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Exam 3 Flashcards

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0
Q

what percent of known fungi are pathogenic?

in what do they cause disease?

A

30%

plants and humans

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1
Q

What is mycology?

What kind of cell are they?

A

the study of fungi

eukaryotes

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2
Q

What are the two types of fungi?

A

yeast and mold

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3
Q

How are fungi different than bacteria?

A

larger, grow slower, and at lower temperature

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4
Q

what are the 3 different roles of fungi?

A
  • decomposers/recylers
  • produce enzymes that we use (beano)
  • produce medications (penicillin)
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5
Q 
How would yeast be described?
shape? 
reproduce?
appearance?
examples?
A

unicellular and non-filamentous

  • oval
  • asexually by budding
  • moist, creamy, and white
  • saccharomyes cerivisae and Candida albicans
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6
Q

How would mold be described?
filaments called?
what is mycelium?
reproduces?

A

multi-cellular and filamentous

  • hyphae
  • a mass of intertwined hyphae
  • asexually via spores which can be inhaled by humans as a means of disease transmission
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7
Q

what is mycoses?
why do we not know how many mycoses cases we have?
how would mycoses happen?
what conditions aid this process?

A
  • fungal disease
  • not reportable to the CDC
  • fungal pathogens are opportunists
  • invasive medical procedures, medical therapy, pre-existing conditions, and life style factors
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8
Q

What are the three classes of drugs used to treat fungal infections?

A

polyenes, azoles, and echinocandins

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9
Q

How do polyenes work?

what are the two most commonly used? and how do they work?

A
  • by attaching to the sterol component found in the fungal membrane, causing the cells to become porous and DIE
  • nystatin-used as a topical agent to treat superficial infections, or orally to treat candidal infections
  • amphotericin B- used to treat severe systemic fungal infections
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10
Q

How do azoles work?

what are the 3 common ones used? what are they effective against?

A
  • by preventing fungi from making an essential part of their cell wall.
  • ketocanazole-oldest, slightly more toxic, not very effective against aspergillosis or others
  • flucanozole-against superficial and systemic candidiasis, but many are resistant to it now
  • itraconazole-newest, effective against a range of different fungal infections , can treat aspergillosis
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11
Q

how to echinocandins work?

what are the 2 kinds and what are they effective against?

A
  • disrupting the wall that surrounds fungal cells

- caspofungin and micafungin effective for sever systemic fungal infections

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12
Q

what is the disease and organism that causes fever, cough, chest pain, chills, night sweats, headache, fatigue, shortness of breath, joint aches, rash 1-3 WEEKS after exposure? how is it transmitted? where is it commonly found? how is at higher risk?

A
  • Coccidoiomycosis (valley fever), Coccidioides immitus (mold), pathogen
  • spores inhaled from disrupted soil, usually after natural disaster
  • southwestern u.s. mexico
  • consruction or farm or mine workers
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13
Q

what disease and organism causes fever, headache, dry cough, chills, chest pain, weight loss, night sweats, 3-17 DAYS after exposure?
how is it transmitted?
where is it commonly found?
who is at higher risk?

A
  • histoplasmosis, Histoplasma capsulatum (mold, pathogen)
  • spores in soil with bat or bird droppings, disturbed soil makes spores airborne and inhaled
  • ohio, missouri, mississippi river valleys
  • infant, young children, older people
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14
Q

what disease and organism causes thick, white, lacey patches in the MOUTH, red, flat rash with scalloped edges on the SKIN, and a thrush extending down ESOPHOGUS into stomach, painful ulcers, difficulty swallowing, and a whit, cheesy discharge, itching and burnign in the VAGINA?
how is it transmitted?
who is at greater risk?

A

candidiasis, Candida albicans (yeast, opportunist)

  • part of NORMAL FLORA, change in environment causes imbalance and overgrowth of candida
  • newborns, immunocompromised people, and common at least once in most women.
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15
Q

what disease and organism causes BLURRED VISION, bone pain, hest pain dr cough, fever, fatigue, headache nausea, night sweats, weight loss, weakness, PNEUMONIA-LIKE ILLNESS, shortness of breath, coughing,fever, skin lesions, and MAY INFECT CENTRAL NERVOUS SYSTEM?

