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Microbiology and Immunology > Bacterial Pathogens and Diseases 1 > Flashcards

Bacterial Pathogens and Diseases 1 Flashcards

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Biology 101 flashcards
1
Q

What is a pathogen ?

A

A micro-organism capable of causing disease

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2
Q

What is pathogenicity ?

A

The ability of an infectious agent to cause disease

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3
Q

What is Virulence ?

A

The quantitive ability of an agent to cause disease. To what extent does it cause disease

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4
Q

Whta is Toxigenicity ?

A

The ability of a micro-organism to produce a toxin that contributes to the development of disease

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5
Q

What are the virulence mechanisms ?

A 
The mechanisms through which a pathogen can cause disease :
Adherence factors (molecules and proteins that allow the attachment of bacteria to find a niche and start colonisation )

Biofilms
(Molecules that allow bacteria to form complex structures for macromolecules)

Invasion of Host cells and tissues
To evade phagocytosis , colonise tissues )

Toxins-Endotoxins and exotoxins

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6
Q

What are exotoxins ?

A

These are a diverse heterogeneous group of proteins produces and secreted by living bacterial cells (not byproducts or waste )

Produced by gram negative and positive bacteria

Cause disease symptoms in host during disease

Act via a variety of diverse mechanisms

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7
Q

What are gram negative bacteria ?

A

Gram negative bacteria have a thin peptidoglycan layer and have no outer lipid membrane
They do not retain the violet stain

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8
Q

What are gram positive bacteria ?

A

Gram positive bacteria have a thick peptidoglycan layer and no outer lipid membrane

These stain violet

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9
Q

What selective advantages do exotoxins give bacteria ?

A 
They help transmission of disease 
They evade immune response 
They enable biofilm formation 
They enable attachment to host cells 
They escape from phagosomes

They allow for colonisation ,niche establishment and carriage -Evolutionary advantage

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10
Q

What is a example of bacteria found on mucosal surfaces ?

A

Staphylococcus aureus

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11
Q

What exotoxins does Staphylococcus auerus contain ?

A

Haemolytic toxins

  • Cause cells to lyse by forming pores
  • Important cause of features of S.aerus disease
  • alpha , beta and gamma toxins , Panton Valentine Leukocidin (PVL) , LukAB, LukED, LukMF

Phenol soluble modulins PSM
-Aggregate the lipid bilayer of host cells -lysis

(Majority of S.aureus in humans is asymptomatic carriage in the nose )

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12
Q

What are some functions of the toxins found in S.aureus ?

A

A. When the S.auerus is phagocytosed , the alpha toxins can block the fusion of lysosomes to phagolysosome so the organism can stay.
Modulins can aid the escape of the S.auereus from the phagolysosome

B. Some molecules e.g. phenol soluble modulins can be harmful to other micro-organisms ( competition).This allows it to find a niche within the nasal cavity. It also allows S.aeurus which is a cocci (no flagella) to slide through surfaces to colonise the nasal mucosa.

C.

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13
Q

What are Cocci bacteria ?

A

A coccus (plural cocci) is any bacterium or archaeon that has a spherical, ovoid, or generally round shape.

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14
Q

Outline the genetics of exotoxins

A

Can be encoded by chromosomal genes Shiga toxin in Shigella dysenteriae, TcdA and TcdB in C.difficile

Many toxins coded by extrachromosomal genes
(these can be transferred /exchanged )
-Plasmids -Bacillus anthracis toxin , tetanus toxin

-Lysogenic bacteriophage
(a virus which infects and replicated within bacteria /archaea)
e.g. streptococcal pyrogenic exotoxins in Scarlet Fever , Diphtheria toxins

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15
Q

Describe the classification of Exotoxins

A

1.Membrane Acting toxins -Type 1
(get in contact with cell surface receptors and interfere with processes)

2.Membrane Damaging Toxins -Type 2
(Physically damage )

3.Intracellular Toxins - Type 3
(Interfere with cellular processes)

Issues with this classification =Many toxins have more than one type activity
As mechanisms better understood this classification tend to break down

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16
Q

Outline the main characteristics of the membrane acting toxins

A

Act :
Act from without the cell
(outside the cell)

Interfere:
Interfere with the host cell signalling by inappropriate activation of host cell receptors

Target :
Target receptors include:
Guanylyl cyclase -increases intracellular cGMP

Adenylyl cyclase - Increases intracellular cAMP

Rho proteins

Ras proteins

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17
Q

Give an example of a type 1 exotoxin

A

E.coli Stable heat toxin

It will affect the downstream signalling .

The toxin affects the cystic fibrosis transmembrane receptor causing changes in important ion transporters within tissues.

E.g. Chlorine , bicarbonate ,sodium transporters are affected

Effect is an increase in sodium chloride ions and this can cause diarrhoea.

18
Q

Outline the Type 2 exotoxins and how they work

A

These cause damage to host cell membrane
They can interact with the receptor a channel
polymerising a channel causing disruption of ions.
(Action potentials )

1.Insert channels to host cell membrane
-Beta sheet toxins S.aureus –Alpha toxin , gamma toxin , PVL
alpha helix toxins -dipheria toxin
-Can produce pores in membrane by polymerising.

