micro test 1 study guide

8/7/2019 Micro Test 1 Study Guide

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Micro Test 1 Study Guide

Borrelia Bergdoferi

y Causes Lyme Diseasey Uses Ticks as its Vector(the bug which spreads the bacteria, infecting severalanimals) and uses

severalanimals such as deer, birds,and rats as its Reservoir(the animals which hold the bacteria

but show no symptoms from it/ a carrier)

y Initial symptoms of infection are a red rash (1st symptom which looks like the target symbol) andconjunctivitis (appears after rash, is a red eye) Other symptoms may include facial paralysis,

arthritis,and cardiac and/or neurological symptoms

y orrelia is not passed down from parent tick to larvae tick, but is acquired after alarvae feedson an infected reservoir

Why is Lyme disease so prevalent in the Northeast?

y Deforestation and reforestation of the areay

Preval

ence of foresteda

rea

all

ows both Vectora

nd Reservoir to sprea

d to newa

rea

sy Residential development of reforested areay orrelias ability to infect multiple species

Opsonization- when a microbe becomes targeted for phagocytosis either by complement binding,

antibody binding, or both at the same time. Complement protein and antibody can thus be referred to

as opsonins.

Complement protein- Can also form the Complent Membrane Attack Complex (MAC) which will make

holes in the pathogen membrane and cause celllysis

How Does Borrelia survive within the host?

a. The tick saliva temporarily inhibits immunityb. Borrelialacks or hides common bacterial surface structures

y Rather than have alipopolysaccharide endotoxin on its outer membrane, Borrelia hasonly a phospholipid bilayer as its outer membrane (so that the host isnt killed and

Borrelia is allowed to continue to thrive)

y Borrelias flagellialies between its inner and outer membranes rather than beingattached to its outer membrane. This hides the flagellar antigens from the immune

system

c. Borrelia prevents attack by the host complement proteiny It has lipoproteins on its surface which recruit host proteins that prevent pores from

being made on its surface. The complement is inhibited by the host protein

d. Borrelia is able to adapt to different hostsy While in the tick Borrelia expresses OspA which is used to bind it to the tick midgut.

When the tick is feeding OspC is expressed which helps Borrelia migrate to the tick

salivary gland,and thus enter the host bloodstream.

y Expression of OspA and OspC is regulated by DNA supercoiling which is due toTopoisomerase, which responds to temperature. In high temperatures there is

decreased supercoiling, so there is an increase of OspCand low amounts of OspA. In

cold temperatures there is increased supercoiling, so there is a high amount of OspA


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and OspC is silenced. Mutants which decrease supercoiling willlead to large amounts of

OspC

e. Borrelia changes its surface proteins by mutationy This keeps it one step ahead of the newly formed antibodies, which will only be

effective against the previous variant

f. Borrelia will hide in Immune Privileged sites (such as the brain, eye, testes,and ovaries) wherean immune response can cause irreversible damage

Why does chronic arthritis sometimes develop after the infection clear?

y Bacterial peptides presented as an antigen may closely resemble a self-peptide of thehost, so the antibodies made against the pathogen willalso attack the host cells

containing the similar self-peptide

Salmonella

Salmonella Typhi/Typhoid Fever

y Causes Typhoid Fevery Only infects humansy Is treated with antibioticsy Caused by focally contaminated food/water

Salmonella Typhimurium/Gastroenteritis

y Has a broad host rangey Infection requires ingestion of 10^5 microbesy Caused by contaminated poultry/eggsy Can be shed in feces for up to 3 months,and very rarely (1-3% of people) for up to a year

Type III Secretion System (TIIISS)

y Injects proteins into mammalian cells which are normally non phagocytic, that inducephagocytosis of the bacterium

y Assembled in parts first in the inner membrane, then the outer membrane, then the periplasm(muramidase is needed to cut the peptidoglycan layer) and finally the extracellular domains.

Virulence Factors

y SPI-1 TIIISS is needed to gain entry/invasion into the host cell(but not if Salmonella isinjected directly into the bloodstream, only if orally ingested)

y SPI-2 TIIISS,PhoQ,PhoP,and pSLT are needed in order to survive within the host cell. PhoQis activated by molecular signals from the host cell(macrophages),and then phosphorylatesPhoP. PhoP then represses SPI-1 TIIISS so that SPI-2 TIIISS can protect Salmonella containing

vacuoles from degradation by the lysosome.

y SPI-2 TIIISS,PhoQ,PhoP,and pSLT are all needed for persistence in the host cellHuman Microflora and Nonspecific Host Defenses

y The normal bacteria which colonize humans are commensal/mutualistic


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y The microbe populations change constantly and vary with type of tissue, condition, presence ofother microbes, ph, moisture,and even food eaten

y If they leave their normallocations they can cause diseaseSkin

y Is difficult to colonize because it is dry, salty,acidic,and contains protective oilsy In the moist areas (such as groin, scalp,armpit,and analareas) there are about 10^12 microbesy Gram + tolerate the salt welly Mostly colonized by anaerobes (in the moist areas)

Proprionibacterium

y Gram + bacteria which lives on the skin and causes acney Feeds on the lipids secreted by oil glands and converts them to free fatty acids

o Free fatty acids smell, trigger inflammation,and inhibit the growth of Gram bacteriaNose and Mouth Defense:

y Nose cilia trap microbesy Mucous in the mouth and throat trap bacteriaand carry it to the acidic stomachy Trachea cilia carry bacteriaaway from the lungsy These microfloraare dangerous if they enter the bloodstreamy Can form biofilm around teeth, causing plaque and gum disease

