system
what type of cells are the main cells in the immune system of nervous system
microglial cells
A network of blood vessels and tissue that is made up of closely spaced cells and helps keep harmful substances from reaching the brain
blood brain barrier
what substances can easily pass through BBB and which can pass via active transport
easy: water and O2
active transport: glucose and amino acids
why is there a reduction in immune protection if a pathogen invades CSF
- CSF has 1/200 the amount of antibody and WBC’s are very low
is there a lymphatic system to protect the brain
no
what are the families of infectious CNS/PNS pathologies
encephalitis
meningitis
poliomyelitis
botulism
tetanus
rabies
shingles
what populations are most commonly effected
can effect children, but more often in adults or immuno-compromised individuals
describe the outcomes of CNS pathologies
varies on pathogen
can be very serious is not dx early and when not appropriately managed
list some differential diagnosis s/s that could indicate CNS infection
- seizure activity
- profound alteration in consciousness (GCS, MMSE, seizure monitoring)
- cognitive and perceptual assessment
- sensory integrity
- cardiopulmonary sequelae
- movement disorders reflect the insult of brain structures (decorticate/decerebrate)
what may be the first sign of CNS infection
seizures
describe encephalitis
an acute inflammation to brain tissue
another name for brain tissue
parenchyma
what matter does encephalitis primarily effect
gray matter
etiology of encephalitis
viruses (mosquitos/ticks), complications from chicken pox, measles or mumps, herpes simples
what can encephalitis lead to
neuronal death, cerebral edema, vascular damage to cerebral vessels
S/S of encephalitis
HA, N/V, elevated temp, lethargy, stiff neck, agitation, confusion and coma, focal signs and paralysis depending on areas of brain most involved, seizure activity
how to dx encephalitis
lumbar puncture, MRI and EEG changes
Tx encephalitis
antivirals, antibodies (IV(, possibly corticosteroids, surgical decompression
- depends on cause
why are corticosteroids not great for treating encephalitis
high dose can decreased immune system function
describe mortality rate and recovery of encephalitis
high mortality rate
10-50% recovery (depends on pathogen)
what is meningitis
inflammation of meninges of brain and spinal cord; some forms can be contagious
etiology meningitis
bacteria, virus, fungus, toxins
meningitis pathogens attack what areas
inner ear, sinus or URI
sudden onset of s/s of meningitis
high fever, HA, photophobia, nucal rigidity (neck stiffness), drowsiness, stupor, seizures
dx meningitis
lumbar puncture, Kernig’s sign, brudsinski’s sign
test that stretches the meninges and will cause severe pain
kernig’s sign
tx meningitis
vaccines for bacterial, meds, quiet dark environment
prognosis meningitis
- bacterial: MEDICAL EMERGENCY - can be fatal in infants and elderly
- viral - has to run its course
what is the hallmark sign of meningitis
nucal rigidity (neck stiffness)
describe kernig’s test
- performed with pt supine or in chair
- hip and knee flexed to 90deg and attempt made to extend knee
- (+) pain in neck or back
describe brudzinksi’s test
flexion of neck causes of hips and knees while pt is supine
- this occurs bc the pain has pain with neck flexion
what is poliomyelitis
viral infection affecting LMN’s in brainstem and spinal cord
how does poliomyelitis enter the body
through mouth and nose (PNS disorder)
list the 3 infection mechanisms for poliomyelitis
- asymptomatic (carrier)
- symptomatic - flu-like
- symptomatic with paralysis (due to virus entering anterior horn cells)
s/s poliomyelitis
mm weakness of UE/LE, neck stiffness, mm atrophy, N&V, respiratory system due to paralysis
dx poliomyelitis
by culture
tx poliomyelitis
braces, respiratory support (ie. iron lung)
describe post-polio syndrome
occurs 20-30 ears after initial infection with new mm weakness and fatigue due to pruning and lack of metabolic support for enlarged motor units
describe zika virus and how is it transmitted
- single strand of RNA virus
- transmitted: mosquito bite, also spread mother to baby, sex, blood transfussion
what % of people infected with zika virus are asymptomatic
80%
s/s zika virus if symptomatic
fever, HA, joint pain, mild rash
what does zika virus cause in fetus/unborn child and why
microcephaly - causes apoptosis and inhibition of neural cell differentiation leading to cortical thinning and microcephaly
tx zika virus
no cure
tx is mosquito eradication
recommended safe sex (M 6mo, W 2mo) post traveling to area of high zika transmission
describe botulism
neuromuscular poisoning resulting from bacteria invasion by clostridium botulinum
