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ESA3 > Infection > Flashcards

Infection Flashcards

1
Q

Define bacteraemia

A

presence of bacteria in the blood

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2
Q

Define septicaemia

A

generalised sepsis

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3
Q

Define sepsis

A

SIRS + documented/presumed infection

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4
Q

Define severe sepsis

A

SIRS + organ dysfunction/hypoperfusion

shown by hypotension, decreased urine output

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5
Q

Define septic shock

A

severe sepsis + persistent hypotension despite the administration of fluids

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6
Q

What are the symptoms and signs of acute sepsis?

A 
Fever
nausea
headache 
weakness
general muscle aches
abdominal pain
pale and cool extremities
fast pulse and respiratory rate
low blood pressure
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7
Q

What does SIRS stand for?

A

Systemic Inflammatory Response Syndrome

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8
Q

What are the criteria for SIRS?

A 
Two or more symptoms present out of:
•	Temperature 38
•	Heart rate >90bpm
•	Respiratory rate >20/min
•	WBC 12x10⁹/l
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9
Q

How do microorganisms trigger the inflammatory cascade?

A

lipopolysaccharide endotoxins on cell wall of gram-negative bacteria trigger the inflammatory cascade

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10
Q

What happens in the inflammatory cascade?

A

endotoxin binds to macrophages
cytokines released into local environment to recruit reticuloendothelial system
cytokines released into circulation

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11
Q

Why does microvascular thrombosis occur as a result of the inflammatory cascade?

A

cytokines inititate the production of thrombin

cytokines inhibit fibrinolysis

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12
Q

What is the Sepsis Six?

A 
B - blood cultures
U - urine output measurement
F - IV fluids
A - empirical IV antibiotics
L - measure serum lactate
O - high flow oxygen
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13
Q

What kind of organism is Neisseria meningitidis?

A

gram negative

diplococcus

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14
Q

What are the symptoms of meningitis?

A
  • a fever, with cold hands and feet
  • vomiting
  • drowsiness and difficulty waking up
  • confusion and irritability
  • severe muscle pain
  • pale, blotchy skin, and a distinctive rash (although not everyone will have this)
  • a severe headache
  • stiff neck
  • sensitivity to light (photophobia)
  • convulsion or seizures
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15
Q

What are the features of innate immunity?

A

fast
lacks specificity
lacks memory
no change in intensity

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16
Q

What are the main types of phagocyte?

A

macrophage
monocyte
neutrophil

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17
Q

How are pathogens recognised by host cells?

A

PAMPs on microbial structures

recognised by PRRs on phagocytes

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18
Q

How is the attachment of phagocytes to microbes enhanced?

A

opsonisation

C3b

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19
Q

What processes are cytokines involved in?

A

chemoattraction
phagocyte activation
inflammation

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20
Q

How is the complement system activated?

A

alternative pathway

MBL pathway

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21
Q

Describe the alternative pathway of complement system activation

A

C3b deposits on microbial surface

Bb protein binds to form Alternative Pathway C3 Convertase

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22
Q

Which complement proteins are involved in phagocyte (neutrophil/monocyte) recruitment?

A

C3a

C5a

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23
Q

Which complement proteins are involved in opsonisation of pathogens?

A

C3b - C4b

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24
Q

Which complement proteins are involved in killing pathogens and the membrane attack complex?

A

C5 - C9

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25
Q

Define a health care infection

A

infection arising as a consequence of providing healthcare
neither present or intubating at the time of admission
onset at least 48 hours after admission

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26
Q

What kind of organism is Clostridium difficile?

A

anaerobic
gram positive
bacillus

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27
Q

What are common causes of a C diff infection?

A

antibiotic treatment with clindamycin, ampicillin and cephalasporins

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28
Q

What toxins are produced by C diff?

What is their effect?

A

Toxin A - enterotoxin causing excessive fluid secretion and inflammatory response

Toxin B - cytotoxin. disrupts protein synthesis. causes disorganisation of cytoskeleton

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29
Q

What is the treatment for C diff infections?

A

not severe = ten day oral metronidazole

severe = ten day oral vancomycin

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30
Q

What kind of organism is Staphylococcus aureus?

A

gram positive
coccus
facultative anaerobic

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31
Q

What kind of organism is Norovirus?

A

single stranded
RNA
non-enveloped

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32
Q

Which type of immunity is activated for extracellular microbes?

A

humoral immunity

antibodies

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33
Q

Which type of immunity is activated for intracellular microbes?