The Stomach:

y Has a very high acidity (low pH) which kills most microbesy Helicobacter pylori can survive at this low pH and is the cause of ulcersy Acidity can be lost because of malnourishment which allows for pathogen growth

The Intestine:

y Contains the vast majority of human microflora(10^9-11 cells/ cubic centimeter)y The bacteria ferment ungested food, provide nutrients and inhibit pathogens

Genitourinary:

y Kidney and bladder are sterile, but the urethraand vagina contain bacteriay Flora changes with female monthly cyclesy Acidic secretions inhibit pathogensy Lactobacillus acidophilus resides in the vaginaand is also used in probiotics,and yogurt

production. Its lactic acid production inhibits the growth of other bacteria

Benefits of Microflora:

y Make vitaminsy Digest foody Prevent colonization of pathogens


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Risks:

y Are opportunistic and will cause disease with surface breach or in immunocompromisedhost

Innate Immunity: barriers to infection, nonspecific reaction to destroy invading cells (such as

complement protein binding). Does not require antibodies

Adaptive Immunity: A reaction to specific antigens

Innate Host Defenses

Physical Barriers

y The Skiny Mucousy Ciliay Toll-like receptor proteins on tissues

Chemical Barriers

y Acidic pH of the stomach, skin,and vaginay Antimicrobial peptides which destroy the plasma mebraney Lysozyme in tears,and on skin

o Destroys peptidoglycan layer by breaking the links between the alternating NAM andNAG sugars of the peptidoglycan. Only works against Gram + since their peptidoglycan is

on the outside

Acute Inflammatory Response:

Damages tissue releases bradykininbradykinin stimulates mast cells mast cells release histamine

histamine causes vasodilation and the release of platelets, plasmaand prostaglandinsprostaglandins

stimulate nerve cells which causes itching and pain

Phagocytes- Phagocytes avoid attacking host cells by recognizing the host self-surface molecule cd47.

However, they will bind and phagocytose opsonized bacteria

y Kill bacteria using digestive enzymes (in the lysosome) as wellas a reactive oxidative burst (fromthe phagosome)

The Complement Membrane Attack Complex may for m against gram bacteria because they do not

have peptidoglycans as their outer layer. Individual complement proteins may act as opsonins for both

Gram and + bacteria

Interferons are synthesized by cells infected by viruses. After the cell is killed by the viruses the

interferon is released to neighboring cells and binds to interferon receptors. This causes the neighboring

cells to activate endoribonuclease which cleaves and destroys viral RNA,and inactivate elF-2 which stops

translation for any of the RNA missed by endoribonuclease

Fever


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y Pyrogens induce temperature riseo Exogenous pyrogens such as LPS (lipopolysaccharide) cause the release of endogenous

pyrogens.

o Endogenous pyrogens such as interferon and TNF signal the brain to raise thetemperature,and also reduce iron availability to bacteria.

y High temperatures stress invading bacteriaThe Adaptive Immune Response

T-Cells mature in the Thymus, while B-Cells (can be phagocytic) mature in Bone marrow

How do T-Cells recognize self?

The Major Histocompatibility Complex

y MHCI proteins are expressed on most cellso MHCIand cd47 are self markerso Are taught to Killer T-Cells (cd8)o Present host cell proteins from the cytoplasmo If missing from a cell or presenting a foreign antigen, the cell will be attacked by Killer t-

cells (cd8) using perforin and granzyme

Perforin has an effect similar to the MACand forms pores in the cell membrane.Granzyme enters through these pours and digests the proteins within the cell

y MHCII is only expressed on cells that interact with T-cells (such as B cells,and macrophages)o It is used to present proteins taken in from the environment/phagolysosome (which

came from invading microbes where were then broken down and displayed as antigens)

to Helper T cells (cd4) (which triggers cytokine release)

y T-Cells have a t-cell receptor which will interact with MHCIand MHCII depending on which t-cell it is

Antibody Production:

Some macrophage will ingest a microbe, degrade it and present a microbial peptide with its MHCII. A

Helper T-Cell(cd4) with a T-cell receptor that matches with the peptide with then join with the MHC

II/peptide complex and become activated, releasing cytokines. This activated Helper T-cell then joins

with an active B-Cell presenting the same peptide in its MHCIIand joins with it. After the activated

Helper T-celland B-cell join,a plasma cell is formed and begins secreting antibodies specific for that

antigen.

Antigens: are usually large complex molecules,and may have more than one site which is capable of

binding an antibody. Can only be a small molecule if it is combined with another carrier molecule such as

a protein. Small molecule attached to carriers are known as haptens

Nonspecific Phagocytosis removes antigens such as whole cells. Uses surface proteins (toll receptors)

which are specific for certain antigens, but are not antibodies.

Superantigens such as LPS cause septic shock. They force empty MHCIIand t-cell receptor as wellas

mismatched t-cell receptor and MHCII to join, triggering an immune response (systemic release of

histamine)


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y There are many t-cells and b-cells in our body at any given time. Each b-cell expresses onespecific antibody determined at random by genetic factors

Antibody Response

y After a primary antigen exposure antibodies willappear after several days due to b-cells bindingthe antigen and making antibodies. The B-cells change to memory cells. Initially IgM levels arehigher than IgG levels.

y After the secondary exposure antibodies appear within a few hours,and IgG levels becomemuch higher than IgM

Antibodies bind foreign antigens harmful to the host cell,and prevent them from binding with host

cells.

Antibodies can also inhibit colonization of epithelial cells by bacteria,and act as opsonins.

micro test 1 study guide

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