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239 terms

Microbiology Final

STUDY
PLAY
viruses
-non-living infectious particles
-obligate intracellular parasites
virus size
20-450 nanometers
(need an electron microscope to see them, however you can see the damage they cause to an infected cell with a light microscope)
what is an envelope
lipoprotein layer that is modified piece of the host's cell membrane
-also frequently covered by glycoproteins
what do the glycoproteins on envelope do
form spike like projections that are used for attachment to cellular receptors
-they are also antigenic
if virus doesn't have a membrane what is it called
naked nucleocapsid
how do envelopes affect viral susceptibility
-confers a level of instability
-more susceptible to heat, detergents and lipid solvents such as alcohol
what is a capsid
protein shell that surrounds the nucleic acid strand of virus
what is name of nucleic acid and capsid together
nucleocapsid
what are the identical building blocks of capsids
capsomers and protomers
what are capsomers and protomers
clusters of small protein or polypeptide molecules
how do capsomers adn protomers make a capsid
they spontaneously self-assemble
what is difference between capsomers and protomers
capsomers-more complex and antigenic (icosahedrons)
protomers-antigenic and more simple
(helical)
what are the two types of capsids
helical
icosahedron
helical capsids
-rod shaped polypeptides called protomers
-hydrogen bond together and to nucleic acid
-form series of hollow discs (bracelet)
-linked in continuous helix - nucleic acid is wound in
can helical capsids be empty
because of arrangement they are incapable of producing an empty capsid
icosahedron
-3D, 20 sided polygon, 12 evenly spaced corners
-no bonding between capsomer and nucleic acid
-use at least 2 different forms of capsomers
-many associate with envelopes
can icosahedrons form empty capsids
yes because no direct bonding b/t capsomer and nucleic acid
what is advantage of structure based on identical protein subunits
-reduction of genetic information needed to reproduce it
-promotes self-assembly
-no energy or enzymes are required to form the viral capsid
functions of envelope and capsid
-protection from acidic and enzymatic fxs of the host
-attachment to host cell
-antigenic
complex viruses
atypical viruses that are more intricate in structure than the helical or icosahedron
poxviruse
-very large
-nucleic acid core
-lack regular capsid->just several layers of lipoproteins and coarse surface fibrils
(primitive membrane)
bacteriophages
-polyhedral head
-helical tail
-fibers for attachment to host cell
defective
-viral nucleic acid and proteins
-cannot replicate without a helper virus
(during course of many human viruses more defective than infectious particles are made)
pseudovirions
-contain host cell DNA rather than viral DNA
viroids
-single molecule of circular RNA
-without protein coat or envelope
-genetic material does not code for any proteins
-replication methodology not understood
-assoc w/ plant diseases-no known human infections
nucleic acids
-RNA or DNA
-number of genes: 4-400
-single strand or double strand
DNA viruses
Parvovirus
Papovirus
adenovirus
hepadnavirus
poxvirus
herpesvirus
parvovirus
-DNA
i.e. B19 virus
papovirus
-DNA
i.e. JC virus, BK virus, human papilomavirus
adenovirus
-DNA
i.e. viral forms of pharyngitis, upper and lower respiratory tract disease
hepadnavirus
-DNA
i.e. hepatitis B
poxvirus
-DNA
i.e. small pox virus
herpesvirus
-DNA
i.e. herpes simplex 1 and 2, varicella-zoster, cytomegalovirus, and Epstein-Barr virus
RNA viruses
picornavirus
calicivirus
reovirus
flavivirus
togavirus
retrovirus
orthomyxovirus
paramyxovirus
rhabdovirus
filovirus
coronavirus
arenavirus
bunyvirus
positive polarity
viral RNA has same make up as cellular mRNA
i.e. picorna, calici, flavi, toga, retro, corona
negative polarity
viral RNA has mirror image of cellular mRNA
i.e. orthomyxo, paramyxo, rhabdo, filo, arena, buny
positive polarity, non-segmented
picorna
calici
flavi
toga
corona
negative polarity segmented
orthomyxo
negative polarity non-segmented
paramyxo
rhabdo
filo
segmented
reo, orthomyxo
non-segmented
picorna,
calici,
flavi,
toga,
corona,
paramyxo,
rhabdo,
filo
single stranded linear
picorna, calici, flavi, toga, retro, orthomyxo, paramyxo, rhabdo, filo, corona
single stranded circular
arena, buny
double stranded
reovirus
Picornavirus
