MICR3001 Past Exam Paper Practices!
bye everyone.
Let’s all keep this civil and remember that the goal is to help each other to each do the best
we can! Best of luck everyone! :)
Jw is candidasis the ‘most common fungal disease’? asspergillus
Do we need to study for clinical module?? SOS!! No telling - theres been 1-2 clinical questions in the
past few exams but that doesnt mean it couldnt change - especially since some of the lectures had
example qs
Good luck everyone <3 <3
Did we get back the fungal report yet?
NO!!!!! ANGERY REACTS ONLY >:( +8
Anger intensifies +1
Any idea what we need to know for module 4 lol? +7
Not gonna study anything from module 4 (wing it) +5 its 3 weeks of content though - literally longer
than the fungal module im worried the yll be a few questions for module 4 - there haven’t been
many in past exams though? - IVE BEEN BURNED BEFORE 😰😰😰
Module 4 stuff is honestly pretty self explanatory except for the last 2 lectures
James better go easy on us for module 3 for giving our marks back so late :(
All these virulence factors are getting mixed together in my head which one belongs to which idk
My plan is to rewrite them over and over again and hope for the best (: aaaaaa
Plus 1 if you’re gonna skip the fungal module all together and hope for the best :) +7
The herpes lecture notes are soo long, and he talked so little hahahah *cries* +1 why havent there
been any herpes questions in the past
Look down at question C2 my friend. He also attached written lecture notes with it with what he
said out loud.
Honestly feel like crying tbh+7
I SHOULD'VE DONE ENGINEERING
Plus 1 if you have given up all hope and must now rely on the Cells at Work
anime +2 yall mind if i hit that YEET
Do we need to know every detail in the herpes lecture notes? +4 Not the molecular names
but the rest of it probably
COMMENT ON THE FUNGAL QNS PLS SO WE CAN WRITE UP THE
ANSWER NICELY. THANKS :)
Added a Gonorrhoeae question as A5, please feel free to answer it
,JAMES FRASER IS GONNA ASK A HARD QUESTION I JUST
KNOW IT :( +1000000000000000000000001 (he is gonna rekt us)
- If he asks about how to make chocolate, i called it first here.
Added module 4 question on genomics + scarlet fever he mentioned
as example in the lecture - D6
LMS if you feel fucked by BIOC3003 :) ← hit the feels
A1. Write about the virulence mechanisms employed by uropathogenic Escherichia coli to
exert its pathogenic effect AND discuss the implications for both treatment and vaccination.
Two types of fimbriae
- Type 1: Bind D-mannose containing glycoproteins in the bladder via FimH tip
adhesin and are associated with bladder colonization (cystitis)
- P fimbriae: Bind gal-gal disaccharide in upper urinary tract via PapG tip adhesin.
Kidney colonisation (pyelonephritis)
- Both phase variable
Toxins
- Hemolysin: Pore forming, inserts into eukaryotic membrane, causes cell lysis and
triggers apoptosis, stimulates cytokine production.
- Cytotoxic necrotising factor 1 (CNF-1): Kills epithelial cells, causes actin
rearrangements and membrane ruffling.
- Secreted autotransporter serine protease (Sat): vacuolation and tissue damage.
Others
- LPS: O antigen (only specific types). Required for serum survival.
- Capsule: Offers resistance from the host immune system.
- Iron acquisition: Power/feed cell, multiple systems, often uses siderophores.
- Antigen 43: causes bacterial clumping, promotes biofilm formation, IBC (intracellular
bacterial communities) formation and therefore persistent infection
Most of these factors are kept in transposable pathogenicity islands.
Treatment
Short term: antibiotics, able to use because it’s uncomplicated and increase antibiotic
strength as strains become resistant.
Catheter infections: Broad spectrum.
Novel Treatments
Mannosides to inhibit fimH adhesion of UPEC (has good oral bioavailability)
Vaccines
FimH: target a vaccine toward fimH adhesin (using antibody specific to those binding sites)
PapG: Target a vaccine toward binding sites of PapG. (have trouble with this because P
fimbriae are phase variable, and not present in all strains)
, Probiotics
Asymptomatic bacteriuria delivered to the site of infection, can inhibit colonization of the
urinary catheter by more virulent/pathogenic strains.
Do you think we should include the stuff about intracellular bacterial communities?
