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Molecular Basis Of Disease > Bacterial Pathogens And Disease 1 > Flashcards

Bacterial Pathogens And Disease 1 Flashcards

1
Q

Define pathogen

A

A microorganism capable of causing disease.

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2
Q

Define pathogenicity

A

The ability of a infectious agent to cause disease

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3
Q

Define virulence

A

The quantities ability of a agent to cause disease

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4
Q

Define toxigenicity

A

The ability of a microorganism to produce a toxin that contributes to the development of disease

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5
Q

What are the 4 virulence mechanisms?

A

Adherence factors

Biofilms

Invasion of host cells and tissues

Toxins- endotoxins and exotoxins

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6
Q

What are exotoxins?

A

Heterogeneous group of proteins produced and secreted by living bacterial cells

Produced by both gram negative and gram positive bacteria

Cause disease symptoms in host during disease

Act via a variety of diverse mechanisms

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7
Q

What is the advantage of bacteria having exotoxins?

A
  • Evade immune response
  • Enable biofilm formation
  • Enable attachment to host cells
  • Escape from phagosomes

All allowing for colonisation, niche establishment and carriage - evolutionary advantage

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8
Q

Do toxins cause disease?

A

No, but may help transmission

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9
Q

How does the case of straphylococcus aureus express the important of exotoxins?

A

Haemolytic toxins cause cells to lyse by forming pores and have a Importance in symptoms of S aureus

Phenol soluble Modular’s PSM - aggregate the lipid bilayer of host cells (lysis)

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10
Q

Describe the function of the different toxins associated with the movement of staphylococcus aureus?

A

Alpha toxin - initial attachment

Beta toxin - accumulation

E DNA - secondary structure formation

PSMs - detachment

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11
Q

How are exotoxins classified?

A

Classification can be by the toxins activity
- membrane acting toxins - type 1
- membrane damaging toxins - type 2
- intracellular toxins - type 3

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12
Q

Where are toxins expressed in the bacterial genome?

A

By extrachronsomal genes

  • Plasmids
  • Lysogenic bacteriophage
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13
Q

What is the problem with classifying exotoxins?

A

Many toxins may have more than one type of activity

As mechanisms better understood this classification tends to break down

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14
Q

How to membrane acting toxins TYPE 1 work?

A

Act:
- act from without the cell.

Interfere:
- interfere with host cell signalling by inappropriate activation of host cell receptors

Target:
- target receptors include:
. guanylyl cyclase (increase intracellular cGMP)
. adenyl cyclase, (increase intracellular cAMP)
. Rho proteins
. Ras proteins

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15
Q

Give a example of membrane acting toxin?

A

E coli table heat toxin

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16
Q

How do membrane damaging toxins TYPE 2 work?

A

Interact with the receptor and form a pore

  1. Insert channels into host cell membrane (beta sheet toxins and alpha helix toxins)
  2. Enzymatical damage

Can be receptor mediated or receptor independent

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17
Q

How do intracellular toxins work?

A

Have 2 components (A and B)

Component B has the capacity to interact with a specific receptor - gets internalised by receptor mediated endocytosis

Component A is a toxigenic (enzymatic) that interfere with cellular processes

AB5 is heat sensitive while the rest are heat resistant

18
Q

Give examples of component A of intracellular toxins

A

ADP - ribosyl transferase

Glucosyltransferase

Deamidase

Protease

Adenylcyclase

19
Q

What are the 2 mechanisms by which exotoxins can induce a inflammatory response?

A
  • Superatigen
  • via activation of the different inflammasome leading to release IL1 and IL18
20
Q

How can exotoxin’s cause inflammation by superantigen?

A

Non specific bridging of the MHC class 2 and class T cell receptor leading to cytokine production.

21
Q

How can toxins be inn-activated?

A

inactivated using formaldehyde or glutaraldehyde → toxoids

22
Q

What are toxoids?

A

Toxoids are inactive proteins but still highly immunogenic – form the basis for vaccines.

23
Q

How are toxin mediated diseases treated?

A

Affected by administering preformed antibodies to the toxin

Eg.
. Diphtheria antitoxin – horse antibodies.
• Tetanus – pooled human immunoglobulin.

24
Q

What is clostridium difficile?

