Infectious disease Flashcards

1
Q

What is infection?
What is an infectious disease?

A

Infection = invasion and growth of an organism in a host
Infectious disease = When an infection leads to host damage and injury

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2
Q

What is pathogenesis?
What is a pathogen?

A

Pathogenesis = the mechanism by which a disease is produced
Pathogen = disease causing organism e.g. bacteria

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3
Q

What is a communicable disease?
What is a zoonotic disease?

A

Communicable = disease that can be spread from one person to another
Zoonotic = Disease spread from animals to humans

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4
Q

What are primary pathogens?
What are opportunistic pathogens?

A

Primary pathogens = cause disease in someone even if they have a fully functioning immune system

Opportunistic pathogens = take the opportunity to cause disease when the immune system is weakened

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5
Q

What is the principle behind Koch’s postulates and what are the 4 Koch’s postulates

A

Principle = figuring out which organism caused the disease

  • Pathogen must be found in all hosts with the disease but not in healthy individuals
  • The pathogen must be isolated from a diseased host and be able to be grown in pure culture
  • When given to a healthy individual, the pathogen must reproduce the disease of the original case
  • The pathogen can be isolated and grown in pure culture from the newly-infected host
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6
Q

What do fimbriae/pili do on bacteria and what is pilin variation?

A

Finger like projections, allow the bacteria to adhere to the host cell

Pilin variation = Bacteria contain different pili that could be expressed, but only one type of pili is actually expressed
Through the course of infection, the bacteria can vary the type of pili protein expressed to a different type at random, preventing the immune system from recognising the different pili proteins
(diagram in jotter)

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7
Q

What is virulence?

A

The severity of disease caused by the pathogen

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8
Q

What are virulence determinants and what are the 2 types?

A

Virulence determinants = component of the bacteria that has the ability to harm the host

2 types:
- Extracellular determinants = products made and secreted by the bacterial cell
- Cell surface determinants = determinants that are held on the surface of bacteria

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9
Q

What are exotoxins and what are the 3 classes of exotoxins, including what effect each class has?

A

Exotoxins = secreted toxins (extracellular determinants)

Classes:
- Neurotoxins = damages the neurons/nervous system
- Cytotoxins = kills the cell
- Enterotoxins = harms the intestines and digestive system

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10
Q

What are the 2 main parts to exotoxins and what are they responsible for?

A
  • B part = binds the exotoxin to the host cell
  • A part = is active and responsible for the specific toxic effects
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11
Q

What are exoenzymes and what do they do?

A

Work more locally by degrading the tissue to promote the spread of the bacteria deeper into the tissue

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12
Q

What type of bacteria are endotoxins found on?
What are endotoxins also referred to as and what are the 3 distinct regions, including what their functions are?

A

Gram-negative
Lipopolysaccharides (LPS)

Contains:
- O-polysaccharide chain = specific to the species of gram-negative bacteria its found on (O-specific chain)
- Lipid A = hydrophobic molecule which anchors the whole LPS molecule to the cell surface of the target cell. Also educes the toxic activity to the target cell (different effects depending on the structure of this part
- Core = links the O-specific chain and Lipid A parts together

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13
Q

What do our cells do in defence of an endotoxic infection? (4)

A
  • Our cells activate macrophages, which release cytokines
  • Cytokines activate complements
  • Compliments activate the coagulation cascade
  • This causes local inflammation and swelling to occur
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14
Q

What is sepsis and what does this cause (5)?

A

When the LPS (endotoxins) spreads from the local inflammation to the rest of the body
Causes fever, vasodilation, hypotension, thrombosis, and organ failure which leads to death

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15
Q

What are the 4 big differences between exotoxins and endotoxins?

A

Table in jotter
Chemical nature :
Exotoxins = proteins which can be denatured
Endotoxins = LPS

Location (on bacteria):
Exotoxins = Extracellular, secreted
Endotoxins = Cell surface attached

Potency (damaging effect):
Exotoxins = Relatively high
Endotoxins = Relatively low

Type of bacteria found in:
Exotoxins = Both gram-positive and gram-negative
Endotoxins = Just gram negative

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16
Q

What is innate immunity?
What are 2 examples of innate immunity components? (just names)

A

Non-specific first line of defence, always present and acts quick. Acts the same way each time.

