Winter 2011 Final Exam

Microbiology 509 with Pradhan at Ohio State University - All Campuses

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By: Summer Jones
Textbook:

Microbiology: A Human Perspective w/ARIS bind in card
Created: 2011-03-14
Size: 114 flashcards
Views: 251

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Innate Immunity

-Doesn't improve overtime
-Lack Memory cells
-Nonspecific Response
-works with several pathogens
-doesn't get built up
-Innert immunity, born with
-fxns same fxn in same fashion and pathogen doesn't change on a diff pathogen
-genes inherited

Adaptive Immunity

-Highly specific- Change with type of pathogen. Only work on that one pathogen
-is memory response--improves quality of immunity
-acquired immunity
-keep building immunity response in life time
-you build it up during your life time

First line of defenses

To prevent entry of microbes
-Cough or sneeze getting rid of bacteria in mucus
1. Physical barriers
2. Chemical Barriers
3. Normal Flora/Microbes

1. Physical Barriers

skin, mucus membrane
--enter in skin, has to be intact for bacteria to enter
--enter thru sweat glands and hair follicles or open wounds

2. Chemical Barriers

Lysozyme: tear, saliva
--Prevent bacterial infection
Lactoferrins and transferrins
--free Fe (non-bound, where bacteria need to grow
Defensins
Peroxidase
--certain enzymes present in body that'll become barriers against microbes trying to enter.

3. Normal Flora/Microbes

1. Competitive Exclusion
2. Production of toxins
3. Alteration of Environment

3. Normal Flora/Microbes-- 1. Competitive Exclusion

very dynamic nature
already in body and fight with invading microbes for food
attach sites, etc

3. Normal Flora/Microbes-- 2. Production of toxins

Collicin--toxic against other microbes but not toxic to humans
belongs to E. Coli and attacks invading microbes

3. Normal Flora/Microbes--3. Alterations of Environment

causes pH to change
when present add acids to decrease likely hood of invading microbes from entering and est. in body

Cells of the Immune System

Hematopoietic Stem cell-gives rise to all blood cells, in bone marrow, where blood components/cells are born from
Blood cells
RBCs-carries O2 and CO2- no role in immune response
platlets- small elements-do have role in IR, form clots
WBCs--players of IR

WBCs/Leukocytes

1. Granulocytes
A. Neutrophils
B. Eosinophils
C. Basophils
2. Mononuclear phagocytes
A. Macrophages
B. Dendritic cells
3. Lymphocytes
A. T an B lymphocytes
--doesnt play rule in innate but do in adaptive, have no ability of phagocytosis

1. Graulocytes

A. Neutrophils--has ability to perform phagocytocis, eat pathogens
B. Eosinophils-- killing parasite protect you from worm, can form phagocytosis
--not as efficient
C. Basophils-- no phagocytosis--cells release Histamine to release allergies

Process of Phagocytosis

1. Chemotaxis--accumulate phagocytic cells at site of infection
2. Recognition & atthmt--pathogen & WBC same escape & cause infection
3. Englufment: phagosome- (vesicle) pathogen moved into the cell
4. Formation of a Phagolysosome (fusion of 2 cells, gets digested/killed)
5. Digestion
6. Exocytosis

Inflammation

Defense mechanism in human body, not turned off in time, persistant
1. Local response--produced only in body of body, flu
2. Symptons--all 4 must be present for inflammation
3. Causes
4. Fxns

Inflammation 2. Symptons

2nd line of defense after phagocytosis
-redness: rubor
-heat:calor
-pain: dolor-- b/c irritation of nerves
-swelling: edema
redness and swelling very common/easy to determine
most critical in innate IR

Inflammation: 3. causes & 4. Fxns

3. Causes
--infection-- damage ( from environment) cells
--Physical damage without infection

4. fxns
--destroy injurious agent
--limit the spread
--repair damaged tissue-- end of inflammation, process

Process of inflammation

1. trigger
2. vasodilation & increased permeability of blood vessels
3. phagocyte migration (diapedesis)
4. phagocytosis (PMN vs. Macrophages)
5. Tissue repair
Pus formation

Process of inflammation 1-3

1. chemicals: released from damaged cells to attack
2. increase diameter of cells what to bring more WBC
3. WBCs ooze out of Blood vessel