-enteroviruses-i.e . poliovirus, coxsackievirus, echovirus, and hepatitis A
-Rhinovirus-common cold
+NS
Calicivirus
i.e. Norwalk virus, and Hepatitis E
+NS
Reovirus
i.e. rotavirus
S
double stranded
Flavivirus
i.e. yellow fever, dengue virus, and st. louis and Japanese encephalitis virus
+NS
Togavirus
i.e. alpha virus (encephalitis) and rubvirus (rubella)
+NS
Retrovirus
oncovirus (sarcoma and leukemia viruses), lentivirus (HIV and certain animal pathogens)
+
Orthomyxovirus
i.e. influenza virus
-S
Paramyxovirus
i.e. measles, mumps, parainfluenza, and respiratory syncytial viruses
-NS
Rhabdovirus
i.e. rabies
-NS
filovirus
i.e. ebola and Marburg virus
-NS
Coronavirus
i.e. respiratory tract infections (common cold)
+NS
Arenavirus
i.e. lassa fever virus and lymphocytic choriomeningitis virus
- (SSC)
Bunyvirus
i.e. encephalitis and Korean hemorrhagic fever
- (SSC)
Eclipse period
from the time of initial entry to the time of the assembly of the first progeny virion
Time of most eclipse periods for human viruses
1-20 hours
Latent period
time from the onset of the infection to the appearance of the virus
Cytopathic effect
CPE; lysis and death of cell (not all viruses have CPE)
Difference between lytic cycle and lysogeny for bacteriophage replication in bacteria
lytic- lyse cell
Lysogeny- enter into incorporation w host genome, lie dormant in genome, replication only during binary fission of host
Aka lytic cycle
virulent phage
Aka lysogeny
temperate phage
Animal viral replication stages
adsorption, penetration, uncoating, replication, assembly, release
adsorption
attachment to host cell through receptors
-enveloped- glycoprotein spikes
-naked- surface proteins-looks like a ligand
receptor mediated endocytosis- penetration
whole virus enters cell
- mimics ligand- multiple virus endocytosed at one time
-for naked viruses
translocation (membrane fusion)- penetration
whole virus enters cell
-for enveloped viruses
uncoating
utilizes lysomal function
(may die at this point)
replication (eclipse)
early and late genes
type I: ssRNA -positive polarity
type II: ssRNA -negative polarity
type III: dsRNA
type IV: ssRNA -positive polarity and DNA intermediate
Early and late genes
early: transcribed before replication
late: transcribed at replication
type I
ssRNA w/ positive polarity
transcribe w cluster of proteins
type II
ssRNA w/ negative polarity
-makes a mirror image
type III
dsRNA
type IV
ssRNA w positive polarity and DNA intermediate
release-non-enveloped
lysis
release-enveloped
budding or exocytosis
stationary vs dissemination
migrates to target tissue and stays there vs all over
virus shedding
skin, respiratory tract, gastrointestinal tract, body fluids, vectored(insect/animal bites)
abortive infection
failed infection
lytic infection
cell death
cell alteration due to infection but no cell death
syncytia
inclusion bodies
malignant transformation
syncytia
multinucleated giant cells
-from fusion of viral infected cells
-fusion from changes in cellular membrane, due to inclusion of viral proteins
syncytia is seen typically in which viruses
herpesvirus
paramyxovirus
inclusion bodies
frequently found in infected cells
-are areas containing viral proteins and viral particles
-abnormal aggregations
examples of viral inclusion bodies in animals
intracytoplasmic eosinophilic, intranuclear acidophilic, intranuclear basophilic, and both intranuclear and intracytoplasmic
negri bodies
rabies
guarnieri bodies
small pox
henderson-peterson bodies
molluseum contagiosum
intracytoplasmic eosinophilic
negri, guarnieri, henderson-peterson
intranuclear acidophilic
cowdry type A, cowdry type B, torres
cowdry type A bodies
herpes simplex virus, and varicella zoster
cowdry type B bodies (IA)
polio
torres bodies
yellow fever
intranuclear basophilic
cowdry type B, "owl eyes"
cowdry type B (IB)
adenovirus
"owl eyes"
cytomegalovirus
both intranuclear and intracytoplasmic
warthin finkeldey bodies in Measles
malignant transformation
unrestrained growth, prolonged survival, and morphological changes
-genetic disruption
-increases likelihood that cell will undergo a cancerous mutation
persistent infection
infection without cell death
-true persistant/chronic carrier infections
-latent virus infections
persistent/chronic carrier infections
-continue to produce significant amounts of virus for long periods of time
-i.e. herpes - lock into nerve endings in region- don't flag cytotoxic T cells- cells don't die, neurons
latent virus infections
