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Semester 2 Missed Lectures > Infection > Flashcards

Infection Flashcards

1
Q

What is the microbiota and when does it become harmful?

A

It is the normal community of microorganisms that are carried on the skin and mucosal surfaces that don’t usually cause harm, and can be beneficial.

The microbiota becomes harmful when they are displaced or when there is multiplication of the microbes.

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2
Q

Explain the two types of inhalation infection mechanisms?

A

Droplets - large particles that are suspended in the air for a short period of time, at a close distance that fall onto surfaces.

Aerosols - small particles that are suspended in the air for a long period of time and can travel a great distance.

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3
Q

What is bacteriology and what are some methods it uses?

A

The detection of a specific bacterium.
It is detected by:
- Taking specimens through swabs, fluids or tissues and culturing.
- Microspcopy of bacterial and patient cells.
- Antibiotic susceptibility testing.
- Antigen detection.
- Nucleic acid detection through PCR.

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4
Q

What is virology and what are some methods it uses?

A

The detection of a specific virus.
It is detected by:
- PCR, detecting the viral nucleic acid.
- Antibody detection.
- Antigen detection, using ELISA.

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5
Q

How do cytolytic toxins cause symptoms?

A

They damage membranes.

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6
Q

How do AB toxins work?

A

They are a two-part toxin, where the B antigen binds to the cell and delivers the A antigen to the cytosol to interfere with cell function.

A toxins are often enzymes.

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7
Q

How do superantigens cause symptoms?

A

They are microbial proteins that bind to MHC class II molecules and T-cell receptors, activating T cells.

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8
Q

How do enzymes cause symptoms?

A

They destroy tissues, facilitating the invasion of bacteria.

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9
Q

What are endotoxins, and how do they cause symptoms? What type of bacteria are they found on?

A

They are cell-wall components, usually lipopolysaccharide complexes, that can damage host cells directly or stimulate an immune response.
They are found on gram negative bacteria.

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10
Q

What are some differences between exotoxins and endotoxins?

A

Exotoxins are released to enhance the survival of a bacterium, whereas endotoxins are released upon cell death.

Exotoxins are more toxic than endotoxins.

Exotoxins are heat labile, whereas endotoxins are heat stable.

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11
Q

How does alcohol gel and soap work?

A

Alcohol gel works by dissolving the lipid membrane of bacteria, killing them.

Soap works by washing the pathogens off the skin, not killing them.

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12
Q

What is debridement?

A

The removal of infectious tissue, preventing the spread of infection.

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13
Q

Physiologically, who are more likely to get infections?

A

Elderly people - over the age of 65.
Children under the age of 5.
Pregnant women.

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14
Q

When the normal flora in the intestine and vagina is depleted by antibiotics, what can happen?

A

In the intestine, clostridium difficile can develop.
In the vagina, vaginal thrush can develop.

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15
Q

Where are monocytes found and what do they become?

A

They are present in the blood.
When they are recruited to the site of infection, they differentiate into macrophages in tissues.

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16
Q

Where are neutrophils predominantly found, and what happens to them during an infection?

A

They are normally present in the blood.
During an infection, they:
- Proliferate.
- Are recruited by chemokines to the site of infection.
- They phagocytose bacteria.

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17
Q

What are the functions of basophils/ mast cells, eosinophils, natural killer cells, and dendritic cells?

A
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18
Q

Which toll like receptor detects lipopolysaccharides of gram-negative bacteria and lipoteichoic acids are gram positive bacteria?

A

TLR4.

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19
Q

Which toll like receptor recognises lipoproteins of gram negative bacteria, peptidoglycans of gram positive bacteria and mycobacteria?

A

TLR2.

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20
Q

What are the oxygen-dependent and oxygen-independent pathways of phagocytes?

A

Dependent - respiratory burst - hydroxyl radicals, superoxide radicals, etc.

Independent - lysozyme, transferrin, cationic proteins, and proteolytic and hydrolytic enzymes.

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21
Q

What is the classical pathway of complement activation?

A

Antibody-antigen interaction.

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22
Q

What are some macrophage-derived cytokines and their systemic and local actions?

