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All TP1 and Some TP2 > Infection 1+2 > Flashcards

Infection 1+2 Flashcards

1
Q

What is infection?

A

Invasion of a host’s tissue by microorganisms

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2
Q

6 microorganism types that can cause infection

A 
• Bacteria - 
	• Viruses  - e.g. covid
	• Fungi 
	• Protozoa = e.g. malaria 
	• Helminths (worms) 
Prions
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3
Q

5 ways of infection transmission

A
  • Person to person (touch, air droplets, sexually)- Influenza, SARS-CoV-2, EBV, HIV
  • Water – Cholera, Hep A
  • Food – E.coli, Salmonella
  • Insects – Malaria (mosquitos)
  • Surface (touching, hand hygiene) – MRSA
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4
Q

2 types of transmission

A

Direct

Indirect

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5
Q

Direct transmission

A

→ disease caused by direct contact to disease from the resevoir (disease carrier) to host

Eg. Droplet transmission - coughing respiratory droplets

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6
Q

Indirect transmission

A

→ diseases caused by transmission through an intermediary source

Eg. Air borne, vehicle (food, water), vectors

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7
Q

6 things to ask about in history taking

A
  • Details of symptoms
  • Time since first exposure
  • Contacts (including sexual partners)
  • Environment (damp building, air conditioner, overcrowding like Tb)
  • Food/drink
  • Travel
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8
Q

What are markers of infection

A

Generalised signs of infection

- not everyone has the exact same

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9
Q

7 markers of infection - patient symptoms

A
  • Rise in temperature
    • (in some cases temperature may go down)
  • General malaise
    • (lethargy, body ache, head ache, loss of appetite, eg influenza)
  • Pain
    • (eg general muscle pain in a number of infections, abdominal pain in Hepatitis, abdomen tender to touch, at site of infection)
  • Breathlessness
    • (chest infection including pneumoniae)
  • Local skin changes
    • (eg impetigo –blisters and sores on the skin Cellulitis- redness, heat, pain at the site of infection necrotising faschiitis – deep skin infection)
  • Cough
    • (dry cough eg whooping cough productive cough - purulent sputum eg tuberculosis)

• Confusion (eg meningitis, sepsis)

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10
Q

Virulence factors

A

→ molecules produced by bacteria’ fungi and protozoa that add to their effectiveness
- enable them to achieve colonisation in the host

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11
Q

3 things that determine severity of disease

Pathogen level

A
  • Virulence factors
  • inoculum size (size of pathogen)
  • antimicrobial resistance
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12
Q

2 things that determine severity of disease

Patient level

A
  • Site of infection

- co-morbidities

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13
Q

2 general tests for infection

A
  • White blood cell count

- c-reactive protein

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14
Q

White blood cell count

A

• Generally increase in WBC when someone has infection BUT in some cases cells may decrease for example CD4+ cells in HIV

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15
Q

C-reactive protein

A

Increase in C-reactive protein is a marker of infection and inflammation).
• In a study by Wang (2020) CRP levels positively correlated with lung lesions and could reflect disease severity in the early stage of COVID-19 infection)

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16
Q

How do doctors know that patients have infection?

A
  • History, examination, investigations
  • full blood count
  • c-reactive protein
  • liver kidney function tests
  • Imaging
  • histopathology
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17
Q

5 ways to identify bacteria

A
  • Direct microscopy after staining (Gram stain, acid fast stain) - look at shape and size
  • Blood culture (growth and identification) let bacteria in blood grow so you can see if it is there
  • Swabs (direct staining and microscopy or growth in appropriate medium)
  • Nucleic acid amplification/PCR (faster genetic methods)
  • Antigen tests
  • Antibody tests
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18
Q

3 ways to identify viruses

A
  • Detection of antigens using Elisa/immunofluorescence - look for antigen and match to virus
  • Nucleic acid amplification/PCR
  • Antibody tests
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19
Q

Features of prokaryotes

A
  • Circular dna and plasmids
  • no nucleus
  • no membrane bound organelles
  • cell wall normally made of peptidoglycan
  • no carbs in plasma membrane
  • 70s ribosomes
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20
Q

Features of eukaryotes

A
  • chromosomes
  • nucleus
  • membrane bound organelles
  • cell wall only in plant cells
  • carbs and sterois in plasma membrane
  • ribosomes 80s
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21
Q

What are commensals?

