Infection Flashcards

(46 cards)

1
Q

Give examples of gram positive bacteria

A

Staphylococcus aureus Streptococcal pneumoniae Clostridium difficle

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2
Q

Give examples of gram negative bacteria

A

Neisseria meningitides Escherichia coli Pseudmonas aeruginosa

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3
Q

Give examples of encapsulated bacteria

A

Staphylococcus aureus Streptococci pneumoniae Neisseria miningitides Pseudomonas aeruginosa

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4
Q

Define SIRS

A

Systemic inflammatory response syndrome. 2 or more of the following:

  • Temp: 38oC
  • HR: >90bpm
  • RR: >20/min
  • WBC: <4 or >12 x 109/L
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5
Q

Define sepsis

A

SIRS + suspect pathogen

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6
Q

Define severe sepsis and septic shock

A

Severe sepsis: SIRS and organ dysfunction/hypoperfusion
Septic shock: Severe sepsis but unresponsive hypotension depsite IV fluid administration

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7
Q

What are the sepsis six?

A

O2 = give oxygen

F = give fluid

L = lactate level

U = urine output

I = infection cultures

D = drugs (antibiotics)

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8
Q

What type of virus is HIV?

A

Enveloped positive single strand RNA

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9
Q

Describe how HIV infects host cells

A
  • HIV virus attaches to CD4 receptor
  • Viral RNA is inserted into host DNA to ensure replication
  • HIV causes tissue destruction from either the virus or host’s response to virus-infected cells
  • Gives immunological state
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10
Q

What type of virus is influenza?

A

Enveloped negative single strand RNA

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11
Q

Explain what is meant by antigenic drift

A

Minor antigenic changes in H and N proteins on outer surface, occurs every year.

Random mutations does not involve change in viral subtype

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12
Q

Explain what is meant by antigenic shift

A

Dramatic changes in antigenic properties of H and N proteins.

From H1N1 to H3N2

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13
Q

What are the treatments for influenza?

A

Neuraminidase inhibitor - prevents release from cell membrane once replicated (e.g. oseltamivir)

M2 ion channel inhibitor - prevents acidification of endosome required for disassembly of virus for replication (e.g. amantadine)

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14
Q

What type of virus is hepatitis B?

A

Enveloped double stranded DNA virus

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15
Q

Give some mechanisms of infection

A
  • Haematogenous
  • Contiguous (direct) spread
  • Inoculation
  • Ingestion
  • Inhalation
  • Vector (e.g. mosquito)
  • Vertical transmission
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16
Q

Generally how to infections cause damage?

A

Either through toxin production or interacting with host defences (e.g. inflammation)

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17
Q

How does the hepatitis B virus cause damage?

A

Infected hepatocytes causing cell-mediated response resulting in inflammation and necrosis

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18
Q

What type of virus is varicella-zoster?

A

Enveloped double stranded DNA virus

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19
Q

What are the most common pathogenic causes of malaria?

A

Plasmodium vivax (80%)

Plasmodium falciparum (15%) - more dangerous

20
Q

Describe transmission of malaria

A

Female anopheles mosquite (vector)

Infected blood products

21
Q

What is the pathogenesis of malaria? And give common signs/symptoms

A
  • Multiply in RBCs
  • Cause haemolysis and cytokine release

Anaemia, jaundice, hepatosplenomegaly

22
Q

Give common pathogenic causes of meningitis

A

Neisseria meningitides

Streptococcus pneumoniae

23
Q

How does neisseria meningitides cause a non-blanching rash?

A

Toxin release causes destruction of blood vessel wall leading to blood release under the skin

24
Q

Give common causes of typical pneumonia

A

Streptococcal pneumoniae

Haemophilus influenza

25
Give causes of atypical pneumonia
Chlamydia pneumoniae Mycoplasma pneumoniae Influenza virus Pneumocystis jiroveci (immunocompromised)
26
What does staphylococcus aureus secrete that aid in its survival?
Catalase - catalyses conversion of peroxide to water and oxygen, prevents damage from neutrophils, oxidative burst Coagulase - localised clotting, restricts access of polymorphonuclear neutrophils
27
What are the common causes of hospital-acquired pneumonia?
Escherichia coli Staphylococcus aureus
28
What type of bacteria is helicobacter pylori?
Gram negative bacilli
29
How does H. pylori ensure it's survival?
Burrows into mucus 'un-stirred' later - more alkali Produces urease to convert urea to carbon dioxide and ammonia - neutralises stomach acid Ammonia toxic to epithelial cells so causes inflammation
30
What are the common pathogenic causes of UTI?
Escherichia coli Staphylococcus saprophyticus Staphylococcus aureus - catheter
31
What are the cells of innate immunity?
* Monocytes/macrophages * Neutrophils * Dendritic cells * Natural killer cells * Degranulating cells (mast cells, eosinophils, basophils)
32
What is chronic granulomatous disease?
Mutation on X chromosome causing defective enzymes involved with respiratory burst Neutrophils are attracted to site of infection and phagocytose but are unable to kill pathogens
33
Explain how phagocytes recognise microbes
Micrboes express pathogen-associated molecular patterns (PAMPs) which are recognised by phagocytes expressing pattern recognition receptors (PPRs)
34
Describe the 2 types of PRRs
Collectin - interact with innate immune system Toll-like receptors
35
What are the molecules are opsonins?
Antibodies - IgG, IgM Complement - C3b, C4b Mannose-binding lectin C-reactive protein
36
What are the 3 types of cytokines that macrophages release?
1. Cytokines acting over distance - G-CSF, increases bone marrow production of neutrophils 2. Cytokines acting locally - TNF, increases stickness of endothelial blood cells, more like neutrophils will enter surrounding tissue 3. Chemokines - IL-8, attract other cells (neutrophils)
37
Explain acute phase response
If infection not cleared then macrophages produce more cytokines (IL-1, IL-6, TNF) which surge into circulation and affect other organs * Liver - increases production of serum acute-phase proteins * Hypothalamus - increases body temperature (inhibits replication of viruses) * Nervous system - shivering and sweating
38
How does complement damage pathogens?
1. Membrane attack complex - forms a polymers that binds to pathogen wall and punches holes in it 2. C3a increases vascular permability 3. Increases opsonisation
39
What condition results from a mutation in complement cascade? (Hint: C1 inhibitor gene mutation)
Herediatory angio-oedema
40
Which MHC class, CD type receptors and T cells are specific for intracellular microbes?
MHC I, CD8 T cells causing cytotoxic T cell response
41
Which MHC class, CD type receptors and T cells are specific for extracellular microbes?
MHC II, CD4 T cells and activates T helper cells
42
What is graft-vs-host reaction
Immune cells of the transplanted tissue recognise the recipitent as foreign, therefore mount immune response
43
What are the 4 P's of infection prevention?
1. Patient 2. Pathogen 3. Practice 4. Place
44
What is the difference between primary immunodeficiencies and secondary immunodeficiencies?
Primary immunodeficiencies are a result of a intrinsic defect (congenital) - usually B cell deficiencies Secondary immunodeficiencies are caused by an underlying disease or condition affecting immune compoenets (decreased production or increased loss/catabolism)
45
Give one example of each primary immunodeficiencies: 1. B cell deficiency 2. Phagocyte deficiency 3. T deficiency 4. Complement deficiency
* B cell deficiency - IgA deficiency (B cell unable to switch to IgA) * Phagocyte deficiency - Chronic granulomatous disease * T deficiency - Di George syndrome (incomplete development of thymus) * Complement deficiency - Herediatary angio-oedema
46
Which interleukin is pyrogenic?
Interleukin-1