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Yr 2 - EMS > Micro-organisms in Disease:Infection > Flashcards

Micro-organisms in Disease:Infection Flashcards

1
Q

Define pathogenicity

A

The capacity of a micro-organism to cause infection Harm is often mediated by host response, rather than by the pathogen itself

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2
Q

What are the requirements of for a micro-organism to cause disease?

A
  • Transmissibility - Establishment in or on a host - Harmful effect(s) - Persistence
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3
Q

Define virulence

A

Virulence is sometimes defined as the degree to which a micro-organism is able to cause disease. Allows a relative description of pathogenic potential

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4
Q

How do Staphylococcus aureus and Streptococcus mutans compare in pathogenicity and virulence?

A

Pathogenicity - both pathogenic Virulence - S. aureus is more virulent than S. mutans, as it causes disease much more readily.

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5
Q

Define infectivity

A

The ability of a micro-organism to become established on/in a host

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6
Q

What is infectivity mediated by?

A
  • Microbial ligand - Host cell surface receptor
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7
Q

Define virulence factor

A

Components of a microorganism which aid its ability to cause infection (infectivity and virulence). Encoded by virulence genes.

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8
Q

What are examples of virulence factor?

A
  • Facilitation of adhesion
  • Toxic effect(s)
  • Tissue-damage
  • Interference with host defence mechanisms
  • Facilitation of invasion
  • Modulation of the host cytokine responses
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9
Q

What is the cycle of infection? Why is it important?

A

Interrupting this cycle can help control infection

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10
Q

What can impact the speed and severity of the cycle of infection?

A

The status of the immune status of the host

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11
Q

What is ‘entry’ regarding the cycle of infection?

A

The point at which the microbe enters the host

E.g:

  • Breathing in respiratory droplets –> entry to URT
  • Touch contaminated surfaces then touch your face
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12
Q

What is ‘spread’ regarding the cycle of infection?

A

Spread within the host: enter host cells and ‘hijack’ host machinery and replicate

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13
Q

What does ‘evading defences’ involve regarding the cycle of infection?

A

Involving the innate immune system if this is a new pathogen:

  • Pathogens try to interrupt innate immune system
    • May interrupt interferon production
    • May interrupt cytokine production
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14
Q

What does ‘multiply and damage’ refer to regarding the cycle of infection?

A

A lot of the damage is done by the immune system instead of the pathogen:

  • Inflammation
  • Can spread (e.g. from URT to LRT causing damage to the lungs, leaving lungs prone to other infections e.g. bacterial pneumonia)
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15
Q

What does ‘disperse’ refer to regarding the cycle of infection?

A
  • Coughs and sneezes
  • Singing, talking
  • Often symtpoms can lead to greater disperse (diarrhoea, coughing)
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16
Q

How can the cycle of infection be interrupted?

A
  • Hygiene measures
  • Reducing interactions (social distancing)
  • Preventing aerosols
  • Vaccine
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17
Q

Infections can arise from endogenous or exogenous sources. What are endogenous sources? What are exogenous sources?

A

Endogenous - Microorganisms from the host getting into the wrong place

Exogenous - Organisms originating from the external environment/infected individuals

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18
Q

What is the incubation period?

A

The period between infection with the organism and manifestation of clinical features

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19
Q

What is the period of infectivity?

A

Period during which a transmissible organism may be transmitted to another person

E.g. chickenpox: from 48 hours before the onset of the rash to when all the lesions have crust over

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20
Q

What is bacterial pneumonia?

A

Infection of the LRT - causes fluid to collect in the alveoli of the lungs

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21
Q

What organisms can cause bacterial pneumonia?

A

– Streptococcus pneumoniae (most common)

– Staphylococcus aureus

– Haemophilus influenzae

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22
Q

Chest x-ray of pneumonia

A
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23
Q

What is gonorrhoea? What is it caused by?

A
  • Sexually transmissible infection (STI)
  • Caused by Neisseria gonorrhoeae
  • Second most common STI in UK
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24
Q

What are the symptoms of gonorrhoea?

A
  • Discharge of pus from urethra
  • Burning sensation
  • Sterility
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25
Q

Describe the ‘encounter/entry/colonisation’ phase regarding bacterial pneumonia

A
  • Inhalation of air-borne droplets containing pathogen
  • Contact with mouth of infected individual
  • Contaminated blood
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26
Q

Describe the ‘encouter/entry/colonisation’ phase regarding gonorrhoea?

