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Microbiology > M21 - Respiratory pathogens 1 (toxins and virulence) > Flashcards

M21 - Respiratory pathogens 1 (toxins and virulence) Flashcards

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Biology 101 flashcards
1
Q

What is virulence mechanisms?

A

The degree of pathogenicity of a disease causing organism is determined by the proteins it expresses & how effectively it can integrate environmental information

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2
Q

What is the cycle of infection?

A
  • Entry
  • attachment
  • Multiplication
  • Evasion of host defences
  • Causes damage
  • release and spread
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3
Q

Name some virulence mechanisms.

A
  • Bacterial adhesion
  • Bacterial invasion
  • Bacterial evasion of host defenses
  • Bacterial toxins
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4
Q

Name 4 of the ligands and their receptors of bacterial adhesion.

A
  • Capsule S.pyogenes / Keratinocytes
  • Fimbriae B. pertusis / Laryngeal epithelial cells
  • Cell wall S. aureus / Epithelial cells
  • Fibrils S. sanguinis / platelets , salivary proteins
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5
Q

Describe bacterial invasion.

A
  • Can be superficial or systemic (metastasis)
  • Can be extra or intra cellular
  • Can gain access via general contact or injection (e.g. arthropods, malaria)
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6
Q

Give 2 examples of bacterial invasion.

A
  • Organism erodes tooth - S.mutans (caries)

- Organism persists in epithelial - P.gingivalis (perio)

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7
Q

What happens in dissemination/metastasis after penetration of epithelium?

A
  • Blood vessel endothelium –> circulates in blood
  • Enter phagocytic cells –> circulates in blood/accumulates in lymph nodes
  • Lymphatic tissue endothelium –>accumulates in lymph nodes
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8
Q

what multiple mechanisms do bacteria have to avoid host defences?

A 
–  Immunity at mucosal surfaces
–  Destroy Immune cells
–  Interfere with inflammatory response 
–  Evade Innate Immunity
–  Overcome acquired Immune Responses
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9
Q

What provides immunity at mucosal surfaces?

A
  • Production of Glycosidases & Sialidases :
    e. g. Streptococci spp. & Veillonella spp

-Proteases -cleave hinge region of IgA1 normally protected by glycosylation (S. sanguini)

-IgA binding proteins :
M Family proteins - bind Fc region of Ig (wrong way round)

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10
Q

what is the key to the immune response?

A

• Cytokine balance is key to immune response
– Integrate & orchestrate myeloid, lymphoid & vascular
response to infection.
– TNF a, Interferon, Interleukins,
– Bacteria can induce septic & toxic shock

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11
Q

What are cytokines?

A

group of regulatory proteins key to immune response

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12
Q

What are endotoxins?

A

-Gram-negative cell wall constituent
-Lipopolysaccharide (LPS) outer membrane complex;
E.coli, Salmonella

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13
Q

Name the LPS components.

A

Toxicity; LipidA

Immunogicity; Polysaccharide

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14
Q

What do endotoxins do?

A

Induces variety of inappropriate inflammatory responses that impair hosts response to pathogen

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15
Q

How do endotoxins interfere with cytokines?

A

Bind to receptors on macrophages, B cells, & other cells that stimulates release of acute phase cytokines.

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16
Q

Describe the outer membrane of gram negative bacteria.

A

– Assymetricmembrane
– Lipopolysaccharides(LPS)
– Peptidoglycan
– Lipoproteins

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17
Q

What causes endotoxin shock or systemic inflammatory response syndrome (SIRS)?

A

Either :

  • endotoxin or lipopolysaccharide and peptidoglycan acting on macrophages to release inflammatory cytokines
  • exotoxins acting on T cells to release inflammatory cytokines
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18
Q

Describe complement evasion as a method to evade innate immunity.

A

Capsules

a) prevent activation via C3 and C3b
b) mask bound C3b

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19
Q

Describe evasion of phagocytic killing as a method to evade innate immunity.

A

PVL -S.aureus

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20
Q

Name 2 variations that can overcome acquired immune responses?

A
  • phase variation

- antigenic variation

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21
Q

Describe phase variation.

A

– switching between “on” and “off” forms of a gene
• flagellin gene of Salmonella typhimurium
• opacity genes of Neisseria gonorrhoea

22
Q

Describe antigenic variation.

A

– allows the bacterium to change the sequence of a gene

• pilin genes of Neisseria gonorrhoea

23
Q

What do these variations make it hard to do?

A

Find effective vaccines

24
Q

What is diphtheria?

A
  • 2-6 day incubation

- mucous membranes infected (tonsils)

25
Q

what are the early symptoms of diphtheria?

A

Sore throat, low fever, swollen neck glands

26
Q

what are the late stages of diphtheria characterised by?

A

– Airway obstruction, breathing
difficulty
– Shock (hypotension, tachycardia, pale, cold skin, sweating, anxious)

27
Q

What are outbreaks of diphtheria associated with?

A

– Unsanitary/crowded conditions

– Immunity gaps, vaccination failure

28
Q

What does the toxin in diphtheria produce and what results from this?

