Biol 121- Impact of Microbes Flashcards

1
Q

which 2 things are hazard groups decided by?

A

whether there is an effective vaccine, and whether or not it has public health importance

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2
Q

How did SARS-CoV-2 infect and what are its effects on respiration?

A

After entering the body through the mouth or nose, SARS-CoV-2 makes its way into the the lungs, where it uses its distinctive spike proteins to infect alveolar cells. In response, the immune system attacks the area of infection, killing healthy alveolar cells in the process. Reduced surfactant from alveolar epithelial type II cells, along with increased fluid accumulation in the alveoli causes reduced or severely hindered gas exchange.
Liquid from peripheral system starts leaking into alveoli, gas exchange way low, patient has to be put onto ventilators and stuff.

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3
Q

why was long covid very hardtop identify?

A

many symptoms, over 200

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4
Q

when coronavirus infects lung cells, immune cells (including macrophages) identify the virus, producing cytokines? Describe the effect of cytokines + formation of a cytokine storm

A

they attract more immune cells, e.g. white blood cells, which produces more, creating a cycle of inflammation damaging lung cells, through fibrin formation (impedes blood flow). The weakened blood vessels allow fluid to fill lung cavities, leading to respiratory failure. This is a cytokine storm, which is more damaging than covid itself. The recovery trial saved 1 million lives and brought billions to the economy.

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5
Q

why was covid quarantine 14 days?

A

About 97% of the people who get infected and develop symptoms will do so within 11 to 12 days, and about 99% will within 14 days.
After 14 days, the SARS-CoV- 2 viral load has dramatically decreased.

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6
Q

what are pathogens?

A

groups of microbes that cause infectious diseases

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7
Q

which places and typically how do infectious diseases spread?

A

places such as homeless shelters, sewage in LMIC’s

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8
Q

what are some pros and cons in terms of food of microbes?

A

food materials e.g. yogurt, beer, cheese, vinegar, etc
cons: microbes grow well in food fit for human consumption, food spoilage, food borne disease

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9
Q

why are agar plates widely used for culturing bacteria?

A

low levels of carbon as high levels can limit their growth. they usually have a lot of bacterial diversity.

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10
Q

what are the 2 ways you can microscopically count bacteria?

A

culturable- not individually counting cells, usually involve dilutions and scaling up
direct- individually counting cells

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11
Q

why do we need to add additives and modifications to media something with bacteria?

A

usually in cultures, there are many different types, with high diversity, that we don’t know the true value of as many of them are lost. modifications bring them through. things like pcr can identify organisms after they’re cultured, to test for antibiotic resistance and things like it

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12
Q

describe a eukaryote, which groups do they/ do they not include?

A

an organism that consists of one or more cells each of which has a nucleus and other well-developed intracellular compartments.
Include all organisms except for bacteria, viruses, certain algae.
They include fungi, plants, animals and some unicellular organisms.

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13
Q

describe Bacteria and their origins

A

they constitute a large domain of prokaryotic microorganisms.
usually a few micrometers long, they are among the 1st life forms to appear on Earth

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14
Q

describe archaea, their size, and name their 4 specific characteristics

A

they are similar to bacteria in size and simple structure but are different in molecular organisation.
1. the presence of characteristic tRNAs and rRNAs
2. absence of peptidoglycan cell walls, replaced by a largely proteinaceous coat usually
3. contains ether-linked lipids built from phytanyl chains
4. occur only in weird habitats, places where there is no oxygen, like peat boxes and cow’s stomach, usually producing methane

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15
Q

which domain to all know disease-causing prokaryotes belong to?

A

Bacteria

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16
Q

what is the typical order of microbial cell sizes?

A

virus- bacteria- yeast- eukaryotes- algae- protists
(Yeast and eukaryotes are very very similar tho)

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17
Q

name 3 properties of all bacterial cells

A
  1. compartmentalisation and metabolism- taking up nutrients from the environment, transforming them and releasing waste back therefore an open system
  2. growth- all bacteria divide by binary fission
  3. evolution- cells contain genes and can display new biological properties, shown by phylogenetic trees.
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18
Q

name 3 properties that only some bacterial cells possess

A
  1. motility- some are capable of self-propulsion with flagella
  2. differentiation- some cells can form new structures e.g. a spore, usually part of a cellular life cycle
  3. communication- many cells communicate or interact baby means of chemicals that are released or taken-up
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19
Q

why do smaller cells have faster growth, and what does this mean for evolutionary populations?

A

higher surface area: volume ratio= faster rate of nutrient exchange, meaning evolution/mutation rates are increased, leading to greater evolutionary possibilities.

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20
Q

label this bacterial cell

A

s-layer: layer of protein where the function isn’t fully understood- crystalline
capsule: polysaccharide, some cells have it

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21
Q

describe the membrane structure in bacteria

A

contains phospholipids, integral membrane proteins.
the inside is negative and the outside is positive.
can be used to drive the formation of atp, while the integral membrane proteins can be used for transport and structure

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22
Q

what is the function of the bacterial cell membrane?

A

separation of cell from environment, the selectively permeable barrier controls movement of molecules in or out of the cell. It is a site of respiration and photosynthesis, and energy conservation (proton motive force). Transport is able to be used instead of just simple diffusion, which allows saturation at low external concentrations.

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23
Q

what is the function of the bacterial cell wall?

A

Determines and maintains the shape of bacteria, and protects the cell from osmotic lysis and water loss.

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24
Q

what is the advantage of filamentous-shaped bacteria?

