Exam 3
Microbiology 200 with Ford at University of Kansas
About this deck
By: Lauren Cox
Created: 2011-04-12
Size: 140 flashcards
Views: 23
Created: 2011-04-12
Size: 140 flashcards
Views: 23
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DNA mutations
DNA mutations can change the information stored in DNA.
Types of DNA mutation
Base substitution
Deletion
insertion
inversion
translocation
duplication
Deletion
insertion
inversion
translocation
duplication
base substitution
take one base and convert it to another. EX. Sickle Cell affect (change in one base)
deletion
removal of a base. Usually really BAD. End up changing all amino acids after removing the base.
Insertion
Add a base
Inversion
rotation in the sequence. EX. ACGTACG changed GCATGCA
Translocation
part of the chromosome is moved to the another.
duplication
duplicating a section of DNA. Important in bacterial evolution.
Consequences of Mutations
Silent mutations
Missense mutation
Nonsense mutation (Frame Shift)
Missense mutation
Nonsense mutation (Frame Shift)
Slient mutations
No change in protein. Most Mutations are silent! Can occur in a noncoding area. Can mutate a promoter and alter transcription levels.
Missense Mutation
change in amino acid (Sickle Cell anemia)
Nonsense mutation
change in frame. Change in stop codon making nonfunctional proteins eventually degrade the cell.
Mutation Related Diseases
Cancer
Genetic diseases
Genetic diseases
Cancer
misregulation of the cell cycle. Mutations can alter the function of the cell cycle. Tumor-suppressor genes can be mutated to become nonfunctional. HIGH RISK! Requires multiple mutations.
Genetic Diseases
Genes can be mutated. the DNA sequence for a gene gets errors, causing it to make a different protein. Can be inherited by family members. EX. Cystic fibrosis and Hemophilia.
Cause of Mutations
Radiation
Chemicals
Reactive Oxygen Species
DNA replication Errors (Not often)
Chemicals
Reactive Oxygen Species
DNA replication Errors (Not often)
Mutagen
a chemical that causes an increase in the mutation rate
Carcinogen
a chemical that can cause cancer. Most are Mutagens but not ALL
Ames Test
Uses bacteria to determine if a chemical compound is a mutagen. (EX. Salmonella with a mutant histidine synthesis gene. Salmonella requires histidine to grow. Some Salmonella revert back to normal. Adding a mutagen will increase the reversion chance.) Chemicals that cause reversions tend to cause cancer.
Recombinant DNA
Genes can be taken from one organism and added to another.
Restriction Enzyme
Can cut DNA. The cut pieces can be repaired with Ligase. Discovered in 1972 and partially banned in 1975.
Green Fluorescent Protein (GFP)
Come from Jelly fish. Added to organisms. Very useful for mapping where genes are expressed.
Transgenic bacteria products:
insulin
Human Growth Hormone
Erthropoietin (RBCs)
Factor 8- blood clotting factor
Human Growth Hormone
Erthropoietin (RBCs)
Factor 8- blood clotting factor
Causes of Food Spoilage:
Enzymatic reactions
Oxidation
Microbes
Oxidation
Microbes
Food Spoilage in Dairy:
Sour taste- lactic acid and acetic acid production
Denaturation- proteolysis of casein and decreased pH
Bitter taste- protein degradation
Denaturation- proteolysis of casein and decreased pH
Bitter taste- protein degradation
Food Spoilage of Meat:
Rancid taste- oxidation of lipids
Smell- degradation of amino acids to make sulfides and amines.
Smell- degradation of amino acids to make sulfides and amines.
Six Traditional Methods of Growth Control:
1. Apply heat
2. Consume Immediately
3. Desiccation (removal of water)
4. Raise Osmolarity ( increase solute concentration) Add salt of sugar
5. Fermentation
6. Increase Acidity
2. Consume Immediately
3. Desiccation (removal of water)
4. Raise Osmolarity ( increase solute concentration) Add salt of sugar
5. Fermentation
6. Increase Acidity
D- Value (On TEST)
Decimal reduction value of time required to kill 90% of cells.
