Module 10 Flashcards
Host microbe interactions
Commensal
host provides shelter/environment for bacteria (benefit bacteria)
Mutualistic
mutual benefit
Pathogenic
damages host
microbiome
functional collection of different microbes in a system
microbiota
community of microorganisms present in a habitat
Metagenomic
genetic material in a given environment
colonization
microbes present and grow on non sterile external body surface
basic steps to infection
enters body sites, overgrows, induces immune response
disease
damages caused by infection
normal microbiota
total microbial population associated with a human
mainly bacteria
10^13 human cells + 10^14 bacteria cells
different classes of microbes and explain
transient: short term, highly variable, high external influence
resident: long term, stable, limited external influence
functions of micrbiota
digest nutrients
provide nutrition
educate/prime host defenses
colonization resistance
how is microbiota esablished
at birth by feeding
how is microbiota unstabilized
hormone fluctuations during puberty
factors in microbiota development
drivers(host and microbiota)
microbe-microbe interactions
habitat filtering
skin microbiome (3)
low diversity (dry and salty)
transient populations on surfaces, resident in pores
mostly commensal, some mutualistic
respiratory tract microbiome (4)
site specific composition
oral cavity: biofilm communities
nasal and upper: similar to skin/mouth
lower: few transient
genito-urinary microbiome
urine is sterile, first 1cm of urethra has transient
vaginal has non specific defenses, acidic
intentional microbiota alteration
fecal transplant
probiotics
prophylactic antibiotics
antispetics
intestinal microbiome
highest populations and great diversity
mutualistic
composition impacted by diet
unintentional microbiota alteration
dysbiosis from antibiotic use
FMT cure rate and use
60-90% cure rate
only used to combat recurring C diff
works by creating competition not wiping out
probiotic
living microorganisms for competitive exclusion
prebiotics
nutrients to help out microbes
symbiotics
mix of pre and probiotics
original koch postualte
suspect causative agent not in healthy
suspect must be isolated, grown, and put into organism to test
issues with koch postulate original
not designed for virus
does not account for asymptomatic carriers
no longer ethical to deliberately infect
pathogenicity
ability to cause disease
virulence
degree of pathogenicity
ID50
infectious dose
LD50
lethal dose
periods of disease
incubation
prodromal (general signs)
illness (severe symptoms)
decline
convalesence
stages of pathogenicity (list)
exposure
adhesion
invasion
disease
transmission
exposure
mode of transmission varies with portal of entry
adhesion
capability of microbe to attach to cell
works with adhesins that bind to certain receptors on host and form biofilm
bacteria adhesins
fibrae, capsules
protozoa adhesin
cilia
virus adhesins
capsid
spike proteins
invasion
dissemination in local tissue using exoenzymes and toxins
disease
successful multiplication
local disease
small near entry port
focal disease
spread to secondary location
systemic disease
disseminated, lesions not at site of entry)
transmission
required for success
molecular koch posulates
-gene is pathogenic members of species
-inactivating/deleting gene decreases virulence
-reversion or allelic replacement can bring back pathogenicity
how do pathogens damage
inject effectors and reprogram cell
enzymes distryo/affect tissue integrity
produce toxins
exoenzymes
act as spreading (invading) factors
intoxication
ingest toxin, rapid (1-12hrs)
infection
bacteria, delayed (12-72hrs)
endotoxins
part of bacterial structure
released by lysis
exotoxins
secreted proteins
type 1 toxin
target cell surface, superantigens
type 2 toxin
target euk cell membrane, pore forming
type 3 toxin
AB type toxin
how do superantigens cause damage
entering blood stream, forming cytokine storm,
what are membrane disrupting toxins, how do they work
kill host cells (phagocytes) and escape phagosome
1. form channel/pore, water rushes in lysing cell
2. attack phospholipids cleaving head
functional subunits of AB toxin
A subunit-toxic enzymatic activity
B subunit- bind to receptor carries A
single peptide AB toxin
gram positive
multiple peptide AB toxin
gram negative
ADP ribosyltransferase
targets NAD+
genotoxin
targets host DNA
deaminases
target rRNA
botulism toxin
flaccid paralysis
stops muscle contration
tetanus toxin
uncontrollable contraction
spastic paralysis
options for pathogen invasion
camouflage
disguise
resistance
camouflage
coating surface with host proteins, host mimicry
disguises
change structures on cell surface
antigenic variation, phase variation, epigenetic variation, LPS modification
resistance
vary LPS length (longer is harder for host to attack)
capsule
surface enzymes
influenzavirus (disease, adhesin, attachment site)
influenza
hemagglutinin
sialic acid of respiratory and intestinal cells
herpes simplex virus 1 or 2 (disease, adhesin, attachment site)
oral/genital herpes
glycoprotein: gB, gC, gD
heparan sulfate on mouth/genital mucosal cells
human immunodeficiency virus (disease, adhesin, attachment site)
HIV/AIDS
glycoprotein: gp120
CD4, CCR5 of immune system cells
mycotoxicoses
poisoning due to consumption of fungal metabolic product
cutaneous mycoses
fungal infection on outermost layers
spreads through direct contact
subcutaneous mycoses
fungal infection of skin and SQ tissues
affects pre existing wounds
systemic mycoses
fungal infection of internal organs
start airborne and spread
very severe to fatal