A

can form mats and cover surfaces

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25
with coccus-shaped bacteria, they can form clusters, name them
diplococci- 2 cocci joined streptococci- many joined in a line clump of cocci- fairly self-explanatory
26
differences between gram-positive + gram-negative cell wall
gram-positive: almost 90% peptidoglycan. many also have trichroic acids embedded. negatively charged so lead to cell surface being negatively charged. Can bind to divalent cations like Mg and Ca. Some covalently bind to lipids- lipoteichoic acids. gram-negative: 10% peptidoglycan, contained between plasma membrane and outer membrane. Mostly outer membrane made of lipids, proteins and lipopolysaccharides. Contains porins, and periplasm which contains enzymes that process nutrients.
27
what are porins?
proteins that allow hydrophilic small molecules to cross the outermembrane
28
describe an archaea cell wall
s-layer consisting of proteins or glycoprotein, no peptidoglycan
29
how does a gram stain work?
stain with crystal violet then rinse with water, add iodine (as forms a complex with crystal violet), wash with ethanol then rinse, counterstain with safranin then rinse and blot. gram +ve= deep purple gram -ve= light pink as they can't retain the stain so are counter stained by the safranin
30
describe structure of peptidoglycan
rigid because glycan strands linked by glycosidic bonds, cross linked. same backbone but over 100 different types due to differences in bridging peptides. lysozymes can break G-M bonds, as a defence against bacteria. G= N-Acetylglucosamine M= N-Acetylmuramic acid
31
how do some antibiotics such as penicillin kill bacteria?
prevent cell wall formation, they are bacteriolytic.
32
why can't lysozymes lyse archaea?
they don't have peptidoglycan
33
why doesn't penicillin kill archaea?
they have a variety of cell walls including a pseudo-peptidoglycan
34
properties and function of capsules
made of polysaccharides. 1. protection of host defences (phagocytosis) 2. protection from harsh environmental conditions (desiccation) 3. attachment to surfaces
35
some bacteria can change shape, how is this a defence mechanism?
changing outward chemical profile to deter predators
36
what are fimbriae and pili?
fimbriae: short, thin, hair-like proteinaceous appendages, recognition and attachment to surfaces pili: similar except longer, thicker, less of them, required for mating
37
what is a polar flagellum?
flagellum at end of cell
38
what is a monotrichous bacteria?
one flagellum
39
what is an amphitrichous bacteria?
one flagellum at each end of the cell
40
what is a lophotrichous bacteria?
cluster of flagella at one/both ends
41
what is a peritrichous bacteria?
spread over entire surface of cell
42
describe bacterial cytoplasm
contains ribosomes + nucleoid, sometimes with cellular inclusions. also macromolecules (proteins, RNA, etc), and organic stuff like lipids and carbs, with inorganic stuff like ions
43
describe the nucleoid
irregularly shaped bit, with 1 (sometimes 2) chromosomes, where all genetic info is held.
44
describe bacterial plasmids?
small, circular DNA molecules, that are independent of the nucleoid chromosome. carry a lot of genes for stuff like antibiotic resistance, and are non-essential for growth and reproduction.
45
describe cellular inclusions
granules of organic/ inorganic material reserved for future use. - glycogen - poly-β-hydroxybutyrate - polyphosphate granules - sulphur granules contain iron in the form of magnetite, used to orient cells in magnetic fields. gas vesicles arranged in bundles- for buoyancy in aquatic bacteria e.g. cyanobacteria performing photosynthesis.
46
describe endospores + their advantages
made by some gram-positive bacteria. when stressed, bacteria form them. 1. can survive for many years and are produced under unfavourable conditions e.g. when cells runs out of nutrients 2. highly resistant to heat, drying, radiation and chemicals very low water content. 3. contain calcium dipicolinate- binds free water and helps dehydrated cell 4. special proteins protect DNA
47
what are halophilic bacteria?
salt-loving bacteria
48
do prokaryotes or eukaryotes have cilia?
eukaryotes
49
what are the 10 macro elements (main nutritional elements of bacteria)?
carbon, oxygen, hydrogen, nitrogen, phosphorus, sulphur, potassium, calcium, magnesium, iron
50
give examples of amino acids sulphur is in?
methionine, cysteine, also present in vitamins. e.g. biotin.
51
name the 5 micro elements (components of various enzymes)
copper, zinc, nickel, vanadium, selenium, etc
52
macro- and microelements can be provided in the laboratory for bacterial growth; name 3 types of bacterial media they can be grown in
1. culture media- nutrient solids that provide all elements needed for growth e.g. agar plates 2. chemically defined media- exact chemical composition is known 3. complex media- exact chemical composition is not known, made of digests of complex material such as milk protein, soybeans, etc
53
describe aseptic technique while working with bacteria
1. flame the loop to sterilise 2. remove tube cap and flame the tube tip to sterilise 3. only sterilised portion enters tube 4. tube is reframed and recapped 5. loop is sterilized loop can be either disposable plastic or washable, but metal washable ones are now favoured as a large percentage of the UK's plastic comes from laboratories.
54
why is culturing in liquid media sometimes favourable to culturing in solid media?
1. gives bacteria easier access to all the nutrients as opposed to when they are in static bacterial colonies 2. liquid is faster and more sensitive 3. it is easy to sterilise with ultra-filtration bacteria growing in liquid media
55
how do some rod cell bacteria become septum-shaped?
through binary fission, the membrane pinches inward and they can grow to almost twice their length, to form a septum.
56
what is generation time?
time needed for a population to double i.e. doubling time. it is affected by availability of nutrients, and varies greatly
57
what is exponential growth?
growth with a constant doubling time
58
what is a batch culture?
culture grown in a "closed system", no additional nutrients added and no bacterial waste products removed during the culture period
59
label the phases on the bacterial population growth curve
A= lag phase, time between inoculation and maximal division rate where the cells adjust to a new environment B= log (exponential) phase, constant doubling time and maximal growth rate C= stationary phase, bacteria can no longer reproduce but are still alive (probs due to no nutrients left or growth inhibited by bacterial products) D= death (decline) phase, bacteria die, typically slower than growth phase
60
some viable cells can be cultured, however why can some not?
1. viable but nonculturable bacteria: bacteria that are in a state of very low metabolic activity and do not divide but are alive and have the ability to become culturable once resuscitated. 2. can't grow in conventional media 3. such bacteria can still cause disease (e.g. cholera)
61
name 3 ways you can count bacteria by microscopy (with dyes)
1. total count: non-specific dye that stains all bacteria. culturable, viable, VBNC and in many cases dead cells 2. viable count: fluorescent activity dyes. counts all cells with activity e.g. enzymatic, active membranes, etc 3. culturable count: counts cells that can form colonies on solid media or increase turbidity in liquid media
62
advantages and disadvantages of microscopic count
advantages: easy and fast disadvantages: uses special microscope counting slide, and doesn't differentiate between living and dead bacteria
63
name some stains used in culturing bacteria
DAPI, acridine orange, live-dead stain
64
what is the assumption made when doing a culturable count on an agar plate?
each culturable cell will grow and divide to yield one colony
65
how many bacterial cells would you expect to see per plate in a serial dilution?
20-200 cfu
66
describe cholera as an illness, with statistics
cholera is an acute, diarrhoea illness caused by infection of the intestine with the toxigenic bacterium Vibrio cholerae serogroup O1 or O139. an estimated 1.3- 4 million people around the world get cholera each year and 21000 to 143000 people die from it
67
in a test for cholera, a positive result means the water is definitely not safe, but what could a negative culture mean?
1. not present i.e. safe 2. viable but not culturable- still pathogenic- not safe
68
what is an indirect method of measuring bacterial growth?
measuring turbidity- when a cell suspension looks cloudy (turbid), Spectrophotometers direct a beam of light at a specific wavelength through the sample. cells scatter light passing through the suspension
69
what are the 3 types of antimicrobial agents and draw graphs for how they affect growth, both total cell count and viable/ culturable cell count
70
what are 5 types of oxygen dependency descriptions for bacteria
1. obligate aerobes- need oxygen for growth 2. obligate anaerobes- can't grow with oxygen 3. facultative anaerobes- can grow with or without 4. aerotolerant anaerobes- don't need oxygen but tolerate 5. microaerophilic- need oxygen but can tolerate at low conc anaerobes don't use oxygen as a (terminal) electron acceptor, and use nitrate, sulphur, carbonate, etc, instead
71
name the 4 groups that describe how well bacteria grow with temperature
1. psychrophiles- grow best in temps close to freezing 2. mesophiles- organism adapted to live in environments both acidic and hot, around 15-45 degrees. many bacteria in body are mesophiles (optimum around 37) 3. thermopile- grows best at warmer than normal temps, max around 80. live in hot springs, compost heaps, etc. THERMUS AQUATICUS TAQ 1 PCR WOOOOOO 4. hyperthermophiles- very hot xxxx e.g. hot springs
72
which bacteria is current record holder for which one can grow in highest temp?
geogemma barossii grows between 80-121 degrees, survives at least 2 hours at 130
73
where do most extreme and non-extreme acidophilus live?
extreme ones (pH 0-2 odd) live in volcanic soils and water, and gastric juices less extreme live in acid soil and stuff
74
where do alkaliphiles live?
more extreme ones (pH 14-11 odd) live in extremely alkaline soda lakes, like natronobacterium gregoryi pH 12
75
why does water diffuse out of halophiles' cells through osmosis?
high salt results in low water activity
76
what is a host?
organism that supports growth of viruses, bacteria and parasites
77
what is a pathogen?
organism that causes disease, by impairing or interfering with the normal physiological activities of the host.
78
what are pathogenicity and virulence?
