Unit 7 Microbiology official Flashcards
(97 cards)
1
Q
characteristics of monera
A
-Prokaryotic
-Unicellular
-2 Phylla
Cyanophyt
Schizophyta
2
Q
Why Only 30,000 Species of Monera?(why it’s hard to speciate them)
A
-Monera are very small and have few visible features, making them hard to tell apart by appearance.
-They also exchange genes between different types, which blurs the lines between species.
3
Q
bacillus
A
rod-shaped bacteria
4
Q
coccus
A
bacteria that is shaped like a ball or a sphere.
5
Q
diplococcus
A
type of bacteria made of two round cells stuck together.
6
Q
streptococcus
A
type of bacteria that forms long chains of round cells.
7
Q
staphlococcus
A
type of bacteria that forms clumps or bunches of round cells, like grapes.
8
Q
vibrio
A
type of bacteria shaped like a curved rod, kind of like a comma.
9
Q
Spirillum
A
type of bacteria that has a spiral or corkscrew shape.
10
Q
Monera cell walls
A
-composed of peptidoglycans
-prevents lysis(bursting open)
-gram positive have thick cell walls made of peptidoglycan
-gram negative have thin cell walls
11
Q
Glycolcalyx
A
-coating prevents disease causing bacteria from being detected by macrophages
12
Q
Flagellates
A
-allow for motility
13
Q
Binary fission
A
-how tiny living things make more of themselves so they can survive, grow, and spread.
1. Bacterial dna is copied
2.Membrane starts to form in between the two identical sets of dna
3.Cells separate into two new identical cells
14
Q
conjugation
A
-one bacterium grows a little tube (called a pilus).
-The pilus connects to another bacterium.
-The first bacterium copies some of its DNA (a plasmid).
-It sends the copy through the tube to the other bacterium.
-Now both bacteria have the new DNA
15
Q
endospores
A
tough shells that bacteria make to stay alive during tough times and can wake up when conditions improve.
16
Q
zoonosis
A
Disease that can be transmitted to humans from animals
17
Q
antigenic shift
A
Mutation in the pathogen population that changes their antigens (i.e. proteins that identify them to our immune systems)
Antigenic shifts allow pathogens to affect more than one species
18
Q
moneran reproduction
A
water
-organic material
-heat
19
Q
viral reproduction
A
-need a living host cell
-genetic code
20
Q
difference between viruses and bacteria
A
Monera
bacteria. They are alive, can eat, grow, and reproduce on their own.
Viruses
not really alive. They can’t do anything alone. They have to invade other living things to make more viruses.
21
Q
how are viruses and bacteria similar
A
both are super tiny and cause sickness,
22
Q
If zoonoses are specific to different animals’ host cells how do they “jump” to other species?
A
-Germs can change through mutations (small mistakes in their genes).
-These changes can let germs jump from one animal to another, like humans.
23
Q
bactierophage
A
a type of virus that specifically infects bacteria by attaching to their surface, injecting its genetic material, and using the bacterial machinery to replicate, often leading to the destruction of the host cell.
24
Q
bacteriophage- function the the tail
A
facilitates the injection of this material into the host bacterium.
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whats in the head of bacteriphage
dna or rna
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whats the head of bactierophage surrounded by
protein coat called capsid
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bacteriophage- function of tail fibers
help the phage attach to the bacterial cell wall.
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Lytic(host bacterial cell)(bacteriophage)
Attachment: The virus (bacteriophage) attaches to the surface of a bacterial cell using specific molecules on the cell's membrane.
Entry: The virus injects its genetic material (DNA or RNA) into the bacterial cell through a needle-like structure.
Replication: The viral DNA hijacks the bacterial cell's machinery, causing it to make copies of the virus's genetic material and proteins.
Assembly: New viral parts are assembled inside the bacterial cell.
Lysis: The bacterial cell is filled with new viruses and bursts open (lyses), releasing the new viruses into the environment.
Infection: The new viruses can now infect other bacterial cells and repeat the cycle.
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lytic(host eukarytoic cell)(like human cells)
Attachment: The virus attaches to a specific molecule (antigen) on the surface of the host eukaryotic cell.
Entry: The virus enters the eukaryotic cell. If it's a DNA virus, the viral DNA enters the nucleus; if it's an RNA virus, it stays in the cytoplasm.
Replication: For DNA viruses, their genetic material is copied inside the nucleus of the host cell. For RNA viruses, replication happens in the cytoplasm.
Assembly: The viral parts (proteins and genetic material) are assembled into new viruses in the cytoplasm.
Lysis: The host cell bursts open (lyses), releasing the new viruses into the body to infect other cells.
Infection: The released viruses can go on to infect new eukaryotic cells, continuing the cycle.
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Lysogenic Cycle in Bacterial Cells
Attachment: The virus (bacteriophage) attaches to the surface of the bacterial cell.
Entry: The virus injects its genetic material (DNA) into the bacterial cell.