  • how is it transmitted?
  • who is at greater risk?
A

Cryptococcosis, cryptococcus neoformans (yeast, opportunist)

  • inhaled spores from environment where soil has bird (PIGEONS) droppings in it
  • immunocompromised people (AIDS)
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16
Q

what disease and organism cause fever, rapid breathing, chills sweats, progressive, profound fatigue?
how is it transmitted?
who is at risk and who is not?

A

Pneumocystis pneumonia, Pneumocystis jiroveci (mold, opportunist)

  • spores common in the environment inhaled
  • immunocompromised (AIDS) people, DOES NOT CAUSE INFECTION IN HEALTHY PEOPLE
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17
Q

what disease and organism causes TINEA CAPTIS (round, scaly lesions on SCALP, hair loss), TINEA CORPORIS (round, scaly red lesions on the BODY), TINEA BARBAE (swelling and crusting around hair follicle in BEARD area, TINEA CRURIS (reddish, brown color in GROIN extends to thigh), TINEA UNGUIUM (yellow, think, crumbly toe NAILS), and TINEA PEDIS (scaling and inflammation of toe webs, thick scaling on heels, and soles, FEET)? (RINGWORM)
-how is it transmitted?

A

Dermatophytosis, Trichophyton OR Microsporum (mold, opportunist)
-direct contact with infected lesions or indirectly through contact with fomites on shoes, towels, showers, etc. COLONIZES ONLY DEAD TISSUE

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18
Q

what disease and organism causes brown/reddish/white patches on skin?
what disease causes patchy scaling or thick crust on scal;, yello/white scales (DANDRUFF) itching
how is it transmitted?
what are factors that encourage this?

A

Tinea Versicolor, Malassizia (yeast, opportunist)
Seorrheic dermatitis, same organism as above
-normally on skin of humans, but will overgrow
-humidity, sweating, oily skin

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19
Q

how are infectious diseases preventable?

A

vaccines

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20
Q

why are developing countries at a greater risk for infectious disease?

A

they face poverty, overcrowding, poor/lack of nutrition, lack of access o health care, chronic disease left untreated.

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21
Q

define infection
disease
can you have infection with out disease?

A
  • invasion or colonization of the boy by a pathogenic microbe
  • any change from a state of health
  • yes
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22
Q 
define acute disease and give example 
chronic disease
latent disease
communicalbe disease
contagious disease
non-communicable disease
A
  • develops rapidly and lasts short time (cold)
  • develops slowly and is continual (hep C)
  • pathogen remains inactive and possibly reactive (herpes)
  • disease that is spread from one host to another (flu)
  • disease that is very EASILY spread from one host to another (measles, chicken pox)
  • disease that can’t spread from one host to another (heart disease, diabetes)
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23
Q

define epidemiology
incidence
prevelance

A
  • study of where and when diseases occur
  • # of NEW cases of a disease in a given population or area
  • total # of cases of disease ina given population or area (existing cases + new cases)
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24
Q

define endemic disease
epidemic disease
pandemic disease
sporadic disease

A
  • diseases that occur at a relatively stable frequency iin a given population or area
  • occurring at a greater than normal frequency in a given population or area
  • epidemic occurring simultaneously on more than one continent
  • only a few cases occur
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25
Q

what is etiology?

how do we determine this?

A

cause of disease

koch’s postulates

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26
Q

What are Koch’s 4 postulates?

A
  1. suspected pathogen must be found in every case of the disease
  2. isolate the pathogen and grow it in pure culture in the lab
  3. inoculate the healthy host with the pure culture and they must get the identical disease.
  4. reisolate the pathogen from the experimental host and compare it to pure culture, MUST be identical.
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27
Q

what are considered signs?

symptoms?

A
  • objective manifestations of disease, can be observed/measured by others
  • subjective manifestation of disease, only be felt by the patient
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28
Q

define pathogenicity

virulence

A
  • ability to cause disease

- degree of pathogenicity

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29
Q

what 3 things increase pathogenicity/virulance of a microbe?

A
  1. extracellular enzymes
  2. toxins
  3. anti-phagocytic factors
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30
Q

what are extracellular enzymes?

what are 4 examples and what do they do?

A
  • produced by some bacteria and secreted into the environment
    1. coagulase-clot former
    2. staphylokinase/streptokinase-clot buster
    3. leukocidin-kills white blood cells, decreases phagocytosis
    4. hyaluronidase- invade deeper into tissues (drills holes)
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31
Q

what are toxins and the 2 types?