pathogenicity: the ability to cause disease, how hard it is to catch and establish itself. virulence: the degree or intensity of pathogenicity (determined by toxicity and invasiveness). the effect the pathogen can have.
79
what is infection?
bacteria persist in host without necessarily causing tissue damage. the bacteria’s invasion and persistence in the host’s system; they don’t necessarily have to cause damage.
80
what is disease?
overt damage to the host, parts of body cannot fulfil their normal functions.
81
describe miasma theory
air is the origin of epidemics from rotting organic matter, meaning eradicating disease needs to be though the preventive approach of cleaning and scouring. Cholera outbreaks specifically in London were blamed on air infection, the not nice smells reinforced miasma theory- sewage. Held until around mid-1800s. Soil at low elevations, especially near the banks of the River Thames, contained much organic matter which produces ‘miasmata’.  The concentration of such deadly ‘miasmata’ would be greater at lower down than in the surrounding hills.
82
describe Robert Koch's work on germ theory of disease
Koch’s postulates- simple methods to show something causes disease. Microorganisms would be isolated, then microscopy. They would then be purified and injected into a healthy animal. The disease would then be reproduced in a lab, and these microorganisms would be isolated and looked at under a microscope and stuff, and if the microorganisms were the same then good. Led to finding causes and treatments of anthrax, cholera and tuberculosis (TB specifically was a problem until around 1950s). Developed simple methods for obtaining bacteria in pure culture.
83
describe the 2 successful bacterial pathogens
1. opportunistic: only cause serious disease when host defences are impaired + often exist in the environment e..g hot tubs, freshers flu, can cause skin disease. 2. primary pathogens (obligate): can cause disease in healthy people, and capable of causing disease in absence of immune defects e..g syphilis. Need to cause disease to survive e.g. human/ animal- human transmission.
84
draw a flow chart for the steps for infectious disease
85
give reservoir examples for anthrax, legionnaire's disease and chlamydia
anthrax: livestock, soil (Although anthrax reservoirs involve livestock and soil, they can infect and kill humans (an anthrax bomb was dropped on some sheep or something in the 40s, killed loads of sheep and downwind as well). Forms spores. legionnaire's: high moisture places e.g. air-con (wasn't discovered until like the 70s because stuff like air-con wasn't a massive thing until then) chlamydia: humans
86
give examples of direct host-to-host transmission
airborne: aerosols (coughing and sneezing) body contact: touching, kissing, sex
87
give examples of indirect host-to-host transmission
vectors-borne: vector= living organism. arthropods (insects and ticks) and vertebrates (rats, dogs, cats, birds). also formites (passive vectors): non-living materials, food and water and soil, eating utensils and surgical instruments
88
what is host colonisation?
establishment of a stable population of bacteria in the host. the human body contains a large number of bacteria, and the pathogen must be able to compete successfully for nutrients and surface attachment sites. Bacteria in the colon and things are already established (skipped colonization), so they have really high competition with other pathogens, which is a good defense mechanism for us.
89
what is the point of adherence?
to overcome flushing mechanisms bacteria must adhere to host cell surfaces. some bacteria adhere to other surfaces e.g. streptococci to tooth surfaces
90
describe step 1 of adherence
association: overcoming non-specific forces such as charge and hydrophobicity
91
describe step 2 of adherence
adhesion: involves specific bacterial adhesins + receptors. Adhesins include fimbriae and pili which stick out with proteins, capsules + slime layers, gram-positives. Antigens specific to blood groups and matrix extracellular proteins are some host receptors. Subsequent stages may result in aggregation to produce a biofilm Biofilms may disperse and seed new sites of infection.
92
describe some barriers to colonisation or infection
1. eyes: lysosome dissolves cells walls 2. skin: physical barrier produces antimicrobials normal flora inhibits pathogens 3. mucus: prevents colonisation in trachea and lungs 4. stomach: pH inhibits and kills bacteria 5. cilia: in lungs wave around and flush out bacteria
93
describe bacterial invasion
some bacteria are able to penetrate into, through, or between cells e.g. epithelial (shigella) or phagocytic (salmonella).
94
how is invasion accomplished by lytic compounds that attack the host tissue?
including lots of enzymes that attack things like collagen. There will be a lot of genes producing collagenase, endotoxins, exotoxins, etc. Invasins= virulence factors.
95
describe some host defences
the immune system is very efficient at eliminating non-pathogenic bacteria. Macrophages and other phagocytes: engulf and kill bacteria Cytotoxic cells: kill cells infected with bacteria
96
describe bacteria avoidance of phagocytosis
bacteria produce structures preventing effective contact: capsules, special surface proteins. they can also survive inside phagocytic cells, often by very pathogenic bacteria. Legionnaire’s are very good at that, when they get taken up into the lungs.
97
describe the 5 different roles antibodies have for host defences
98
describe 3 factors of antibody avoidance
Capsules (sometimes not immunogenic because they resemble host structures) Antigenic variation: bacteria can switch between different types of a surface structure E.g. : Streptococcus pneumoniae can make > 50 capsule variants Sometimes degradation of antibodies.
99
give an example of capsules preventing complement activation
lipopolysaccharides (gram -ves) sometimes hinder pore formation
100
give 4 ways tissue damage occurs
1. Iron acquisition- iron is essential for bacterial growth, binds with high affinity. Tissues: free iron levels are below that required to support bacterial growth To acquire enough iron to grow, bacteria express high affinity iron uptake systems. a. Siderophores: bind iron with high affinity b. Direct binding of iron transport proteins e.g. transferrin 2. Direct effects of bacterial toxins- Exo- + endotoxins- exotoxins act on specific targets, gram-positive or gram-negative. They are heat labile because they are proteins. Endotoxins bind to cells, causing damage indirectly, usually gram-negative. Penicillin releases a lot of lipopolysaccharides when the cells burst. 3. Indirect effects of bacterial toxins 4. Induction of autoimmune responses TOXINS = VIRULENCE FACTORS
101
Compare exo- and endotoxins in terms of: gram test, complex molecule, where they are produced, heat, immuno-resistance, lethality
exo; made by gram +ve and -ve, protein, secreted by living bacteria, usually heat labile, highly immunogenic, potentially lethal end: made by gram -ve, lipopolysaccharide, part of cell membrane released on cell lysis, usually heat stable, weakly immunogenic, lethal at higher concentrations
102
name 3 ways exposure to exotoxin can occur in different ways
Ingestion of preformed exotoxin Example: food poisoning by Staphylococcus aureus - cannot colonise the gut, but toxin in food causes poisoning Colonisation of mucosal surface or tissue followed by toxin production Example: Vibrio cholerae, cause of cholera - colonises the gut but does not invade, cholera toxins leads leads hypersecretion of water and chloride ions and dehydration Colonisation of wound followed by toxin production Example: Clostridium perfringens, grows in wound or abscess, exotoxin causes tissue destruction
103
give 2 examples of exotoxins irl
tetanus: a neurotoxin, interferes with synapse function and mess with the nervous system. diphtheria toxin: inhibits mammalian protein synthesis. has mortality of up to 20% in very young/old people.
104
why are endotoxins called endotoxins + explain some of the lore
105
what do the lipid a part and the o-polysaccharide part do in endotoxins?
Generally considered less potent/specific than exotoxins. Lipid A is the toxic part but the O-polysaccharide part affects the immunogenicity and hence the virulence. Lipid A binds to immune system receptors and stimulates the immune system leading to the physical effects.
106
what can endotoxins cause?
fever, shock and many other bad things, e.g. meningitis, even though a lot of them are needed to cause lots of disease.
107
give examples of exit routes for pathogens for the continued life of a pathogen
tears, nose secretions, saliva, ear wax, blood, skin flakes, faeces, urine, milk and vagina (blood) for women and semen for men
108
how do the structure and functional adaptations of bacteria contribute to success
Circular chromosome with plasmids Fimbria adhesion, pili conjugation, flagella motility Capsule adhesion/evasion No nucleus or membrane enclosed organelles Short doubling time- binary fission- rapid reproduction and mutation.
109
what is a protist?
a eukaryote that doesn't class as fungi, plant or animal.
110
what is a cytoskeleton in a eukaryotic cell?
organises the other organelles of the cell, like train tracks, moves other organelles to the right place in the cell
111
name the 2 parts of the eukaryotic cell that not all of them have
cell wall: plants and fungi, gives structural strength chloroplast: plants and algae, photosynthesis
112
state the 3 groups of protists when it comes to feeding
Photoautotrophic: from chloroplasts (green plastids) and photosynthesis. use inorganic carbon source (usually carbon dioxide). Transform inorganic carbon to organic e.g. glucose. ANYTHING that photosynthesis is algae (not a taxonomic group). Note- any swimming algae have a cell wall. Heterotrophic: protists that can’t photosynthesize so need to feed on bacteria, fungi and other protists. Termed protozoa (no cell wall). Mixotrophic: do both, and can change the ratio of eating to photosynthesis at will, also don't have a cell wall.
113
how big are protists?
larger than 5 micrometers usually, largest amoeba recorded is 10cm though
114
what are the advantages and disadvantages of a direct microscopic count for protists?
+: easy and fast -: uses special microscope counting slide and doesn't differentiate between live and dead bacteria. also near enough all protists are motile, so they need to be killed to count them microscopically: total cell count
115
name the organelles protists have in common with bacteria