A
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23
Q

What is the cell wall of bacteria?

A

A peptidoglycan layer.

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24
Q

What is the capsule of bacteria, and what does it do?

A

A polysaccharide, that facilitates adherence to surfaces and protection from antibodies and phagocytosis.

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25
Q

What is the gram stain for streptococcus mutans and where is it normally found?

A

Gram positive cocci in chains.
It is normally found in the oral cavity.

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26
Q

When should a patient be screened for sepsis?

A

They have a presumed or confirmed infection with:
- NEWS score of 5 or more.
- At risk of neutropenia.
- Clinician is concerned about the patient.
- Evidence of organ dysfunction, e.g., raised lactate.

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27
Q

What do the NEWS2 score test on?

A

Breathing rate.
Oxygen saturation.
Heart rate.
Temperature.
Level of consciousness.
Systolic blood pressure.

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28
Q

What is red flag sepsis?

A

NEWS2 being 7 or above, or 6 and above with one of:
- Lactate over 2mM.
- Chemotherapy in the last 6 weeks.
- Organ failure.
- Patient looks unwell (grey and mottled).
- Patient is deteriorating.

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29
Q

What is amber flag sepsis?

A

NEWS2 5 or above, or 1-4 with at least one of:
- Lactate > 2mM.
- Chemotherapy in the last 6 weeks.
- Patient looks unwell (grey and mottled).
- Patient is deteriorating.
- Organ failure evident.

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30
Q

What is the sepsis 6?

A

Get senior help.
Give oxygen.
Take bloods and cultures - look at lactate and for specific bacteria.
Give IV antibiotics.
Give IV fluids if required to correct hypovolaemia.
Monitor urine output.

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31
Q

Which organisms commonly cause sepsis?

A

Neisseria meningitidis
Streptococcus pyogenes/ pneumoniae.
Staphylococcus aureus.
Enterococci.

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32
Q

What types of infections are more common in HIV?

A

Opportunistic infections, such as Candida albicans.
Latent infections, such as with varicella zoster.

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33
Q

What is the structure of HIV?

A

It is a single stranded RNA retrovirus.

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34
Q

Why do other STIs increase the risk of HIV contraction?

A

They can cause breaks in the skin or mucosa.

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35
Q

What is the definition of hepatitis?

A

Inflammation of the liver.

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36
Q

What does an increased alkaline phosphate show?

A

Biliary tract damage.

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37
Q

What are the 3 causes of an ALT>1000?

A

Viral hepatitis.
Blood clots.
Drugs/ medication.

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38
Q

What is the most common transmission of hepatitis B?

A

Vertical transmission.

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39
Q

What is the significance of the e-antigen for hepatitis B?

A

It is highly infectious.

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40
Q

What are naive T cells and effector T cells?

A

Naive T cells are T cells that have not previously encountered an antigen.

Effector T cells are T cell that have previously encountered the antigen and are capable of performing effector functions during an immune response.

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41
Q

What is the innate and adaptive response to extracellular microbes?

A

Innate = phagocytosis and complement system activation.

Adaptive = humoral response - antibody production.

42
Q

What is the innate and adaptive immune response to intracellular microbes?

A

Innate = natural killer cells, and interferons.

Adaptive = cell-mediated immunity - cytotoxic T cells.

43
Q

What gives MHC molecules their highly polymorphic ability?

A

They have variable peptide binding clefts, which can be different for different people.

44
Q

What are the different HLA types of MHC class I and MHC class II molecules?

A

Class I = HLA-A, -B, -C.
Class II = HLA-DP, -DQ, -DR.

45
Q

What types of cells express MHC class I and MHC class II molecules?

A

MHC class I = all nucleated cells.
MHC class II = antigen-presenting cells.

46
Q

Outline some persuasive interventions for antimicrobial stewardship.

A

Education.
Reminders.
Audits.
Feedback.

47
Q

Outline some restrictive interventions for antimicrobial stewardship.

A

Automatic stop orders.
Prior authorisation.
Formulary restriction.
Restricted susceptibility reporting.

48
Q

Outline some structural interventions for antimicrobial stewardship.

