Microbiology
cont. protozoa diseases
trichomonas vaginalis
sti, men often carriers, often dont know because asymptomatic
women have effects (irritation/discharge)
easily spread bc take time show symptoms
foul odor, discharge, painful pee, misdiagnosed as uti, no good generic drug for protozoal disease
Leishmanii
leishmaniiasis
inflammation of spleen, could result in deterioration of spleen, further complications
Entamoeba Histolytica
tissue lysis
amebic dysentary, bloody diarrhea
associated w/ water, pond/water
Cryptosporidium
cryptosporidiosis
diarrhea, stomach cramps, first established when water treatment plant fail
“boil alert”, fear of cryptosporidia
immunocompromised cause further complications
Toxoplasma gandi (different from others)
toxoplasmosis
reason why pregnant ppl shouldnt deal with litter box
think kitty litter, wick moisture from waste
cat defecate, in feces have protozoa, in cyst form ( protective layer survive w/o water)
then cysts mature and enter into mouse, cow, to human (litterbox) inhale dust
lead to developmental issues, fetal termination
cow also susceptible, can get into food supply
protozoa go into muscle tissue, eat uncooked meat, toxoplasmosis introduced to human body
strongly encourage individuals to report feral cats, protozoa could continue to persist
mostly impact immunocompromised and developing individuals
Malaria
often misdiagnosed, people contribute it to the flu, malaria is treatable in early stages
misdiagnosed, person will likely die
transmitted by bite of mosquito, bite introduce protozoa to bloodstream
migrate to liver where continue to grow (weeks to months to show)
in liver continue to grow, damage liver, enter into circulatory system
rbc lyse, causes people to feel tired, have pain, slight fever
mosquito not native to US, prevalent to african nations, people travel it gets spread
as travel through circulatory system, can be transmitted by another mosquito (bite and spread)
all living members need to know, must know diseases names and characteristics
ch.5, nonliving members microbrial world
do not fit scientific definition of life
independent, replicate on their own
viruses, viroids, prions
nonliving, obligate intracellular parasites
must be inside another host cell to gather nutrients and make more of itself
outside host cell inert, cant do anything, cant replicate, cant gather nutrients, cant seek
anything could be host cell
once enter host cell become parasite
eventually damage host cell
they are inactive, no abilities whatsoever
Viroids
genetic material single strand rna
will fold upon itself for more stability
impact humans directly and indirectly
indirectly: affect plants, potatoe/tomatoe plants, viroid disease kill plants, highly contagious (contact)
affect food supply
directly: viroid in combination w hepatitis b virus cause hepatitis d
hepatitis affect liver
treatment: very difficult, dont really understand how works
Prions
no genetic material
only made up of protiens, prion protien is ncredibly resistant to all know protien treatments
sterilization kill all microbe except prion
prion prpc, prpsc (diseased)
difference in tertiary structure (structure determine function)
prpc: normal form tertiary structure, associated w/ our neurons
neurons have cell body, axon, terminals
prion protien associated w/ movement action potential down axon
when person eat something w/ diseased prion (prpsc)
prpsc:
come in contact w/ neuron, cause diseased ones to interact with normal prions
causes normal protien to unfold and refold into diseased form
change tertiary structure normal to disease
affect nervous system
cause spongiform encephalitis
brain becomes holey
can be lethal, human form called Creutzfeldt Jakob
sheep form called scrapie, cow form mad cow disease
deer form can be found in ohio region
no way to treat, could char the meat and wouldn’t work
transmission through contaminated meat products
fist detected in wild elk in Scandinavian area
elk would act strangely
certified slaughterhouses in US not supposed to supply brain matter, check make sure no prions
transmission through organ transplants
indirectly affect food sources, affect directly by causing creutzfeld jakob
Virus terminology
can be treated, but are specific to virus, viruses change quickly
virion: is a single copy of a virus
virus: single or multiple copies of the virus
bacterial virus: virus infects bacterial host cells
animal virus: virus infect animal host cells
we have to be concerned over this
bacteriophage: is a bacterial virus with a lysogenic and lytic cycle
phage: bacterial or animal virus w/ lytic and lysogenic phase
viral load: amount of virus within host organism/cell
how have viruses impacted us?
genetically engineered food
research perspective, how world works
covid
viruses impact humans on a molecular level
infect cells and influence their genetic makeup
8% human genome consist of viruses, integrated themselves in our human DNA
10-20% bacterial dna contain viral sequences
everywhere
not isolated to humans
Virus Taxonomy
living taxonomy? identification, classification, naming
viruses outside host have no capabilities, non living
how classify?
