Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Sem 2: Microbiology > Week 7 > Flashcards

Week 7 Flashcards

(87 cards)

Start Studying
1
Q

What is an overview of the human-microbe relationship?

A

Microbes colonize the human host
Either as members of the normal flora in harmony with the host Or subverting host defenses and causing disease
Few microbes able to invade tissues, produce toxic substances, or inflict noticeable damage
Pathogens - The minority of microorganisms can cause us harm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is needed in a bacteria for a sucessful infection?

A

Sense environment (virulence factors are expensive so needed to know when triggered)
Need to know where they are
Must express proteins to survive stress
Must express proteins required for adhesion or invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What may be needed in a bacteria for a sucessful infection?

A

May make toxins
May enter host cells and replicate
May spread through host cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are different ways microbes have to influence virulence?

A

Production & delivery of various virulence factors
Attachment to host tissues
Replication & evasion of immunity
Damage to host tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 4 main mehcanisms for bactrial pathgenicity?

A

Toxin ingestion following production- Bacillus cereus
Toxin production following colonization- Clostridium botulinum
Invasion of host tissues without toxin production- Mycobacterium tuberculosis
Tissue invasion followed by toxin production- Vibrio cholerae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes disease?

A

Microbes cause disease while stealing space, nutrients, and/or living tissue from their symbiotic hosts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the process of disease in microbes?

A

Contamination - gain access to the host
Adherence - adhere to host
Colonisation - Replicate on the host
Invasion - invade tissue
Damage - Produce toxins, proteins or other agents that cause host harm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are common virulence factors?

A

Endotoxin
Capsule
Antigenic phase variation
Sequestration of growth factors
Resistance to serum killing
Antimicrobial resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are factors associated with specfic bacteria?

A

Exotoxin production
Expression of adhesion factors
Intracellular survival and multiplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Whats an overview of adherence?

A

Adhesins attach to host cell receptor
Often located at tips of fimbriae
Can be component of capsules or various cell wall proteins
Binding highly specific; exploits host cell receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an overview of colonisation?

A

Growth in biofilms
Siderophores bind iron
Avoidance of secretory IgA - Rapid pili turnover, antigenic variations, IgA proteases
Compete with normal microbiota, tolerate toxins (colonisation resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an example of free iron in the body?

A

Free iron (Fe2+) levels very low in body fluids
Iron overload increases susceptibility to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Whats is an overview of bacterial systems for scavenging iron?

A

Siderophores chelate available iron & transport into bacteria
Iron can be scavenged direct from host iron-binding proteins e.g by lactoferrin-binding proteins
Often very tightly regulated
Some pathogens avoid the problem by cutting out need for iron e.g. Treponema pallidum (Syphilis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Whats an overview of bacterial response to low iron levels?

A

Low levels of iron switches on aggressive virulence factors ( a signal they are in the host) eg Diphtheria toxin , Shiga-like toxin, Pseudomonas aeruginosa exotoxin A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is requires for bacteria to avoid physical and immunological removal?

A

Must stick to:
Cell surfaces and extracellular matrix e.g. in respiratory, gastrointestinal & genitourinary tracts
Solid surfaces e.g. teeth, heart valves, catheters
Other bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can occur at the same time as adherence?

A

Adherence often combined with manipulation of host cell signalling and cytoskeleton (Salmonella)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the impact of afimbriating bacteria?

A

Afimbriated bacteria have much lower adhesion sucess compared to fimbriated bactria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is an overview of penetrating the skin?

A

Difficult barrier to penetrate; bacteria rely on injuries
Staphylococcus aureus enters via cut or wound; Yersinia pestis is injected by fleas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an overview of penetrating mucous membrane?

A

Entry point for most pathogens
Directed Uptake by Cells
Pathogen induces cells to engulf via endocytosis
Salmonella uses type III secretion; actin molecules rearrange, ruffling of membrane, uptake of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the function of type III secretion systems?

A

Effector proteins induce changes (altering of cell’s cytoskeleton structure)
Can induce uptake of bacterial cells into host cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of bacteria have TSIII secretion systems?

A

Secretion systems in Gram-negative bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an overview of exploit antigen-sampling process?

A

Host mucosal-associated lymphoid tissue (MALT) sample the
lumen of the intestine.
Some pathogens use these M cells to cross intestinal barrier
Shigella survives phagocytosis by macrophages; induces
apoptosis; binds to base of mucosal epithelial cells and
induces uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the function of capsules?

A

Capsules are Involved in avoidance of phagocyte-mediated recognition and attachment.
Diplococcus produce a clear capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are ways to avoid phagocytosis?