A

• Commensals are microorganisms (normally bacteria) that live on the surface of our bodies and in specific areas eg intestinal tract, oral cavity, vagina

  • Known as microbiome = all of the commensals together
    • Live in harmony with us don’t normally cause disease
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22
Q

Antibiotics and commensals

A

• Antibiotics can destroy commensals, e.g. leave to yeast infections and thrush in cavities

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23
Q

Naming organisms

A
  • Genus + species. (“Surname + first name”) for example: Staphylococcus aureus (Staph aureus, S. aureus)
    • Names are sometimes supplemented by adjectives describing growth, typing or antimicrobial susceptibility characteristics, for example E coli 0157, MRSA (methicillin resistant Staph aureus)
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24
Q

bacteria cell structure

A
  • Plasmids
    • Ribosomes
    • Cell wall - peptidoglycan
    • Food granule
    • Plasma membrane
    • Chromosome – nucleoid region
    • Flagellum
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25
Q

4 categories of oxygen tolerance

A
  • Aerobes – can survive in the presence of oxygen
    • Obligate aerobes –require oxygen for survival
    • Anaerobes – can survive in the absence of oxygen - gas gangrene release gas results in amputation
    • Obligate anaerobes –require oxygen-free environment for survival (unless able to form spores)
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26
Q

3 bacterial shapes

A

Coccus = bacteria in circular shape ( clusters or chains)
Spirillus= bacteria in spiral shape
Bacillus - bacteria in a rod shape

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27
Q

Arrangement of cocci bacteria

A
  • Clusters = cocci like a bunch of grapes

* Chains = cocci in a row

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28
Q

5 mechanisms of bacterial pathogenesis

A

Virulence factors –> enable bacteria to establish and cause infection chostentry)

  • Evasion of immune system – bacteria escapes immune system(e.g. polysaccharide capsule outside bacteria, so antigens are covered)
  • Adherence to host cells (e.g. pili and fimbriae)
  • Invasiveness (e.g. enzymes such as collagenase – to breakdown collagen)
  • Toxins
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29
Q

2 types of toxins

A

Endotoxins

Exotoxins

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30
Q

Exotoxins

A

→ toxin secreted by bacteria, released outside the cell
- damages host by destroying cells or disrupting normal cellular metabolism

e.g.diphtheria toxin – produced into environement

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31
Q

Endotoxins

A

→ bacterial toxins consisting of lipids loccited within a cell

Eg. Lipopolysaccharide

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32
Q

Endospores

A

-> almost go to sleep in bad environments and then wake up in suitable environments
• Some bacteria develop endospores to survive lack of nutrients or other adverse environmental factors
• The genetic material is preserved within spores
• spores are Highly resistant form which can withstand chemicals and extremes of temperature

Examples are Clostridium difficile, Bacillus cereus

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33
Q

What are gram positive bacteria

A

• Thick outer layer of peptidoglycan which can retain blue dye (methodine blue) so bacteria appear purple

  • lack an outer membrane space
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34
Q

What are gram negative bacteria

A
  • Much thinner outer layer of peptidoglycan, methodine blue purple colour is removed as it doesn’t stick to the layer
    • When counterstaining with pinkish dyes, these counter dyes are retained so bacteria appears pink
  • have an extra periplasmic space between peptidoglycan layer and outer membrane
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35
Q

Gram positive cocci

A
  • Staph aureus
  • coagulase negative staph
  • alpha haemolytic strep
  • beta haemolytic strep
  • strep pyogennes
  • strep pneumoniae
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36
Q

Gram postive baccili

A

Bacillus cereus

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37
Q

Gram negative cocci

A
  • Neisseria meningitidis

- neisseria gonorrhea

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38
Q

Gram negative bacilli

A
  • E.coli
  • salmonellas typhi
  • naempphilius influenzas
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39
Q

4 things that antibiotics interfere with

A

– Cell wall synthesis
– Protein synthesis
– Nucleic acid synthesis
– Cell membrane function

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40
Q

Properties of viruses

A

Intracellular obligate parasites – can’t exist on their own, need a host cell
• Genetic material is DNA or RNA – never both
• Enveloped or non-enveloped
• Non enveloped – capsid protein surrounds genetic material
• Enveloped – has capsid encasing genome but also an envelope made of lipid bilayer and proteins
• Capsid symmetry can be helical or icosahedral which gives viruses their shape

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41
Q

Enveloped virus

A

→ lipid bilayer envelope and capsid

* enveloped viruses are more sensitive to harsh environments, for example, heat, dryness, compared to non-enveloped viruses 
* These are generally transmitted by respiratory, parenteral and sexual routes
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42
Q