Process of inflammation 4-5

4. body polymorphonuclear need macro b/c neut are killed to save you. help still needed?macrophages then take over can go multiple stages
PMN= neutrophils, 1st respond
pus formation-- see alot/depends on accumulation of dead RBC, WBC, Blood vessels. indication of rapid cell death

Chemicals released by damaged cells

Histamine-- vasodilation, increased permeability of blood vessels
Kinins--vasodilation, increased permeability of blood vessels
prostaglandins--intesity histamine and kinin effect
leukotrienes--increased permeability of blood vessels, phagocytic atthmt

Fever

mechanism of defense, body temp increases response to infection
once serves its purpose it must be turned off
1. systemic response to an infection--involves entire body
2. what causes? Macrophages-- IL1-->hypothalamus
3. how is host helped?

Fever 2. What causes 3. how is host helped

2. IL1--interleukins 1
part of brain that regulates body
secreted ion 1- travels to brain b/c thermostat is at
temp, increase body temp
3. more production at bone marrow for more WBC
using enzymes to kill
can accelerate some IR
increase immune cell #
enhance killing of microgranisms

interferons

1. who produces?
cell itself, proteins that are cytochines (msgrs), many anial species and humans, 3 types: alpha, beta, & gamma
2. what are they and how do they act
chemical msgs
AVP kill infections

2 categories of interferons

IFN-alpha and beta--cause cells to produce antiviral proteins that inhibit viral replication
gamma ifn: causes neutrophils and macrophages to phagocytize bacteria

The complement system

are innate, present in blood, grp of proteins
1. what is it? C1, C2, C3.....C9, system of proteins present in blood
2. Activated in 3 different ways--in response to pathogen/infection
a. classical pathway
b. lectin pathway
c. alternative pathway

The complement system 2. activated 3 diff ways

a. classical pathway--presence of pathogen and antibody
need antibodies to work
b. lectin pathway--presence of pathogen
c. alternative pathway--presence of pathogen

lower case letter with complement protein
indicates activated
eg. C3--> C3a or C3b

Consequences of complement activation

1. opsonization: C3b is an opsonin
2. inflammation: C3a and C5a
3. Cytolysis: membrane attack complex

1. opsonization

makes easiest to capture bac
coat outside surface of bac/pathogen
antibodies serve as opsonin
protein or antibody called obsornins
works by 1. flagging bac 2. tightly atth to the cells to increase the rate of catching the bac
fxn of complement proteins

2. inflammation

increase permeability of blood vessels
participates in chemotaxis
provides help in vasodilation

3. cytolysis

lysis of target--pathogen
forms in membrane of bacterial cell
proteins activated
punches hole (bac) cell membrane
cell causes infection to lyse
MAC--> C5b, C6, C7, C8, C9

The complement system

C3b causes opsonization
C3a + C5a cause inflammation
C5b + C6 + C7 + C8 + C9 cause cell lysis--- get together to form MAC
G neg more susceptible to the complementary proteins
--create hole in membrane, directly killing bacteria

Some bacteria evade complement

able to avoid complement proteins
--capsules preven C activation
--surface--lipid carbohydrates prevent membrane attack complex (MAC) formation
--enzymatic digestion of C5a-- process of inflammation
how? prevent formation of MAC

Adaptive/Acquired immunity

1. naturally acquired active immunity
2. naturally acquired passive immunity
3. artificially acquired active immunity
4. artificially acquired passive immunity

Naturally acquired active immunity

your own immune system actively involved in producing antibodies
eg. chicken pox
microbes naturally introduced to system
immunity acquired w/daily basis exposure to bacterial infections
passive-present in the body

Naturally acquired passive immunity

antibodies stay for a few months (6) in the new born child
receiving premade antibodies
fetus gets antibodies from mother
mothers milk baby gets antibodies
mothers antibodies cross placenta and vie to the fetus (only some types)

Artificially acquired active immunity

eg. vaccines
body actively fighting infection but did not get the exposure by daily exposure

Artificially acquired passive immunity

eg. snake bite-- premade antibodies
elderly--premade antigens are introduced to body
studying abroad--get vaccines, or premade antibodies
immune response occurs outside your body. Natural and artificial based on how introduced to body