A
  • chemicals secreted by some gram (+) and (-) bacteria, can harm teh host, trigger inflammation in host
  • exotoxins and endotoxins
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32
Q

what are exotoxins and what are the 3 types (how do these work?)?

A
  • secreted by the bacteria into the environment, can spread using the circulatory system.
    1. cytotoxins-kill cells, interfere with cell function
    2. neurotoxins-interfere with synapse
    3. enterotoxins-kill cells that line the GI tract
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33
Q

what are endotoxins and an example and what it does?

A
  • part of bacterial structure

- lipid A of LPS of gram(-) bacteria outer membranes can cause fever, clots, hemmerage, inflammation, death

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34
Q

what do anti-phagocytic factors do and what is an example?

A
  • decrease phagocytosis

- glycocalyx (capsule/slime layer)

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35
Q

what is symbiosis and what are the 3 types (explain them)?

A

2 different organisms living together

  1. mutualism-both organisms benefit
  2. commensalism-one organism benefits, other organism neither benefits nor is harmed (neutral)
  3. parasitism-one organism benefits, the other organism is harmed
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36
Q

what is a reservoir of infectious disease?

3 kinds?

A
  • sites where pathogens are maintained as a source of infection
    1. animal reservoirs- zoonotic disease (animal-human, human-animal)
    2. human carriers-asymptomatic carriers
    3. non-living carriers-water, soil, food
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37
Q

what are 4 portals of entry for pathogens? what is the most common way pathogens enter?

A
  1. broken skin
    * 2. mucous membranes
  2. placenta
  3. parenteral route
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38
Q

what are mucous membranes?

what are the 5 mucous membranes of the body?

A
  • line all body cavities open to exterior

- respiratory tract, GI tract, urinary tract, reproductive tract, conjuctiva

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39
Q

what is the parenteral route?

examples?

A
  • means by which a portal of entry is circumvented by depositing pathogen directly into tissue,
  • needle, mosquito bite
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40
Q

once a pathogen enters via a portal of entry how do they stay there?
what can the pathogen form that makes it hard to fight?

A

glycocalyx, fimbrae, suckers/hooks

-biofilm-web of bacteria and debris

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41
Q

how do portals of exit work?what is used?

A
  • must exit in order to infect a new host

- usually exit the same way they entered via secretions (respiratory droplets, semen, vaginal secretions, feces, urine)

42
Q

what are the 5 stages of infectious disease, describe them, and when are you contagious?

A
  1. incubation period-infected with pathogen until s&s begin, length varies depending on virulance of pathogen, initial dose, state of health, site of infection, and how quickly pathogen divides/replicates
  2. prodromal period-not in all infectious diseases, short periodo very mild and general S&S
  3. illness-S&S most evident/severe
  4. decline-S&S are decreasing as body begins to return to normal
  5. convalescence-S&S are gone, body returns to normal
    * you are likely contagious the ENTIRE time!!
43
Q

what are the 3 modes of transmission?

A
  1. contact transmission
  2. vehicle transmission
  3. vector transmission
44
Q

what are the 3 kinds of contact transmission? describe each

A
  1. direct contact transmission-person to person via body contact between hosts (kiss, handshake, sexual intercourse)
  2. indirect contact transmission-person to person via a fomite (inanimate object) (kleenex, toothbrush, glass, money)
  3. droplet transmission-cough/sneeze (respiratory droplets), person to person via oral/nasal secretions that travel 3 feet or less
45
Q

what are the 4 kinds of vehicle transmission? describe each

A
  1. airborne transmission-spread via air, travel great distance, survive outside body
  2. waterborne transmission-contaminated water, fecal-oral
  3. foodborne transmission-improperly processed food, improperly handled/cooked food
  4. body fluid transmission-bloood, seme, vaginal secretions, braskmilk
46
Q

what are the 2 kinds of vector transmission? describe each

A
  1. biological vector-arthropod (insect) serves as part of pathogen’s life cycle
  2. mechanical vector-insect passively carries the pathogen (flies, roaches)
47
Q

what are nosocomial infections?
why are they a problem?
how do they happen?
what are some common sites of infection?

A
  • healthcare acquired infections (HAI)
  • pathogens are always present in health care environments, and there are a lot of immunocompromised patients there, transmission comes from (staff-patient, patient-staff, staff-staff, patient-patient, visitors)
  • invasive medical procedures (surgery, catheters, trachs/respirators, inapropriate atibiotic usage)
  • urinary, surgical site, lungs, blood stream
48
Q

what are 8 ways nosocomial infections can be decreased?

