VL19: Bioweapons Flashcards
Describe the infection cycles of Bacillus anthracis and Yersinia pestis
B. anthracis:
- cattle are host
- inhale spores while grazing
- spores germinate
- bacteria kill host
- humans can be exposed to spores from environment, animal products
Yersinia pestis:
- rodents are host
- fleas are vector
- always cycles between host and vector without staying in environment
- usually infection through vite from flea, contact with infected rodent or other host
What disease is caused by yersinia pestis
bubonic plague
Describe 3 ways how the yersiniae infection can occur + what the disease looks like under these circumstances
- bite from flea: årpöoferates in lymph nodes
- if flea insert Y.pestis directly into blood stream, septicemic infection
- Respiratory most deadly, death in 24 h (if not treated), can be trasmitted through respiratory droplets (possibly artifically generated aerosols=
Is the pest still a thing?
yes
deadly, treatable, still with us
How did yersinia evolve?
HGTm (virulence plasmid pYV),
the different pathogenic strains all evolved via HGT
Describe bacillus, which species are harmles and harmful, what is the difference
B.subtilis well studied, extremley harmless, model bacterium
B.anthracis, Bereus cause disease, B thuringiensisd
common structures: endospores, d
Describe bacillus cereus
soil bacterium
colonize invertebrate guts as symbiont
cause of food poisoning (emetic toxin, enterotoxin)
other virulence factors: phospholipases, hemolysins, proteases
What is interesting about bacillus turingiensis
commonly as biopesticide
produces parasporal crystals made up of indescticidal toxins (cry and Cyt, located on plasmid)
basic info about B. antrhacis
-sporulating, gram positive
-
Describe the B.anthtracis life style
- short replication phases of 20-40 generations, requires infection of host, usually causes death
- interrupted by long dormant phases as spores in the environment
- genome is highly homogenous
- virulence gene on 2 plasmids: pXO1 pXO2, both plasmids required to cause anthrax
Give some information about the origin and geography of B.anthracis
recently emerged (13,000-26,000 years ago)
cluster A strain (associated wirh wool production) found all over world (trade)
origin due to pXO1 and pXO2
less than one generation per year ->slow mutation rate
How is B anthracis different from other bacilli? + 4 properties
- pXO1 carries the toxin genes and pXO2 encodes capsule, essentialfor toxicity
- inactivity of PlcR regulon, controls transcription of secreted virulence factors in B.cereus, B.thuringiensis
- non-motile, non-hemolytic, negative for phospholipase C sensitive to gamma phage (due to PlcR inactivation)
Describe the PlcR-PapR QS system
- PlcR is transcriptional regulator
- PlcR is functional protein in B-cereus, B-thuringiensis, but not in B.anthracis
- plcR is part of 2 gene operon with papR, which encodes small QS protein (exported via Sec, reimported as heptapeptide
- PlcR-PapR=activates genes by binding to PlcR-box upstream of genes
- B.cereus has 28 functional PlcR-boxes, controls at least 45 genes, many virulence factors
What do pXO1 and pXO2 do?
pXO1: encodes anthrax toxin components on pathogenicity island
-PA, protective antigen (adhesive subunit of the 2 toxins)
-LF. lethal factor
-EF, edema factor
+transcriptional activator AtxA
+repressor PagR
pXO2: carries capBCADE for capsule + its transcriptional regulators, allows survival in macrophages
capsule is also regulated by AtxA from pXO1
AtxA is global transcription regulator, important for virulence
PA binds to host cell, is cleaved, then either LF or EF bind to PA -> internalization (endocytosis), complexes dissolve LF, EF cause toxicity
EF: increase in cAMP -> affects signaling pathway
LF: release of pro-inflammatory cytokines, cleavage of MAPKK -> apoptosis
How is B anthracis diagnosed?
WHO recommends plasmid ID