2.Enzymatical damage e.g. S.aureus beta -haemolysin, PSM

Not receptor function but receptor itself
Receptor mediated

Receptor independent

19
Q

How do Membrane damaging toxins function ?

A

Receptor Mediated interaction

Polymerise a pore , forms a hole in the membrane .
Doesn’t affect function of receptor.

Receptor independent may attach to membrane and alter the phospholipid bilayer structure .

20
Q

Outline the type 3- Intracellular toxins function

A

These are active within the cell which means they need to gain access.

Usually two components -AB toxins

Receptor binding and translocation function -B
(can bind to host cell receptor) -Internalised through receptor mediated endocytosis

Toxigenic (enzymatic )- A

May be single or multiple B units e.g. Cholera toxin AB(5)- has electrostatic interactions and this makes it heat sensitive.

AB are covalently linked and heat resistance

21
Q

What are some example of the enyzmatic A componenet of intracellular toxins ?

A

Wide variety of activities
These can modify enzymatic activity

ADP-ribosyl transferases -Exotoxin A of Pseudomonas aeruginosa
pertussis toxin

Glucosyltransferases e.g. TcdA and TcdB of Closetridium difficile.
can affect ribosomal Rna and inhibit protein synthesis

Deamidase - dermo necrotic toxin of Bordetella pertussis

Protease -Clostridial neurotoxins :botulism and tetanus
These can destroy proteins
and affect presynaptic structure

Adenylcyclase -e.g. EF toxin of Bacillus anthracis
This can affect production of cAMP which is a key messenger for many processes

22
Q

Give some further examples of intracellular toxins -type 3 other

A

Type 3 secretion and toxin injections
e.g. YopE in Yersinia species

This bacteria has managed to inject its toxins into host cells.
Produce multi-protein complexes which anchor to the membrane. Inner membrane and outer membrane + protein complex which forms a needle and injects the toxins.

Type IV secretion and toxin injection

e. g. CagA in Helicobacter pylori
- This is a different secretion process

23
Q

Outline super antigens and inflammatory cytokines

A

Exotoxins are able to induce inflammatory cytokine response.

Antigen presenting cell

Cytokines which are released:
IL1, IL1 beta , TNF, IL6 , interferon gamma , IL18

Due to hyperactivation of T cells which is not antigen specific

Mechanisms :
Super antigen : non specific bridging of the MHC class 2 and T-cell receptor leading to cytokine production e.g. Staphylococcal exfoliative toxin A , Toxic shock syndrome Toxin 1 (TSST1)

Via activation of the different inflammasome leading to release of IL1 beta and IL18 e.g. S.auereus toxin A, PVL

Activate cell upon detection of pathogen patterns, death by paraptosis

24
Q

What are toxoids?

A

Toxins can be inactivated by using formaldehyde/glutaraldehyde which creates toxoids

These are inactive proteins but still highly immunogenic - form the basis of vaccines.

E.g.
Tetanus Vaccine
Diphtheria
Pertussis (Acellular)

Treatment of toxin mediated disease can be affected by administering preformed antibodies to the toxin

Diphtheria antitoxin-horse antibodies
Tetanus-Pooled human immunoglobulin (specific /normal)
Botulism-horse antibodies

Experimental and research-Monoclonal antibodies

25
Q

Give an example of a toxin mediated disease

A

Toxins in Clostridium dificile disease:

This is a gram positive bacillus (rod shaped0
Anaerobic
Spore forming -highly resistant
Toxin-producing
Can be carried asymptomatically in the gut -if controlled by microbiota
3 toxins

26
Q

What is the epidemiology of C.dificile ?

A

Common hospital acquired infection worldwide
Spread through ingestion of spores-dormant in environment
Coloniser of the human gut up to 5% in adults
Risk factors-Antibiotic use, age ,antacids and prolonged hospital stay

27
Q

How can C.difice be caused by antibiotics?

A

They act to destroy the microbial ecosystem within the gut

Antibiotics provide a competitive advantage to spore forming anaerobes over non spore forming anaerobes.

Allows C.dificile colonisation +growth

All antibiotics have potential for causing disease.

Examples:

Some antibiotics are worse:
2nd and 3rd generation cephalosporins
Quinolones
Clindamycin
Aminoglycosides
Trimethoprim
Vancomycin
28
Q

Outline the pathogenesis of C.dificle (Toxin-mediated disease)

A

Mediated by the toxin it contains:
Cytotoxin A- TcdA coded by the tcdA gene

Cytotoxin B-TcdB coded by tcdb gene

Binary toxin-C.diff transferase (CDT)-minor role in disease

Tcd A and Tcd B -Type 3 AB toxins
The A component of toxins are glycosylating enzymes

There is a receptor binding domain which binding domain which interacts with the cell for internalisation.

