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Microbiology > Bacteria General + Pathogenesis > Flashcards

Bacteria General + Pathogenesis Flashcards

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Biology 101 flashcards
1
Q

how are bacteria named and classified

A

Phylum
Class
Order
Family
Genus
Species
Strain (subset of species differentiated by a small diff)

!!! putting spp. at the end of the species (eg. Staph spp) = AL STRAINS

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2
Q

GENERAL description of prokaryotic structure

A

-usually smaller in size
-no membrane bound organelles including nucleus
-circular DNA free in cytoplasm + extra-chromosomal DNA in the form of plasmids
-cell membrane + cell wall (diff to euk) + capsule or slime coat
-70S ribosomes (50+30)
-Asexual rep through binary fission (variability given due to plasmid conduction)
-flagellum (some)

!!! RESPIRATION USING MEMBRANE NOT MITOCHONDRIA

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3
Q

describe the DNA of prok cells

A

-single circular chromosome with no histones
-no introns
-genes arranged in operons
-NPAs (nucleoid associated proteins, help participate in transcription or affect chromosome organisation)

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4
Q

operon def

A

MONOCISTRONIC TRANSCRIPTION UNIT - clustered genes that code for structural proteins, all share a common promoter which allows them to be controlled together –> commonly the proteins encoded by the clustered genes have similar functions

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5
Q

describe plasmids

A

-extrachromosomal DNA
-mostly circular (but can be linear)
-each cell can have more than 1
-can carry advantageous genes:fantimicrobial resistance/ increased virulence / toxin production
-passed to other bacteria using CONDUCTION (cell to cell contact using pili)

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6
Q

what is the composition of the prok cytoplasm (3)

A

-glycogen and starches (as carbon source)
-inorgnic Pi (metabolism)
-ENDOSPORES: asexual spores that can develop inside certain families of bacteria (Bacilli and Clostridium) - usually triggered by a starvation of nutrients, and can be released and germinate under favourable conditions

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7
Q

what is the composition of the prok cell membrane

A

LIPIDS (40%), PROTEINS (60%), SMALL CARB AMOUNT

-lipids are mainly simple, rarely polyunsaturated
-unglycosylated proteins

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8
Q

what enzymes does the cell membrane of prok cells contain and why (2)

A
  1. enzymes for peptidoglycan synthesis (needed for cell wall)
  2. enzymes for ATP production (resp occurs in membrane bcos prok dont have mitochondria)
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9
Q

3 shapes of bacteria

A
  1. cocci (spherical)
  2. bacilli (rods)
  3. spirochetes (coils)
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10
Q

structure of bacteria cell walls + what wall determines

A

RESPONSIBLE FOR SHAPE OF BACTERIUM + GRAM+/-

  1. NAG/NAM joined by beta 1-4 bonds makes PEPTIDOGLYCAN
  2. tetrapeptide (4aa)

IN GRAM+: pentapeptide

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11
Q

method for gram staining

A
  1. add crystal violet (purple)
  2. decoloration using alcohol wash
  3. add safranin (pink)
  4. observe final color

GRAM+: retain the purple GRAM-: pink

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12
Q

layers of cell wall of G+/- bacteria

A

G+: 2 LAYERS - cell wall of peptidoglycan (thick)

G-: 3 LAYERS - peptidoglycan (thin), periplasmic space (empty), outer membrane (virulence factor with lipopolyssacharide)

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13
Q

G+ wall structures

A

-contains teichoic acid: this increases peptidoglycan rigidity, gives negative charge and is HIGHLY ANTIGENIC (and highly variable between diff species)

-peptidoglycan thicker than that of G-

-highly polar and binds cations (bcos enzymes to make peptidoglycan require Mg2+)

-allows G+ to tolerate higher salt environement concs

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14
Q

G- wall structure

A
  • General enzymes (detox and other functions)

-Outer membrane: 1st virulence factor bcos it contains liposaccharide (O-side chain, core, lipid A)

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15
Q

structure and function of lipopolysaccharide

A

PRESENT IN G- WALLS, THREE COMPONENTS:

  1. O-side-chain: long polyS chain with ANTIGENIC properties (highly variable)
  2. Core polysaccharide: short central chian connecting 1/2
  3. Lipid A: endotoxin that contributes to virulence factors
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16
Q

Mycobacteria wall

A

-peptidoglycan
-myolic acids
-porins

!!structure doesnt allow easy entry of nutrients so growth is VERY slow, advantageous bcos it is very small and can be invisible to the system + hard for drugs to enter

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17
Q

what is the staining used for mycobacteria

A

Zhiel-Nielsen staining

18
Q

Describe the layers present outside of the cell wall of bacteria + functions (4)

A
  1. Capsule (tightly attached)
  2. Slime layer (loosely attached)
    -both made of polyssacharides

FUNCTIONS:weakly antigenic properties, adherence to surfaces + formation of biofilm, antiphagocytic + prevents dehydration

19
Q

describe the filamentous appendages of a bacterium

A
  1. Pili (long protein projections for conjugation - adherence and transfer of plasmids)
  2. Fimbriae (short protein projections for adherance)
  3. Flagellae (propellers for movement, characteristic of cylindrical bacteria like bacili but NOT cocci)
20
Q

what is the term for a bacteria without a flagellum

A

ATRIC (eg cocci)

21
Q

3 basic rules for bacteria metabolism of all human pathogenic bacteria

A
  1. chemosynthetic (obtain energy for atp from demolition of substances)
  2. heterotrophs (need source of C)
  3. organotrophes (need pre-formed organic compounds as energy sources)
22
Q

ways in which bacteria can produce ATP (2)

