8.0 Multiple Choice Questions (MCQs) I Flashcards
Viruses that cause zoonotic infections:<div>A. have non-humans as natural hosts</div><div>B. cause diseases with high mortality/morbidity</div><div>C. include influenza virus</div><div>D. may be transmitted by insects</div><div>E. include measles virus</div>
<div>Viruses that cause zoonotic infections:<div>A. have non-humans as natural hosts (TRUE)</div><div>B. cause diseases with high mortality/morbidity (TRUE)</div><div>C. include influenza virus (TRUE)</div><div>D. may be transmitted by insects (TRUE)</div><div>E. include measles virus (FALSE)</div></div>
The group of reversiviruses includes<div>A. human immunodeficiency virus</div><div>B. variola virus</div><div>C. hepatitis C virus</div><div>D. Rous sarcoma virus</div><div>E. hepatitis B virus</div>
<div>The group of reversiviruses includes<div>A. human immunodeficiency virus (TRUE)</div><div>B. variola virus (FALSE)</div><div>C. hepatitis C virus (FALSE)</div><div>D. Rous sarcoma virus (TRUE)</div><div>E. hepatitis B virus (TRUE)</div></div>
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<div>Reversiviruses replicate their genome via a reverse transcriptase step - and shares this property with retroviruses.</div>
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<div>B - F; variola virus is a poxvirus e.g. smallpox</div>
<div>C - F; a flavivirus</div>
These viruses commonly enter their host via the alimentary canal<div>A. Rotavirus</div><div>B. Blue tongue virus</div><div>C. Hepatitis B virus</div><div>D. Rhinovirus</div><div>E. Poliovirus</div>
<div>These viruses commonly enter their host via the alimentary canal<div>A. Rotavirus (TRUE)</div><div>B. Blue tongue virus (FALSE)</div><div>C. Hepatitis B virus (FALSE)</div><div>D. Rhinovirus (FALSE)</div><div>E. Poliovirus (TRUE)</div></div>
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<div>B - F; transmitted by blood biting insects</div>
<div>C - F; transmitted via blood e.g. iatrogenic</div>
<div>D - F; transmitted via the respiratory tract e.g. common cold</div>
<div>Viruses that commonly enter via the alimentary canal include poliovirus, hepatitis A virus, rotavirus, enteric adenoviruses</div>
Interferon beta<div>A. Is induced following activation of Toll-like receptors</div><div>B. Induces expression of interferon stimulated genes (ISGs) via NFkB</div><div>C. Signals through type 1 IFN receptors</div><div>D. Directly binds viruses and blocks entry</div><div>E. Up-regulates class I MHC</div>
<div>Interferon beta<div>A. Is induced following activation of Toll-like receptors (TRUE)</div><div>B. Induces expression of interferon stimulated genes (ISGs) via NFkB (FALSE)</div><div>C. Signals through type 1 IFN receptors (TRUE)</div><div>D. Directly binds viruses and blocks entry (TRUE)</div><div>E. Up-regulates class I MHC (FALSE)</div></div>
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<div>B - F; NFkB leads to the production of IFN alpha/beta which then goes on to stimulate ISGs through JAK-STAT pathway and ISGF-3</div>
<div>D - F; they induce downstream pathways that leads to increased likelihood of recognition by the immune system (MHC-class I indirectly upregulated) and they inhibit viral protein synthesis via production of OAS, Mx, PKR</div>
Yellow Fever Virus<div>A. Is a zoonotic infection</div><div>B. Is commonly transmitted congenitally</div><div>C. Causes respiratory infection</div><div>D. Is a non-enveloped RNA virus</div><div>E. Causes haemorragic fever</div>
<div>Yellow Fever Virus<div>A. Is a zoonotic infection (TRUE)</div><div>B. Is commonly transmitted congenitally (FALSE)</div><div>C. Causes respiratory infection (FALSE)</div><div>D. Is a non-enveloped RNA virus (FALSE)</div><div>E. Causes haemorragic fever (TRUE)</div></div>
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<div>B - F; it is transmitted by the female aedes aegypti mosquito</div>
<div>C - F; causes haemorrhagic fever<br></br>D - F; is a flavivirus which are enveloped viruses; they are positive strand ssRNA viruses</div>
Influenza Virus<div>A. Is an RNA virus</div><div>B. Encodes an ion channel protein that promotes un-coating of the virus</div><div>C. Causes disease with high seasonality in temperate climates</div><div>D. Requires a high pH environment to activate membrane fusion</div><div>E. Pandemics are associated with HA drift</div>
<div>Influenza Virus<div>A. Is an RNA virus (TRUE)</div><div>B. Encodes an ion channel protein that promotes un-coating of the virus (TRUE)</div><div>C. Causes disease with high seasonality in temperate climates (TRUE)</div><div>D. Requires a high pH environment to activate membrane fusion (FALSE)</div><div>E. Pandemics are associated with HA drift (FALSE)</div></div>
<br></br><div>D - F; it requires a low pH. Low pH leads to a conformational change in the HA2 subunit that allows the fusion peptide (N terminal part) to integrate into the endosomal membrane. This destabilises the membrane and promotes fusion between the viral envelope and the endosomal membrane.</div><div>E - F; pandemics are associated with HA shift; shifts results in production of new strains due to reassortment of RNA segments between two virions of different strains within a cell infected by them both at the same time</div>
Pattern-recognition receptors (PRRs)<div>A. Are important for viral entry</div><div>B. Mediated phagocytosis of free virus particles</div><div>C. PRRs activate the JAK-STAT signalling pathway within the infected cell</div><div>D. Detect viral DNA in the cytoplasm</div><div>E. Activate the IRF3 TF within the infected cell</div>
<div>Pattern-recognition receptors (PRRs)<div>A. Are important for viral entry (FALSE)</div><div>B. Mediated phagocytosis of free virus particles (TRUE)</div><div>C. PRRs activate the JAK-STAT signalling pathway within the infected cell (FALSE)</div><div>D. Detect viral DNA in the cytoplasm (TRUE)</div><div>E. Activate the IRF3 TF within the infected cell (TRUE)</div></div>
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A - F; PRRs are important host cell viral recognition proteins that detect PAMPS such as nucleic acids in the cytoplasm, and they activate the innate immune system.<div>C - F; the JAK-STAT pathway is activated in neighbouring cells, that helps to protect them from viral infection</div>
Human immunodeficiency virus (HIV)<div>A. Binds to macrophages using the CCR5 cytokine receptor</div><div>B. Is a zoonotic infection</div><div>C. Converts its positive sense RNA genome into DNA via reverse transcription</div><div>D. Is controlled by CD8+ cytotoxic T lymphocytes in patients termed ‘slow progressors’</div><div>E. Requires ribosomal frame-shifting to express env</div>
<div>Human immunodeficiency virus (HIV)<div>A. Binds to macrophages using the CCR5 cytokine receptor (TRUE)</div><div>B. Is a zoonotic infection (TRUE)</div><div>C. Converts its positive sense RNA genome into DNA via reverse transcription (TRUE)</div><div>D. Is controlled by CD8+ cytotoxic T lymphocytes in patients termed 'slow progressors' (TRUE)</div><div>E. Requires ribosomal frame-shifting to express env (FALSE)</div></div>
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<div>E - F; expression of env protein requires splicing, expression of gag vs. gag-pol requires frame-shifting</div>
In viral infection:<div>A. Herpes virus establish persistent (latent) infections</div><div>B. Hepatitis B establishes persistent (chronic) infection in about 90% of normal adults</div><div>C. Measles virus always causes an acute infection</div><div>D. Varicella zoster virus establishes latency in sensory ganglia</div><div>E. Influenza viruses always cause acute infection</div>
<div>In viral infection:<div>A. Herpes virus establish persistent (latent) infections (TRUE)</div><div>B. Hepatitis B establishes persistent (chronic) infection in about 90% of normal adults (FALSE)</div><div>C. Measles virus always causes an acute infection (FALSE)</div><div>D. Varicella zoster virus establishes latency in sensory ganglia (TRUE)</div><div>E. Influenza viruses always cause acute infection (TRUE)</div></div>
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A - they establish latent infection in sensory nerves<div>B - it establishes chronic infection in about 90% of neonates but the rates are much lower in adults [~10%]</div><div>C - if people are vaccinated they won’t necessarily get the acute infection + measles virus mutants can persist in the CNS and cause a chronic demyelinating disease (SSPE) with a frequency of about 1/million infections</div><div>D - hence classic dermatomal pattern of reactivation</div><div>E - T</div>
The following statements are true:<div>A. Cryptococcus neoformans causes a slowly progressive meningo-encephalitis</div><div>B. Invasive infections with Aspergillus fumigatus has high fatality</div><div>C. Candida albicans is a common commensal organism of human mucous membranes</div><div>D. Structural barriers play a minor role in innate protections from fungal infection</div><div>E. Protein synthesis in fungi can be blocked by nystatin</div>
<div>The following statements are true:<div>A. Cryptococcus neoformans causes a slowly progressive meningo-encephalitis (TRUE)</div><div>B. Invasive infections with Aspergillus fumigatus has high fatality (TRUE)</div><div>C. Candida albicans is a common commensal organism of human mucous membranes (TRUE)</div><div>D. Structural barriers play a minor role in innate protections from fungal infection (FALSE)</div><div>E. Protein synthesis in fungi can be blocked by nystatin (FALSE)</div></div>
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A; T - abundant in bird droppings and possesses a thick polysaccharide capsule that is an important virulence determinant. Infection is acquired by inhalation. The organism has a strong tendency to spread from the lungs through the circulation to the CNS. In people who are HIV positive, or immunosuppressed it can cause a slowly worsening meningo-encephalitis, with progessively worsening headache, fever, confusion, hydrocephalus (insufficient reabsorption of CSF), and then coma. 20% fatality; survivors often have persistent neurological disability including blindness. Can treat with amphotericin plus flucytosine, followed by long-term high-dose fluconazole.<div>B; T - an environmental mould that occurs worldwide and produces abundant air-borne spores which are inhaled by people every day (hospital re-building work, mouldy hay, compost heaps), causes airway colonisation, aspergilloma and invasive infection of lung or paranasal sinuses and spreads along blood vessels leading to dissemintated infection. Invasive infection has a very high fatatlity. Treatment is with amphotericin or voriconazole, and surgery if possible.<br></br>C; T - moist epithelial surfaces, usually restrained by host defences and bacterial competition<br></br>D; F - the intact epithelium of the skin or moist mucosal surfaces of the mouth, intestine, genital tract are key structural barriers to prevent fungal entry. Damage to it can lead to fungal invasion, through the epithelium, into the connective tissue and blood vessels followed by dissemiantion to other parts of the body.<br></br>E; F - nystatin blocks ergosterol function in fungal membranes.</div>
Regarding fungal infection:<div>A. Ringworm is a superficial fungal infection</div><div>B. The candidate albicans toxin candidalysin targets endothelial cells</div><div>C. Cryptococcus neoformans is abundant in bird-droppings</div><div>D. Aspergillus fumigatus is a filamentous saprophyte</div><div>E. Filamentous fungi are common components of the normal human flora</div>
<div>Regarding fungal infection:<div>A. Ringworm is a superficial fungal infection (TRUE)</div><div>B. The candidate albicans toxin candidalysin targets endothelial cells (FALSE)</div><div>C. Cryptococcus neoformans is abundant in bird-droppings (TRUE)</div><div>D. Aspergillus fumigatus is a filamentous saprophyte (TRUE)</div><div>E. Filamentous fungi are common components of the normal human flora (FALSE)</div></div>
Regarding Fungi<div>A. Most are saprophytes</div><div>B. Many are parasites of humans and animals</div><div>C. They can be eukaryotes or prokaryotes</div><div>D. They have a cell wall containing both chitin and glucans</div><div>E. Many, but not all, are dimorphic</div>
<div>Regarding Fungi<div>A. Most are saprophytes (TRUE)</div><div>B. Many are parasites of humans and animals (FALSE)</div><div>C. They can be eukaryotes or prokaryotes (FALSE)</div><div>D. They have a cell wall containing both chitin and glucans (TRUE)</div><div>E. Many, but not all, are dimorphic (TRUE)</div></div>
In fungi<div>A. DNA is organised in chromosomes within a membrane-bound nucleus</div><div>B. Hyphae are branching cylinders that grow by cell division</div><div>C. At 37 degrees the spores of dimorphic fungi germinate into yeasts</div><div>D. The azole toxin drug Fluonazole inhibits the synthesis of fungal microtubules</div><div>E. The anti-fungal drug Caspofungin inhibits the synthesis of glucan, a component of the cell wall</div>
<div>In fungi<div>A. DNA is organised in chromosomes within a membrane-bound nucleus (TRUE)</div><div>B. Hyphae are branching cylinders that grow by cell division (TRUE)</div><div>C. At 37 degrees the spores of dimorphic fungi germinate into yeasts (TRUE)</div><div>D. The azole toxin drug Fluonazole inhibits the synthesis of fungal microtubules (FALSE)</div><div>E. The anti-fungal drug Caspofungin inhibits the synthesis of glucan, a component of the cell wall (TRUE)</div></div>
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<br></br>D - F; fluconazole is an azole class but it inhibits synthesis of ergosterol which is part of the cell membrane. Ergotamine is a toxin produced by fungi.<br></br>
In haematopoiesis<div>A. NK cells derive from the common lymphoid precursor</div><div>B. Platelets are derived from erythroblasts</div><div>C. Macrophages and dendritic cells are both derived from monocytes</div><div>D. Plasma cells give rise to B cells</div><div>E. The common myeloid progenitor gives rise to both granulocytes and monocytes</div>
<div>In haematopoiesis<div>A. NK cells derive from the common lymphoid precursor (TRUE)</div><div>B. Platelets are derived from erythroblasts (FALSE)</div><div>C. Macrophages and dendritic cells are both derived from monocytes (TRUE)</div><div>D. Plasma cells give rise to B cells (FALSE)</div><div>E. The common myeloid progenitor gives rise to both granulocytes and monocytes (TRUE)</div></div>
The cell surface molecule<div>A. LFA-1 is a marker for T cells</div><div>B. CD8 binds to MHC class II molecules</div><div>C. ICAM-1 binds to LFA1</div><div>D. CD4 is expressed on helper T cells</div><div>E. CD3 is expressed on the majority of NK cells</div>
<div>The cell surface molecule<div>A. LFA-1 is a marker for T cells (FALSE)</div><div>B. CD8 binds to MHC class II molecules (FALSE)</div><div>C. ICAM-1 binds to LFA1 (TRUE)</div><div>D. CD4 is expressed on helper T cells (TRUE)</div><div>E. CD3 is expressed on the majority of NK cells (FALSE)</div></div>
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A - F; LFA-1 is a marker for neutrophils. They are integrin family adhesion molecules that bind to Ig superfamily molecules, ICAMs. They mediate tight binding. Initially the interactions are weak but signalling through chemokine receptors causes a conformationl changes in LFA-1 that reuslts in a high affinity binding state.<div>B - F; CD8 binds to MHC class I molecules.</div><div>E - F; FCgammaRIII is involved; it recognises antigen/antibody complexes. Ligation of this receptor leads to release of cytoplasmic granules containing lytic enzymes. This leads to ADCC.</div>
Pattern recognition receptors include:<div>A. TLR5 which binds flagellin</div><div>B. TLR3 which in conjunction with CD14 recognises LPS</div><div>C. NOD2 which recognises muramyl dipeptide</div><div>D. TLR9 which binds methylated CpG-rich DNA</div><div>E. NLRP3 (also known as NALP3) which recognises cholesterol crystals</div>
<div>Pattern recognition receptors include:<div>A. TLR5 which binds flagellin (TRUE)</div><div>B. TLR3 which in conjunction with CD14 recognises LPS (FALSE)</div><div>C. NOD2 which recognises muramyl dipeptide (TRUE)</div><div>D. TLR9 which binds methylated CpG-rich DNA (FALSE)</div><div>E. NLRP3 (also known as NALP3) which recognises cholesterol crystals (TRUE)</div></div>
<br></br>B - F; TLR3 recognises double-stranded viral RNA and it forms a homodimer. LPS is recognised by TLR4 homodimer.<br></br>D - F; TLR9 recognises unmethylated CpG-rich DNA because methylated is eukaryotic.
In the acute inflammatory response:<div>A. Histamine comes from stored sources</div><div>B. Leukotrienes are actively synthesised</div><div>C. C3a, C3b, C5a are derived from precursors present in plasma</div><div>D. Mast cells release endogenous pyrogens to activate the acute phase response</div><div>E. Histamine is released from mast cells by substance P released from nerve fibres</div>
“<div>In the acute inflammatory response:<div>A. Histamine comes from stored sources (TRUE)</div><div>B. Leukotrienes are actively synthesised (TRUE)</div><div>C. C3a, C3b, C5a are derived from precursors present in plasma (TRUE)</div><div>D. Mast cells release endogenous pyrogens to activate the acute phase response (FALSE)</div><div>E. Histamine is released from mast cells by substance P released from nerve fibres (TRUE)</div></div><div><br></br></div><br></br>D - F; macrophages release endogenous pyrogens [e.g. molecules/cytokines that induce fever]. These include IL-1beta, TNF-alpha and IL-6.”
In the complement system:<div>A. The classical pathway is always first to act</div><div>B. The alternative pathway is the main pathway responsible for generating C3b</div><div>C. Factor H speeds up activation of the alternative pathway</div><div>D. DAF disrupts the C3 convertase C3bBb</div><div>E. MCP makes C3b susceptible to cleavage by factor I</div>
“<div>In the complement system:<div>A. The classical pathway is always first to act (FALSE)</div><div>B. The alternative pathway is the main pathway responsible for generating C3b (TRUE)</div><div>C. Factor H speeds up activation of the alternative pathway (FALSE)</div><div>D. DAF disrupts the C3 convertase C3bBb (TRUE)</div><div>E. MCP makes C3b susceptible to cleavage by factor I (TRUE)</div></div><div><br></br></div>A - F; the first to act is the alternative pathway, then the lectin pathway and then finally the classical pathway<div>C - F; factor H antagonises the alternative pathway. It is the main control factor responsible for regulating complement activation in solution. It is a soluble cofactor for factor I that attaches to sialic acid on host membranes. It causes dissociation of C3bBb (the alternative pathway C3 convertase) and makes C3b susceptible to cleavage by factor I.</div>”
The following statements regarding cytokines are true:<div>A. IL-12 activates NK cells.</div><div>B. IL-4 inhibits the generation of Th1 cells</div><div>C. IL-8/CXCL8 is referred to as an endogenous pyrogen</div><div>D. Neutrophils follow a concentration gradient of IL-8/CXCL8</div><div>E. IL-6 activates the acute phase response</div>
“<div>The following statements regarding cytokines are true:<div>A. IL-12 activates NK cells. (TRUE)</div><div>B. IL-4 inhibits the generation of Th1 cells (TRUE)</div><div>C. IL-8/CXCL8 is referred to as an endogenous pyrogen (FALSE)</div><div>D. Neutrophils follow a concentration gradient of IL-8/CXCL8 (TRUE)</div><div>E. IL-6 activates the acute phase response (TRUE)</div></div><div><br></br></div><br></br>C - F; CXCL8 activates and recruits NK cells, as well as neutrophils. It is a chemokine e.g. controlled in cell movement.”