Integration: Instead of immediately taking over the bacterial cell, the viral DNA integrates into the bacterial DNA. This new combined DNA is called a prophage.
Replication: Every time the bacterial cell divides, the viral DNA (prophage) is copied along with the bacterial DNA. The virus is now passed on to the daughter cells without causing immediate harm.
Triggering: At some point, environmental factors (like stress or damage to the bacteria) can trigger the prophage to exit the bacterial DNA.
Activation: The viral DNA becomes active, and the virus switches to the lytic cycle, producing new viruses and eventually causing the cell to burst open.
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Lysogenic Cycle in Eukaryotic Cells (Like Human Cells)
Attachment: The virus attaches to specific molecules (antigens) on the surface of the host eukaryotic cell.
Entry: The virus enters the eukaryotic cell, and if it's a DNA virus, the viral DNA enters the nucleus.
Integration: The viral DNA integrates into the host cell's genome, becoming a part of the host's DNA. This stage can last for a long time without the virus causing harm.
Replication: As the eukaryotic cell divides, the viral DNA is copied along with the host’s DNA, passing the virus to new cells.
Dormancy: The virus stays hidden in the cell, not producing new viruses. This is called the latent phase.
Activation: Environmental factors (like stress or immune system changes) can trigger the viral DNA to become active again, starting the lytic cycle and producing new viruses.
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retrovirus
Viruses that transduce cells “in reverse” by injecting RNA into the host cell
RNA is written back into DNA via the enzyme reverse transcriptase
The new viral “DNA” becomes a PROVIRUS and is copied by host cells into their daughter cells
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Envelope of a disease
Form: glycoprotein shell around capsis and nucleic acid code
Function: coat the virus with proteins that facilitate the binding of the virus to the host cell
34
Why are host cells so important for viruses?
-they need to sneak into a living cell and use the cell's stuff to make more viruses. Without a host cell, a virus is basically useless.
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kirby-Bauer Antibiotic Sensitivity Test Evaluation,
A petri dish is covered with bacteria.
Little paper discs soaked in different antibiotics are placed on the dish.
if an antibiotic works, it kills bacteria around the disc — creating a clear zone (no bacteria).
Bigger clear zone = More effective antibiotic
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broad v narrow spectrum antibiotics
Broad-spectrum: Attacks many types of bacteria (good when unsure what’s causing the infection).
Narrow-spectrum: Targets specific bacteria (better when you know the bug – fewer side effects).
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sensitive vs. resistant strains
Sensitive bacteria: Bacteria that Dies when exposed to the antibiotic → ✅ antibiotic works.
Resistant bacteria: bacteria that Survives even with the antibiotic → ❌ antibiotic doesn’t work.
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antibiotic resistance
when bacteria change so that antibiotics no longer kill them.
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VIREMIA
Concentration of viral particles in the blood of the host. Also called viral load
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T LYMPHOCYTES
White blood cells
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CD4
Assessment of the concentration of T lymphocytes in the bloodstream.
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Prevalence-
how many cases relative to the population size?
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Morbidity-
What portion of cases were symptomatic?
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Mortality-
What portion of the cases were fatal?
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Case fatality ration
what portion of symptomatic cases were fatal?
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george soper 1906
Used maps to determine how a disease was being spread
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epidemiological triangle
a model used in epidemiology to understand the factors that contribute to disease
-host -
-environment
-agent
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pathogen
The causative agent of disease
One pathogen: One disease
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Koch’s Postulates (1876)
To prove that a given microorganism is the pathogen for a certain disease one must
1. Isolate from afflicted individual
2. Culture the suspected pathogen away from the afflicted individual
3. Infect previously un-afflicted individual with the cultured pathogen
4. The previously un-afflicted individual must develop the same symptoms/disease state as the original host
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Host
-Individual afflicted with the pathogen
-genetic predisposition, active immunity, could decide whether you show symptoms of the pathogen
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vector
-The agent that transfers the pathogen from host to host
-one vector- many diseases
-Ex: mosquitoes carry malaria, encephalitis, heart worms etc.
-Ex: saliva carrys mumps tuberculosis and influenza
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resevoir
Naturally occurring population that carries the pathogen
Continual source of the pathogen for its vectors
Ex: cows carry anthrax but are not affected by anthrax
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virulence
How much does the pathogen affect the host?
Higher virulence=person has a lot more symptoms
Higher virulence will lead to a low R0 number because if a person dies from the disease they won't be able to pass it on.
Ex: Ebola is so virulent, killing the host so rapidly, that it is difficult for the disease to spread to other hosts
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Virulence Trade-Off Theory
If a virus makes you too sick or kills you fast, it might not spread to others.
If it's too gentle, it might not spread well either.
viruses evolve to be just sick enough to spread without stopping themselves.
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R0
Basic reproductve number
How many cases will derive from a single case of a given disease
R0>1= diseases will spread
R0<1= disease won't spread
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endemic
Constantly present in a population or region
Relatively low spread
Ex: Malaria in parts of sub-Saharan Africa is endemic, meaning it is consistently present in those regions at a relatively stable rate.
