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PPE Revision > Infection > Flashcards

Infection Flashcards

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
Q

Give causes of atypical pneumonia

A

Chlamydia pneumoniae

Mycoplasma pneumoniae

Influenza virus

Pneumocystis jiroveci (immunocompromised)

26
Q

What does staphylococcus aureus secrete that aid in its survival?

A

Catalase - catalyses conversion of peroxide to water and oxygen, prevents damage from neutrophils, oxidative burst

Coagulase - localised clotting, restricts access of polymorphonuclear neutrophils

27
Q

What are the common causes of hospital-acquired pneumonia?

A

Escherichia coli

Staphylococcus aureus

28
Q

What type of bacteria is helicobacter pylori?

A

Gram negative bacilli

29
Q

How does H. pylori ensure it’s survival?

A

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
Q

What are the common pathogenic causes of UTI?

A

Escherichia coli

Staphylococcus saprophyticus

Staphylococcus aureus - catheter

31
Q

What are the cells of innate immunity?

A
  • Monocytes/macrophages
  • Neutrophils
  • Dendritic cells
  • Natural killer cells
  • Degranulating cells (mast cells, eosinophils, basophils)
32
Q

What is chronic granulomatous disease?

A

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
Q

Explain how phagocytes recognise microbes

A

Micrboes express pathogen-associated molecular patterns (PAMPs) which are recognised by phagocytes expressing pattern recognition receptors (PPRs)

34
Q

Describe the 2 types of PRRs

A

Collectin - interact with innate immune system

Toll-like receptors

35
Q

What are the molecules are opsonins?

A

Antibodies - IgG, IgM

Complement - C3b, C4b

Mannose-binding lectin

C-reactive protein

36
Q

What are the 3 types of cytokines that macrophages release?

A
  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
Q

Explain acute phase response

A

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
Q

How does complement damage pathogens?

A
  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
Q

What condition results from a mutation in complement cascade? (Hint: C1 inhibitor gene mutation)

A

Herediatory angio-oedema

40
Q

Which MHC class, CD type receptors and T cells are specific for intracellular microbes?

A

MHC I, CD8 T cells causing cytotoxic T cell response

41
Q

Which MHC class, CD type receptors and T cells are specific for extracellular microbes?

A

MHC II, CD4 T cells and activates T helper cells

42
Q

What is graft-vs-host reaction

A

Immune cells of the transplanted tissue recognise the recipitent as foreign, therefore mount immune response

43
Q

What are the 4 P’s of infection prevention?

A
  1. Patient
  2. Pathogen
  3. Practice
  4. Place
44
Q

What is the difference between primary immunodeficiencies and secondary immunodeficiencies?

A

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
Q

Give one example of each primary immunodeficiencies:

  1. B cell deficiency
  2. Phagocyte deficiency
  3. T deficiency
  4. Complement deficiency
A
  • 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
Q

Which interleukin is pyrogenic?

A

Interleukin-1

PPE Revision (16 decks)

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