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Unit 3 > W1 Microbiology and pathogenicity lecture > Flashcards

W1 Microbiology and pathogenicity lecture Flashcards

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1
Q

Define microbe.

A

Any organism that is too small to be seen by the visible eye, this includes some bacteria, viruses, fungi and parasites.

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2
Q

What is a pathogen?

A

A microorganism that parasitizes a host and causes disease.

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3
Q

What are the two single-celled morphologies for bacteria?

A

cocci (round/circle)
bacilli (rod shaped)

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4
Q

What are the different formation of cocci bacteria?

A

Monococcus - single cell
Dicoccus - paired cell
Staphylococcus - grouped cells
Streptococcus - chained cells aka one long line.

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5
Q

How do the different formulations of bacteria arise?

A

Depend on how the bacteria replicate.

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6
Q

What are the different formulations of rod shaped bacteria?

A

single rod - bacillus
Grouped / clustered
Chain - in one long continuous line.

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7
Q

Draw a diagram with labelled components of a typical bacterial cell.

A
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8
Q

What is significant in regards to protein synthesis about a prokaryotic cell having a nucleoid rather than a nucleus?

A

Genetic material is more accessible.
More rapid protein synthesis - also explained by ribosomes free in cytoplasm, lack secluded membrane bound organelles.

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9
Q

What is the role of pilli?

A

Mobility and adhesion (not in all bacteria)

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10
Q

What is an inclusion body in relation to a prokaryote?

A

An aggregate of recombinant protein found in the cytoplasm, often made from the expression of genes that the bacteria has taken in from another species or bacterium (non-self).

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11
Q

Describe the cell wall complex structure of gram-positive and gram-negative bacteria?

A

Gram-positive have a thicker outer layer of peptoglycan in their cell wall, with an inner cell surface plasma membrane
Gram-negative bacteria have a thin outer plasma membrane, then a thinner peptoglycan cell wall, followed by the inner cell surface membrane.

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12
Q

What is the periplasmic space?
What is its function?

A

In gram negative bacteria the periplasmic space is the space between the inner and outer membrane including the peptoglycan cell wall.
In gram positive bacteria the periplasmic space is the smaller gap between the inner membrane and the peptoglycan cell wall.
This space contains enzymes and substances that could be toxic within the cell cytoplasm. This allows it to play a role in protein processing, molecule synthesis and protection from turgor pressure.

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13
Q

What is the significance in the difference in size in the periplasmic space between gram-positive and gram-negative bacteria?

A

Gram-negative bacteria have a larger periplasmic space, so are more protected from turgor pressure and have a higher level of protein manipulation and synthesis before molecules enter the cytoplasm.

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14
Q

Explain how the outer and inner membrane both play a role in substances entering a gram-negative bacterial cell?

A

Outer membrane has larger pores, allows larger substances to enter the periplasmic space.
Larger molecules are broken down or processed by proteins/enzymes in the perisplasmic space.
This means they are made smaller so are able to enter through the smaller pores found in the inner membrane.

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15
Q

What are bacterial spores?

A

Spores are produced by SOME bacteria during environmental hostility.
They contain a copy of bacterial DNA.
Often dehydrated with little cytoplasm or content.
They are released in the dormant form and are surrounded by multiple layers that make them more resistant to conditions such as high temperature, UV and oxidation.
Hence are more likely to survive the extreme environment conditions.
Spores are able to sense a relaxation in environmental conditions then change their mechanisms to germinate another bacterial colony.

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16
Q

Why are bacterial spores important clincally?

A

Allow bacteria to survive more hostile conditions, meaning specialist cleaning methods are often needed if contamination occurs.
Bacteria that produce spores are more likely to survive and spread so are more difficult to treat.
Bacteris that produce spores are more likely to have a less controlled spread.

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17
Q

What are the stages of treatment for an infectious disease?

A

Observations of patients symptoms
Take a sample of bacteria from patient
Grow a culture in a lab, make observations and test to identify the bacteria.
Give appropriate treatment often antibiotics.
Observe the wider population (epidemiology)
Prevent further transmission.

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18
Q

What is empirical prescription and why is this important to antibiotic resistance?

A

Prescribing a treatment based only on symptoms, no identification test.
More likely to prescribe antibiotics for a viral infection.

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19
Q

How does a hospital infection outbreak vary from a community outbreak?

A

Hospital is a more closed environment.
Patients more vulnerable to infection
More likely to be an antibiotic resistant strain.
Faster pace of spread.

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20
Q

What is an infectious disease?

A

Due to infection by a pathogen.

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21
Q

What is meant by infection?

