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Microbiology and Parasitology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

The three major phyla of pathogenic bacteria are:

A

Spirochetes, proteobacteria, gram positives

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2
Q

Describe the chromosomes of bacteria (shape/number/introns)

A

1 circular chromosome without Introns

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3
Q

Describe the bacterial ribosome (S value and subunits) – Bonus: what is it for Eukaryotes?

A

70S with 50S and 30S subunits – Eukaryotes are 80S with 60S and 40S subunits

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4
Q

Describe the process of gram staining

A
  • Crystal violet stains peptidoglycan layer
  • Iodine fixes CV
  • ETOH wash erodes CV unless “protected” in cell wall
  • Safarain/Fucsin counter stain
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5
Q

Break down the meaning of the word “staphylococcus”

A

Clustered rounds

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6
Q

What are some advantages to first doing a gram stain before a culture?

A
  • Etiology (possible identity of disease cause)
  • Management
  • Bacterial count (extent of infection)
  • Elaboration (what to test next)
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7
Q

Patient has a purpuric rash, and headache; what bacteria (and gram stain) do you expect on CSF examination?

A

Neisseria meningitidis (G -ve diplococci)

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8
Q

A patient with Pneumonia shows G +ve Diplococci in their sputum. What is the likely organism?

A

Streptococcus pneumoniae

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9
Q

What is the thickness of the peptidoglycan layer in G +ve vs G -ve bacteria?

A

100nm vs 10 nm

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10
Q

Name the layers making up the cellular envelope of the gram negative bacteria.

A

Outer membrane, periplasm, thin peptidoglycan layer, cytoplasmic membrane.

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11
Q

Describe the structure of the Glycan backbone of peptidoglycan

A

N-Acetylglucosamine(NAG) linked with an N-Acetylmuranic acid (NAM), B1-4 glycosidic link. Lactyl ether attached to NAM acid. Small peptide chain attached to lactyl ether. Peptide side chains form cross links

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12
Q

What enzyme group catalyse peptide crosslink in peptidoglycan and why are they important?

A

Transpeptidases, which are inhibited by Beta-Lactam antibiotics

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13
Q

Describe teichroic acids (including bacterial type)

A

Found only in G +ve, give cell wall -ve charge. Pathogenicity factor in that they increase adhesion to host membrane. Called Lipoteichoic acids if bound to cell mbn, Wall trichroic acids if bound to peptidoglycan.

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14
Q

MSCRAMMs … shudder

A

“microbial surface components recognizing adhesive matrix molecules” are adhesins which are part of the peptidoglycan layer, primarily in G +ve bacteria. Initial adhesion to host mbn and formation of biofilms. External ligand binding domain, within cell wall, repeat LPXTG domain (potential drug target), Proline rich cell wall associated region, hydophorbic transmbn region, charged cytoplasmic region. Anchored in cell wall viar action of sortase enzyme.

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15
Q

Describe lipopolysaccharides

A

aka: Endotoxin, found only in G-ve. Consists of lipid A base with a core polysaccharide and O antigen. Critical to bacterial mbn stability. Highly immunogenic.

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16
Q

OmpA

A

Outer Membrane Protein A - Found in E. Coli. Highly immunogenic.

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17
Q

What stain is typically used for mycobacteria?

A

Ziehl-Nelson stain

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18
Q

Describe the staining of mycobacteria. Why?

A

Not stained by Gram method, due to waxy mycolic acid layer Some do not have any cell wall.

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19
Q

What gives mycobacteria their name?

A

Free mycolic acids in cell envelope, which causes a waxy surface.

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20
Q

Define the term monocistrionic.

A

One gene mRNA transcript encodes for one protein (as opposed to one transcript multiple proteins). Usually found in Eukaryotes.

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21
Q

Define the term polycistrionic.

A

One gene mRNA transcript encodes multiple proteins (as opposed to one transcript encoding one protein). Usually found in Prokaryotes.

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22
Q

Describe how transcription levels can be altered with positive and negative regulators. (Bonus: give example)

A

Positive and negative gene regulators may bind upstream to increase/decrease then binding/activity of RNA polymerase. Multiple genes may be controlled simultaneously as part of a “regulon.” PhoP in Salmonella is a positive regulator than regulated > 50 genes (disabling it makes the bacteria virulent).

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23
Q

Transcription and translation are __________ in bacteria. Explain.

A

“coupled” When mRNA is produced, ribosomes attach immediately and start making proteins.

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24
Q

What is the average and range of sizes for bacterial genomes?