Six Modern Methods of Growth Control:
1. Aspesis
2. Decrease temperature
3. Anitmicrobial chemicals
4. Radiation
5. Filter Sterilization
6. Antibiotics
2. Decrease temperature
3. Anitmicrobial chemicals
4. Radiation
5. Filter Sterilization
6. Antibiotics
Aspesis
avoid contamination
Dienococcus radiodurans
Resistant to desiccation, low temperatures, vaccum, low pH and radiation. Non pathogenic. Can survive 5,000 Gray. Killed 1/3 at 15,000 Gray radiation.
Bacteriocidal
Antibiotic that kills bacteria
Bacteriostatic
Antibiotic stops bacterial growth
Glycolysis
ten step process that breaks glucose down into 2 pyruvate molecules.
Fermentation
Anaerobes (dont require oxygen) will not use citric acid cycle of electron transport chain. Some can get ATP from Glycolysis alone!
Saccharomyces cerevisiae (On TEST)
Bakers or Brewers Yeast! Facultative anaerobe. Produces ethanol as a byproduct of fermentation. Acquires ATP from glycolysis alone.
THREE Problems of Bakers/ Brewers Yeast:
1. Pyruvate waste product
2. NADH waste product
3. Limited NAD+
2. NADH waste product
3. Limited NAD+
Ethanol Fermentation
-Carbon dioxide is removed to form Acetaldehyde
-Acetaldehyde is reduced to form ethanol (receives electrons).
-Acetaldehyde is reduced to form ethanol (receives electrons).
Ethanol
-soluble in fats and waters
-Increase membrane fluidity, loose integrity
-no wine of beer over 12% ethanol
-Higher concentrations are made from distillation
-Depressant for some and a stimulant for others
-Increase membrane fluidity, loose integrity
-no wine of beer over 12% ethanol
-Higher concentrations are made from distillation
-Depressant for some and a stimulant for others
Ethylene Glycol
antifreeze. EXTRA OH
Methanol
rubbing alcohol. ONE Carbon. Produced by wood fermentation. causes Blindness
Alcohol Flush Reaction
turn bright red because Acetaldehyde is not being broken down effectively. Jump to hangover state.
action potential
transmits an electrochemical signal from the cell-body to the axon.
synapse
space where the dendrite of one neuron meets the axon of another neuron.
Neurotransmitter of Ethanol
1. Serotonin- increase signaling
2. Dopamine- increase signaling
3. GABA- decrease
4. NMDA (formation of memories)- decrease
5. Glutanate (slowed speech)- decrease
2. Dopamine- increase signaling
3. GABA- decrease
4. NMDA (formation of memories)- decrease
5. Glutanate (slowed speech)- decrease
Cause of Hangover
1. other fermentation products
2. Acetaldehyde
3. Disruption of REM and Non REM sleep
4. Accumulation of waste products
5. Dehydration
6. Withdraw
2. Acetaldehyde
3. Disruption of REM and Non REM sleep
4. Accumulation of waste products
5. Dehydration
6. Withdraw
Spontaneous Generation
thought that microbes arose without cause through environmental conditions.
Antony Van Leeuwenhoek
Discovered the first bacteria
Louis Pasteur
Discovered that microbes did not arise spontaneously. ALL life arises from other life.
Joseph Lister
Tried Phenol on wounds
Types of Antimicrobials:
1. Disinfectants- sterilize objects (fomites) EX Phenol and Formaldehyde. High Concentrations!
2. Antiseptics- Sterilize living tissue. EX. iodine, alcohols, hydrogen peroxide. Low concentration!
3. Antivirals
4. Antifungals
2. Antiseptics- Sterilize living tissue. EX. iodine, alcohols, hydrogen peroxide. Low concentration!
3. Antivirals
4. Antifungals
Alexander Fleming
Discovered Penicillin in 1928.