characteristics
host: single virus doesnt affect everything, is specific to a host, looking for specific combo of receptors (will detect for right combination, virus can enter)
different combo receptors, virus will fall off host cell
once enter, type disease caused depends on host and virus
structures
composition: what are they made up of? what do they look like
genetic makeup
viruses are incredibly diverse, no generic viral drug
bacteria can change very quickly, viruses change even quicker
flu virus changes year to year, covid changed dramatically since 2020
able to change quickly because they’re non-living
bacteria still living, virus is just an entity
no need to survive
size
potency/virulence not reflective of size
viruses are smaller than living things but just as potent
envelope vs. naked virus
envelope or no envelope
considered “naked” virus
virus always has protein coat (capsid)
inside protein coat have some sort genetic information (DNA or RNA)
considered enveloped virus
other kind have envelope (usually made up of lipid), capsid, and genetic material
lipid protein coat usually very similar to host cell membrane
enveloped: more sensitive to soap/detergents
covid 19
remove envelope (but apply to envelope and naked), unable to infect the cell
outermost layer have spikes (proteins), recognize receptors on host cell
soap remove lipid layer enveloped, no spikes = no infection
never dna and rna, could have very small amount of protein inside (negligible)
genetic material is limited, how much can be inside virus depends on capsid
bigger capsid= more genetic info
think like cup
information in genetic material contains:
information virus needs to replicate, can not get from host cell
naked virus would last longer in environment, encapsulated lipid could dry out, spikes fall out
shape
isohedral vs helical shape
isohedral: can remove panels and see genetic meterial inclosed
is completely enclosed
helical: ends open, genetic material is not enclosed
2 main shapes, some have combo, no definitive shape
combo: complex shapes
isohedral head and helical end
head have genetic material, helical filamental prortion is hollow
base plate underneath
spiked are located under base plate, only underneath base plate
supported by fibers “tail fibers”
looks like spider
effectiveness of virus determined by shape, structure of this virus function as hypodermic needle
head will push down through hollow tube, inject genetic material into host cell
composition viruses
protein coat capsid
single or double strand dna
genetic material determined by size capsid
proteins very limited
only have genetic material cant get from host cell
goal? make more copies
smallpox? 2x dna (stable)
single stranded dna are parvoviruses
cause skin infections
problem? not as stable
single stranded rna viruses
polio
2x stranded rna viruses
2x stranded dna most stable, changes less frequently
viral protiens:
protiens needed for early infection
used immediately, can not wait to hijack protien from host cell, very unique to virus
virus carry almost no protien tries to use what it can from host cell
how interact with host
recongize right host cell, infection will continue/take, depending on virus what will happen to host cell
in general one option is for virus to enter host cell and immediately cause productive infection
more copies of virus made immediately
2 routes differentiate
1 option: keep making copies, accumulate in host cell, cause host cell burst open
kills host cell, virus not has lots of copies released all at once rather than small amount, could bump into other host cells
lytic cycle (lysis)
2 option: extrusion budding cycle, as more viruses produced, slowly released from host cell into environment
does not kill host cell immediately, over time it will
3rd: instead enter productive infection, go into lysogenic cycle, virus hide in host cell and wait until conditions change
latent state, nothing happens
productive infections
bacterial viruses (unicellular)
all have these 5 steps
attachment
penetration
synthesis
assembly
release
lytic cycle: kill host cell
attachment: timepoint in which virus bumps into potential bacterial host cell
spikes interact w/ receptors, right combo go to next step
penetration: the genetic material of the virus enters into the host cell (hypodermic needle)
capsid stays on outside bacterial cell, only viral genetic material enter
biosynthesis: hijack everything in host cell, doesn’t need to survive/long term, needs to utilize everything host cell has
shit down host cell biological processes to synth more virus
assembly and maturation: needs to put components together to make new functional viruses
take place in host cell, once done will release
release: host cell lyses, new virions released, host cell is dead
influenza release ab 10,000 virion copies for each lytic cycle
each virion potentially infect another host cell
fast infection rate, looking at something with big burst size
extrusion budding cycle
5 stages
attachment
penetration
synthesis
assembly
release
key difference, no big burst, host cell doesnt die
attachment: spikes of virus recognize combo receptors on host cell
penetration: virus injects genetic material into host cell, capsid stay on outside host cell
synthesis: will start using components host cell, borrow/use not hijack, host cell metabolism still working, start synthesizing viral components
assembly: take place at host cell cell surface
make small hole on surface bacterial host cell, releases virus into environment
holes cause damage to host cell, slowly weaken host cell
also host cell can still do binary fission, divide, now have 2 infected cells
Latent stage: the virus hides inside host cell and waits, willattach, penetrate, but will then change
after penetration, viral genetic info become circle, evaluate conditions host cell
good conditions will go into lytic cycle
in bad condition will go into lytic cycle
if host cell in moderate condition, go into lysogenic cycle
will hide and wait until conditions become terrible or perfect, then go lytic
long periods of time
bacterial and viral genome become one, lysogenic
lysogenic stage can give new qualitites to bacterial cell
lysogenic conversion
new qualities to bacterial cell
C botulinum
only cause botulism in lysogenic phase
when toxin created
botulism = muscle cells wont contract
cholera: only cause cholera with virus
how do bacterial viruses cycles relate to animal viruses cycles
host cell die doesn’t mean host itself will die
Viroids, Prions, and Viruses Pt.2
bacterial cell host cell, bacteria is found everywhere
virus randomly interacts and goes through process
host human? so many cells, not every type of cell is host cell for virus
flu: epidermal cell? sex cell? not target for virus, but can interact
needs to interact with target cells in order for infection to take place
how come in contact
transmission: how things are transmitted from one place to the next
reservoir and host
reservoir: where pathogen naturally found
rhinovirus (common cold): naturally found humans
host: who receives it
how transmitted?
direct transmission: reservoir → host
indirect transmission: reservoir →intermediate→ host
rhinovirus has direct transmission
vectors: things that carry the pathogen from reservoir to host, not infected, only carrier
airborne, droplet
vertical transmission: (direct)transmitted from mother to child, within blood relationship
horizontal transmission: direct/indirect, between individuals
respiratory droplet: form direct transmission from person to person
cough/sneeze/talk, respiratory droplet travel 3 feet
3 ft radius distance between next person
rhinovirus (common cold), influenza
sexual transmission: direct form transmission, sexual contact (vaginal, anal, oral), blood
HIV (AIDS), herpes (cold sores, genital warts)
droplet nuclei: indirect form transmission
sick person produce mucus, mucus comes out w/ respiratory droplet when cough, mucus dries very quickly
mucus becomes platform for pathogen to travel on, can travel infinite distance
respiratory droplet just liquid, droplet nuclei is dry (airborne), follow air current
enteric transmission: form indirect transmission, fecal-oral transmission
why wash hands, hospital and daycare setting
rotavirus: target little kids ( dont have great immune responses), polio
food industry
zoonotic: indirect form transmission, animal or insect form
rabies: transmitted by dogs/raccoons/ medium/large mammal
can bite and be bitten/survive
lyme disease: ticks (deer/mice)
west nile: mosquito
fomite borne: indirect form transmission, inanimate objects
desk, chair, floor
controlling transmission?