patients recover from initial infection and virus production stops
-enters cells- no flags- goes dormant and then latter becomes active
i.e. varicella zoster, or when chicken pox resurfaces as shingles
natural barriers
skin,
mucous,
ciliated epithelium,
gastric, bile, etc
nonspecific defenses
fever
interferon
macrophages
natural killer cells
fever
mechanism not completely known
thought to inhibit virus particles and replication
interferon
set of glycoproteins that inhibit growth of viruses by blocking translation of viral proteins
-interferon 2,5-oligonucleotide synthetase, endonuclease, and protein kinase trigger three proteins
-these proteins act to degrade and phosphorylate viral RNA but not cellular RNA
antigen-specific immune response
adaptive immunity
antibodies, T-cells
-hypersensitivity and inflammatory response
-partial immunity
-children's lower severity
hypersensitivity and inflammatory response
symptoms often from immune response to virus not from virus itself directly
partial immunity
may change glycoproteins
-system recognizes half of it- response slower than secondary/memory response but not as slow as primary response
children's lower severity
i.e. chicken pox- less severe reaction than in adult
susceptibility and severity factors
immune status
age
general health
viral dose
genetics of virus-host specific
genetics of host-immunity
antiviral drug therapy
-interferon, antiviral drugs
-there currently is no cure- only management and viral load reduction
-can only give interferon in limited amts before becoming dangerous to the host
-only defeat percentage of virus not all of it
viral cultivation
-needs living system to grow!!!
-bird embryos, cell culture
localized infection
remains confined to a specific tissue
generalized/systemic infection
when organism spreads to other tissue or fluids
-generally only one organism
focal infection
when a localized infection breaks loose and spreads to another tissue
toxemia
infection remains localized but a toxin is produced and travels to different tissue group
mixed infection
(synergistic mixed infection)
several agents establish themselves simultaneously at the infection site
primary infection
first infection
secondary infection
when primary infection is complicated by a second microbe
acute infection
infections that come on rapidly with severe but short lived effects
chronic infection
progress or persist over long periods of time
sign
OBJECTIVE evidence of disease noted by an observer
symptom
SUBJECTIVE evidence of disease as sensed by a patient
early warning symptoms and signs
fever, inflammation, leukocytosis, leukopenia, antibody titer
leukocytosis
abnormal increase of white blood cells
leukopenia
lowering of white blood cells
asymptomatic
infected but showing no signs of the infection
portals of exit
-respiratory, salivary, mucous, sputum, nasal discharge,
-skin scales,
-fecal,
-urogenital,
-blood
prevalence
total number of existing cases with respect to the
entire population
incidence
number of new cases over a certain time period
mortality
number of deaths
morbidity
number afflicted with infectious disease (symptomatic and asymptomatic)
endemic
infectious disease that exhibits steady frequency over a long period in a particular geographic locale
sporadic
occasional cases are reported at irregular intervals in unpredictable locales
epidemic
prevalence of an endemic or sporadic disease- increasing beyond what is expected for that population
pandemic
epidemic that spreads across continents
living reservoirs
(people)
asymptomatic, incubation, covalescent, chronic, passive carriers
asymptomatic carrier
hard to find and treat
incubation carrier
will eventually develop signs and symptoms
convalescent carrier
has recovered from signs and symptoms but still capable of transmitting infection to others
chronic carrier
an individual who acts as host to pathogenic organisms for an extended period without displaying any signs of disease
passive carrier
persons who mechanically transfer a pathogen without ever being infected by it
animal reservoirs
vectors
-biological and mechanical
vector
animal that transmits microbe from one host to another
biological vector
participates in life cycle
mechanical vector
no participation in life cycle
zoonosis
indigenous to animals but transmissible to humans
non-living reservoir
fomite-
-an inanimate object i.e. pens clothes
communicable
an infected host can transmit the infectious agent to another host and establish an infection