cytoplasm, cytoplasmic membrane, LOADS of ribosomes for protein synthesis (however, they are 80s instead of 70s). They both also carry out asexual reproduction.
116
what are the differences between protist and bacterial asexual reproduction?
bacteria: binary fission, protists: mitosis. bacteria doubling time is about 20 mins at 37 degrees, whereas protists take hours or days. bacteria daughter cells are identical, whereas protists are genetically identical but may vary in other components
117
do protists divide or multiply?
The cell divides, the population multiplies
118
describe the population growth curve for protists
Same population growth curve as bacteria, may have to make more enzymes in lag phase as their food they have to eat isn’t ideal in their new environment. When entering stationary phase, some cells will die and some will live, but there will be no net increase or decrease in cells, it all evens out.
119
what are the advantages of protist cysts?
same as bacterial endospores Produced under unfavourable conditions Highly resistant to heat, drying & radiation Very low water content Can survive for 20 years in the environment Good resistance to antibiotics/disinfectants Effective dispersal mechanism Can be transmitted to others via faeces
120
name the (at least) 7 organelles protists can have that bacteria don't
cytoskeleton, nucleus, endoplasmic reticulum, mitochondrion, Golgi apparatus, chloroplast, cell wall Protists in general have a lot more membrane than bacteria due to most of the organelles having their own membranes.
121
describe cell wall presence in protists
Cell wall always present in… Non-motile photosynthetic protists E.g. Diatoms (cell walls usually made of silica) Different structure to bacteria (e.g. cellulose, silica) All cysts have cell walls Cell wall not present in... Motile photosynthetic protists Heterotrophic protists Mixotrophic protists …need to overcome osmosis
122
problems with no cell wall xxxxxx
no cell wall leads to osmosis. Water moves into the cell via osmosis down the water potential gradient. The cell may burst if too much water enters, so they need a mechanism to pump water out.
123
describe the importance for contractile vacuoles
When the contractile vacuole is empty, water will fill it and continue to do so and will increase in size until the contractile vacuole contracts, expelling water. No osmosis will occur if there is a cell wall. Some protists will not have a contractile vacuole due to the environment they live in e.g. isotonic. Sea water, for example, is the same water content as inside the cell, so marine protists don’t need a contractile vacuole. Some pathogenic protists in the blood also don’t need one, as they have the same water content in the cytoplasm as the blood.
124
describe optimum temperatures of protists
No hyperthermophiles: can’t tolerate heat very well. Majority are mesophilic, can tolerate temperature until about 40 degrees. Cut off is around 60 degrees.
125
describe how the types of protists relating to oxygen dependency compare to bacterial ones
there are only obligate aerobes and obligate anaerobes, not facultative anaerobes, aerotolerant anaerobes, microaerophilic. some scientists say we have microaerophilic protists but the evidence isn't great
126
how do protists respire?
normal aerobic respiration with mitochondria producing carbon dioxide. in anaerobic cells, they basically have an anaerobic mitochondrion called hydrogen some, producing hydrogen, acetate, carbon dioxide.
127
describe endosymbiont theory for mitochondria and plastids
Bacteria originally living as endosymbiont in cells, dependency then became permanent. Alpha-proteobacterium became a mitochondrion. Hydrogenosome evolved from a mitochondrion Cyanobacterium became a chloroplast, and were originally thought to be algae. Evidence: size for organelle= size of bacterium, and phylogeny analysis relates their DNA to their bacterial origin. There are great similarities between the RNA of mitochondria and proteobacteria, and cyanobacteria and chloroplasts. Have own circular DNA and replicate by binary fission= unequal distribution in daughter cells. Contain same ribosomes as bacteria. They have a double membrane (engulfing mechanism).
128
describe the food vacuole (phagosome) dynamics in protists
With the food vacuole in protists, the lysosomes will digest food, and the environment will become acidic, and some other stuff will happen, and the debris will be taken out by exocytosis. The membrane will eventually be recycled. Mitochondria and chloroplasts all have a double membrane, showing evidence for the digestive phagosome mechanism. Selective digestion or no digestion- leads to mixotrophy.
129
describe the 3 types of mixotrophy
organellar: (selective digestion). Eats algal cells and does not digest plastids (“Kleptoplastids”). Plastids fix CO2. Plastids do not encode for polymerases. Die and need replenishing (so eats more). Protist can live without the plastids. Cellular mixotrophy: (no digestion). Eats algal cells but doesn't digest them. Algae fix CO2 and divide in cell. “Endosymbiosis". Protist can live without the algae. Both organellar + cellular= ciliates and amoebae. Constitutive mixotrophs: (algae evolve into organelles). Over time, endosymbiotic algae become true organelles, and the protist can't live without them. They make a sort of agreement that the host cell will provide the DNA polymerase for the plastids and stuff to divide. Only seen in flagellates.
130
how does light affect mixotrophs ratio of photosynthesis and feeding?
High light: Photosynthesis > feeding Low light: Feeding > photosynthesis
131
describe some features of ciliates
Covered in cilia (tiny hairs), used for movement and feeding. Most developed protozoan, due to prehistoric mouth (cytostome) and anus (cytoproct) heheheheh. Contains macronuclei and also micronuclei, unlike other protozoa, used for sex heheheh.
132
describe motile cilia
“9+2”- 9 microtubule pairs on the outside they also contain a dyneim motor protein for movement. Cilia are positioned in very orderly strict lines, to allow efficient movement. Sessile ciliates don’t move a lot, and instead attach to other things. Present in humans (bronchial and oviduct epithelium, to move the egg down the fallopian tube)
133
describe non-motile cilium
9+0, no dynein motor protein. ‘Primary cilium’ on all human cells- senses changes in external environment.
134
describe general features of cilia
used for movement to go back and forward, some fuse to form cirri (thick cilia), allowing ciliates to walk/ scurry. they are also very important for feeding, as they direct prey towards the cytostome, which contains stiffer cilia (membranelles) that act like a sieve and only allow specific prey to go through down the mouth: “filter feeding”. They’re eaten, and anus is close to mouth, so the waste is expelled easily.
135
what are sessile ciliates?
encased in a vase-shaped lorica (shell) that is also provided with a lid, which the cell can shut behind itself after it retracts into the lorica.
136
describe how some sessile ciliates use their shape for feeding.
prey are drawn towards their cell, and Cilia do a little Mexican wave and move one by one, creating a vortex, spinning food towards its mouth e.g. Vorticella
137
describe how Suctorian ciliates are an exception to the rule
No cilia what the frick. it has numerous microtubule tentacles, each one ending with a cytostrome. The tentacles are kind of like straws to suck in prey and stuff- raptorial feeding. Release extrusomes which kill the cell and dissolves all its contents and uses tentacles to suck it up. Similar to peristalsis. Doesn’t divide into 2 like normal ciliates, produces little ciliates inside that have cilia, that are released from the mother cells.
138
what are mixotrophic ciliates?
Do not contain their own plastids. Acquire photoautotrophic ability two ways. Organellar mixotrophy and Cellular mixotrophy
139
ciliates can reproduce sexually and asexually, describe them both
asexual: the ciliates divide across the waist bit, in transverse binary fission, and involves mitosis. sexual: conjugation, involves meiosis and mitosis, where 2 cells lying against each other= having sex because they never divide like that. Involves a micronuclei swap that produces genetically different ciliates from when they first met- allows for a lot of diversity with ciliates.
140
describe how anaerobic ciliates (sulphur ciliates) respire
hydrogensomes convert pyruvate into hydrogen, acetate and carbon dioxide. then, the vast majority of sulphur ciliates in archaea domain contain methanogenic bacteria to make methane from the carbon dioxide and hydrogen (will use acetate if not much of the others but its slower).
141
explain how UV light can be used to identify methanogenic bacteria in ciliates
Coenzyme F420 fluoresces blue with UV light, loads of them in the ciliates.
142
explain general features of flagellates
possess flagella, like cilia except longer and fewer, the max a cell can have is 8 but most have 1 or 2. Also has the 9+2 structure but move in a rotational way, whereas cilia move backwards and forwards. Ciliates can reverse and stuff but flagellates cant- easy way to tell them apart. They only possess macronucleus so can't sexually reproduce, and divide longitudinal (tip to toe). They're mainly aerobic and feed by heterotrophy, photoautotrophy and mixotrophy
143
describe heterotrophic flagellates (zoo flagellates)
most are aerobic, the only anaerobic one is sexually transmitted. most are aerobic, and they respire carbon dioxide converted to prey's carbon. they both raptorial feed and filter feed also
144
explain differences between naked and hipsid flagellum + how raptorial feeding can be increased because of them
The hairy ones create more efficient feeding e..g they create feeding currents and the prey will be drawn to the flagellum base, and they will be ingested via cytoplasmic extensions (pseudopedia). However, naked ones can be covered in drawing pin things that can move around the cell, piercing bacterial cells and taking them to the base of the flagellum and depositing it.
145
explain filter feeding with naked flagella
they can have their own little fishing net; some cells will have a collar of microvilli tentacles, and prey will get caught and go through the tentacles. They contain actin, making to good for contracting.
146
what are choanoflagellates?
has a collar of tentacles, with a single naked flagellum, attached to the center by a stalk thing, most closely related to humans and animals than protists. In a sponge, the choanocytes are very similar to choanoflagellates in the way they feed (filter feeding). Silica lorica, for example, makes its own glass woven basket kind of thing to hide from predators. Before division, they can make more strips for the daughter cell, so that when they divide, they have their own little basket. Increases the strength of the lorica.