In the complement system:<div>A. The membrane attack complex is initiated by cleavage of factor C5.</div><div>B. C3b and C5b increase inflammation and enhance vascular permeability.</div><div>C. Mannose-binding lectin interacts with MASP-1 and MASP-2.</div><div>D. The alternative pathway C3 convertase is C4bC2a.</div><div>E. C-reactive protein on bacterial surfaces recruits complement component C2.</div>
“<div>In the complement system:<div>A. The membrane attack complex is initiated by cleavage of factor C5. (TRUE)</div><div>B. C3b and C5b increase inflammation and enhance vascular permeability. (FALSE)</div><div>C. Mannose-binding lectin interacts with MASP-1 and MASP-2. (TRUE)</div><div>D. The alternative pathway C3 convertase is C4bC2a. (FALSE)</div><div>E. C-reactive protein on bacterial surfaces recruits complement component C2. (FALSE)</div></div><div><br></br></div><div>B - F; C3a and C5a are anaphylatoxins which stimulate inflammation; not the b parts<br></br>D - F; the classical C3 convertase is the C3bC2a. The alternative pathway C3 convertase is C3bBb<br></br>E - F; CRP on bacterial surfaces recruits complement component leads to activation of the classical pathway. Cq1 can bind to CRP, and this leads to activation of C1r and C1s subunits. C1s is able to cleave C4 to expose a reactive thioester group which can covalently attach C4b to the pathogen surface. Activated C1 then associates with and cleaves C2 depositing the C2a fragment on C4b forming C4bC2a, the classical C3 convertase. This can cleave C3 and deposit C3b on the microbial surface, and then membrane associated C3b generated can utilise the alternative pathway amplification loop by binding to factor B to generate C3bBb. The classical convertase C3bC2a can also associate with C3b to generate C4bC2aC3b, a classical pathway C5 convertase.</div>”
Immunological tolerance:<div>A. Can involve regulatory T cells which have the signature transcription factor GATA3.</div><div>B. In pregnancy involves IDO which catabolises tryptophan.</div><div>C. Depends on the transcription factor IPEX being expressed in the thymus</div><div>D. Requires that all B cells with receptors that recognise self undergo apoptosis or anergy</div><div>E. Can be induced if T-cells receive signalling through MHC 1 in the absence of costimulation</div>
“<div>Immunological tolerance:<div>A. Can involve regulatory T cells which have the signature transcription factor GATA3. (FALSE)</div><div>B. In pregnancy involves IDO which catabolises tryptophan. (TRUE)</div><div>C. Depends on the transcription factor IPEX being expressed in the thymus (FALSE)</div><div>D. Requires that all B cells with receptors that recognise self undergo apoptosis or anergy (FALSE)</div><div>E. Can be induced if T-cells receive signalling through MHC 1 in the absence of costimulation (TRUE)</div></div><div><br></br></div>A - F; T regs are positive for FOXP2. GATA3 transcription factor is the signature Th2 TF.<br></br>C - F; Depends on the TF AIRE in the thymus. IPEX is an X-linked disease that only occurs in boys in which there is a lack of Tregs due to mutations in FOXP3; they die by two years unless treated due to lymphoproliferation and autoimmunity because of a lack of self-tolerance<br></br>D - F; because they require T cell activation if the T cell is tolerised then the B cell is not a worry”
Regarding autoimmunity:<div>A. C1, C2 or C4 complement deficiency predisposes to SLE</div><div>B. Type 1 diabetes is more prevalent in individuals with an aspartate residue in position 57 in DQB1</div><div>C. EAE (experimental autoimmune encephalomyelitis) is predominantly due to TH2 T cells</div><div>D. Myasthenia gravis involves antibodies to TSH recepetor</div><div>E. TFH (T-follicular helper) cells principally activate macrophages</div>
“<div>Regarding autoimmunity:<div>A. C1, C2 or C4 complement deficiency predisposes to SLE (TRUE)</div><div>B. Type 1 diabetes is more prevalent in individuals with an aspartate residue in position 57 in DQB1 (FALSE)</div><div>C. EAE (experimental autoimmune encephalomyelitis) is predominantly due to TH2 T cells (FALSE)</div><div>D. Myasthenia gravis involves antibodies to TSH recepetor (FALSE)</div><div>E. TFH (T-follicular helper) cells principally activate macrophages (FALSE)</div></div><div><br></br></div><br></br>B - F; less prevalent with the charged aspartate<br></br>C - F; predominantly due to CD4+ T helper cells, but not specific to Th2 cells<br></br>D - F; Grave’s disease<br></br>E - F; they principally activate B cells; they are responsible for antibody development, isotope switching and affinity maturation”
In transplantation:<div>A. Direct recognition of allogeneic transplants requires donor derived dendritic cells.</div><div>B. Indirect recognition occurs only when MHC molecules are mismatched</div><div>C. HLA matching is more important for haemopoietic stem cells transplants than for liver transplants</div><div>D. HLA typing is not necessary in the autologous situation</div><div>E. A GvH response is never advantageous</div>
<div>In transplantation:<div>A. Direct recognition of allogeneic transplants requires donor derived dendritic cells. (TRUE)</div><div>B. Indirect recognition occurs only when MHC molecules are mismatched (FALSE)</div><div>C. HLA matching is more important for haemopoietic stem cells transplants than for liver transplants (TRUE)</div><div>D. HLA typing is not necessary in the autologous situation (TRUE)</div><div>E. A GvH response is never advantageous (FALSE)</div></div>
The endogenous pathway of antigen presentation involves:<div>A. Mostly peptides derived from extracellular pathogens</div><div>B. Presentation of antigen on MHC class I molecules<br></br></div><div>C. Presentation of antigen to cytotoxic T cells</div><div>D. Presentation of antigen to TH1 cells</div><div>E. Presentation of antigen to B cells</div>
“<div>The endogenous pathway of antigen presentation involves:<div>A. Mostly peptides derived from extracellular pathogens (FALSE)</div><div>B. Presentation of antigen on MHC class I molecules (TRUE)<br></br></div><div>C. Presentation of antigen to cytotoxic T cells (TRUE)</div><div>D. Presentation of antigen to TH1 cells (FALSE)</div><div>E. Presentation of antigen to B cells (FALSE)</div></div><div><br></br></div>A - F; presents intracellular antigens, on MHC I molecules for CD8 cells. Proteins within the cytosole are continually being degraded into peptides by the proteasome. These peptides are moved from the cytosol into the ER via TAP [transporter associated with antigen processing]. Suitable peptides are then loaded onto partially folded MHC class I molecules in a process that is assisted by chaperone proteins known as the peptide loading complex [PLC]. Fully loaded MHC peptide complexes are released from the chaperones, pass through the golgi, and then follow the secretory pathway to the cell surface. See diagram.<br></br>D - F; Th1 cells are CD4 cells and so interact with MHC class II<br></br>E - F; B cells do not bind to antigen presented on MHC molecules. B cells binds antigen via its specific surface BCR/Ig and internalises it. The endocytosed antigen is then processed and presented on the surface MHC class II peptide complex. This peptide is then recognised by T helper cells which interacts with the MHC II molecules with its TCR. Also requires co-stimulatory moelcules to provide signal 2. This promote B cell proliferation, B cell survival signals and promotes Ig class switching. This interaction also leads to activation of the T cell.”
Antigen presentation:<div>A. Professional antigen presenting cells include macrophages, dendritic cells and B-cells.</div><div>B. Co-stimulatory molecule expression is a defining feature of professional antigen presenting cells.</div><div>C. Foreign antigen presented by B lymphocytes is mainly taken up by phagocytosis.</div><div>D. Peptide anchor residues interact with pockets in the MHC peptide binding groove.</div><div>E. The proteasome generates the majority of peptides presented by MHC class II molecules</div>
“<div>Antigen presentation:<div>A. Professional antigen presenting cells include macrophages, dendritic cells and B-cells. (TRUE)</div><div>B. Co-stimulatory molecule expression is a defining feature of professional antigen presenting cells. (TRUE)</div><div>C. Foreign antigen presented by B lymphocytes is mainly taken up by phagocytosis. (FALSE)</div><div>D. Peptide anchor residues interact with pockets in the MHC peptide binding groove. (TRUE)</div><div>E. The proteasome generates the majority of peptides presented by MHC class II molecules (FALSE)</div></div><div><br></br></div><br></br>C - F; B cells are non-phagocytic. They have BCRs that can interact with a wide variety of molecules in their native conformation. Antigen bound to the BCR is endocytosed and processed to be presented on MHC II molecules for presentation to B cells.<br></br>E - F; the proteasome generates the majority of peptides presented by MHC class I molecules. Peptides presented on MHC II molecules are taken up into the cell by endocytosis and are then degraded into peptides by proteases.”
MHC class II molecules<div>A. Are highly polymorphic and show more variation than TCR molecules</div><div>B. Are expressed on all cell types</div><div>C. Present peptides to CD4 restricted T cells</div><div>D. Can undergo somatic hypermutation</div><div>E. Are present on follicular dendritic cells</div>
“<div>MHC class II molecules<div>A. Are highly polymorphic and show more variation than TCR molecules (FALSE)</div><div>B. Are expressed on all cell types (FALSE)</div><div>C. Present peptides to CD4 restricted T cells (TRUE)</div><div>D. Can undergo somatic hypermutation (FALSE)</div><div>E. Are present on follicular dendritic cells (FALSE)</div></div><div><br></br></div>A - F; they are highly polymorphic with many different alleles in the population - 9,342 protein variants. However, TCR molecules show the most variation with up to 1018variants.<br></br>B - F; they are expressed on professional antigen presenting cells e.g. macrophages, B cells and dendritic cells. Class II molecules can be induced to be expressedon other cells in the presence of IFNgamma.<br></br>D - F; B cells undergo somatic hypermutation in their production of antibodies. Point mutations are introduced into heavy and light chain variable regions. This involves deamination of cytosine to uracil by the enzyme activation induced cytidine deaminase (AID). Antibodies with increased affinity are selected by affinity maturation. The mutation rate is abut 1/1000 BP per cell division.<br></br>E - F; they are present on dendritic cells NOT follicular dendritic cells. These two types of cell are from different lineages and are not related either structurally or functionally.”
Regarding the MHC.<div>A. Every individual possesses hundreds of different MHC I and II alleles</div><div>B. A particular MHC molecule will be specific for only one peptide</div><div>C. Exposure of DCs to PAMPs decreases surface expression of MHC class I molecules</div><div>D. Polymorphism in MHC class I molecules is concentrated in the a1 and a2 domains</div><div>E. MHC class I molecules binds peptides in the ER</div>
“<div>Regarding the MHC.<div>A. Every individual possesses hundreds of different MHC I and II alleles (FALSE)</div><div>B. A particular MHC molecule will be specific for only one peptide (FALSE)</div><div>C. Exposure of DCs to PAMPs decreases surface expression of MHC class I molecules (FALSE)</div><div>D. Polymorphism in MHC class I molecules is concentrated in the a1 and a2 domains (TRUE)</div><div>E. MHC class I molecules binds peptides in the ER (TRUE)</div></div><div><br></br></div>A - F; every individual possesses 3 MHC class I isotypes and 3 MHC class II isotypes and hence each individual has 6 different MHC class molecules. I = A, B, C. II = DP, DQ, DR.<br></br>B - F; a particular mHC molecule will be specific for anchor residues, and for particular lengths of peptide but it will not be specific for the residues in between these anchor residues meaning that it can present a wide array of peptide fragments.<br></br>”
Pathogen associated molecular patterns<div>A. Can evolve quickly to counter new pathogens</div><div>B. Are present in vertebrate hosts</div><div>C. Are specific to the individual organism</div><div>D. Can recognise double stranded RNA</div><div>E. Include lipopolysaccharide</div>
“<div>Pathogen associated molecular patterns<div>A. Can evolve quickly to counter new pathogens (FALSE)</div><div>B. Are present in vertebrate hosts (FALSE)</div><div>C. Are specific to the individual organism (FALSE)</div><div>D. Can recognise double stranded RNA (FALSE)</div><div>E. Include lipopolysaccharide (TRUE)</div></div><div><br></br></div>A - F; they are highly conserved which helps our cells to detect PAMPS regardless of the exact type of pathogen present/or regardless of slight mutations between different pathogens.<div>B - F; they are a sign of infection hence are not normally present. DAMPS are normally present.<br></br>C - F; they are highly conserved across different classes of organisms. This means that we don’t need as many different PRRs to detect them.<br></br>D - F; PRRs can recognise double stranded RNA. Double stranded RNA might however act as a PAMP e.g. from RNA viruses e.g. TLR3.<br></br></div>”
Prions:<div>A. Are infectious proteins that can be transmitted by ingestion</div><div>B. Have a mainly alpha-helical structure in the disease form of the protein</div><div>C. Are expressed at high levels in the CNS</div><div>D. Are inactivated by UV irradiation</div><div>E. Can cause progressive neurodegenerative diseases</div>
“<div>Prions:<div>A. Are infectious proteins that can be transmitted by ingestion (TRUE)</div><div>B. Have a mainly alpha-helical structure in the disease form of the protein (FALSE)</div><div>C. Are expressed at high levels in the CNS (TRUE)</div><div>D. Are inactivated by UV irradiation (FALSE)</div><div>E. Can cause progressive neurodegenerative diseases (TRUE)</div></div><div><br></br></div>B - F; the PrP has a mainly beta-sheet structure in the disease form. This form is very stable (resistant to protease digestion) and catalyses the conversion of the normal protein.<br></br>D - F; infectivity is not destroyed by irradiation that would destroy nucleic acids<br></br>”
Influenza Virus<div>A. can have filamentous or spherical morphology</div><div>B. encode an RNA-dependent DNA polymerase<br></br>C. require a high pH environment to fuse with cellular membranes<br></br>D. encode 3 viral envelope proteins<br></br>E. cause seasonal epidemics due to the process of antigenic drift</div>
“<div>Influenza Virus<div>A. can have filamentous or spherical morphology (TRUE)</div><div>B. encode an RNA-dependent DNA polymerase (FALSE)<br></br>C. require a high pH environment to fuse with cellular membranes (FALSE)<br></br>D. encode 3 viral envelope proteins (TRUE)<br></br>E. cause seasonal epidemics due to the process of antigenic drift (TRUE)</div></div><br></br>B - F; encode an RNA-dependent RNA polymerase made up of PB1, PB2 and PA polypeptides<br></br>C - F; they require a low pH<br></br>”
Measles virus:<div>A. Is controlled by a subunit vaccine</div><div>B. Is highly infectious</div><div>C. Is enveloped</div><div>D. Can infect neurons</div><div>E. Is a cell associated virus</div>
“<div>Measles virus:<div>A. Is controlled by a subunit vaccine (FALSE)</div><div>B. Is highly infectious (TRUE)</div><div>C. Is enveloped (TRUE)</div><div>D. Can infect neurons (TRUE)</div><div>E. Is a cell associated virus (TRUE)</div></div><div><br></br></div>A - F; by a live vaccine - all MMR are live<br></br>”
Viruses that often establish chronic or latent infections include:<div>A. Foot and mouth disease virus</div><div>B. Rotavirus<br></br>C. Herpes simplex virus<br></br>D. Human cytomegalovirus<br></br>E. Hepatitis C virus</div>
<div>Viruses that often establish chronic or latent infections include:<div>A. Foot and mouth disease virus (FALSE)</div><div>B. Rotavirus (FALSE)<br></br>C. Herpes simplex virus (TRUE)<br></br>D. Human cytomegalovirus (TRUE)<br></br>E. Hepatitis C virus (TRUE)</div></div>
<div>Gene transfer by transduction is mediated by</div>
<div><div>A. Sex pili</div> <div>B. Contact between bacteria</div> <div>C. Bacteriophages</div> <div>D. Naked DNA</div> <div>E. Bacterial plasmids</div></div>
“<div>C. Bacteriophages<br></br></div><div><br></br></div><div>- Transduction = via bacterial viruses e.g. bacteriophages</div><div>- Transformation = from dead (lysed) bacteria</div><div>- Conjugation = direct transfer between two bacteria via sex pili</div>”
<div>Pathogenic bacteria have evolved in close association with their host. Which is the most accurate description? They…</div>
<div><div>A. Are simple eukaryotic cells</div> <div>B. Use mitochondria to generate energy</div> <div>C. Are often obligate intracellular parasites</div> <div>D. Do not undergo meiosis</div> <div>E. Have a large number of introns in their genome</div></div>
“<div>D. Do not undergo meiosis<br></br></div><div><br></br></div><div>- Bacteria are prokaryotes not eukaryotes</div><div>- They do not contain mitochondria because they don’t have intracellular membrane bound organelles</div><div>- Some bacteria are obligate intracellular parasites - e.g. chlamydia. However, most can make ATP and protein and hence are not intracellular pathogens. Chlamydia has lost many of the metabolic enzymes and pathways and is adapted to scavenge essential metabolites from the host cell.</div><div>- Bacteria do not have as many introns as eukaryotes</div>”
<div>Bacterial endotoxins are clinically important. Which best describes a property of endotoxins?</div>
<div>A. They are more heat stable than exotoxins</div>
<div>B. They are lipopolysaccharide</div>
<div>C. They are characteristic of gram-positive bacteria</div>
<div>D. They are cytolysin</div>
<div>E. They are secreted from the bacterial cell</div>
“<div>A. They are more heat stable than exotoxins<br></br></div><div><br></br></div><div>- Endotoxin is lipid A which is a component of the gram-negative bacterial cell wall e.g. lipopolysaccharide (e.g. it is not a lipopolysaccharide, it is a component of lipopolysaccharides)</div><div>- It is released from dying bacteria and is a major alarm signal that triggers a wide-ranging immune response</div><div>- It is not a pathogen specific toxin since lots of bacteria have this lipid A; however, it is unique to bacteria and hence acts as a good host alarm signal</div><div>- Endotoxin overload can occur as large numbers of bacteria die e.g. in septicaemia, causing septic shock</div><div>- Exotoxins are pathogenic protein toxins secreted by bacteria and can be denatured by heat to produce non-toxic immunogenic forms used for vaccination</div><div>- Exotoxins can be divided into cytolysins and intracellular enzymatic toxins</div>”
<div>Cholera toxin is an important virulence factor. Which best describes a property of the protein? It…</div>
<div>A. Enters host cells by receptor-mediated endocytosis</div>
<div>B. Is a single polypeptide</div>
<div>C. ADP ribosylates translation elongation factor 2</div>
<div>D. Cleaves synaptobrevin</div>
<div>E. Causes net influx of chloride ions into host cells</div>
“<div>A. Enters host cells by receptor-mediated endocytosis<br></br></div><div><br></br></div><div>- V. cholerae colonises the small intestine via fimbrial adhesin</div><div>- V. cholerae is a gram -ve curved rod with a polar flagellum</div><div>- The principal disease symptoms are caused by secreted cholera toxin (CTX)</div><div>- CTX genes are carried on a bacteriophage integrated into the bacterial chromosome and are co-regulated with adhesin and other genes by a HAP signal transduction system</div><div>- Toxin structure is AB5; B binds to the host receptor GM1-ganglioside and is taken up via receptor-mediated endocytosis and retrograde transport to the ER where A and B dissociate; active A subunit is translocated into the host cell cytosol</div><div>- Not a single peptide because of the AB5 structure e.g. 6 peptides in total</div><div>-A subunit is an ADP-ribosylase and it activates stimulatory G protein Gs, fixing it on the on state e.g. inhibits GTP hydrolysis thereby leading to GTP bound to G protein</div><div>- Results in uncontrolled high levels of cAMP which leads to increased activity of the CFTR channel and causes net efflux of Cl- from the epithelial call</div><div>- Ion imbalance leads to water/electrolyte loss (up to 20 L/day) into the lumen which leads to copious watery diarrhoea (rice water), shock, collapse and cardiac failure</div><div>- Diphtheria toxin ADP-ribosylates translation elongation factor-2</div><div>- Synaptobrevin is cleaved by botulinum and tetanus [botox on peripheral nerves and tetanus on centrla nerves]</div>”
<div>Helicobacter pylori</div>
<div>A. Survives by producing spores</div>
<div>B. Is motile by flagella</div>
<div>C. Is associated with colon cancer</div>
<div>D. Causes antibiotic-associated diarrhoea</div>
<div>E. Produces uric acid</div>
“<div>B. Is motile by flagella<br></br></div><div><br></br></div><div>- H. pylori causes gastric and duodenal ulcuers [90% are associated w/ infection]</div><div>- Half of the human poopulation is colonised</div><div>- It colonises the mucin layer near gastric mucosal cells in the lower stomach antrum - although only a few percent will get ulcers</div><div>- Very motile by means of flagella and binds to cells via adhesins</div><div>- Gram negative bacteria that is spiral shaped</div><div>- Neutralises acid by urease which splits urea into ammonia, thereby raising the pH, which makes the gastric mucous less viscous and so it is easier for the H. pylori to swim to the epithelium</div><div>- Associated with gastric cancer; chronic inflammation may expose proliferating mucosal stem cells to dietary carcinogens and generate mutagenic reactive oxygen, in addition, bacterial effector CagA delivered into gastric epithelial cells interferes with signalling pathways and may lead to increased cell proliferation</div><div>- Destroys epithelial cells via VacA which is a pore-forming vacuolating cytotoxin; secreted by H. Pylori, it inserts into the membrane to form anion selective channels that are endocytosed; these disturb the ion balance of late endosomes and water flows in, swelling the endosomes to form characteristic vacuoles</div><div>- H. Pylori also attracts PMNs via stimulating epithelial cells to produce IL-8</div><div>- C. diff induced diarrhoea is associated with antibiotic use</div><div>- Spore forming bacteria: clostridium tetani, clostridium perfringens, clostridium botulinum, bacillus anthracis [e.g. some bacteria produce dormant endospores to survive the environment]</div>”