Humoral Response

1. involves the production of antibodies
2. key cell type: B lymph
3. Tends to be most effective against bacterial toxins, bacteria, and viruses before they enter cells
extraC--freely circulate body
using C-M IR if becomes intra or cellular level

Cell-mediated Response

1. involves the production of specialized lymphocytes
2. key cell type: T lymphocytes 1. TH 2. TC
3. effectiveness: useful at the cellular level

Antigen Characteristics

1. maybe foreign to the body 99.9% non "self"
2. maybe self autoimmune diseases--body produces auto anti bodies against organs
3. Macromolecules: usually proteins or lipoproteins
4. maybe particulate (insoluble) or soluble (like albumin)
circulate around

Mechanism of humoral response

1. characteristics of B lymphocytes
2. Primary humoral response
3. antibody production in primary humoral response
4. plasma cells vs. memory cells

Characteristics of B lymp

type of WBC
non phagocytic secrete antibody proteins, made in bone marrow
goes thru stages
originate and mature in bone marrow

Primary humoral response

what happens if lymp do not encounter their specific antigen? are eliminated
what happensif lymphocytes recognize self-antigen?formed in system

Antibody production in primary humoral response

1st time production against pathogen
predominate Ab (first antibody IgM- produced)

1. plasma cells vs 2. memory cells (eg. 1&2)

1. secrete antibody proteins and release outside of plasma cells. Chasing pathogens in your body = humoral response. dont remain in system-- they disappear
2. life long protection. Remain in body for years 10-12years

Humoral response: 2 kinds

b.c depends on antigens
1. T-independent humoral response: 5-10% produce
T-independent antigens-- bacteria capsules pili
made of polysaccharides
2. T-dependent humoral response--90% produce this
made up of protein antigens
more powerful

Immunoglobulins (Ig) /antibodies (Ab)--protein cells

1. antibodies are proteins made in response to an antigen that can bind w/that antigen (highly specific)
1 antigen, 1 epitope
2. a single antibody unit is a monomer which is bivalent
3. 5 types/classes of antibody: may have diff #'s of binding sites

basic structure of antibody #1

1. a typical antibody monomer has 4 protein chains: 2 heavy+2 light chains (disulfide links)

basic structure of antibody #2

2. w/in each chain is a variable region (V) & a constant region (C)
light & heavy bind to antibody
Fc region only binds- 2 fxns
-classify Ab into 5 grps
-dont by Fc region
-Activate complement

basic structure of antibody #3, 4, 5

#3 a variable region (V) is where antigen binding occurs

#4 a constant region (Fc) serves as a basis for classifying antibody

#5 The Fc region can attach to a host cell or a complement

Classes of Immunoglobulins 1. IgG

a. about 80% of total serum antibody
b. predominant antibody of secondary humoral response
c. crosses the human placenta to produce natural, passive, acquired immunity valency is 2
only crosses blood placenta

Classes of Immunoglobulins 2. IgM

a. found in serum, lymph and on B-cell surfaces
b. first & predominant antibody of primary humoral response
c. pentamer; valency is 10

Classes of Immunoglobulins 3. IgA

a. found in secretions:mucus, tears, saliva, milk (especially colostrum); blood; lymph
acquired immunity b/c milk
b. especially important in protecting upper respiratory tract
c. dimer, with secretory component (monomer in serum)
4 antigen molecules

Classes of Immunoglobulins 4. IgD

serves as B cell receptor
a. minor serum antibody
b. found on B-cell surfaces: presumed antigen receptors on B lymphocyte surfaces
c. no known fxn in serum
d. valency is 2
small quantities not in secreted forms
not on B cell dont know fxn

Classes of Immunoglobulins 5. IgE

a. .002% of serum antibody; generally not circulating
b. most bound tightly by Fc region to mast cells
c. participate in allergic reactions
d. valency is 2
least amt of antibody except if allergic then IgE increases
bound at surface of Mast cells

Protective outcome of antibody 1&2

1. Neutralization--of toxins viruses/ bacterial
2. immobilization and prevention of adherence--bacteria flagella bound to Ab if becomes immobile

Protective outcome of antibody 3-5

3. Agglutination and Precipitation-- bring 100s increase of antigen together-- make insoluble if soluble then precipitation
removed by phago
binding to antigen not enough need phaocytic cells to remove them
4. Opsonization
5. Complement Activation