Cell Wall Inhibitors:
1. B-lactam Antibiotics
2. Vancomycin
3. Bacitracin
2. Vancomycin
3. Bacitracin
B-lactam Antibiotics
-Half of all antimicrobial drugs.
-Penicillin and cephalosporins
-inhibit the formation of peptidoglycan cross links
-Penicillin and cephalosporins
-inhibit the formation of peptidoglycan cross links
Vancomycin
-Binds to the peptide links that hold sugar subunits of peptidoglycan together.
-Not effective against Gram Negative bacteria.
-Can ruin Kidneys
-Used to treat Staphylococcus aureus.
-Not effective against Gram Negative bacteria.
-Can ruin Kidneys
-Used to treat Staphylococcus aureus.
Bacitracin
-prevents peptidoglycan subunits from being transported across the inner membrane
-ONLY topical
-ONLY topical
Cell Membrane Disrupters
Gramicidin
Gramicidin
-forms channels in membrane
-Ions leak in and out
-also works on eukaryotes
-lyse red blood cells
-ONLY topical
-Ions leak in and out
-also works on eukaryotes
-lyse red blood cells
-ONLY topical
Protein Synthesis Inhibitors
1. Aminoglycosides
2. Tetracyclines
3. Macrolides
2. Tetracyclines
3. Macrolides
Aminoglycosides
-inlcude gentamicin and kanamycin
-Bind to the small subunit of the ribosome and prevent it from joining with the -large subunit.
-No exchange of info from mRNA to Protein.
-Bind to the small subunit of the ribosome and prevent it from joining with the -large subunit.
-No exchange of info from mRNA to Protein.
Tetracyclines
-Bind to small subunit
-Prevent tRNA from binding
-Most are Bacteriostatic
-Prevent tRNA from binding
-Most are Bacteriostatic
Macrolides
-includes erythomycin
-binds to the large subunit of ribosome
-blocks polypeptide chain from leaving
-Can be both Bacteriocidal or Bacteriostatic
-binds to the large subunit of ribosome
-blocks polypeptide chain from leaving
-Can be both Bacteriocidal or Bacteriostatic
DNA Synthesis Inhibitors
1. Sulfa Drugs
2. Fluroquinolones
3. Metronidazole
2. Fluroquinolones
3. Metronidazole
Sulfa Drugs
-prevent the formation of nucleic acids by inhibiting the synthesis of folic acid.
-PABA- precursor to make folic acid which sulfa drugs prevent
-Competitive inhibitor.
-PABA- precursor to make folic acid which sulfa drugs prevent
-Competitive inhibitor.
Fluroquinolones
-include ciprofloxacin
-inhibits DNA gyrase from resealing nicks
-inhibits DNA gyrase from resealing nicks
Metronidazoles
-activated by flavodoxin
-damages DNA by causing nicks
- humans given the inactive form
-damages DNA by causing nicks
- humans given the inactive form
RNA Synthesis Inhibitors:
1. Rifampin
Rifampin
-Binds to the B subunit of RNA polymerase
-Blocks the emergence of mRNA (blocks pores)
-prevents RNA from being created
-Blocks the emergence of mRNA (blocks pores)
-prevents RNA from being created
General Causes of Antibiotic Resistance:
1. Overuse of Antibiotics
2. Misuse of Antibiotics
3. Human population density and interactions
4. Immune-suppressed individuals
5. Frequent Mutations
6. Bacterial populations densities
7. Short replication time
8. Horizontal Gene Transfer
2. Misuse of Antibiotics
3. Human population density and interactions
4. Immune-suppressed individuals
5. Frequent Mutations
6. Bacterial populations densities
7. Short replication time
8. Horizontal Gene Transfer
5 Mechanisms fro Antibiotic Resistance
1. Restriction of Access
2. Enzymatic Inactivation
3. Target Modification
4. Failure to Activate
5. Alternate Pathway
2. Enzymatic Inactivation
3. Target Modification
4. Failure to Activate
5. Alternate Pathway
porins (Restriction)
found in gram negative outer membranes. Some antibiotics are too large to diffuse the membrane
Reduced uptake (restriction)
Some antibiotics gain access to the cell through receptors on the inner membrane can be mutated to not bind to the drug. RARE mechanism
Antibiotic Efflux Pump (restriction)
Removes the drug from the cell as it diffuses in.