respiratory: cover mouth when cough (elbow), distance
droplet nuclei: blow/cough into something disposable
sexual transmission: protected sex
enteric transmission: wash hands/food
fomite transmission: clean items
zoonotic: can’t control nature, most challenging to control
multiplication cycles in animal virus
has attachment, but process different
has penetration
uncoating
synthesis
assembly
release is different
length replication cycle vary from 8 hrs (poliovirus) to 36 hrs in herpesvirus
faster virus replicates, sooner see signs/symptoms, can treat/control
long replication process, longer to see signs/symptoms, don’t realize you are transmitting
influcences how well control transmission
attachment: bacterial process (virus randomly bump into cell, recognize receptors w/in cell)
humans: virus must come in and be targeted to potential host cell
virus must come in individual and get targeted to host cell, depends on how body is working, reach potential host cell, spike attachment proteins interact w/ receptors on host cell
could stay in body without right host cell but cant establish infection (Hepatits B: bloodborne, still has to make it to host liver cells, dpesnt reach cant cause onfection)
poliovirus: target is intestinal/nerve cells
spikes must rcongze recpetor combination on hsot cell
penetration: bacterial cell, virus inject viral genetic material, capsid stay outside
animal virus: penetration take place 1 of 2 methods
receptor mediated endocytosis: spikes of virus interact with receptors on host cell membrane, interaction causes cell membrane to change shape
make little pocket around virus, seal off, brought in completely
fusion: takes place between virus w/ lipid envelope and host (outer layer has spikes)
viral envelope and cell membrane fuse together, only the capsid and genetic material enter the host cell
capsid keep virus protected
uncoating: seperation viral dna from capsid ( only found animal virus)
eukaryotes: organelles/nucleus
during synthesis, have to target right location
nucleus or ribosomes
assembly: bacterial virus (make virus)
eukaryotic virus: take place inside host cell
release:
lytic, extrusion budding, lysogenic, release virus
release just from host cell , will spread to other host cells
accumulate infections, host won’t die but host cell will
howmuch release depends on virus
single poliovirus release 100,00 copies per cycle (8hr replication process)
have immense potential for rapid viral proliferation
many times, if enveloped virus: will release through extrusion budding method (sometimes incude vesicles, nucleus, endoplasmic reticulum),
use membranes, form pouch, bud off host cell
non-enveloped: can do extrusion budding but mostly do lytic cycle (release all at once, kill host cell)
productive infection:
attachment, penetration (receptor mediated of fusion), uncoating, biosynthesis, mature/release
Latent stage: lysogenic phase
attachment, penetration, uncoating
during uncoating makes detection condition hsot cell
moderate, integrate into membrane and wait
conditions favorable/bad, will go through lytic cycle
Infections
where pathogen can replicate and make more of self, while at same time can damage host
animal virus: can have infections, multicellular organ
bacteria virus: can have infections
acute v persistent infection
acute: short periods of time, person immune repsonse kick in, eliminates virus
persistent: last long periods of time, avoid immune response
chronic/latent
acute infections often associated with lytic infections
virus dissapears after disease ends, immune system recognize
rhinovirus, measles
chronic infections often associated with extrusion budding
slow release of virus over long period time, make more of virus as cell divide
once hit plateau see signs/symptoms, sign/symptom eventually decline, viral load remain high
balanced pathogenicity
body replaces damaged cells, still have functional cells
hepatitis (sign/symptom: jaundice, abdominal pain)
remains high within the body at all times
latent infection: will integrate, associated with lysogenic cycle (followed up by lytic)
increases, see signs and symptoms, then virus dissapear from cirulation
still on body, as immune system decline viral load increase dramatically
reach pateau sign/symptom, as decline, virus hide inside host cell
cold sores, chickenpox/shingles
phenotype mixing
single host cell can e host to multiple different viruses
virus 1 and 2 can enter simultaneously ( good host cell have combo receptors)
goal virus make more of itself
have 2 virus enter same host cell, will do regular cycle
during process take over host cell, only restriciton capsid have is size, gen material is nonspecific
capsid can take different types genetic material, spikes and attachment protiens, can introduce new genetic material to host cell not intended to enter
viruses can go into different hosts
then during biosynthesis, can make more
host has never been introduced to the new virus before (jump species barrier)
can not be stopped, recognize same host cell, capsid have no selection beside size, can take whatever genetic information
how get variety of same virus
Genome exchange (genomic recombination)
have 2 virus enter same host cell
blue gen material→ blue capsid
not all, just a little bit
will have red and blue gen material
genetic combo will make virus never seen before, no protection against it
can not be stopped
phenotype mixing: change capsid and genetic material
genome exchange: mixture genetic material
Viruses Pt. 3
flu virus (influenza)
takes place yearly (new strain)
effects not too severe, immune response partially recognize
haven’t had flu in long time will have more severe complications
slight point mutations year to year ( change in nucleotide sequence)
made up of 8 pieces of RNA (single stranded, unstable and mutate easily)
is enveloped, have lipid layer
outside lipid layer have spikes and other protiens
hemagluttin (protien, antigen our immune response recognizes)
as long as exact same hemagglutinin present, body will recognize
if chnage protien, body would not recognize fully
neuraminidase (specialized spike, recognize receptors on host cell for influenza virus)
signs/symptoms for flu
begin in upper espitroy tract, progress to lower
similar symptom to common cold
body aches, fever, tired, headache, chills, dry cough, stuffy nose, sore throat
people do not die of flu, people die of complications associated
secondary complications, pneumonia
Antigenic drift/shift
slight change on annual basis
antigen change: hemagglutinin
stay inside winter time, need 3 ft seperation, influenza spread by respiratory droplet
periodically will get antigenic shift
can get genome exchange and phenotype mixing
virus never seen before, no protections
wide spread infection
ex. 1918 flu: spanish flu
1950s, people already exposed, cases will drop over time as ability to develop flu vaccine continue
become smarter
drift: small change, drift: big change
antigenic shift will occur within next 5-10 yrs
Antigenic Shift event
phenotype mixing, genotype mixing, will have no protection against it
2009 antigenic shift, can go back to 1918 flu strain
spanish flu: origionated in turkey, then went to pigs, then humans
can tell that this started with avain flu
transmission ,pathogenesis, virulence
mostly through respiratory and fomites
direct/indirect
target cell: cells of respiratory tract (cells w/ cilia, ex. throat)
damage can take up to 1-2 weeks, can transmit to others
have flu vaccine every year, rely on prediction
make in eggs, make prediction on what flu virus will look like in the following year
sometimes right, sometimes wrong
flu vaccine recongize ab 60%, good vaccine
this year have influx of common flu
viruses and tumors
can a virus cause tumor?