contagious
if agent is highly transmissible
non-communicable
does not arise from transmission
horizontal transmission
disease spread through a population from one infected individual to another
vertical transmission
from parent to offspring
direct transmission
touch
indirect transmission
conveyor is used
nosocomial infection
infection acquired as a result of a hospital stay
iatrogenic
effects resulting from treatment by a physician
physical agents
heat and radiation
chemical agents
disinfectants, antibiotics and other drugs that affect microbial growth
sterilization
removal of all micro-organisms and infectious particles, including spores and viruses
bacterialcidal
destruction of vegetative forms of bacteria
bacteriostatic
prevention or slowing of bacterial reproduction and metabolism
germicide
any chemical agent that is used to kill pathogens
disinfection
a physical process used to destroy vegetative forms of pathogens
sepsis
growth of micro-organisms, and/or toxins in the blood or other sterile tissues
antiseptics
chemical agents applied directly to the body
moist heat
a variety of methodologies that range from boiling, autoclaving, pasteurization
moist heat temperature range
usually 60-135 degrees C
moist heat vs dry heat
generally considered more effective
-works faster at similar temperatures
how does moist heat function
by coagulating and denaturing proteins
-as well as secondary damage to cell membrane, ribosomes, DNA and RNA
thermal death time
the shortest period of time required to all the micro-organisms in a sample, when exposed to a specific temperature under standard conditions
autoclaving
use of pure steam under pressure
-most practical and dependable way to apply moist heat
-closed system, constant volume
-increase pressure allows for increases temperature
what can you achieve w steam under pressure
higher temperatures than those possible with non-pressurized steam or boiling water
added advantages of autoclaving
rapid heating
greater penetration
autoclave operation pressure and temp
15lb/in(squared)
at which pure steam is 121 degrees C
boiling water
100 degrees C
-kill vegetative micro-organisms
-destroy some exotoxins
-cannot guarantee sterilization
-some bacterial endospores can withstand 100 degrees for more than an hour
(not good for endotoxins or endospores)
pasteurization
developed as alternative treatment to reduce microbial contamination because temperature needed to achieve sterilization have adverse affects on many foods
flash method
71.6 degrees C
15secs
batch method
63-66 degrees C
30min
goal of pasteurization
prevent contamination by:
salmonella
cmpylobacter jejuni
listeria monocytogenes
brucella
coxiella burnetti
mycobacterium bovis
mycobacterium tuberculosis
where is pasteurization ineffective
endospores, thermophiles
i.e. lactobacilli, micrococcus, and yeasts
dry heat
variety of methods that use process of incineration
how does dry heat function
by oxidizing cells or reducing them to ash
incineration
destruction of micro-organisms by burning
drying oven
170-180 degrees
1-2 hours
-highly destructive to materials that cannot withstand high temperatures
refrigeration/freezing
-some can grow at zero degrees C
-subzero temps will inhibit metabolism of most micro-orgs
-standard freezer -20 degrees C
-will not kill them- will often preserve them
desiccation
drying stops metabolic activity
what determines length of time microbes can survive after dessication
-species
-material in or on which orgs are dried
-completeness of drying
-physical conditions involved
radiation
-ionizing
-non-ionizing
ionizing radiation
gamma rays, X-rays, and cathode rays
-atoms of cell absorb energy from radiation and eject an orbital electron(s) causing ions to form
-causing protein failure
-deep penetration
-more dangerous
wavelength range of ionizing radiation
.001-100nm
cell structure susceptibility (ionizing radiation)
-DNA most, then organelles
what does ionizing radiation allow for without heat
deep penetration
drawbacks of ionizing radiation
can change flavor and nutrient composition
ionizing radiation currently used mostly for-
drug, equipment and spice sterilization
non-ionizing radiation
excites atoms by raising them to higher energy state causing abnormal linkages within molecules such as DNA
i.e. UV
wavelength range of non-ionizing radiation
136-400nm (most 260nm)
non-ionizing radiation absorbed directly by
DNA