Non - enveloped virus

A

→ capsid protein

non enveloped viruses are more stable in adverse environments
These are generally transmitted by the fecal-oral rout

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43
Q

Single stranded non - enveloped

Dna viruses

A

Parovirus 19

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44
Q

Double stranded non enveloped

Dna viruses

A

Adenovirus
Hpv
virus jc
Bk virus

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45
Q

Double stranded enveloped

Dna viruses

A

Herpes
Hepatitis B
Molluscum
Contagiosum

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46
Q

Single stranded, positive strand, lcosanedral non c enveloped

Rna viruses

A 
Hep A, e
Norovirus
Echovirus
Enterouirus
Coxsackievirus
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47
Q

Single stranded, positive strand icosanedral or helical enveloped

A 
Hiv
Hep C
Rubella
Yellow fever
West nile
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48
Q

Single stranded, negative strand, helical , enveloped

A 
Ebola
Measles
Mumps
Influenza
Parainfluenza
Rsv
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49
Q

Double stranded. Icoschedral, non - enveloped

A

Rotavirus

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50
Q

Virus growth

A

Need living cells to replicate (obligate intracellular parasites) = different viruses grow in different types of cells
• Use the living cells to synthesise all the constituents of the virus
• Different viruses grow in different types of cells
• In the laboratory:
– Vero cells
– HeLa cells
– Baby hamster kidney cells (BHK)

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51
Q

Viral replication - steps

A
  1. Attachment to the appropriate cells (eg haemagglutinin of influenza virus or glycoprotein GP 120 of HIV to appropriate cell receptor)
    1. Penetration of virus into cell (endocytosis or fusion of envelope with host cell membrane)
    2. Uncoating viral capsid is removed by viral enzymes or host enzymes leading to release of their genome and other materials such as enzymes into host cell
    3. Replication Initiation of transcription or translation of the viral genome resulting in the manufacture of virus components and genome
    4. Assembly of components into new virions which a ready for the release
      Release of the virions by lysis or budding from the target cells and further infection.
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52
Q

Dna virus replication

A

—> Transcription and replication occurs in the nucleus of the infected cells
• Most DNA viruses assemble in the nucleus
• Early Transcription (Translation of proteins for DNA replication)
• Late Transcription (Translation of structural proteins)
Assembly and release

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53
Q

Rna virus replication

A

—-> RNA viruses normally undergo transcription, translation and replication in the cytoplasm.
• Positive sense single stranded RNA can function as mRNA and get translated into proteins by the host ribosomes
• Negative sense RNA has to be changed to positive mRNA using the enzyme RNA dependent RNA polymerase to make a positive strand copy
• which can be read by the ribosomes and result in the manufacture of proteins

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54
Q

Latency

A

—> Latent viral infection – the virus can remain dormant within cells and does not cause symptoms until it is activated by some factor(s)
• Immunosuppression (chemotherapy or infections such as HIV result in reactivation of latent viruses)

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55
Q

Examples of latent virus

A
  • Herpes simplex viruses
    • Varicella zoster virus (chickenpox and reactivation causes shingles.) - in ganglia
    • Cytomegalovirus (in myeloid progenitor cells)
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56
Q

Bacteriophage

A
  • DNA is injected into bacteria
    • Shape is characteristic like a spaceship
    • DNA inside viral head
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57
Q

Yeast

A
  • Candida albicans (thrush) = affects immunocomprised people or those on long term antibiotics as it removes cammensals
  • Cryptococcus neoformans (usually affects the lungs or the central nervous system)
  • Pneumocystis jiroveci (pneumonia) - in younger people and Hiv patient
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58
Q

Fungi features t examples

A
  • Produce spores = sometimes spores are infection causing vehicle
  • Cell wall (chitin) and cell membrane (ergosterol) different from bacteria and other eukaryotic cells

Yeast -candida albicans
Molds

59
Q

Protozoa

A
  • unicellular eukaryotic organism
    • Giardia lamblia – parasitic intestinal disease
    • Cryptosporidium parvum – intracellular parasite – epithelial cells of the villi in lower small intestine
    • Plasmodium falciparum - malaria (more detail later)
60
Q

Helminths - 3 worms groups t examples

A
  • Cestodes: ribbon-like, segmented intestinal parasites
    • Tapeworms (e.g. Taenia saginata – beef tapeworm)
  • Nematodes: long non-segmented worms
    • Roundworms (e.g. Enterobius vermicularis - pinworm)
  • Trematodes: small, flat leaf-like worms that can infect urinary bladder, liver, lungs, blood vessels in the intestine
    • Flukes (e.g. Schistosoma mansoni - blood fluke)
61
Q

