Path & host Flashcards

1
Q

Pathogenicity factors

A

How likely is an organism to cause an illness?

  1. Infectivity, ability to become established on or within host
  2. Virulence, ability to cause harmful effects once established
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2
Q

Infectivity factors

A
  • Attachment e.g. E.coli have P-fimbriae

- Acid resistance e.g. H.pylori, has urease which makes ammonia from urea

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3
Q

Virulence factors

A
  • Invasiveness, reproduces rapidly
  • Toxin production, infects immune system
  • Exotoxins released extracellularly by the microorganism
  • Enterotoxins are exotoxins which act on the GI tract
  • Endotoxin is structurally part of the Gram negative cell wall, Lipid A is the nasty bit
  • Evasion of immune system
  • These are specific to strains, not species
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4
Q

Streptococcus pyogenes

A
  • Highly invasive
  • Enterotoxin, superantigen
  • Necrotising fasciitis
  • Cellulitis
  • Connective tissue breakdown by enzymes
  • Fibrinolysis - enzymatic breakdown of fibrin in blood clots
  • Stimulate division of T cells in the absence of specific antigen
  • Overwhelming cytokine production - toxic shock
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5
Q

Tetanus

A
  • Clostridium tetani
  • High virulence
  • Infects dirty wounds
  • Toxin production, binds to nerve synapses, inhibits release of inhibitory NTs
  • Death by respiratory paralysis
  • Rx by debridement and abx and antitoxin
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6
Q

Cholera

A
  • Vibrio cholera
  • High virulence
  • Enterotoxins
  • Colonises small intestine
  • Toxin production, increases cAMP levels, inhibits uptake of Na+ and Cl- ions. Stimulates secretion of Cl- and HCO3- ions.
  • Passive, massive outflow of H2O
  • Death by dehydration
  • Rx - rehydration
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7
Q

Staph aureus

A
  • Highly virulent
  • Enterotoxin
  • Stimulate division of T cells in the absence of specific antigen
  • Overwhelming cytokine production - toxic shock
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8
Q

E.coli

A
  • O157 is the nasty one
  • Induces severe uncontrolled host repose
  • Cytokine production
  • Fever, rigors, hypotension, tachycardia, collapse
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9
Q

Mechanisms of viral pathogenesis

A
  • Cell destruction following virus infection, death of T4 cells by HIV
  • Virus-induced changes to cellular gene expression, cellular transformation by tumour viruses
  • Immunopathogenic disease, Influenza A, induced myocarditis
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10
Q

Sites of viral entry

A
  • Conjunctiva
  • Arthropod, insect bite
  • Capillary
  • Respiratory tract
  • Alimentary tract
  • Skin
  • Urinogenital tract
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11
Q

Types of viral infection

A
  • Acute
  • Latent
  • Chronic
  • Tumour virus infection
    NB: symptoms arise at peak of virus in body
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12
Q

Acute viral infection

A
  • Localised, specific to site

- Development of viraemia can go to other tissues

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13
Q

Examples of acute viral infections

A
  • Influenza A, resp. infection. Virus infects cells of respiratory tract, destruction of respiratory epithelium, altered cytokine expression leading to fever
  • Enterovirus. Virus is normally excreted in faeces but if viraemia occurs then it can get into non-neuronal tissues and neuronal tissues.
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14
Q

Enterovirus examples

A

Poliomyelitis, aseptic meningitis, myocarditis, pancreatitis, respiratory infections

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15
Q

Latent viral infections example and life cycle

A
  • Herpes simplex virus: primary infection in epithelium
  • Virus migrates to ganglia and stays latent in nucleus, no virus replication
  • Stimulus occurs e.g. stress, life events, immunosuppressants, sunlight
  • Virus migrates back to epithelium and it is released, results in replication
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16
Q

Tumour virus infections examples

A
  • Papilloviruses: cervical carcinoma
  • Retroviruses: lymphomas and leukaemieas, causes the cells to be transformed from normal:
    1. Virus infects cell, virus nucleic acid, as DNA, integrates into cellular genome
    2. Virus causes changes in cellular gene expression
    3. Uncontrolled cell multiplication and tumour formation
17
Q

Antigenic drift

A

Gradual evolution of viruses to generate antigenic variants

You might have partial immunity

18
Q

Antigenic shift

A

Significant changes in virus antigenic structure
Complete change, no immunity
Avian flu and swine flu are examples where non-human hosts for influenza A play a key role in new types of virus