A

Prevent phagosome-lysosome fusion: avoid destruction
Salmonella sense ingestion by macrophage, produce protein that blocks fusion process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are ways to escape from phagosome?
Escape from phagosome: prior to lysis with lysosomes Listeria monocytogenes produces molecule that forms pores in membrane; Shigella species lyse phagosome
26
What are ways to escape within phagolysome?
Survive within phagolysosome: few can survive destructive environment Coxiella burnetii (Q fever) can withstand; delays fusion, allows time to equip itself to survive
27
What is a case study of serum resisting bacteria?
Neisseria gonorrhoeae hijacks host system, binds to complement regulatory proteins to avoid membrane attack complex
28
What is a case study of avoiding antibodies?
IgA protease: cleaves IgA, found in mucus, secretions Produced by Neisseria gonorrhoeae and others Antigenic variation: alter structure of surface antigens, stay ahead of antibody production Neisseria gonorrhoeae varies antigenic structure of pili
29
What is an overview of mimicking host molecules?
Bacteria cover their surface with molecules similar to those found in host cell, so they appear to be “self” Streptococcus pyogenes form a capsule from hyaluronic acid
30
What are ways a pathogen can harm a host?
Direct (toxins produced) Indirect (immune response) Damage may help pathogen to exit and spread. Vibrio cholerae induces watery diarrhea, up to 20 liters/day, which contaminates water supplies Bordetella pertussis triggers severe coughing, pathogens released into air
31
What are exotoxins?
Toxins acting on cell membranes Toxins active inside cells
32
What is an overview of Lipid A?
Endotoxin the lipid A component of lipopolysaccharide (LPS) (gram negative) Lipid A triggers inflammatory response - When localized, response helps clear infection and when systemic, causes widespread response: septic shock or endotoxic shock Lipid A released following cell lysis - Activates innate and adaptive defenses Heat-stable; autoclaving does not destroy - Causes fever and disseminated intravascular coagulation Lipid A stable so can stay around and cause endotoxic shock
33
What is an overview of peptidoglycans for immunity?
Peptidoglycans and other components of the bacterial cell wall can also trigger fever, sepsis and septic shock
34
What is an impact of endotoxin?
Fever Hypotension Life-threatening complication of septicaemia e.g. in meningococcal infection, in ITU or oncology patients Endotoxic shock (hyperimmuno response) seen with dirty intravenous equipment
35
What causes the effects of endotoxin?
Most of the effects of endotoxin are mediated by tumour necrosis factor Attempts at therapy using anti-endotoxin or anti-TNF antibodies
36
What are an overview of Gram positive bacteria toxins?
Exotoxins are proteins that are exported out of cells and which can damage body tissues. Exotoxins (along with exoenzymes) are more associated with Gram-positive bacteria than Gram-negative, though pathogens of both Gram types display Exotoxins.
37
How are some toxins described in terms of their action site?
Neurotoxins affect neurons. Enterotoxins affect the gastrointestine. Cytotoxins damage cells.
38
How is the mechanism for damaging membranes in exotoxins?
Many bacterial toxins form pores in eukaryotic cell membranes, producing oligomeric rings: Streptolysin O of Streptococcus pyogenes Listeriolysin of Listeria monocytogenes Alpha-toxin of Staphylococcus aureus Other toxins, such as phospholipases, degrade components of the membrane e.g. Clostridium perfringens alpha toxin
39
What is an overview of A-B toxins?
A-B exotoxins have two parts A (active) subunit is toxic, usually an enzyme (is ejected into cytoplasm to exert toxic effect) B subunit binds to cell, determines cell type to be infected
40
What is an overview of Vibrio cholerae A-B toxins?
B component binds to GM1 A toxin impacts CFTR causing more Cl- to be pumped outside of cell causing osmotic differences there for water and Na+ move to balance everything out causing diarrhoea
41
Whats are the differences between Exotoxins and endotoxins?
Exo - Gram + and - Endo - only Gram neg Exo - protein Endo - Liposaccaharide (Lipid A component) Exo - very potent Endo - small amounts - immune response spread large amounts can be deadly
42
What are damging effects of immune response?
Phagocytic cells can release enzymes and toxic products Immune complexes: antigen-antibody complexes can form, settle in kidneys and joints, and activate complement system leading to inflammation - acute glomerulonephritis following skin, throat infections of S. pyogenes Cross-reactive antibodies: may bind to body’s own tissues, promote autoimmune response - acute rheumatic fever following S. pyogenes infection
43
What is EPEC?
Enteropathogenic Escherichia coli
44
What is an overview of EPEC?