HPV: human pappilomavirus
yes but rare
what is tumor/cancer?
cancerous cell is cell that doesn’t take on normal role
cells start dividing faster, will damage good cells
can have viruses that cause tumors
retroviruses, rna viruses
MOST DONT
why important to note?
human cell do g1, s, g2, mitosis, cytokenisis
tightly controlled, dont undergo mitosis unless strictly neccessary
each cell have very specific role, need to be replaced by specific cell
cell division
group genes proto-oncogenses
encourage cell division
tumor supressor supressor genes
stop cell division
when cells mutate (maybe through virus) chnage how function
tumor supressor genes turn into protooncogenes, cell divide unneccesarily
proto-oncogenes can increase, turn super green light
oncology: study of cancers
one cell get virus, mutates, will divide uncontrollably, damage good cells
stay same location, tumor is benign
can eventually metastisize
move away from origional tissue, can enter other areas, enter circulatory and lymphatic system, spread to other locations
move location = bad
Human Papillomavirus Infection
vaccine encouraged (as young as eight)
most people exposed to some form at some point in life time, may not be aware
does not always cause signs and symptoms
signs/symptoms
genital warts
females: associated vulva region in/around vagina
males: associated with penis/scrotum
also associated anal region/around groin
through sexual contact
flat, grouped, can be obstructive
urination, sexual contact
most strains not harmful, but some can lead to formation cancers
why strongly encouraged women have pap smear (check cervix)
looking for abnormal cells/structures, will ask to do more tests to verify
cervical cancers, if undetected usually because not being checked on regular basis
not detected early enough, can progress, metastasize, lead to death
4300 women die cervical cancer per yr
men less likely to die from cancer associated with HPV
genital warts not lethal
increase number of reporting of mouth and throat cancers, looking for connection HPV
is non enveloped DNA virus
is harmful because contains oncogenes
encourage more cell division
lots of strains more than 100, only 5 cause cancer
target host cell mucous membranes and epithilial cells
at some point people get exposed, ab 14% female college students become infected with incurable condition
made transmission: sexual contact (including oral)
auto inoculation is possible
self inoculation, can transmit virus from own wart to other regions of body
sexual/physical contact
indirect transmission can occur: other sexual activities w/ inanimate object
prevention: vaccinate, very effective, also protect against other non cancerous strains
age 8
100% effectiveness
avoid sexual contact
auto inoculation: wash hands
100% effective, should it become childhood vaccine?
today health administration (department HHS) unlikely
before change 42 US jurisdictions introduced legislation require HPV vaccine/educate children/school on it
a few states have required HPV vaccine to allow entry into public system
Virginia requirement is only for girls, others are both boys and girls
strong support for school entry requirements for HPV vaccine with opt out options
Contagion
Wednesday
coughing, sexual intercourse og from affair partner (Chicago- Hong Kong)
respiratory/fomite
r-not
reproductive rate, how many people 1 infected can infect (4, 1/12 people on planet will contract)
bats and pig, receptors found respiratory tract and cns
lung/brain (lock/key)
sweating, seizure, dizziness, fatigue, foaming at mouth
Monday
virus highly adaptable
epidimiologist- Hong Kong
virus kills every cell try grow in, cant tret/vaccine until grow
grew in bsl3
mev1 virus now has breakthrough, able to grow
virus started in hong kong, someone gave it to minnisotta lady, gave to man hit by. bus, she also gave to ukranian woman
conspiracy theorist take forcythia? stop onset of virus (allegedly)
¼ die from virus
forcythia doesnt work ☹
homeopathic treatments being observed
deforestation, minnosota lady company, led to bat infecting pig farms, infectong people, chef touch minnosota lady
CH12
Immune Response
we can recognize our own human cells
how know which micorbes are harmful v helpful
immune function
white blood cells constantly ove through body, searching for potential pathogen
must be able to differentiate self, healthy cells, damaged cells, foreign materials bad v harmless
must be able to get rid of cells that aren’t functioning properly
cancer cells avoid this
autoimmune disorder
immunse system recognizing healthy/own cells (mistakenly attack body own tissue and organ)
lupus
rheumatoid arthritis
celiac disease
if not harmful immune system signaled not to react/react differently
recognition+response
allergy: body recognizing spore/pollen as dangerous
hypersensitivity: increased sensitivity to something that is not dangerous
How does immune response start
must be able to differentiate betwee foreign and self
antigens: antibody generator
protiens/polysachharides, look different from our own protiens/polysacch, will stimulate production of antibody
something that comes within/outside the cell
endogenous antigen: protien bacterium produces and inserting in cell, when displayed
exogenous antigen: nail/rust particles
recognition lead to phagocytosis
molecular recognition: pathogen associated molecular patterns (PAMPs)
peptidoglycan, dna sequenc
not found in humans
pattern recognition receptors (PRRs)
channels moving material along cell membrane
we dont have
Immunity
involve many different systems
skin: system is integumentary
circulatory/lymphatic system
why call immune response
immunity: ability of an organism to resist a particular infection or toxin by the action of specific antibodies or sensitized white blood cells (leukocyte)
blood has leukocytes, thrombocytes, erythrocytes
adaptive v innate immune response
innate immunity: first line defense
things physically block the portal of entry
way the agent enters the body (respiritory, sexual)
nose hairs, saliva, mucus, skin, bacteria
innate immunity: second line defense
internalized system of protective cells and fluids
monocytes, cranulocytes, cynophil, basophil, fever,
adaptive immunity: third line defense
have to recognize very specific antigen
1st and 2nd line are more generic (born with it, no exposure necessary)
third line defense provide long term immunity
not born with it, must learn how to recognize and defend
learn and remember response
once learn will remember forever
Host defenses
innate
1st line
things anatomical and physiological
physical barrier, microbiota barrier, chemical barriers
2nd line
cellular/chemical
phagocytosis, inflamation, fever, antimicrobrial products
3rd line
specific, b/t cell
Mandate immune system
constant patrol, surveillance of body
recognize foreign material
go after something actually dangerous
destruction of entities deemed to be foreign/pathogenic
( although can place into distinct groups, they overlap and work together)
Innate
First line of defense
born with it, nonspecific
physical and chemical barriers prevent microbes/pathogens (living/nonliving) from entering
stomach acid, earwax, nose hairs, intestinal microbes, flushing out waste
Skin
2 main categories, epidermis/dermis
epidermis: outer
dermis: inner
skin is dry, watr beads (waterproof), constantly sloughig away top layer (tough and non easily penetrated), sweat flush microbes (digestive enzymes like lysosyme)
sweat in salt cause bacterial cell to shrink