A
  1. HAND WASHING
  2. good housekeeping
  3. PPE-personal protective equipment (gloves, masks, gown, shoecovers, face shield)
  4. disposables
  5. isolation of patients
  6. educate patients, staff, visitors about nosocomials
  7. use antibiotics apropriately
  8. surveillance
49
Q

what is an example of an occupational exposure to blood-borne pathogens?
what are the 3 blood-borne pathogens, what percent chance of transmission and what is done about it?

A
  • needlesticks
    1. hep B virus-6-30%, vaccine and HBV gamma globulin (90% effective in preventing transmission)
    2. hep C virus-1.8%, anti-viral meds
    3. HIV virus-0.3%, anti-viral meds
50
Q

define immunity

A

body’s ability to resist infectious disease through innate and acquired mchanisms

51
Q

define innate (non-specific) immunity
when is it acquired?
specificity?
what lines of defense?

A
  • an inborn set of pre-existing defenses against infectious disease
  • present at birth, immediate protection
  • relatively non-specific, works agains any pathogen
  • includes 1st and 2nd line of defense
52
Q

what is included in the first line of defense?

A

skin and mucous membranes

53
Q

SKIN
how effective?
what are 7 things that make skin so effective?

A
  • intact skin is an excellent barrier against infections disease
    1. multi-layered-epidermis, dermis, subcutaneous tissue
    2. collagen and elastin fibers in skin-give strength and pliability
    3. sweat glands produce sweat-high salt environment
    4. sebaceous glands produce sebum-oily secretion softens skin, and decreases tearing
    5. produce dermicidins-kill bacteria
    6. dendritic cells ready to do phagocytosis
    7. normal flora out compete pathogens
54
Q

what are the 5 mucous membranes?

what are 5 ways that mucous membranes protect itself?

A
  • respiratory, GI tract, urinary tract, reproductive tract, conjunctiva
    1. cells are tightly packed together, and continuously shed
    2. mucous membranes produce mucous, trap pathogens, cilia propel mucous
    3. tears, saliva, mucous all contain lysozyme (destroys peptidoglycan)
    4. pH of stomach is very acidic, most microbes are neutrophiles
    5. dendritic cells in mucous membranes (phagocytosis)
55
Q

define blood
plasma
formed elements

A
  • plasma and formed elements
  • liquid portion of blood
  • blood cells and cell fragments
56
Q

where is blood formed?

what are the 3 types of blood cells? other names and functions

A
  • bone marrow
    1. RBC-red blood cells, erythrocytes, carry O2 / CO2
    2. platelets-cell fragments-clotting
    3. WBC-white blood cells, leukocytes, immunity
57
Q

what are the 6 types of leukocytes and their functions?

what are the 2 most important ones?

A

basophils-inflammation, allergy
eosinophils-worm and fungal infections, allergy
*neutrophils-phagocytosis
macrophages and monocytes-phagocytosis
dendritic cells-phagocytosis
lymphocytes-T cells, B cells, acquired or specific immunity

58
Q

what are the 6 parts of the second line of defense?

A
  1. phagocytosis,
  2. extracellular killing
  3. complement
  4. interferon
  5. inflammation
  6. fever
59
Q

what is phagocytosis?
what is phagocytized?
what are the most important phagocytes?

A
  • cellular eating by surrounding and ingesting foregn/unwanted material
  • unwanted items, pathogens, pathogen products (extracellular enzymes, exotoxins)
  • neutrophils and macrophages
60
Q

what are the 5 steps in phagocytosis? describe

A
  1. chemotaxis-attract phagocytes to arrive where they are needed via chemicals
  2. adherence- phagocyte attaches/adheres to unwanted/foreign substance
  3. ingestion-phagocyte uses a pseudopodia (false foot, membrane extension) to surround and bring in unwanted/foreign material
  4. killing-send foreign/unwanted material to lysosomes, enzymes in lysosomes kill most pathogens in about 30 min
  5. elimination-remnant exit phagocyte via exocytosis
61
Q

what decreases adherence in phagocytosis, what increases it?

A
  • glycocalyx/slime layer/ capsule

- antibody or complement bound to unwanted/foreign material

62
Q

what are the two types of extracellular killing cells, what do they kill and how, where are they found?