A
  • Sexual contact with infected individual
    • Contact with urethral exudate
  • Vertical transmission (mother to child during birth)
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27
Q

What part of the cycle are pilli and fimbriae essential in?

A

Entry and colonisation

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28
Q

Define tropism

A

The turning of all or part of an organism in a particular direction in response to an external stimulus.

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29
Q

What are adhesins?

A
  • Proteins that are present on the surface of bacteria or fungi that help in attaching to biotic or abiotic surfaces –> require specific resceptor
  • Adhesins are involved in determining tissue tropism of bacterial infection
    • Preference for specific tissue
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30
Q

What is tissue tropism?

A

Tissue tropism is the cells and tissues of a host that support growth of a particular virus or bacterium:

  • Some bacteria and viruses have a broad tissue tropism and can infect many types of cells and tissues
  • Other viruses may infect primarily a single tissue
    • For example, rabies virus affects primarily neuronal tissue.
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31
Q

It can be difficult to discriminate between spread & evading defences when categorising virulence factors. What are examples of spread/evade defences?

A
  • Flagella
  • Capsule
  • Pneumococcal surface protein A
  • IgA protease
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32
Q

What is the ‘capsule’ of bacteria?

A

A layer of polysaccharide found on the outside of S. pneumoniae and other pathogens

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33
Q

What is the purpose of the capsule?

A

Important in evading defences:

  • Prevents phagocytosis
  • Allows S. pneumoniae to pass through mucus in lungs due to sugar layer
  • Prevents complement-mediated killing
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34
Q

What is Pneumococcal surface protein A (PspA)? Which bacteria is it seen in?

A

A surface-exposed protein virulence factor for Streptococcus pneumoniae

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35
Q

What is the function of Pneumococcal surface protein A?

A

Prevents complement-mediated killing by interrupting the complement system

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36
Q

What is the complement system?

A
  • Part of innate immunity
  • Enhance phagocytosis (opsonisation)
  • Directly kill cells (membrane attack complex)
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37
Q

Where is IgA located? What is its function?

A
  • Secretory immunoglobulin A that is found in the mucosal secretions of the respiratory tract and urogenital tract
  • Binds to pathogens and prevents them from adhering to host tissues
  • IgA is the first line of defence in the resistance against infection:
    • Inhibits bacterial and viral adhesion to epithelial cells
    • Neutralises bacterial toxins and virus, both extra- and intracellularly.
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38
Q

What is IgA protease? What does it target?

A
  • An endopeptidase that degrades IgA
  • Targets the amino acid sequence Pro-Pro-Y-Pro (Y = threonine, serine or alanine)
    • Hinge region of heavy chain
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39
Q

3 major bacteria release the IgA protease which destroys IgA. What are they?

A
  1. S. pneumoniae
  2. N. gonorrhoeae
  3. H. influenzae type B
40
Q

What is effect of IgA protease degrading IgA?

A

Interrupts IgA –> pathogen can infect cells more easily

41
Q

What is Pneumolysin? What is it secreted by?

A

A cholesterol-dependent cytolysin (CDC) toxin (virulence factor) secreted by S. pneumoniae

42
Q

What are the effects of Pneumolysin?

A

Multiple monomers come together (multimerise) and bind to cholesterol in host plasma membrane, forming lytic pores in host membranes. This causes host cells to release internal contents (e.g. nutrients) and dies.

43
Q

What are Hyaluronidases and Neuraminidases??

A

Hyaluronidases are a family of enzymes that catalyse the degradation of hyaluronic acid.

Neuraminidases are enzymes capable of degrading Sialic/neuraminic acid

44
Q

Why do many pathogenic bacteria able to establish infections at the mucosal or skin surface produce the enzyme hyaluronidase or neuraminidase?

A

Hyaluronic acid and neuraminic acid are both components of interstitial cement in connective tissue (hyaluronic) or epithelial cells (neuraminic). The breakdown of these can:

  1. Provide nutrients
  2. Provide more space for organisms to grow
  3. Activate immune system
45
Q

What is an endotoxin?

A
  • A toxin present in a bacterial cell
  • Is released on cell death/lysis –> NOT actively secreted
46
Q

What is effects of endotoxins?

A

Can cause uncontrolled activation of immune response:

  • Inflammation
  • Severe tissue damage
  • Multiple organ failure (endotoxic shock, sepsis)

An example of when killing bacteria is actually harmful to host.

47
Q

What is endotoxic shock?