mucous membranes
digestive, urinary, respiratory tracts and eye
block entry bacteria, digestive qualities, help pass materials out of body
respiratory tract: columnarcells, mucus producing cells, cilia, help move materials out
GI tract: have normal microbes, mucus (urine, intestional fluid, vaginal secretions)
all contain normal microbes
normal flora
structural barrier, use up nutrients/space avaliable
competitive
can produce toxins that prevent other pathogens from entering the space
can control environmental conditions
temperature/pH
probiotic diet
fresg fruit/salads/meats (sushi/beef tartar)
food can help restore lost microbes
Nonspecific Chemical defenses
stomach acid, ph of vagina/chem substances of semen, lysozyme
Second line defense
pathogen has passed through 1st line
how wbc might respond to it (generic)
cells of the blood
all originate from bone marrow
hematopoietic stem cells: have the ability to become any type of blood cell
lymphocytes
granulocytes: spotted/grainy undermicroscope
neutrophil, basophil, eosinophil
monocytes: one cell
macrophages, dendritic cells
lymphocytes
t/b cells (usually part of adaptive)
Natural killer cells
usually part of innate response
multiple cells involved, must communicate with one another
signaling (instigator, signal , receiver, response)
cell communication
some sort of cell must start communication
not pathogen, must be immune cells
cytokines: some sort cellular signaler
chem/protien, what is being relayed
receptor: how percieve signal, protiens that can recieve signals and cause some sort of response
response: one type is adhesin
add portusions to cell that can grab onto another cell
need neutrophil, grab neutrophil
sensor system
toll like receptor: receive signal, pathogen get through 1st line→ enter body, lookin for characteristics unique to something foreing
flagellum, cell walls, sequences, lps, generic qualities of toxins
nonspecific to one microbe
stimulate receptor to change and send out cytokins
constantly patrolling body
sensory system: complement system
made up of numerous complement proteins (work togther)
funtion in cascade formation
can go from dormant to activated state, when interact with other dormant cause to activate
increases activated complement protiens
can do 3 things
stimulate inflammation
form membrane attack complex (cytolysis)
form pores on foreign entity in hopes of ruining integrity
opsinozation
complement protien coat entire surface of foreign entity, serve as an attractnt for phagocytic cells
all require recruition (except cytolysis)
Phagocytosis
taking in large objects (up to cell) bringing them into the cell, nd breaking them down
cell keep what can use, expel what it can not
many type phogocytic cell (neutrophil, macrphages0
can be localized
macrophages : tissues
neutrophils: circulatory
when damage occurs, pathogen enter whatever space, must have some sort of stimulation to bring in phagocytic cells
come to area, attracted by chemotaxis
based on chem. concentration
once reach will be adheranse ( attraction between agent and phagocytic cell)
phagocytic cell form pseuodpods
surround agent, create vesicle, bring agent inside cell
phagosome
phagosome+lysosome: break down and digest agent
phagolysosome
exocytosis waste, keep what want
Leukocytes
neutrophil
granulocyte, found in circulatory system
professional phagocytic cells
relatively short life span
bc contain lots of materials for phagocytosis
lots of digestive enzymes
very dedicated to phagocytosis, is main goal
patrol, circulate, movement
macrophages
have to develop to do phagocytosis, not proffessional
regular, need to go through developmental process to become proffessional
live relativley long time bc not professional phagocyte
have other roles, no digestive enzymes
in tissues
tend to be more localized in their tissues
present during injury, recruit other cells to get rid of pathogen in tissue
cytokines: signals eneter circulatory system, recruit neutrophil bc proffessional phagocytic cells
chemotaxis
monocyte
Natural Killer Cells
derivative of the early lymphocyte
all the cells started in the bone marrow
are part of innate response bc generic, looking for any type of cell that doesn’t look healthy
not phagocytic cells
release enzymes that cause the cell to form holes
pores
the cell will lose its integrity and be terminated
Inflammatory response
inflammation, most of the time is induced (innate response stimulate) but can be chronic
cardiovascular disease, chronic
most time stimulated bc of innate response
localized (inflammation of injury site) or systemic (throughout a system)
can be induced by injury, necrosis, can take place after trauma/infection
not just innate, takes place when stimulate adaptive response
1. want to bascially let cells of body know injury has taken place, recruit cells involved
neutrophils
2. to start proccess of needing to fix area damaged
stimulate clles needed to heal
3. physically block microbe/destroy
powerful defensive reaction but can cause injury
rerut phagocytic (proffessional)to eliminte infection, may need to destroy surrounding cells
A means for the body to maintain stability and restore itself after injury
by taking antiinflammatories could be causing issues
macrophages able to detect invading micorbe, make cytokines, can enter vessels and travel ciruilitory stsyem to recruit more cells
Vasodilation
causes the blood vessels in the earea to expant, as cytokines enter easily, there will be swelling, crached. increased blood flow = heat
phagocytic cells
neutrophila move w/ chemotaxis
diapedisis, phagocytimc ell allow for neutrophil to slip w/in connecitve/barrier, to enter patogen
leuokocyte move into tissue from blood vessels
response is adhesins
more cells recruited,
Fever
usually treated wit tylenol of cough serup,too high mcan harm developmenty
controled by hypothalamus
release pirigins (increase temp)
low v hide degree
reflection that bpdy has felt dome sort of action
normally 83.3degrees
form energy can provide cells w energy, stimulate ummune system to work faster
when take tylnol/advidl may be causing more harm (pathogen start causig issuse
Pyrons
Exogenous pyrogens:
roducts of infectious agents such as viruses, bacteria, protozoans, fungi, endotoxin, blood, blood products, vaccines, or injectable solutions coming from outside the body •
Endogenous pyrogens:
liberated by monocytes, neutrophils, and macrophages during phagocytosis such as interleukin-1 and tumor necrosis factor
Benefits fever:
inhibit multiple temp sensitive microorganism (poliovirus, cold virus, herpes zoster virus, systemic and subcutaneous fungal protien
interfere w nutriton bacteria
influecne how iron is valiabe
increase metabolism , stimulate immune reaction, naturaly protective of physiological processes
treatment fever
meds can influence heart rate, respiratory rate
negative side effects (heart beat too fast)
complications, in gneeral if low grade fever, can let it continue before uncomfortable or too high
Interferons
usually activated when viral infection
attachment, penetration, uncoating, maturation, assembly, release
host cell can detect vira; genetic material, and infection
virus does biosynthesis, can tell cell is functioning abnorammly
stimulate self to rpoduce interferon
infected cell still doomed, but interferons cn release back inside affected cell
reciever is neighborig cells
interferon signal to neighboring cell that
1. infection has taken place
2. infection stimulate cell to do apoptosis (neighboring)
