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Sem 2: Microbiology > Week 7 > Flashcards

Week 7 Flashcards

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

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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

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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

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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

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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

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6
Q

What causes disease?

A

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

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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

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8
Q

What are common virulence factors?

A

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

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9
Q

What are factors associated with specfic bacteria?

A

Exotoxin production
Expression of adhesion factors
Intracellular survival and multiplication

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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

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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)

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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

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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)

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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

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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

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16
Q

What can occur at the same time as adherence?

A

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

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17
Q

What is the impact of afimbriating bacteria?

A

Afimbriated bacteria have much lower adhesion sucess compared to fimbriated bactria

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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

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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

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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

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21
Q

What type of bacteria have TSIII secretion systems?

A

Secretion systems in Gram-negative bacteria

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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

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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

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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

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25
Q

What are ways to escape from phagosome?

A

Escape from phagosome: prior to lysis with lysosomes
Listeria monocytogenes produces molecule that forms pores in membrane; Shigella species lyse phagosome

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26
Q

What are ways to escape within phagolysome?

A

Survive within phagolysosome: few can survive destructive environment
Coxiella burnetii (Q fever) can withstand; delays fusion, allows time to equip itself to survive

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27
Q

What is a case study of serum resisting bacteria?

A

Neisseria gonorrhoeae hijacks host system, binds to complement regulatory proteins to avoid membrane attack complex

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28
Q

What is a case study of avoiding antibodies?

A

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

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29
Q

What is an overview of mimicking host molecules?

A

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

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30
Q

What are ways a pathogen can harm a host?

A

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

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31
Q

What are exotoxins?

A

Toxins acting on cell membranes
Toxins active inside cells

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32
Q

What is an overview of Lipid A?

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

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33
Q

What is an overview of peptidoglycans for immunity?

A

Peptidoglycans and other components of the bacterial cell wall can also trigger fever, sepsis and septic shock

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34
Q

What is an impact of endotoxin?

A

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

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35
Q

What causes the effects of endotoxin?

A

Most of the effects of endotoxin are mediated by tumour necrosis factor
Attempts at therapy using anti-endotoxin or anti-TNF antibodies

36
Q

What are an overview of Gram positive bacteria toxins?

A

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
Q

How are some toxins described in terms of their action site?

A

Neurotoxins affect neurons.
Enterotoxins affect the gastrointestine.
Cytotoxins damage cells.

38
Q

How is the mechanism for damaging membranes in exotoxins?

A

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
Q

What is an overview of A-B toxins?

A

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
Q

What is an overview of Vibrio cholerae A-B toxins?

A

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
Q

Whats are the differences between Exotoxins and endotoxins?

A

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
Q

What are damging effects of immune response?

A

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
Q

What is EPEC?

A

Enteropathogenic Escherichia coli

44
Q

What is an overview of EPEC?

A

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
Q

What is an overview of EPEC infection?

A

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
Q

What is an overview of actin pedestals in EPEC?

A

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
Q

What is a downside of the T3SS?

A

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
Q

What are the 5 main components of the T3SS?

A

Regulators (sensory)
Chaperones (assmble proteins)
Secretion Apparatus
Translocators
Effectors

49
Q

What are the 5 main functions of the T3SS?

A

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
Q

What is an overview of Type III secretion systems?

A

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
Q

What are pathogenicity islands?

A

Cluster of all the genes for similar function related to pathogenicity eg T3SS
Can be transferred through horizonal transer

52
Q

What is the function of intimin (EPEC)?

A

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
Q

What is the purpose of EPEC creating cellular pedastals?

A

Loss of absorptive surfaces
Reduces integrity of tight juncitons
Altered Cl- or HCO3- ion secretion
Water movement across membrane
Creates Diarrhea

54
Q

What are an overview of the Helicobacter pylori?

A

Microaerophilic (5% O2, 10%CO2)
Cork-screw morphology
Highly motile (flagella)

55
Q

What are an overview of the Helicobacter pylori infection?

A

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
Q

What happens during Helicobacter pylori infection?

A

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
Q

What is an overview of peptic ulcer disease pre 1990s?

A

Caused by stress/environmental factors
Incurable disease, often requiring surgery
Ulcers often returned despite surgery
Debilitating disease, often lethal in long term

58
Q

What was the work by Marshall and Warren for peptic ulcer disease in 1984?