<div>Which statement most accurately relates to corynebacterium diphtheriae infection?</div>
<div></div>
<div>A. Toxic shock syndrome can develop</div>
<div>B. Toxin production is repressed in the presence of iron</div>
<div>C. Cytotoxic T cells play a major role in host defence</div>
<div>D. The toxin gene is carried on a plasmid</div>
<div>E. Bacteria induce their own uptake into epithelial cells</div>
“<div>B. Toxin production is repressed in the presence of iron<br></br></div><div><br></br></div><div>- Corynebacterium diphtheriae is a gram-positive rod</div><div>- Not many cases any more due to toxoid vaccination but it is still a major kill worldwide, especially in children</div><div>- It has a close counterpart in animals e.g. C. ulcerans and C. pseudotuberculosis which leads to a range of diseases in sheep, goats, cows and horses</div><div>- Produces diphtheriae toxin - DTX</div><div>- Toxin gene is carried on bacteriophage, not a plasmid; DTX gene is controlled by a bacterial transcription factor; DtxR which represses gene expression when bound by iron e.g. transcription is switched on in the host where the concentration of free iron is low</div><div>- Bacteria colonise the nasopharyngeal epithelium and secrete A-B toxin which results in intense local inflammation and damage to mucosal cells and growth of bacteria in inflammatory exudate, and formation of pseudo-membrane which occludes the airway</div><div>- Toxin can lead to irregular heartbeat, coma and death</div><div>- Bacteria don’t actually enter the epithelial cells themselves; but the A-B single polypeptide binds to the HB-EGF receptor (via B peptide); host furin protein then nicks the A-B but A-B remains covalently attached via a disulphide bridge; toxin is then taken up by endocytosis; acidification of the endosome then occurs; by V-ATPase; then B-dependent translocation of A across vesicle into the cytosol; in the cytoplasm the disulphide bond is reduced and A is released and blocks protein synthesis by ADP-ribosylating translation elongation factor-2 (EF-2)</div><div>- Toxic shock syndrome is associated with Staph. Aureus infection</div><div><img></img>- Cytotoxic T cells are important in viral infections/intracellular infections but C. diptheria is not an intracellular pathogen<br></br></div><div>- Not all strains of corynebacterium diphtheriae are toxigenic –> depends whether they have the bacteriophage with the DTX on within it or not</div>”
<div>Regulation of cAMP levels is important for controlling ion balance. Which of the following induce elevated cAMP levels without targeting host adenylate cyclase.</div>
<div>A. Shigella</div>
<div>B. Vibrio cholerae</div>
<div>C. Bordella pertussis</div>
<div>D. Enterotoxigenic E. Coli</div>
<div>E. Clostridium difficile</div>
“<div>C. Bordella pertussis<br></br></div><div><br></br></div><div>- B. Pertussis (whooping cough) and bacillus anthracis (anthrax) actually produce toxins that are adenylate cyclases, thereby not directly interacting with the host AC but mimicing it</div><div>- B. Pertusis also produces a toxin that does ADP-ribosylate regulators of host AC as well</div><div>- Enterotoxigenic E. Coli (ETEC) produces cholera-like enterotoxin LT (labile toxin) which causes a similar diarrhoea in children in developing countries, as well as travellers’ diarrhoea</div><div>- V. Cholerae induces high cAMP via increasing the activity of the G-protein and thereby indirectly increasing host AC activity</div><div>- C. Difficile toxins glycosylate small GTPases involved in regulation of signal transduction - it disrupts actin cytoskeleton and tight junctions</div><div>- Shigella produces shiga toxin (produces bacterial dysentery) which is a glycosidase that depurinates 28s rRNA. Blocks protein synthesis of the host cell.</div>”
<div>Some diseases are characteristically spread by propagated outbreaks. Which of the following is least likely to be spread by this route?</div>
<div>A. Dysentery</div>
<div>B. Cholera</div>
<div>C. Whooping cough</div>
<div>D. Typhoid</div>
<div>E. Bubonic plague</div>
“<div>E. Bubonic plague<br></br></div><div><br></br></div><div>- Propagated outbreaks, where host-to-host transmission results in ever greater numbers of infection is common for whooping cough, TB, gonorrhoea, dysentery, cholera and typhoid</div><div><div>- Dysentery + Cholera are spread by faecal-oral route via water</div><div>- Whooping cough is spread by respiratory tract (air-borne droplets)</div></div><div>- Typhoid is spread by faecal-oral route</div><div>- Bubonic plague is spread from rodents (point/continuous source) to humans, in which the disease becomes pnuemonic –> and then can cause propagated outbreaks, but this is penumonic plague NOT bubonic plague</div>”
<div>Which of the following most accurately describes properties of pathogenic bacteria</div>
<div>A. Genomes contain between 300 and 600 genes</div>
<div>B. Genomes are usually DNA but sometimes RNA</div>
<div>C. Genomes contains blocks of virulence genes separated by introns</div>
<div>D. Transduction of genes is effected by bacteriophage</div>
<div>E. Transduction of genes requires contact between bacteria</div>
“<div>D. Transduction of genes is effected by bacteriophage<br></br></div><div><br></br></div><div>- Genomes typically contains ~ 4,500 genes (Salmonella)</div><div>- Genomes are DNA</div><div>- There are not many introns in bacterial genomes</div><div>- Transduction of genes is via bacteriophages</div><div>- Conjugation allows for transferral of plasmid; bacteria contact via a pilus</div>”
<div>Cholera toxin</div>
<div>A. Undergoes retrograde transport</div>
<div>B. Is injected into host cells</div>
<div>C. Inhibits host protein synthesis</div>
<div>D. Disrupts control of host protein production</div>
<div>E. Is related to an E.Coli heat stable toxin</div>
“<div>A. Undergoes retrograde transport<br></br></div><div><br></br></div><div>- The toxin is endocytosed into the epithelial cells of the host; not injected</div><div>- Diphtheria toxin ADP-ribosylates EF-2 to inhibit host protein synthesis</div><div>- Is related to E. Coli heat labile toxin [enterotoxin]; e.g. not heat stable</div><div>- Acts to alter ion balance, but doesn’t directly act upon host protein production just cAMP</div>”
<div>Diptheria is a respiratory tract infection</div>
<div>A. Is caused by a gram-positive rod-shaped bacterium</div>
<div>B. Diphtheria toxin acts by activating host protein synthesis</div>
<div>C. Diphtheria toxin activity requires endosome acidification</div>
<div>D. Infection is especially common in patients with cystic fibrosis</div>
<div>E. Diptheria toxoid vaccination is ineffective in the developing</div>
“<div>C. Diphtheria toxin activity requires endosome acidification<br></br></div><div><br></br></div><div>- It is caused by a gram positive rod but not rod shaped; tennis racket/club shaped</div><div>- Diptheria toxin acts by inhibiting host protein synthesis</div><div>- Acidification of the endosome (by a V-ATPase proton pump) triggers B-dependent translocation of A across the vesicle membrane into the cytosol where it can then inhibit EF-2 and hence inhibit elongation</div><div>- Pseudomonas infection is particularly common in people with CF; P. aeruginosa biofilms form in the lungs</div><div>- Diptheria toxoid vaccination is effective in preventing the disease; and has significantly lowered rates where it is used</div>”
<div>Which of these bacteria best fits the criteria of being an obligate aerobe and also have an outer cell membrane</div>
<div>A. Salmonella typhi</div>
<div>B. Shigella dysenteriae</div>
<div>C. Pseudomonas aeruginosa</div>
<div>D. Corynebacterium diphteriae</div>
<div>E. Staphylococcus aureus</div>
“<div>C. Pseudomonas aeruginosa<br></br></div><div><br></br></div><div>- Outer cell membrane = gram negative</div><div>- Salmonella = gram negative + facultative anaerobe</div><div>- Shigella = gram negative + facultative anaerobe</div><div>- Pseudomonas = gram negative + obligate aerobe</div><div>- Corynebacterium diphtheriae = gram positive + facultative anaerobe</div><div>- Staphylococcus aureus = gram positive + facultative anaerobe</div><div>- TB is also an obligate aerobe</div>”
<div>Transmission from animals is characteristic of human disease outbreaks caused by which bacteria?</div>
<div>A. Vibrio cholerae</div>
<div>B. Salmonella typhi</div>
<div>C. Shigella dysenteriae</div>
<div>D. MRSA</div>
<div>E. Yersinia pestis</div>
“<div>E. Yersinia pestis<br></br></div><div><br></br></div><div>- Yersinia pestis causes pneumonic plague; infecting bacteria in flea spread through lymphatics to form enlarged lymph nodes which we call buboes; then haemorrhagic inflammation occurs with spread of the bacteria to the blood and the lungs; can also cause meningitis, septiciaemia, and multi-organ failure. The necrotic lesions give it the name black death.</div><div>- Cholera is spread by the faecal oral route via infected water</div><div>- Salmonella is spread by food/water borne infection</div><div>- MRSA is caused by staph aureus, an opportunistic infection which is often nosocomial e.g. hospital acquired; e.g. it is spread via inanimate objects e.g. in burns, surgical wounds and following catheterization</div><div>- Shigella dysenteriae is spread via faecal oral route of infected water</div>”
<div>The bacterial cell wall is a major target for antimicrobial agents. Which of these binds to bacterial D-ala-D-ala containing tetrapeptides?</div>
<div>A. Trimethoprim</div>
<div>B. Methicillin</div>
<div>C. Lysozyme</div>
<div>D. Vancomycin</div>
<div>E. Beta-lactamase</div>
“<div>D. Vancomycin<br></br></div><div><br></br></div><div>- Vancomycin is a glycopeptide that binds to D-Ala-D-Ala and blocks access to the transpeptidase, preventing crosslinking of PG; vancomycin resistant gram-positive pathogens produce different peptidoglycan biosynthesis enzymes that synthetise D-Ala-D-Lac alternative peptide crosslinks</div><div>- Trimethoprim inhibits DHFR (dihydrofolate reductase) thereby inhibiting folate synthesis [conversion of dihydrofolic acid to tetrahydrofolic acid] which is an essential step in the synthesis of nucleotides</div><div>- Methicillin - a penicillin type antibiotic that inhibits the transpeptidase enzyme and hence inhibits cell wall synthesis</div><div>- Lysozyme is produced in host tears and splits bacterial peptidoglycan</div><div>- Beta-lactamase is not an antibiotic but a produce produced by bacteria that hydrolyse beta-lactam based antibiotics e.g. penicillins to produce penicilloic acid</div>”
<div>These bacteria are the most common cause of chronic disease resulting in immune mediated pathology?</div>
<div>A. Mycobacterium leprae</div>
<div>B. Clostridium tetani</div>
<div>C. ETEC</div>
<div>D. Vibrio cholerae</div>
<div>E. Treponema pallidum</div>
“<div>A. Mycobacterium leprae<br></br></div><div><br></br></div><div>- Mycobacterium leprae causes leprosy which is chronic, the condition involves granuloma formation</div><div>- C. tetani doesn’t produce chronic infection</div><div>- ETEC (enterotoxigenic E. Coli) causes travellers’ diarrhoea, but doesn’t produce chronic infection</div><div>- Cholera doesn’t produce chronic infection</div><div>- Treponema pallidum causes syphilis –> which is chronic, however, it is not as immune mediated as mycobacterium leprae e.g. in mycobacterium leprae there is granuloma formation etc. whereas there are no granulomas in syphilis</div>”
<div>Which of these is most important with respects to pathology associated with bacterial endotoxin?</div>
<div>A. Is a secreted protein</div>
<div>B. Is a component of lipopolysaccharide</div>
<div>C. Activates macrophages</div>
<div>D. Forms pores in host cell membranes</div>
<div>E. Contributes to the inflammation characteristic of Salmonellosis</div>
“<div>C. Activates macrophages<br></br></div><div><br></br></div><div>- It is not a secreted protein; LPS is released from dead bacteria</div><div>- Acute inflammation is triggered by the lipid A component of gram-negative bacterial LPS</div><div>- LPS released is bound by LPS-binding protein and is delivered to macrophage receptors, CD14 and TLR4, which triggers signalling pathways that activate cytokine genes</div><div>- Lipid A is unique to gram negative bacteria and so it is a very good host alarm signal, triggering a strong innate immune response - overload can lead to sepsis/shock</div><div>- It does contribute to the inflammation characteristic of Salmonellosis but this is not the most important aspect of its pathology since it is not specific to salmonella infection</div><div>- Salmonella induces host ctoskeletal rearrangement via SP-1 encoded needle and effectors SipA, SipC, it forces entry directy via the apical surface epithelial cells of the distal ileum and proximal colon; it then remains within membrane bound vacuolles in a replicate niche and multiplies. It is then released from epithelial cells by lysis and induces inflammation principally by LPS-lipid A, producing gastroenteritis</div><div>- Lipid A does not form pores in host cell membranes</div>”
<div>Which of the following best describes features of infection by Mycobacterium Tuberculosis? It…</div>
<div>A. Is caused by a gram positive rod shaped bacteria</div>
<div>B. Results in damage to the lungs by a bacterial exotoxin</div>
<div>C. Is resolved by a strong TH17 response</div>
<div>D. Requires an effective IL-12 response for control</div>
<div>E. Is spread to humans from cattle</div>
“<div>D. Requires an effective IL-12 response for control<br></br></div><div><br></br></div><div><div>- Mycobacterium is neither gram +ve or -ve because the waxy impermeable cell envelope made up of mycolic acid prevents staining and also making it more resistant to immune attack; it is therefore referred to as acid fast and is stained with Ziehl-Neelsen stain</div> <div>- It results in damage to the lungs through granuloma formation and cavitation; persisting M. tuberculosis leads to type IV granulomatous inflammation in which activated macrophages are surrounded by fibroblasts and a few lymphocytes ‘wall off’ the pathogen. Granulomas show ongoing tissue destruction (necrosis), repair (fibrosis, scarring) and inflammation</div> <div>- There is a separate mycobacterium bovis which is in cattle and is closely related - it can be spread through unpasteurised milk but this is still M. Bovis and not M. Tuberculosis</div> <div>- M. Tuberculosis is an obligate aerobe</div> <div>- Bacteria spread by small droplets and are ingested by alveolar macrophages; virulent strains can resist intracellular killing by establishing safe uptake pathways that arrest phagosome-lysosome fusion; the bacteria can cross the alveolar epithelium and enter the lymphatics, drain to the regional lymph nodes and may enter the blood to disseminate around the body to produce new foci of infection</div> <div>- Lysis of host cells and dissemination is facilitated by small secreted ESAT6 protein, that forms pores to interfere with macrophage signalling pathways e.g. down-regulates ROS</div> <div>- When infection persists there is a shift as CD4+ TH2 cells produced in addition to protective Th1 cells; however, normally Th1 cells activate macrophages via IFNy. TNFalpha and NO are produced and bacteria are phagocytosed and killed and cell-mediated immunity is established</div> <div>- IL-12 is important in inflammatory Th1 responses - it is released by activated macrophages and leads to activation of NK cells, as well as differentiation of CD4 T cells into Th1 cells</div> <div>- Th17 responses are involved in the removal of extracellular bacteria and fungi at epithelial surfaces</div></div>”
<div>Which of the following is least likely to cause disease of the GI tract by attaching to endothelial cell using pili?</div>
<div>A. EPEC E. coli</div>
<div>B. Salmonella typhi</div>
<div>C. Clostridium difficile</div>
<div>D. Vibrio cholerae</div>
<div>E. Vac A expressing H. pylori</div>
“<div>C. Clostridium difficile<br></br></div><div><br></br></div><div>Only gram negative bacteria form pili and all of the other bacteria in the list are gram negative and hence C. diff must be the answer since this is gram positive</div>”
<div>Bacterial virulence genes are important for host colonisation. Which best describes a genetic feature that allows bacterial effector gene expression to be coordinated? Genes are…</div>
<div>A. Located on introns</div>
<div>B. Located on pathogenicity islands</div>
<div>C. Located on plasmids</div>
<div>D. Subject to global regulation</div>
<div>E. Spread between bacteria without cell-to-cell contact</div>
“<div>B. Located on pathogenicity islands<br></br></div><div><br></br></div><div>- Bacteria don’t have introns in their genome</div> <div>- Genes required for infection and survival in the host are grouped on pathogenicity islands; they have evolved by integration of transposons, plasmids and bacteriophage and incorporation of transformed DNA; they typically have a high G+C content that differs from the surrounding chromosomal DNA; they increase dissemination of virulence traits and facilitate virulence gene co-regulation</div>”
<div>Diptheria is generally well controlled by vaccination. Which feature is most important for the pathogenicity of diphtheria toxin?</div>
<div>A. The toxin causes bacterial secretion of a pseudomembrane</div>
<div>B. The toxin undergoes retrograde transport to the endoplasmic reticulum</div>
<div>C. The toxin requires a low iron environment for release of the A subunit</div>
<div>D. The diphtherias vaccine prevents infection with corynebacterium diptheriae</div>
<div>E. The toxin is encoded by a gene carried on a bacterial virus</div>
“<div>E. The toxin is encoded by a gene carried on a bacterial virus<br></br></div><div><br></br></div><div><div>- The formation of the pseudomembrane in the airway leads to occlusion which can lead to death </div> <div>- The toxin requires a low iron environment for transcription e.g. DTX gene is controlled by bacterial transcription factor DtxR which represses gene expression when bound by iron (Fe)</div> <div>- The toxin undergoes retrograde transport but not via the ER; it is taken in via an endosome and then is released into the cytosol</div> <div>- Vaccination does not prevent infection, but means that the individual has pre-existing immunity to infection</div> <div>- The toxin is encoded on a bacteriophage gene that is then integrated into the genome; hence some strains are not pathogenic because they don’t have the virulence gene incorporated; non-toxigenic strains</div></div>”
<div>Which of the following statements about cholera is untrue</div>
<div>A. Can be endemic</div>
<div>B. Can be epidemic</div>
<div>C. Can be pandemic</div>
<div>D. Involves bacterial entry into host cells of the GI tract</div>
<div>E. Produces diarrhoea as a result of a protein toxin</div>
<div>D. Involves bacterial entry into host cells of the GI tract</div>
<div>Which of the following statements about salmonella species is true. They…</div>
<div>A. Produce spores</div>
<div>B. Have between 250 and 300 genes</div>
<div>C. Have a capsule</div>
<div>D. Are obligate intracellular pathogens</div>
<div>E. Can grow anaerobically</div>
“<div>E. Can grow anaerobically<br></br></div><div><br></br></div><div><div>- They do not produce spores</div> <div>- They do not have a capsule</div> <div>- They have around 4,500 genes</div> <div>- They are not obligate intracellular pathogens</div> <div>- They are facultative anaerobes</div></div>”
<div>Which of the following does not cause food-borne disease</div>
<div>A. Clostridium botulinum</div>
<div>B. Clostridium tetani</div>
<div>C. Salmonella enterica</div>
<div>D. Listeria monocytogenes</div>
<div>E. Staphylococcus aureus</div>
“<div>B. Clostridium tetani<br></br></div><div><br></br></div><div><div>- You get tetanus from soil getting into a wound via spores</div> <div>- Listeria can be found in unpasteurized cheese, salad and hence why pregnant women don’t eat this cheese</div> <div>- Salmonella is food-borne via chicken/eggs</div> <div>- C. botulinum can be via food e.g. old home canned food</div> <div>- Staphylococcal food poisoning is also a thing</div></div>”
<div>Which of the following statements about streptococcus pyogenes is most accurate</div>
<div><div>A. Survives by producing endospores</div> <div>B. Forms clusters of cells</div> <div>C. Is a coccobacillus</div> <div>D. Causes fasciitis</div> <div>E. Can be an intracellular pathogen</div></div>
“<div>D. Causes fasciitis<br></br></div><div><br></br></div><div><div>- Can cause pharyngitis, tonsillitis, scarlet fever, necrotizing fasciitis, erysipelas and impetigo</div> <div>- Is a gram positive cocci</div> <div>- Staphylococci forms clusters of cells</div> <div>- Extracellular pathogen</div> <div>- Does not produce spores</div></div>”
<div>Which of the following do not specifically inhibit protein synthesis</div>
<div>A. Trimethoprim</div>
<div>B. Tetracycline</div>
<div>C. Chloramphenicol </div>
<div>D. Streptomycin</div>
<div>E. Gentamycin</div>