Hydrophobic domain which allows the escape of the active A component into the intracellular space. The GTD and CPD domain (A part of the toxin which mediate disease)

29
Q

What are the components of the TcdA and TcdB ?

A

GTD_glucosyltransferase domain
CPD-Cycteine protease domain
DD-delivery hydrophobic domain
RBD-receptor binding domain

There is a receptor binding domain which binding domain which interacts with the cell for internalisation.

Hydrophobic domain which allows the escape of the active A component into the intracellular space. The GTD and CPD domain (A part of the toxin which mediate disease)

30
Q

How does the toxin interact with the membrane and get internalised ?

A
  1. The toxin will bind to specific host cell receptors
  2. Receptor mediated endocytosis =internalised and cause damage
  3. Endosome will acidify which leads to creation of a pore-mediated by hydrophobic domain
  4. This allows release of active component A of toxin
  5. GTD will interact with Rho GTPases
  6. Deactivation effects within the host cell

Consequences:
Cytopathic effects changing structure of cell
cytoskeleton breakdown, epithelial cell permeability increase ,epithelial to epithelial cell contact loss

Cytotoxic
Activation of production of reactive oxygen species which are very toxic and damaging -can induce apoptosis

31
Q

Outline cytopathic and cytotoxic

A

Patchy necrosis with neutrophil infiltration
Epithelial ulcers
Pseudomembranes,leuokocyes
fibrin mucous cell debris

May be asymptotic
Watery diarrhoea
dysentery
Pseudomembranous colitis

32
Q

How can C.dificiel be diagnosed ?c

A

Clinical signs and symptoms
Raised white cell count in the blood
Detection of organisms and toxins in stool
2 phase test :
Glutamamte dehydrogenase -detects if C.dificile organism present
2.Toxin enzyme linked immunosorbent assay (ELISA) for TcdA and TcdB toxins)

Detection of tcdA/tcdB gene -PCR
Colonoscopy-pseudomembranous colitis

33
Q

How can c.dificiel be treated ?

A

Treatment is dependent on severity and presence of surgical complications
Ideally removal of offending antibiotic -not always possible
Antibiotics : fidaxomicin or metronidazole or vancomycin.
Surgery-Partial , total colectomy
recurrent-Faecal transplant (recover microbiota from a patient )

34
Q

What is the Veroocytotoxin Escheria coli (VTEC) disease ?

A

VTEC or Shiga-toxin (Stx) producing E.coli (STEC) can cause disease mild to life threatening disease

Stx carried by some E.coli -most commonly 0157:H7

  • Identified usually by growth on sorbitol MacConkey agar (SMac) -does not feremtn sorbitol and hence is clear
  • other less common types n
35
Q

What is the epidemiology of VTEC disease

A

E.coli 0157:H7 naturally colonises the gastrointestinal tracts of cattle who are generally asymptomatic
Transmission :
Predominantly via consumption of contaminated food/water
Person to person
Animal to person

Low infectious dose

36
Q

What is the pathogenesis of VTEC diseases?

A

Toxin -Shiga like toxin (SLT)= shigatoxin (STx) = Verocytotroxin

Stx,Stx1,Stx1a,1c,1d Stx2a,2c,2d -variations in a.a sequence

gene carried on lysogenic bacteria

Type 3 exotoxin -AB 5

Enzymatic component A= N-Glycosidase

Bound to 5 B subunits

37
Q

What is the Mechanism of VTEC disease?

A

Bind to receptor globotriaosylceramide Gb3 or glovbotetraosylceramide (Gb4) on host cell membrane

Bound toxin internalised by receptor mediated endocytosis

Carried by retrograde trafficking via the Golgi apparatus to the endoplasmic reticulum

The A subunit is cleaved off by membrane bound proteases

Once in the cytoplasm A1 and A2 dissociate

A1 binds to 28S RNA subunit -blocks protein synthesis

This can also cause a haemolytic uermic syndrome ( condition that affects blood /blood vessels )

38
Q

Outline STEC pathogenesis

A

STEC closely adheres to the epithelial cells of the gut mucosa.

Stx is transported from the intestine to the kidney and other tissues is possibly through polymorphonuclear neutrophils (PMNs).

Bind to glomerular endothelial cells of kidney,cardiovascular and central nervous system.

very high levels of Gb3 in kidey so kidneys most affected.

Thought that Stx favours inflammation resulting in microvascular thrombosis and inhibition of fibrinolysis.

39
Q

What can STEC disease lead to ?Symptoms

A 
Abdominal cramps
Watery diarrhoea
Haemolytic uraemic syndrome 
Anaemia 
Renal failure 
Thrombocytopenia 
Lethargy 
Severe headache 
Convulsions 
Encephalopathy
40
Q

How can STEC be diagnosed and treated ?

A

Clinical signs and symptoms
Haemotological and biochemical evidence
Stool culture -Grow on SMAc
PCR for Stx genes

Treatment :
Supportive including renal dialysis and blood product transfusion
Antibiotics have little to no role

Microbiology and Immunology (16 decks)

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