micro exam 3

Obligatory intracellular parasite

need a living host to multiply

contains wither DNA or RNA

contains protein coat

no ribosomes

no ATP requiring

Host range

the spectrum of host cells a virus can infect

Bacteriophages

virsues that infect bacteria

virus size

nm

nanometer

bacteria size

um

micrometer

bigger than the virus

Viral structure

nucleic acid, DNA or RNA never both

linear or circular

Viral structure: capsid

protein coat made of capsomeres (subunits)

Viral structure: envelope

lipid, protein, and carbohydrate coating on some viruses

help protect

Viral structure: spikes

projections from outter surface

help attach spikes are found on the envelope (protein coat)

complex viruses

bacterial virus

complicated structures

bacteriophage (these viruses can grab the bacteria)

viral species

a group of viruses sharing the same genetic information and host

plaques

what bacteriophages form, are clearings on a lawn of bacteria on the surface of agar

each plaque corresponds to a single virus, can be expressed as plaque-forming units (PFU)

Where are bacteriophages grown?

in bacteria (a host)

growing animal viruses

in embryonated eggs viruses are injected into egg

viral growth is signaled by changes or deaths of the embryo

animal=host

cell cultures

tissues are treated with enzymes to separate cells

virally infected cells are detected via their deterior

cell lines

chicken embryotic eggs

How to identify virus

virus needs host

Serological test (draw blood) reaction of the virus with antibodies

cytopathic effects: kill the cell line

• certain type of virus kills a specific cell line

How to identify bacteria

• gram stain

• biochemical test (phenol red, OF test, Triple sugar iron, methol red citus, enzym)

what are Continuous cells

cancer cells (tumors)

continuous= tumor cells keep growing

Viral multiplication (what does it need)

• host cell

• must overtake the hosts metabolic machinery

Viral multiplication: lytic cycle

Multiplication of bacteriophages

phage causes host DNA to break causing lysis and death of the host cell

1. attachment : phage attaches to host cell

2. penetrates: phage penetrates host cells injection DNA into host

3. Biosynthesis: synthesis bacterphage DNA and proteins, production of phage DNA and proteins

4. Maturation: assembly of phage particles

5. Release: host cell dies (lysis) phage lysozyme breaks the cell wall. **this is when I see virus*

Viral multiplication: latent cycle/lysogenic cycle

no virus

phage DNA is incorporated in the host dna

phage conversion

specialized transduction

1. attach

2. penetrate

3. incorporate to host

viral Multiplication: animal virus

1) Attachment: bacteriophage/virus attach to animal cell
2) Enter: whole virus enters host (pinocytosis)
3) Uncoating: remove protein coat around the virus using enzymes

4) Biosynthesis: synthezise virus DNA/RNA/protein
5) Maturation: assemble
6) Release (w/o envelop): release by budding (takes host plasma membrane from envlope and puts it around itself)

• no envelope = host lysis

Viral one step growth curve

Eclipse period:

acute infection:

goes down: when the host dies

biosynthesis DNA virus : steps

dna virus:

1. attach

2. uncoating

3. viral DNA go in nucleus to be syntheised

4. viral DNA goes to mRNA then to viral protein

5. once all is syntheised then assemble

6. lysis host dies , virus is released

biosynthesis RNA virus : steps

rna→ reverse transcription→ produces DNA → makes mRNA→ then finally makes protein

why can virus cause cancer?

virus cause infection which changes the hosts DNA causing mutation which is cnacer

oncogenes

transform normal cells into cancerous cells

oncogentic viruses

become integrated into the host cells DNA and induce tumors

latent viral infections

remains in asymptomatic host cells for long periods

• cold sores

• luekemia

• shingles

remains inside the host cell in a dormant state without actively producing infectious virus particles

persistent (chronic) viral infection

occur gradually over a long period, is general fatal

• HIV

• liver cancer

Chpt 15;

Pathogenicity

the ability to cause disease

Virulence

the degree of pathogenicity

How microorganisms enter a host: portals of entry

– Mucous membranes
– Skin
– Parenteral route
Deposited directly into tissues when barriers are
penetrated

ID50:

infectious dose for 50% of a sample population
– Measures virulence of a microbe

LD50:

lethal dose for 50% of a sample population
– Measures potency of a toxin

How microorganisms enter a host: Adherence

Almost all pathogens attach to host tissues in a
process called adherence (adhesion)

How microorganisms enter a host: Adhesins (ligands)

Adhesins (ligands) on the pathogen bind to
receptors on the host cells
– Glycocalyx
– Fimbriae

How bacterial pathogens penetrate host defenses: Capsules

• Glycocalyx around the cell wall
• prevent phagocytosis

Cell Wall Components: M protein

resists phagocytosis
– Streptococcus pyogenes

Cell Wall Components: Opa

proteins that allow attachment to host cells
– Neisseria gonorrhoeae

Cell Wall Components: Waxy lipid

(mycolic acid) resists digestion
– Mycobacterium tuberculosis

Antigenic Variation

Pathogens alter their surface antigens (and antibodies
are rendered ineffective)