non-ionizing radiation penetration
shallow penetration
non-ionizing radiation drawbacks
production of toxic photochemical products
current uses of non-ionizing radiation
room disinfection and treatment of liquids
filtration
are a physical process involving porous material and suction system
-can be designed to filter all manner of bacteria but not viruses or toxins
-keys; pore size and suction
membrane filters
cellulose esters made into extremely thin disks with pores small enough to prevent the passage of microorganisms
high-efficiency particulate air filters (HEPA)
consists of a cellulose acetate disk pleated around an aluminium foil
-designed to capture 99% of all particulate matter exiting a system
phenol- mode of action
damage microbial cells- altering the normal selective permeability of the cytoplasmic membrane
-leakage of vital intracellular substances
-also denature and inactivate enzymes
-bacteriocidal or static depending on concentration
phenol aqueous solution
5%
lysol
soap solution containing phenol like compounds
hexachlorophene
bacteriostaic agent for gram positive bacteria
-prolonged usage proved to be toxic
phenol coefficient technique
gold standard to judge all else
alcohols
-poor efficiency - which increases with length of exposure
alcohol mode of action
protein denaturant
lipid solvent
alcohol types
ethyl alcohol (70-90%)
methyl alcohol
propyl and isopropyl alcohol (40-80%)
halogens mode of action
-strong oxidizing agent
-can destroy essential metabolic compounds of microorgs
-light sensitive
-iodine and chlorine
iodine mode of action
reacts with amino acid tyrosine to inactivate many enzymes and proteins
chlorine mode of action
formation of hydrochlorous acid when reacts w water
-also produces nascent oxygen (O): powerful oxidizing agent
heavy metals
-mercury, lead, zinc, silver, copper
-not used mainstream - replaced by antibiotics
-oligodynamic action
heavy metal mode of action
inactivate cellular proteins by combining w some component of the protein
detergents soaps
removal of transient flora
- not anti- any such thing
-just disrupts attachment
anionic detergents
negatively charged
cationic detergents
positively charged
nonionic detergents
do not ionize when dissolved in water
quaternary ammonium compounds
special group of cationic detergents
-related structure to ammonium chloride
-are antimicrobial
prophylaxis
a process that prevents infection or disease
narrow-spectrum
effective against a limited number of microbial types
broad-spectrum
effective against a wide variety of microbial types
(most commonly used)
microbial drug drawbacks
selection of drug resistant strains
systemic allergic reaction
drug toxicity
destruction of normal flora
PrP
protein that prions are made of
-found throughout body
-resistant to proteases
PrPc
normal form
c=cellular or common
-structurally well defined
-209 amino acids, one disulfide bond
-alpha helical structure
-not sedimentable
-binds copper ions with high affintiy
-readily digested by proteinase K
-may play important role in cell-cell adhesion and intracellular signaling
PrPsc
infectious form
sc=scrapie (from prion disease occurring in sheep)
-polydisperse-defined at a relatively poor level
-is able to convert normal to infectious form
-predominantly beta-sheet conformation
-highly amyloid fibers
major difference between normal and abnormal prion isoforms
secondary level of structure
PrPc- high alpha protein
PrPsc- beta motif
what happens with PrPsc
spongiform encephalitis
prion diseases (TSE)
transmissible spongiform encephalopathies
-family of rare progressive neurodegenerative disorders
-long incubation periods
-failure to induce inflammatory response and characteristic spongiform changes associated with neuronal loss
what do abnormal prions induce
abnormal folding of normal cellular prion proteins in the brain
-rapidly progressive and always fatal
human prion disease
-creutzfeldt-jakob (CJD), variantCJD (vCJD), -gerstmann-straussler-scheinker syndrome
-fatal familial insomnia
-kuru
animal prion diseases
-bovine spongiform encephalopathy (BSE)
-chronic wasting disease (CWD)
-scarpie
-transmissible mink encephalopathy
-feline spongiform encephalopathy
-ungulate spongiform encephalopathy
Prions
highly conserved molecule
prion mode of infection
ingestion (oral)
(NOT fecal oral)
-corneal transplant, contaminated instrument, and growth hormone
prion infection symptoms
loss of motor control, dementia, paralysis, death