Pathogens & hosts Flashcards

1
Q

<p>What is clinical infection characterised by?</p>

A

<p>Inflammation</p>

<p>Pain</p>

<p>Pyrexia (raised body temperature)</p>

<p>Tachycardia (increased heartrate)</p>

<p>Rigors (sudden feeling of cold with shivers)</p>

<p>Increased white cell count</p>

<p>Increased C reactive protein (CRP)</p>

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2
Q

<p>What is pyrexia?</p>

A

<p>Raised body temperature</p>

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3
Q

<p>What is tachycardia?</p>

A

<p>Increased heartrate</p>

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4
Q

<p>What are rigors?</p>

A

<p>Sudden feeling of cold with shivers</p>

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5
Q

<p>What is a pathogen?</p>

A

<p>An organism that can cause disease</p>

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6
Q

<p>What is a commensal?</p>

A

<p>An organism which is part of normal flora</p>

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7
Q

<p>What are examples of commensals?</p>

A

<p>E coli in the gut</p>

<p>Staph aureus in the nose</p>

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8
Q

<p>What is a skin commensal?</p>

A

<p>Coagulase-negative staphyloccii</p>

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9
Q

<p>When can coagulase-negative staphyloccii be pathogenic?</p>

A

<p>In the presence of foreign bodies (such as prosthetic heart valves)</p>

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10
Q

<p>What is Koch's postulates?</p>

A

<p>The criteria used to identify the agent of a particular disease</p>

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11
Q

<p>What are the principles of Koch's postulates?</p>

A

<p>Organism must be found in all cases of the disease</p>

<p>Able to be cultured outside the body for several generations</p>

<p>Should reproduce the disease on inoculation (vaccination)</p>

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12
Q

<p>What do non-sterile sites contain that sterile sites do not?</p>

A

<p>Commensals</p>

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13
Q

<p>What do we need knowledge of to determine if something is a pathogen?</p>

A

<p>Normal flora for the site</p>

<p>Organisms pathogenicity</p>

<p>Clinical context</p>

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14
Q

<p>What is pathogenicity?</p>

A

<p>Ability of an organism to cause disease</p>

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15
Q

<p>What is flora?</p>

A

<p>Collective bacteria and other microorganisms in an ecosystem</p>

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16
Q

<p>What does an organism need to be to cause an infection?</p>

A

<p>Infectivity (ability to become established)</p>

<p>Virulence (ability to cause harmful effects once established)</p>

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17
Q

<p>What is infectivity?</p>

A

<p>Ability to become established</p>

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18
Q

<p>What is virulence?</p>

A

<p>Ability to cause harmful effects once established</p>

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19
Q

<p>What are things that help infectivity?</p>

A

<p>Attachment (such as P-fimbriae on E coli)</p>

<p>Acid resistance (such as urease on helicobacter pylori)</p>

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20
Q

<p>What is an example of attachment helping infectivity?</p>

A

<p>P-fimbriae on E coli</p>

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21
Q

<p>What is an example of acid resistance helping infectivity?</p>

A

<p>Urease on helicobacter pylori</p>

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22
Q

<p>What is urease?</p>

A

<p>An enzyme that catalysis urea to ammonia and carbon dioxide</p>

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23
Q

<p>What is virulence supported by?</p>

A

<p>Invasiveness</p>

<p>Toxin production</p>

<p>Evasion of immune system</p>

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24
Q

<p>What is virulence specific to?</p>

A

<p>Strains, not species</p>

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25
Q

<p>What is an example of invasiveness?</p>

A

<p>Streptococcus pyogenes causing:</p>

<p>Necrotising fascilitis (flesh eating disease)</p>

<p>Cellulitis</p>

<p>Connective tissue breakdown</p>

<p>Fibrinolysis</p>

<p></p>

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26
Q

<p>What is haemolysis?</p>

A

<p>The rupture or destruction of red blood cells</p>

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27
Q

<p>What are the 3 types of haemolysis?</p>

A

<p>Alpha haemolytic (partial haemolysis, turns blood agar green)</p>

<p>Beta haemolytic (complete haemolysis, turns blood agar clear)</p>

<p>Non haemolytic</p>

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28
Q

<p>What is alpha haemolytic?</p>

A

<p>Partial haemolysis</p>

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29
Q

<p>What colour does alpha haemolytic turn blood agar?</p>

A

<p>Green</p>

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30
Q

<p>What is beta haemolytic?</p>

A

<p>Complete haemolysis</p>

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31
Q

<p>What colour does beta haemolytic turn blood agar?</p>

A

<p>Clear</p>

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32
Q

<p>What may different species of strepococci be?</p>

A

<p>Alpha, beta or non haemolytic</p>

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33
Q

<p>What is an example of an alpha haemolytic streptococci and what does it cause?</p>