A

• Toxin produces acute inflammation & formation of pseudomembrane
– Dead tissue, fibrin, polymorphs & bacteria
• Swollen neck
• Complications, breathing obstruction, cardiac arrhythmia, coma

29
Q

Describe the features involved in diphtheria.

A

– Life threatening disease
– Cause toxigenic Corynebacterium diptheriae
• Gm +ve bacilli
• Chinese lettering morphology
• Aerobic, non-motile
• Tellurite agar (toxic for other throat flora)
• Albert s stain (metachromatic granules)
• Confirmation of Toxin production
– Transmitted by direct contact droplets/skin, or indirect via contaminated object

30
Q

Describe corynebacterium diphtheria.

A 
•  DT Type III
•  Soluble 3 domain protein
–  Receptor-binding, translocation, & catalytic,
•  Heparin-binding EGF-receptor
•  Endocytosed
•  Proteolytic cleavage
•  Fragment A carries Catalytic domain
•  Fragment B Receptor domain and Translocase Domain
31
Q

what is the treatment for corynebacterium diphtheriae?

A

– Immediate inoculation with diptheria
antitoxin
– Administer Penicillin or Erythromycin to eliminate bacteria

32
Q

what is the prevention of corynebacterium diptheriae?

A

– Activeimmunisation
– Diptheria Formal Toxoid (DPTvaccine)
– Part of multiple vaccine, diptheria, tetanus & whooping cough given at 2, 3 & 4 months.
– Booster at approximately 5 years

33
Q

What is whooping cough?

A

highly contagious, life threatening disease

34
Q

what bacteria is associated with whooping cough?

A

Bordetella pertusis small Gm-ve cocci

35
Q

how is infection of whooping cough caused?

A

exposure to infected individual

36
Q

what population is whooping cough highly significant in?

A

children < 2 years old with the possibility of secondary bacterial pneumonia and neurological complications that may prove fatal

37
Q

What are the characteristics of the disease for >15 years?

A

symptoms are milder, similar to viral upper

respiratory tract infection

38
Q

what are the symptoms of whooping cough?

A

• Severe cough that persists for >7 days
• Low or no fever (limited to first week)
• Major Symptoms
– >2 weeks choking cough attacks (whoop in 50% of cases)
– Persist for 3 weeks to 3 months (100 day cough)

39
Q

what symptoms may adults with whooping cough present?

A

– Shortness of breath during coughing
– Nocturnal coughing
– Tingling sensation in back of throat
– Post-tussive vomiting

40
Q

how does bordetella pertusis enter the body?

A

respiratory tract

41
Q

what does bordetella pertusis attach to?

A

ciliated epithelial cells of respiratory tract

42
Q

what is bordetella pertusis mediated by?

A

Filamentous Hemagglutinin (FHA)

43
Q

what is the outer membrane protein of bordetella pertusis that promotes atthachment to tracheal epithelial cells?

A

Pertactin (PRN)

44
Q

what toxins are involved in bordetella pertusis?

A

– Pertusis Toxin
– Adenylate Cyclase/hemolysin
– Lethal (or Dermonecrotic) Toxin
– Tracheal cytotoxin (TCT)
( Kills ciliated cells & stimulates their extrusion (loss) from the
mucosa)
– Lipopolysaccharide (endotoxin) also contributes to disease

45
Q

Describe the pathogenesis of bordetella pertusis.

A

• Growth on ciliate epithelial & toxin production
– Paralyse cilia Tracheal cytotoxin (TCT)
• Kills the ciliate epithelial cells
• Induce mucus secretions
– Stimulate inflammatory response
– Kill leukocytes (Pertusis toxin)

46
Q

Describe the structure of the pertusis toxin.

A

-classically one A unit and five complex B units
-Bordetella pertusis:
>PT toxin
>A subunit S1
>B composed of S2,S3, S5 and 2 x S4
>S1 ADP-ribosyltransferase
>leads to increase in cAMP

47
Q

what does pertusis toxin do?

A

– Disrupts cell function, increases mucus secretion, incapacitates phagocytes
– Systemic consequences, increase in insulin (hypoglycemia) & sensitivity to histamine

48
Q

How do you diagnosis bordetella pertussis?

A

• Cough plate
– (hold BG culture plate in front of mouth when coughing)
• Perinasal swab of posterial pharyngeal walls

49
Q

What is the treatment for bordetella pertusis?

A

• Erythromycin for 14 days
– (ideally pre-paroxysmal stage)
• Skilled nursing, remove mucus & vomit
• Antibiotic therapy for secondary infections

50
Q

Describe the vaccination of B. pertusis.

A

– Includes 3 main antigenic types (acellular vaccine)
– Given as part of multiple vaccine
• (diptheria, tetanus, whooping cough, polio & Hib))
– 2, 3 or 4 months

51
Q

Describe virulence mechanisms and what is included.

A

• Understanding molecular basis of disease, informs prevention, treatment & development of new mechanisms to control disease.

  • • Bacterial adhesion
  • • Bacterial invasion
  • • Bacterial evasion of host defenses
  • • Bacterial toxins & definition of an endotoxin

Microbiology (30 decks)

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