Flashcards in Unit 5 - Chapter 22 Deck (43)
structure and significance of blood-brain barrier
drugs must be:
special carrier mechanisms for:
barrier which prevents many substances, including antibiotics, from entering the brain.
Capillaries are less permeable than others within the body, and more selective in passing materials.
Drugs cannot cross blood-brain barrier unless they are lipid soluble.
There are special carrier mechanisms for glucose and some amino acids
inflammation and the blood-brain barrier
tends to alter blood-brain barrier to allow antibiotics to cross that would not be able to cross if there were no infection
chloramphenicol w/ respect to the blood-brain barrier
antibiotic that enters brain readily b/c it is lipid soluble
penicillin w/ respect to the blood-brain barrier
only slightly lipid-soluble, but if taken in large enough doses, may cross the barrier to be effective
how do microorganisms invade the CNS?
1. through trauma (skull fracture or fracture of the vertebral column);
2. by a medical procedure (spinal tap);
3. microorgs can move along peripheral nerves; and
4. via bloodstream or lymphatic system when inflammation alters the permeability of the blood-brain barrier.
bacterial meningitis: bacterias that cause 70% of the cases and 70% of the related deaths
1. gram+ diplococcus Streptococcus pneumoniae;
2. Gram- Haemophilus influenzae;
3. Gram- neisseria meningitidis
How do those 3 cause meningitis?
last part: they might enter:
All 3 possess a capsule that protects them from phagocytosis as they replicate rapidly in the bloodstream from which they might enter the cerebrospinal fluid.
Death & meningitis
speed at which it occurs
due to what symptoms
caused by release of what
Death from bacterial meningitis often occurs very quickly, probably from shock and inflammation caused by release of endotoxins of the gram-negative pathogens or the release of cell wall fragments (peptidoglycan and teichoic acids) of gram-positive bacteria.
fever, headache, stiff neck... followed by nausea and vomiting
diagnosis based on gram stain and serological tests of the bacteria in CSF
cephalosporins may be administered before identification of the pathogen.
local infection of a would by Clostridium tetani. Obligate anaerobe grows in deep, unclean wounds. It is endospore-forming, gram+, and rod-shaped (bacillus)
Clostridium tetani pathogenic effects
pathogenic effects due to:
C. tetani is not invasive, does not spread from the site -- pathogenic effects are due to toxicity. C. tetani produces the neurotoxin tetanospasmin--spreads via neural cells and causes spastic paralysis, which causes the symptoms of tetanus
C. tetani toxin
exotoxin, A-B toxin, blocks nerve impulses to muscle relaxation pathway, results in noncontrollable muscle contractions
Muscle contraction normal vs tetanus
normal: inhibitory interneuron releases glycine that binds to motor neuron and blocks excitation signals from CNS and stops release of acetylcholine so muscles relax.
tetanus: toxin binds to interneuron and inhibits release of glycine so motor neuron continues to release acetylcholine, thus muscle contractions continue
Tetanus immunization, unimmunized people, and control of infection
acquired immunity results from DPT immunization and booster (every 10 years). unimmunized persons can get tetanus immune globulin. Debridement (removal of tissue) and antibiotics may be used to control infection.
toxin (endo/exo) inhibits:
Anaerobe Clostridium botulinum that grows in canned goods under anaerobic conditions - has endospores
exotoxin (neurotoxin) that inhibits transmission of nerve impulses.
blurred vision for 1-2 days;
progressive flacid paralysis follows for 1-10 days,
possibly resulting in death from respiratory and cardiac failure
diagnosed by inoculating mice with samples from patient serum, stool, or vomit specimins. Different sets of mice are immunized with type A, B, or E antitoxin. All the mice are innoculated w/ test toxin; if those protected w/ type A antitoxin are the only survivor, then the toxin is type A.
toxin of C. botulinum used to decrease wrinkles
viral diseases of the nervous system
most enter via:
some can enter:
most enter by circulation of the blood or lymph; some viruses can enter peripheral nerve axons and move along them toward the CNS
old people vs young people
best known for causing paralysis, which only affects 1% of those infected w/ polio. most cases are asymptomatic or exhibit mild symptoms such as headache, sore throat, and nausea, and happens in young people. older people will exhibit more of the paralytic form of the disease.
transmitted by ingestion of contaminated feces water.
first invades lymph nodes of neck and small intestine.
viremia and spinal cord involvement may follow
based on isolation of the virus in feces and throat secretions
Salk vaccine (inactive polio vaccine, or IPV) involves injection of formalin-inactivated viruses and boosters every few years.
Sabin vaccine (oral polio vaccine, or OPV) contains three live, attenuated strains of poliovirus and is administered orally.
spasms of mouth and throat muscles,
virus multiples in skeletal muscles and connective tissue. results in fatal encephalitis when virus moves along peripheral nerves to the CNS.
extensive brain and spinal cord damage and death
through bite of rabid animal (esp dangerous when bitten in areas rich in nerve fibers (hands/face));
by inhalation of aerosols when macerating infected tissue in a laboratory blender;
invasion through minute skin abrasions.
Mostly from dogs, cats, domestic cattle; but also happens by bats, skunks, foxes, raccoons, silver-haired bats and vampire bats.
Never in squirrels, rabbits, rats, or mice.
When patient/animal is alive, diagnosis is sometimes confirmed by immunofluorescent studies, in which viral antibodies are detected in saliva, serum, or CSF.
After death, diagnosis is confimed by fluorescent-antibody (F-A) test performed on brain tissue.
postexposure: PEP (postexposure prophylaxis -- administration of human rabies immune globin (RIG) along with multiple intramuscular injections of vaccine. Preexposure consists of vaccination, but only for high-risk individuals (lab workers, animal control professionals, veterinarians) are routinely vaccinated before known exposure.
Arboviral encephalitis causative agent
mosquito borne viruses (arboviruses)
Arboviral encephalitis symptoms
encephalitis (brain swolls); increases in summer months when mosquitos are more prevalent
most notable arboviral infections
eastern equine encephalitis (EEE); western equine encephalitis (WEE), St. Louis encephalitis (SLE); California encephalitis (CE); west nile virus (WNV)
arboviral encephalitis diagnosis
arboviral encephalitis control
control of the mosquito vector is the most effective way to control encephalitis
abnormally folded self-replicated proteins with no detectable nucleic acid that can induce change in the shape of a normal protein, causing proteins to clump
nervous system diseases caused by prions
incubation time, measured in (unit of time)
have long incubation times, measured in years. CNS damage is insidious and slowly progressive, with the fever and inflammation seen in encephalitis.
prion autopsies shows what characteristics?
show characteristic spongiform (porous, like a sponge) degeneration of the brain, as well as characteristic fibrils in brain tissue.
transmissible spongiform encephalopathies (TSE)
disease caused by prions
occurs in animals, infected animal scrapes itself against fences and walls until areas of its body are raw. Animal gradually loses motor control and dies. Infection can be experimentally passed to other animals by injection of brain tissue from one animal to the next.
Creutzfeldt-Jakob disease (CJD)
caused by what?
some cases traced to injection of what:
TSE disease that humans suffer from that is similar to scrapie. Transmission is via corneal transplants and accidental scalpel nicks from a surgeon during autopsy. Some cases are traced to injection of growth hormone derived from human tissue.
TSE disease of humans in new guinea, Transmission is related to cannabalistic rituals