B-lactamase (Enzyme inactivation)
Cleave the beta lactam ring
Clavulanic acid- inactivated B-lactamase
Clavulanic acid- inactivated B-lactamase
Penicillin- Binding Protein Resistance (Target Modification)
Alters the shape of the protein so that penicillin can't fit into the binding site.
Vancomycin Resistance (Target Modification)
-Prevents the peptide interbridge from forming.
-Vancomycin resistant bacteria can alter the peptide bond.
-Vancomycin resistant bacteria can alter the peptide bond.
Metronidazole Resistance (Failure to activate)
-Bacteria can mutate to not express flavodoxin
-mutate promoter region of gene itself
-mutate promoter region of gene itself
Sulfa drug resistance (Alternate pathway)
bacteria use another metabolic pathway to make folic acid
Transduction
involves use of a virus; SAME species
Types of Viral Infection
1. The Lytic Cylce
2. The Lysogenic Cylce
2. The Lysogenic Cylce
The Lytic Cylce
bacteriophages replicate inside a cell and cause it to lyse
The Lysogenic cycle
the viruses integrate their DNA into the host genome. Pull of genes form the host as the virus leaves transfering genes to another organism. EX: Diphtheria
Transformation
involves the up take of DNA/ PLASMIDS
Plasmids
small pieces of circular DNA
Have a size of 2kb to 50kb (killa base)
Have a size of 2kb to 50kb (killa base)
Common Plasmid Genes
1. Antibiotic Resistance
2. Metabolic Enzymes
3. Adhesion Factors
4. Toxins
2. Metabolic Enzymes
3. Adhesion Factors
4. Toxins
Competence
Ability of bacteria to take up free DNA (Plasmids) from the environment.
Artificial Competence:
1. Calcium Chloride- make membrane more permeable
2. Electroporation- Short burst of electricity, puts holes in membrane
2. Electroporation- Short burst of electricity, puts holes in membrane
Non- Plasmid Transformation
Some bacteria can take up linear pieces of DNA and integrate them into their DNA.
Plasmid Transformation
Bacteria can take up plasmids
Conjugation
-Species, Genus, and Families trade genes
-Direct transfer of DNA between bacteria.
-Performed using sex pilus
-Direct transfer of DNA between bacteria.
-Performed using sex pilus
F-factor
-transmitted plasmid is much larger
-fertility factor
-allows bacteria to make sex pilus
-fertility factor
-allows bacteria to make sex pilus
Transposons
-small pieces of DNA that can insert themselves into a chromosome
-can land inside genes and inactivate them
-carry antibiotic resistant genes
-can land inside genes and inactivate them
-carry antibiotic resistant genes
Types of Transposition
1. Nonreplicative Transpostion
2. Replicative Transpostion
2. Replicative Transpostion
Nonreplicative Transposition
The transposable element is moved. Transposon jumps from plasmid to chromosome
Replicative Transposition
The transposable element is duplicated. Tansposon jumps into chromosome while in the plasmid and can replicate themselves.
pathogen
any biological agent that can cause a disease. (prions, virus, bacteria)
MOST microbes are NOT pathogens
MOST microbes are NOT pathogens
virulence
ability of a pathogen to cause a disease
Virulence factor
natural traits a pathogen can us to establish itself in a host. (Ex. Toxins)
Possible Reasons for Virulence:
1. bacteria have evolved to cause human disease (Primary pathogen)
2. Bacteria are attempting to create a non parasitic association, but fail.
3. Bacteria normally live in another niche, but have accidentally entered and caused an immune response.
2. Bacteria are attempting to create a non parasitic association, but fail.
3. Bacteria normally live in another niche, but have accidentally entered and caused an immune response.
Tuskegee Syphilis Experiment (ethical problem)
Black men with syphilis go untreated so that the government can track the progression of the disease.