“<div>A. Trimethoprim<br></br></div><div><br></br></div><div><div>- Trimethoprim - inhibits DHFR</div> <div>- Tetracycline - inhibits binding of amino acyl tRNA to ribosome; 30S subunit; inhibits translation</div> <div>- Chloramphenicol - inhibits peptidyl transferase activity of 50S subunit; inhibits translation</div> <div>- Streptomycin + gentamycin - alter conformation of 16S rRNA in 30s subunit so inhibits tRNA binding and hence translation</div></div>”
Which of the following infections is most likely to be involved in granuloma formation<div>A. Neisseria meningitidis</div><div>B. Pseudomonas aeruginos</div><div>C. Mycobacterium leprae</div><div>D. Bordetella pertussus</div><div>E. All bacteria producing superantigens</div>
“<div>C. Mycobacterium leprae<br></br></div><div><br></br></div><div>- Leprosy also causes granuloma formation and causes chronic bacterial infection</div><div>- Neisseria meningitidis causes meningitis –> it can colonize several percent of the population, but meningococcal disease is uncommon. Neisseria meningitidis strains have sialic acid capsules, an example of host mimicry. Polysaccharides are weakly immunogenic, but anti-capsular antibodies can protect against specific serotypes.</div><div>- Pertussus causes whooping cough but this is an acute severe disease of young children which involves colonisation of the respiratory epithelium, damage to epithelial cells by LPS lipid A, and production of pertussis toxin and adenylate cyclase. Produces fever and bronchitis. This and toxin action on neurons promotes paroxysms of coughing. Life-threatening in infants with underlying disease, can lead to neurological sequelae.</div><div>- Superantigens can lead to shock due to SAg bridging weakly interacting MHC II molecules and TCRs by binding outside the normal antigen-binding pocket. This leads to activation of useless T cells by promoting tighter binding and stronger singalling in T cells. This results in a cytokine storm.</div>”
Which of these diseases/infections is least likely to be spread by propagated outbreaks<div>A. Gonorrhoea<br></br>B. Influenza<br></br>C. Meningitis<br></br>D. Botulism<br></br>E. Typhoid<br></br></div>
“<div>D. Botulism<br></br></div><div><br></br></div><div><br></br></div><div>- Botulism is caused by food poisoning –> so unless you also eat the toxins then you will not get it from an infected person</div><div>- C.f. all the other which can be transmitted between humans</div><div>- Typhoid is spread is spread by water via the faecal-oral route</div><div>- Gonorrhoea is sexually transmitted</div><div>- Influenza is spread via inhalation of air-droplets and is easily spread</div><div>- Meningitis may be caused by several pathogens, some of which colonize the nasopharynx asymptomatically (carriers can therefore be important in outbreaks). Pathogens that can cause meningitis include:</div><div><br></br></div><div>1) Neisseria meningitidis</div><div>2) Haemophilus influenza type B (Hib)</div><div>3) Streptococcus pneumoniae</div><div>4) E. Coli</div>”
Which of the following is the most accurate statement<div>A. Lipid A is part of the bacterial cell wall peptidoglycan</div><div>B. Obligate aerobic bacteria have a mitochondrion</div><div>C. Pathogenic bacteria have between 8,000 and 12,000 genes</div><div>D. Bacteria take up free DNA by transduction</div><div>E. Salmonella uses the usher secretion pathway</div>
“E. Salmonella uses the usher secretion pathway<div><br></br></div><div>All gram negative bacteria use the usher secretory pathway to get things from the periplasm to the outer membrane<div><br></br></div><div>- Lipid A is a component of LPS not PG</div><div>- Bacteria don’t have mitochondria</div><div>- Bacteria take up free DNA released by dead cells by transformation</div><div>- Pathogenic bacteria can have a variety of genome sizes e.g. Salmonella genome is ~ 4,500 genes but chlamydia has a smaller genome ~ 900 genes and makes up for the loss of proteins via being an obligate intracellular bacteria</div></div>”
The following cause infections of the respiratory tract<div>A. Bordetella pertussis and streptococcus pyogenes</div><div>B. Salmonella typhi and Yersinia pestis</div><div>C. Legionella pneumophila and staphylococcus aureus</div><div>D. Vibrio cholerae and streptococcus equi</div><div>E. Pseudomonas aeruginosa and Helicobacter pylori</div>
“<div>A. Bordetella pertussis and streptococcus pyogenes<br></br></div><div><br></br></div><div>- Pertussis causes whooping cough.</div><div>- Streptococcus pyogenes can produce a number of different things including pharyngitis + Scarlet fever + Necrotising fasciitis, puerperal fever, eryseipela and impetigo.</div><div>- Salmonella typhi causes gastroenteritis.</div><div>- Yersinia pestis causes bubonic plague (can then spread to pneumonic plague).</div><div>- Legionella pneumophila causes an atypical pneumonia.</div><div>- Streptococcus equi causes strangles in horses which is a severe upper respiratory tract infection.</div><div>- Pseudomonas aeruginosa can cause conjunctivitis, UTI, infect burns, wounds. It can also produce lung infection.</div><div>- Helicobacter pylori causes gastric ulcers + cancer.</div><div>- Staphylococcus aureus can cause erysipelas, impetigo, skin infection and toxic shock syndrome. Also causes severe diarrhoea and vomitting.</div><div>- Cholera causes diarrhoea and vomitting</div>”
The following specifically inhibit synthesis of the bacterial cell wall<div>A. Tetracyclin</div><div>B. Ciprofloxacin</div><div>C. Trimethoprim</div><div>D. Cephalosporin</div><div>E. Neomycin</div>
“<div>D. Cephalosporin<br></br></div><div><br></br></div><div>- Tetracyclin inhibits the amino-acyl tRNA binding to the 30S subunit thereby inhibiting translation</div><div>- Ciprofloxacin is a fluoroquinolone that inhibits DNA topoisomerase II (DNA gyrase) + IV this inhibits replication and transcription since these enzymes are important in controlling DNA topology</div><div>- Trimethoprim inhibits DHPR thereby interferring with folic acid and thus pyrimidine synthesis</div><div>- Cephalosporin is a beta-lactam antibiotic</div><div>- Neomycin is an aminoglycoside like gentamicin and alters the conformation of teh 16S rRNA in the 30S subunit where the ribosome ‘reads’ mRNA and recruits aminoacyl-tRNA. This inhibits tRNA selection and polypeptide elongation.</div>”
Which of these bacteria is least likely to be considered part of the normal microflora of humans<div>A. Bacteroides fragilis</div><div>B. Staphylococcus epidermidis</div><div>C. Salmonella typhi</div><div>D. Streptococcus viridans</div><div>E. Streptococcus pneumoniae</div>
“<div>C. Salmonella typhi<br></br></div><div><br></br></div><div>- Bacteroides fragilis –> part of normal gut microflora</div><div>- Staphylococcus epidermidis –> part of the normal human skin flora + sometimes mucosal too</div><div>- Salmonella typhi</div><div>- Streptococcus viridans –> commensal found in the mouth/gut/genital region</div><div>- Streptococcus pneumoniae –> this is the cause pneumonia/meningitis, however, it can also be a commensal</div>”
Which of the statements regarding Typhoid is least accurate<div>A. Can be endemic</div><div>B. Can be epidemic</div><div>C. Is characterised by the action of a protein toxin</div><div>D. Involves survival of bacteria in host macrophages</div><div>E. Can involve a host carrier state</div>
“<div>C. Is characterised by the action of a protein toxin<br></br></div><div><br></br></div>It is a protein toxin, however, the toxin does not appear to influence disease severity; strains that are deficient in the toxin seem to be pretty much indistinguishable from those producing the toxin and hence typhoid is not really characterised by its actions.<div><br></br></div><div>- Typhoid causes typhoid fever</div><div>- Salmonella typhi replicates in macrophages and is spread locally and systemically via blood stream to liver and spleen; but not always</div><div>- Severe symptoms are caused by typhoid toxin (CDT - cytolethal distending toxins) that cleaves DNA and response to LPS lipid A</div><div>- Bacteria are shed in bile, returning to the intestine and environment</div><div>- Carriers can be important (typhoid Mary)</div><div>- Up to 50% of the world is in a typhoid endemic region</div><div>- Spread by water via faecal-oral route</div><div>- Can be a point source or a continuous source outbreak, or propagated outbreaks (if the carrier for example is not isolated)</div>”
Which statements about Infection with Mycobacterium tuberculosis is most accurate? Infection<div>A. Is eliminated by formation of epithelioid granulomas</div><div>B. Is preventable by a toxoid vaccine</div><div>C. Leads to ingestion of the bacteria by macrophages</div><div>D. Leads to immunity through development of specific antibodies</div><div>E. Is detected by a type 2 hypersensitivity reaction in response to BCG</div>
“<div>C. Leads to ingestion of the bacteria by macrophages<br></br></div><div><br></br></div><div>- The response to persistance (not elimination) of TB is via type IV granulomatous inflammation in which aggregates of activates macrophages (which may differentiate to epithelioid cells or multi-nucleate giant cells), surrounded by fibroblasts and a few lymphocytes that ‘wall-off’ the pathogen</div><div>- Granulomas show ongoing tissue destruction (necrosis), repair (fibrosis, scarring) and inflammation</div><div>- Leads to caseous necrosis aids spread of the bacterium (Miliary TB)</div><div>- Antibodies against TB are not very effective due to the mycolic acid coat –> instead the immune response to is primarily via Th1 cells that activate macrophages and produce IFNgamma</div><div>- It is detected by a type IV hypersensitivity reaction in the Mantoux test against a small amount of injected tuberculin into the skin of the forearm e.g. memory Th1 cells release cytokines that recruit and activate macrophages</div><div>- The vaccine is M. bovis not a toxoid vaccine (e.g. a vaccine made from a toxin that has been made harmless but that still elicits an immune response)</div>”
Which of the following statements about Salmonella is least accurate?<div>A. Salmonella can cause food-borne infections</div><div>B. Can be typed using the O cell surface lipopolysaccharide antigen</div><div>C. Can invade intestinal epithelial cells</div><div>D. Can resist killing by macrophages</div><div>E. Can cause gastric ulceration</div>
“<div>E. Can cause gastric ulceration<br></br></div><div><br></br></div><div>- Salmonella is found in chicken and eggs</div><div>- Salmonella is a gram negative bacteria meaning that it will have the O cell surface LPS antigen; see diagram</div><div>- Salmonella can induce host cytoskeletal rearrangement and forces entry directly via the apical surface of epithelial cells of the distal ielum and proximal colon; requires SPI-1 encoded needle and effectors e.g. the actin binding SipA and SipC</div><div>- Salmonella remains within a membrane-bound vacuole - a ‘replicative niche’ and multiplies</div><div>- Released from epithelial cells by lysis and induces inflammation via LPS lipid A</div><div>- It is then taken up by macrophages where it replicates. It survives intracellulary by switching on SPI-2 genes encoding effectors that inhibit maturation of the phagolysosome and confer resistance to defensins and oxidative burst (pumps, superoxide dismutase, catalase)</div>”
Which of the following statements about E. Coli infections of the GI tract is most accurate<div>A. ETEC colonises by fimbrial (pili) adhesions<br></br>B. EPEC produces a cholera-like enterotoxin LT (labile toxin)<br></br>C. EHEC produce yellow colonies on McConkey agar<br></br>D. ETEC produces a shiga-like toxin (SLT) that accentuates inflammation<br></br>E. E. Coli 0157 is an ETEC found in beefburgers</div>
“<div>A. ETEC colonises by fimbrial (pili) adhesions<br></br></div><div><br></br></div><div>- ETEC colonises by fimbrial pili adhesions –> it is a common cause of diarrhoea in children as well as Traveller’s diarrhoea. It is spread by contaminated water</div><div>- Labile toxin is an E. coli entertoxin e.g. ETEC<br></br></div><div>- E. coli are lactose fermenting and hence they will be red on McConkey agar<br></br>- EHEC produces shiga like toxin that is a glycosidase that depurinates 28S rRNA thereby blocking protein synthesis<br></br>- E. Coli 0157 is an EHEC found in beef</div>”
Which of the following statements about diphtheria toxin is most accurate? The toxin:<div>A. Forms large pores in host cell membranes</div><div>B. Acts as an ADP-ribosylase in the host cell</div><div>C. Targets epithelial cells of the intestine</div><div>D. Is produced by all strains of cornebacterium diphtheriae</div><div>E. Targets the host cell adenylate cyclase</div>
“<div>B. Acts as an ADP-ribosylase in the host cell<br></br></div><div><br></br></div><div>- It ADP-ribosylates elongation factor 2 thereby preventing protein synthesis</div><div>- It is not produced by all strains; just the toxigenic strains that have been infected with the bacteriophage carrying the toxin</div><div>- It is a respiratory tract disease that is air-borne –> it colonises the nasopharyngeal epithelium, not the intestine</div>”
The following do not cause disease by infecting the GI tract<div>A. Vibrio cholerae</div><div>B. Salmonella typhimurium</div><div>C. Helicobacter pylori</div><div>D. Clostridium botulinum</div><div>E. Shigella dysenteriae</div>
“<div>D. Clostridium botulinum<br></br></div><div><br></br></div><div>- C. botulinum does not infect the GI tract</div><div>- It grows anaerobically in food and produce botulinum toxin that is then ingested</div><div>- Botulinum toxin is a neurotoxin</div><div>- Bacterial dysentery, caused by invasive shigella causes highly infectious disease characterised by acute inflammation of the colon and low-volume diarrhoea containing blood mucus and PMNs. Damage is caused directly by the shiga toxin and indirectly by the inflammatory response</div>”
Which of the following is false - the bacterial cell wall is:<div>A. Disrupted by lysozyme</div><div>B. Disrupted by tetracycline</div><div>C. Disrupted by penicillin</div><div>D. Made of peptidoglycan</div><div>E. Strengthened with a pentaglycine cross-link</div>
“<div>B. Disrupted by tetracycline<br></br></div><div><br></br></div><div>- Tetracyline binds to the amino-acyl tRNA binding of the 30S subunit thereby inhibiting elongation</div><div>- Lysozyme in tears splits bacterial peptidoglycan</div>”
Which statement regarding Salmonella is most accurate. Salmonella:<div>A. Like shigella causes zoonotic infections</div><div>B. Causes disease by secreting many enzymatic toxins</div><div>C. Can enter epithelial cells by inducing cytoskeletal change</div><div>D. Has a single cell membrane</div><div>E. Causes toxic shock syndrome</div>
“<div>C. Can enter epithelial cells by inducing cytoskeletal change<br></br></div><div><br></br></div><div><br></br></div><div>- It is caught via ingesting chicken and eggs but is not directly zoonotic</div><div>- Toxic shock syndrome is caused by Staph. Aureus</div><div>- It has an inner and outer membrane because it is a gram negative bacteria</div><div>- It causes disease primarily by release of Lipid A which leads to gastroenteritis</div><div>- It can enter epithelial cells by inducing cytoskeletal change; in order to do this is uses SPI-1 (pathogenicity island) needle and injects SipA and SipC which bind to actin; this occurs within the distal ileum and the proximal colon; within these cells salmonella remains within membrane bound vacuoles where it multiplies.</div>”
Which statement regarding bacterial cells is least accurate? They<div>A. often contain extrachromosal DNA</div><div>B. divide by binary fission</div><div>C. are haploid</div><div>D. possess intermediate filaments</div><div>E. contain mitochondria</div>
E. contain mitochondria
Which statement regarding bacterial exotoxin is least accurate? They…<div>A. Are secreted from the bacterial cell</div><div>B. Are heat labile</div><div>C. Are proteins</div><div>D. Have similar effects regardless of the bacterial species of origin</div><div>E. May be encoded by plasmids</div>
“<div>D. Have similar effects regardless of the bacterial species of origin<br></br></div><div><br></br></div><div>- There are lots of different types of bacterial toxins which are all exotoxins</div><div>- They are all secreted</div><div>- They are heat labile because they are proteins –> can be used to form non-toxic immunogenic proteins</div><div>- Two broad groups</div><div><br></br></div><div>1) cytolysins</div><div>2) intracellular enzymatic toxins</div>”
Which statement regarding bacterial evasion of host defences is least accurate? They…<div>A. Subvert macrophage function</div><div>B. Avoid phagocytosis</div><div>C. Integrate DNA into the host genome</div><div>D. Destroy antibody</div><div>E. Undergo phase variation</div>
“<div>C. Integrate DNA into the host genome<br></br></div><div><br></br></div><div>- Retroviruses can integrate their DNA into the host genome</div><div>- Lots of bacteria subvert macrophage function e.g. Yersinia injects multiple effectors into macrophages:</div><div><br></br></div><div>1) YopT, a protease that targets small GTPases to disrupt the cytoskeleton</div><div><br></br></div><div>2) YopP an acetyl transferase that inhibits signalling, triggering apoptosis.</div><div><br></br></div><div>- Bacteria can inactivate antibody e.g. secretory IgA is cleaved by specific proteases of mucosal pathogens e.g. strep pneumonia, H. influenzae, N. gonorrhoea, N. meningitidis</div><div><br></br></div><div>- Bacteria can avoid phagocytosis by shielding with antiphagocytic capsules e.g. polysaccharides:</div><div><br></br></div><div>1) Steric hindrance e.g. physical block</div><div>2) Non-immungenic polysaccharide e.g. sialic acid</div><div>3) Lack of affinity for complement factor B: C3b not formed</div><div><br></br></div><div>- Bacteria can shut off or switch on expression of surface antigens via phase variation e.g. Salmonella flagelline</div><div><br></br></div><div>1) Rearrangement of an invertible promoter region, flanked by recombination sequences recognised by site-specific DNA recombinase</div>”
Which statement regarding bacterial virulence genes is least accurate?<div>A. Can be acquired by transformation</div><div>B. May be grouped in pathogenicity islands</div><div>C. May be carried on plasmids</div><div>D. Are involved in the establishment of maintenance of infections</div><div>E. Evolve less rapidly than other genes</div>
“<div>E. Evolve less rapidly than other genes<br></br></div><div><br></br></div><div>- Transformation is when genes are taken up from DNA released from dead/lyesd bacteria</div><div>- They will involve more rapidly since this is important in evading host responses</div>”
Which statement regarding tetanus toxins is most relevant to its function?<div>A. it is produced by spores of C. tetani in anaerobic wounds</div><div>B. the ‘A’ chain acts on peripheral nerves, causing spastic paralysis</div><div>C. it is a protease cleaving synaptobrevin</div><div>D. it inhibits a small GTPase in the CNS, disrupting neurotransmitter release</div><div>E. The ‘A’ chain undergoes retrograde transport and blocks release of inhibitor neurotransmitters in the CNS, causing flaccid paralysis</div>
“<div>C. it is a protease cleaving synaptobrevin<br></br></div><div><br></br></div><div>- Tetanus neurotoxin is made during anaerobic growth of the pathogen in a wound</div><div>- The ‘A’ chain acts on central nerves/intermediate neurons</div><div>- It reduces neurotransmitter release from the inhibitory interneuron</div><div>- It causes spastic paralysis</div>”
Regarding these infections which statement is least accurate?<div>A. Streptococcus pyogenes is beta-haemolytic, forms gram-positive chains, and is Lancefield-typed by cell surface M proteins</div><div>B. Pneumonia and meningitis are caused by streptococcus pneumoniae and haemophilus influenza both of which have a capsule and secrete IgA protease</div><div>C. Protection against whooping cough caused by Bordetella pertussis is provided by the DPT combination vaccine</div><div>D. Diphtheria toxin is a single polypeptide A-B toxin that glycosylates translation elongation factor EF-2, inhibiting protein synthesis</div><div>E. Antigen-antibody complexes resulting from streptococcus pyogenes infection cause type III hypersensitivity, specifically glomerulonephritis</div>
“<div>D. Diphtheria toxin is a single polypeptide A-B toxin that glycosylates translation elongation factor EF-2, inhibiting protein synthesis<br></br></div><div><br></br></div><div>- Diphtheria toxin ADP-ribosylates EF-2</div><div>- Streptococcus pyogenes causes pharyngitis acutely but can lead to glomerunephritis and rheumatic fever more long term</div>”
This organism is an obligate anaerobe that produces endotoxin:<div>A. Salmonella typhi</div><div>B. Clostridium tetani</div><div>C. Bacteroide fragilis</div><div>D. Vibrio cholera</div><div>E. Clostridium sporongenes</div>
“<div>C. Bacteroide fragilis<br></br></div><div><br></br></div><div>- Salmonella typhi is an gram negative facultative anaerobe</div><div>- Clostridium tetani is a gram positive obligate anaerobe</div><div>- Bacteroides fragilis is a gram negative obligate anaerobe; see diagram</div><div>- Vibrio cholera is a gram negative facultative anaerobe</div><div>- Clostridium sporongenes is a gram positive obligate anaerobe</div>”
In pathogenic bacteria, which statement is most accurate?<div>A. Growth involves haploid chromosome replication and binary fission</div><div>B. Virulence genes are typically distributed randomly on the chromosome</div><div>C. Between 4000 and 6000 genes are arranged without introns in the nucleus</div><div>D. Transformation involves bacterial pili</div><div>E. Transduction requires contact between bacterial cells</div>
“<div>A. Growth involves haploid chromosome replication and binary fission<br></br></div><div><br></br></div><div>- Virulence genes are found on pathogenicity islands</div><div>- Pathogenic bacteria can vary in the number of genes they have ~500-7,500 (depending to an extent on whether they are intracellular or extracellular bacteria)</div><div>- Transformation involves taking up genes that have been released by lysed bacteria</div><div>- Transduction requires contact via pili between bacterial cells</div>”
