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Host Pathogenesis 1&2
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- 11) What are normal flora? 2) What is virulence? 3) What is the difference between primary pathogens and opportunistic pathogens?1) Microorganisms that have a commensal relationship with humans, and provide beneficial functions.
2) virulence is the quantitative measure of the pathogenicity of a particular microbe.
3) Primary pathogens are those that invade and colonise a new host (normal immune system); opportunistic pathogens take advantage of the an already compromised host. - 2Give a brief overview of the steps resulting in a pathogenic infection by a microbe.1) Exposure
2) Adhesion (through skin or mucous)
3) Invasion (through epithelial cells)
4) Colonisation (systematic -- circulatory system)
5) toxicity -- toxin effects are local/invasiveness -- pathogen spreads to other organs systems relative to primary site of infection. - 3Name the three adherence surface molecules.1) Fimbriae
2) Pillus
3) Glycocalyx - 4Describe three characteristics each of the following surface adherence proteins. 1) Fimbriae 2) Pillus 3) Glycocaylx1) Fimbriae -- i) structurally related to pillus, not involved in motility. ii) binds host glycoproteins for adherence
iii) many in number
2) Pillus -- i) longer, fewer in number
ii) binds host glycoproteins for adherence.
3) Glycocalyx -- i) secretes gooey substances on the cell for adherence.
ii) has anti-phagocytic potential - 5Can microorganisms uses multiple systems of adherence or only 1? Give an example of one such microorganism.Microorganisms can use multiple systems of adherence.
Example: Gonorreiha has Opa protein which binds to CD6 receptors. or use pillus. - 6Explain the difference in how Strep Kinase vs. Coagulase help microbes in the invasion of host cells.Strep Kinase digest fibrin clots because they resist microbial growth.
Coagulase on the other hand builds clots on the site of entry to protect itself from the host defence mechanism. - 7Name two host proteins that limit Fe levels to prevent microbial growth1) transferrin and lactoferrin
- 8What is the meaning of 'attenuation of virus' ?'attenuation means that the virus has been passaged so many times that it has accumulated mutations over time, and has now adapted to new environment. It will now be non-infectious in its original environment.
- 91) What is the meaning of LD50? 2) What is the difference between toxicity and invasiveness?1) LD 50 is the dose at which 50% of the test group population is killed.
2) Toxicity is the ability of the microbe to cause a disease within the host
Invasiveness is the ability of the organism to multiply in the host. - 10List three of Koch's Molecular Postulates.1) The pathogenic phenotype in consideration should be associated with a pathogenic member of the genus or pathogenic strain of a species.
2) inactivation of the specific pathogenic gene should result in a considerable loss of virulence in appropriate model system.
3) complementation of mutation either via plasmid or allelic replacement of mutated gene should result in restoration of pathogenicity. - 11Give three characteristic features of Endotoxins.1) Endotoxins are toxic structural components.
2) Exhibited as LPS on gram - bacteria
3) Released in large quantities when the cell is lysed.
4) presence tested by limulus assay - 12i) What are exotoxins? ii) What are the two kinds of exotoxins?i) exotoxins are released extracellularly as the organism grows.
ii) two kinds -- cytolytic (enzymes that attack cell components during lysis) and A-B exotoxins (consists of two subunits; A - active, B - binding). - 13Describe the mechanism employed by the A-B toxin in Diptheria.1) Toxin enters the cell, B subunit binds to cytoplasmic membrane and shuttles the A subunit across the membrane.
2) A subunit then inhibits cellular translation by ribosylating eiF2.
3) toxin is carried by the B phage
4) bacterial gene encodes for the repressor of the Tox gene, in addition to iron co-repressor. - 14Describe the A-B subunit in Botulinum vs. Tetanus.In Botulinum, the B subunit binds to receptors on pre-synaptic membrane of motor neuron.
2) A subunit blocks the release of acetylcholine; muscles fail to contract and patients die of respiratory fever.