147
describe photoautotrophic flagellates
own green or gold plastids to help photosynthesise (they don't feed). All of them are aerobic and pretty much just use their flagella or movement towards light and nutrients.
148
explain how photoreceptor can aid photoautotrophic flagellates
With photoreception, the light detector in the flagellate can change the direction of the flagellate and direct it to where there is the most amount of light.
149
what is special and cool about dinoflagellates?
they have a 2nd flagellum around their waist, meaning they can spin as well as go backwards and forwards.
150
how do protists live and congregate?
some protists live alone e.g. ochromonas with few plastids and prefers to feed on prey some form colonies of cells e.g. SYNURA (remember pls xxx), and dinobryon with loads of plastids, that prefer to photosynthesise
151
what are mixotrophic flagellates?
phytoflagellates that eat (best of both however usually one is over-riding xxxx), 'constitutive mixotrophy'- have their own plastids that can divide. they also do raptorial feeding. whichever feeding type dominates is affected by light regime and temperature
152
describe general features of amoebae
Very simple protists with only one macronucleus like the flagellates. Most are aerobic so will use mitochondria, and most are heterotrophic so will eat prey (mixotrophic ones are usually organellar or cellular). Amoebae divide in any plane in asexual reproduction. Some move and some are stationary.
153
describe features of naked amoebae, and how they move, and the 3 cell forms
basically a blob of cytoplasm with cytoplasmic membrane. when the cytoplasm moves, the cell is elongated and produces pseudopodia that creep along surfaces, they are also used for catching prey. they can ingest anywhere. the feeding form is called trophozoites, all produce cysts (sleeping) and there is also a floating form (non-feeding form). Floating form is not epic as it protrudes its pseudopodia, making star shapes, and then they stiffen to allow maximum floating- they can’t feed in this state. Floating form is used to basically just float between attachment of different surfaces.
154
describe general features of shelled amoebae
Shelled amoebae are enclosed in a test (good for predators) and they can move and bring their shell with them which can be made of anything. Intrashellular cytoplasm in the test, project extrashellular cytoplasm to move/feed. Can feed by 2 mechanisms- raptorial (grabbing) and diffusion feeding. Foraminiferans (they diffusion feed) make their shell out of calcium carbonate (chalk), if the amoebae died inside, the shell won’t dissolve and instead becomes fossilized. Diffusion feeding- the amoebae protrude sticky flexible filaments of extrashellular cytoplasm (axopodia), increasing surface area for prey capture, they become stuck. Radiolarians and heliozoans use silica (glass). Can also produce cysts.
155
describe advantages of protists in terms of ecological impact
basically all of them are good. microbes: base of every food chain keep bacterial populations healthy important in nutrient cycling
156
describe disadvantages of protists in terms of ecological impact
mainly amoebae. allow the evolution of new bacterial pathogens. act as a reservoir for them too e.g. legionella, salmonella
157
describe the microbial loop in terms of protist ecological loop (draw if can)
“The Microbial Loop”: base of loop is anything that can photosynthesize e.g. primary producer. They utilize an inorganic carbon form (usually carbon dioxide) to make way more sugar (DOC) than they need, constantly leak sugar out of their cells, which is bacteria’s primary organic carbon source. Heterotrophic protozoa eat the photoautotrophs and the bacteria, which are eaten by metazoa. With growth curve, all organisms in the environment must be active, so the protists prevent the bacterial numbers hitting carrying capacity, forcing them to stay in their dividing state. Remineralization: carbon, nitrogen, phosphorus assimilated into the cytoplasm. Predation keeps bacteria in ‘log phase’: Bacteria are constantly feeding and dividing so they are constantly ‘active’. They need to maintain their ratio, but they will naturally lose carbon dioxide through respiration, so they also pump out phosphorus and nitrogen as well to keep up with it as waste, which bacteria likes.
158
how do amoebae link with bacteria in the evolution of pathogens?
amoebae and macrophages share many similarities. normal bacteria can develop into pathogenic bacteria by basically practicing on amoebae in the environment by evading either being eaten or being digested. Usually change their antigens on their surface so they can’t be picked up by receptors. Can also have this sugary casing thing to protect receptors. If they get eaten, fusion of lysosomes with the phagosome can be stopped. If they still survive that, they can just divide in the phagosome or escape into the cytoplasm and start doing dastardly things (trojan horse).
159
90% of human cells are bacterial, which one protist is naturally present?
E.coli (amoeba), it exists in the gut so isn't pathogenic. the gut is the site of most bacteria, and an attractive location for parasitic protists.
160
name some gut infections caused by protists, give examples of the protists, reservoirs and transport
one ciliate amoebae e.g. balantidium cell, and flagellates e.g. Giardia lambia , which 2 macronuclei which is quite epic, and they feed on bacteria, and divide quickly forming a block in your intestine- diarrhea. All produce cysts. reservoir: water, animals, humans transport: contaminated water, faecal-oral route
161
describe an example of eye infections caused by protists, give example of protist, reservoir and transport
amoebae belonging to acanthamoeba, causing keratitis (hence why hydrogen peroxide must be in contact lens cleaner) reservoir: water transport: dirty contact lenses it is treatable but can lead to glaucoma.
162
describe a brain infection caused by protists, give examples of protist, reservoir and transmission
one amoeba- naegleria fowler 'brain eating amoeba', causing primary amoebic meningoencephalitis (PAM). reservoir: warm water transmission: flagellate swims up nose fatal in 2 weeks
163
give an example of an STD caused by a protist, give example of the reservoir and transmission
one flagellate- trichomonad vaginalis, causes trichomoniasis (anaerobic and no cysts). Infects the urethra, vagina and prostate. reservoir: humans (males are asymptomatic) transmission: sexual intercourse treatable
164
give an example of blood/ tissue infections caused by protists, give examples of reservoir and transmission
flagellates e.g. leishmania mexicana, causes leishmania (aerobic, no cysts). reservoir: dogs transmission: sand fly (vector) 'visceral': attacks tissues e.g. spleen and liver. 'cutaneous': infects macrophages and divides within treatable
165
what is the range of fungi sizes, from unicellular yeasts to humongous fungi?
unicellular yeasts are microns big (around 1/1000 of a mm), while humongous fungi e.g. amillaria can be just under 100 tons.
166
are fungi prokaryotes or eukaryotes?
eukaryotes
167
what are fungi cell walls made of?
chitin and polysaccharides
168
do fungi reproduce sexually and asexually, and are the resulting nuclei haploid or diploid?
they reproduce both sexually and asexually, and the nuclei are usually haploid (one chromosome set), as opposed to animals which are diploid and plants which are polyploid.
169
fungi are heterotrophs, what does this mean?
they obtain energy by degrading complex organic molecules from the environment. they're very successful heterotrophs, as they are complex organisms that can build up all the nutrients they need, so they occupy a large range of niches. They contain no chlorophyll, can't use carbon dioxide as a single carbon source, and are not nitrogen-fixing
170
what are the 3 types of heterotrophic parasitic fungi in terms of feeding?
saprophytes- derive nutrients from dead remains necrophytes- derive nutrients from organisms they have killed biotrophs- derive nutrients from living host
171
key differences between plants and fungi in terms of feeding, shape, cell wall, division
plants are photo-autotrophs (photosynthesisers), while fungi secrete enzymes and digest/ absorb organic material. fungi are usually filamentous in form, while plants are made up of box-like cells. fungi cell walls are composed of chitin and polysaccharides, while plant cell walls are made of peptin and cellulose. fungal nuclear mitosis takes place within the nucleus, while in other eukaryotes the nuclear envelope breaks down.
172
what is the closest relative to fungi?
animals
173
describe yeasts, in terms of shape and reproduction
single cell/ nucleus, oval or spherical, reproduces asexually by producing an identical but separate daughter cell. they can also aggregate to form a colony or 'pseudohyphae'. in reproduction, yeasts typically bud a daughter cell.
174
describe the shape of filamentous fungi, and how they reproduce
this is the vast majority of fungi, and are multicellular. they grow with long 'thread-like' filaments- hyphae, and have polarised tip growth forming mycelia (colonies or masses of hyphae), and can grow further to form large complex bodies (interwoven). for reproduction, they generate light weight spores for effective dispersion and colonise food supply rapidly, they are haploid and are formed from specialised aerial extensions from mycelia.
175
describe how dimorphic yeasts/ fungi form
environmental cues (e.g. temperature, carbon dioxide) trigger transition between yeast and filamentous form, for example Candida albicans becomes aggressive when it changes from yeast to fungi. they are medically important.
176
fungi can reproduce sexually or asexually, describe sexual reproduction for fungi in general and heterothallism/homothallism
union of compatible nuclei to form diploid (2n) state usually when nutrients are in poor supply, sexual spores are usually more hardy structures allowing survival in adverse conditions. heterothallism- results in exchange of genetic material and requires 2 different mating types homothallism- some fungi are able to self-fertilise and produce sexual spores
177
draw a diagram showing the generalised overview of sexual reproduction in fungi
178
what are the 3 divisions of fungi?
zygomycota, ascomycota, basidomycota
179
describe the process of asexual reproduction in zygomycetes