Regarding TB, which statement is least accurate?<div>A. M. tuberculosis is spread by small droplets and is ingested by alveolar macrophages</div><div>B. Chronic granulomatous disease is typically resolved by a Th1 response</div><div>C. M. tuberculosis resists macrophages by means of an alignate polysaccharide coat</div><div>D. Caseous necrosis aids spread of the pathogen and is associated with miliary TB</div><div>E. The presence of immunity is detected as a T cell response by the tuberculin skin test</div>
“<div>C. M. tuberculosis resists macrophages by means of an alignate polysaccharide coat<br></br></div><div><br></br></div><div>- Pseudomonas aeruginosa produces an alginate polysaccharide ‘slime’ coat during lung infections; this protects the bactera in the biofilm from the host immune response and antimicrobials</div>”
Which of the following most typically causes propagated outbreaks of food-borne disease in humans?<div>A. Streptococcus aureus</div><div>B. E. coli 0157 (EHEC)</div><div>C. Helicobacter Pylori</div><div>D. Vibrio Cholerae</div><div>E. Clostridium difficile</div>
“<div>B. E. coli 0157 (EHEC)<br></br></div><div><br></br></div><div>- E. Coli 0157 is commonly found in beef</div><div>- Staph. aureus can grow in custard and processed meats</div><div>- Cholera is from water borne</div><div>- C. Diff is antibiotic associated not food associated</div><div>- H. Pylori doesn’t produce propagated outbreaks of disease</div>”
In antibiotic action and resistance which statement is most accurate?<div>A. TolC is an inner membrane transporter in efflux pumps conferring multi-drug resistance</div><div>B. Vancomycin mimics D-Ala-D-Ala crosslinks to inhibit peptidoglycan synthesis, and resistance to it is mediated by altered crosslinks</div><div>C. Rifampicin and ciprofloxacin both act on the DNA-dependent RNA polymerase</div><div>D. Trimethoprim and sulphonamide inhibit dihydrofolate reductase and thus folate synthesis</div><div>E. Chloramphenicol acts at the bacterial ribosome to prevent translation, and resistance to it typically involves antibiotic modification by an acetyl transferase</div>
“<div>E. Chloramphenicol acts at the bacterial ribosome to prevent translation, and resistance to it typically involves antibiotic modification by an acetyl transferase<br></br></div><div><br></br></div><div>- TolC is a transporter which spans the periplasm and the outer membrane. It confers multi-drug resistance e.g. in gram negative pseudomonas and E. Coli; see diagram</div><div>- Penicillin mimics the D-Ala-D-Ala peptidoglycan crosslink. It binds to the active site of the transpeptidase irreversibly inhibiting PG crosslinking.</div><div>- Vancomycin binds to D-Ala-D-Ala and resistance is mediated by production of D-Ala-D-Lac via different peptidoglycan biosynthetic enzymes</div><div>- Rifampicin blocks bacterial DNA-dependent RNA polymerase but ciprofloxacin is a fluoroquinolone that inhibits topoisomerases</div><div>- Trimethoprim inhibits DHFS but sulphonamides inhibit DHPS</div><div>- Resistant bacteria produce acetyl transferases that modify (acetylate) chloramphenicol + aminoglycosides (gentamicin, neomycin) to prevent ribosome binding</div>”
Regarding gastrointestinal infections which statement is least accurate?<div>A. Helicobacter pylori is a motile gram-negative bacteria that causes inflammation of the gastric mucosa and gastric ulcers</div><div>B. ETEC causes traveller’s diarrhoea colonizes host cells by modulating the actin cytoskeleton to form pedestals and secreting a cholera-like ADP-ribosylating toxin</div><div>C. Cholera toxin A subunit short-circuits adenylate cyclase control, so disturbing the activity of membrane ion pumps</div><div>D. C. Diff causes inflammation of the colonic mucosa and secretes glycosylating toxins that disrupt epithelial tight junctions</div><div>E. Shiga toxin is a glycosidase that blocks host cell protein synthesis, causing kidney damage</div>
“<div>B. ETEC causes traveller’s diarrhoea colonizes host cells by modulating the actin cytoskeleton to form pedestals and secreting a cholera-like ADP-ribosylating toxin<br></br></div><div><br></br></div><div>- EPEC + EHEC produces pedestal formation: the bacterium uses specialised needles to ‘inject’ proteins into the host cell, including a specific Tir (translocated intimin receptor). Tir then binds to the bacterium via bacterial surface protein intimin and promotes actin polymerisation</div><div>- ETEC produces LT (labile toxin) which is the cholera like ADP-ribosylating toxin. It causes traveller’s diarrhoea.</div><div>- C. Diff secretes a toxin that glycosylates small GTPases involved in signal transduction - this disrupts the actin cytoskeleton and tight junctions</div><div>- Shiga toxin produced by Shigella that causes dysentery is a glycosidase that depurinates 28s rRNA and blocks protein synthesis. This leads to renal failure. Shiga like toxin is produced by EHEC and also damages the kidney.</div>”
Regarding bacterial toxins, which statement is most accurate:<div>A. Pneumolysin, streptolysin O and E. Coli haemolysin all form pores in the cell membranes</div><div>B. Staphylococcal and botulinum toxins are both superantigens causing food poisoning</div><div>C. Endotoxin (lipid A) can be converted to a protective vaccine by heating</div><div>D. C. perfringens alpha-toxin is a phospholipase that can be detected by its actions on egg yolk agar (ELEK test)</div><div>E. Pertussis and cholera toxins are multimeric ATP-ribosylate enzymes that target adenylate cyclase</div>
“<div>A. Pneumolysin, streptolysin O and E. Coli haemolysin all form pores in the cell membranes<br></br></div><div><br></br></div><div>- Pneumolysin = streptococcus pneumoniae, streptolysin O + S = streptococcus pyogenes, haemolysin = E. Coli (UPEC)</div><div>- Staph aureus produces a superantigen but botulinum toxin is not a superantigen. Staph aureus bacteria are ingested in food but do not colonise while botulinum toxin is found in food.</div><div>- Exotoxins can be converted to a vaccine via heating e.g. toxoid vaccines</div><div>- Clostridium perfringens does produce an alpha-toxin. It enzymatically degrades membrane phospholipids. However, the ELEK test is used to looks for toxigenic strains of corynebacteria diphtheria.</div><div>- Pertussis and cholera toxins produce multimeric ADP-ribosylating enzymes that target adenylate cyclase</div>”
Among pathogenic bacteria which statement is most accurate?<div>A. Mycoplasma do not gram stain as they do not have a cell wall, but rather a waxy lipid coat</div><div>B. Treponema pallidum is a spiral shaped spirochaete that causes tick-borne Lyme’s disease</div><div>C. Bacillus anthracis and cornebacterium diphtheriae are spore-forming bacteria producing enzymatic protein toxins</div><div>D. Botulinum toxin cleaves a neuronal SNARE so preventing release of acetylcholine, causing flaccid paralysis that is exploited in cosmetic procedures</div><div>E. Shigella is a zoonotic infections that also transmits person-to-person</div>
“<div>D. Botulinum toxin cleaves a neuronal SNARE so preventing release of acetylcholine, causing flaccid paralysis that is exploited in cosmetic procedures<br></br></div><div><br></br></div><div>A - Mycobacteria are referred to as ‘acid-fast’ because they are difficult to destain due to a waxy impermeable cell envelope (mycolic acid) that makes the pathogen resistant to disinfectants and protects it from immune attack; they do however still have a cell wall</div><div>B - Treponema pallidum causes syphillis. It is a spirochaete (e.g. spiral shaped). Lyme’s disease is caused by Borrelia Burgdorferi.</div><div>C - Bacillus anthracis is a pore forming bacteria but cornebacterium diphtheriae is not.</div><div>E. - Shigella is a very infectious disease that transmits via the faecal-oral route. Man is the main reservoir.</div>”
NK cells<div>a. kill target cells using perforin and granzymes</div><div>b. kill target cells by antibody dependent cell cytotoxicity (ADCC)</div><div>c. kill virus infected cells through recognition of MHC class I molecules presenting virus-derived peptides</div><div>d. have inhibitory receptors that recognise classical MHC class I molecules</div><div>e. activate macrophages by secreting IFN-γ</div>
A - T; perforin forms pores in the cell membrane and allows apoptosis inducing granzymes into the cell<div>B - T; NK cells have FcyRIII receptor that binds to Ab Fc regions –> this binding activates the NK cell and leads to release of perforin and granzymes</div><div>C - F; Th1 cells do this. Virally infected cells therefore decrease MHC1 exression but NK cells recognise this as ‘missing self’ and kill cell</div><div>D - T; thereby not killing normal host</div><div>E - T</div>
<div>In the complement system</div>
<div>A. generation of C3(H2O) is a reversible reaction</div>
<div>B. C4b can covalently attach to pathogen surfaces</div>
<div>C. mannose-binding lectin is a soluble pattern recognition receptor</div>
<div>D. deficiency in factor I results in uncontrolled alternative pathway activation and C3 depletion</div>
<div>E. individuals deficient in complement component C1 are predisposed to immune-complex disease</div>
A - ?; it’s hydrolysis so probably if you remove H2O again?<div>B - T; C1s can cleave C4 to expose reactive thioester group which can covalently attach C4b to pathogen surface</div><div>C - T; it binds close knit arrays of mannose and fucose residues found on microbial surfaces of bacteria, yeast and fungi and some viruses (important in lectin pathway)</div><div>D - T; because factor I is a serine protease that degrades C3b and C4b (with help of cofactors MCP and factor H)</div><div>E - T; also C2 and C4 deficiency</div>
Pattern Recognition Receptors<div>a. include TLR4 which recognises components of Gram–negative bacterial LPS</div><div>b. include NOD2 which recognises muramyl dipeptide and is often mutated in individuals with Crohn’s disease</div><div>c. recognise either pathogen associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), but not both</div><div>d. are all transmembrane signalling receptors</div><div>e. that recognise bacterial cell wall components often activate proinflammatory responses through NF-kB</div>
“A - T; homodimer<div>B - T; NOD1 and 2 recognise fragments of peptidoglycan from bacteria. NOD2 detects muramyl dipeptide (found in most bacteria) released from gut microbiota and is involved in gut homeostasis</div><div>C - F</div><div>D - F; some are soluble e.g. CRP or MBL</div><div>E - T; bacterial produce MYD88 –> NF-kB and AP-1 while viral produce TRIF –> IRFs</div><div><img></img><br></br></div>”
Of the T cell subsets<div>A. TH17 cells promote neutrophil recruitment and are involved in defence against extracellular bacteria and fungi</div><div>B. TH2 cells express GATA3</div><div>C. TH1 cells promote responses against intracellular bacteria and protozoa</div><div>D. TH2 cells express MHC class I</div><div>E. natural regulatory T cells (Tregs) are thought to be educated in the periphery when they meet antigen</div>
A - T<div>B - T</div><div>C - T</div><div>D - T; and MHC class II</div><div>E - F; natural Tregs develop in the thymus. Tregs have an intermediate affinity for self antigens in MHC molecules and are not deleted by negative selection</div>
In transplantation<div>A. hyperacute rejection can be complement-mediated</div><div>B. HLA matching is very important in liver transplants</div><div>C. syngeneic transplants are transplants between two genetically identical individuals</div><div>D. minor transplantation antigens may be derived from MHC molecules</div><div>E. chronic rejection may be due to gradual damage to the blood vessels of the graft</div>
A - T; results from pre-existing Abs e.g. ABO or HLA antigens that are expressed on ECs. Tissues are damaged by complement activation, coagulation and leakage of fluid, as well as aggregation of platelets that block the microvasculature<div>B - F; very important in haemopoietic stem cells, and significant in kidney and heart</div><div>C - T</div><div>D - T; minor antigens (H antigens) are proteins that vary in sequence and where one of the allomorphs contains a peptide which binds to the MHC of the recipient.</div><div>E - T; can occur years later. May involve immune respones against blood vessels leading to ischaemia and loss of function. It may be due to type III hypersensitivity due to IgG antibodies against allogeneic HLA class I molecules on the graft, forming immune complexes that deposit in blood vessels. Indirect allo-recognition is important for chronic rejection as B cells binding shed donor HLA proteins are helped by T cells. Kidney damage can also affect loss via non-immune mechanisms.</div>
The following purified virus genomes are infectious if artificially introduced into cells<div>A. herpes simplex virus</div><div>B. vaccinia virus</div><div>C. poliovirus</div><div>D. influenza virus</div><div>E. HIV</div>
“<div>The following purified virus genomes are infectious if artificially introduced into cells<div>A. herpes simplex virus (TRUE)</div><div>B. vaccinia virus (TRUE)</div><div>C. poliovirus (TRUE)</div><div>D. influenza virus (FALSE)</div><div>E. HIV (FALSE)</div></div><div><br></br></div><div>D - F; -ve sense are non-infectious as need virally encoded RNA-dependent RNA pol</div><div>E - F; retroviruses are non-infectious as require virally encoded reverse transcriptase</div>”
These are obligate anaerobes producing endospores and enzymatic toxins<div>A. Clostridium difficile</div><div>B. Clostridium botulinum</div><div>C. Bacteriodes fragilis</div><div>D. Streptococcus pneumoniae</div><div>E. Clostridium tetani</div>
<div>These are obligate anaerobes producing endospores and enzymatic toxins<div>A. Clostridium difficile (TRUE)</div><div>B. Clostridium botulinum (TRUE)</div><div>C. Bacteriodes fragilis (FALSE)</div><div>D. Streptococcus pneumoniae (FALSE)</div><div>E. Clostridium tetani (TRUE)</div></div>
<div>In gastrointestinal infections<br></br></div>
<div>a. Helicobacter pylori is a motile Gram-negative bacterium for which VacA is a key virulence factor</div>
<div>b. ETEC causes travellers’ diarrhoea by bacteria entering host intestinal cells and inducing inflammation</div>
<div>c. Listeria invades intestinal cells by receptor-mediated endocytosis to establish an intracellular infection, but it can become systemic and cross the blood-brain barrier</div>
<div>d. Clostridium difficile secretes toxins that disrupt the actin cytoskeleton and epithelial tight junctions</div>
<div>e. Shiga toxin inhibits Rho/Ras GTPases, causing kidney damage</div>
A - T; pore-forming vacuolating cytotoxin<div>B - T; via fimbrial pili adhesins. Spread by contaminated water.</div><div>C - T</div><div>D - T; TcdA and TcdB that are small glycosylases leading to diarrhoea and inflammation of colonic mucosa. Cell damage is indirect via inflammation and pseudomembrane formation.</div><div>E - F a glycosidase that depurinates 28S rRNA thereby blocking protein synthesis but does cause renal failure</div>
The following are pro-thrombotic<div>A. microparticles</div><div>B. plasminogen activator inhibitors</div><div>C. nitric oxide</div><div>D. fibrin</div><div>E. Von Willebrand factor</div>
<div>The following are pro-thrombotic<div>A. microparticles (TRUE)</div><div>B. plasminogen activator inhibitors (TRUE)</div><div>C. nitric oxide (FALSE)</div><div>D. fibrin (TRUE)</div><div>E. Von Willebrand factor (TRUE)</div></div>
The following statements are true<div>A. Bcl2 is a pro-survival protein</div><div>B. P53 inactivates p21</div><div>C. the APC gene is often mutated by frameshift mutations</div><div>D. Bcr-Abl is formed as the consequence of a chromosomal inversion</div><div>E. Ras proteins are activated by GTP hydrolysis</div>
<div>The following statements are true<div>A. Bcl2 is a pro-survival protein (TRUE)</div><div>B. P53 inactivates p21 (FALSE)</div><div>C. the APC gene is often mutated by frameshift mutations (FALSE)</div><div>D. Bcr-Abl is formed as the consequence of a chromosomal inversion (FALSE)</div><div>E. Ras proteins are activated by GTP hydrolysis (FALSE)</div></div>
<div><div>Which gene/genes are mutated in Lynch Syndrome?</div></div>
<div><div><div>A.BRCA 1/ BRCA 2</div><div>B.Rb1</div><div>C.KRAS</div><div>D.APC</div><div>E.MLH1/ MLH2</div></div></div>
E.MLH1/ MLH2
<div><div>Which statement is true?</div></div>
<div><div><div>A. BCL-2 is pro-apoptotic</div><div>B.Oncogene mutations are loss of function</div><div>C.Telomeres lengthen with each cell division</div><div>D.Activation of the Wnt signalling pathway leads to B-catenin degradation.</div><div>E.Rb1 acts at the G1/S checkpoint</div></div></div>
<div>E.Rb1 acts at the G1/S checkpoint</div>
<div><div>Which statement is true?</div></div>
<div><div><div>A.BRAF is classically mutated in breast carcinomas</div><div>B.E-cadherin is a DNA repair protein</div><div>C.MYC is a tumour suppressor gene</div><div>D.The translocation (8;14) is known as the Philadelphia chromosome<i></i></div><div>E.Isocitrate dehydrogenase (IDH) mutations leads to a block in cell differentiation</div></div></div>
E.Isocitrate dehydrogenase (IDH) mutations leads to a block in cell differentiation<br></br>
<div><div>Which statement is true?</div></div>
<div><div><div>A.RAS acts in the nucleus to regulate the cell cycle</div><div>B.TMPRSS2-ERG is a fusion gene is found in ~50% of leukaemias</div><div>C.Cyclin D1 complexes with CDK2 to regulate Rb1</div><div>D.PTEN is often over expressed in cancers</div><div>E.BCR-ABL fusion protein is a tyrosine kinase</div></div></div>
E.BCR-ABL fusion protein is a tyrosine kinase<br></br>
<div><div>Which statement is false?</div></div>
<div><div><div>A.Xeroderma pigmentosum patients lack excision repair</div><div>Β.Dimethyl nitrosamine is a carcinogen found in meat products</div><div>C.Aflatoxin B1 is produced by Aspergillus flavus</div><div>D.Aristolochic acid commonly causes lung cancer<i></i></div><div>E.Beta-naphthylamine is a bladder carcinogen</div></div></div>
D.Aristolochic acid commonly causes lung cancer
<div><div>Which of the following does not cause cancers in humans?</div></div>
<div><div><div>A.EBV</div><div>B.HBV</div><div>C.HHV8</div><div>D.HTLV1</div><div>E.CMV<i></i></div></div></div>
E.CMV<br></br>
Regarding complement<div>A. C1q and mannose binding lectin (MBL) participate in the alternative pathway</div><div>B. self cells are protected by decay accelerating factor (DAF) and properdin</div><div>C. C3 is the central component of the complement system</div><div>D. C3a and C5a cause anaphylactic shock by systemic stimulation of mast cells</div><div>E. C3b, C-reactive protein (CRP) and MBL are opsonins</div>
A - F; MBL is lectin and C1q is classical<div>B - F; properdin is a positive regulator of C3bBb. DAF does protect and dissociates classical and alternative C3 convertases.</div><div>C - T</div><div>D - T</div><div>E - T</div>
Inflammation<div>a. symptoms include calor, rubor, tumor, dolor</div><div>b. involves the pro-inflammatory cytokines IL-1, IL-6 and tumour necrosis factor (TNFα)</div><div>c. leads to the chemokine CXCL8 attracting mast cells</div><div>d. occurs only in response to a pathogen</div><div>e. from a systemic infection can lead to TNFα in the blood, giving rise to septic shock<br></br></div>
A - T<div>B - T; IL-1beta, TNF-alpha, IL-6, CXCL8 and IL-12 all released by macrophages</div><div>C - F; neutrophils</div><div>D - F; pancreatitis for example</div><div>E - T</div>
Innate immunity<div>a. can result from pattern recognition receptor recognition of pathogen associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs)</div><div>b. can be initiated by TLR4 and NOD-like receptor (NLR) recognition of LPS in endosomes</div><div>c. stops most microorganisms before adaptive immunity is stimulated</div><div>d. in response to viral RNA through TLR3 leads to interferon response factor 3 (IRF3) activation and production of type I interferon</div><div>e. is necessary for the activation of adaptive immunity</div>
A - T<div>B - F; NOD-like receptors are cytosolic that recognise both PAMPS and DAMPS<br></br><div>C - T; physical and chemical barriers prevent the vast majority of infections and then oroganisms that do penetrate are usually elminated by the innate immune system</div></div><div>D - T; TLR3 recognises ds viral RNA –> TRIF –> IFNs</div><div>E - T</div>
Regarding cell death<div>a. apoptosis is always due to disease</div><div>b. perforin and granzymes cause necrosis through the action of caspases</div><div>c. the inflammasome activates caspases to cause apoptosis</div><div>d. synergistic cytokines lead to cell survival while antagonistic cytokines lead to cell death</div><div>e. necrosis initiates inflammation</div>
A - F<div>B - F; apoptosis not necrosis</div><div>C - F; induces inflammation by causing caspase 1 to activate IL-1beta. Other caspases lead to apoptosis.</div><div>D - F (?); not totally sure but I think it’s more about whether the responses of each cytokine promotes or hinders the other</div><div>E - T</div>
During an adaptive immune response<div>a. antigen is carried in the lymph to regional lymph nodes</div><div>b. follicular dendritic cells (FDCs) hold antigen/antibody complexes on their surface for presentation to T cells</div><div>c. B and T lymphocytes mainly enter lymph nodes via the afferent lymph</div><div>d. T helper cells are found in germinal centres</div><div>e. naïve T cells are activated by monocytes</div>
A - T<div>B - F</div><div>C - F</div><div>D - T; T follicular helper cells</div><div>E - F; macrophages</div>