In Tetanus, B subunit binds to inhibitory interneurons; A subunit internalises, and blocks the release of glycine. This leads to an uncontrolled release of acetylcholine, and results in lock jaw. - 15i) Describe the A-B subunit toxin effect exhibited by Cholera. ii) what therapy is used to treat cholera?1) the B subunit binds to GM 1 ganglioside
2) the A subunit is internalised, and induces the production of adnylate cyclase.
3) increased cyclic amp blocks NA uptake
4) as a result, Cl- diffuse to the lumen, as does water.
ii) rehydration therapy. - 16What are the 5 key differences between exo/endotoxins?1) exotoxins are proteins and endotoxins are LPS
2) exotoxins are heat sensitive and endotoxins are heat stable
3) exotoxins are immunogenic and endotoxins are weakly immunogenic
4) exotoxins are released from a live bacterium; endotoxins released when the bacterial cell lyses.
5) endotoxins cause a fever and exotoxins don't. - 17What is the difference between intracellular obligate and intracellular facultative pathogens.intracellular obligate pathogens can only survive intracellularly but facultative pathogens can survive intracellularly and extracellularly.
- 18List three advantages and disadvantages of a cell residing intracellularly.Advantages -- 1) intracellular environment is a good source of nutrients
2 ) there aren't other competing microbes
3) conditions are relatively stable
Disadvantages -- 1) have to avoid host defence mechanisms
2) need to gain entry
3) need an exit strategy. - 19Give a brief overview of the 4 cellular entry mechanisms employed by pathogens.1) phagocytosis
2) receptor mediated endocytosis
3) macropinocytosis
4) active invasion - 20Describe in as much detail possible the mechanism behind phagocytosis.1) the bacterial cell envelope comprises 'invasin' which helps the bacteria enter the host cell via a zipping mechanism.
2) the bacterial cell is first in the primary phagosome
3) it is then transferred to a secondary phagosome, which comprises a proton pump. Pumping of protons acidifies the vacuole.
4 ) the secondary phagosome fuses with a lysosome, which causes killing of the cell. - 21Describe in as much detail possible the mechanism behind macropinocytosis.1) In macropinocytosis, the bacteria ruffles around the cell membrane and induces endocytosis (forces itself in)
2) it does so by forming a needle complex.
3) the bacteria inserts the needle into the host cell, and releases effector proteins that modulate the host actin causing it to polymerise -- leading to 'ruffling' of cell membrane. - 221) The needle complex is evolutionarily related to which cellular component? 2) Given this evolutionary linkage, what can we say about the effector proteins that pass through the needle complex?1) the needle complex is related to the flagella.
2) the effector proteins are small, and barely fold. They can easily easily be unfolded into a linear form. - 23List down three functions of the needle complex.1) the complex results in a directional exchange of material from pathogen to host.
2) in the absence of the host cell, it stops the delivery of effector proteins.
3) upon contact with host, forms a pore in the membrane and releases effector proteins. - 24Name the four survival strategies employed by cells.1) reside in the phagosome
2) escape the phagosome
3) modify the phagosome
4) exit the endocytic pathway. - 25Describe the autophagic pathway.Under conditions of starvation, the cell recycles its nutrients by digesting its own organelles in the ER.
- 26List down the protein markers for each stage of phagocytosis.1) primary phagosome marker is Rab5
2) secondary endosome markers are ATPase and immature cathepsin
3) phagolysosome marker is mature cathepsin. - 271) Name the microbe that exhibits survival strategy 1. 2) Describe the mechanism this microbe employs as a part of survival strategy 1.1) C. burnetti
2) Tha bacteria resides in the phagolysosome.