Phagocytic cells and complement

17
Q

What are 2 examples of phagocytic cells?
How does phagocytosis work (include examples 2 of phagocytic receptors)? (3)

A

Examples = Macrophages and Neutrophils

  • Cell have pattern recognition receptors to recognise “foreign” molecular patterns from pathogens (recognises when a foreign molecule binds to the receptor) - including C3b and Fc receptors
  • Cell holds the pathogen in a vacuole and a reactive oxygen species/enzymes are released into the vacuole to destroy the pathogen
  • Danger signals are also released to attract more immune cells to the site of infection
18
Q

What is compliment?
How is the signal amplified?

A

Family of enzymes that are present in blood as an inactive precursor
Become active upon stimulation by a signal

Initial small signal can simulate many molecules through a positive compliment cascade

19
Q

What are the 3 pathways that active compliment and how does each activate the compliment?
What is the active enzyme formed called?

What are the 3 outcomes of this?

A

Classical = Antigen/antibody complex
Alternative = Surface of pathogen
Lectin = Mannose sugar on pathogen surface

Active enzyme = C3 Convertase

Outcomes:
- Vascular permeability is increased to recruit immune cells to site of infection
- Opsonization = coats foreign organisms in compliment protein to help phagocytes recognise the organism as foreign and engulf it
- Membrane Attack Complex (MAC) = punches hole in the pathogen membrane, causing lysis of the pathogen (destroys it)

Diagram of this on summary sheet

20
Q

What is adaptive immunity?
What are the 2 molecules involved in adaptive immunity?

A

Specific, second line of defence, takes longer to develop and produces a quicker response on second exposure (memory)

B Cells - Antibodies
T cells - Helper cells (cytotoxic/regulatory cells)

21
Q

What does the variable region of B-cells (antibodies) contain?

What does the constant region determine and what are the 4 different types?

How does the antibody change during the course of infection, and what does this depend on?

A

Variable region = VDJ recombination, random combinations of segments of the V, D, and J genes join together to make the variable part specific

Constant region determines the class of antibody
3 Classes:
- IgM, always the first antibody produced in the immune response
- IgA
- IgE
-IgG

Class switches from IgM to IgG, IgE, or IgA
Depending on the environment the B cell is in (on the type of infection)

22
Q

What do T cell receptors recognise and what are these?

What type of receptors on which molecules recognise which class of MHC?

What does the class of MHC indicate?

A

Recognise surface markers: MHC and processed antigens displayed on the surface of infected cells

CD8 receptors on T Cytotoxic (Tc) cells recognise MHCI
CD4 receptors on T helper cells (Th) cells recognise MHCII

Class of MHC indicates the peptide origin and helps for an appropriate response to be initiated
(all on summary sheet)

23
Q

What type of cells produce MHCI surface signals and how are they produced?

A

All nucleating cells

Cytosolic proteins, including intracellular pathogens, are degraded to peptides via the proteosome.
These peptides then bind to MHCI on the surface of the cell, and the peptide-MHCI complex acts as a cell surface marker to indicate the cell is infected
(on summary sheet)

24
Q

What response is initiated when Tc cells recognise MHCI surface markers?

A

Tc cells kill the infected cell by inducing apoptosis through the use of perforin, granzymes and FAS ligands
(On summary sheets)