3. do so other neighboring cell can not get infected
will form physical barrier for virus to stop from affecting surrounding cells
take one for the team
viral and innate
how recognize between self and foreign cells
contain MHC class 1
major histo combatibility complex
2 main type
complex of protiens on surface of cell, they display endogenous antigen
endogenous: cell produced antigens that could potentially signal immune response
demonstarte what kind of cell, if cell belongs to you, represents condition of cell (doing normal cell function, developed properly)
wot keep cells that dont fucntion correctly
display endogenous antigens
pattern recognition, natural killer will leave healthy alone, but if cell infected, will have different endogenous antigen
natural killer dont recognize, kill
MHC class 1 vert important
automiimune disease, cells cant recognize our own cells
Adaptive Response
specific, need to be exposed to potential athogen/antigen in order to be stimulated
must be taught, body needs to remember
next exposure to same antigen already has a defense for it
3rd line of defense
oftentimes uses lymphocytes (not exclusive, uses some cells part of innate response)
innate and adaptive overlap
t/b cells
key characteristics
is specific: recognizes one particular agent
has memory: ability to remember antigen and be able to defend against it immediately
has to be diverse:
not just one cell that responds, multiple respond
has to be induced (not always on)
has mechanism in which antigen is exposed and system decides whether to respond
once whole system is stimulated must be able to replicate itself
so have great response
has to have tolerance: know when response needed/not needed
cells
all cells from blood come from bone marrow, hematopoetic stem cells
cells that can mature into other types of cells
think fertilization: 1 cell develop into person
1 cell had potential to become every type of cell in human body
our cells now have become differentiated
cell has a particular role, can not convert to another type of cell
stem cells are undifferentiated, have ability to become other types of cells
b cells are somewhere inbetween
in process of being differentiated
process called: development/learning
T/C cell development
all start from hematopoetic stem cells in bone marrow
develop into naive B cell and naive T cell
b cell stay in bone (naive), t cell go to thymus (naive)
havent learned anything, from there will move to their secondary lymphatic organs, will wait until stimulated
like spleen, lymph nodes
Lymphatic System
lymphatic capillary take sample of blood/fluids, take to secondary lymphatic organs
where naive b/t cell will be exposed to antigens
antigen presenting cells also found in lymphatic fluid
present peices of the antigen on the surfac of the cell
come from person, will endocytose antigens and make decision of whether is antien that need/dont need defense’
antigen presenting cell usually first cell to make decision if antigen is needed
if needed will present on mhc2, if not nothing eill happend
ex. dendritic cell. macrophages, b cell
cell communication
receptors and cytokines
cytokines: chemical signalers
receptor: recieve and cause change
no receptor, signal dont get perceived
MHC class 1: what our cells display to show condition/characteristics
if display worng, need to be eliminated
Antigen presenting cells
MHC class 2: make decision ab antigen, present on MHC class 2
own andogenous smaterial
Lymphocyte receptors
recieve signal and order some kind of response
multiple types, need to be able to percieve signals
adaptive respons e
humoral and cellualry immunity
Humoral Immunity
body
extracellular antigen stimulate
antigen→ enter lymphatic vessles———→ travel through lymphatic syystem to secondary organs
secondary lymphatic antigen
secondary myohatic system will need naive B cell
anrtigen and naive b cell interact
if no need for anitgen, nothing happen, if needed will be macrphaged and presented on mch2
naive t helper v cytotoxins
helper: antigen present on NHC class2 , is yes need antigen, cell divide/develop, turn into activated t hekper cells
will keep dividing, some will devellop into membrane
for future use
activated t helper cell will start to release cytokines
receptor must receive cytokines, recieved by naive b cells, will divide and develop into activated b cells
some develop i to memory sales, some develop into plasma cells
plasma cells produce antibodies, need specialized antibodies
do clonlal selection, choose best of best
choose cell that produced the best antibody
will continue to divide, outcome lots and lots of the best antibody
will release antibodies, make them release
antibodies have to make it back out through lymphatic system to the body
come out through secondary lymph system, amybe to circulatory, to lymhatic system to antigen
bind to antigen, impact directly and indirectly
b cells dont exist? this process wont take place
clonal selection
process of selecting best plasma cell to continue to divide and make more of tiself
antibodies
will divide and release antibodies (are protiens, structure determine function)
Antibodies
y shaped protien
c shape portion: constant, determine whch class antibody it is
IgG,IgM,IgA,IgD,IgE
needs to be able to make all 5 classes
antigen bind to variable regions
5 classes:
IgG: monomer, work as single antibody
make up 80% found antibody
found in blood/lymph/intestines
longest lasting antibody, 23 days
can be activated and used w complement proteins
crosses placenta, developing fetus will get it too, infant born w/IgG
involved phagocyosis and neutralization
IgM: 1st antobody prodiced when exposed to antigen
pentamer: 5 binding site to grab antigen
glutamer
IgA: dimer
2 together, found saliva/tears/mucus/breast milk
why encouraged to breastfeed, IgA can be passed on to child
IgE: least amount found in body
found bound to mast/basophil, throughout body
associated allergic rxtn
IgD: monomer, development humoral response
direct v indirect:
direct:
agglutination, pulls antigen out of solution, cause clump together
neutralization: block antigen/product and prevent from impacting target
indirect:
opsonization: antibody coat antigen, attract phagocytic cell
complement: coat antigen, attract complement protiens to damage antigen
antibody dependent cell mediated cytotoxicity: antiboyd bind to antigen, attract natural killer cells or cynophils, cause those cells to release their damaging enzymes
Cellular Immunity
intracellular antigen
antigen presenting cell: dendritic cell (expert)
antigen and dendritic cell interact, if dendritic cell decides no, no further response
if yes will enddocytose the anitgen and present pieces of it on its MHC2s
travel through lymphatic system to secondary lymphatic organs
show it to naive t helper cell, interact, naive t helper cell needs to make decision
if yes will divide and develop into activated helper t cell
some will develop into memory cells to be used later (learn and remeber response)
others wil continue dividing and developing until they release cytokines
cytokines get recieved by naive t cytotoxic cell
causes naive t cytotoxic cell to divide and develop into activated t cytotoxinc cell
some will develop into memory cells (used for future)
active t cytotoxic cell will travel through lymphatic system (vessels) and come out
will release cytokines into body to signal to cells
signal so all cells will present their MHC class 1
condition? foreign?