3) the virus needs a low pH to actively replicate. - 281) What kind of an intracellular pathogen is C.burnetti? 2) What does it cause in humans? 3) What is a special characteristic about that makes it potential biowarfare.1) obligate intracellular pathogen
2) it causes Q fever in humans (mild flu like symptoms)
3) it has ID50 of 1, meaning only take 1 bacteria to cause infection. - 291) Name the microbe that exhibits survival strategy 2. 2) Describe the mechanism this microbe employs as a part of survival strategy 2.1) Lysteria (bacteria)
2) This microbe punches holes in the endosomal membrane, escapes into the cytoplasm where it replicates in a nutrient rich environment. - 30Give a detailed account of the mechanism Lysteria employs to punch holes in the phagosomal membrane.1) Lysteria's invasion of the host cell is dependent on inIA expression.
2) Once inside a vacoule, it releases specific homolytic factors such as LLO -- which degrades the endosomal membrane.
3) Key point about LLO is that it is only active in an acidic pH, and this is how the bacteria ensures its degrading the endosomal membrane and not the host membrane.
4) Once in the cytoplasm, lysteria secretes Act2 protein that polymerises actin to facilitate cell to cell spread. - 31How is survival strategy III exercised by M. tuberculosis different from HGE and Ehrlichia?--> survival statergy III comprises modifying the phagosome.
--> M. tubercolosis fails to acidify the endosome because it doesn't uptake the proton pump. As a result, the immature cathepsin never matures and is always inactive.
Therefore, bacteria have a neutral pH and an inactive protease.
--> HGE manages to acidify the endosome but fails to progress into phagolysosomal compartment.
Therefore, the vacuole has a low pH but is lacking a protease. - 321) Describe the two ways bacterial cells can make use survival strategy 4. 2) Also mention the microbe associated with each mechanism of survival strategy 4.1) In survival strategy 4, the bacterial cell avoids the endocytic pathway by either adapting to the exocytic pathway or the autophagy pathway.
2) i) Chlamydomonas leaves the endocytic pathway and subvert to the exocytic pathway. it gains vesicular cargo, and camps out near the golgi.
ii) legionella and B.abortus avoid the endocytic pathway by hijacking the autophagy pathway. As soon as the bacteria enters the host cell, it is surrounded by the ER -- which feeds off the phagosomal membrane. The pathogen is remodelled, and the cell now confuses it for one of its own's components. As a result, it forms its own replicative niche. - 331) What is an exocytic marker seen in Chlamydomonas? 2) Why does Chlamydomonas lack endocytic markers?1) sphingomyelin.
2) This is because the cell evades the endocytic pathway all together and instead subverts to excocytic pathway. It gains vesicular cargo. - 34Desccribe the microneme complex T.gondii establishes to interact with the actin-myosin motor of the host cell.i) T. gondii displays gliding motility. When it needs to invade the host, instead of moving across the surface, it now points downwards.
ii) It uses its surface adhesion protein (Microneme) to bind to the cell, and makes use of GAC to interact with actin-mysosin motor. - 351) What is the purpose of rhoptries in T.gondii invasion of the cell?The rhoptries are secreted at the time of the invasion, and invaginates the host membrane by forming a moving junction.
- 36What are the two functions of the moving junction made by the rhoptries?1) The parasite holds onto the moving junction as a means of entering the cell.
2) The moving junction also acts like a molecular seive, wherein lips can pass through but the transmembrane proteins are prevented from passing through. - 37What is the consequence of the moving junction acting like a molecular sieve?The moving junction doesn't let the transmembrane proteins pass through, into the vacuole. The parasite thus evades host cell defence mechanism because the vacuole is non-fusogenic, and thus cant be destroyed by the lysosome.
- 38What protein helps in parasite egression of the host cell?PLP 1 which is a pore-forming molecule that is only active in low pH. This molecule however doesn't help in entry because the parasite enters through an empty vacuole.
This vacoule, in turn, acidifies much later in the lytic life cycle.
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- Fichas sobre Host Pathogenesis 1&2, creado por Anahita Sehgal el 19/03/2019.
- Creado por
- Anahita Sehgal · mar 2019
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- 20 mar 2019
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