A

The invasion by and multiplication of a pathogenic microbe within a host.

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22
Q

What is contamination?

A

The presence of microbes in an environment/location.

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23
Q

What are Koch Postulates?

A

The four criteria Koch used to prove a microbial cause behind a disease.
1. The microbial cause must be observed in every incidence of the disease
2. Microbe must be isolated from diseased host and grown in a culture.
3. Culture when given to a healthy person must cause the same disease
4. Microbe must be re isolated from the second individual.

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24
Q

What are some faults in Koch’s Postulates?

A

It is difficult to isolate microbes in their pure form.
The way a disease presents itself may vary from person to person.
Bacteria mutates quickly, genetic fingerprint may change between hosts so no-longer be an identical cause.

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25
What is an important note from looking at the different sites and types of infections?
The same pathogen can infect multiple different sites. Similarly the same body site can be infected by multiple different pathogens.
26
What does the iceberg concept of infection show?
Only a small proportion of people exposed to an infection will get severe symptoms are seek help. There will be increasing more people who have mild symptoms, do not have symptoms, were exposed but did not catch the infection.
27
Why is the icebergy concept of infection important clinically?
Shows the difficulties of controlling infection rates. A larger proportion will have an infection than the number that presents to medical services.
28
What are the key stages in disease progression?
1. Encounter 2. Entry/establishment 3. Colonisation (including spread, multiplication, damage and outcome) - may be commensal or pathogenic.
29
What does successful transmission for a microbe depend on?
The number of microbes (higher=more likley) The size, density and surface features. Hydrophobicity( water borne only) Resistance to dessication, spore formation and ahesion to surfaces (contact) Open routes into host e.g cuts Vector availiability.
30
How does hydrophobicity impact has easily a microbe pass between hosts?
A more hydrophobic microbe will float on the surface of the water, so is more likely to be included in drinking water taken from open sources, so is more likely to have a successful transimission.
31
What factors affect adherence and invasion of a microbe to a host?
Depend on microbe and host features Break is host surface layer Attachment is often by pilli Proteases to penetrate epithelium Capsules increase chance of survival increase phagosomes and have sticky carbohydrates for adhesion Some virus may injected epithelial cells with molecules (DNA) to change surface features e.g transcribe for receptors for viral attachment.
32
What are some consequences of disease success? What factors influenced how successful a disease is?
A microbe may or may not be pathogenic Host cells resist defences e.g neutralising toxins, adaptive and innate immunity. Microbe growth may also be limited by the availability of nutrients such as iron. Microbes may cause tissue damage by accumulation of toxins or digestive enzymes.
33
What is normal or commensal flora?
Organisms that live in benign symbiosis with the host. Same microbes may be pathogenic but unable to enter the disease process, conditions may change e.g during stress, which causes the microbes to become pathogenic.
34
What is tissue remodelling?
Causes by prolonged inflammation leading to tissue damage, structure and function of tissue is damaged and changes.
35
Define pathogenicity
The ability of a pathogen to create an infectious disease in an organism.
36
Define virulence.
The severity of disease/degree of damage caused by a microbe.
37
Define virulence/pathogenicty factor
A microbial property or process that contributes to the virulence/pathogenicity of a pathogen.
38
What are the different molecular determinants of pathogenicity?
Attachment to host cell Production and delivery of factors (toxins etc) to the host cell Replication and evasion of immunity Degree of damage to host cells.
39
What is LD50?
The lethal dose of a microbes toxin that will kill 50% of experimentally inoculated animals
40
What is ID50?
The dose of a microbe required to infect and cause disease in 50% of experimentally inoculated animals.
41
What are adhesions?
Molecules produced by the bacteria to attach to the host cell, often found on the end of pilli. Pilli have glycocalax and glycoprotein.
42
What is the role of capsule?
Contain carbohydrates Aid attachment and evasion of phagocytosis.
43
What is the function of hemolysins and how does this apply to alpha/beta hemolytic streptococci?
Hemolysins lyse erythrocytes, causing anemia and weekend host defences. Makes iron available for host growth. In alpha - red blood cells are only incompletely lysed In beta - red blood cells are fully lysed.
44
What is the function of coagulase?
Clots the fibrinogen into fibrin in plasma (fibrin =clot). This protects the microbe from phagocytosis and isolates it from other host defences. Staphylocossus aureus are often coagulase positive.