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epidemic
Sudden increase in cases spreading through a large population
Ex: The Ebola outbreak in West Africa in 2014-2016 is considered an epidemic because it was a sudden, widespread occurrence of the disease in specific areas but did not spread globally like a pandemic.
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pandemic
Sudden increase in cases across several countries and continents
Ex: The COVID-19 outbreak, which spread worldwide, affecting millions of people across many countries and continents, is a pandemic.
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EPI curve assesment
An EPI curve shows the number of cases (prevalence) in a given period of time.
Depending upon how many cases you get in a period of time, it allows you to determine what kind of disease it is
endemic (small cases, long time, same frequency),
epidemic (many cases, short time, infrequent)
pandemic (many cases, long time, widespread).
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lazaretto
quarantine
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city of ferrara
-no deaths fromBubonic Plague from 1576-1750
-How?- they had strict rules about who and what could enter the city
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How does our body defend itself against pathogens?
The immune system
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Functions of the immune system
1. Isolate, neutralize and destroy pathogens and invasive particles
2. Remove damaged cells/tissues
3. Maintain a “memory” of previous invaders
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active immunity
Your body makes its own antibodies after getting sick or after a vaccine.
(It takes time but lasts a long time.)
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passive immunity
You get antibodies from another source (like from your mom through breastmilk or from medicine).
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autoimmune disorder
-immune system does too much
-mis identifies parts of you as pathogens and destroys parts that should not be destroyed
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immunocomprimised
-immune system doesnt do enough
-Immune system doesnt do what is supposed to do
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Causes of a compromised immune system
cancer
Aging
AIDS
Chemotherapy
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innate immunity
-It’s ready from birth.
-It fights anything bad right away.
-first line of defense
-Example: skin, mucus, fever, inflammation, and cells like neutrophils and macrophages.
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Adaptive Immunity (slow at first, but smart
-It learns and remembers specific germs.
-It uses special cells like B cells and T cells.
- After it fights a germ once, it remembers how to beat it faster next time
-targets specific invaders
-Ex: T and B lymphocytes
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POSSIBLE PATHOGEN
Virus
Bacteria
Fungi
Work
Protist
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1st level of defense
-skin and muccus membrane -pathogen often passes through this
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antigen
Pieces on the surface of pathogens (like ID tags) that show they are bad.
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Cytotoxic t-cell(killer t cell)
find infected cells and release cytotoxins that destroy them.
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which types of cells are part of out innate immunity
Basophils, macrophages, neutrophils, dendritic cells
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Humoral immunity
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Helper T cell
-Help by sending signals to b cells
-help by sending signals to macrophages
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macrophages
Big cells that eat pathogens
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basophils
Cells that cause inflammation and allergic reactions by releasing chemicals like histamine.
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why is it good that basophils release histamine?
Basophils release histamine to open blood vessels so macrophages can quickly reach and fight infections.
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memory b cells
Special B cells that remember a pathogen.
If the same germ tries to attack again, they quickly make lots of antibodies to fight it fast!
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antibodies
Y-shaped proteins made by B cells.
They stick to specific antigens to block the pathogen and mark it for destruction.
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vaccines
-vaccines look like a pathogen to the immune system but doesnt make it sick
-the vaccine exposes the body to antigens that are similar to the antigens found on a pathogen
-your body learns to fight this pathogen
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lymphatic system
Moves immune cells around the body
Filters out germs and waste
Lymph nodes detect and fight pathogens
Helps start immune responses
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heard immunity
enough people in a community are immune to a disease, making it harder for the disease to spread and protecting those who aren’t immune.
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virgin field
because none of the population had been prevously exposed to the pathogen theres no immunity.
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nuetraphils
kill pathogens by swallowing them (phagocytosis), releasing toxic chemicals, and trapping them in sticky nets (called NETs).
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Why do neutrophil levels increase after macrophages?
Macrophages have a limit to how many viruses they can destroy (~100), so neutrophil levels increase when macrophages reach that limit and need reinforcement
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Why is this swelling important?
Swelling helps fight infection and repair tissue by delivering immune cells and nutrients to the wound.
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Bone marrow
This is where your body makes T cells, B cells, and macrophages
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Thymus
production of Helper T cells
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Lymph nodes
These are spots in your body where pathogens collect. Immune cells like T cells, B cells, and macrophages gather here to attack the pathogens.
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Spleen
holds Natural Killer T cells
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peyers patches
specialized areas of lymphoid tissue in the small intestine that help monitor and respond to pathogens, playing a key role in immune defense and the regulation of intestinal health.
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filoviruses
such as Ebola and Marburg, are highly virulent, thread-shaped viruses that cause severe hemorrhagic fevers and can spread through direct contact with infected bodily fluids, posing significant public health risks and potential as bioterrorism agents.
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