Regarding antibody generation<div>A. the heavy chain is generated by splicing together different V, D and J exons</div><div>B. IgG is the first antibody isotype to be produced</div><div>C. somatic hypermutation requires the enzyme activation-induced cytidine deaminase (AID)</div><div>D. B cells arriving in regional lymph nodes undergo VDJ recombination</div><div>E. humans have an antibody repertoire estimated to comprise at least 1011 different specificities</div>
<div>Regarding antibody generation<div>A. the heavy chain is generated by splicing together different V, D and J exons (TRUE)</div><div>B. IgG is the first antibody isotype to be produced (FALSE)</div><div>C. somatic hypermutation requires the enzyme activation-induced cytidine deaminase (AID) (TRUE)</div><div>D. B cells arriving in regional lymph nodes undergo VDJ recombination (FALSE)</div><div>E. humans have an antibody repertoire estimated to comprise at least 1011 different specificities (TRUE)</div></div>
MHC class I molecules<div>a. are expressed on most cells of the body</div><div>b. may be recognised by receptors present on NK cells</div><div>c. present peptides to CD8+ cytotoxic T cells</div><div>d. primarily present peptides derived from antigens that enter the cell by endocytosis</div><div>e. use invariant chain as a chaperone</div>
“A - T<div>B - T</div><div>C - T</div><div>D - F; this is MHC II e.g. non-self</div><div>E - F; MHC II associates with invariant chain within ER to prevent binding of ER peptides</div><div><br></br></div><div><br></br></div><div><img></img><br></br></div>”
Regarding the immune system<div>a. a haplotype refers to a combination of MHC alleles that are inherited together</div><div>b. MHC polymorphism refers to variation in the sequence of genes at the same genetic locus</div><div>c. co-dominant expression refers to the expression of both maternal and paternal MHC haplotypes on the same cell</div><div>d. an anchor residue refers to an amino acid in the peptide-binding groove that binds the peptide</div><div>e. antibody affinity is the strength of binding of a single antibody binding site to a single monovalent epitope on an antigen</div>
“A - T<div>B - T; e.g. different alleles</div><div>C - T</div><div>D - T</div><div>E - T; c.f. avidity which is a measure of the strenght of interaction due to recognition of these polyvalent epitopes. IgM antibodies are low affinity but high avidity</div><div><img></img><br></br></div>”
Professional antigen-presenting cells (APCs)<div>A. include B lymphocytes, mast cells and dendritic cells</div><div>B. express CD40 ligand and CD28</div><div>C. express both MHC class I and MHC class II molecules</div><div>D. originate from haematopoietic stem cells in the bone marrow</div><div>E. can be activated in the absence of infection</div>
<div>Professional antigen-presenting cells (APCs)<div>A. include B lymphocytes, mast cells and dendritic cells (FALSE)</div><div>B. express CD40 ligand and CD28 (FALSE)</div><div>C. express both MHC class I and MHC class II molecules (TRUE)</div><div>D. originate from haematopoietic stem cells in the bone marrow (TRUE)</div><div>E. can be activated in the absence of infection (TRUE)</div></div>
These statements about cytokines are correct<div>A. CXCL8 is chemotactic for neutrophils</div><div>B. interferon gamma (IFNγ) suppresses Th2 responses</div><div>C. IL-6 induces the acute phase response</div><div>D. IL-12 and IL-10 are pro-inflammatory</div><div>E. IL-2 induces T cell proliferation</div>
A - T<div>B - T</div><div>C - T</div><div>D - F; IL-10 is anti-inflammatory</div><div>E - F; IL-2 leads to Treg increase which decrease T cell proliferation</div>
Regarding tolerance<div>A. autoimmune regulator (AIRE) expression allows peripheral antigens to be expressed in the thymus</div><div>B. the majority of developing thymocytes fail positive selection</div><div>C. high doses of soluble self-antigen leads to B cell anergy</div><div>D. Tregs typically express the Foxp3 transcription factor</div><div>E. immunodysregulation polyendocrinopathy enteropathy X-linked (IPEX) syndrome is due to defective AIRE expression</div>
A - T; turns on peripheral genes in the thymus so that developing T cells may be exposed to their products<div>B - T</div><div>C - T</div><div>D - T</div><div>E - F; AIRE lack –> APECED while loss of FOXP3 leads to IPEX</div>
In the response to infection<div>A. IL-4 and IL-13 are important cytokines for controlling helminth infections</div><div>B. clearance of protozoan infections is generally helped by Th1 responses and hindered by Th2 responses</div><div>C. NK cells release interferon gamma (IFNγ)</div><div>D. most vaccines against virus infection protects via the generation of neutralizing antibody</div><div>E. alternatively-activated macrophages are associated with Th2 responses</div>
A - F; IL-5 and IL-13 are important for helmniths<div>B - T; anything intracellular = Th1</div><div>C - T</div><div>D - T</div><div>E - T</div>
Regarding immunity to pathogens<div>A. cytotoxic T cells (CTLs) kill virus-infected cells</div><div>B. Th1 cells are MHC class II-restricted and a major role is to activate macrophages</div><div>C. Th17 cells promote neutrophil recruitment to sites of fungal infection</div><div>D. TNFα stimulates dendritic cell activation and migration to lymph nodes</div><div>E. type I interferons induce an antiviral state by preventing virus attachment to the host cell</div>
“A - T<div>B - F</div><div>C - T</div><div>D - T</div><div>E - F; I’m not sure if this actually occurs?</div><div><img></img><br></br></div>”
Regarding autoimmunity<div>A. CD4+ Th1 cells are responsible for causing disease in the rat model of multiple sclerosis</div><div>B. myasthenia gravis is caused by autoantibodies that activate the acetylcholine receptor</div><div>C. environmental factors contribute about 50% of the susceptibility towards type I diabetes</div><div>D. mutant MHC molecules are the most important genetic risk factor in autoimmune disease</div><div>E. deficiencies in complement components predispose towards the immune complex disorder systemic lupus erythematosus (SLE)</div>
A - T; CD4+ T cells specific to MBP (myelin basic protein) can subsequently cause disease if injected into another animal<div>B - F</div><div>C - T; MHC contributes other 25% and other genes the final 25%</div><div>D - F</div><div>E - T; C1, C2 and C4 deficiency all can lead to problems with immune complex disease</div>
Regarding transplantation<div>A. hyperacute rejection can result from pre-existing antibody</div><div>B. minor transplantation antigens result from allelic differences in proteins expressed in the recipient and donor</div><div>C. a syngeneic transplant refers to a transplant between genetically identical individuals</div><div>D. direct recognition of MHC alloantigen involves donor dendritic cells presenting antigen to and activating host T cells</div><div>E. non-depleting anti-CD4 antibodies preferentially induce Th1 responses in transplant patients</div>
A - T<div>B - T; where they vary in sequence and one of the allomorphs contains peptides which binds to the MHC II of the recipient and then stimulate a CD4 T cell alloreaction</div><div>C - T</div><div>D - T</div><div>E - F; a new antibody approach –> anti-CD4 non-depleting antibodies favours less harmful Th2 reponses over Th1</div>
Regarding blood groups<div>A. an individual, who has not been previously transfused, is likely to have antibody to the O antigen blood group</div><div>B. an individual with blood group AB is a universal donor</div><div>C. the population frequency of AB individuals is low</div><div>D. a child who is blood group A (phenotypically) may have a mother who is blood group O</div><div>E. rhesus (Rh) antigen incompatibility is not a consideration in blood transfusions</div>
A - F<div>B - F; universal receiver</div><div>C - T; 4%</div><div>D - T</div><div>E - F</div>
Regarding viruses<div>a. the genome of a positive-strand RNA virus is complementary to mRNA</div><div>b. influenza virus and rotavirus both have segmented RNA genomes</div><div>c. a haemagglutination assay is performed by infecting red blood cells with influenza virus</div><div>d. enveloped viruses can have icosahedral capsids</div><div>e. electron microscopy can be used to observe viruses</div>
A - F; negative strand RNA virus is complementary<div>B - T; influenza RNA ss -ve sense 8 segments while rotavirus is RNA ds with 11 segments</div><div>C - F; HA assay where you get haemagglutination from RBCs with sialic acid on their surface binding to HA of influenza</div><div>D - T; e.g. herpes simplex</div><div>E - T; used in counting virus particles especially if attached by antibody with gold bead attached</div>
Viruses modify infected cells<div>a. herpesviruses encode a thymidine kinase (TK) enzyme that directly converts NTPs to dNTPs</div><div>b. adenoviruses stimulate infected cells to enter the cell cycle</div><div>c. poliovirus cleaves the cap of cellular mRNAs to promote viral gene translation</div><div>d. measles virus spreads by causing infected cells to fuse with neighbouring cells</div><div>e. poxviruses inhibit interferon signalling by blocking the pattern recognition receptors NF-κB and interferon response factor 3 (IRF3)</div>
A - F; this is ribonucleotide reductase –> see diagram<div>B - T</div><div>C - F; poliovirus encodes a protease that cleaves a component of the cap-binding complex so host mRNAs are not recognised, it is poxivurs that cleaves off the 5’ capps completely</div><div>D - T<br></br>E - F; these are downstream of the PRRs –> however, pxo virus does target this parthway</div>
These viruses are sexually transmitted<div>A. herpes simplex virus (HSV)</div><div>B. hepatitis A virus</div><div>C. Ebola virus</div><div>D. human papilloma virus</div><div>E. dengue virus</div>
These viruses are sexually transmitted<div>A. herpes simplex virus (HSV) (TRUE)</div><div>B. hepatitis A virus (TRUE)</div><div>C. Ebola virus (FALSE)</div><div>D. human papilloma virus (TRUE)</div><div>E. dengue virus (FALSE)</div>
Hepatitis B virus<div>a. is spread via the faeco-oral transmission route</div><div>b. causes persistent (chronic) infection</div><div>c. has an RNA genome</div><div>d. encodes a reverse transcriptase essential for virus replication</div><div>e. can be effectively cured by drug treatment</div>
A - F; contaminated needles, mother to child, during first years of life from family, sexually trasnmitted, blood products<div>B - T; 90% chronic if young and 10% if older</div><div>C - F; partially ds DNA</div><div>D - T; polymerase gene</div><div>E - F; effecive vaccine –> genetically engineered subunit cavvine (HBsAg)</div>
Regarding infection by human immunodeficiency virus (HIV):<div>a. binding of the HIV attachment protein gp120 to cellular CD4 is sufficient to allow cell entry</div><div>b. in rapid progressors, primary infection causes a sharp decline in the CD4+ cell count that rapidly rebounds to pre-infection levels</div><div>c. rapid replication followed by virus-induced cell lysis destroys infected CD4+ cells</div><div>d. during infection the ratio of capsid (gag) to envelope (env) protein expression is regulated by ribosomal frameshifting</div><div>e. error-prone reverse transcription of HIV genomes means that the infection cannot be controlled by drug treatment</div>
A - F; gp120 binds to CD4 and also CCR5 of CXCR4 chemokine co-receptors<div>B - F; CD4 count drops massively</div><div>C - T; in the early period the virus continues to replicate but is controlled by CD8+ CTL cells but then as the virus escapes from the immune system and replicates more extensively then more CD4+ cells are destroyed.</div><div>D - F; gag to env is determined by splicing while gag-pol is frameshifting</div><div>E - F; reverse transcriptase inhibitors are important for HIV treatment e.g. AZT</div>
A farm worker with a deep wound in his hand has developed tetanus. Which statement best describes the properties of tetanus toxin that give rise to these features?<div>A. it is produced by spores of Clostridium tetani under anaerobic conditions</div><div>B. it acts on peripheral nerves, causing spastic paralysis</div><div>C. it is a peptidase cleaving small GTPases involved in signal transduction</div><div>D. it is an adenylate cyclase, inactivating synaptobrevin</div><div>E. it blocks release of inhibitory neurotransmitters</div>
“<div>E. it blocks release of inhibitory neurotransmitters<br></br></div><div><br></br></div><div>A - spores are in relation to germination and not the toxin action although this statement is otherwise correct</div><div>B - it acts on spinal interneurons –> botulinum works on peripheral nerves</div><div>D - it cleaves synaptobrevin</div>”
A woman presents with a sore throat and lesions on her tonsils after a few days. A throat swab is inoculated onto a sheep blood agar plate and a blood sample is taken. Which of the following provides the strongest specific evidence that the infection is caused by Streptococcus pyogenes?<div>A. bacteria isolated from the infection site are Lancefield Group B based on cell surface carbohydrate antigens</div><div>B. bacterial colonies show complete haemolysis on blood agar</div><div>C. Gram staining reveals chains of Gram-positive rod-shaped cells</div><div>D. bacterial colonies are small, translucent and concave</div><div>E. titration of the patient’s serum against Streptolysin O reveals a high titre of antiStreptolysin O antibodies</div>
“<div>E. titration of the patient’s serum against Streptolysin O reveals a high titre of antiStreptolysin O antibodies<br></br></div><div><br></br></div><div>A - they are Lancefield group A</div><div>B - true but not specific</div><div>C - cocci</div><div>D - sure… non-specific</div>”
A middle-aged man is suffering from severe bloody diarrhoea and stomach cramps after attending a barbecue the previous evening. Which of the following would be the most likely causative agent?<div>A. Staphylococcus aureus</div><div>B. Salmonella enterica</div><div>C. Escherichia coli 0157:H7</div><div>D. Campylobacter jejuni</div><div>E. Listeria monocytogenes</div>
“<div>C. Escherichia coli 0157:H7<br></br></div><div><br></br></div><div>A - skin infections –> in custard and processed meats but is superantigen and hence more sepsis type presentation?</div><div>B - chicken/egg</div><div>D - does produce bloody diarrhoea</div><div>E - it is food borne</div>”
A virus infection of the liver in early childhood resulted in chronic liver inflammation and dysfunction as well as subsequent liver cancer in later life. Which of the following viruses is the most likely cause of these clinical outcomes:<div>A. Hepatitis A virus</div><div>B. Hepatitis B virus</div><div>C. Hepatitis C virus</div><div>D. Human cytomegalovirus</div><div>E. Yellow fever virus</div>
B. Hepatitis B virus
An outbreak of highly pathogenic influenza virus infection in a poultry farm was identified as the H5N1 strain of avian influenza virus. Which best describes the replication of the influenza virus genome:<div>A. Negative sense single stranded RNA that is copied into positive sense RNA and then copied back into negative sense RNA genomes</div><div>B. Negative sense single stranded RNA that is translated directly by the host ribosomes to generate the viral RNA polymerase required to copy the viral RNA genome</div><div>C. Reverse transcription of a segmented negative sense RNA genome into DNA followed by transcription of the DNA copies into RNA genomes</div><div>D. Segmented double stranded RNA that replicates in the cytoplasm through the activity of RNA-dependent RNA polymerase that is packaged into the virion</div><div>E. Single-stranded DNA the replicates in the nucleus through the activity of host RNA polymerase II</div>
A. Negative sense single stranded RNA that is copied into positive sense RNA and then copied back into negative sense RNA genomes
Scientists are studying a virus that infects lymphocytes and in rare circumstances can cause lymphoma. The virus that is most likely the focus of this research is:<div>A. Cytomegalovirus</div><div>B. Epstein-Barr Virus</div><div>C. Human immunodeficiency virus</div><div>D. Human papillomavirus 18</div><div>E. Rous sarcoma virus</div>
B. Epstein-Barr Virus
A key component of an innate immune response to viruses is the interferon pathway. The production of type I interferon in response to virus infection:<div>A. Activates pathogen recognition receptor signalling cascades</div><div>B. Causes rapid cell division due to the release of growth factors C. Is blocked by viral proteins that destroy MHC class I molecules</div><div>D. Stimulates the synthesis of antiviral proteins such as protein kinase R</div><div>E. Stimulates virus gene expression through the activation of the JAK-STAT signalling pathway</div>
D. Stimulates the synthesis of antiviral proteins such as protein kinase R
Strain A mice make TH2-type responses in reaction to helminth infections. When infected with the murine whipworm Trichuris muris, what is the expected response?<div>A. The mice will make IFNγ and clear the parasite</div><div>B. The mice will make TNFα and suffer persistent infection</div><div>C. The mice will make IFNγ, IL-4 and IL-13 and establish an asymptomatic longlived infection.</div><div>D. The mice will make IL-4 and IL-13 and clear the infection</div><div>E. The mice will make IL-4 and IL-13 and suffer persistent infection</div>
<div>D. The mice will make IL-4 and IL-13 and clear the infection<br></br></div>
NK cells function in early defence against viruses that have not previously been encountered. They do this by:<div>A. expressing activatory receptors that recognise the presence of MHC class I on infected cells.</div><div>B. expressing activatory receptors that recognise virus encoded molecules.</div><div>C. expressing activatory receptors that recognise self molecules induced in stressed cells.</div><div>D. expressing Fc receptors that are capable of inducing perforin and granzymes release thereby inducing apoptosis of the infected cell.</div><div>E. interacting with dendritic cells and initiating their migration to regional lymph nodes.</div>
“<div>C. expressing activatory receptors that recognise self molecules induced in stressed cells.</div><div><br></br><div>A - MHC I are everywhere so this doesn’t make sense</div><div>B - virus tries to reduce expression of signals so don’t think this makes sense</div><div>D - no because antibodies have not yet been made</div><div>E - they interact with macrophages</div></div>”
The complement system is a collection of proteins that work together to provide protection from infection. Which statement most correctly describes the listed activity?<div>A. C3, C4 and C5 are structurally related complement components that can covalently attach to pathogen surfaces<br></br></div><div>B. DAF and factor H regulate C3 convertase activity by recruiting the protease activity of factor I</div><div>C. patients deficient in C4 would be predicted to suffer from immune complex diseases such as contact hypersensitivity</div><div>D. patients deficient in factor I would be predicted to suffer from over activation of the alternative pathway</div><div>E. properdin is one of a group of complement control proteins that increase the activity of the complement pathways by stabilising the alternative pathway C3 convertase</div>
“<div>D. patients deficient in factor I would be predicted to suffer from over activation of the alternative pathway<br></br></div><div><br></br></div><div>A - they all attach but not sure if structurally related because maybe just C3 that has the internal thioester bond</div><div>B - Factor H and MCP are cofactors for factor I (soluble serine protease) and then degrades C3b and C4b. DAF dissociates classical and alternative C3 convterases and is present on host cells.</div><div>C - contact hypersensitivity is IV e.g T cell mediated but C4 deficiency does lead to immune-complex disease</div><div>E - it’s not one of a group but it does do this</div>”
The following viruses can transform cells<div>A. Measles virus</div><div>B. Rabies virus</div><div>C. Papilloma virus</div><div>D. Avian retrovirus</div><div>E. Rhinovirus</div>
<div>The following viruses can transform cells<div>A. Measles virus (FALSE)</div><div>B. Rabies virus (FALSE)</div><div>C. Papilloma virus (TRUE)</div><div>D. Avian retrovirus (TRUE)</div><div>E. Rhinovirus (FALSE)</div></div>
Concerning vaccines and vaccination<div>a. smallpox eradication was facilitated by the development of a freeze-dried vaccine</div><div>b. the Salk polio vaccine is a live attenuated vaccine</div><div>c. the current hepatitis B vaccine is a genetically-engineered subunit vaccine</div><div>d. an advantage of dead vaccines is that they induce humoral and cellular immunity</div><div>e. eggs are used during the production of the influenza virus subunit vaccine</div>
A - T<div>B - F; sabin is the live attenuated virus, salk is the inactivated virus</div><div>C - T; made by expressing HBsAg in yeast, purifying and injecting with adjuvant</div><div>D - F; live vaccines do this</div><div>E - T</div>
Regarding innate and adaptive immune responses to virus infection<div><br></br></div><div>a. antibodies are usually involved in killing virus-infected cells</div><div>b. cytoplasmic viral DNA can be sensed by pattern recognition receptors</div><div>c. NK cells generally play a role late in infection once an antigen-specific CD8+ T-cell response has developed</div><div>d. adenoviruses evade immune attack by preventing the transport of MHC class I molecules to the cell surface</div><div>e. Epstein-Barr virus (EBV) encodes a viral cytokine that drives the immune system towards a Th1 response</div>
A - F<div>B - T; TLR9 senses DNA viruses via unmethylated CpG rich DNA</div><div>C - F</div><div>D - T; block transport of peptides into ER for presentation, retain MHC I intracellularly so preventing their transport to the cell surface</div><div>E - F; vIL-10 –> Th2</div>