1. aerial hypha produces a sporangium 2. sporangium bursts to release spores 3. spore germinates to produce aseptate mycelium 4. vegetative mycelium grows 5. gamete forms at tip of hyphae (haploid nucleus)
180
describe sexual production in zygomycetes
1. aerial hypha produces a sporangium 2. sporangium bursts to release spores 3. spore germinates to produce aseptate mycelium 4. vegetative mycelium grows 5. GAMETE FORMS AT TIP OF HYPHAE 6. mating hyphae join and fuse (dikaryon n+n) 7. zygosporangium 8. mature zygosporangium 9. nuclear meiosis (not shown) 10. zygosporangium produces an asexual sporangium 11. spores (1n) are released from sporangium
181
describe features of zygomycetes, the smallest phyla of fungi
aseptate haploid hyphae. asexual features- haploid sporangiospores from sporangia sexual features- diploid zygospore most are saprophytes, and contain glomus (important mycorrhizal fungi) which improves nutrient uptake, resistance to drought and disease.
182
describe ascomycetes asexual reproduction
1. hypha produces conidiophore and conidiospores 2. conidiospores released from conidiophore 3. conidiophore germinates to produce mycelium and mycelium grows
183
describe ascomycetes sexual reproduction
1. hypha produces conidiophore and conidiospores 2. conidiospores released from conidiophore 3. conidiophore germinates to produce mycelium and mycelium grows 4. cytoplasmic fusion with opposite mating type 5. dikaryon (n+n) 6. nuclei fuse in terminal cells to form 2n nuclei 7. meiosis produces 4 haploid (1n) cells 8. mitosis produces 8 haploid ascospores on each tip 9. ascus opens to release ascospores
184
describe general features of ascomycetes, including sexual and asexual features
septate hyphae (haploid) asexual features- haploid conidospores from conidiophores sexual features- haploid ascospores (meiosis followed by mitosis) most are saprophytes, and model organisms, with many important plant pathogens
185
describe basidiomycetes sexual reproduction
1. basidiospore released 2. basidiospore germinate to produce mycelia 3. hypha of opposite mating fuse below ground to produce eukaryotic mycelium 4. dikaryon mycelium produces basidiocarp (mushroom) 5. pair of haploid nuclei fuse to form diploid (2n) 6. meiosis produces 4 haploid nuclei 7. 4 basidiospore (1n) develop
186
describe general features of basidiomycetes including sexual and asexual features
septate hyphae (dikaryons) asexual cycle is uncommon, but sexual features include haploid basidiospores (meiosis). various types of fruiting body (basidiocarps) e.g. toadstools, brackets and puffballs most are saprophytes (lignin decomposers) and have many important plant pathogens e.g rusts. they can also act as food for us e.g. mushrooms
187
describe general features of deuteromycetes including sexual and asexual reproduction
sexual reproduction cycle absent, however asexual spores formed in various ways (e.g. conidiophores and arthroconidia). fungi imperfecti. most were ascomycetes and did include the important food spoiler Aspergillus flavus, and the industrial workhorse Aspergillus niger.
188
what are the impacts of fungal infections?
species extinction, food security, loss of fixed carbon (carbon dioxide released)
189
describe true pathogens e.g. Histoplasma
they are usually asymptomatic in the healthy host. Physiological adaptations to high temperature and low oxygen tension, with a limited number of species known the cause systemic infections in humans. fungal infections have adaptations to deal with this stuff. Restricted to geographical places, a lot of America and some of Africa (mainly endothermic places). Not obligate parasites, digesting environmental nutrients, don’t have to infect hosts to complete life cycle they can just chill (saprophytic).
190
describe how an increase or decrease in temperature can lead to a true pathogens' change from a natural habitat to an animal habitat
true pathogens are in the hyphae form (brown and filamentous) in their natural habitat at temperatures usually below 30. They reproduce via spores and are saprophytic. when temperature increases, they change to their animal habitat (waxy yeast form) , usually around 35-40 degrees. They reproduce via budding or endospores, and are parasitic. A decrease in temp will change back to the hyphal form.
191
give examples of true pathogens, and the events in its infection
histoplasmosis (histoplasma capsulatum)- most common, 500,000 cases in USA per year. 1. Soil containing bird shit is whipped up by wind, so microconidia are inhaled. 2. The patient will develop mild pneumonia. 3. In the tissue has of infection, the yeast is phagocytosised, and multiplies by budding. 4. In some cases, phagocytes enter the blood and cause disseminated disease. Coccidioidomycosis- common in alkaline desert soils in southwestern US. Forms endospores in sporangia in yeast form. 1. Digging in soil produces aerosol of arthrospores, which cause a lung infection when inhaled. 2. Arthrospores develop into spherules which release endospores into the lungs, which immunocompetent people can just fight and be done with. But unhealthy people can develop meningitis, osteomyelitis and skin granulomas.
192
what are opportunistic pathogens?
the host defences need to be impaired to infect. there are many species distributed world-wide. In terms of adaptations, they don’t change morphology with changes to host environments but tolerate changes and can sometimes thrive in them. Poor prognosis- limit with drug treatments, can expect mortality rate to be around 50-60%. Superficial/ benign to chronic system infections.
193
Describe infection and features of the opportunistic pathogen Candida albicans
Candidiosis- widespread (around 20% of us have it)+ most common fungal pathogen causing life loss. 4th biggest killer in tertiary care hospitals. if you’re immunocompetent, can be an aggressive but not harmful infection, but if not it can be systemic and cause organ failure. Oral thrush on HIV patient for example. It goes through thermal dimorphism, where it goes to aggressive hyphae form to create damage. Invades wounds/ burns.
194
Describe the infection and general lore of opportunistic pathogen Aspergillus spp.
Aspergillosis- there are 600 Aspergillus/ 8 species that cause human disease, e.g. A.fumigatus is a thermophile that produces small spores. Produces small spores that get lodged into lungs (aspergilloma- fungal ball), also likes room temperature which is not good. Hospitals have been closing because of these infections frfr. Aggressive invasion using hyphae- tissue necrosis. Colonises lungs then disseminates to brain/heart.
195
describe dermatophytes
superficial infections on a healthy host (non-invasive). World-wide distribution- most common are those causing Ringworm and Athletes foot (Trichophyta spp). Also 1 million nail infections in the UK. Its not life-threatening, just slight discomfort- affects like keratin and stud.
196
why are human mycoses a mounting clinical problem?
More immunocompromised hospital patients. A relatively poor understanding of fundamental fungal biology- limited anti fungal treatments.
197
describe control of fungal disease in humans with azoles
E.g. ketoconazole, flucoazole interrupt enzymes. ERGOSTEROL DEPENDENT- fungus form of cholesterol. fungi are killed because the azaleas remove cholesterol.
198
describe control of fungal diseases (mycoses) of humans with polyenes
e.g. nystatin, amphotericin B forms a pore so all the ergosterol leaks out and the fungus will die. Ergosterol= fungus form of cholesterol.
199
how does 5-fluorocytosine control mycoses of humans?
inhibits RNA synthesis- fungistatic.
200
what are the 2 major groups of phytopathogenic fungi?
1. pathogens of immature (or compromised tissue) 2. pathogens of mature and non-compromised tissue (where the plants don’t know it’s infected) e.g, neurotrophic pathogens and biographic pathogens.
201
describe pathogens of immature tissue (phytopathogenic fungi)
they have a broad host range, soil-borne pathogens attack roots e.g. Phythium and Phytophora spp.) they express aggressive invasion of root tips with extensive destruction, particularly in water-logged soils.
202
describe pathogens of mature tissue (phytopathogenic fungi)
usually high degree of host specificity Neurotrophic pathogens- excrete toxins and cell-wall-digesting enzymes. Host cell dies and tissue is invaded. EVOKE HOST RESISTANCE MECHANISMS. Biographic pathogens- maintain host viability. There is limited tissue invasion, and the DO NOT EVOKE RESISTANCE MECHANISMS. life cycle depends on living host, and they arrive as spores on leaves.
203
give and describe an example of a nectrophic pathogen
Armillaria melles (honey fungus)- major root rot pathogen of broad leaved trees. Rhizomorphs are made up of loads of tubes. They are sent out and the honey fungi affect underneath the bark of a tree (phloem system), killing the tree. Excrete ligninases, cellulase and pectinases.
204
give and describe examples of biographic pathogens- the haustoria biotrophs
Puccinia graminis- via stomatal opening. they infect mesophyll cells. When leaves are infected, this forms a nutrient sink which diverts nutrients from growth and grain yield- reduced photosynthesis. Erysiphe graminis- infect directly through the cuticle epidermal layer. Affects like wheat and such. They don’t kill plants, but they compromise them e.g. yield of grain and stuff will be reduced. They don’t evoke resistance mechanisms anyway, so the plants wouldn’t know if it was being affected. Haustorial because they produce a haustorium. They punch a hole through the cell wall, leaving the inside and everything else intact, depleting the plant’s nutrients, reducing crop production.
205
how are fungi used to control insect pests (stats)?
For fungi to infect, they require a stable environment, high humidity and controlled temperature, so glasshouses are a way of ensuring. Soil is also a stable environment. 1 billion dollars spent each year in USA to control insect pests- only 5% of this on BCAs. E.g. Koppert (brand)- Mycotal kills whitefly and thrips in 10-14 days and Vertalec kills aphids in 7-10 days. Over 400 species of fungi attack insects and mites.
206
give the typical infection cycle or fungi killing pests and stuff I fear
1. spore attachment 2. germination to intersegmental region- usually includes extending a hypha to one of the weaker parts of the insect like a hole or something 3. penetration of cuticle (lipases, chitinases, proteases) 4. hyphal invasion beneath cuticle 5. sporulates 6. proliferation into blood (yeast phase) 7. death (toxins/ sugar levels) 8. saprophytic stage- spores must do this to keep the life cycle going