A
  • eosinophils-worm infections-attach to helminth, release extracellular toxin, weaken/kill worm
  • natural killer cells (NK cells)-secrete a toxin that can kill infections and tumor/cancer cells-found in tonsils, spleen, lymph nodes, lymph, blood
63
Q

what is complement?
how does it work?
what are the 2 pathways?

A
  • 25 proteins that circulate in the blood in an inactive state that complement or assist in the destruction of pathogenic bacteria and products of pathogenic bacteria (exotoxins, extracellular enzymes)
  • domino effect, if first protein is activated, all others are activated.
    1. classical pathway-antibody bound to antigen
    2. alternative pathway-pathogen or pathogen product
64
Q

once activated, what does complement do? (3)

A
  • cell/bacterial product lysis
  • call other immune cells to area (phagocytes)-increase phagocytosis
  • increase inflammation
65
Q 
what is interferons?
what does it mean for the cell producing it?
how does it work?
who does it work against?
what does it cause?
how is it used?
A
  • anti-viral proteins produced by some viral-infected animal cells
  • too late for cell producing interferon, producing the interferon to help neighboring cells.
  • interferons interfere with viral replication in neighboring cells
  • any virus
  • S&S-malaise, muscle aches, chills, fever, headache
  • treat viral infections
66
Q

what are the 3 purposes of inflammation?

A
  1. localize the infection, reduce the spread of the pathogen
  2. neutralize exotoxins
  3. aids in repair of damaged tissue
67
Q

what triggers inflammation?

S&S?

A
  • heat, chemicals, uv light, cut/abrasion, pathogen

- redness, swelling, heat, pain

68
Q

what 3 chemicals do damaged cells in an area where inflammation is going on produce?
what do these chemicals do?

A
  • prostaglandins, histamine, leukotrienes

- vasodilation of vessels in area-increase blood flow to area, bring in clotting factors, phagocytes enter area.

69
Q

what is pus?

what is pus under the skin called?

A
  • dead tissue + pathogen+leukocytes

- abscess

70
Q

what does inflammation have to do with healing?

A

inflamed tissue heals faster, aids in repair of damaged tissue

71
Q

what are some anti-inflammatory meds, how do they work?

A

-ibprofin, aspirin-anti-prostiglandins

72
Q 
what is a fever?
how is body temp controlled?
what are pyrogenes? examples?
what is the purpose of a fever?
what are some concerns?
what is a fever reducing med?
A
  • body temperature greater than 100 degrees
  • by the hypothalamus in the brain
  • cause hypothalamus to increase body temperature-exotoxins, antibody/antigen complexes, pathogens
  • slow growth rate/kill pathogen, increase the effect of interferons, increase phagocytosis, increase specific immunity, increase tissue repair
  • very high, prolonged fever can lead to- increased heart rate, increased metabolism/caloric demand, dehydration, malaise, body aches, chills, hallucinations, coma, convulsions, death
  • tylenol
73
Q

define specific (acquired) immunity
when does it develop?
what is different about the second time a pathogen enters?
how can you acquire specific immunity?

A
  • the ability to recognize and defend against pathogens
  • in response to a pathogen—takes time
  • it is MUCH faster and more powerful
  • Naturally (infection) or artificially (vaccination)
74
Q

Define antigen.
what are some examples?
what does the term antigen derive from?

A
  • anything that triggers a specific immune response
  • pathogen, pollen, dander
  • ANTIbody GENerator
75
Q

define epitope.

antibodies (another name for) define

A
  • small parts of an antigen that triggers a specific immune response.
  • aka immunogobulins (Ig), proteins that bind to an antigen and tag the antigen for destruction by the immune system.
76
Q

what does the lymphatic systerm include?
what is it involved in?
what does it do?
what kind of system is it?

A
  • lymphatic vessels, lymph nodes, lymphoid organs/tissues
  • directly involved in specific immunity-screen for antigens
  • returns leaked fluid to circulatory system, screens that fluid for antigens.
  • a one-way system returns leaked fluid to circulatory system
77
Q

what does lymph travel through?
what happens when an antigen is found in the lymph?
what is the function of the different lymphatic organs/tissues?

A
  • lymph nodes that cluster at portals of entry
  • they mount a specific immune response
  • spleen-filter blood and removes pathogens
  • tonsils, peyer’s patches= trap pathogens, cells with in them screen for pathogens and mount a specific immune response
78
Q

What are the two parts of humoral immunity?

what kind of pathogens does it work best against?