A

• gram-positive bacillus.
• anaerobic.
• spore-forming.
• toxin-producing.
• can be carried asymptomatically in the gut. • 3 toxins.

25
Q

What is the epidemiology of C. difficile?

A

. Common hospital acquired infection worldwide.
• Spread by ingestion of spores

Risk factors
- antibiotic use,
- age,
- antacids
- prolonged hospital stay.

26
Q

How can antibiotics contribute to the spread of C. difficile?

A

. Thought to act by disrupting the microbial ecosystem within the gut.

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

• Allows C. difficile colonisation and growth.

• All antibiotics have potential for causing disease.

27
Q

What are the cytotoxins of C. difficile?

A

Cytotoxin A - TcdaA coded by TcdaA gene

Cytotosin B - TcdB coded by TbdaB gene

Binary toxin C - minor role in disease

28
Q

Describe the process by which TedA/TedB cause down stream effects within the host cell.

A
  1. Toxins binding to specific host cell receptors
  2. Toxins internalisation
  3. ENDO some acidification
  4. Pore formation in the endosome
  5. GTD release from the endosome to the host cell cytoplasm
  6. Rho GTPase inactivation by
  7. Downstream effects within the host cell.
29
Q

What is the symptoms of C. difficile?

A

Asymptomatic

Watery dihoreah

Dysentery

Pseudomembranous Colitis

Toxic Megacolon and Peritonitis

30
Q

How is C. difficile diagnosed in patients?

A

• Clinical signs and symptoms
• Raised white cell count in blood.
• Detection of organisms and toxins in stool
• Detection of tcdA and tcdb genes – PCR
• Colonoscopy – pseudomembranous colitis

31
Q

How is C. difficile detected with its toxin using the 2 stage test?

A
  1. Glutamate dehydrogenase – detects if C. difficile organism present.
  2. Toxin enzyme linked immunosorbent assay (ELISA) for TcdA and TcdB toxins.
32
Q

How is C. difficile treated?

A

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.

33
Q

What is VTEC disease?

A

Also known as Shiga-toxin (Stx) producing E. coli (STEC) can cause disease mild to life threatening disease.

• Identified usually by growth on sorbitol MacConkey agar (SMac) – does not ferment sorbitol and hence is clear.

34
Q

What is the epidemiology of VTEC disease?

A

naturally colonizes the gastrointestinal tracts of cattle who are generally asymptomatic.

Transmission
• Predominantly via consumption of contaminated food and water
• Person to person, particularly in child day-care facilities, and from
• Animal to person. E.g. in petting zoos, dairy farms, or camp grounds.

35
Q

What is the pathogenesis of the toxin causing VTEC?

A

Toxin – Shiga like toxin (SLT) = shigatoxin (Stx) = verocytotoxin (VTEC)

. Type III exotoxin – AB5
• Enzymatic component A = N-Glycosidase
• Bound to 5 B subunits

36
Q

What is the mechanism by which Stx toxin effects cells?

A

• Bind to receptor globotriaosylceramide Gb3 or globotetraosylceramide (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 disassociate

• A1 binds to 28S RNA subunit – blocks protein synthesis.

37
Q

Describe the pathogenesis of STEC

A

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

• The route by which Stx is transported from the intestine to the kidney and other tissues is debated, possibly polymorphonuclear neutrophils (PMNs)

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

• Very high levels of Gb3 in kidney so kidneys most affected.

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

38
Q

What is STEC disease?

A

Children under 5 years are at greater risk

Can be severe and life threatening
Abdominal cramps, watery or bloody diarrhoea - may not be present

39
Q

How is STEC diagnosed?

A

•Clinical signs and symptoms
•Haematological and biochemical evidence.
•Stool culture – Growth on SMac
•PCR for Stx genes

40
Q

How is STEC treated?

A

•Supportive including renal dialysis and blood product transfusion

•Antibiotics have little to no role

41
Q

What are the symptoms of STEC disease?

A

• Haemolytic uraemic syndrome
• Anaemia
• Renal Failure
• Thrombocytopaenia

• Less common are neurological symptoms
• lethargy,
• severe headache,
• convulsions,
• encephalopathy.

Molecular Basis Of Disease (32 decks)

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