207
how does the fungus Verticillium lecanii help to control biological agents
Produce spores in liquid fermentors, making the production of the spores commercially viable. Fresh spores are sticky so they attach to the insect which becomes contagious. As spores don’t need to be ingested, targeting the organism is easy. Germination also requires lower humidity (lower temperature, approx. 15-18 for 12 hours)
208
What are the mechanisms of control for phytopathogenic fungi?
1. Parasitism of the pathogen by the BCA 2. Production of antibiotics, BCA poisons the pathogen 3. Competition for nutrients, water, space
209
describe parasitism to control phytopathogenic fungi (mechanism 1)
"mycoparasites"- many are zygomycetes which are biotrophic and produce haustoria, meaning they can grow inside of an organism and infect it from there. most potential shown by neurotrophic mycoparasites. E.g. Pyhtium oligandrum (oomycete). Only reason Pythium oligandrum isn’t used is because the spores produced aren’t hardy enough, making it difficult to get it to market.
210
describe the specific example for production of antibiotics as a mechanism (2) of phytopathogenic fungi
e.g. Trichoderma spp. (trichodermin; gliotoxin). "Trianum"- Koppert- sold for control for a range of fungal diseases including B. cinerea infection of grapes. Trianum lowers competition and stops other fungi from infecting grapes.
211
explain fungal competition in the context of butt rot control in conifers
With deforestation, the stump after needs to be treated as pathogens such as Heterobasidion (butt rot) will colonize and produce spores, and many more will try to colonize as well. To treat, you paint Phlebiopsis gigantea onto the stump, letting it grow on the stump which isn’t pathogenic so won’t infect neighboring trees, and will compete with the Heterobasidion for infection of neighboring trees. Blue dye is used with the Phlebiopsis, so we know that the stump has been treated. Found in like Norfolk in a pine plantation, and a forest canopy where loads of trees have died. As the trees die, Heterobasidium annosum grows up to the soil surface and produces bracket-shaped fruitbodies just above or within the forest litter layer. The fruiting bodies release basidiospores that can be wind-dispersed and infect freshly exposed stump surfaces to spread the infection. The cultures of Phlebiopsis can be fluorescently dyed to see.
212
how does fungi help with food and drink?
baking and brewing e.g. Saccharomyces cerevisiae like marmite, gives fluffy and non-flat bread. glucose -> 2C2H5OH + 2CO2 also like soya bean products- improved fermentation of beans with Aspergillus oryzae (aerobic) and Zygosaccharomyces (anaerobic)- a halophile so can stand high salt conditions and makes it unlikely for any other pathogens to grow. also quorn lets go: mycelia of Fusarium graminearum (venenatum). On the back of rationing after World War 2, at first there was high demand for protein hence the development of mycoproteins. However, in the 80s, there was demand for low fat as well which wasn’t a massive concern when rationing. Grows on glucose syrup- made from a cheap source of carbohydrate. Ammonia- nitrogen source. Filaments can be spun and flavoured to resemble meat.
213
describe how fungal cell factories commercially produce enzymes with Aspergillus niger
Glucoamylases: liquid starch to high glucose syrup (baking and brewing and stuff), cheap alternative to glucose. Pectinases: breakdown pectins in plant cell wall (fruit juices)- removes cloudiness. Glucose oxidase: food preservation; diagnostic tests. The reaction it catalyzes is glucose + oxygen -> gluconate + hydrogen peroxide. It is highly specific for glucose as a sugar and doesn’t accept any other sugars like fructose. Used in urine tests and keeps meat red instead of going a weird grey color, also due to removal of oxygen, which extends shelf life. Phytases: improvement of animal feed. Good at storing phosphate from soil, in a vacuole in the form of phytases. It is difficult to digest, so to improve the nutritional value of food, you can treat the food with phytases.
214
what is the problem with fungal cell factories?
starch-based foods cooked at high temperatures (e.g. crisps, biscuits etc) recently discovered high levels of acrylamide- carcinogen. Aspergillus niger was tampered with, changed the metabolism to produce Asparaginase, which removes the amide group from asparagine, removing acrylamide.
215
describe how citric acid is produced commercially by Aspergillus niger
baso Krebs cycle; excess sugar Citric acid is way easier to produce from Aspergillus niger instead of extracting all of it from lemons and stuff, very acidic as it is a tricarboxylic acid. Grown in limited supply of trace metals.
216
describe how fungal cell factories produce antibiotics
antibiotics- penicillin, which interrupts the bacterial cell wall, so it doesn’t develop, and the bacteria can’t survive. 1928- Alexander Fleming. 1941- saved first life + widely used by the end of WWII. Improved yields from 2 mg to 30 g per litre. Chemically altered semi-synthetic pencillins (methicillin; ampicillin).
217
describe how fungal cell factories an produce statins
High plasma cholesterol levels is an important risk factor in coronary heart disease Most of the body’s cholesterol is synthesised directly from intracellular pre-cursors. Statins are fungal metabolites that inhibit the biosynthesis of cholesterol and are used to reduce plasma cholesterol levels. E.g. Lovastatin (R group= CH3. Aspergillus terreus). Mevastatin (R group= H. Penicillin citrinum).
218
why are viruses described as molecular fossils?
they contain preserved organic material that has been transformed into fossils or has mostly decayed.
219
what is a virus?
A simple, miniscule, infectious, obligate intracellular parasite comprising of genetic material (DNA or RNA) surrounded by a protein coat (capsid) and/or an envelope derived from a host cell membrane.
220
describe like the general features about virus genomes
Viruses have a very small genome (influenza has 11 genes it can code for compared to 22000 from humans), as they don’t need to code for lots of proteins that code for structures; they’re simple. They hijack metabolic machinery from other organisms to reproduce. The way they infect hosts is also very simple.
221
around how big are viruses?
around like 20-200 nm (1um= 1000nm), can be seen with an electron microscope
222
which is bigger a bacteriophage or smallpox virus?
smallpox, around 200nm while bacteriophages are 50 nm
223
describe the big fat giant viruses
mimiviruses- like 750 nm which is bigger than bacteria crazyyyyyy. they can even be seen under a light microscope pandoravirus: a little less than 1000 nm which is large and hefty. 2.9 megabytes genome size which is like 2556 genes. thank golly they only infect amoeba.
224
describe the 2 phases of viruses
1. extracellular virion- outside the host cell- for transmission. 2. intracellular virus- after infecting the host cell- for replication When you cough and sneeze and stuff, what is ejected is an extracellular virion, which is used for transmission. Viruses specifically are used for replication and are not the usual shape that we think they are.
225
explain like viral replication vs bacterial multiplication
viral replication is the formation of biological viruses during the infection process in the target host cells. bacterial multiplication is the asexual reproduction, or cell division, of a bacterium into two daughter cells, in a process called binary fission.
226
describe the tool used to view viral structural biology (like 4 things)
1. electron microscopy 2. X-ray crystallography 3. cryo-electron microscopy 4. NMR
227
draw out the structure of the virion and label functions
Capsomers are arranged in a very specific orientation, that defines the shape of the virion, (e.g. rabies is bullet-shaped, adenovirus for covid is polyhedral, etc.).
228
describe some cool different shapes of capsids
1. helical- capsomers are bond together in a spiral fashion e.g. TMV 2. polyhedral- capsid is roughly spherical (Icosahedron symmetric carry 20 faces and 12 corners e.g. adenovirus) 3. binal (complex)- neither helical or the other one, irregular + complex. may consist of both helical and isometric symmetries e.g. bacteriophages
229
what are the functions of capsids?
1. protects the nucleic acid from digestion by enzymes 2. contains special sites on its surface that allow the virion to attach to a host cell. 3. provides proteins that enable the virion to penetrate the host cell membrane and, in some cases, to inject the infectious nucleic acid into the cell's cytoplasm. Under the right conditions, viral RNA in a liquid suspension will self-assemble a capsid to become a functional and infectious virus.
230
draw the kind of contrast in structures between a naked and enveloped virions + give examples
enveloped ones usually acquire their envelopes from the host cell. Eclipse period: when the viruses are being formed in the host cell, nothing is happening on the exterior.
231
what are the shapes of rabies virus, measles, and ebola?
rabies- like a bullet thing measles- sphere ebola- long ahh snake
232
describe different host cells for viruses (7)
1. bacteria- bacteriophages 2. protozoa- e.g. leishmania. can't infect vertebrates but dsRNA can be sensed by vertebrates and thus leads to complications. 3. algae- members of Phycodnaviridae family infect algae, are dsDNA viruses of 100–560kb. Can infect human) 4. fungi- mycoviruses are either dsRNA or +ssRNA, human infection? 5. plants- TMV, can't infect humans 6. animals- avian influenza virus, can transmit to human-zoonotic viruses 7. virophage- viruses that infect viruses. dsDNA Sputnik virophage infect giant Mimivirus EACH VIRUS ONLY INFECTS A SPECIFIC GROUP OF HOSTS/ SINGLE HOST.
233
describe general features of a bacteriophage
More than 10^30 bacteriophage particles in the world’s waters. A bacteriophage particle weights about a femtogram (10-15 grams). 10^30 x 10^-15= the biomass on the planet of bacterial viruses alone exceeds the biomass of elephants by more than 1000-fold! There are only a few with envelopes, most have dsDNA and many are complex.
234
explain the replication cycle of the lytic bacteriophage T4
1. adsorption: attachment to specific receptors 2. penetration (entry of DNA) 3. replication: synthesis of viral nucleic acids and protein 4. maturation: assembly and packaging of new virions 5. release: release of new virions (lysis) 6. reinfection
235
describe the lore of the epic bacteriophage T4 and the whole temperate and lysogenic phage thing