A

<p>Streptococcus pneumoniae which causes:</p>

<p>Pneumonia</p>

<p>Meningitis</p>

<p>Septicaemia</p>

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34
Q

<p>What are beta haemolytic bacteria further identified by?</p>

A

<p>Lancefield groupings</p>

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35
Q

<p>What are lancefield groupings based on?</p>

A

<p>Surface antigens</p>

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36
Q

<p>What groups are in lancefield groupins?</p>

A

<p>A to G</p>

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37
Q

<p>What are the clinically most important lancefield groups?</p>

A

<p>A, B and D</p>

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38
Q

<p>What is a major group A beta haemolytic streptococci and what does it cause?</p>

A

<p>Streptococcus pyogenes which causes:</p>

<p>Sore throats</p>

<p>Cellulitis</p>

<p>Necrotising fascilitis</p>

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39
Q

<p>What is a toxin?</p>

A

<p>A poison that acts as an antigen in the body</p>

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40
Q

<p>What are the 3 kinds of toxins?</p>

A

<p>Exotoxins (released extracellularly)</p>

<p>Enterotoxins (exotoxins which act on the GI tract)</p>

<p>Endotoxins (structurally part of the gram negative cell wall)</p>

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41
Q

<p>What are exotoxins?</p>

A

<p>Toxins that are released extracellularly</p>

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42
Q

<p>What are enterotoxins?</p>

A

<p>Exotoxins that act on the GI tract</p>

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43
Q

<p>What are endotoxins?</p>

A

<p>Toxins that are structurally part of the gram negative cell wall</p>

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44
Q

<p>What does clostridium tetani produce?</p>

A

<p>Toxins that cause tetanus</p>

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45
Q

<p>What is tetanus?</p>

A

<p>Uncontrolled muscle spasm due to loss of inhibition at the neuromuscular junction</p>

46
Q

<p>What is used for the immunisation of tetanus?</p>

A

<p>Antigenically modified toxin</p>

47
Q

<p>What is a toxoid?</p>

A

<p>A chemically modified toxin that is no longer toxic but is still antigenic and can be used as a vaccine</p>

48
Q

<p>What are examples of bacteria that produce toxins?</p>

A

<p>Clostridium tetani</p>

<p>Clostridium perfringes</p>

<p>Clostridium difficile</p>

49
Q

<p>What does vibrio cholerae cause?</p>

A

<p>Uses enterotoxins to colonise in the small intestine and cause:</p>

<p>Increases cAMP levels (inhibits uptake of Na and Cl ions, and secretion of Cl and HCO3ions)</p>

<p>Passive outflow of water</p>

<p>Cause of death by dehydration</p>

50
Q

<p>What are superantigens?</p>

A

<p>Class of antigen that cause non-specific activation of T cells resulting in massive cytokine release causing toxic shock</p>