45
What is the function of collagenase?
Breaks down collagen which is found in the connective tissue, allows the pathogen to spread throughout the tissue.
46
What is the function of leukocidins?
Pore forming esotoxins that kill leukocytes and degranulate lysosomes within leukocytes, decreases the host defences.
47
What is the function of porins?
Inhibit leukocyte phagocytosis by activating adenylat cyclase system.
48
What are toxins?
The primary factor of pathogenicity. Poisonous substances produced by microbes.
49
What is toxemia?
When toxins are in the bloodstream.
50
What is toxigenicty?
The capacity of microorganisms to produce toxins.
51
What are exotoxins?
Toxins produced inside gram positive bacteria, are released into the surrounding medium.
52
What are endotoxins?
Toxins found in the outer portion of gram negative bacteria cell walls. Are released when the bacteria dies and cell wall breaks apart *must be mindful of this when giving antibiotics - symptoms of too much toxin release.
53
What is the general virus structure?
Genetic material (RNA/DNA) Protein coat - capsid Lipid membrane (optional)
54
What are the different structures of protein coats?
Mainly helixical and ixosahedral (20 sided) More complex shapes are available. As self formed give a regular structure.
55
What is HIV?
An enveloped ssRNA genome virus. Contains a nucleocapsid, capsid and matrix.
56
What are the different types of ssRNA?
Positive sense - translated straight into protein, directly Negative sense - must become positive sense before protein biosyntheis
57
What is a bacteriophage?
A virus that infects bacteria. Has role in bacterial virulence and able to spread pathogenic genes between bacteria. Found in human gut. Used in phage therapy to treat bacterial infections (not in UK) - potential to reduce strength of antibiotic resistance.
58
What is the latent period?
Part of viral replication. All changes occur in the cell, can see changes from outside the cell. Virus replicates within the cell.
59
Why is there a rapid increase in virus numbers after the latent period?
New replicated Viruses are released (burst) out of host cells. A single virus may be replicated many times within a single host cell. The initial increase is not a straight line as release is dependent on the host cell cycle stage.
60
What does it meant that viral infection occur in step wise processes?
Viral numbers are changed by a repeating latent period (stable numbers) to rapid increase as released from cells to latent period and so on.
61
What are early enzymes in viral replication?
Enzymes found preformed in the virus. When infects the cell may play a role in uncoating the virus or early replication.
62
What are the different processes that fit into the viral latent period and exponential increase?
Latent period: Early enzymes Nucleic acid replication and protein synthesis Protein coat synthesis Latent and rapid increase: Assembly and release - not assembly is random, may contain non-viral DNA from host cell.
63
What are the different phases of viral replication?
Adsorption phase - binds to and enters host cell Eclipse phase- genome replication and proteins synthesis starts Maturation - viral formation in the cell.
64
What are the different stages of viral replication?
Recognition absoprion and pentration Release of DNA/RNA DNA/RNA synthesis Synthesis of viral subunits may include protease action on polypeptides Assembly of the virus Lysis of cell and release of mature virus.
65
Why is a virus often nat surrounded by a lipid envelope?
Released during cell lysis so is not pinched off through the cell membrane.
66
What is meant by the lytic cycle of viral replication?
Virus injects DNA into cell DNA remains separate to host cell DNA. Viral DNA replicates and new viruses are formed. The cell lyses releasing the new viral componenets.
67
What is meant by the lysogenic cycle of viral replication?
Virus injects DNA into a cell. Viral DNA becomes incorporated into host genome Host cell divides, viral DNA is passed to host cell offspring Under stressful conditions the virus DNA is exercised from the host DNA and enters the lytic cycle.
68
What is viral pathogenesis?
The process by which a viral infection becomes a disease. Causing a disease has no value to the virus, in fact most viruses are subclinical as it is not in their interest to kill the host.
69
What is an acute viral infection?
A rapid onset of infection, with: Quick development and cure of symptoms (with or without residue effects) Rapid death. Effects may lead to chronic infection
70
What is a chronic infection?
A silent subclinical infection for life A disease with a long dormant stage Chronic infections can be reactivated to become acute Cancer causing viruses, have a long timer before symptoms show.
71
How can viruses cause cancer?
By lysogenic pathway, insertion of viral DNA interrupts and causes a mutation in host TSG or POG.
72
What are the different factors in viral pathogenesis?
Effects on host cell Course of infection Cell/tissue tropism Cell/tissue damage Host immune response Viral clearance / persistant
73
What is cellular pathogenesis?
How a cell responds to being infected by a virus. 1) No apparent change 2) Death 3)Transformation
74
What are he direct ways in which a virus can cause cell damge/death?