A
  1. SUBTSTRATE LEVEL PHOSPHORYLATION:
  2. ETC PHOSPHORYLATION
23
Q

classification of bacteria based on mode of respiration (5)

A
  1. Obligate aerobe: must have oxygen
  2. obligate anaerobes: must use fermentation
  3. facultative aerobes: can do either (most common)
  4. aerotolerant anaerobes: use anaerobic fermentation but tolerate O2
  5. micro-aerophilic: grow very slowly in O2 but do well in 10% CO2
24
Q

phases of bacterial growth

A
  1. lag (adjestments)
  2. exponential (cell division every 20 mins)
  3. stationary (equilirium)
  4. death (over competition)
  5. long-term stationary (highly dynamic period where birth and death are balanced)
25
Q

method of bacteria reproduction

A

binary fission (asexual rep producing 2 genetically identical daughter cells)

26
Q

nature of DNA rep of bacteria

A

semi conservative, begins at a single replication origin (oriC) and then continues until a full cycle is made

it uses DNA polymerase
+ is regulated by replisome (coordinates rep so that leading and lagging strand are going at the same rate)

27
Q

what gives bacteria genetic diversity

A

GENE SHARING:
1. transformation: takes in free DNA from environment (proved by Griffith experiments)

  1. transduction: infection by bacteriophage and insertion of the viral DNA (lithic of temperate phages)
  2. conjugation: attachment via pili and passing of plasmid

!! always affects only a PORTION of the genome, transfer is polarised and unidirectional

28
Q

2 types of phage cycles during transduction

A
  1. LYTIC phages: generalised transduction where the phage’s entire genome will be copied into the host
  2. TEMPERATE phage: specialised transduction where only selective genes are internalised
29
Q

Different ways to classify pathogens

A
  1. True/opportunistic (always cause infection vs only cause disease in vulnerable hosts)
  2. Site of infection: extracellular, intracellular (facultative and obligate with either preferential or obligatory internal rep) or toxigenic
  3. Based on their host: exogenous (sick host to carrier), exogenous (migration of flora) or zoonosis (animals to humans)
30
Q

3 virulence factors

A
  1. structural: capsule, cell wall, lipopolyssacharide, outer membrane
  2. biochemicals: exotoxins and enzymes
  3. genetic: transferable plasmids with advantageous genes (eg antibiotic resistance)
31
Q

what does the degree of virulence of a pathogen depend on

A
  1. invasivity (ability to proliferate)
  2. toxigenicity (toxin production for host damage)
  3. specific virulence factors

(presence of specific or non-specific defenses shown by the host can also modulate sensitivity to the pathogen)

32
Q

OVERVIEW OF INFECTION PROCESS

A
  1. entry
  2. cell adhesion
  3. colonisation of tissues (via biofilm production /
  4. immune system evasion
  5. intracellular multiplication and persistence (spread to other tissues) in certain cases
33
Q

descirbe the entry of pathogens

A

-mouth/ears/eyes/nose
-urogenital tract
-open wounds or broken skin

!! will have to overcome host’s mechanisms of defense once in contact wiht the surface epithelium

34
Q

describe the adhesion of pathogens during process of infection

A

-bacterium-cell contact is established via receptors on bacteria cell wall
-occurs through appendages: fimbria, pilli, adhesins (monomeric proteins)
-components of the capsule can facilitate this

ADHESINS RECOGNISE THE HOST: ECM components, glycoproteins (fibronectin) and integral receptors

35
Q

describe the colonisation of tissues during the process of infection

A

COLONISATION: replication of pathogen within the host despite a harsh extracellular milieu (low pH, mucus, antimicrobial peptides, immune cells, microbiota for competition)

BIOFILM FORMATION: thin ECM film that helps aggregate bacteria and protect from eniroment (contains superficial cells inside matrix, intermediate cells and profound cells that are the initiators of biofilm formation). Cell dispersion releases cells to a diff site to repeat process

36
Q

reasons why a biofilm is advantageous to the bacteria

A

protects from environment:
-architecture/stability
-dessication tolerance
-antiphagocytotic
-nutrient acquisition
-antimicrobial agents
-pH changes
-intracellular communication
-remodelling and invasion

37
Q

how do bacteria evade the immune system after colonisation

A

VIA AGGRESINS:
-capsules and slime coats
-secreted enzymes (eg. hyaluronidases, coagulases, catalases)
-toxins

38
Q

endo vs exotoxins

A

ENDO: are inherent components of the gram NEGATIVE cell wall (eg lipid A and O-antigents)

EXO: produced and released into the environement (usually gram POSITIVE bacteria) - usually encoded by plasmids

39
Q

types of exotoxins

A
  1. acting on cell surface - bacterial superantigens: bind onto MHCII receptors, activate Th cells in an antigen INDEPENDENT manner and the surplus of Th activated causes rash/ shock/ fever
  2. damage cell membrane - cytolytic: phospholipid destruction, hemolysins, pore forming
  3. intracellular - AB toxins: B subunit binds to host cell and A penetrates cell, targeting nervous system (Eg tetanus), digestive system (eg cholera) or other (eg diptheria)
40
Q

Is lipid A always harmful?

A

in small amounts it can induce immune stimulation (like fever) HOWEVER in high amounts it causes pathogenic cascade leading to eventual septic shock

Microbiology (5 decks)

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