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70 Cards in this Set
- Front
- Back
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Describe B. anthracis
G+/- Spores? Shape? |
G+
Spore forming Rod |
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What is the infectious dose for this organism?
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2,500 - 10,000 bact
(~8000) |
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Where does this bact usually cuase disease?
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In herbivores
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How is this transmitted?
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Animal to human if in contact with infected animal or contaminated animal products
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What is the reservoir for this bacteria?
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Soil
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Describe the life cycle of this bact
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Spores in the ground
Get ingested by cow Germination and multiplication of the bacilli Cow dies, spores released Spore is what infects the organism |
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What are factors thatinduce sporulation?
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O2
Temp Nutrients Sunlight Ca2+, H2O pH Mn2+ |
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Where do the spores go once they're ingested?
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Go to the distal alveoli (perfect size to reach there)
Once there, get engulfed by macs Goes from spore -> vegetative state and produces toxins One of these toxins (LT), is a metal protease that cleaves MAPKK Some macs go to megasomal LN and the bact get into the blood stream Can get pulmonary edema Can go to brain and kill you |
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What are the 2 toxins produced by B. anthracis?
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Edema toxin (ET)
Lethal toxin (LT) |
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What does the CHR part of the bact include?
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2 plasmids
pX01 pX02 |
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What does pX01 make?
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Edema and lethal factor
Can also cause disease in intestine (not as bad because doesn't cause infection a s fast) |
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When do flies play a role in transmission of this bacteria?
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In enzootic areas
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What are the initial symptoms of inhalation of this bacteria?
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Fever
Cough Myalgia Malaise => looks like a cold or the flu |
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What are the terminal symptoms?
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High fever, dyspnea, cyanosis
Hemorhagic mediastinitis, pleural effusion Rapid progression to shock, death ->100% mortality even with aggresive treatment |
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How do you diagnose clinical inhalation of B. anthracis?
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Immunochemical staining
B anthracis detected by PCR Rise of anti-PA IgG |
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What kind of a disease is this?
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Lung disease (not just a LN disease)
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What is a dominant radiological feature of some patients?
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Pulmonary infiltrates
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What is an important feature of the illness?
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Pleural effusion
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What does acutaneous infection result in?
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Black scar
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What is the mortality rate of cutaneous anthrax infection?
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20% if untreated
0% if treated |
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Which toxin is involved in cutaneous infection?
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Edema toxin
->Causes swelling |
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How is gastrointestinal infection caused by this baceria?
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Eat contaminated meat
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What happens in this infection?
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Same thing as in cutaneous infection
Intestinal eschar Can lead to generalized toxemia |
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How can this be treated?
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Doxycyclin
Fluroquinolone -Usually use one of these in conjunction with 1 or 2 other drugs, to make sure that the drugs go into the CSF (also don't want disease resistance) Can also use steroids -Don't use cephalosporins |
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Is quarantine required for this bacteria?
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No
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What other treatment should be given?
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Supportive care
Standard precautions (gloves etc) Early treatment improves prognosis |
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What post-exposure treatment should be given?
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Oral antibiotics: Ciprofloxacin or Doxycycline
Antibiotics for at least 100 days without vaccine Antibiotics for 40 days with 3 doses of vaccine |
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Describe the current vaccine vs B. anthracis
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FDA approved
Active component is protective Ag (PA) from an attenuated non-encapsulated strain Protective vs cutaneous and maybe inhalation anthrax -> Limited availability |
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What is the laboratory risk of B anthracis?
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Lvl 2
(but once you grow it, it should be lvl3, since the spores can go everywhere) |
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What is a lvl A lab?
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BSL-2 with class II bio saftey cabinets
Trained personnel in handling pathogenic agents Containment practices to prevent aerosol transmission |
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What general tests are used to distinguish B. anthracis?
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Phenotype (G stain)
Immunodetection: use enz assays Sequence detection: genomics |
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What are key level A tests performed on B. anthracis?
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G stain
Growth characteristics on agar Catalase + Sporulation in air Lack of motility Penicillin inhibition zone Capsule formation |
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What are the presumptive identification characteristics of B anthracis?
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Spores are oval
Non-swelling of vegetative cell Ground glass morphology |
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What is the india ink stain for?