In a three hour exam with 7 other questions???? Nah defs not. That above is defs worth the
12.5 marks.
I mean personally I would because it’s only like 2 sentences. +1
A2. Neisseria meningitidis is an important human pathogen that causes significant morbidity
and mortality. Discuss the virulence factors that enable Neisseria meningitidis to cause
disease. What vaccines are used to prevent infections caused by Neisseria meningitidis?
Outer Membrane
- Pili: typical family of adhesins (type IV), crucial role in colonisation of host. Long
polymeric proteins.
- Opa & Opc: outer membrane protein, variable in number, size and antigenicity. Act
as adhesins. Adherence is mediated by Opc and other factors, and it can also cause
cytoskeletal changes that facilitate epithelial invasion. (Opa: CD66, Opc: Heparin)
- Porins: Two major (PorA and PorB), human antibodies recognise both of them.
React with antibodies which can enhance the immune response.
- Iron Acquisition: Grows in iron restricted environments, has receptors which can bind
hemoglobin (intracellular) and transferrin/lactoferrin (extracellular).
- Capsule: anti-phagocytic, resistant to bactericidal activities of the complement
system. Resistant to engulfment by macrophages. (composed of sialic acid
derivatives which are poorly immunogenic)
- LPS: Endotoxin (only known toxin produced by this bacterium). OM vesicles
released from cell surface, direct relationship between the blood LPS content and
patient outcomes. It activates a cytokine cascade, leading to inflammation which can
lead to death.
-
Treatment
Can be treated with antibiotics if caught early enough, however it can be hard to diagnose it
early on in the disease, as many of the early symptoms present themselves as the flu.
Vaccines
Vaccines exist for C strain and combined ACYW strains (based on capsule, don’t provide
long lasting immunity). However the serogroup B capsule is poorly immunogenic, and has
structures identical to human cells (meaning it could lead to immunopathology)
- New group B vaccine in the pipeline. This one is based on the outer membrane
proteins, the major antigens which exist on the cell surface. Currently approved for
use in Australia.
A3. Recent evidence demonstrates that at approximately 96 hours following internalization
by macrophages, Mycobacterium tuberculosis can breach the phagosomal membrane and
bye everyone.
Let’s all keep this civil and remember that the goal is to help each other to each do the best
we can! Best of luck everyone! :)
Jw is candidasis the ‘most common fungal disease’? asspergillus
Do we need to study for clinical module?? SOS!! No telling - theres been 1-2 clinical questions in the
past few exams but that doesnt mean it couldnt change - especially since some of the lectures had
example qs
Good luck everyone <3 <3
Did we get back the fungal report yet?
NO!!!!! ANGERY REACTS ONLY >:( +8
Anger intensifies +1
Any idea what we need to know for module 4 lol? +7
Not gonna study anything from module 4 (wing it) +5 its 3 weeks of content though - literally longer
than the fungal module im worried the yll be a few questions for module 4 - there haven’t been
many in past exams though? - IVE BEEN BURNED BEFORE 😰😰😰
Module 4 stuff is honestly pretty self explanatory except for the last 2 lectures
James better go easy on us for module 3 for giving our marks back so late :(
All these virulence factors are getting mixed together in my head which one belongs to which idk
My plan is to rewrite them over and over again and hope for the best (: aaaaaa
Plus 1 if you’re gonna skip the fungal module all together and hope for the best :) +7
The herpes lecture notes are soo long, and he talked so little hahahah *cries* +1 why havent there
been any herpes questions in the past
Look down at question C2 my friend. He also attached written lecture notes with it with what he
said out loud.
Honestly feel like crying tbh+7
I SHOULD'VE DONE ENGINEERING
Plus 1 if you have given up all hope and must now rely on the Cells at Work
anime +2 yall mind if i hit that YEET
Do we need to know every detail in the herpes lecture notes? +4 Not the molecular names
but the rest of it probably
COMMENT ON THE FUNGAL QNS PLS SO WE CAN WRITE UP THE
ANSWER NICELY. THANKS :)
Added a Gonorrhoeae question as A5, please feel free to answer it
,JAMES FRASER IS GONNA ASK A HARD QUESTION I JUST
KNOW IT :( +1000000000000000000000001 (he is gonna rekt us)
- If he asks about how to make chocolate, i called it first here.