25
What type of cells produce MHCII surface signals and how are they produced? (4 steps)
Only occurs in macrophages and B cells - Antigens from outside the cell are taken up into intracellular vesicles - Proteases degrade the antigen into fragments (peptides) - Vesicles containing the antigen fragments fuse with vesicles containing MHCII, allowing the fragments to bind to MHCII - MHCII, containing antigen fragments, is then presented to the cell surface to be recognised by a Th cell (all on summary sheet) (diagram in jotter)
26
What response is initiated when Th cells recognise MHCII surface markers? How does memory work and what do stimulated B cells mature into?
Th cells tell other cells to release cytokines (to induce apoptosis) and tell B cells to produce antibodies (on summary sheet) Mature onto plasma cells and memory cells Memory cells on repeat exposure to the same pathogen rapidly secrete high levels of antibody
27
How do natural killer cells work? (3)
- Recognise infected cells - Kills infected cells by releasing granules containing perforins and granzymes - Induces apoptosis of the infected cell
28
What are the 3 main differences between Innate and Adaptive immune responses?(table in jotter)
Innate = quick response time Adaptive = longer response time Innate = responds the same way with repeated exposure Adaptive = Adapts to repeated exposure Innate = non-specific Adaptive = specific
29
What are the 5 ways pathogens can evade the immune system? (just names)
- Antiphagocytic strategies (inhibit the functions of phagocytes) - Anti-complement structures - Molecular mimicry/camouflage - Release of soluble antigen - Antigenic variation (changes antigens)
30
What are the 4 pillar of control?
Diagnosis, Treatment, Prevention, and Education
31
What are the 2 types of antimicrobials and how are they different? What can resistance be acquired from?
Cidal = kills the pathogen Static = stops the pathogen from replicating, allowing the immune system more time to kill it naturally May be natural, or acquired from mutations or gain of extrachromosomal DNA
32
What are vaccines based off of and what is the lag phase? What is herd immunity?
Memory - Mimics natural infection so that the immune system is prepared and can produce a quick secondary response Lag phase = time taken for the immune system to react to the infection and produce enough antibodies to fight the infection. Lag phase is much shorter in secondary response Herd immunity = Transmission of a disease is reduced/stopped in a population if enough individuals are immunised against that disease
33
What are the 6 different types of vaccines and what do they contain?
- Inactivated/dead pathogens - Toxoids - vaccines against exotoxins - DNA/RNA that codes for specific antigens from a pathogen - Attenuated line = pathogen is still kept alive but virulence of it is reduced (made less harmful) - Subunit (conjugate - parts of pathogens) - Viral vectors = delivers DNA for an antigen into a host cell
34
What disease does the variola virus cause?
Small pox
35
What is HIV and how is it transmitted? What does HIV cause? What is the mechanism of HIV?
Retrovirus - has RNA dependant DNA polymerase Transmission = sexual contact/blood/giving birth Causes many opportunistic infections such as AIDS Mechanism: Gp120 binds to the CD4 receptor and causes a conformational change, allowing the coreceptor to binds and for the viral membrane to fuse with the host cell membrane, allowing the virus to infect the cell.
36
How do antimicrobials work against HIV and what other treatments can be used + what do they do? What are the issues with trying to create a HIV vaccine? (2)
Antivirals stop the virus infection at different stages of the HIV life cycle Treatments = ART/HAART and drug combinations that delays resistance to the antimicrobials Issues = No one can naturally clear HIV from their system, so we don't have a reference for what we want the vaccine to do Genetic variability is also a challenge
37
What is Malaria caused by? What is the treatment available? What prevention methods are in place? (3)
Caused by organism called plasmodium falciparum which is transmitted by the bite of a female mosquito. Has a complex life cycle. Treatment = chemical based therapies, drug resistance can be an issue Prevention = prophylactic drug treatment (prevent the disease before it occurs), reduce vector, vaccines
38
What is Tuberculosis caused by (incl. how the organism is weird) and how does it spread? What does it cause? How can the tuberculosis by reactivated?
Caused by a microbe called myobacterium tuberculosis, which have unusual cell walls containing Arabinogalactan and Mycolic acids Spread by infected aerosols Causes lung disease, but can also spread to other parts of the body Reactivated as the microbe can survive intracellularly in macrophages and inhibit the fusion of lysosomes with phagosomes
39
What treatment is available for tuberculosis and what does it do? What is the vaccine available for it, what is it made of and how is it affective or not?
Treatment = drugs such as Isoniazid, which inhibits mycolic acid synthesis, problems with resistance BCG vaccine, made from weakened from of a closely related bacteria called M.Bovis Only effective for severe TB forms, not against common versions