it do be virulent and kills the host (a lytic phage). Many bacteriophages have an alternative life cycle where they don’t kill the host: temperate phages or lysogenic phages. After infection, the genome of a temperate phage can integrate into the host’s chromosome; it is then termed a “prophage” - prophage produces a repressor protein - repressor blocks lytic genes. The prophage replicates with the host chromosome: lysogeny or lysogenic cycle The bacterial hosts that harbour a prophage are termed lysogens, they are immune against infection with the same phage because of the repressor. Stresses (UV light, toxin) initiate induction to resume lytic cycle.
236
how do we quantify bacteriophages?
same as bacteria just nutrient agar plate, produces bacteriophage plaques
237
describe some uses of phages in biomedicine
1. concentrated solution of bacteriophage specific for Listeria monocytogenes. for use on unprocessed foods like cheese, meats, fish. 2. a bacteriophage enzyme (phage lysin gamma, PylG) detects and kills Bacillus anthracis spores 3. Display of the immunodominant region of HBV on bacteriophage T7.
238
give 3 general epic things about viruses about how abundant they are
1. they are "planetary force"- 10 million of them in like a drop of seawater 2. they keep control of bad bacteria- 10 million phages on a normal hand 3. they're primarily known for "impact on health"- covid, hiv/aids.
239
give some of the ways that viruses are named like things they're named after + a few examples
1. geographic location they were first isolated e.g. Newcastle disease virus lol 2. host organism e.g. African horse sickness virus 3. scientists that discovered e.g. Epstein-Barr virus 4. type of disease e.g. Hepatitis A,B,C 5. sites of the body e.g. rhinovirus (upper respiratory tract) + adenovirus
240
what are the 2 main epic methods for taxonomy of viruses?
1. International Committee on the Taxonomy of Viruses (ICTV) 2. Baltimore System of Virus Classification They are used together I fear
241
describe how phenotypic and genotypic factors can distinguish one virus from another just generally
phenotypic: molecular composition, virion/ capsid structure, envelop or not, host range, pathogenicity genotypic: sequence similarity, gene contents and synteny and expression, PHYLOGENETIC RELATIONSHIPS.
242
explain (with monkeypox as an example) how phenotype and genotype can go into the classification of the virus
phenotype: natural host ranges (subfamily), mortality and morbidity characteristics genotype: amino acid sequence identity, nucleotide sequence, PHYLOEGENETIC ANALYSIS
243
what is like the main big thing about virus classification with the Baltimore system?
viral genome MUST MAKE MRNA that can be read by host ribosomes, doesn't concern phenotype or genotype or genetic material
244
describe that weird + and DNA and RNA thing for the baltimore system
3 species of RNA- mRNA has an open frame which can code for the protein, 5’ cap and 3’ tail, and Poly A tail. Also, single stranded!!!!!!! It is positive meaning it is ready to be ready and translated. If it is negative, it’s not ready to be read.
245
which level of the Baltimore system diagram thing are most viruses that infect humans?
like 5/6 e.g. coronavirus Adenoviruses are those that contain double-stranded DNA with a gap.
246
give possible ways viruses can infect cells (4)
1. transformation into tumour cell 2. lysis (death of cell + release of virus) 3. persistent infection (slow release of virus without cell death 4. latent infection (virus present but not causing harm, latent infections can develop into persistent e.g. HIV to AIDS but need a trigger)
247
what are the 3 general stages and 6 sub-stages of the virus life cycle?
1. ENTRY- attachment, uncoating, replication 2. REPLICATION- replication (transcription) and biosynthesis (translation) 3. EXIT- assembly, budding
248
describe step 1 entry of the virus life cycle
1. attachment- all viruses require a receptor to attach, except for fungal viruses (no extracellular phase) and plant (entry by mechanical damage). The receptors that the virus attaches to aren’t exactly made for this e.g. receptors can be made for plasma membranes. They each usually have their own function. Some viruses also use multiple receptors e.g. rhinovirus + retrovirus, and some viruses can bind to same receptors e.g. influenza and measles. 2. entry- either inject nucleic acid (polio), fuse the envelope to the host membrane (measles) or endocytosis (herpes). With endocytosis, due to the change in osmotic pressure, the nucleic capsid will burst, and the nucleic acid will be released.
249
explain step 2 (replication) in the viral life cycle
1. viral proteins- synthesis of mRNA (unanimous) 2. viral genome- generation of viral genetic material (virus-dependent) proteins + genome= assembled epic virus.
250
explain step 3 (exit) of the viral life cycle
naked viruses will just be released in cell lysis I fear. enveloped ones: 1. viral glycoproteins re added to the envelope of the virus 2. the virus buds intracellularly, which includes Golgi apparatus and ER, and shit is released.
251
which genome were viruses first identified in?
dinosaurs xxxxxx, probs the oldest form of biomaterial and are billions of years old
252
give 3 examples of old ahh viral diseases and 3 of new re-emerging ones
old: polio, hepatitis, influenza new: covid, West Nile fever, dengue fever some new and epic diseases are re-emerging due to things like deforestation that put us in closer contact with animals and stuff that could pass something one.
253
which hosts can rabies infect?
animals, plants, humans, very not good stuff like cats, dogs, horses, wolves, bears and bats (covid lol), more than 99% cases in humans are transmitted by dogs though.
254
describe the replication of rabies virus
1. RNA polymerase forms mRNA (+ssRNA) 2. translation into protein by host 3. transcription of viral RNA from -ssRNA to +ssRNA , then back to -ssRNA viral genomes 4. assembly of progeny virus
255
how does rabies virus cause encephalitis?
Virus enters the peripheral nervous system, migrates to the central nervous system to the brain up the spinal cord. Cause swelling of the brain (encephalitis) – almost always results in death.
256
describe the 2 forms of rabies
1. furious- takes the same course as human- this is like 80-90% of rabies cases (100% mortality). Change in behaviour and voice because the neurons near the vocal cords are affected by the disease, paralytic stage. 2. dumb- 10-20% cases- predominantly paralytic, lapse into stage of sleepiness, death within 3 days.
257
describe the general historical lore of monkeypox virus
first identified in 1958 in Denmark, however 1st human case reported in 1970, gave the impression that it was a zoonotic infection (animals->humans). 2 distinct clades have emerged- the Congo basin or Central African clade + West African clade. In clade 1, the average mortality is around 4% but it can be up to 10%. New case in the UK lets go. Cases in USA from 2003, and between 2018-2021, there were a handful cases with no fatalities have been reported from some countries (1 in Israel, 1 in Singapore, 7 in the UK); 5 were in returning travellers from Nigeria.
258
describe the animal-human transmission and human-human transmission of monkeypox
1. animal-human: bites and scratches from infected animals. Usually rodents, rats and ferrets. Preparation and handling of infected animal products (bushmeat) may also result in transmission. 2. human-human: skin to skin contact like sex hhehehhe with lesions on the skin. through indirect contact with contaminated fomites such as bedding or clothing.
259
describe the 3 vaccines we have for monkeypox (smallpox)
1. ACAM2000- single dose producing a lesion at the inoculation site. can replicate so not recommended for immunocompromised + pregnant women, etc. 2. Modified Vaccinia Ankara- 2 doses 4 weeks apart, no lesion. doesn't replicate so safe. 3. LC16m8- (modified vaccinia virus)- single dose, less replication ability than the first one so safer
260
what are viroids?
infectious agents that resemble virus Smallest known pathogens ever with small circular ssRNA + no capsid. Resistant to proteases + nucleases and only infect plants (potato spindle tuber viroid). Don't encode proteins (regulatory RNA?) and mode of action is unknown but replicate autonomously.
261
what are obelisks?
a new class of viroid-like elements that are first identified in human oral and stool metatranscriptomic data. 1. circular RNA 2. predicted rod-like secondary structure 3. open reading frames coding for a novel protein superfamily called "Oblins". Can form their own distinct phylogenetic group with no detectable sequence or similarity to known biological agents. Very new for real, early 2024 or something.
262
what are prions?
small proteinaceous infectious particles which resist inactivation and contain no genetic material. Prion diseases are often called Spongiform Encephalopathies because the shape they form in the brain kinda spongy. - Cellular prion localize on the neurons synapses between neurons or facilitate the uptake of copper into the cell. - Caused by the accumulation of the misfolded protein scrapie prion protein (PrPsc), which damages the CNS of animals.
263
describe the mechanism of prion diseases
264
describe Scrapie disease in sheep (caused by a prion)
It is a degenerative, fatal disease in the CNS- causes ataxia and recumbency. No treatment currently, selective breeding for genetic resistance, surveillance and depopulation are the primary means of control for this diseases
265
describe bovine spongiform encephalopathy (BSE) in cattle (caused y a prion
mad cow disease due to animals erratic behaviour. first diagnosed in the UK 1986, about 4 mill cows killed in the eradication process rip Classical BSE, H-type atypical BSE, L-type atypical BSE. Classical BSE is the only form that can be transmitted to humans through the consumption of contaminated meat causing variant Creutzfeldt-Jakob disease.
266
describe Kuru disease in humans (caused by a prion)
means "trembling", reported in “Fore” tribe of Papua New Guinea via ”funerary cannibalism”
267
describe CJD disease in humans (caused by a prion)
Creutzfeld-Jacob Disease: Those affected lose the ability to think and to move properly and suffer from memory loss. It is always fatal, usually within one year of onset of illness. 1. Sporadic CJD: most common 2. Familial/ Inherited CJD: rare genetic condition where one of the genes a person inherits from their parent. 3. Variant CJD: likely to be caused by consuming meat from a BSE cow 4. Latrogenic CJD: when the infection is accidentally spread from someone with CJD through medical or surgical treatment.