One of several categories of diarrheagenic E. coli. EPEC is a well established cause of human diarrhea, particularly in young children. The hallmark of EPEC infection is the A/E histopathology often observed in small bowel biopsy specimens from infected patients, and seen after the infection of epithelial cells in tissue culture
45
What is an overview of EPEC infection?
Infection generally causes acute diarrhea, but severe cases can lead to a protracted disease. Aside from profuse watery diarrhea, both vomiting and the development of fever are common symptoms of EPEC infection. EPEC strains remain a significant health threat to children worldwide
46
What is an overview of actin pedestals in EPEC?
The host cell undergoes a number of alterations during infection by EPEC, but the most striking change is the formation of actin pedestals. In fact, the resulting localized actin accumulation is distinct that it forms the basis of an in vitro diagnostic test for EPEC Actin pedestals are raised actin structures formed by the dynamic polymerization of host actin
47
What is a downside of the T3SS?
Metabolically demanding, so bacteria have to look for specific signals to produce the protein as if produced all the time would reduce growth and fitness
48
What are the 5 main components of the T3SS?
Regulators (sensory) Chaperones (assmble proteins) Secretion Apparatus Translocators Effectors
49
What are the 5 main functions of the T3SS?
Export proteins across bacterial envelope Bring bacterial & host cells close together Translocate proteins between bacterial and host cells Translocate proteins across host cell membrane Translocated proteins subvert host cell functions
50
What is an overview of Type III secretion systems?
Type III Secretion Systems are multi-protein complexes connecting bacteria to host cells Mediate protein secretion and translocation from bacterial cytoplasm to host cell interior Effector proteins subvert cellular functions Therefore, important not just to bacterial pathogenesis, but to the wider field of eucaryotic cell biology
51
What are pathogenicity islands?
Cluster of all the genes for similar function related to pathogenicity eg T3SS Can be transferred through horizonal transer
52
What is the function of intimin (EPEC)?
Intimin binds to intimin receptors in the epithelial cell memebrane. The receptors where inserted there by bacteria to allow for the intimin to bind to the cell membrane. Cellular rearraging occurs resulting in actin remodelling to produce a pedastal through recruiting of actin beads pushes membrane up
53
What is the purpose of EPEC creating cellular pedastals?
Loss of absorptive surfaces Reduces integrity of tight juncitons Altered Cl- or HCO3- ion secretion Water movement across membrane Creates Diarrhea
54
What are an overview of the Helicobacter pylori?
Microaerophilic (5% O2, 10%CO2) Cork-screw morphology Highly motile (flagella)
55
What are an overview of the Helicobacter pylori infection?
An example of a bacterial pathogen that does not enter human cells, but causes inflammation Colonizes mucus layer Able to grow at moderate acidity Adheres to epithelial cells
56
What happens during Helicobacter pylori infection?
Stomach acid secretions maintain a low pH to aid food digestion Helibacter infection, gastrin secreted by G cells stimilates excess acid production Continused excess to stomach acid causes tissue damage and ulceration, peptic ulcer disease eventually leading to malignant outgrowths and gastric tumour
57
What is an overview of peptic ulcer disease pre 1990s?
Caused by stress/environmental factors Incurable disease, often requiring surgery Ulcers often returned despite surgery Debilitating disease, often lethal in long term
58
What was the work by Marshall and Warren for peptic ulcer disease in 1984?
Marshall and Warren describe isolation and culture of Campylobacter-like micro-organism from patients with peptic ulcer disease
59
What can be caused by Helicobacter pylori infection?
Impacts neutrophil and chemotaxis recruitment Cytokine siganlling (IL-8) Severe inflamation of epithelial cells in epithelial cells
60
What can cause gastrointestinal disease?
Environmental conditions eg stress H.pylori Host factors
61
What are examples of gastrointestinal disease cause by H.pylori?
Peptic ulcer disease Chronic gastritis MALT-lymphoma Atrophic gastritis - gastric carcinoma
62
How did B.Marshall attempt to fulfil Koch's postulates for Helicobacter pylori?
He drank H.pylori solution Caused gastric inflammation Cured with antibiotics Fulfiled Koch's postulates (other methods were used)
63
What are the main types of plant diseases?
Fruit rot Stalk rot Mildew Wilt Leaf blight
64
Why are plant diseases significant in agriculture?
Plant pathogens can impair the quality of crop plants. Plant diseases can drastically reduce crop yield (e.g. Irish potato famine)
65
Whats an overview of Airborne fungi?
Air-born fungi cause recurrent seasonal epidemics on e.g. small grain cereals. e.g. Blumeria spp. on small grain cereals (causes mildew.)
