host-microbe interactions Flashcards
types of interactions
mutualism, commensalism, competition, parasitism, pathogenesis
commensal vs synergism vs mutualism
commensal = 0/+
syn: +/+ - protocooperation
mutualism (symbiosis) +/+
competition
amensalism
predation
parasitism
c: -/-
a 0+/-
p +/-
p +/-
rumen microbiology - mutualism in cows.
rumen is 1 part of cow stomach.
ton of bacteria in there - fermentation. lots of methane release
what is endosymbiosis
1 guy lives in the other. both act as 1 - benefit
human-microbe interactions
-application of ecological principles
many interactions btw human + normal microbial flora.
- human body is diverse enviro for microbes. usually benign
Normal human flora
microorganisms living on body surfaces of healthy individuals
- 10^3 bacteria + archaea in average adult
- most in gut, some on skin, mouth, resp tract, urogenital tract.
- normal are opportunistic pathogens
bacteria associated with mucous membranes
- frequent sites of infection bc favourable for bacterial growth.
bacteria can grow - close access to epithelial resources. invade = infect
mouth microbes - adhere to?
adhere to gums + teeth
- > not removed by brushing. acidify = plaque, cavities, gingivitis, periodontal disease
- mouth covered in microorganisms from surrounding enviro within hours following birth
how bacteria bind to tooth?
attach to glycoprotein deposited by saliva.
- oral microbes continue to grow = thick bacterial layer AKA dental plaque. hard, strong biofilm. if thick enough = anaerobic - fermentation = degrade teeth
GI tract microbes
stomach: high acidity kills most microbes.
- some survive if pass thru quick, or in food particles.
- H.pylori is exception.
- small intestine: few organisms
- large intestine: larges microbial popln in body (10^13 -10^14)
large intestine - elimination, replaced, metabolism?
eliminated by peristalsis, desquamation + movement of mucus
- replaced rapidly due to quick doubling times (similar to continuos culture
- most are anaerobes
name few large intestine bacteria
streptococcus, enterococcus, escherichia, lactobacillus,
methanobrevibacter
what things do large intesince bacteria do?
vitamin synthesis gas production odour production organic acid production glycosidase reactions steroid metabolism
H.pylori
- characteristics + functions
flagella - motile, chemotaxic
urease- neutralize gastric acid
lipopolysaccharides - adhere to host cell
-type 4 secretion system: like pillus= changes in host , virulence factor kills host cell.
H.pylori - how to get ulcers? then + now
past: stress caused. take antacid to healh
now: H.pylori infection = ulcer. inflammation, could be painful, perofation, bleeding etc.
bacteroides thetaiontaomicron
colonizes exfoliated host cells, food particles + sloughed mucus.
- attach or eliminated
- adhere to particles in gut, not gut itself.
- degrades complex carbs along with methanogens
microbe diversity in body
areas we though were sterile are not.
ex: brain, stomach, skin, repro system..
- aura of bacteria match microbial fingerprint.
bacteria make habitat in warm, dark , wet enviros
biodiversity + functional genomics in human microbiome - stage of life
young - low microbiome diversity
mddle age = greatest diversity in gut.
old - lower diversity = more infection
human microbiome project
generally found microbiome is stable over time.
- more diverse microbiome = healthier you are.
- diff area of body - diff microbiomes, but same area of body across popln is v simiar microbiome
babies birth - c-section vs vaginal
diff microbiome. bc diff inoculation of bacteria.
same w formula vs bottle fed
dysbiosis
imbalance in microbiome
theory of dysbiosis linked w disease
distinct pattern due to habitat, live w animals? diet, health.
- microbes evolve with us.
need to know what homeostasis is for individual to know what dysbiosis looks like
rebiosis
return of microbial community ecology to “normal”
- infant anitbiotic in 1st year = may affect health long term
dysbiosis linked to disease
bowel disorders, crohns, obesity, celiac, allergies, autism, depression, parkinsons
pathogenicity
ability of organism to produce pathological change or disease that impars host function
- disease-producing, parasite, opportunistic
define virulence
quantitative measure of pathogenicity
define infection
any situation in which organism is established + growing.
- doesnt have to be pathogenic
attenuation
decrease or loss of virulence
toxicity
ability of organism to cause disease through making toxin that inhibit host cell function/kills host cells
= toxins can travel
invasinveness
ability of pathogen to grow in host tissue at densities that inhibit host function
- damage without toxin
steps to pathogenic life cycle
- exposure
- adherence to skin/mucosa
- invasion through epithelium
- colonizaiton + growth => back to 1 or
- toxicity, invasiveness
- tissue damage, disease
adherence of pathogen
needed to gain access to host tissue - attach to epithelial cell.
-direct attachement: to surface cell/host
indirect attachment: capsule attaches to host
four factors involved in adherence to host cells
- capsule/slime layer
- adherence proteins
- lipoteichoic acid
- fimbriae (pili)
invasion
starts at site of adherence.
- spread through circulatory, lymphatic systems
= availability of nutrients important in affecting pathogen growth.
