导图社区 how pathogens pass through one
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how pathogens pass through one
这是一篇关于how pathogens pass through one的思维导图，主要内容有Quantification、some check points、Pathogens just give up?。
编辑于2022-06-11 15:43:06- pathogens
- Virulence
- Pathogeni…
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how pathogens pass through one to others?
Quantification
Pathogenicity
The ability of a pathogen to produce a disease by overcoming the defenses of the host.
ID 50
infectious dose required to cause disease in 50% of inoculated test animals
ex.
10^8 cells for Vibrio cholerea
5,000 to 10,000 spores for Inhalation Anthrax
Virulence
The degree of pathogenicity
LD 50
Lethal Dose of a microbes toxin that will kill 50% of experimentally inoculated test animal
ex.
Subtopic
some check points
transmittion
vehicals
foodbone
food that is usually incompletely cooked, poorly refrigerated, or prepared under unsanitary conditions
Cooking
cross contamination
inadequate heating
Storage
animal vectors
2 types of foodbone diseases
Food-bone infection
Bacteria
Usually entero bacteria
Salmonella typhi
Typhoid fever
Salmonella paratyphi
Paratyphoid fever
cholera
dehydration
E. coli
4 serotypes
antigens
O-somatic antigens
H-flaggela antigens
Enteropathogenic E. coli (EPEC)
O157:H7
Heat sensitive, freeze resistant
Bovine reservoir
inadequately cooked hamburger meat, raw milk, cream and cheeses made from raw milk.
low infectious dose<100cells
Enterotoxigenic E. Coli (ETEC)
Enterohemorrhagic E. coli (EHEC)
O157:H7
Shiga-like toxins (SLT) provoke cell secretion and kill colonic epithelial cells.
Enteroinvasive E. coli (EIEC)
Campylobacter
Low infective dose 500 cells
kill below 25℃， grow best under 45℃
poultry intestine
Yersina enterocolita
in pork
maybe waterborne
survive and grow during refrigerated storage
resistance to complement and phagocytosis
all may induced by fecel contamination
Virus
Helmins
features
incubation period: hours to days
inadequate cooking, cross contamination , poor personal hygiene , bare hand contact.
may further comunication
only infection has fever(gram-)
Food-bone intoxications
Toxic synthetic chemicals
Natural food toxins
Bacterial toxins
Staphylococcus aureus enterotoxin
Staphylococcus grow at 12-44oC (optimum 37oC); pH: 4.0-9.83 (optimum 7.4-7.6),18% NaCl
found in varying numbers in air, dust, water, food, feces and sewage.
found in the nose, skin, saliva, intestinal contents and in feces
poor competitor
Common feature of toxin
Heat stable
PH stable
irradiation stable
Proteolysis stable
Vehicle foods:
milk, food, egg
disease
1-6 hrs after consumption and duration of illness is 24-72 hrs..
nausea, headache, vomiting and diarrhea
infectious dose: 1 micro Gram
detection
probing
nestcal PCR
Bacillus cereus
Clostridium botulinum
Heat shock (cooking) leads to spore germination, and then refragerate leads to vegiterian growth
gram + releases exotoxin
Very toxic
likely to grow in food with out air
spores very heat resistence
direct toxin igestion
Clostridium perfringens
Toxin released in guts after ingestion of cells
Fungal toxins
features
incubation period: minutes to hours
inadequate cooking , improper handling temperatures
no fever
waterbone
water contaminated usually with untreated or poorly treated sewage
airbone
transmission via small droplets that travel more than 1 meter from reservoir to host
droplets
moisure particle
dust particle
contact
direct
physical contact between microorganisms source(the host) and susceptible host
like you touch/eat a shit
indirect
when microorganism transmitted from reservoir to susceptible host by means of nonliving object
but their effective distance is too close, and less that common like food so can't be vehicals
big droplets
microorganisms spread by droplets that travel only short distance
different from airbone
sneeze
needles & other nonliving object
animal vectors
Arthropods
passive
on insects feet or other body parts
active
enter
attachment
most bacterias colonise mucosal surfaces (adhere, compete for nutrients, multiply)
adhesin
one of the 3 virulence factors
The number and adherece ability determine the number of tissue entry
Entry
parallel potals
Respiratory Tract
nose, mouse, lungs
airbone difussion
path respiratory tract
ex. pneumonia
some times path also digestive tract
ex. tuberculosis
really "born" in air?
bone means one pathogen can pass through that media
ex.
measles
e.x.