51
Q

<p>What are superantigens produced by?</p>

A

<p>Certain exotoxins of strep pyogenes and staph aureus</p>

52
Q

<p>What do endotoxins cause?</p>

A

<p>Severe uncontrolled host response such as:</p>

<p>Cytokine production</p>

<p>Fever</p>

<p>Rigors</p>

<p>Hypotension</p>

<p>Collapse</p>

53
Q

<p>What are examples of gram negative cocci?</p>

A

<p>Neisseria spp</p>

<p>Moraxella catarrhalis</p>

<p>E coli</p>

54
Q

<p>What is the name of E coli?</p>

<p></p>

A

<p>Escherichia coli</p>

55
Q

<p>What kinds of reserves does E coli have?</p>

A

<p>Human and animal reservoirs</p>

56
Q

<p>What virulence machanisms does E coli have?</p>

A

<p>Pili</p>

<p>Capsule</p>

<p>Endotoxins</p>

<p>Exotoxins</p>

57
Q

<p>What does E coli do?</p>

A

<p>Ferments lactose</p>

58
Q

<p>What is a serotype?</p>

A

<p>Serologically distinguishable strain</p>

59
Q

<p>How many serotypes of E coli are there?</p>

A

<p>Over 160</p>

60
Q

<p>What are different kinds of virus pathogenic mechanisms?</p>

A

<p>Cell destruction following virus infection</p>

<p>Virus induced changes to cellular gene expression</p>

<p>Immunopathogenic disease</p>

61
Q

<p>What are different kinds of virus infections?</p>

A

<p>Acute infections</p>

<p>Latent infections</p>

<p>Chronic infections</p>

<p>Tumour virus infections</p>

62
Q

<p>What is an example of virus pathogenisis?</p>

A

<p>The transmission of influenza A:</p>

<p>1) Virus infects cells of the respiratory tract</p>

<p>2) Destruction of respiratory epithelium</p>

<p>3) Secondary bacterial infection</p>

<p>4) Altered cytokine expression leading to fever</p>

63
Q

<p>What can the generation of novel influenza be caused by?</p>

A

<p>Antigenic drift (minor changes, natural mutations in the genes of flu viruses over time)</p>

<p>Antigenic shift (abrupt major changes in virus antigenic structure)</p>

64
Q

<p>What is antigenic drift?</p>

A

<p>Minor changes, natural mutations, in the genes of flu viruses over time</p>

65
Q

<p>What is antigenic shift?</p>

A

<p>Abrupt major changes in the virus antigenic structure</p>

66
Q

<p>What are enteroviruses?</p>

A

<p>Single stranded sense RNA viruses</p>

67
Q

<p>What are examples of enteroviruses?</p>

A

<p>Poliovirus</p>

<p>Coxsackie B viruses</p>

68
Q

<p>What are some conditions caused by enteroviruses?</p>

A

<p>Poliomyelitis (caused by poliovirus)</p>

<p>Aseptic meningitis</p>

<p>Myocarditis (caused bu coxsackie B virus)</p>

<p>Pancreatitis (caused by coxsackie B virus)</p>

<p>Respiratory infections</p>

69
Q

<p>What is viraemia?</p>

A

<p>The presence of viruses in the blood</p>

70
Q

<p>What can viruses do from the blood?</p>

A

<p>Infect neuronal tissues which will cause paralysis</p>

71
Q

<p>What is paralysis?</p>

A

<p>Loss of muscle function in part of your body</p>

72
Q

<p>What is a latent virus infection?</p>

A

<p>Virus that lies dormant in a cell and can start expressing genes in the future (reactivation)</p>

73
Q

<p>What is an example of a latent virus infection?</p>

A

<p>Herpes simplex virus</p>

74
Q

<p>What are the 2 types of herpes simplex virus?</p>

A

<p>Cold sores (type 1)</p>

<p>Genetial lesions (type 2)</p>

75
Q

<p>What is the pathogenisis of herpes virus infections?</p>

A

<p>1) Primary infection on epithelial cells</p>

<p>2) Virus migration to the ganglia</p>

<p>3) Virus reamins latent in nucleus (no virus replication)</p>

<p>4) Stimuli causes reactivation of the virus</p>

<p>5) Virus migration to epithelial cells leading to virus replication</p>

<p></p>

76
Q

<p>What are examples of viruses that can induce tumours?</p>

A

<p>Papilomaviruses (cervical carinoma)</p>

<p>Reteroviruses (lymphomas and leukaemias)</p>

77
Q

<p>What is the pathogenisis of human T-lymphotropic virus-1?</p>

A

<p>1) Transmission by blood and mother to child</p>

<p>2) Infects T cells</p>

<p>3) Modifies host cell gene expression using transactivating proteins (ones that cause transactivation, increased rate of gene expression)</p>

<p>4) Causes a variety of disease such as leukaemia</p>

<p>5) Directly responsible for the tumour</p>

78
Q

<p>What are the 2 kinds of host defence mechanisms?</p>

A

<p>Innate immunity</p>

<p>Acquired immunity</p>

79
Q

<p>What is innate immunity?</p>

A

<p>The non-specific first line of defence</p>

80
Q

<p>What is responsible for innate immunity?</p>

A

<p>Physical barriers such as the skin, gastric acid and mucus</p>

<p>Phagocytic cells that ingest foreign bodies (such as polymorphs and macrophages)</p>

81
Q

<p>What are different kinds of polymorphs?</p>

A

<p>Neutrophils</p>

<p>Eosinophils</p>

<p>Basophils</p>

82
Q

<p>What is opsonisation?</p>

A

<p>Immune process where particles are targeted for destruction by a phagocyte</p>