informs all cells that an activated t cytotoxicvcell has been released
interacts with the cells and possibly the antigen
your cells? nothing happens
unhealhty cell? wrong MHCclass 1? will kill that cell
if interact w/ antigen t cytotoxic will destroy
can hide, can pretend/go undetected if hiding in healthy cells
is humoral response totally seperate from cellular response?
no, will connect (cytokines) with naive b cells, can activate humoral response
if have something attack common naive t helper cell, bad (but come from bone marrow, so body cna replace what is lost)
if can not, become problem
HIV patients show symptoms at first, but over time stop bc bone marrow replace
start facing complications again bc bone marrow can not keep up
as long as memory cells exist, body will remember how to fight off pathogen
when get old, they decline, similar to immune response
antigen presenting cell
bits of antigen presenting on MHC2s
t helper cell interact and gets activated, the whole shebang typed out, eventually other cells noeed to present MHC1 or will kill cell
needs to display right MHC1, if infected will not
macrphages
associated w/ innate, but can function as antigen presenting cell
can potentially leave tissue, eneter circulatory system, go into lymhatic system, and show MHCII, cytokines stimulate macropage, become activated
in the precense of cytokines can divide and develop into activated macrophages
better phagocytosis than regular macrophages
innate and adaptive is not totally seperate, have same goal
multi organ system
Outcome t helper cell
help stimulate macrophage, cytokines can stimulate other types of cells
neutrophils, mast cells,
humoral response, celular response, needs 2 cells to make decision on whether response is needed
humoral : naive b and t helper
cellular: naive t helper and antigen presenting cells
make sure repsonse is needed
allergies: immune response is recongizing something harmless as dangerous
sometimes immune response doesnt require to cell, can skip one and still ilicite response even if agent doesnt need defense against
cant make b cells? cellular or macrophages step in
have other protective measures
Building Immunologic diversity
in secondary lymphatic organs many naive b/t cells waiting to learn different responses
many different combinations out there
ex. spanish flu, all we coud do is protect from exposure, until started to figure out how to develop vaccine (think contagion, stayed isolated unti the got the vaccine)
no good treatment, need to wait for vaccine’
learn and remeber: adaptive repsonse
Igm is the one 1st intoriduced 1st exposure, Idg second exposure
Outcomes of Immune response
immunity: can recognize recruit, contain, remove, and repair
sometimes immune repsonse doesnt work perfectly
sometimes get hypersensitivity
havng high immune response to somehtign that is avirulent
not disease causing
think pollen, food allergy, blood typing,
autoimmune: attack own cells/tissue
immunodeficiency: doesnt develop response to somethign pathogenic
4 general outcome, ideally gives you immunity, sometimes ge these repsonses
if just wait until encounter pathogen, then will have signs and symptoms until 3rd line defense
Vaccines
how aquire immunity
naturally aquired immunity: immunity aquired thorugh normal biological experiences
think respiratory
artifical aquired immunity: protection rom inection abotained through med. procediures like vaccine/immune serum
active immunity
when individual recieve immune stimulus activat b/t cell to produce immune substances like antibodies
memory, rneder person ready for quick action upon reexposer
several days develop
last long time
stimulated by natural/artificial mean
passive immunity
occure when individual recieve antibody from another human/animal
recipeint protected for short period time, even if no prior exposure to antigen
lack emmory for og antigen
lack antiboyd production against disease
immediate onset of protection
short term, natural/artificial in origion
think breast milk
natural active: immumity ofllowing attack measles
natural passive: temp. immunity from antibody of mother transfer to infant through plcenta/milk
active artificial: deliberate exposre, immunization
artificial passive: antibody in immune serum intoduced to body, injection rabies immune globulin
immunization history
around for wiute some time, started in th centruy variolation (take remnant of someoen who had disease and forcefully intoduce to other individuals) still some ppl who developed the disease
edward jenner: vaccine (use something similair to disease causing agent to stimulate immune response)
vaccination: any immunity obtained by inoculation with selected anttigens
artificially aquired, looks like virulent pathogen (aviruletn strand/portions of pathogen)
trick immune response to preempt
vaccines
about whole population, not just individual, role as nurse proffesional is to protect population
want to acheive herd immunity
going to vaccinate certian percentage of population so that disease does not spread
ab 70%
with 70% of population vaccinated, when in contact virulent pathogen will not develop disease
other 30% will develop disease but wont spread
everyone does not need to be vaccinated, contain the spread
think covid: herd immunity was at 80-85%, when look at covid it transmitted very easily
pathogens have ID (infectious dose)
number of copies of virulent pathogen you need in order to establish disease
ID: 70 copy, if you only get 50 wont get disease
covid had low ID number
transmitted much easier than womething w/ high ID
needed to rise herd immunity percentage to mitigate this
vaccine needs to stimulate memory cells
avirulent/portions, sometime body doesnt recognize, not good vaccine
bc stimulate memory, memory doesnt last forever
tetnus: every 10 years, memory cells wont remeber for longer than that
vaccine act as boost
want memory cells to be long lasting
vaccine needs to be able to be distributed with ease
covid vaccine: had to be stored minus 80 degree celcius, very particular
cant start degrading the moment it gets made, by time get to distribution will be useless
vaccine can not have severe side effect: mild symptom okay
convulsions/seizure/cardiac problems, people refrained from taking
need to eterime if any long term unknown
insurance compant wont cover if not aware of vaccine
antivaxxers: worry about long term effects (whatevr still losers)
vaccine must be affordable (without insurance)
artificially active immunity
atimulate primary adaptive response, stimulate memory
immediate/powerful sustained repsonse
when think ab how to get vaccine 2 ways
attenuated vaccine: ones that are avirulent pathogen, still replicate, trick body to recognize virulent one
subunit vaccine (fractionated): killed cells/portions of pathogen
attenuated: can still replicate, trick into recognize virulent one
look for similair sign/symptom/structure
fractionated: multiple boosters
trying to kill pathogen, take key components
sometimes have to genetically engineer fractionated for body to recognize as something to develop defense against
attenutated vaccine
avirulant pathogen, ability to replicate
long lasting defense
if not aware of somethign similair have to encourage to take place
intorduce mutations to virulent form of pathogens
hope for avirulent form
trial and error
if can find.make one, person will have lifetime effects (no need long term booster)
will naturally transmit
when look at them, have really good effect
some downsides
avirulent fomr could eventially go back through reversion
these tyoe of caccine need refridgeration
really do way to contain spread
tend to have more complications
good outweigh disandvantage
Inactivated vaccine (subunit/fractionated0
killed/portions virulent pathogen
but can not replicate, need a little bit of help
best antigen protien and polysacharides
sometimes need to engineer inactivated vaccine
adjuvent: something added to protien/polysachharide to make more noticable
allum: derivative aluminaum, easily recognized by innune resoponse
defense against adjuvent/not against actual agent
genetically engineera; recombinant
add protien componenent to the poriten antigen
conjugate vaccine: add protien component to polysacharride antigen
less side effects, good to giev to people eho are too immunocomporomised, cant reverb,/ go back to virulet form
easy to store
need boosters (disanvantage(
no natural transmission
Inactivated vaccine
whole agen vaccinem killed version
can not infect a shost girl
toxoid vaccine: pathogen itself is not harmufl but its fathersashes dont,
protien subunint vaccine
polyscharride vaccie, polysacch
dna based vaccine: inject dna into cell
stable and long effect
Killed cell or inactivated virus vs attneuated calls or virus
attentuated grow
prpe immune system to recognize virulent pathogen
subunit: need to engineer sometimees/polysach/toxin
DNA vaccine
goal is to intorduce dn a, go into your boyd, your, will theoretically protect you
rna vaccine: covid vaccine, rna is unstable (degraded)
idea is dna and rna vaccine will be great asset for future, can design them more easily (your body makes critical protiens/wont reject, accelerated process)
attenuated vs inactivated
table 17.2 know
How adminster
subcutaneous: under skin
intramuscular: in muscle
intradermal: deeper in skin
where living cells are
nasal/oral vaccine
sniff, individuals who cant take injeciton, not avaliable for all diseases
stimulate mucus membranes, antiboyd produced from vaccine is iGa
more readily accepted
side effects
trials, experimental animals, humans
then go to market
mild side effect vs strong/adverse
MMR (measle, mump, rubella)
very affective, misinformation cause people to not want to get
measles is on rise as effect
not able to acheive herd immunity
fluctuation immunization rates
pertussis immunization: whooping cough, can crack elderly individual rib, violent cough
vaccine caused covulsions/seizures, vaccine remade, is fractionated form (acellular)
measles immunization: no connection, does not need to be remade, maybe rebranded
R not value
number individuals infected by one person having the virulent pathogen
prior to vaccine, rnot value high
when herd immunity, rnot should decrease (after vaccine)
relationship between rnto value and ID, if ID value is low, rnot value is high
dont know everyhting
role of science: where the vaccines are going
cytokinese vaccine, vaccine that can activate receptor, protien vaccines, dna/rna based vaccine
edible vaccine: genetically engineer plants to overcome disease, diseased food
rice: staple food aroung the worl, modiycy rice to mke america
distribusion: what foods native to each caramel
shipping (cold)
Antimicrobrial Grugs:
all against grudgery, have selecttive toxicicty
can be synthesized articicially
antibiotics: derivedin only from nsturre
can bet antibiotics from bactheria
know 3 main things
1. what is the pathigen dausing drred,
2. degree migvro
3. overall medical condition pf patient
in gen. antimicrobrial grugs follow process
give drg to patient, drug geths targetded to pathogen, will bind to it to tar
celll way syhnthesis, translation/transcrotpion same time
plasma membrane protien ( cant just tanregt lipicd,target an enxyme that is. potentional
we can tmake follic acid, by targeting thivr rd
selective toxicity: nee to know
repsonse to treatment
sometimes drug cant get to site, sometime person doesnt respond will ( drug selective tocicity
in output is issue, some patients can manage
how patient become antimicrobrial drug resistant
makes the mcirobe multidrug resistant, cant stop natural selection
can slow down but not stop
eventually will reach circumstance where no drugs to use
need to slow down process
process
our drug (if we have sensitive microbe) and apply drug, micorbe will now be destroyed
s long as population maintian sensitivity were toogh
when things mutate?
bacteria mutates, faster and easier than we do
these pathogens were sensitive, pathogen takes root, resistant drug keeps dividing anf dividing
vertical relationship, can also do horizontal transfer
can transmit to toher psecies(resistant)
timeframe between developig destance, though something coud change/mutate
apply drug, only resistant population remain, can reproduce
can not stop this process but can slow it down
methids: bacteria to become
drug could come in, spin right back out instead of in
oftentimes impcts whey is called eflux, eflex complex is nonspecific, works again against multiple drugs (like revolcing doow)
method of coming ins blocked
bacteria changes, could also inactivate the drug
Increased elimination: drug enter, efflux pump kik me out
alteration in target molecule: drug can not bind to target
decreased uptake (porin protienprevent entry into the cell
once resistant can transmit to other microbes, you need to be aking care of thi
no good comon antiviral vaccine, need to be specific
viral infections often go unnoticed/
Facts:
with time it will appear, pathogen will have progressive resistance over time, get stronger
progressive resistantce:
multidrug resistance
frequency may fuctuate, affects evryone,
see resistance at high
affect everytbody
nosocomial infection
Bad bugs and no drugs
last 2 yrs only to yrs closer but, no antimicrobrial drugs
people dont realze how important it is to be wass, cant slow it down, must think aboyt clinituan
narrow spectrum, rotate drgugs to read patient info
need to educate patients, stad ground
public awareness, tking drugs to completion as prescribed
take drugs as supposed to
dont share meds, dont throw it away/dispose, take it to reputable location og fisposal
public awareness
that drugs are not curing everything, that there is problem,
aware that getting meds cheaply isnt the solution, can be expensive but not that car from the canadian border
fowllows what they sugjested
global regulation
must be mulsitple countries addrssing and workign together
slowing it down
narrow down pathogen: narrow spectrum
prenvet infection:
prescribe antimiccrobrial drug carefully
prevent ransmission