A

cell dependent immunity

cytotoxic T cells

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34
Q

What are MHC molecules?`

A

molecules inside cells coded for by HLA genes
Selectively bind to peptides produced when proteins are processed inside the host cell
present peptides on the cell surface to T cells with the appropriate TCRs

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35
Q

Which cells express MHC Class I molecules?

A

all nucleated cells

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36
Q

Which cells express MHC Class II molecules?

A

antigen presenting cells

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37
Q

Which cells do MHC Class I molecules interact with?

A

CD8+ - cytotoxic

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38
Q

Which cells do MHC Class II molecules interact with?

A

CD4+ - T helper

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39
Q

What kind of microbes do MHC Class I molecules present peptides from?

A

intracellular

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40
Q

What kind of microbes do MHC Class II molecules present peptides from?

A

extracellular

41
Q

What is the function of CD4+ cells?

A

Release cytokines that regulate the proliferation and differentiation of T cells into helper, memory and regulatory T cells
Cooperate with B cells to enhance the production of antibodies.
induce the migration and activation of monocytes and macrophages, leading to inflammation

42
Q

What is the function of CD8+ cells?

A

On contact with their target cell, they are able to kill the cell.
use granzymes and perforins

43
Q

Which cytokines induce the proliferation of CD4 cells?

A

TNF-alpha

IL-6

44
Q

Where does B cell activation occur?

A

Secondary Lymphoid Organs - spleen, lymph nodes

45
Q

What is the function of plasma cells?

A

antibody production

46
Q

Relate the structure of the spleen to its function

A

red pulp - removal of dead or damaged cells

white pulp - lymphoid tissue

47
Q

What kind of bacteria does the spleen specifically protect against?

A

encapsulated

48
Q

Describe the structure and function of IgA

A

monomer in blood
dimer in secretions

neutralisation on mucosal surfaces (first contact!) and in blood

49
Q

Describe the structure and function of IgG

A

monomer

opsonisation
complement activation
neutralisation

crosses placenta
most abundant

50
Q

Describe the structure and function of IgM

A

pentamer

initial response (Thinking)

51
Q

Describe the structure and function of IgE

A

monomer

mast cell degranulation in parasitic infections and allergic response

52
Q

Describe the structure and function of IgD

A

B cell antigen receptor on cell surface

53
Q

What initiates the production of TH1 Helper cells?

A

IL-12 release by APCs

54
Q

What is the function of TH1 Helper Cells?

A

release of cytokines!!!

produce INF-gamma, TNF beta and IL2
activates macrophages
promotes cytotoxic CD8+ and NK cells
promotes phagocytosis

55
Q

What initiates the production of TH2 Helper cells?

A

IL-4 and IL-5

56
Q

What is the function of TH2 Helper Cells?

A

produce IL-4 and IL-5, IL-10, and IL-13

promotes antibody production by plasma cells
promotes eosinophil recruitment

57
Q

What type of hypersensitivity reaction are TH1 Helper Cells seen in?

A

Type IV

58
Q

What type of hypersensitivity reaction are TH2 Helper Cells seen in?

A

Type I

59
Q

What happens when a macrophage is activated?

A

increased phagocytic ability
increased respiratoty burst activity
increased MHC expression
increased release of cytokines

60
Q

Describe the action of granzymes

A

enter cells

initiate apoptosis

61
Q

Describe the action of perforins

A

form a pore in cells

62
Q

What is the cause of chronic granulomatous disease?

A

unable to produce ROS due to defect in NADPH oxidase
no oxidative burst
phagocytized bacteria cannot be destroyed so granulomas form

63
Q

What is hereditary angioedema caused by?

A

autosomal dominant disease
low levels of the plasma protein C1 inhibitor
inflammatory system activated
episodic swelling of subcutaneous tissue

64
Q

What causes a malaria infection?

A 
Plasmodium:
falciparum, 
vivax, 
ovale 
Malariae
65
Q

What are the presenting features of malaria?

A 
six days to six months post exposure
anaemia
fever
chills
sweats
splenomegaly
hepatomegaly
headache
cough
jaundice
66
Q

Describe the pathogenesis of a malaria infection

A 
mosquito bite
EXOERYTHROCYTIC sporozoites enter blood stream
dormant in liver = hypnozoite
mature and release merozoites
ERYTHTROCYTIC 
invade red blood cells
asexual reproduction inside cell
mosquito bites and ingests
sexual reproduction inside mosquito to from sporozoites
67
Q

What are the risk factors for malaria?