Enzymes: Coagulases

coagulate fibrinogen

Enzymes: Kinases

digest fibrin clots

Enzymes: Hyaluronidase

digests polysaccharides that hold cells together

Enzymes: Collagenase

breaks down collagen

enzymes: IgA proteases

destroy IgA antibodies

How bacterial pathogens penetrate host cells: Invasions

Surface proteins produced by bacteria that rearrange
actin filaments of the cytoskeleton
 Cause membrane ruffling

How bacterial pathogens damage host cells: Siderophores

proteins secreted by pathogens that bind iron more tightly than host cells

How bacterial pathogens damage host cells: toxins

poisonous substances produced by
microorganisms
– Produce fever, cardiovascular problems, diarrhea,
and shock

Toxigenicity

ability of a microorganism to produce a toxin

Toxemia

presence of toxin in the host’s blood

Intoxications

presence of toxin without microbial growth

Antitoxins

antibodies against specific exotoxins

Toxoids

inactivated exotoxins that are used in vaccines

A-B toxins

contain an enzyme component (A part)
and a binding component (B part)
– Diphtheria toxin

Genotoxins

damage DNA (causing mutations,
disrupting cell division, and leading to cancer)

Membrane-disrupting toxins

lyse host cells by
disrupting plasma membranes

Leukocidins

kill phagocytic leukocytes

Hemolysins

kill erythrocytes by forming protein channels

Streptolysins

hemolysins produced by streptococci

Superantigens

cause an intense immune response
due to release of cytokines from host cells (T cells)
– Cause symptoms of fever, nausea, vomiting,
diarrhea, shock, and death

Limulus amebocyte lysate (LAL) assay

is used to test for endotoxins

Lysogenic conversion

changes characteristics of a
microbe due to incorporation of a prophage

three portals of entry for microrganisms

skin

inhaling

ingesting

biofilms

resists phagocytosis

resist antibiotics

streptococcus pneumoniae

gram positive

cause Pneumonia

endotoxins

gram negative, contain lipid A (LPS)

endotoxins are apart of the cell wall of gram negative bacteria

only r released when cell death/division

LPS is released when endotoxins are destroyed

lower toxicity

resistant to heat (heat stable)

cant use antibiotide to block

Causes fever because once endotoxin dies it releases cytokin

*be able to give an example

exotoxin

Proteins produced and secreted by bacteria
– Soluble in bodily fluids; destroy host cells and
inhibit metabolic functions

is a protein

can use antibodie

gram positive or negative

high toxicity

can denature from heat

cant cause fever

*be able to give an example

food infection

bacteria is in the food and u eat it

signs and symtombs = long

food intoxication

eat a toxin

no bacteria

sign and symptoms = short (much quicker)

cytopathic effects (CPE)

are visible effects of viral infection on a cell

infect of the host

• creates inclusion bodies (cell swells)

• fusing cells to create a syncytium (cell swells even more)

• loss of contact inhibition in the cell, leading to cancer

Interferons

tell the neighboring cells which prevent viral infection of neighboring cells. Or tell the neighbor cell to die (apoptosis)

portals of exit

coughing, sneezing, urine, saliva, feces, skin, blood, needles, syringe

most common: respiratory exit

How to stop portals of entry

wear mask, wear gloves, PPE

how to stop penetration of evasion

get vaccines, shots

goal of viruses/primary microbe

wants to multiply inside u not destroy u

capsid

virus protein (virus)

capsule

carried by bacteria (bacteria)

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8. le 2. c (its 50%) 5. c 2. food one ((A) food infection) B = food intoxication ) intoxication=fast, u eat it directly 8. small pox (e)

Virion

fully developed infectious particle composed of nucleic acid and surrounded by a protein coat outside a host cell

How are viruses classified

nucleic acid and protein coat (how the capsomeres are arranged)

plaque method

host bacteria and bacteriophages are pored onto a Agar plate medium. then the bacteria mixture hardens into a thin layer one cell thick. Each virus infects a bacterium, multiplies, then releases more viruses. All the bacteria from the viruses are destroyed creating plaques (clearings that are visible

three ways to grow animal viruses

cell culturees

embryonated eggs

using living animals

Living animals

animal is inoculated with the speciment then the animal is observed for signs of disease or is killed so infected tissues can be studied

Embryonated eggs

virus containing tissue is injection into egg, Growth is signals by the death of the embryo

cell culture lines

treating a slice of animal tissue with enzymes that separate individual cells , then these cells are suspended into a culture medium , nromal cells will grow while while continuous cells wont grow and will appear

primary cell lines

tissue cells from tissue slices that die after a few generations

diploid cell lines

develop from human embryos and live for 100s of generations

continuous cells lines

primary used because they can live infinitely

Best way to identify viruses: Serological methods

viruse is detected and identified based on its reaction to antibodies

plaque method defeniton

a method for counting the number of bacteriophages in a sample using bacterial growth in a solid media

Multiplication of bacteriophages: 2 mechanisms:

lytic cycle or lysogenic cycle