A
  • b lymphocytes (b cells) and antibodies

- exogenous pathogens

79
Q

where are B cells produced? where do they go after that?
what is on B cells that allows it to bind to an antigen?
How many B cells do you have in your body?
what is the main function of B cells?

A
  • stem cells in the bone marrow, then travel to lymph nodes/lymphoid organs and tissues
  • 100,000 copies of that one specific antigen.
  • millions of different B cells which recognize and bind millions of different antigens
  • antibody production
80
Q

How many B cells are there for a specific antigen before the first time it enters the body?
describe what happens to existing B cells after pathogen enters body. (2)

A
  • before exposure, there are 1-3 cells that can recognize and bind to an antigen
    1. the antigen selects an existing B cell binding to the receptor on the B cell
    2. Antigen binding to the B cell receptor stimulates that B cell to divide by mitosis. Produces millions of identical B cells called B cell clones.
81
Q

What happens to the B cell clones?

A
  • some clones become PLASMA CELLS, function 4-5 days, secrete antibody against the antigen, secrete 2000 antibodies/second. Antibodies circulate in blood, lymph, mucus, colostrum, breast milk in search of their antigen. find it, bind to it, and tag it for destruction.
  • some become MEMORY B CELLS. Don’t secrete antibodies, just stay around (long lived) in case you encounter the same antigen again. if you do encounter same antigen, b memory cells very quickly divide and produce plasma cells that secrete antibodies agains the antigen and more memory B cells.
82
Q

what are antibodies?
how many antigens can one antibody bind to?
what do antibodies do?

A
  • y0shaped protein molecules
  • binds to 1 SPECIFIC antigen
  • binds to its antigen and tags it for destruction by the immune system.
83
Q

what 5 things happen when antibody binds to its antigen?

A
  1. can prevent viral attachment to receptor host cell.
  2. neutralizes bacterial exotoxins
  3. prevents bacterial attachment
  4. agglutination (clumping) of antigen, decreasing movement of the antigen.
  5. increases phagocytosis
84
Q

what are the 5 types of antibodies and describe them.

A

IgM- 1st antibody produced, short lived,
IgA-respiratory tract, Gi tract, mucus, tears, saliva, colostrum, breast milk, prevents attachment of pathogens
IgD-acts as antigen receptor of B cells
IgE-allergic response, helminth response
IgG-produed 24-48 hours after antigen exposure, most (80%) o f circulating antibodies, main component of secondary immune response, crosses the placenta, booster shots increase IgG

85
Q

what is the primary response?

secondary response?

A
  • 1st encounter of antigen, has a lag and takes time, produces memory B cells, IgM and IgG against antigen
  • 2nd and any additional time you encounter the antigen, rapid response, memory B cells, IgG lots of it that stays behind
86
Q

what two things make up cell-mediated immunity?

what does it work best against?

A
  • T cells and antigens

- against endogenous pathogens-infected cells (virus, bacteria, parasite) and abnormal cells (tumor cells, cancer cells)

87
Q

where do T cells come from? where do they go?

what about their receptors and number of them?

A
  • arise from stem cells in bone marrow, go to thymus, mature and educated (self vs non-self) then go to lymphatic system
  • each have t-cell receptors that bind 1 SPECIFIC antigen, there are 100,000 copies of this receptor on its surface.
88
Q

what are the 2 types of t-cells describe and what is funciton?

A
  1. cytotoxic t-cells-have t-cell receptor and CD8 co receptor on their surface
    - recognize and eliminate infected and abnormal cells
  2. helper t-cells-have t-cell receptor and CD4 co receptor on their surface
    - help in humoral and cell-mediated immunity
89
Q

what is the major histocompatability complex (MHC)?

A
  • proteins embedded in membrane of cells,

- genetic, multiple genes determine your MHC, completely UNIQUE to you.

90
Q

what are the 2 types of MHC? where are they found

A
  1. MHC class II- found on the surface of antigen presenting cells (APC) (B cells macrophages, neutrophils, dendritic cells) it folds and forms a groove that an antigen (epitope) can fit into
    - cells present epitopes in MHC II to CD4 helper T Cells .
  2. MHC class I-found of surface of all nucleated body cells, folds to form a groove that an antigen (epitope) can bind to
    - cells present epitope in MHC I to cytotoxic (CD8) T cells.
91
Q

what are APC cells? examples? what kind of MHC do they have?

A
  • antigen presenting cells
  • B cells, macrophages, neutrophils, dendritic cells
  • BOTH MHC II and MCH I
92
Q

what are the 9 steps of helper t-cell activation?