Regarding virus evolution and virus adaptation to their hosts<div>a. virus infections associated with high morbidity and/or mortality are often zoonoses</div><div>b. antigenic drift is the process by which influenza virus can acquire a HA gene from another influenza virus</div><div>c. changes in the influenza PB2 gene can affect influenza virus replication efficiency in human cells</div><div>d. acquisition of cellular genes from their hosts explains the existence of RNA virus genomes of over 100 kilobases (kb)</div><div>e. following its introduction to Australia, myxoma virus mutated to become a more virulent pathogen</div>
A - T<div>B - F</div><div>C - T; PB2 makes up part of the RNA-dependent RNA polymerase –> E = avian while K = human</div><div>D - F; the largest RNA viruses are just > 30 kb and these are due to proof reading activity of RNA polymerase</div><div>E - F</div>
Tetanus toxin<div>a. is a single polypeptide A-B toxin produced by spores of Clostridium tetani in anaerobic wounds</div><div>b. B subunit binds to a receptor on peripheral nerve membranes c. is a protease that cleaves synaptobrevin, blocking release of inhibitory neurotransmitters in the CNS</div><div>d. A chain causes spastic paralysis by acting on peripheral nerves</div><div>e. has the same proteolytic action as Botulinum toxin</div>
A - T<div>B - T</div><div>C - T</div><div>D - F</div><div>E - T</div>
In respiratory infections<div>a. Streptococcus forms hemolytic colonies, pairs or chains of Gram-positive cocci, and is Lancefield Group A</div><div>b. Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenza, all secrete IgA protease and have polysaccharide capsules</div><div>c. whooping cough is caused by Bordetella pertussis, which secretes ADPribosylating pertussis toxin and an adenylate cyclase toxin</div><div>d. Legionella pneumophila initiates propagated outbreaks from infected water (for example, from air conditioning units)</div><div>e. diphtheria toxin ADP-ribosylates rRNA and thus inhibits translation</div>
A - F; they all have different groups surface carbohydrates e.g. equi is C while pyogenes is A<div>B - F; they all have IgA proteases; they all have capsules (Neisseria = sialic acid one which not polysaccharide?)</div><div>C - T</div><div>D - T</div><div>E - F; ADP-ribosylates EF2 so preventing protein synthesis</div>
These are rod-shaped cells that have an outer membrane<div>A. Salmonella typhi</div><div>B. Clostridium perfringens</div><div>C. Bacillus anthracis</div><div>D. Bacteriodes fragilis</div><div>E. Neisseria meningitidis</div>
<div>These are rod-shaped cells that have an outer membrane<div>A. Salmonella typhi (TRUE)</div><div>B. Clostridium perfringens (FALSE)</div><div>C. Bacillus anthracis (FALSE)</div><div>D. Bacteriodes fragilis (TRUE)</div><div>E. Neisseria meningitidis (FALSE)</div></div>
In Gram-negative bacteria such as Escherichia coli<div>a. haploid chromosome replication and binary fission result in population doubling times of two minutes in laboratory culture</div><div>b. virulence genes can be located on bacteriophage, on plasmids and on pathogenicity islands</div><div>c. LPS lipid A activates macrophages via CD14 and TLR4</div><div>d. lipid A protects the cell from damage by the complement membrane attack complex</div><div>e. DNA acquisition by conjugation requires bacterial contact, but transformation allows DNA uptake from the environment</div>
A - F; every 20-30 mins<div>B - T; weird Q</div><div>C - T</div><div>D - F; LPS-O antigen and capsules prevent complement (lipid A is inner, not outer coat)</div><div>E - T</div>
In tuberculosis<div>a. Mycobacterium tuberculosis is spread in propagated outbreaks by droplets, and survives in alveolar macrophages by inhibiting phagosome-lysosome fusion and resisting the oxidative burst</div><div>b. chronic disease involves granulomatous inflammation which is often resolved by shifting to a Th2 response</div><div>c. Mycobacterium bovis can be a zoonotic disease of humans</div><div>d. mycobacteria grow slowly, they do not Gram stain due to cell wall lipid content, but are visible microscopically after Albert staining of cytoplasmic granules</div><div>e. immunity is indicated by a cell-mediated response in the tuberculin skin test, and is conferred by the live attenuated DPT vaccine</div>
A - T; TB, gonorrhoea, dysentery, cholera, typhoid all examples<div>B - F</div><div>C - T</div><div>D - F; Albert stain is for the polyphosphate granules of Corynebacterium diphtheriae<br></br>E - F; BCG</div>
Regarding antibiotics and bacterial resistance<div>A. TolC is an inner membrane transporter in multidrug efflux pumps</div><div>B. vancomycin mimics D-Ala-D-Ala crosslinks to inhibit peptidoglycan synthesis, but resistance is mediated by synthesis of alternative peptide crosslinks</div><div>C. ciprofloxacin, a fluoroquinolone, inhibits gyrase and thus gene expression</div><div>D. resistance to Trimethoprim, an inhibitor of folate synthesis, is conferred by expression of a ‘bypass’ dihydrofolate reductase</div><div>E. tetracycline binds the 30S ribosomal subunit and blocks aminoacyl tRNA entry</div>
Regarding antibiotics and bacterial resistance<div>A. TolC is an inner membrane transporter in multidrug efflux pumps (FALSE)</div><div>B. vancomycin mimics D-Ala-D-Ala crosslinks to inhibit peptidoglycan synthesis, but resistance is mediated by synthesis of alternative peptide crosslinks (FALSE)</div><div>C. ciprofloxacin, a fluoroquinolone, inhibits gyrase and thus gene expression (TRUE)</div><div>D. resistance to Trimethoprim, an inhibitor of folate synthesis, is conferred by expression of a ‘bypass’ dihydrofolate reductase (TRUE)</div><div>E. tetracycline binds the 30S ribosomal subunit and blocks aminoacyl tRNA entry (TRUE)</div>
In gastrointestinal infections<div>a. Helicobacter pylori is a motile Gram-negative rod that causes chronic inflammation of the gastric mucosa</div><div>b. enterotoxigenic Escherichia coli (ETEC) causes diarrhoea in children and piglets, colonizing host cells by inducing Tir-dependent pedestals and secreting cholera-like toxin</div><div>c. Listeria is a food-borne organism that establishes an intracellular infection in the GI tract, but can become systemic and cause meningitis</div><div>d. Clostridium difficile causes inflammation of colonic mucosa after antibiotic treatment, and secretes toxins that target small GTPases, leading to disruption of epithelial tight junctions</div><div>e. the predominant enterohaemorrhagic Escherichia coli (EHEC) serotype O157 is transmitted from beef, and in addition to inflammatory disease it produces a ADP-ribosylating toxin that can cause renal failure</div>
A - T<div>B - F; colonises via fimbrial (pili) adhesins and then cholera-like enterotoxin (LT). EPEC delivers Tir as does EHEC</div><div>C - T</div><div>D - T; glucosylate small GTPases thereby disrupting actin cytoskeleton and tight junctions</div><div>E - F; it does cause renal failure but shiga toxin (assuming similar to shiga like is a glycosidase that depurinates 28S rRNA rather than ADP-ribosylating)</div>
Regarding toxinogenic bacteria<div>a. pneumolysin, streptolysin O, Helicobacter VacA and Clostridium perfringens alpha-toxin all form pores in host cell membranes</div><div>b. uropathogenic Escherichia coli (UPEC) bind kidney cells via adhesins on the tip of P-pili and produce cytotoxic necrotizing factor, a deamidase that targets host cell GTPases</div><div>c. staphylococcal toxic shock syndrome toxin (TSST) is a superantigen that stimulates a cytokine storm after binding major histocompatibility complex (MHC) class I and T cell receptor molecules</div><div>d. shiga toxin is a glycosidase that modifies small GTPases, inhibiting protein synthesis</div><div>e. Corynebacterium ulcerans and Corynebacterium diphtheriae cause respiratory disease in which an ADP-ribosylating toxin targets host translation</div>
A - F; clostridium perfrigens alpha toxin apparenty degrades the membrane but is not in the list of pore forming toxins<div>B - T</div><div>C - F</div><div>D - F</div><div>E - T; related to the pathogen C. pseudotuberculosis</div>
The following statements are true<div>A. Salmonella enterica and Salmonella typhi cause zoonotic gastrointestinal disease in humans</div><div>B. Neisseria generates antigenic variation of surface pili by recombining silent pilin genes into active expression loci</div><div>C. Chlamydia trachomatis causes trachoma and urethritis, and is an obligate intracellular pathogen</div><div>D. both streptococcal glomerulonephritis and arthropod-borne Lyme’s disease caused by Borrelia involve type III hypersensitivity</div><div>E. cholera toxin, pertussis toxin and diphtheria toxin are multimeric</div>
<div>The following statements are true<div>A. Salmonella enterica and Salmonella typhi cause zoonotic gastrointestinal disease in humans (FALSE)</div><div>B. Neisseria generates antigenic variation of surface pili by recombining silent pilin genes into active expression loci (TRUE)</div><div>C. Chlamydia trachomatis causes trachoma and urethritis, and is an obligate intracellular pathogen (TRUE)</div><div>D. both streptococcal glomerulonephritis and arthropod-borne Lyme’s disease caused by Borrelia involve type III hypersensitivity (TRUE)</div><div>E. cholera toxin, pertussis toxin and diphtheria toxin are multimeric (FALSE)</div></div>
In fungal infections<div>a. a dimorphic fungus exists as a mould at 37°C and as a yeast at 24°C</div><div>b. Cryptococcus is a yeast</div><div>c. asymptomatic persistent Aspergillus infection of alveolar macrophages is common</div><div>d. Sporothrix infection is acquired by inhalation</div><div>e. the azole anti-fungal Fluconazole inhibits the synthesis of cholesterol</div>
A - F; e.g. histoplasma –> when warm they are yeasts<div>B - T</div><div>C - F; it occurs in those with lung cavities, asthma, or severe deficiencies in neutrophils and it has a very high fatality</div><div>D - F; you get it from cuts e.g. rose picker’s disease</div><div>E - F; ergosterol</div>
In fungal infections<div>a. CD4+ T cells are essential for host defence against systemic (deep) yeast infections</div><div>b. superficial fungal infections of the skin are often transmitted indirectly by spores on inanimate surfaces</div><div>c. the echinocandin anti-fungal Caspofungin inhibits the synthesis of β-glucan</div><div>d. Th17 cells are essential for host defence against superficial fungal infections</div><div>e. the polyene anti-fungal Amphotericin damages the fungal cell membrane</div>
A - T; CD4+ –> Th17 –> IL-17 and IL-22<div>B - T; e.g. dermatophyte moulds such as microsporum, trichopyton and epidermophyton</div><div>C - T</div><div>D - T</div><div>E - T</div>
Regarding helminths<div>a. dogs are a definitive host for Echinococcus tapeworms</div><div>b. Schistosoma japonicum infection is associated with bladder cancer</div><div>c. Trichuris trichuria infection can last for decades</div><div>d. Enterobius vermicularis infections are rare in the UK</div><div>e. Taenia solium causes neurocysticercosis</div>
A - T<div>B - T; not sure if this one is true because we learn about S. Mansoni but hopefully</div><div>C - T; e.g. whipworm</div><div>D - F; most common worm infection, especially in young children</div><div>E - T; epilepsy, seizures and blindness</div>
Regarding schistosomiasis<div>a. the adult worm protects against immune attack by secreting proteases that cleave iC3b</div><div>b. granulomas are characteristic of the immune response to schistosome adult worms</div><div>c. Albendazole is the drug of choice for treatment</div><div>d. resistance to Schistosoma mansoni re-infection is highest in adolescent children</div><div>e. severe fibrosis is associated with a sustained Th2 cell response</div>
A - T; apparently m28 protein cleaves<div>B - T; Th2</div><div>C - F; praziquantal</div><div>D - F? not really sure on this</div><div>E - T</div>
Regarding tapeworms<div>a. the scolex maintains the adult tapeworm position in the gut</div><div>b. adults are hermaphrodites</div><div>c. hydatid cysts are a major cause of epilepsy</div><div>d. the proglottid is a male reproductive unit</div><div>e. Echinococcus granulosus causes alveolar disease that can result in jaundice</div>
A - T<div>B - T</div><div>C - T; cystercerci can cause epilepsy</div><div>D - F; they are eggs –> think there’s not really sexes</div><div>E - F; alveolar disease isn’t gonna cause jaundice</div>
Regarding Apicomplexa<div>A. micronemes, apicoplasts, and rhoptries are all secretory organelles of the apical complex</div><div>B. bradyzoites and sporozoites are the dividing forms of Toxoplasma gondii in intermediate hosts</div><div>C. the phylum includes Eimeria, Babesia and Theileria species</div><div>D. Plasmodium falciparum CpG DNA and haemazoin are recognised by TLR9</div><div>E. during invasion Plasmodium vivax merozoites bind to the human Duffy antigen receptor for chemokines</div>
A - F; apical complex = microneme, rhoptry and dense granule<div>B - F; bradyzoites are normally quiescent tissue cysts while the oocysts are formed by the gametocytes that fuse to form an oocyst. Also the cat is the definitive host and this is where the sexual cycle occurs.</div><div>C - T</div><div>D - F; CpG DNA will be be for TLR9 but I think the haemazoin will be TLR-2 or TLR1/6 –> see diagram</div><div>E - T</div>
Malaria in humans<div>a. is most commonly caused by Plasmodium vivax and Plasmodium falciparum</div><div>b. is a major cause of childhood fatality in sub-Saharan Africa</div><div>c. includes cerebral malaria caused by red blood cell sequestration mediated by variable PfEMP adherence to the vascular endothelium</div><div>d. has selected for changes in haemoglobin, some of which act to decrease red blood cell sequestration by reduced adherence to the vascular endothelium</div><div>e. is a disease found only in sub-Saharan Africa</div>
A - T; 40-50% for falciparum and 15-20% for vivax<div>B - T</div><div>C - T</div><div>D - F; PfEMPs that increase adherence via iCAM-1 to reduce clearance by the spleen</div><div>E - F</div>
Regarding control or treatment of parasitic infections<div>a. the African Programme for Onchocerciasis Control provides mass Praziquantel administration</div><div>b. Lumefantrine and Amodiaquine are used in artemisinin-based combination therapies</div><div>c. the “Roll Back Malaria” initiative has a major emphasis on long-lasting insecticidal nets containing DDT and indoor residual spraying</div><div>d. chloroquine in the first-line drug of choice for Plasmodium vivax</div><div>e. since publication of the Millennium Development Goals, the death rates amongst under 5 year olds from malaria has decreased by 65%</div>
A - F; Ivermectin acn be used against a range: worm parasites –> arthropod ectoparasites<div>B - T</div><div>C -F; nets contains pyrethroid insecticides while indoor residual spraying uses DDT</div><div>D - T; also P. ovale</div><div>E - T</div>
A brain infarct<div>A. may be a complication of coronary artery thrombosis</div><div>B. may produce a cyst</div><div>C. usually heals by regeneration</div><div>D. is characterised by caseation necrosis</div><div>E. may be due to atherosclerosis in a common carotid artery</div>
<div>A brain infarct<div>A. may be a complication of coronary artery thrombosis (FALSE)</div><div>B. may produce a cyst (TRUE)</div><div>C. usually heals by regeneration (FALSE)</div><div>D. is characterised by caseation necrosis (FALSE)</div><div>E. may be due to atherosclerosis in a common carotid artery (TRUE)</div></div>
A thrombus in the left ventricle may<div>A. heal by organisation</div><div>B. embolise to the lungs</div><div>C. cause a cerebral infarct</div><div>D. become infected</div><div>E. be due to an aneurysm</div>
<div>A thrombus in the left ventricle may<div>A. heal by organisation (TRUE)</div><div>B. embolise to the lungs (FALSE)</div><div>C. cause a cerebral infarct (TRUE)</div><div>D. become infected (TRUE)</div><div>E. be due to an aneurysm (TRUE)</div></div>
In dyserythropoiesis:<div>a. normal folate stores last for five years</div><div>b. disease of the small bowel may lead to iron deficiency</div><div>c. folate deficiency may lead to iron deposition in the liver</div><div>d. iron deficiency causes macrocytosis</div><div>e. folate deficiency is exacerbated by pregnancy</div>
A - F; vit B12<div>B - T; e.g. coeliac</div><div>C - T; in both B12 and folate deficiency iron cannot be utilised normally and so is deposited in various organs</div><div>D - F; microcytosis</div><div>E - T</div>
The following are pro-thrombotic<div>A. microparticles</div><div>B. prostacyclin</div><div>C. protein C</div><div>D. thrombomodulin</div><div>E. thromboplastin</div>
<div>The following are pro-thrombotic<div>A. microparticles (TRUE)</div><div>B. prostacyclin (FALSE)</div><div>C. protein C (FALSE)</div><div>D. thrombomodulin (FALSE)</div><div>E. thromboplastin (TRUE)</div></div>
Atheromatous plaques<div>A. can affect the media of blood vessels</div><div>B. are more likely to occur if levels of blood triglycerides are elevated</div><div>C. may be calcified</div><div>D. are more likely to occur in individuals with diabetes mellitus</div><div>E. only develop in arteries or veins</div>
<div>Atheromatous plaques<div>A. can affect the media of blood vessels (FALSE)</div><div>B. are more likely to occur if levels of blood triglycerides are elevated (TRUE)</div><div>C. may be calcified (TRUE)</div><div>D. are more likely to occur in individuals with diabetes mellitus (TRUE)</div><div>E. only develop in arteries or veins (FALSE)</div></div>
A malignant growth<div>A. can form metastases</div><div>B. is contained in a capsule</div><div>C. invades surrounding tissue</div><div>D. can be called a leiomyoma</div><div>E. is always caused by inherited genetic mutations</div>
<div>A malignant growth<div>A. can form metastases (TRUE)</div><div>B. is contained in a capsule (FALSE)</div><div>C. invades surrounding tissue (TRUE)</div><div>D. can be called a leiomyoma (FALSE)</div><div>E. is always caused by inherited genetic mutations (FALSE)</div></div>
In cancers<div>a. an adenoma is a malignant growth of colorectal tissue</div><div>b. cervical cancer is a malignancy of squamous epithelium</div><div>c. a neoplasm is always malignant</div><div>d. leukaemia can derive from myeloid or lymphoid cells</div><div>e. metaplasia describes the proliferation status of tumour cells</div>
A - F<div>B - F; 90% are squamous but 10% are adenocarcinoma</div><div>C - F</div><div>D - T; liquid haemopoietic neoplasm e.g. CML and CLL</div><div>E - F; change from one differentiated cell type to another due to the presence of a stimulus</div>
Concerning mutations underlying cancer<div>a. all mutations contribute to tumour growth</div><div>b. the majority of mutations detected in cancer are in tumour suppressor genes</div><div>c. activation of DNA damage repair genes is an important source of mutation</div><div>d. genetic instability can be caused by defects in mismatch repair</div><div>e. genetic instability is essential for the development of malignancies</div>
A - F<div>B - F</div><div>C - F</div><div>D - T</div><div>E - F; can have growth control or genetic instability and they are separate mechanisms</div>
The hallmarks of cancer<div>A. include independence of growth–stimulating signals</div><div>B. include increased sensitivity to apoptosis</div><div>C. can be induced by bcl2 translocations</div><div>D. include block in cellular differentiation</div><div>E. include angiogenesis</div>
<div>The hallmarks of cancer<div>A. include independence of growth–stimulating signals (TRUE)</div><div>B. include increased sensitivity to apoptosis (FALSE)</div><div>C. can be induced by bcl2 translocations (TRUE)</div><div>D. include block in cellular differentiation (TRUE)</div><div>E. include angiogenesis (TRUE)</div></div>
Mutations associated with cancer include<div>a. gain of function mutations in PTEN</div><div>b. amplification of cyclin D1</div><div>c. loss of function mutations in Rb1</div><div>d. inactivating mutations of APC and β-catenin</div><div>e. epigenetic modifications</div>
A - F; loss of function as TS<div>B - T</div><div>C - T</div><div>D - F; activation of beta-catenin is pro-proliferative</div><div>E - T; 30-50% of colon cancers show epigenetic instability e.g. methylation of MLH1</div>
Drugs used to treat cancer<div>a. can activate the immune system by inhibiting PD-1</div><div>b. can function by inhibiting the ATP-binding pocket of phosphatases</div><div>c. can induce DNA damage</div><div>d. such as Vemurafenib, the BRAF inhibitor, activates growth of cells with RAS mutations</div><div>e. such as platinum compounds, inhibit mitotic spindles</div>
A - T; inhibit PD-1 thereby leading to increased T cell activation<div>B - F; I think if this was kinases then it might be true but PTEN is anti-cancer and is the only phoshatase mentioned</div><div>C - T; e.g. cis-platin</div><div>D - F</div><div>E - F; taxanes</div>
Concerning environmental agents and cancer<div>A. ultraviolet (UV) light induces guanine dimers</div><div>B. exposure to aflatoxins is associated with bladder cancer</div><div>C. mutagens can be identified by the Ames test</div><div>D. human T lymphotropic virus 1 (HTLV-1) is associated with Kaposi’s sarcoma</div><div>E. causes of cancer can be identified by epidemiological studies</div>
<div>Concerning environmental agents and cancer<div>A. ultraviolet (UV) light induces guanine dimers (FALSE)</div><div>B. exposure to aflatoxins is associated with bladder cancer (FALSE)</div><div>C. mutagens can be identified by the Ames test (TRUE)</div><div>D. human T lymphotropic virus 1 (HTLV-1) is associated with Kaposi’s sarcoma (FALSE)</div><div>E. causes of cancer can be identified by epidemiological studies (TRUE)</div></div>
Regarding the status of signalling pathways in cancer<div>a. the mitogen-activated protein (MAP) kinase pathway is often inactivated</div><div>b. activation of p53 can result in cell cycle arrest or apoptosis</div><div>c. DNA damage increases p53 activity</div><div>d. p53 is a negative regulator of mdm2</div><div>e. mixed lineage leukemia (MLL) is associated with activation of a histone lysine acetyltransferase</div>