Jewish Chronic Disease Hospital (ethical problem)
old people with dementia injected with cancer
Willowbrook State School (ethical problem)
Injected mentally disabled kids with hepatitis A without parents permission
50% Lethal Dose (LD 50)
amount of pathogenic bacteria required to cause a terminal infection in half of the animals
LOWER LD50 MORE virulent
LOWER LD50 MORE virulent
50% Infectious Dose (ID 50)
Dose of bacteria required to infect half of the animals.
LOWER ID 50 MORE virulent
LOWER ID 50 MORE virulent
Germ Theory of Disease
Koch's postulates required to link a microorganism to a disease.
Koch's Postulates:
1. Microorganism must be found in all cases of the disease
2. It mush be isolated and grown in culture
3. It must reproduce the disease when introduced to a host
4. It must be reisolated from the host with the disease
2. It mush be isolated and grown in culture
3. It must reproduce the disease when introduced to a host
4. It must be reisolated from the host with the disease
Postulate Problems:
1. Some strains of microbes are pathogenic while others are not. (Ex. E. coli)
2. Some microbes can be very difficult to culture (EX. Syphilis)
3. Genetics can make a person more or less susceptible to the disease
4. Age can also make someone more or less susceptilble
5. An animal model may not exist (ex. Cholera)
2. Some microbes can be very difficult to culture (EX. Syphilis)
3. Genetics can make a person more or less susceptible to the disease
4. Age can also make someone more or less susceptilble
5. An animal model may not exist (ex. Cholera)
Ulcer Causes:
1. Non steroidal Anti-inflammatories
2. Helicobacter pylori
2. Helicobacter pylori
Helicobacter pylori
penetrates the mucus and adheres to the epithelial cells and produce urase in the stomach.
Salmonella
- motile with peritrichous flagella
-moves with run and tumble motility
-infects small intestine
-causes gastroenteritis
-Gram negative facultative anaerobe
-survive water at cold temps
-moves with run and tumble motility
-infects small intestine
-causes gastroenteritis
-Gram negative facultative anaerobe
-survive water at cold temps
Salmonella typhi
-incubation for a month
-rash on abdomen
-Bacteria travel from liver and spleen
-Delirium and convulsions
-rash on abdomen
-Bacteria travel from liver and spleen
-Delirium and convulsions
Mary Mallon
-Typhoid Mary
- Asymptomatic/ chronic carrier- no symptoms
- Asymptomatic/ chronic carrier- no symptoms
Five F's of food poisoning:
1. fluids
2. food
3. fingers
4. flies
5. fecal material
2. food
3. fingers
4. flies
5. fecal material
Reservoir
natural host or habitat of a pathogen (Ex. person infected, animal, part of the environment)
Source
organism or object responsible for transmitting the disease. (Ex. contaminated food)
Reservoir types:
1. Carrier: spread- infection without showing symptoms
2. Biological vector- plays a direct role in pathogen's life (mosquitoes and ticks)
3. mechanical vector- transports the pathogen (house fly)
2. Biological vector- plays a direct role in pathogen's life (mosquitoes and ticks)
3. mechanical vector- transports the pathogen (house fly)
Toxins
Chemical products produced by an organism, which have a poisonous effect on other organisms . FIRST virulence factor discovered!