- pathogens grow locally at invasion or spread throughout body
measure virulence
LD50 - lethal dose that kills 50% of animals in test group
- lower number? more virulent
high virulence + # of cells for LD100
small range. hgihly virulent, kill in small quantities
enzyme virulence factors
- enhance virulence by breaking down/altering host tissue to provide accessto nutrient
= hyaluronidase breaks down hyaluronic acid that glues animal cells together
-protect pathogen by interfering w normal host defense mechanisms
= coagulase breaks down collagen netwrok
virulence factors in bacteriophage
erythrogenic toxin, shiga-like toxin, enterotoxins, neurotoxins ,diphtheria toxin
plasmin virulence factors
enterotoxins, hemolysin, urease, edema factor, coagulase, fibrinolysin
transposon virulence factors
enterotoxin
shiga toxin
cholera toxin
salmonella virulence factors
o antigen = inhibits phagocyte killing in LPS layer of g(-) CW
endotoxin in LPS layer = fever
enterotoxin = diarrhea (symptom) - effect small intestine
siderophores = pick up Fe to aid growth
type 1 fimbriae = adherence
exotoxins + 3 categories
proteins released from pathogenic organism as it grows
- cytolytic toxin
- AB toxin
- superantigen toxin
cytolitic toxins work
by degrading cytoplasmic membrane integrity
- host cell lysis + death
- hemolysins too.
cytolytic toxin ex:
staphylococcal a-toxin
form mutlimer in PM = pore.
what is AB toxin do?
A + B units.
B binds to host cell receptor
A transfers damaging agent to host
ex of AB toxin
diphtheria toxin
- catalyze ADP-ribosylation of elongation factor 2 + prevent aa transfer to grwoing peptide chain in ribosome
ex of botulinum toxin
blocks release of aCh to muscle tissue = permanent relaxed state
superantigen toxins
stimulate large numbers of immune cells
- result in extensive inflammation + tissue damage = cells gorw elsewhere cause not viable there
endotoxins
lipopolysaccharide portion of CW of certain g(-) bacteria. toxin when solubilized.
- less toxic than exotoxins.
- only when cells are present
innate resistance to infection
nonspecfic barriers prevent colonizationof host by most pathogens
- lack of defenses = more susceptible to infection + colonization
risk factors for infection
compromised host: 1+ resistance mechanisms inactive = infection increases (AIDs, pregnant)
age: young + old more susceptible
stress: decrease immune function due to cortisol
diet + lifestyle affect microbiome
genetic condition
specific (adaptive) immunity
complex, mutli-path systems
- innate immunity
- t-cell immunity
- antibody-mediated immunity
- organism recognized, person is immune . immune memory is specific
immunization - vaccination
inoculation with attenuated/killed pathogen or chemically modified exotoxin
immune system response
recognize specific antigens - develops antibodies against.
- flu/antigens can mutate = need new flu vaccine yearly
herd immunity
when 90% or more of popln have immunization/vaccine against - infection cant pass easily. non-immune not as susceptible.
transmission mechanisms
person-to-person zoonotic + vectorborne soilborne waterborne foodborne
types of person-to-person transmission
airborne
direct contact
sexually transmitted
diff vtw zoonotic + vectorborne
zoo: animals.
vector = insect usually. animals can be vectors tho too
airborne pathogens
smaller particles, stay in air longer. more dangerous bc aerosolized
seasonal flu - kind of virus? characteristics?
RNA virus. ss, negative sense, helical RNA
- surrounded by envelope - protein + lipid bilayer + glycoproteins
- DNA on 8 segments = high reassortment between strains
antigenic shift vs drift
shift: unique reassortments
drift: minor mutations in envelope genes (cell recognies this slow change)
endemic, epidemic, pandemic - timig?
en: annual
epidemic: 2-3 years (large regions)
pandemic - 10-14 years (widespread infection
why were so many killed in 1918 flu pandemic?
secondary bacterial pneumonia
- new virus occurred at time
H1N1
combo of human avian.
- reassorted in swine.
- majority of infections are mild or have no symptoms
who does H1N1 tend to afffect?
younger, healthier ppl. more from H1N1 than seasonal flu
- may be penetrate deeper into lungs?
infection + fatality rate or seasonal flu vs H1N1
more ppl infected with seasonal flu. but proportionally, 1% ppl died from H1N1, less than 01% died from seasonal flu
HIV AIDS - what is it?
HIV: virus infects immune system cells
= macrophage + t-cells.
= CD4 surface protein
leads to AIDS (immune deficiency)
- death due to secondary opportunistic infections.
secondary opportunistic infections assoc w HIV/AIDs
kaposi’s sarcoma = co-infection of herpes + HIV = specific cancer
penumocystic carnii pneumonia
tuberculosis
gastorintestinal and neurological infections
HIV/AIDs disease progression
- RNA retrovirus. copies itself + makes RNA. makes cDNA and inserted into genome.
= slowly replicates.
= need protease to inhibit progression of disease.
symptom free: normal range or t-cells.
swollen lymph nodes = increase in t-cells
subclinical immune function - severe t-cell depletion.
opportunistic infections and systemic immune deficiency = lots of HIV RNA copies, few t-cells
Malaria
parasitic infection - deadly, transmitted by insect vector.
sporozite is most infectious.
- grows in liver of human, infects RBC - parastie grows + lyses cell = anemia.