A

Marshall and Warren describe isolation and culture of Campylobacter-like micro-organism from patients with peptic ulcer disease

59
Q

What can be caused by Helicobacter pylori infection?

A

Impacts neutrophil and chemotaxis recruitment
Cytokine siganlling (IL-8)
Severe inflamation of epithelial cells in epithelial cells

60
Q

What can cause gastrointestinal disease?

A

Environmental conditions eg stress
H.pylori
Host factors

61
Q

What are examples of gastrointestinal disease cause by H.pylori?

A

Peptic ulcer disease
Chronic gastritis
MALT-lymphoma
Atrophic gastritis - gastric carcinoma

62
Q

How did B.Marshall attempt to fulfil Koch’s postulates for Helicobacter pylori?

A

He drank H.pylori solution
Caused gastric inflammation
Cured with antibiotics
Fulfiled Koch’s postulates (other methods were used)

63
Q

What are the main types of plant diseases?

A

Fruit rot
Stalk rot
Mildew
Wilt
Leaf blight

64
Q

Why are plant diseases significant in agriculture?

A

Plant pathogens can impair the quality of crop plants.
Plant diseases can drastically reduce crop yield (e.g. Irish potato famine)

65
Q

Whats an overview of Airborne fungi?

A

Air-born fungi cause recurrent seasonal epidemics on e.g. small grain cereals. e.g. Blumeria spp. on small grain cereals (causes mildew.)

66
Q

Whats an overview of soil borne fungi?

A

Soil-borne fungi tend to cause chronic (persistent) infections e.g. Fusarium and Verticillium. Often cause wilt diseases.

67
Q

How much impact do fungi have on agricultural breeding?

A

More than 50% of breeding for disease resistance has been for fungal resistance

68
Q

Whats an overview of oomycetes?

A

Dispersed via asexual zoospores
Produce oospores (for sexual reproduction)
Cellulose cell walls
Diploid
Cause downy mildew diseases and blights
Not fungi (Stramenopiles)

69
Q

What is an overview of biotrophic?

A

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
Q

What is an overview of necrotrophic?

A

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
Q

What is an overview of hemi-biotrophic?

A

Hemi-biotrophic pathogens. Grow biotrophically at first and then switch to necrotrophy
Intermediate host range
Tomato leaf spot (Septoria lycopersici)

72
Q

What are the key processes of fungal pathogenesis?

A

Attachment
Penetration
Invasive growth within the plant
Suppression/inactivation of host defences

73
Q

What is an overview of infection cycle of rice blast fungus?

A

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
Q

How much pressure does the appressoria generate?

A

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
Q

What is an example of powdery mildews?

A

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
Q

What is an overview of Haustoria?

A

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
Q

What is an overview of the structure of haustroria?

A

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
Q

What is an example of biotrophic pathogen that doesnt produce a haustoria?

A

The tomato leaf mould pathogen Cladosporium fulvum.
No haustoria are produced.
Extracellular hyphae do form contacts with leaf mesophyll cells enter through stomata

79
Q

What is an overview of a necrotrophic fungi?

A

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
Q

How do fungi effectors enter plant cells?

A

Proteins directly cross the extrahaustorial membrane (1) or enter the cell endomembrane system via vesicles (2)

81
Q

What is an example of virulence gene in Phyphthora infestans?

A

AVR3a from Phytophthora infestans:
When silenced fungi lesions do not form so AVR3a are required for virulence

82
Q

What is an example of a effectors that responds to a plant response system?

A

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
Q

What is an example of an enzyme virulence factor?

A

The AVN1 gene - avenacinase - a b-glucosyl hydrolase
Avenacinase from Gauemannomyces. graminis f.sp avenae (Gga) degrades the antifungal compound avenacin

84
Q

What is an overview of green revolution?

A

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
Q

What traits were bred for in the Green revolution?

A

Higher yield
Improved grain quality
Multiline varieties for resistance to diseases/pests
Tolerance of abiotic stresses

86
Q

What are examples of R gene ‘Boom and busts’?

A

Lr1, 13 released 1970 breakdown 1973
Lr13, released in 1971 and breakdown in 1975
Lr23 released in 1982 and breakdown in 1985

87
Q

Why do host resistance genes breakdown?

A

This is due to evolution of the pathogen, not a change in the host resistance gene.

Sem 2: Microbiology (12 decks)

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