A

4Mbp average, range 0.5-10Mbp

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25
Discuss "Function Unknown" genes
Up to ~30% of proteins may have unknown but necessary functions. Even in synthetic genomes which have been rid of "junk DNA."
26
Describe the various ways in which genes may be transferred from one bacteria to another.
- Horizontal transfer (F+ makes pilus, transfers one strand of plasmid to F-, duplication) - Generalised transduction (Virus degrades host DNA, packs piece of host DNA in envelope, injects host DNA into new bacteria) - Transformation (Bacterial lysis leads to free DNA, "naturally competent" bacteria takes up DNA).
27
Describe plasmids
Small self-replicating DS circular DNA. Copy number 1-400.
28
Discuss lysogenic vs lytic viral replication.
In lysogenic the viral DNA is integrated into the host chromosome and is stably replicated as part of the continuing host. In lytic; the virus hijacks machinery and produces purely viral proteins, resulting in eventual lysis, releasing huge numbers of viral particles.
29
Describe how gene transfer could affect virulence using an example.
A commensal E-coli ancestor gained SH1/SH2 and a virulence plasmid while losing ompT and cadA in order to become Shigella
30
Describe Hospital vs community acquired MRSA in regards to their resistance and virulence genes
Hospital acquired: mecA of other resistance gene | Community: PVL toxin and resistance gene
31
Define Disease
A disorder of structure or function in a human, especially one that produces specific symptoms or that affects a specific location and is not simply a direct result of physical injury.
32
Define Pathogen
A microbe that can cause disease
33
Define an opportunistic pathogen
Causes disease only in immunocompromised patients, usually NOT in healthy people.
34
Define infection
Colonization with a microbe, not necessarily causing symptoms.
35
Define Pathogenicity
The frequency with which a microbe to cause disease (e.g. S. Aureus is often not pathogenic but some strains will have pathogenicity).
36
Define Virulence
The degree of pathology caused by a microbe (e.g. Ebola is highly virulent because it causes very serious sx).
37
List 5 virulence factors (broad types).
Adhesins, Invasins, Evasins, Aggresisn, Modulins
38
What are the 4 components of Koch's Postulates?
1) Microbe found in all cases of disease 2) Microbe isolated and grown in pure culture 3) Microbe reproduces sx when introduced into healthy host 4) Re-isolate in pure culture to re-identfy same microbe
39
Describe host defence properties of skin.
- High [NaCl] in sweat - Sebum fatty acids - Low moisture - Antimicrobial peptides (e.g. Lactoferrin, lysozyme. SLP)
40
What is the gram stain of normal skin flora? Give 2 of the most common species
Gram +ve. Staphylococcus , propionbacteria acnes
41
Describe host defence properties of mucosa.
- Tight junctions between epithelial laters - Competition from normal flora - Stomach acidity - Mucocillary escalator - Fluid flow (e.g. tears/saliva/urine/gut fluid) - Metal sequestration - Antimicrobial peptides (eg lysozyme) - IgA
42
What is disbiosis? Why does it matter?
Disruption of the normal bacterial flora. Allows more pathogenic bacteria to take hold and cause disease. Normal flora would outcompete pathogens as well as inhibit through other mechanisms.
43
Which physiochemical forces are most important for bacteria?
Hydrophobic forces, cation bridging, and specific interactions.
44
Describe some of the structures used in bacterial adhesion.
``` Fimbrae: Multisubunit surface appendages - Often for distant binding/bringing close Afimbrial adhesins (e.g. OmpA) - Often for close binding Capsule polysaccharide ```
45
Describe the features of type P, S, and I pili
Adhesin: PapG Receptor: Glycolipids Tissue affinity: Urinary tract Adhesin: SAFS Receptor: Sialic acid on glycoproteins Tissue affinity: Meninges Adhesin: FimH Receptor: Mannose Tissue affinity: UT & Gut --Often in commensals
46
Describe the antimicrobial properties of intestinal mucosa.
Small intestine has steep oxygen gradient within mucosa, which also contains antimicrobial proteins. Colon contains deep thick mucous which is colonized by commensals and superficial thin mucous layer.
47
What are mucins?
Complex polymorphic glycoproteins responsible for holding water in mucous layer. Both transmbn and secreted types.
48
What processes might bacteria use to overcome a mucous barrier?
Secrete mucinase proteins to break down mucous and ease penetration. "Swim" through mucous using flagella.
49
Host cells detect flagellar proteins via ______. Flagellar proteins would be classified as a _ _ _ _.
TLR 5. PAMP (pathogen associated molecular protein)
50
What are siderophores? Briefly describe their function/action and potential as a drug target.
Low MW proteins that can bind Fe at [very low]. Strong Fe affinity than hosts. Bind to siderophore receptor on bacterial mbn. Many different species specific siderophores. Could be used as a trojan horse to deliver drugs selectively into bacterial cell.