A

Rapid lab tests.
Expert systems.
Quality monitoring.
Computerised records.

49
Q

What could some problems with ineffective antimicrobial stewardship be?

A

Under-prescribing antibiotics, worsening health outcomes.
Automatic stop orders could prevent immediate action when required.

50
Q

Where are B and T lymphocytes produced and matured, respectively?

A

They are both produced by the bone marrow.
T-cells are matured in the thymus.
B-cells are matured when they come into contact with antigens.

51
Q

Where are B and T lymphocytes found?

A

Mucosa-associated lymphoid tissue.
Lymph nodes.
Spleen.

52
Q

When does lymphadenopathy occur?

A

When B and T cells are activated and proliferate.

53
Q

What 3 signals are required for T-cell activation?

A

1) MCH class I molecules displaying the peptides to T-cell receptors.

2) CD28 protein is activated by the B7 protein.

3) Cytokines released.

54
Q

What do the cytokines released to CD4+ cells determine?

A

The different T-helper cells that are formed.

55
Q

What cytokines are required for the formation of T-helper cell 1, and what is its functions?

A

IL-12.

Functions:
- IgG and IgA production from B-cells.
- Activation of cytotoxic T cells.
- Recruitment and activation of macrophages.

56
Q

What cytokines are required for the formation of T-helper cell 2, and what are its functions?

A

IL-4.

Functions:
- Production of IgE from B cells.
- Activation of eosinophils.
- Activation of mast cells.

57
Q

What cytokines form T-helper cell 17, and what are its functions?

A

IL-1 or IL-6.

Functions:
- Neutrophil recruitment and activation.

58
Q

What cytokines stimulate naive T-cells to form Treg, and what are its functions?

A

IL-10 and TGF-beta.

Functions:
- Immune suppression.
- Tolerance.

59
Q

What types of molecules are recognised by B-lymphocytes?

A

Macromolecules like proteins, lipids and nucleic acids.
Micromolecules.

60
Q

Explain the 3 stages of B-lymphocyte activation.

A

1) B-cell receptor engagement - antigens binding to the B-cell receptor.

2) T-cell receptor engagement - antigen from the T-cell activate the T-cell receptor, and B7 proteins are activated by CD28 proteins.

3) Cytokines and CD40 activation.

61
Q

What cytokine stimulates the production of IgG?

A

IFN-gamma.

62
Q

What cytokine stimulates the production of IgA?

A

TGF-beta.

63
Q

What is a surface?

A

An interface between a solid and a liquid or gas.

64
Q

What feature on bacteria allow for adherence to the human cell membrane?

A

Pili or fimbriae.

65
Q

What does quorum sensing control?

A

Sporulation.
Biofilm formation.
Virulence factor secretion.

66
Q

What are the 3 methods that quorum sensing produces its effects?

A

Signalling molecules such as autoinducers.
Receptors.
Gene expression.

67
Q

What are the requirements for it to be classed as a healthcare infection?

A

They did not have the infection or incubated with the infection prior to hospital admission, meaning that they developed symptoms at least 48 hours after admission.

68
Q

Give an example of a viral, bacterial, fungal and parasitical healthcare infection pathogen.

A

Viral = influenza, varicella zoster, norovirus.
Bacterial = MRSA, clostridium difficile, mycobacterium tuberculosis.
Fungal = Candida albicans and aspergillus.
Parasitical = malaria.

69
Q

What are some interventions of the built environment that prevent healthcare infections?

A

Toilet availability.
Wash hand basins.
Space for patients.
Pressure differences in rooms.

70
Q

What 3 cleaning methods should be used?

A

Disinfectants.
Steam cleaning.
Hydrogen peroxide vapour.

71
Q

What causes an infectious dose to vary?

A

The type of micro-organism it is.
Immunity of the host.
Where the micro-organism infects.
The presentation of the micro-organism.

72
Q

What are neglected tropical diseases?

A

Diseases that have very little funding, and have certain stigma associated to them. They are associated with poor outcomes.

73
Q

Give an example of an acute, sub-acute and chronic incubation period disease.

A

Acute = shigella.
Sub-acute = malaria.
Chronic = HIV.