A - F<div>B - T</div><div>C - T</div><div>D - F; MDM2 is a negative regulator of p53</div><div>E - F; MLL is a histone methyase that is fused to other genes in leukaemias that turns a gene on</div>
<div>Concerning cancer therapy</div>
<div>A. the Kaplan-Meier curve relates cancer incidence to radiation dose</div>
<div>B. Glivec (a.k.a. Gleevec) targets K-RAS</div>
<div>C. PARP inhibitors activate the immune response to cancers</div>
<div>D. PD-1 and CTLA-4 are found on certain T cells</div>
<div>E. platinum compounds such as cis-platin cross-link DNA strands<br></br></div>
<div><div>Concerning cancer therapy</div><div>A. the Kaplan-Meier curve relates cancer incidence to radiation dose (FALSE)</div><div>B. Glivec (a.k.a. Gleevec) targets K-RAS (FALSE)</div><div>C. PARP inhibitors activate the immune response to cancers (FALSE)</div><div>D. PD-1 and CTLA-4 are found on certain T cells (TRUE)</div><div>E. platinum compounds such as cis-platin cross-link DNA strands (TRUE)</div></div>
The following agents are implicated in increasing the risk of the stated cancers<div>a. hepatitis B virus and liver cancer</div><div>b. napthylamine and bladder cancer</div><div>c. aflatoxin and liver cancer</div><div>d. Epstein-Barr Virus and Kaposi’s Sarcoma</div><div>e. asbestos and breast cancer</div>
A - T<div>B - T</div><div>C - T</div><div>D - F</div><div>E - F</div>
Concerning inherited predisposition to cancer<div>a. the inherited mutation is usually loss-of-function and heterozygous</div><div>b. in patients with hereditary predisposition to retinoblastoma, retinoblastomas are usually homozygous for loss of RB1</div><div>c. mutations that cause inherited predisposition may either be in growth-control pathways or DNA-repair pathways</div><div>d. breast cancer predisposition due to mutated BRCA1 or BRCA2 is among the most prevalent genetic diseases in the UK</div><div>e. most patients with a strong hereditary predisposition to colon cancer inherit a defect in mismatch repair</div>
A - T<div>B - T</div><div>C - T</div><div>D - T</div><div>E - T</div>
Malignant colorectal or colon tumours often<div>a. arise from papillomas</div><div>b. have truncation of K-RAS</div><div>c. have mutation of both p53 (TP53) and APC</div><div>d. have mutation of both B-RAF and K-RAS</div><div>e. have chromosome rearrangements</div>
A - F<div>B - F; K-ras is mutation in a range of cancers but is usually activated by point mutations that block hydrolysis</div><div>C - T</div><div>D - T; also in 60% of melanomas</div><div>E - T; not totally sure</div>
Examples of oncogene activation include<div>a. point mutation of B-RAF</div><div>b. promoter methylation of p16Ink4a (also known as p16 or CDKN2A)</div><div>c. deletion of SMAD4</div><div>d. fusion of B-RAF by tandem duplication</div><div>e. amplification of HER2 (also known as ERBB2)</div>
A - T<div>B - F; it is often deleted completely</div><div>C - T; it inhibits proliferation and survival and is downstream of the TGF beta pathway (e.g. tumour supressor gene)</div><div>D - T; to KIAA1549 in paediatric astrocytomas</div><div>E - T; 10-20% of breast cancers</div>
Concerning genetic instability in cancer<div>A. microsatellite instability arises from defects in mitosis</div><div>B. mismatch repair deficiency occurs in the majority of colon cancers</div><div>C. activation of telomerase leads to genetic instability</div><div>D. genetic instability is occasionally caused by mutations in DNA polymerases</div><div>E. BRCA2-deficiency is associated with chromosome instability</div>
<div>Concerning genetic instability in cancer<div>A. microsatellite instability arises from defects in mitosis (FALSE)</div><div>B. mismatch repair deficiency occurs in the majority of colon cancers (FALSE)</div><div>C. activation of telomerase leads to genetic instability (FALSE)</div><div>D. genetic instability is occasionally caused by mutations in DNA polymerases (TRUE)</div><div>E. BRCA2-deficiency is associated with chromosome instability (TRUE)</div></div>
Concerning neoplasia<div>a. leiomyoma is a benign tumour arising from muscle</div><div>b. an adenoma is a benign tumour of glandular epithelium</div><div>c. adenocarcinoma of the cervix does not require metaplasia</div><div>d. adenocarcinoma of the cervix is a benign neoplasm</div><div>e. lipoma is a benign neoplasm</div>
A - T<div>B - T</div><div>C - T</div><div>D - F</div><div>E - T</div>
The following distinguish malignant from benign neoplasms<div>a. ability to metastasize</div><div>b. ability to kill a patient</div><div>c. invasion of the surrounding normal tissue</div><div>d. in the uterine cervix, papillomavirus infection</div><div>e. presence of tumour suppressor mutations</div>
A - T<div>B - F</div><div>C - T</div><div>D - F</div><div>E - F</div>
A lung infarct<div>A. Usually heals by regeneration</div><div>B. May be accompanied by pleurisy (pleuritis)</div><div>C. May produce heart failure</div><div>D. Typically appears pale after 24 hours</div><div>E. Is at high risk of infection</div>
<div>A lung infarct<div>A. Usually heals by regeneration (TRUE)</div><div>B. May be accompanied by pleurisy (pleuritis) (TRUE)</div><div>C. May produce heart failure (FALSE)</div><div>D. Typically appears pale after 24 hours (FALSE)</div><div>E. Is at high risk of infection (TRUE)</div></div>
Concerning anaemia<div>A. folate deficiency is common in vegans</div><div>B. B12 deficiency leads to macrocytosis</div><div>C. iron deficiency can affect cytochrome function</div><div>D. beta thalassaemia is characterised by both reduced production and increased destruction of red blood cells</div><div>E. angina may worsen if anaemia develops</div>
<div>Concerning anaemia<div>A. folate deficiency is common in vegans (FALSE)</div><div>B. B12 deficiency leads to macrocytosis (TRUE)</div><div>C. iron deficiency can affect cytochrome function (TRUE)</div><div>D. beta thalassaemia is characterised by both reduced production and increased destruction of red blood cells (TRUE)</div><div>E. angina may worsen if anaemia develops (TRUE)</div></div>
Atheromatous plaques<div>A. can arise in arteries, veins or capillaries</div><div>B. are more likely to occur if levels of blood high density lipoproteins are elevated</div><div>C. may lead to embolism</div><div>D. can cause aneurysms</div><div>E. are more likely to occur in post-menopausal women than in pre-menopausal women</div>
<div>Atheromatous plaques<div>A. can arise in arteries, veins or capillaries (FALSE)</div><div>B. are more likely to occur if levels of blood high density lipoproteins are elevated (FALSE)</div><div>C. may lead to embolism (TRUE)</div><div>D. can cause aneurysms (TRUE)</div><div>E. are more likely to occur in post-menopausal women than in pre-menopausal women (TRUE)</div></div>
Ischaemia<div>A. may be a consequence of a myocardial infarct</div><div>B. can cause coagulative necrosis</div><div>C. is tolerated better by neurones than by myocardial cells</div><div>D. can cause cell swelling</div><div>E. leads to a low concentration of blood haemoglobin</div>
<div>Ischaemia<div>A. may be a consequence of a myocardial infarct (FALSE)</div><div>B. can cause coagulative necrosis (TRUE)</div><div>C. is tolerated better by neurones than by myocardial cells (FALSE)</div><div>D. can cause cell swelling (TRUE)</div><div>E. leads to a low concentration of blood haemoglobin (FALSE)</div></div>
A thrombus in a leg vein may<div>A. be a complication of hypertension</div><div>B. embolize to the kidney</div><div>C. be due to inherited deficiency of protein C</div><div>D. be associated with Factor VIII deficiency</div><div>E. become infected</div>
<div>A thrombus in a leg vein may<div>A. be a complication of hypertension (FALSE)</div><div>B. embolize to the kidney (FALSE)</div><div>C. be due to inherited deficiency of protein C (TRUE)</div><div>D. be associated with Factor VIII deficiency (FALSE)</div><div>E. become infected (TRUE)</div></div>
<div>Concerning eukaryotic parasites and the human host<br></br></div>
<div>A. humans are the definitive hosts of Plasmodium vivax</div>
<div>B. microfilaria are micro-parasites capable of multiplying within human host</div>
<div>C. humans can be both the intermediate and definitive host of Taenia solium</div>
<div>D. vertical transmission of Toxoplasma gondii can occur in humans</div>
<div>E. prevalence rather than intensity of helminth infection is strongly associated with severe human morbidity</div>
<div><div>Concerning eukaryotic parasites and the human host<br></br></div><div>A. humans are the definitive hosts of Plasmodium vivax (FALSE)</div><div>B. microfilaria are micro-parasites capable of multiplying within human host (FALSE)</div><div>C. humans can be both the intermediate and definitive host of Taenia solium (FALSE)</div><div>D. vertical transmission of Toxoplasma gondii can occur in humans (TRUE)</div><div>E. prevalence rather than intensity of helminth infection is strongly associated with severe human morbidity (FALSE)</div></div>
Schistosoma haematobium can cause the following<div>A. haematuria</div><div>B. Symmers clay pipestem fibrosis</div><div>C. hydronephrosis</div><div>D. bladder transitional cell carcinoma</div><div>E. Katayama Fever</div>
A - T<div>B - F</div><div>C - F</div><div>D - T</div><div>E - T</div>
Concerning Plasmodium falciparum<div>a. PfEMP-1 is encoded by at least 50 var genes</div><div>b. liver schizonts rupture to release up to 30,000 hypnozoites</div><div>c. prophylactic chemotherapy is important for disease control in endemic countries</div><div>d. in placental malaria PfEMP-1 binds chondroitin sulphate A</div><div>e. individuals lacking the Duffy blood group antigen are resistant to infection</div>
A - T; around 60<div>B - F; they release around 10,000 merozoites in a schizont</div><div>C - T</div><div>D - T</div><div>D - F</div>
The following are stages within insects during the Plasmodium life cycle<div>A, Ookinete</div><div>B. Amastigote</div><div>C. Sporozoite</div><div>D. Sporocyst</div><div>E. Kinetoplast</div>
<div>The following are stages within insects during the Plasmodium life cycle<div>A. Ookinete (TRUE)</div><div>B. Amastigote (FALSE)</div><div>C. Sporozoite (TRUE)</div><div>D. Sporocyst (TRUE)</div><div>E. Kinetoplast (FALSE)</div></div>
The following are transmitted by vectors<div>A. Necator americanis (hookworm)</div><div>B. Wucheria bancrofti (Elephantiasis)</div><div>C. Trypanosoma cruzi (Chagas’ disease)</div><div>D. Plasmodium ovale (Malaria)</div><div>E. Taenia saginata (beef tapeworm)</div>
<div>The following are transmitted by vectors<div>A. Necator americanis (hookworm) (FALSE)</div><div>B. Wucheria bancrofti (Elephantiasis) (FALSE)</div><div>C. Trypanosoma cruzi (Chagas’ disease) (TRUE)</div><div>D. Plasmodium ovale (Malaria) (TRUE)</div><div>E. Taenia saginata (beef tapeworm) (FALSE)</div></div>
The following are neglected tropical diseases caused by protozoan parasites<div>a. Dracunculiasis</div><div>b. Echinococcosis</div><div>c. Malaria</div><div>d. Chagas’ disease</div><div>e. Onchocerciasis</div>
A - F; worm<div>B - F; not tropical</div><div>C - F; not neglected</div><div>D - T</div><div>E - F; worm</div>
Regarding antibiotics<div>A. resistance to trimethoprim, the inhibitor of folate synthesis, is conferred by a ‘bypass’ dihydrofolate reductase</div><div>B. tetracycline binds the 30S ribosomal subunit, inhibiting the peptidyl transferase</div><div>C. chloramphenicol binds the large ribosomal subunit and blocks host cell translation, but resistance follows antibiotic modification by an acetyl transferase</div><div>D. fluoroquinolones like ciprofloxacin inhibit gyrase and block transcription</div><div>E. vancomycin mimics D-Ala-D-Ala crosslinks to prevent peptidoglycan crosslinking, but variant transpeptidases make vancomycin-resistant peptide crosslinks</div>
<div>Regarding antibiotics<div>A. resistance to trimethoprim, the inhibitor of folate synthesis, is conferred by a ‘bypass’ dihydrofolate reductase (TRUE)</div><div>B. tetracycline binds the 30S ribosomal subunit, inhibiting the peptidyl transferase (FALSE)</div><div>C. chloramphenicol binds the large ribosomal subunit and blocks host cell translation, but resistance follows antibiotic modification by an acetyl transferase (FALSE)</div><div>D. fluoroquinolones like ciprofloxacin inhibit gyrase and block transcription (TRUE)</div><div>E. vancomycin mimics D-Ala-D-Ala crosslinks to prevent peptidoglycan crosslinking, but variant transpeptidases make vancomycin-resistant peptide crosslinks (FALSE)</div></div>
In host defence against bacteria<div>a. IFN and NK cells are usually the most important components b. neutralizing antibodies block cell adhesion and also toxin action</div><div>c. lysozyme breaks down bacterial surface capsular polysaccharide</div><div>d. TLR5 recognizes flagellin</div><div>e. the commensal flora of the gut comprises only obligate anaerobic bacteria</div>
A - F<div>B - F</div><div>C - F; peptidoglycan</div><div>D - T</div><div>E - F</div>
Uropathogenic E.coli<div>a. are typically commensals of the lower urinary tract, causing ascending infection to the bladder (causing cystitis) and kidney (causing pyelonephritis)</div><div>b. colonize the kidney using adhesins on the tip of P-pili, binding receptors on kidney epithelial cells</div><div>c. P pili are assembled from subunits incorporated by the chaperone-usher pathway</div><div>d. kidney damage is largely caused directly by a bacterial pore-forming toxin and indirectly by the inflammatory response</div><div>e. commonly cause kidney stones if infection recurs and inflammation persists</div>
A - F<div>B - T</div><div>C - T</div><div>D - T; haemolysin for pore and LPS for inflammation</div><div>E - F; proteus</div>
The following typically cause outbreaks of human disease after ingestion of contaminated meat or dairy products<div>A. Legionella pneumophila</div><div>B. Enterohemorrhagic E.coli (EHEC)</div><div>C. Salmonella enterica</div><div>D. Staphylococcus aureus</div><div>E. Vibrio cholera</div>
<div>The following typically cause outbreaks of human disease after ingestion of contaminated meat or dairy products<div>A. Legionella pneumophila (FALSE)</div><div>B. Enterohemorrhagic E.coli (EHEC) (TRUE)</div><div>C. Salmonella enterica (TRUE)</div><div>D. Staphylococcus aureus (TRUE)</div><div>E. Vibrio cholera (FALSE)</div></div>
In gastrointestinal infections<div>a. Helicobacter pylori is a motile Gram-negative bacterium for which VacA is a key virulence factor in causing gastric ulceration b. ETEC, which cause traveller’s diarrhoea, colonizes host cells by a fimbrial adhesin and secretes an ADP-ribosylating toxin</div><div>c. Listeria invades intestinal cells by receptor-mediated endocytosis to establish an intracellular infection, but it can become systemic and cross the bloodbrain barrier</div><div>d. Clostridium difficile causes inflammation of the colonic mucosa and secretes toxins that disrupt the actin cytoskeleton and epithelial tight junctions</div><div>e. circulating Shiga toxin secreted by Shigella inhibits Rho/Ras GTPases, disrupting the cellular cytoskeleton and causing kidney damage</div>
A - T<div>B - T</div><div>C - T</div><div>D - T</div><div>E - F; glycosidaase that depurinates 28S rRNA –> shiga like toxin of EHEC does cause kidney failure though</div>
In respiratory infections<div>a. diphtheria toxin is an ADP-ribosylating enzyme that modifies host ribosomal RNA and blocks translation</div><div>b. chronic granulomatous disease caused by M. tuberculosis is typically resolved by a TH2 response</div><div>c. pharyngitis is caused by the Gram-positive bacterium Streptococcus pyogenes, which is Lancefield group A based on cell surface carbohydrate</div><div>d. Mycobacteria do not Gram stain, but are visible after Ziehl-Neelsen staining of polyphosphate granules in the cytosol</div><div>e. immunity to M. tuberculosis is detected as a T cell response by the tuberculin skin test, and conferred by the live BCG vaccine</div>
A - F<div>B - F</div><div>C - T</div><div>D - F</div><div>E - T</div>
In pathogenic bacteria<div><br></br></div><div>a. growth typically involves haploid chromosome replication and binary fission to generate two identical progeny cells</div><div>b. Salmonella enterica has c.5-6000 genes, with many that are involved in disease located on SPI-1 and SPI-2 pathogenicity islands</div><div>c. endotoxin is the lipid A component of bacterial LPS, and activates macrophages via CD14</div><div>d. transformation involves DNA uptake following contact between two bacterial cells</div><div>e. Chlamydia have less than 200 genes and consequently are obligate intracellular parasites</div>
A - T<div>B - F</div><div>C - T</div><div>D - F</div><div>E - F</div>
These are obligate anaerobes that produce endospores<div>A. Staphylococcus aureus</div><div>B. Clostridium perfringens</div><div>C. Bacteriodes fragilis</div><div>D. Streptococcus viridans</div><div>E. Clostridium tetani</div>
<div>These are obligate anaerobes that produce endospores<div>A. Staphylococcus aureus (FALSE)</div><div>B. Clostridium perfringens (TRUE)</div><div>C. Bacteriodes fragilis (FALSE)</div><div>D. Streptococcus viridans (FALSE)</div><div>E. Clostridium tetani (TRUE)</div></div>
Regarding bacterial toxins<div>A. pneumolysin, streptolysin O, staphylococcal alpha-toxin and E. coli hemolysin all form pores in host cell membranes</div><div>B. tetanus toxin is a protease that cleaves synaptobrevin, blocking release of inhibitory neurotransmitters in the CNS</div><div>C. Bordetella pertussis produces toxins that, respectively, subvert adenylate cyclase regulation and mimic activity of the mammalian enzyme</div><div>D. membrane-damaging Clostridium perfringens alpha-toxin is a phospholipase detected on egg yolk agar (the Nagler test)</div><div>E. the DPT vaccine comprises toxoid preparations of diphtheria, pertussis and tetanus toxins</div>
A - T<div>B - T</div><div>C - T</div><div>D - T</div><div>E - F; killed pertussis and then toxoid D and T</div>
Fungal infections<div>a. can be detected by recognition of fungal cell wall polysaccharides by lectins on the surface of neutrophils</div><div>b. activate the complement enzyme cascade through DC-SIGN recognition of mannose-rich structures</div><div>c. can be diagnosed by examining morphology using a microscope</div><div>d. by Histoplasma capsulatum can lead to granuloma formation e. by Pneumocystis jirovecii is associated with airway colonization in asthma suffers</div>
A - T; lectins are PRRs that can be in the plasma or on the surface of DCs, macrophages, neutrophils, some epithelial<div>B - F; MBL but if on surfacethen you get a cascade that leads to production of CD4+ T cells and IL-17 and IL-22</div><div>C - T</div><div>D - T</div><div>E - F; HIV</div>
Regarding fungi<div><br></br></div><div>a. dimorphic fungi such as Histoplasma capsulatum primarily adopt a filamentous mould morphology in the body of a mammal b. filamentous moulds can form a mycelium (an interwoven mass of hyphae)</div><div>c. the yeast Schizosaccharomyces pombe undergoes mitosis by asymmetrical budding</div><div>d. Candida albicans is present as part of the normal flora on human mucous membranes</div><div>e. spores are fungal cells that are adapted to survival in a hostile environment</div>
A - F<div>B - T; hyphae can form an interwoven mass called a mycelium</div><div>C - F; symmetrical budding</div><div>D - T; in the throat, gut and vagina</div><div>E - T</div>
Smallpox<div>A. was caused by vaccinia virus</div><div>B. presented with skin pustules evenly spread over the body, similar to chickenpox</div><div>C. was eradicated using a virus vaccine that was inactivated by freeze-drying</div><div>D. was only a disease of humans with no animal reservoir</div><div>E. vaccine induces both cellular and humoral immunity</div>
A - F<div>B - F; centrifugal pattern</div><div>C - T</div><div>D - T</div><div>E - T</div>
In a multicellular host with a competent immune system<div>a. pattern recognition receptors (PRRs) can recognise virus pathogen associated molecular patterns (PAMPs) in the cytoplasm or in endosomes</div><div>b. different cell types produce different types of interferon molecules in response to infection</div><div>c. cytotoxic T lymphocytes efficiently recognise and destroy free virus particles</div><div>d. viruses directly inhibit the action of complement by down-regulating MHC class I molecules</div><div>e. the interferon-stimulated gene product protein kinase R (PKR) requires activation by viral double-stranded RNA</div>
A - T; RIG for viral RNA in cytoplasm and then TLR<div>B - T; IFN alpha and beta produced by infected cell, IFN gamma relased by activated T cells and macrophages, IFNdeltas produced by epithelial cells</div><div>C - F</div><div>D - F</div><div>E - T</div>
Histopathological features associated with virus infection include<div>a. nuclear inclusion bodies caused by molluscum contagiosum (a poxvirus)</div><div>b. cytoplasmic inclusion bodies termed Negri bodies in poliovirus infected Purkinje cells</div><div>c. syncytia (fused cells) caused by varicella-zoster virus infection d. mitotic figures in cells adjacent to sites of vaccinia virus infection</div><div>e. owl-eye inclusion bodies in cytomegalovirus infected cells</div>
A - F; cytoplasmic inclusions<div>B - F; rabies</div><div>C - F; measles</div><div>D - T; epidermal growth factor to stimulate division of neighbouring cells</div><div>E - T</div>
Regarding virus infections of the liver<div>A. hepatitis B virus replication requires reverse transcription</div><div>B. chronic infection by hepatitis C virus is rare in people infected after 5 years of age</div><div>C. hepatitis A virus is a non-enveloped positive strand RNA virus</div><div>D. hepatitis B virus causes acute infection and jaundice</div><div>E. translation of the hepatitis C virus polyprotein is controlled by an internal ribosome entry site (IRES)<br></br></div>
A - T<div>B - F</div><div>C - T</div><div>D - T</div><div>E - F; think this is just poliovirus</div>