A 
poor
young children
pregnancy
elderly
non-immune eg. travellers
68
Q

Explain, in relation to time of presentation, the most likely causative organism of malaria

A 
falciparum = 7-14 days
vivax = 12-17 days
ovale = 15-18 days
malariae = 18-40 days
69
Q

Explain, in relation to the fever cycle, the most likely causative organism of malaria

A 
falciparum = daily
vivax = tertian (relapse due to dormant parasites in liver)
ovale = tertain
malariae = quartan
70
Q

How is malaria diagnosed?

A

thin blood film

71
Q

State the treatment of malaria

A

Non-falciparum = chloroquine, primaquine

Falciparum = quinine

72
Q

What organism causes typhoid fever?

A

Salmonella enterica serovar Typhi

73
Q

What kind of organism is Salmonella enterica?

A

gram negative
bacillus
facultative anaerobic
fimbriae

74
Q

Why is lymph node enlargement seen is Typhoid fever?

A

Ingested salmonella enter the small intestinal cells via endocytosis.
The bacteria then pass through the endothelial cells to the submucosa
taken up by macrophages which carry the salmonella to the reticuloendothelial system where bacteria multiply intracellularly,

75
Q

What are the symptoms of typhoid fever?

A 
•	Systemic disease – bacteraemia
•	Severe fever
•	Abdominal discomfort
•	Constipation
•	Dry cough
•	Chills and sweats
•	Faint rash on trunk
anaemia
lymph node enlargement
raised LFTs
76
Q

What is the incubation period for Typhoid?

A

10-20 days

77
Q

How is Typhoid treated?

A

axithromycin

ceftriaxone

78
Q

What kind of organism is influenza?

A 
RNA
negative strand
segmented
spherical 
enveloped

Type A B and C

79
Q

What type of influenza is the most common cause of major outbreaks?

A

A

80
Q

What type of influenza is the most common cause of yearly oubreaks?

A

B

81
Q

How are Influenza A serotypes categorised?

A

H - facilitates entry of virus into host cell

N - facilitates release of virions from infected host cells

82
Q

What is antigenic drift?

A

minor mutations to one or both of its surface antigens

83
Q

What is antigenic shift?

A

major and sudden changes in the H and N antigens to produce a new virus subtype

84
Q

What is the incubation period for influenza?

A

1-3 days

85
Q

What are the presenting features of influenza?

A 
Anorexia.
Malaise.
Headache (retro-orbital).
Fever.
Myalgia.
Non-productive cough and sore throat.
86
Q

How is influenza managed?

A

Conservative

Oseltamivir and zanamivir reduce replication of influenza A and B

87
Q

what does it mean if a patient is immunocompromised?

A

the patient’s immune system is unable to respond appropriately and effectively ot infectious organisms

88
Q

What organism is often the cause of infection in those with cystic fibrosis?
why?

A

Pseudomonas aeruginosa

produces mucopolysaccharide, forming a biofilm, making it hard to phagocytose.

89
Q

What is the difference between a primary and secondary immunodeficiency?

A 
primary = intrinsic 
secondary = underlying disease or condition affecting the immune components. Decreased production or increased loss/catabolism.
90
Q

What are the causes of neutropenia because of deceased production?

A 
b12/folate deficiency
malignancy infiltrating bone
aplastic anaemia
drugs
viruses
congenital disorders
91
Q

What are the consequences of neutropenia?

A

severe life threatening bacterial or fungal infections

92
Q

Name infections that patients with a neutropenia get

A

catalase positive staphylococcal

invasive Aspergillus

93
Q

What leads to suspicion that a patient immunocompromised?

A 
Infections that are:
Severe
Persistent
Unusual
Recurrent
94
Q

If a patient is T cell deficient, what kind of infections are they susceptible to?

A

viral and fungal infections

PCP, VZV, CMV and EBV

95
Q

How are patients with T cell deficiency managed?

A

no live vaccines
CMV- blood products
prophylactic antibiotics
bone marrow/stem cell transplants

96
Q

If a patient is B cell deficient, what kind of infections are they susceptible to?

A 
frequent LRT and URT infections 
GI complications (Giardia).
97
Q

How are patients with B cell deficiency managed?

A

antibiotic prophylaxis

Ig replacement

98
Q

If a patient is phagocyte deficient, what kind of infections are they susceptible to?

A

prolonged and recurrent infections
catalase positive staphylococcal
invasive Aspergillus
SEPSIS

99
Q

How are patients with phagocyte deficiency managed?

A

prophylactic antibiotics
interferon-g (increases phagocyte activity)
stem cell transplant

ESA3 (5 decks)

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