A
  1. antigen enters body
  2. phagocyte phagocytizes antigen via lysozymes which digest by degredative enzymes
  3. phagocyte displays the epitope of antigen in MHC-II
  4. Phagocyte ends up in lymphatic system in search of the correct inactive helper T-cell to activate, mixes and mingles with inactive helper T-cells in lymphatic system looking for a match
  5. match happens when phagocyte epitope in MHC-II matches inactive helper T-cell receptor and CD4 co receptor
  6. this match causes cytokines/ymphokines (chemical signals) to be produced, T-cell now activated!
  7. active t-cell divides by mitosis and produces clones
  8. some t-cells become memory t-cells and stay behind, most become TH1 or TH2 cells
  9. TH2 cells produce cytokines that stimulate plasma cells to produce antibodies, TH1 cells produce cytokines that activate macrophages, or cytotoxic T-cell, or NK cells
93
Q

what are the 6 steps of cytotoxic t-cell activation?

A
  1. when a cell is infected it displays an “i am infected’ epitope on its surface in MHC-I (if abnormal, it displays an “i am abnormal” epitope on its surface in MHC-I)
  2. A search for correct cytotoxic t-cell
  3. match happens when infected/abnormal cell with its epitope in MHC-I meets up with the inactive cytotoxic T-cell and it’s correct t-cell receptor and CD8 coreceptor, cytotoxic t-cell is now ACTIVATED
  4. cytotoxic t-cell divids by mitosis to produce clones
  5. some clones become memory T-cells, most become active, killing cels
  6. travel through the body in search of more of the infected/abnormal cells, kill immediately when match happens.
94
Q

how do cytotoxic t-cells kill infected/abnormal cells?

A

use chemicals to kill!

  • perforins=make holes in infected/abnormal cell membrane
  • granzymes=cause apoptosis of infected/abnormal cell.
95
Q

define active immunity
what is produced?
time frame?
how is it acquired?

A
  • develops when your specific immune system (cell-mediated and humoral) recognize and respond to a pathogen (antigen)
  • memory b and T cells, IgG against eh antigen
  • take hours to days to develop (time lag)
  • naturally (infection) or artificially (vaccine)
96
Q

define passive immunity
time to be efective?
how long does it last?
how can it be acquired?

A
  • give you antibodies against the antigen
  • immediate protection
  • last days to weeks
  • artificially (gamma globulin shot-shot of pre made antibodies), naturally (mom to fetus-IgG crosses placenta, mom to baby-colostrum and breast milk)
97
Q

what is a vaccination?
what does this produce in the body?
what is the goal?
what are the 5 types?

A
  • inoculate with a weakened/inactive pathogen or epitopes of a pathogen to produce a specific immune response
  • memory B and T cells and IgG against the pathogen
  • eliminate infectious disease
  • attenuated, inactivated, toxoid, subunit, and conjugate
98
Q 
define attenuated vaccines
can virus replicate?
symptoms?
how long dos it last?
why is it hard for developing world?
who can't use it?
A

-weaken a virus in the lab so it can no longer cause disease
-virus will still replicate at a very slow rate
-no symptoms
-life-long immunity because produces a very strong specific immune response
-requires refrigeration
-immunocompromised people
EXAMPLES: oral polio, MMR, chicken pox, shingles, rota virus

99
Q

define inactivated vaccine.
what happens to the epitopes?
why booster shot?
store temp?

A

-“kill” the pathogen using heat/chemical radiation
-alter the epitopes of pathogen slightly because of
-needed to increase IgG, memory B and T cells
-stored at room temp
EXAMPLE: polio shot, hep A

100
Q

define toxoid vaccine

eptiopes? boosters?

A

-bacterial exotoxin, inactivate it using chemicals (formalin)
-alter epitopes slightly
- boosters needed
EXAMPLE- tetanus, diptheria

101
Q

define subunit vaccine
boosters?
EXAMPLES hep B, gardasil

A
  • vaccine includes only the epitopes of hte pathogen

- boosters needed

102
Q

conjugate vaccine
why needed?
how does it work?
EXAMPLES: hemophilus influenzae type b, neisseria meningitis

A
  • pathogen that is a bacteria that has a capsule
  • because capsules are non antigenic
  • they conjugate (attach) the capsule to an inactivated toxin

Microbiology (6 decks)

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