74
Q

What is the most severe species of malaria, and what is the species associated with zoonotic transfer?

A

The most severe is plasmodium falciparum.
The species associated with zoonotic transfer is plasmodium knowlesi.

75
Q

What is the blood film appearance of malaria?

A

They are ring-like structures within red blood cells, due to the development of merozoites.

76
Q

Why would primaquine be given to a patient with malaria?

A

It is good for killing malaria that is dormant in the liver.

77
Q

What is given as a first line treatment for malaria?

A

Quinine and doxycycline.

78
Q

What is the vector for malaria?

A

Female anopheles mosquitos.

79
Q

What should be done before giving primaquine to a patient?

A

Ensure that they do not have a G6PDH deficiency as primaquine requires GSH to be removed from the body.

80
Q

What are the types of salmonella that cause food poisoning?

A

Salmonella enteritidis.
Salmonella typhimurium.

81
Q

What are the complications of food poisoning salmonella?

A

Bacteraemia and sepsis.
Deep-seated infections for immune compromised hosts.

82
Q

What sex does Burton’s disease more commonly affect?

A

Males.

83
Q

What is the most common immunodeficiency in antibody production that requires treatment?

A

Common variable immunodeficiency.

84
Q

What is the most prevalent primary antibody deficiency?

A

Selective IgA deficiency - this often is asymptomatic.

85
Q

What chromosome is affected by DiGeorge syndrome, and what does it lead to?

A

Chromosome 22 defect, leading to a T-cell defect.
This is because there can be developmental defects in bodily systems, such as the thymus and splenic deficiencies.

86
Q

What non-infectious conditions are associated with antibody deficiencies?

A

Autoimmune conditions.
Malignancies.

87
Q

What is the genome of the influenza virus?

A

Orthomyxovirus.

88
Q

What is the incubation period of influenza?

A

1-5 days.

89
Q

What investigations can be done to diagnose flu?

A

Rapid diagnostic tests for antigen detection.
RT-PCR.
Rapid molecular assay for viral RNA detection.

90
Q

What is the breakdown for trivalent and quadrivalent influenza vaccines, and who are each given to?

A

Trivalent = 2 A strains and a B strain. It is given to adults.

Quadrivalent = 2 A strains and 2 B strains. It is given to children.

91
Q

What is the replication time of influenza?

A

6 hours.

92
Q

What does antigenic drift and antigenic shift of influenza cause, respectively?

A

Antigenic drift causes seasonal epidemics.
Antigenic shift causes pandemics.

93
Q

What is the major surface antigen of COVID-19?

A

Spike glycoprotein.

94
Q

What do lateral flow tests detect for COVID-19?

A

The spike protein.

95
Q

Where is E. Coli normally found in the microbiota, and what can it protect against?

A

The large bowel.
It can protect against salmonella.

96
Q

What colour do alpha-haemolytic, beta-haemolytic and gamma-haemolytic streptococci turn a blood agar plate?

A

Alpha-haemolytic turn the plate green due to partial haemolysis.

Beta-haemolytic turn the plate white due to complete haemolysis.

Gamma-haemolytic do not change the colour of the agar as they do not cause haemolysis.

97
Q

Why are bacteria haemolytic?

A

Because it breaks down the red blood cells, releasing haemoglobin, which contains iron. Iron is required for bacterial replication.

98
Q

What are the Lancefield and Sherman classifications?

A

Lancefield is a serological classification of streptococci, looking at the different bacterial antigens.

Sherman is a classification, splitting streptococci into pyogenic, viridans and, enterococcus and lactic streptococci.

99
Q

How can streptococcus pyogenes keep causing infections?

A

As there are over 150 serotypes of the M-protein, different strains can keep causing the infections.

100
Q

How is streptococcal pharyngitis diagnosed?

A

A swab of the exudate can be cultured and tested via a gram stain.

101
Q

How do streptococcal pyrogenic exotoxins cause infection?

A

It cleaves IgG bound to streptococcus pyogenes, preventing it from being opsonised and phagocytosed.

Semester 2 Missed Lectures (5 decks)

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