66
Whats an overview of soil borne fungi?
Soil-borne fungi tend to cause chronic (persistent) infections e.g. Fusarium and Verticillium. Often cause wilt diseases.
67
How much impact do fungi have on agricultural breeding?
More than 50% of breeding for disease resistance has been for fungal resistance
68
Whats an overview of oomycetes?
Dispersed via asexual zoospores Produce oospores (for sexual reproduction) Cellulose cell walls Diploid Cause downy mildew diseases and blights Not fungi (Stramenopiles)
69
What is an overview of biotrophic?
Intimate intracellular contact with plant cells. Biotrophic pathogens require a living host to grow and reproduce. Includes obligate parasites that can only grow on a specific host (e.g. Blumeria species)
70
What is an overview of necrotrophic?
Necrotrophic pathogens - kill host cells through the action of lytic enzymes and toxins, colonise and reproduce on dead tissue Broad host range Rotting fungi (e.g. Botrytis cinerea).
71
What is an overview of hemi-biotrophic?
Hemi-biotrophic pathogens. Grow biotrophically at first and then switch to necrotrophy Intermediate host range Tomato leaf spot (Septoria lycopersici)
72
What are the key processes of fungal pathogenesis?
Attachment Penetration Invasive growth within the plant Suppression/inactivation of host defences
73
What is an overview of infection cycle of rice blast fungus?
Conidia attach and germinate in a few hours. Germ tube ceases growth -> develops into an appressorium Turgor pressure increases forcing a penetration peg into underlying tissues. Invasive growth. Re-emergence of conidiophores (asexual spores).
74
How much pressure does the appressoria generate?
Appressoria can generate a very high turgor pressure of 6-8 Mpa which results in penetration of the cuticular layer Magnaportha accumulates large amount of glycerol to generate the pressure
75
What is an example of powdery mildews?
Blumeria graminis Infects barley, wheat, rye, oat Several forma specialis (informal taxonomic grouping applied to a fungus that is adapted to a specific host e.g. B. graminis f. sp. hordei on barley). Biotrophic
76
What is an overview of Haustoria?
Haustoria are specialised structures formed specifically by biotrophic and hemibiotrophic fungi e.g. B. graminis. Increase the surface area of contact between the fungus and host cell to allow the exchange of nutrients and signal molecules.
77
What is an overview of the structure of haustroria?
Haustoria invaginate the cell following cell wall penetration. The fungus is still extracellular. Comprises two membrane systems from the fungus and the plant. Separated by the extracellular haustorial matrix. Site of delivery for effector molecules and uptake nutrients
78
What is an example of biotrophic pathogen that doesnt produce a haustoria?
The tomato leaf mould pathogen Cladosporium fulvum. No haustoria are produced. Extracellular hyphae do form contacts with leaf mesophyll cells enter through stomata
79
What is an overview of a necrotrophic fungi?
The grey mould fungus, Botrytis cinerea Macerates plant tissue Broad host range Botrytis can infect c.200 different plants. Produces cell wall degrading enzymes that destroy plant tissue in advance of the colonising hyphae
80
How do fungi effectors enter plant cells?
Proteins directly cross the extrahaustorial membrane (1) or enter the cell endomembrane system via vesicles (2)
81
What is an example of virulence gene in Phyphthora infestans?
AVR3a from Phytophthora infestans: When silenced fungi lesions do not form so AVR3a are required for virulence
82
What is an example of a effectors that responds to a plant response system?
Rice recognises chitin, a component of fungal cell walls. Chitin is bound by chitin elicitor binding protein (CEBiP), initiating defence Rice blast fungus (Magnaporthe oryzae) Slp1 protein binds to chitin and suppresses the chitin-induced defence response in the plant
83
What is an example of an enzyme virulence factor?
The AVN1 gene - avenacinase - a b-glucosyl hydrolase Avenacinase from Gauemannomyces. graminis f.sp avenae (Gga) degrades the antifungal compound avenacin
84
What is an overview of green revolution?
The ‘Green Revolution’ in the first half of the 20th Century was initiated by breeders like Norman Borlaug This led to significant achievements in breeding wheat, maize and rice Selected traits
85
What traits were bred for in the Green revolution?
Higher yield Improved grain quality Multiline varieties for resistance to diseases/pests Tolerance of abiotic stresses
86
What are examples of R gene 'Boom and busts'?
Lr1, 13 released 1970 breakdown 1973 Lr13, released in 1971 and breakdown in 1975 Lr23 released in 1982 and breakdown in 1985
87
Why do host resistance genes breakdown?
This is due to evolution of the pathogen, not a change in the host resistance gene.

Sem 2: Microbiology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions