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
cervicals cancers, if undetected usually because not being checked on regular basis
not detected early enough, can progress, metastisize, lead to death
4300 women die cervical cancer per yr
men less likley to die from cancer associated with hpv
genital warts not lethal
increase number of reportings of mouth and throat cancers, looking for connection HPV
is nonenveloped 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
mde transmission: sexual contact (including oral)
autoinoculation 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
autoinnoculation: 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 (affair)
respiratory/folmite
r-not
redroductive rate, how many people 1 infected can infect
bats and pig, receptors found respiratory tract and cns