Vaccines 1&2

1. Heat-killed/inactivated vaccines--pathogen is dead not capable causing anything
Hepatitis A- flu injection
2. Attenuated vaccines
MMR, flu mist -- virus is alive-- it is weakened, lost pathogenistic
genic changes to virus

Vaccines 3&4

3. Toxoid vaccines
form of toxin introduced of pathogen
tetnas shot
4. subunit vaccines
protein of pathogen--epitope introduce it to your body=will be response
hepititis B

Cell-mediated immunity 1&2

1. offers protection against intracellular antigens or at cellular level
2. not transferable through placenta

Cell-mediated immunity 3

3. T lymphocytes and cytokines are the players
chem msg--interlukins
fever production
cytokines that are communicators between leukocytes are interleukins (IL) eg. IL-1 IL-2

T lymphocytes

1. T lymp-made in bone marrow but migrate to thymus to mature
2. surface receptor and Co-receptors of T lymph
TCR+CD4 or TCR + CD 8
3. Helpter T cells CD4
4. Cytotoxic T cells CD8
5. HIV targetscells with CD4 co-receptors
CD4 will be eliminated = AIDS

Antigen Recognition by T lymp

Antigen can not be free-floating (not recognized unless MHC on it ) but needs to be presented to T lymph along with MHC complex

MHC complexes are of 2 types

1. Class I: on surfaces of most nucleated cells of the body
2. Class II: on surfaces of APCs (antigen presenting cells): Dendritic cells, B-cell, macrophages
2 possible ways of APC to T lymph: Ag+MCH I or Ag+ MHC II
then present to T lymph

1. Antigen presentation to T lymp: Ag+ MHC I

Ag + MHC I complex will be presented by an infected cell or an abnormal cell to CD8 + TCR containing T cell

Cytotoxic T lymph Tc (CTL)

a. after recognition of an antigen, 2 cell types produced: effector (CTL) and memory cells
b. fxn of CTL: destruction of target cells virus-infected cells, cancer cells, incompatible tissue grafts

Cytotoxic T lymph Tc (CTL) c &d

c. when target cell is spotted, granules with perforin (holes in PM and lysis) are released by CTL-- takes place before viruses are mature
d. this protein is inserted into the membrane of the offending cell, to form a pore leading to death of target

2. Abtigen presentation to T lymph: Ag + MHC II

Ag+MHC II complex will be presented by an APC, antigen presenting cell, to CD4 +TCR containing T cell
only helper T cells b/c CD4

Helper T cells (TH)

a. after Ag recognition, differentiates into 2 types: effector and memory therefore, 1 and 2 degree responses here
b. fxn: helper T cells produce cytokines to influence the activity of
macrophages
other T cells and
B cells: overlap with humoral response

Natural Killer cells (NK) a&b

innate immunity
capture microbe trying to cause infection
a. dont have markers on surface
Kind of WBC, Neither T nor B interms of surface markers.
dont recognize target, recognition not by antigen receptors
b. no memory response, adaptive category

Natural Killer cells (NK) c&d

c. fxn: perforin- released by cytotoxic T cells
removal of offending cells by lysis using perforin
eg. viruses containing and tumor cells
d. however, able to kill in the absence of stimulation by specific Ag

Epidemiology

study the cause and distribution of disease in population (eg. spread of pathogens)

Transient microbiota

may be present for days, weeks, or months
temporarily associated with our body

normal microbiota

permanently colonize the host
on surface or inside (gut)

symbiosis

is relationship between normal microbiota and the host
can become pathogenic
normal microbiota can become bad
if immune system is down

normal microbiota protect the host by

occupying niches that pathogens might occupy
producing acids
producing bacteriocins
compete with invading pathogens

Composition of normal flora changes due to

hormonal changes
type of food consumed
antibiotics
can change if under stress, normal flow changes

probiotics

live microbes applied to or ingested into the body, intended to exertabeneficial effect

Pathology, infection, and disease 1-4

1. infection--entry of pathogen--colonized body procedures further becomes disease
2. disease-- damage of host body. departure of health status
3. symptons--felt by patient but others cant see that like headache.nauseated
4. signs-- procedures done

Pathology, infection, and disease #5

5. syndrome-- measured by 3rd person
inflammatino--swelling, fever fell temp and measure it
combination of sympton andsigns