Added module 4 question on genomics + scarlet fever he mentioned
as example in the lecture - D6
LMS if you feel fucked by BIOC3003 :) ← hit the feels
A1. Write about the virulence mechanisms employed by uropathogenic Escherichia coli to
exert its pathogenic effect AND discuss the implications for both treatment and vaccination.
Two types of fimbriae
- Type 1: Bind D-mannose containing glycoproteins in the bladder via FimH tip
adhesin and are associated with bladder colonization (cystitis)
- P fimbriae: Bind gal-gal disaccharide in upper urinary tract via PapG tip adhesin.
Kidney colonisation (pyelonephritis)
- Both phase variable
Toxins
- Hemolysin: Pore forming, inserts into eukaryotic membrane, causes cell lysis and
triggers apoptosis, stimulates cytokine production.
- Cytotoxic necrotising factor 1 (CNF-1): Kills epithelial cells, causes actin
rearrangements and membrane ruffling.
- Secreted autotransporter serine protease (Sat): vacuolation and tissue damage.
Others
- LPS: O antigen (only specific types). Required for serum survival.
- Capsule: Offers resistance from the host immune system.
- Iron acquisition: Power/feed cell, multiple systems, often uses siderophores.
- Antigen 43: causes bacterial clumping, promotes biofilm formation, IBC (intracellular
bacterial communities) formation and therefore persistent infection
Most of these factors are kept in transposable pathogenicity islands.
Treatment
Short term: antibiotics, able to use because it’s uncomplicated and increase antibiotic
strength as strains become resistant.
Catheter infections: Broad spectrum.
Novel Treatments
Mannosides to inhibit fimH adhesion of UPEC (has good oral bioavailability)
Vaccines
FimH: target a vaccine toward fimH adhesin (using antibody specific to those binding sites)
PapG: Target a vaccine toward binding sites of PapG. (have trouble with this because P
fimbriae are phase variable, and not present in all strains)
, Probiotics
Asymptomatic bacteriuria delivered to the site of infection, can inhibit colonization of the
urinary catheter by more virulent/pathogenic strains.
Do you think we should include the stuff about intracellular bacterial communities?
In a three hour exam with 7 other questions???? Nah defs not. That above is defs worth the
12.5 marks.
I mean personally I would because it’s only like 2 sentences. +1
A2. Neisseria meningitidis is an important human pathogen that causes significant morbidity
and mortality. Discuss the virulence factors that enable Neisseria meningitidis to cause
disease. What vaccines are used to prevent infections caused by Neisseria meningitidis?
Outer Membrane
- Pili: typical family of adhesins (type IV), crucial role in colonisation of host. Long
polymeric proteins.
- Opa & Opc: outer membrane protein, variable in number, size and antigenicity. Act
as adhesins. Adherence is mediated by Opc and other factors, and it can also cause
cytoskeletal changes that facilitate epithelial invasion. (Opa: CD66, Opc: Heparin)
- Porins: Two major (PorA and PorB), human antibodies recognise both of them.
React with antibodies which can enhance the immune response.
- Iron Acquisition: Grows in iron restricted environments, has receptors which can bind
hemoglobin (intracellular) and transferrin/lactoferrin (extracellular).
- Capsule: anti-phagocytic, resistant to bactericidal activities of the complement
system. Resistant to engulfment by macrophages. (composed of sialic acid
derivatives which are poorly immunogenic)
- LPS: Endotoxin (only known toxin produced by this bacterium). OM vesicles
released from cell surface, direct relationship between the blood LPS content and
patient outcomes. It activates a cytokine cascade, leading to inflammation which can
lead to death.
-
Treatment
Can be treated with antibiotics if caught early enough, however it can be hard to diagnose it
early on in the disease, as many of the early symptoms present themselves as the flu.
Vaccines
Vaccines exist for C strain and combined ACYW strains (based on capsule, don’t provide
long lasting immunity). However the serogroup B capsule is poorly immunogenic, and has
structures identical to human cells (meaning it could lead to immunopathology)
- New group B vaccine in the pipeline. This one is based on the outer membrane
proteins, the major antigens which exist on the cell surface. Currently approved for
use in Australia.
A3. Recent evidence demonstrates that at approximately 96 hours following internalization
by macrophages, Mycobacterium tuberculosis can breach the phagosomal membrane and