Flu/Tuberculosis/Pneumonia Measles/Strep Throat Diphtheria
Gastrointestingal Tract
throat, stomach, intestine
water&food
path digestive tract
ex. hepatisis A
they may infected by another host used to eat/ drink them
defense system
mucus
HCl, enzymes in stomoch
Bile, enzymes in small intestine
e.x.
Salmonellosis (Salmonella sp); Shigellosis(Shigella sp); Cholera (Vibrio cholorea); Ulcers(Helicobacter pylori); Botulism (Clostridium botulinum)
Urogenital tract
misplace oppotunistic pathogens
Mucous Membranes
nose,eyes, etc
direct contacts
Influenza virus
Then you may inhale it, any way it's air bone, and path through respiratory tract
Skin Penetration
into blood
bites, cuts, injection
living animals
mosquito bite
malaria protozoa
direct into blood
through host body fluids
classicle HIV
violate sexual behaviors
blood transfaction
any way, once lot viruses get in your blood, then you are done
tough natural opening: hair follicles and sweat glands
vertical-parental route
deposited directly into tissues beneath the skin or mucous membranes
Specific
microorganisms can cause infections only when they gain access through their specific portal of entry.
Damage
impedin
Function
resist host defence
one of the 3 virulence factors
specific subdivision
Capsules
Cell wall components
Enzymes
Cytoskeleton
toxin
one of the 3 virulence factors
specific subdivisions
endotoxin
exotoxin
Other Damage methods
Direct Damage
Hypersensitivity
exit
generally same as the parallel portals
Pathogens just give up?
Never: they evolve faster
They damage host faster
They prevent host immune synstem
against phagocytosis
capsules
against T cells
superantigens
against antibodies
Antigenic variations
alter surface antigen
virulence factors
adhesin(adhesion)
Structure
ex.–Glycocalyx: Streptococcus mutans –Fimbriae (pili): Escherichia coli –M protein: Streptococcus pyogenes –Opa protein: Neisseria gonorrhoeae –Tapered end: Treponema pallidum
most are cell wall/ capsule components, some times pili
Capsule
–Streptococcus pneumoniae –Klebsiella pneumonia –Baillus anthracis –Yersinia pestis
function
Adhesin function as a ligand and binds to tissue cell surface receptor
impedin(evasion)
Structures
Capsule
Loose network of polysaccharide anchored to outer membrane or cell wall
not essential to normal growth
Each capsule contains only one type of polysaccharide comprising repeating oligosaccharide units joined by glycosidic linkages
Immune evation methods
Use negative charge surface repels phagocytes
use structures similar to host – e.g. sialic acid
Inhibit opsonization, poor activators of complement
But still weak immune generate
shedding removes bound antibodies and complement/oposonin
Cell wall components
M proteins on cell surface and fimbriae of Streptococcus progenes.
Mediates attachment and helps resist phagocytosis.
Waxes on Mycobacterium tuberculosis
helps resist digestion after phagocytosis.
Enzymes
most release trigured by adhesion
ex
Leukocidins
Destroy certain WBCs
destroy phagocytes by inserting porin
reptures of lysosymes cause more tissue damages
exotoxin
Staphylococci and Streptococci
Hemolysins
Lyse RBC by porin inserted
isn't this virulence...?
yes exotoxin
C. perfringens, Staphylococci, Streptococci
coagulase
forms fabrin clot protects pathogens
blocks phagocytes and other immune attacks
Staphylococci
Kinases
Destroy blood clot
Those clots are produced by body to isolate infection.
helps bacteria spread
S. pyogenes, S. aureus
Hyaluronidase
Breaks down hyaluronic acid
which holds cells together in connective tissue
let pathogens infect deeper tissues
part of tight junctions?