Classifying infectious diseases occurrence of a disease

1. communicable disease
2. endemic --diff in every location, local diseases present
3. epidemic--explodes in large #'s small/sharp duration in a given area/location
4. pandemic

Severity or Duration of a Disease #1-3

1. acute disease: symptoms develop rapidly, dissolves rapidly, quickly
2. chronic disease: disease develops slowly
multiplying, last long time
3. subacute disease: Symptoms btwn acute and chronic

Severity or Duration of a Disease #4

4. latent disease: disease w/a period of no symptoms when the causative agent is inactive
not multiplying, pathogens dormant
no symptoms

extent of Host involvement

1. local infection:
2. systemic infection:
3. focal infection:

local infection

pathogens are limited to a small area of the body
not widely spread

systemic infection

an infection throughout the body
thru blood
bad b.c difficult to control
affecting multiple organs

focal infection

systemic infection that began as a local infection

Extent of host involvement

1. sepsis
2. bacteremia: bacteria in the blood
3. septicemia: growth of bacteria in the blood
actively multiplying in blood
4. toxemia: toxins in the blood
5. Viremia: viruses in the blood

sepsis

toxic inflammatory condition arising from the spread of microbes, especially bacteria or their toxins, from a focus of infection

primary infection

viral infection

secondary infection

occurred because of primary infection

subclinical disease

no noticeable signs or symptoms (inapparent infection)
carrier
infecting others with disease

Reservoirs of infectious agents 1&2

infected w/pathogenic agents or carriers and spreading it-- bad cause cant control
1. human reservoirs: patients, carriers
2. non-human animal reservoir--primary reservoirs
sick or carriers
-rabbies virus, plague -- rodents involved

Reservoirs of infectious agents 3

3. environmental reservoirs
microbes found in soil (& even water)

Transmission

contact: direct and indirect
food and water: can carry microbes, if not cooked thoroughly you can eat it
Air: most difficult to control
Vectors

direct contact

1. physical contact--btwn individuals
2. droplet transmission--short distance droplets travel

indirect contact

non living objects
1. transmission via inanimate objects or fomites
nonliving poor handles faucet, pens, etc
2. handwashing: a preventative measure

vectors--living objects

arthropods, especially fleas, ticks, and mosquitoes
transmit disease by
1. mechanical transmission: arthropods carries pathogen on feet--fly transmits pathogen
2. biological transmission: pathogen reproduces in vector--mosquito bites

Nosocomial infections

1. hospital acquired disease
2. hospitals are reservoirs of infectious agents
3. hospitals enable transmission of infectious agent

Pathogenicity

the ability to cause disease

Virulence

the extent of pathogenicity
measure of pathogenicity--ability

primary pathogen

infections in individuals with weak immune system

opportunistic pathogen

own normal flora microbes

How microbes enter a host portals of entry

mucous membranes
skin-intact barrier unless broken
parenteral route-- broken skin barrier
preferred portal of entry--hair follicle, ducts or glands

ID50

infectious dose for 50% of the test population
# of microbes leading to infection

LD50

lethal dose (of a toxin) for 50% of the test population

How pathogens penetrate host defenses

1. capsules and cell wall components contribute to pathogenicity
2. effects of coagulases, kinases, hyaluronidase, and collagenase.
produced by bacteria
3. antigenic variation
mutatio, change themselves to avoid
4. production of toxins, doesnt fit tho

kinases

digest fibrin clots

coagulase

coagulates fibrinogen

hyaluronidase

hydrolyzes hyaluronic acid

collagenase

hydrolyzes collagen

IgA proteases

destroy IgA antibodies
avoid immune responses

Exotoxin

source: mostly gram +
relation to microbe: by-products of growing cell
chemistry: protein
fever?no
neutralized by anitoxin? yes
LD50 small

Endotoxins

source: gram -
relation to microbe: outer membrane
chemistry: lipid a
fever? yes
neutralized by antitoxin? no
LD 50 relatively large

About this deck

By: Summer Jones
Textbook:

Microbiology: A Human Perspective w/ARIS bind in card
Created: 2011-03-14
Size: 114 flashcards
Views: 251

About StudyBlue

“Simply amazing. The flash cards are smooth, there are many different types of studying tools, and there is a great search engine. I praise you on the awesomeness.”
Dennis