Unit 5 - Chapter 22

Question 1

structure and significance of blood-brain barrier

prevents:
capillaries are:
drugs must be:
special carrier mechanisms for:

Answer 1

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

Question 2

inflammation and the blood-brain barrier

Answer 2

tends to alter blood-brain barrier to allow antibiotics to cross that would not be able to cross if there were no infection

Question 3

chloramphenicol w/ respect to the blood-brain barrier

Answer 3

antibiotic that enters brain readily b/c it is lipid soluble

Question 4

penicillin w/ respect to the blood-brain barrier

Answer 4

only slightly lipid-soluble, but if taken in large enough doses, may cross the barrier to be effective

Question 5

how do microorganisms invade the CNS?

Answer 5

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.

Question 6

bacterial meningitis: bacterias that cause 70% of the cases and 70% of the related deaths

Answer 6

1. gram+ diplococcus Streptococcus pneumoniae;
2. Gram- Haemophilus influenzae;
3. Gram- neisseria meningitidis

Question 7

How do those 3 cause meningitis?

last part: they might enter:

Answer 7

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.

Question 8

Death & meningitis

speed at which it occurs
due to what symptoms
caused by release of what

Answer 8

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.

Question 9

meningitis symptoms

Answer 9

fever, headache, stiff neck… followed by nausea and vomiting

Question 10

meningitis diagnosis

Answer 10

diagnosis based on gram stain and serological tests of the bacteria in CSF

Question 11

meningitis treatment

Answer 11

cephalosporins may be administered before identification of the pathogen.

Question 12

Tetanus cause

endospore status
gram status
aerobic status
shape

Answer 12

local infection of a would by Clostridium tetani. Obligate anaerobe grows in deep, unclean wounds. It is endospore-forming, gram+, and rod-shaped (bacillus)

Question 13

Clostridium tetani pathogenic effects

invasiveness
pathogenic effects due to:
neurotoxin produced:
spreads via:
causes:

Answer 13

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

Question 14

Tetanus symptoms

Answer 14

spasms
lockjaw
death

Question 15

C. tetani toxin

Answer 15

exotoxin, A-B toxin, blocks nerve impulses to muscle relaxation pathway, results in noncontrollable muscle contractions

Question 16

Muscle contraction normal vs tetanus

Answer 16

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

Question 17

Tetanus immunization, unimmunized people, and control of infection

Answer 17

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.

Question 18

Botulism cause

aerobic
causative agent
spores
toxin (endo/exo) inhibits:

Answer 18

Anaerobe Clostridium botulinum that grows in canned goods under anaerobic conditions - has endospores

exotoxin (neurotoxin) that inhibits transmission of nerve impulses.

Question 19

Botulism symptoms

Answer 19

blurred vision for 1-2 days;

progressive flacid paralysis follows for 1-10 days,

possibly resulting in death from respiratory and cardiac failure

Question 20

Botulism diagnosis

Answer 20

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.

Question 21

botox

Answer 21

toxin of C. botulinum used to decrease wrinkles

Question 22

viral diseases of the nervous system

most enter via:
some can enter:

Answer 22

most enter by circulation of the blood or lymph; some viruses can enter peripheral nerve axons and move along them toward the CNS

Question 23

poliomyelitis symptom

old people vs young people

Answer 23

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.

Question 24

poliomyelitis invasion

1st
2nd

Answer 24

transmitted by ingestion of contaminated feces water.

first invades lymph nodes of neck and small intestine.

viremia and spinal cord involvement may follow

Question 25

poliomyelitis diagnosis

Answer 25

based on isolation of the virus in feces and throat secretions

Question 26

poliomyelitis treatment

S: IPV
S: OPV

Answer 26

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.

Question 27

rabies symptoms

Answer 27

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

Question 28

rabies contraction

Answer 28

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.

Question 29

rabies diagnosis

alive
dead

Answer 29

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.

Question 30

rabies treatment
post
pre

Answer 30

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.

Question 31

Arboviral encephalitis causative agent

Answer 31

mosquito borne viruses (arboviruses)

Question 32

Arboviral encephalitis symptoms

Answer 32

encephalitis (brain swolls); increases in summer months when mosquitos are more prevalent

Question 33

most notable arboviral infections

Answer 33

eastern equine encephalitis (EEE); western equine encephalitis (WEE), St. Louis encephalitis (SLE); California encephalitis (CE); west nile virus (WNV)

Question 34

arboviral encephalitis diagnosis

Answer 34

serological tests

Question 35

arboviral encephalitis control

Answer 35

control of the mosquito vector is the most effective way to control encephalitis

Question 36

prions

Answer 36

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

Question 37

nervous system diseases caused by prions

incubation time, measured in (unit of time)
Damage is:
Symptoms:

Answer 37

have long incubation times, measured in years. CNS damage is insidious and slowly progressive, with the fever and inflammation seen in encephalitis.

Question 38

prion autopsies shows what characteristics?

Answer 38

show characteristic spongiform (porous, like a sponge) degeneration of the brain, as well as characteristic fibrils in brain tissue.

Question 39

transmissible spongiform encephalopathies (TSE)

Answer 39

disease caused by prions

Question 40

sheep scrapie

Answer 40

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.

Question 41

Creutzfeldt-Jakob disease (CJD)

who suffers?
caused by what?
some cases traced to injection of what:

Answer 41

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.

Question 42

Kuru

Answer 42

TSE disease of humans in new guinea, Transmission is related to cannabalistic rituals

Question 43

Bovine spongiform encephalitis (BSE)

Answer 43

aka mad cow disease, origin is from feed supplements contaminated with prions from sheep infected w/ scrapie