Diversion of cells energy Shutoff of cell molecular synthesis Competition of viral mRNA with cellular mRNA for ribsomes Competition between genetic materials for hosts promoters and transcription factors.
75
What are the indirect ways a virus can cause cell damage/death?
Integration of viral DNA in host genome Usage of host nutrients Inflammation Host immune response.
76
What is cell tropism? What is it determined by?
The range of cells and the affinity for each cell in which a virus can replicate. Determined by cell receptors for virus, transcription factors that recognise viral DNA, ability of cell to support viral replication, physical barrierto enter cell, cell environmental conditions, digestive enzymes and bile in the digestive tract inactivate some viruses.
77
How does the type of virus affect the level of cell damage caused by a virus?
Retroviruses - do not normally causes cell death as lysogenic, are persistent infections so chronic, RNA virus that insert a copy of their DNA into host cell Picornaviruses - causes lysis and death of cells, leading to fever, paralysis, death and tissue damage (poliovirus), very small RNA viruses
78
What are the two types of persistent viral infection?
Both are chronic infections True Latency - the virus remains completely latent after primary infection Persistence - the virus replicates continuously but at a very low level in the body.
79
What are some mechanisms of viral persistence?
Antigenic variation Immune tolerance Direct infection of cells of the immune system so decreased immunity Down regulation of immune molecules such as MHCs and LFA-3. Infection of immunopriviliged sites (less action from immune system here).
80
Give an overvoew of the Hepatitus B virus.
Is a partially double-stranded relaxed circular DNA virus (rcDNA), mainly infected hepatocytes and has high latence hence is passed to progeny cells. HBV polymerase Symptoms include: Jaundice, hives, fever, pain over liver, tiredness and sickness.
81
How does Hepatitis B act in the body?
Enters cell by binding to NTCP receptor rcDNA is delivered inot the host nucleus and converted into full double stranded DNA. DNA is ligated to become stable closed circular DNA. When active is DNA is replicated, new proteins are made, encapsinated then bud off in the cell surrounded by a lipid envelop from the cell membrane and ER.
82
What is the spectrum of Chronic Hepatitis B disease?
Chronic Persistance Hepatitius B - asymptomatic Chronic Active Hepatitus - symptomatic exacerbation Cirrhosis (scaring due to long term damage) in Liver Hepatocellular Carcinoma.
83
What is the basic biology of the influenza virus?
ssRNA consisting of 10 genes on eight strands Three types, A B and C A causes most infections Infects cells of the respiratory tract, Budds off from host cells.
84
What is latency?
Infected to infectious
85
What is incubation?
Infected to symptoms.
86
What are some of the general impacts of influenza?
Acute highly contagious respiratory infections Seasonal Very young and very elderly are at the highest risk Weakens host defenses so more likely to develop secondary infections such as pneumonia.
87
What does infleunza do inside the body/cell?
Binds to cilliated cells of respiratory mucosa, binds by hemagglutinin spikes and fuses with the membrane. Enters by endocytosis and is uncoated. ssRNA transported to nucleus, negative strand RNA becomes positive strand then translated into viral proteins in cytoplasm. Glycoproteins spikes are inserted into host cell membrane, this section of cell membrane budds of around new viral components. Causing rapid shedding of cells so less epithelium, severe inflammation.
88
What are some symptoms of influenza infection?
Fever, headache, pharyngeal pain, shortness of breath and coughing, myalgia (muscle aches and pain).
89
What are the different glycoprotein spikes on influenza?
Hemagglutinin - 15 different subtypes, aids virulence as binds to host cell Neuraminidase - 9 subtypes, hydrolysis mucus and assists viral budding and release.
90
How do influenza glycoproteins underpin the antigenic viability of influenza?
Antigenic drift - constantly mutated to change amino acid composition Antigenic shift - one of the genes or RNA strand is substituted from another strand in a different host.
91
Why does COVID only affect respiraoty cells?
Entry into cell requires TMPRS2 receptor which is only found on respiratory cells.
92
Explain how SARS-CoV-2 infects the cell?
CV spike proteins bind to ACE2 receptors on host Spike proteins are cleaved between S1 and S2 domain by TMPRSS2 (protease transmembrane serine protease 2) and lysosomal Cathespin, hence fuses with the host membrane This either creates a pore for RNA entry or triggers endocytosis then capside dissolved in acidic lysosome. Viral genome is replicated by host mechanisms, Virus is released by vascular exocytosis.
93
What are the physiological and organ impacts of SARS-CoV-2?
Brain fog, headache, fatigue, cough Neuro and GT inflammation, lung fibrosis, liver disorder and heart conditions.
94
What affects does SARS-CoV-2 have on a cellular level?
Blood clots as platlets activated Inflammation Vascular damage Coagulation factor release Neutrophil accumulation and NETS Fibrosis ECM deposition. Eosinophils

Unit 3 (18 decks)

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