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See if it has a capsule
-> if it does, will be a white clearance around the cell because ink can't go through |
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Is this bacteria motile?
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No
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How do you confirm if its a level B organism?
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Phage lysis and Capsule tests
OR DFA: Capsule Ag and Cell wall Ag Phage lysis important |
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What's the problem with doing a bunch of biochemical tests on bacillus?
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The species are very similar and produce similar results
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What happpens when you look at the 16S rRNA?
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B. cereus and B. anthracis have the same
And this test doesn't tell us if toxins are being produced |
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What is the test of choice?
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PCR
-> look for B. anthracis DNA -> can locate a plasmid |
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What is MLVA?
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Multi-locus variable number tandem repeat analysis
-Have 8 markers |
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What can a spore resist?
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Heat
UV and ionizing radiation Pressure Chemical agents Survive decades |
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Describe B. anthracis interaction with macrophage.
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Confocal mic
Phagolysosome Express toxin genes gerX on pX01 ->Delete gerX, get reduced virulence in mice 5 loci other than GerXA/B/C encoding germination-like ptns on chr -Germination loci |
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What factors are involved in the 2 toxins?
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Lethal toxins: PA + LF
Edema toxins: PA + EF |
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What is PA?
EF? LF? |
PA: protective Ag, cell binding domain
EF: edema factor, enz LF: lethal factor, enz |
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What is this toxin "trinity" required for?
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Germination and survival in macrophages
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What kind of toxins are the anthrax toxins?
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Binary toxins
Effector + transporter |
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What does PA alone cause?
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Immunity in guinea pig
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Can EF or LF on its own, without PA, cause disease?
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No, can't cuase either edma or lethality
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What is the result of EF + PA?
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Edema in skin of rabbit
Some immunity in pig |
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What is the result of LF + PA?
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Lethality in mice
some immunity in guinea pig |
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What happens when EF + LF are combined together?
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Can't get into the cell because there isn't any PA
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What happens when EF + LF +PA are combined?
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Increased lethality
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What is the structural organization of PA, LF and EF?
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PA has ATR-Type 1: mb ptn that binds to EF and LF
ATR: mb ptn with ectracellular von Willebrand factor A domain |
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What happens if a soluble receptor for the toxins is added to the culture?
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Get decreased amount of toxin in the cell
.: cell is better protected |
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What is the cellular model of action of anthrax toxins?
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83 unit PA attached
Furin-like enz cleave off 20 units -> PA63 (can be soluble) PA63 becomes a heptamer tht can attach a total of 3 units (3EFs or 3 LFs or 1EF, 2 LFs etc) At lower pH, form pore and toxins leave |
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What does EF affect?
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ATF, cAMP is blocked through blockage of calmodulin
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What does LF affect?
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methylo enz proteases
Affects MAPKK, get death etc |
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What happens if inhibitors of endosomal acidification are added?
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Prevent cytotoxicity
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What happens if PA is blocked with Anti-PA antibodies?
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No disease
Protection vs anthrax toxin PA fcts as an adjuvant for LF Ab response |
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What are the targets of anthrax toxins?
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All MAPKK (Meks1-7) except Mek5
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What is involved in the action of anthrax toxins?
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can have apoptotic factors
Affect many cytokines Ltx1: mouse mac resist LT NF-kB: TF regulating Immune Response |
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What ptn does edema factor need?
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Calmodulin
-> Principal mediator of Ca2+ signalling -> involved in gene T, ion conductivities, vesicular fusion and cytoskeleton fcts |
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What does EF-CaM do?
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Inhibits Ca2+ binding and CaM fct (ex: cAMP ATP)
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What is most importnat to the virulence of anthrax?
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Plasmids
-> required to make toxins Without them, no disease |
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What is important to plasmid virulence?
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Temperature
Bicarbonate influences of capsule formation AtxA: major regulator |
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What does pX02 encode?
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Capsule
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What happens if no pX02?
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Bacteria exist without a capsule
Can cause disease in lung, but cannot disseminate everywhere |
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Is there a lot of spotaneous loss of pX01?
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No
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What does AtxA do?
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Regulates capsule synthesis/degradation and germination
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What do the plasmids encompass?
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Pathogenicity island that can transpose
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