some streptococci, gangrene causing clostridia
Collagenase
similar to breaks down collagen in connective tissues
Necrotizing Factor
Cause tissue cell necrosis
Necrotizing fasciitis/ flesh eating bacteria
Complement C5a inhibition
S. aureus CHIPS protein
inhibits activated complement C5a protein through binding to C5aR
at least inhibited neutrophile chemotaxis observed
IgG fcγ binding
S. aureus Protein A
released from cell wall
Results
form immune aggregates
consume complement
limits IgG opsonization
Reduce phagocytes phagocytosis
IgA hinge region cleavage
convergent evolution
Different species with different proteases all target IgA hinge region
proteolytic sites are differrent
Non-pathogenic relatives lack these proteases
results
we don't know why, it dramatic inhibits the mucus defence
Antigen variation
Some bacteria change surface antigens with time
Super antigen
first binds to the MHC Class II and then coordinate to the variable alpha or TCR beta chain ex.SAg+
Leads to massive clonal expanssion of CD4+ cells~~~~
poly clonal expansion
non specific to any epitopes on SAg.。。
activates 83% of the body’s T-cells
Massive cytokines IFN-gamma/-alpha/IL-1/IL-6 released
deadly
Fever, nausea, vomiting, diarrhea, shock, and death
Sometimes direct activates TCR with out link to MHC-II
ex. SAg+
exist in wide range of microbes
viruses, mycoplasma, and bacteria exotoxin
toxin
exotoxin
identity
Proteins for Gram+(mostly) bacteria grows and metabolism
secreted continously
also may released when cell lysis
can be neutrolized by antibodies
called Antitoxin
toxicity
effects
Cytotoxins
Kill cells
Destroying Particular Parts of the Hosts Cell or by Inhibiting Metabolic Functions
ex. Ulcer
Enterotoxins
damage surface cells of G.I tract, and induce fluid and electrolites loss
IBD
ex. Cholera toxin
enterotoxin Converts ATP into cAMP
causes cells to excrete Cl- ions and inhibits absorption of Na+ ions
severe dehydration~ 10-20L loss in one day。。。。
natural motality 50%
E. coli (0157:H7): Heat-stable enterotoxins (ST)-withstand heat treatment at 100 °C.
alters the host cell 60S ribosomal subunit and inhibits protein synthesis
causes a hemolytic inflammation of the intestines
bloody diarrhea
Neurotoxins
inhibits/prevents nerve impulses
e.x. tetnus
Clostridium botulinum
neurotoxin acts on neuromuscular junction and inhibits muscle relaxation
Molecular
host plasma membrane disruption
inserts porins on host
leukocidins, hemolysins
Disrupting phospholipid bilayer.
cause cell lysis
intracellular A-B toxin
A for active domain, B for binding domain
Binding domain binds to host surface receptor, and trigger receptor mediated endocytosis
In cytoplasma, A and B domains are seperated
A domain inhibits host protein synthesis
toxicity
B domain is released from host cell
A-B
One A binds to one B
Tetanus, Botulinum, Diphtheria
A-B5
One A binds to 5 Bs
Cholera, Shiga
Super antigen
Very toxic with very small LD50
most encode on plasmids or phages
exotoxins are less heat resistence
endotoxin
identify
Outer structural lipids of Gram- bacteria cell walls
because cell wall only breaks when bacteria die
septicaemia
so endotoxin ONLY released When bacteria die
tricky...endotoxin actually locate out side, but exotoxin resides inside
ex. LPS
Toxic portion
Lipid A
Pathogenicity
Activates complement
Triggers coagulation
PAMP recognized by macrophages' TLRs
Releases IL-1
Cause fever
Releases Tumour Necrosis Factor
Damage blood vessels
Causes septic shock
targets of antibiotics
Antigen portion
Can cause fever
with relatively big LD50
Some endotoxins are very heat resistence
statistics
primary virulence factors
220 toxin known
40% damaging host plasma membrane
tricky terms
Antitoxin
antibodies against only exotoxin
Toxoid(Vaccine)
Vaccine can be made by inactivated exotoxin
heat, formalin or phenol
Toxigenicity
Ability to produce toxin
Toxemia
Presence of toxin in the host's blood.
Other damaging perspectives
Direct
Cell lysis
ex. viral productive infection