- neurotoxin (neuromuscular poison) interferes with releease of acetylcholine at peripheral N endings
etiology botulism
- food borne: improper canning procedures, raw honey
- wound borne: bacteria invades wound and secretes neurotoxin
- infant botulism: bacteria grows in intestnes of children; also associated with ingestion of honey in infants < 1 year
s/s botulism
double vision, blurred vision, droopy eyelids, slurred speech, difficulty swallowing, dry mouth, respiratory decline, progressive muscle weakness starting at shoulders
mortality rate botulism
60-70% if not treated immediately
tx botulism
- food borne: toxins are readily destroyed by exposure to heat - cooking foods at temperatures at 176deg for 30 minutes
- induce vomiting to expel toxins
- close monitoring of respiratory status - may require intubation and respiratory support
- antibiotics and vaccines are useless - effect is from toxins
- trivalent antitoxin from CDC in pandemics to slow progression
describe tetanus
acute infectious disease characterized by convlusions and intermittent spasms of voluntary muscles
- bacterial infection - clostridium tetani found in soil and animal feces
what does tetanus produce that effects skeletal muscles and blocks release of inhibitory neurotransmitters
toxin - tetanospasmin
transmission tetanus
acquired from open wound infection (rusty nail, tin can lid, barbed wire)
s/s tetanus
contractions of muscles of mastication (lock-jaw), general muscle spasms
tx tetanus
life supporting procedures, wound debridement, penicillin and tetracycline
outcomes of tetanus
fatal due to paralysis of respiratory muscles if not treated
preventative tx tetanus
keep up with shots, need booster every 10 years at minimum
describe rabies
acute infectious disease of mammals characterized by CNS irritation followed by paralysis and death
- virus carried in saliva of infected animals (dogs, raccoons, squirrels, cats, skunks)
what does rabies cause
encephalomyelitis - neuro and muscular system inflammation
s/s rabies
fever, pain, paralysis, convulsions, rage, mm spasms especially of swallowing (foaming at mouth), hydrophobia
what is the incubation period of rabies
3-10 days
tx rabies
immediately washing wound, anti-rabies injections before virus spreads to brain, confine and tx or destroy the biting animal
prognosis rabies
can be fatal if untreated ASAP
describe shingles (herpes zoster)
actue CNS infection involving DRG resulting in vesicular eruptions and severe pain along the cutaneous areas supplied by the nerve root
etiology shingles (herpes zoster)
caused by varicella zoster - same as chickenpox may be dormant for years; may be activated by systemic diease or in persons receiving immunosuppressive therapy
prevalence shingles (herpes zoster)
1/3 persons who had chickenpox, increased with age over 60
s/s shingles (herpes zoster)
itching, sharp stabbing pain, red rash with pustules along the path of sensory N (dermatome) running toward midline (often trunk)
tx shingles (herpes zoster)
anti-virals (acyclovir), analgesics, meds for itching, isolation precautions must be observed during active infection, vaccine for persons 50+
describe ramsey-hunt
shingles virus affecting facial N (paralysis)
possible hearing loss (CN 8 - 7 and 8 pass through same foramen)
prognosis shingles (herpes zoster)
may recur anytime immune system is depressed or stressed, may develop post-herpetic neuralgia
describe brain abscess
space-occupying lesion of local infection with effects similar to a brain tumor
what population does brain abscess affect
individuals with compromised immune system, persons with systemic illness (HIV)
etiology brain abscess
bacteria, fungi, parasites, sinusitis, mastoiditis, infections from heart/lungs, cranial osteomyelitis (bone infections)
presentation brain abscess
evolves over 1-14 days where capsule of necrotic tissue develops as a result of inflammatory process
S/S brain abscess
may not have fever or increased WBC, HA, disturbed consciousness, nuchal rigidity, N/V, seizures, visual disturbances, dysarthria, hemiparesis, sepsis
tx brain abscess
identification of mass via MRI, antibiotics, surgical drainage, or excisions of capsule, tx of other areas of infection
outcomes brain abscess
50% will be left with some neurologic sequelae, mortality increases if there is hemorrhage
describe prion disease
included a family of encephalopathies to include Creutzfeldt-jakob disease, kuru, and mad cow disease
a protin that can replicate in the nervous system and results in neuronal cell death
prion
etiology of prion disease
ingested from infected beed or protein products containing infected material (hormone therapy)
tx prion disease
no known tx, sx management focus on
clinical presentation/prognosis prion disease
abnormal movement, ataxia, progressive
usually fatal