Toxinoses
diseases caused my toxins
Toxemias
the toxin is spread by the flow of blood. (EX tetanus and Diphtheria)
Intoxication
caused by ingestion. EX. Botulism
Exotoxins
-disrupt cellular process
-include Botulism, Diphtheria, tetanus
-inactivated by heat
-include Botulism, Diphtheria, tetanus
-inactivated by heat
Endotoxins
non protein toxins
gram negative bacteria
gram negative bacteria
Lipopolysaccharid
gram negative bacteria causes massive inflammatory response. Septic shock
Lipoteichoic acid
component of cell wall causes inflammatory response
Pore-forming exotoxin (membrane disrupting)
forms pores in membrane with protiens composed of alpha helices and beta sheets
Phospholipase Exotoxin (membran disrupting)
Also called hemolysins or ctyolysins, can cleave the phosphate from the lipid disrupts the cell membrane. (EX. Gangreen)
A-B toxins
-A (active)- has enzyme activity
-B (binding)- binds to a receptor and moves A into the cell
-A-B subunits separated by proteolysis
-A chain can only get into a certain type of tissue because of B chain
-B (binding)- binds to a receptor and moves A into the cell
-A-B subunits separated by proteolysis
-A chain can only get into a certain type of tissue because of B chain
Flora
organism that lives in a particular region. Not involved in pathogenic processes. Colonize particular regions so pathogens can't grow.
Opportunistic infection
normally non pathogenic microbe can cause a disease
nosocomial infections
acquired in the hospital
Skin Flora
-arid, acidic, aerobic
-Staphylococcus epidermidis- forms biofilms on implants and catheters
-Propioribactrium acnes- Anaerobic lives in pore and hair follicles
-Staphylococcus epidermidis- forms biofilms on implants and catheters
-Propioribactrium acnes- Anaerobic lives in pore and hair follicles
Nasopharynx Flora
Staphylococcus aureus- 1/3 of people
Oral Flora
Streptococcus mutans- tooth decay; ferments sucrose to lactic acid and creates dextran which allows a biofilm to form.
Urinary Tract Infection Causes:
1. More frequent in women
2. Travel upward along urinary tract
3. E. coli MOST common cause
4. Spermicides
2. Travel upward along urinary tract
3. E. coli MOST common cause
4. Spermicides
Escherichia coli
-urine washed bacteria away
- Type 1 Pili- allows E. coli to bind to the mucosa of the urethra.
- Type 1 Pili- allows E. coli to bind to the mucosa of the urethra.
Staphylococcus aureus
-Gram positive Facultative anaerobe
-Golden Cluster Seed
-Infects cuts, glands, and hair follicles
-may require surgery
-Golden Cluster Seed
-Infects cuts, glands, and hair follicles
-may require surgery
Staphylococcus aureus infections:
1. toxic shock syndrome
2. Furuncles
3. Meningitis
4. Endocarditis
2. Furuncles
3. Meningitis
4. Endocarditis
Staphylokinase Toxin
-Dissolves blood clots
-Assists in colonizing new tissues and migrating out of abscesses
-Assists in colonizing new tissues and migrating out of abscesses
fomite
-object (non living) that can carry a pathogen
-Staphylococcus aureus can live on fomites
-Staphylococcus aureus can live on fomites
MRSA
-Mec A gene- penicillin binding protein with a modified target, resistant to B lactams.
-Frequently resistant to other antibiotics as well
-Frequently resistant to other antibiotics as well
About this deck
By: Lauren Cox
Created: 2011-04-12
Size: 140 flashcards
Views: 23
Created: 2011-04-12
Size: 140 flashcards
Views: 23
About StudyBlue
STUDYBLUE makes things that make you better at school.
Things like online flashcards with photos and audio.
Things like personalized quizzes and friendly reminders about when (and what) to study next.
Think of it as a digital backpack™: access to all of your study materials online and on your phone.
STUDYBLUE exists to make studying efficient and effective for every student, for free. Join us.
“I have used this website for three exams, and I see a huge difference in my test results.”
Naj
Naj