83
Q

<p>What is the process of optimisation?</p>

A

<p>1) Organism coated with antibody or compliment</p>

<p>2) Phagocyte has receptors for both and targets them</p>

<p>3) Efficiency of phagocytosis has improved</p>

84
Q

<p>What is acquired immunity?</p>

A

<p>A specific immune response to the antigen concerned and an immunological memory is created</p>

85
Q

<p>What is acquired immunity composed of?</p>

A

<p>Humoral (antibodies)</p>

<p>Cellular (T cells)</p>

86
Q

<p>What does humoral mean?</p>

A

<p>Relating to body fluids</p>

87
Q

<p>What is each organism a mix of? And what is this a mix of?</p>

A

<p>Each organism is a mix of antigens, and each antigen is a mix of epitopes</p>

88
Q

<p>What is an epitope?</p>

A

<p>Part of an antigen which an antbody attaches itself</p>

89
Q

<p>What is an antibody?</p>

A

<p>Y shaped protein used to neutralise pathogens, also known as immunoglobin</p>

90
Q

<p>What is an antibody also known as?</p>

A

<p>Immunoglobulin</p>

91
Q

<p>What are different kinds of antibodies?</p>

A

<p>Immunoglobulin M (primary response)</p>

<p>Immunoglobulin G (secondary response)</p>

<p>Immunoglobulin A (mucosal immunity)</p>

<p>Immunoglobulin E (allergy and helminth infections)</p>

92
Q

<p>What do B cells do when they recognise a specific epitope?</p>

A

<p>Differentiate into a plasma cell</p>

93
Q

<p>What is the differentiation of B cells into plasma cells initiated by?</p>

A

<p>Helper T cell</p>

94
Q

<p>What is a monoclonal antibody?</p>

A

<p>Specificity for a single epitope</p>

95
Q

<p>What is a polyclonal antibody?</p>

A

<p>Multiple specificity</p>

96
Q

<p>What is a plasma cell?</p>

A

<p>Fully differentiated B lymphocyte which produces a single type of antibody</p>

97
Q

<p>What does the compliment system form?</p>

A

<p>A cascade of 20 proteins</p>

98
Q

<p>What is the compliment system triggered by?</p>

A

<p>The combination of an antigen and its antigen trigger</p>

99
Q

<p>What are some functions of antibodies in infection?</p>

A

<p>Neutralising bacterial toxins</p>

<p>Neutralising viruses</p>

<p>Prevents adherance of microorganisms</p>

<p>Opsonises capsulated organisms</p>

<p>Useful means of diagnosis (serology)</p>

100
Q

<p>What does opsonises mean?</p>

A

<p>Makes more susceptible to the action of phagocytes</p>

101
Q

<p>What are functions of compliment proteins in infection?</p>

A

<p>Opsonisation</p>

<p>Lysis of gram negative organisms</p>

<p>Attracts polymorphs</p>

102
Q

<p>What is lysis?</p>

A

<p>Degradation of a cell by rupture of th cell wall or membrane</p>

103
Q

<p>Where does the humoral response happen?</p>

A

<p>Extracellularly</p>

104
Q

<p>When is humoral immunity mostly used?</p>

A

<p>In bacterial infection, causing acute inflammation</p>

105
Q

<p>What does humoral immunity cause?</p>

A

<p>Acute inflammation</p>

106
Q

<p>What is cell mediated immunity?</p>

A

<p>Immune response that does not involve antibodies but the activation of phagocytes and cytotoxic T cells and the release of various cytokines</p>

107
Q

<p>What is the process of cell mediated immunity?</p>

A

<p>1) Macrophages present antigen and stimulate T cells</p>

<p>2) Cytokines are produced and control the response</p>

<p>3) Th1 cells activate macrophages to ingest and kill pathogens</p>

<p>4) Cytotoxic T cells kill infected host cells or foreign cells</p>

108
Q

<p>What are the 2 kinds of active immunisation?</p>

A

<p>Natural (exposure/infection)</p>

<p>Artificial (vaccination)</p>

109
Q

<p>What are different kinds of vaccines?</p>

A

<p>Live attenuated</p>

<p>Killed, inactivated</p>

<p>Toxoid, modified toxin</p>

110
Q

<p>What are common vaccines for travellers?</p>

A

<p>Hepatitis A</p>

<p>Typhoid</p>

<p>Yellow fever</p>

<p>Rabies</p>