51
Briefly describe the structure of sIgA. Where is it generally found?
A linear homodimer joined via a J chain, resists degradation in harsh environments. Found in secretions.
52
Which bacteria typically have IgA protease activity?
Mucosal pathogens. Eg Strtococci, nusseria, hemophillus.
53
List the 3 classes of AMPs (antimicrobial peptides)
``` alpha-defensins: found in granulocytes/paneth cells beta-defensins: found in skin/gut/lung Cathelicidin family (aka LL-37) ```
54
What are defensins and how do they work?
Small AMPs with three disulphide bonds and +vely charged AA. Attracted to -vely charged bacterial mbn then dimerize to form pore.
55
List three ways in which a bacteria may avoid AMPs.
Alteration of Lipid A, proteolytic enzymes (eg Aureolysin), ABC transporters (remove AMP from inside bacteria).
56
Briefly describe the process of phagocyototic killing.
1) Engulfement of bacteria into phagosome 2) Fusion with lysosome to form phagolysosome - Use of AMPs, ROS & RNS 3) Digestion of bacteria 4) Residual body remnant.
57
List 6 ways in which a bacteria may interfere with phagocytosis.
1) Toxin release to kill phagocyte (eg alpha/delta toxin) 2) Opsonization prevention 3) Contact prevention (eg capsule produced by S/ pneumo.) 4) Phagolysosome inhibition (eg mycobacterium tuberculosis) 5) Escape into cytoplasm (eg. Leishmania) 6) Résistance to killing (Eg Mycobacterium leprae scavenges free radicals)
58
Briefly describe exotoxins and the three classes.
Proteins secreted by bacteria which are able to travel. Called enterotoxins when secreted into small intestine (result in V/D). Type I: Mbn acting - Induce cellular processes (eg Superantigen produced by S. Aureus induces massive cytokine release and toxic shock) Type II: Mbn damaging - Either pore forming or phospholipase (aka cytolytic) Type III: Translocated into cell to interfere with cellular processes (eg AB aka "activity binding" toxins -- cholera toxin increases adenyl cyclase activity to inc cAMP and results in watery diarrhea).
59
What is an endotoxin?
Protein toxin bound to bacterial cell wall. Eg. LPS.
60
What is the difference between a toxin and a toxoid?
A toxoid is a toxin which has been treated with heat or chemicals to eliminate the pathogenic effect while retaining the immunogenicity (therefore can be used for vaccines).
61
What is the largest and most heterogeneous group of medically important microbes? (Bonus: how many genera and species?)
Enterobacteriaceae (aka enterobacteria) 40 Genera, 150 species
62
Which Enterobacteriaceae are most common in hospital?
Enterobacter, Klebsiella, Citrobacter, Vibrio
63
Which Enterobacteriaceae are generally the most common in the community?
Escherichia coli, Salmonellae species.
64
Which family of bacteria are responsible for most urinary tract infections? What is this groups Gram stain?
Enterobacteriaceae.
65
Enterobactericeae species most commonly cause which types of infections?
GI tract, UTI, ~30% of septicemias.
66
Give 2 examples of gram -ve Bacilli
Klebsiella, Shigella.
67
Give three examples of Gram +ve cocci
Staphylococcus, streptococcus, enterococcus.
68
Give 4 examples of gram -ve cocci.
ClostridiAH! Bacillus Corynebacteria Listeria
69
What are some shared characteristics of gram negative Bacilli?
1-6 u long, motile, facultative anaerobes, ???Glucose metabolism???
70
Describe how lactose fermentation is used to differentiate bacterial species. (Bonus: give examples of each)
Bacteria cultured on MacConkey agar (which selects for Gram -ve bacter with lactose + neutral red. L-ve uses peptone in agar; alkaline products turn colony white. (eg Salmonella/Shigella) L+ve ferments lactose; acidic products turn colony red. (eg E. Coli, klebsiella, Enterobacter).
71
What are the 7 major contributors to gram -ve bacterial pathogenesis?
Endotoxin (aka LPS) Exotoxins Capsule (Usually blood-born bacteria eg Escherichia, klebsiella, some salmonella) Adhesion pili or fimbriae Type three secretion systems (cellular invasion) Sequestration of growth factors (eg. Siderophores) Resistance to antimicrobials (esp complement)
72
Describe the three groups of E. Coli WRT their pathogenicity in humans. Generally, what feature causes this difference in pathogenicity between groups?
Large group of commensals, of which a small number may cause extra-intestinal infection. Another small group of non-commensals which cause intestinal infection. A possible tiny overlap between the intestinal and extra-intestinal groups. Difference caused by varying virulence factors.
73
How is E. Coli serotyped? (Bonus: include numbers).
Based on the surface proteins. 170 types of O antigen (LPS associated), 50 types of H antigen (flagellar), 30 types of K antigen (capsule),

Microbiology and Parasitology (2 decks)

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