A

A complex phenomenon resulting from systemic release of inflammatory mediators. Endotoxin interacts with inflammatory cells, platelets, and vascular endothelium.

48
Q

How can endotoxins lead to severe sepsis and/or septic shock?

A
  • T lymphocyte response
  • Activation of the clotting cascade
  • Activation of complement
49
Q

Endotoxins cause a T-lymphocyte response. What are the effects of this?

A
  • Cytokine release e.g. TNF-a, y-interferon, interleukin-1
  • Fever, rigors, hypotension, tachycardia, collapse
  • Cardiac and/or renal failure
50
Q

Endotoxins cause activation of the clotting cascade. What can this lead to?

A
  • Disseminated intravascular coagulation (DIC)
  • Depletion of clotting factors
51
Q

What syndromes can be caused by Streptococcus pyogenes?

A
  • Erysipelas
  • Streptococcal sore throat
  • Scarlet fever
  • Necrotising fasciitis
52
Q

What are the virulence factors of S. pyogens?

A
  • Hyaluronidase and streptokinase
  • Toxic shock syndrome toxin
  • Erythrogenic toxin (phage-encoded)
  • C5a peptidase
  • Streptolysins -O and –H
53
Q

What is purpose of S. pyogenes producing hyaluronidase and streptokinase?

A

Break down connective tissue components – facilitate tissue invasion

54
Q

What is purpose of S. pyogenes producing toxic shock syndrome toxin?

A

Superantigen. Causes a syndrome very similar to that caused by endotoxin release

55
Q

What are erythrogenic toxins?

A

Secreted by strains of the bacterium Streptococcus pyogenes. Induce inflammation by nonspecifically activating T cells and stimulating the production of inflammatory cytokines.

  • Causes the rash of scarlet fever
56
Q

What is the purpose of S. pyogenes secreting C5a peptidase?

A

Inactivates complement component C5a

57
Q

What is the purpose of S. pyogenes secreting Streptolysins -O and –H?

A

Lyse red and white blood cells and platelets

58
Q

What is an abscess?

A

An enclosed collection of pus –> a consequence of inflammatory response with phagocytosis of organisms

59
Q

What does pus consist of?

A

consists of living and dead white blood cells, exudate, dead tissue and micro-organisms

60
Q

What are abscesses surrounded by?

A

Surrounded by inflammation, so are associated with all the manifestations of inflammation

61
Q

What are the clinical features of abscesses?

A
  • The lesion itself (fluid filled fluctuant mass)
  • Surrounding inflammation
  • Non-specific symptoms of infection (e.g. anorexia, sweats, malaise, fatigue)
62
Q

What pathogens are superficial abscesses mainly caused by?

A

Staph. aureus and Strep. pyogenes

63
Q

What are pyogenic organisms?

A

Organisms causing the production of pus

64
Q

What are exotoxins?

A

Proteins produced (and usually secreted) by living bacteria –> actively secreted

Typically have quite a specific effect on host (e.g. may only affect nerve cells)

65
Q

What is diptheria? How does it lead to cell death?

A

A serious infection caused by strains of bacteria called Corynebacterium diphtheriae that make toxin (poison). It can lead to difficulty breathing, heart failure, paralysis, and even death.

Inhibition of protein synthesis

  1. Diptheria toxin inactivates elongation factor-2
  2. This prevents protein synthesis
  3. Cell death
66
Q

How does the cholera toxin act?

A

Hyperactivation:

  • Toxin binds to cell and part of the toxin is taken up
  • This increase cAMP activity
  • Leads to loss of cell nutrients –> diarrhoea
67
Q

How does the tetanus toxin work?

A

Effects on nerve-muscle transmission:

  1. Inhibitory transmitter blocked
  2. Continuous stimulation by excitatory transmitter
68
Q

What is the botulinum toxin?

A
  • Incredibly potent - a neurotoxic protein produced by the bacterium Clostridium botulinum
  • It prevents the release of acetylcholine at the neuromuscular junction
    • Causes flaccid paralysis and respiratory failure
    • Infection with the bacterium causes the disease botulism
69
Q

How is the botulinum toxin involved in Botox?

A

Injected into skin causing paralysis –> prevents movement of facial muscles

70
Q

What is treatment for the botulinum toxin/botulism?

A

Treated with penicillin and botulinum antitoxin

71
Q

What toxin causes tetanus?

A

Clostridium tetani - causes infection of wounds (may even be trivial wounds)

72
Q

What are effects of Clostridium tetani?