19
Q

Define pathogen

A

Organism which can cause disease

20
Q

Define commensal

A

Organism which is part of the normal flora e.g. E.coli in gut, Staph aureus in nose, axilla

21
Q

Examples of innate immunity

A
  • Skin, gastric acid, muco-ciliary escalator
  • Phagocytic cells
  • Other white cells (T cells, B cells, these aren’t phagocytic)
  • Opsonisation
22
Q

Phagocytic cells examples

A
  • Polymorphs (acute, short lived): neutrophils, eosinophils, basophils
  • Macrophages (chronic, long lived): monocytes in blood mature into macrophages
  • Fixed macrophages (liver, spleen, lymph nodes) of the mononuclear phagocytic system
  • Free macrophages in the tissues
  • Mononuclear phagocytic system
23
Q

Mononuclear phagocytic system examples

A
  • Spleen clears blood (why you get overwhelming Strep pneumoniae infection in splenectomy)
  • Liver clears entero-hepatic circulation
  • Regional lymph node drain peripheral sites
24
Q

Opsonisation

A
  • How a phagocyte recognises and destroys an antibody
  • Phagocytic cell has receptors for both
  • Efficiency of phagocytosis is greatly improved
  • Important for capsulate bacteria as you can get around the problems with phagocytosis and intracellular killing e.g. Strep pneumoniae and haemophilus influenzae
25
Q

Process of phagocytosis

A
  1. Phagocytosis (ingestion), cell engulfs particle in vesicle
  2. Organism held in phagosome
  3. Fusion with lysosome, in case of macrophage
  4. Phagolysosome is formed
  5. Intracellular killing
26
Q

Organisms resistant to phagocytosis

A
  • Capsulate organisms e.g. strep pneumoniae

- Mycobacterium tuberculosis is resistant to intracellular killing

27
Q

Acquired immunity

A
  • Specific response to antigen concerned
  • Immunological memory created
  • Humoral and cellular
  • Each organism is a complex mixture of antigens
  • Each antigen is a mixture of epitopes, bits that recognise immune system
28
Q

What do antibodies do?

A
  1. Neutralise bacterial toxins
  2. Neutralises viruses in viraemic stage
  3. Prevent adherence of mircoorganisms
  4. Opsonises capsulate organisms (Strep pneumoniae, Haemophilus influenzae)
  5. Useful means of diagnosis with serology
29
Q

5 classes of immunoglobulins

A
  • IgM: eliminates pathogens with B cells before there are any IgG cells
  • IgG: majority of antibody-based immunity against invading pathogens
  • IgA: mucosal immunity
  • IgE: allergy and helminth infection
  • IgD: antigen receptor on B cells that have not been exposed to B cells
30
Q

B-lymphocytes

A
  • Differentiate into plasma cells when they recognise a specific epitope
  • B-lymphocytes require T cell help
31
Q

Monoclonal antibody vs polyclonal antibody

A

Monoclonal -from one clone of plasma cell which has specificity for a single epitope
Polyclonal antibody - multiple specificity

32
Q

Antibody and complement in infection

A
  1. Opsonisation by complement
  2. Lysis of Gram negative organisms by complement
  3. Complement cascade by-products are chemotactic (attract polymophs)
33
Q

Humoral immunity

A
  • Found in body fluids
  • Mostly used in bacterial infection
  • Extracellular
  • Acute inflammation
  • Neutrophilia
34
Q

Cell mediated immunity

A
  • Combats intracellular infection (viruses, certain bacteria and fungi)
  • Lymphocytosis
  • e.g. Mycobacterium tuberculosis is resistant to intracellular killing, Legionella pneumonphila and Candida albicans
35
Q

How cell mediated immunity works

A
  • Macrophages ‘present’ the antigen and this stimulates the T-cells
  • Two T cells: CD4 helper and CD8 suppressor and cytotoxic cells
  • Cytokines are produced and control the response
36
Q

Define colonisation

A
  • No signs or symptoms
  • MRSA can cause infection or colonisation
  • Infection is opposite as you get signs and symptoms
37
Q

Define asymptomatic infection

A

Infection without symptoms

38
Q

Define latent infection

A

Asymptomatic infection capable of manifesting symptoms under particular circumstances or if activated