A
  • Tetanospasmin
    • Produced on germination of spores
    • Binds to nerve synapses
    • Inhibits release of inhibitory neurotransmitters (e.g. gamma-amino butyric acid) in the central nervous system
    • Death by respiratory paralysis
73
Q

What is treatment for Clostridium tetani?

A

metronidazole and tetanus antitoxin

74
Q

What is a granuloma?

A

A focal compact collection of inflammatory cells, mononuclear cells predominating, usually as a result of the persistence of a non-degradable product and of active cell mediated hypersensitivity.

75
Q

What are granulomas formed in response to?

A

a number of inflammatory stimuli

76
Q

What are manifestations of granulomas?

A
  • Radiological manifestations: “nodule” (pulmonary, hepatic, renal, splenic etc)
  • Clinical/pathological manifestations: tissue necrosis (“caseation”)
77
Q

What are intracellular pathogens?

A

Intracellular pathogens are organisms that are capable of growing and reproducing inside host cells.

78
Q

What is the bacteria causing tuberculosis?

A

Mycobacterium tuberculosis

79
Q

What accounts for the main clinical and radiological features of tuberculosis?

A

Granulmoma production

80
Q

What is primary TB?

A

Primary lung infection caused by mycobacterium tuberculosis

  • Ranke/Ghon complex: solitary granuloma (nodule) with hilar granulomatous lymphadenopathy
81
Q

What is Ghon’s complex?

A

A lesion seen in the lung that is caused by tuberculosis. The lesions consist of a Ghon focus along with pulmonary lymphadenopathy within a nearby pulmonary lymph node

82
Q

What is ‘Ranke complex’?

A

Seen in ‘healed’ primary pulmonary tuberculosis and is a later manifestation of the Ghon complex.

83
Q

What is post-primary / reactivation of TB?

A

Widespread granulomatous inflammation +/- cavitation, often apical

84
Q

What is miliary TB?

A

Multiple disseminated 1-3 mm pulmonary granulomas causing infection throughout the body (not just lungs)

85
Q

What is extrapulmonary TB?

A

Diverse manifestations in bone, liver, kidneys, CNS etc.

86
Q

How can lung inflammation promote disperal of pathogens?

A
  • Production of fluid containing pathogen
  • Induction of coughing
  • Dispersal of pathogen via respiratory droplets
87
Q

How can damage to tissues of the genital tract promote disperal of pathogens?

A

Induction of immune response:

  • Production of urethral discharge
  • Dispersal via sexual contact
88
Q

What are other routes of dispersal?

A
  • Diarrhoeal disease and production of liquid faeces
    • Greater dispersal
    • Contamination of food and water
  • Skin infection and production of vesical fluid
  • Pathogens capable of gaining access to the circulatory system
    • Blood transfusions
    • Sharing needles
89
Q

What are P fimbrae / P pilli? Where are they found?

A
  • Tiny hair-like structures on surface of bacterial cells expressing specific adhesions
  • Found on E. coli bacteria
90
Q

How do P fimbrae/pilli function as one of the most important virulence factors in E. coli? Which infection do they aid them in?

A
  • The P fimbriae is considered to be one of the most important virulence factors in uropathogenic E. coli
  • Mediate adherence to host cells –> adhere to glycolipids on human uroepithalial cells –> upper UTIs
91
Q

Which bacteria causes scarlet fever?

A

Group A Streptococcus (S. pyogenes)

92
Q

Which virulence factor of S. pyogenes enables it to cause the rash seen in Scarlet Fever?

A

Erythrogenic toxins –> these induce inflammation by non-specifically activating T cells and stimulating the production of inflammatory cytokines

93
Q

Which bacteria is known as ‘Group B Strep’?

A

Streptococcus Agalaictiae

94
Q

Endotoxins vs exotoxins?

A

Endotoxin: Released during cell death/lysis, NOT actively secreted

Exotoxin: Protein actively secreted by bacteria

95
Q

Function of C5a?

A

A strong chemoattractant and is involved in the recruitment of inflammatory cells, in activation of phagocytic cells and release of granule-based enzymes and generation of oxidants.

96
Q

Which 2 major bacteria can produce TSS toxins and therefore cause TSS?

A
  1. S. pyogenes
  2. S. aureus
97
Q

What is arguably the major virulence factor of S. pneumoniae?

A

Polysaccharide capsule –> shields it from the host immune system and allows it to pass through mucous membrane of lung

Yr 2 - EMS (60 decks)

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