Prions

A

Unconventional infectious agents
• Prions are infective proteins with no nucleic acid
• Causative agent of Transmissible Spongiform Encephalopathies
• Accumulation of prion protein in the grey matter and in extracellular amyloid plaques in the brain

– Scrapie in sheep
– Bovine Spongiform Encephalopathy (BSE) in cattle
– Creutzfeldt-Jakob Disease (CJD)

62
Q

Epidemic

A

Widespread disease within a community e.g. Uk

63
Q

Pandemic

A

An epidemic which has spread beyond one community eg. All of eu

  • an-epidemic that has become widespread
64
Q

What is the infection model?

A

-> factors that come together that result in infection
How is it managed
How is it treated
Patient outcome

65
Q

Process of the infection model

A

Infectious agent and patient converge
Patient becomes infected
Accesses medical personnel for treatment
Patient is treated for infection

66
Q

6 parts of the infection model

A

• The patient (age, immune status, comorbidities)

  • The pathogen (bacteria, virus, fungus, parasite)
    • What it is, how does it produce infection
  • Mechanism of infection
    • How is the infection spread from person to person
  • Process of infection
    • How the organise establishes infection within the host
    • Damage host, fight against hosts immune system
  • Management of the patient (history, examination, investigations, specific and supportive treatment)
    • History to identify infectiona dn organism

• Patient outcome (cure, disability, chronic infection- low lying infection that never goes away, death)

67
Q

Pathogen class

A
  • Bacteriua
    • Virus
    • Yeast
    • Mould
    • Protozoa
    • Helminth
68
Q

Opportunist pathogens

A

Enhance function of the body but change and become virulent with a particular environment

69
Q

3 categories of patient factors

A

Person
Time
Place

70
Q

Patient factors - person

A
  • Age = older and younger people more prone to infection
    • Gender = more females have autoimmune disease (immunosuppressant medication = more infection)
    • Social factors = housing, mold growth, malnourishment
    • Immune status = due to other disorders cancer, HIV that affect immune system
    • Co morbidities
71
Q

Patient factors. - time

A
  • Time of year = influenza is a seasonal virus winter,
    • Time since exposure to pathogen (incubation time of microorganisms e.g. tb is slow growing symptoms occur a while after infection
72
Q

Patient factors - place

A
  • Current – where are they community, care home, hospital = you can pick up infections in environements
    • Travel - from good history
73
Q

Give 8 Mechanisms of infection transmission

A
  • Vertical transmission = mother to baby
    • Contiguous = direct spread, coughing and sneezing
    • Inoculation = vaccination leading to infections, contaminated needles
    • Hematogenous = blood borne infection spread
    • Ingestion = worm infection the gut, poor hand hygiene and then touching food
    • Inhalation = cold, flu, pneumonia
    • Vector = infection being carried by something else – food poisoning, foreign body
    • Autoinfection = transferring cheminselles (organisms living on your skin into your body)
74
Q

Pathogen host interaction

A

Invasion/ attachment —> how it enters body and causes problems

Damage:
• Pathogen that causes cholera produces toxins causing diarrhea
• Others produce toxins causing host damage, e.g. damaging the skin necrosis
• Inflammatory response of organisms infection
• Interaction with the host defenses (immune system)
= neutrophils can phagocytose or inactivate pathogens

75
Q

4 categories of patient management

A

Questions
Diagnosis
Treatment
Infection prevention

76
Q

Patient management - questions

A
  • Where is the infection?

* What is the Infection?

77
Q

Patient management - diagnosis

A
  • History = environment, travel, symptoms
  • Examination = of the right organ to see if it is affected
  • Investigation = target exact organism
78
Q

Patient management - treatment

A
  • Specific = treatment specific to that organism e.g. specific antibiotic (antivirals, antibiotics)
  • Appropriate = something the patient can take e.g. if they are allergic to penicillin
  • Supportive = treatment given may not be instant or give instant results, so support them (provide hydration, water or IVF, or pain medications)
79
Q

Patient management - prevention

A
  • How to prevent infection in community education
    • How to prevent infection in hospital = infection control mechanisms
  • Vaccination
  • sterilization
  • proper hygiene
80
Q

2 types of investigations

A

Specific investigations —> tests to identify the actual infecting agent that causes problems

Supportive investigations –> other investigations that indicate infection

81
Q

Specific investigations - examples

A

For bacteria:
• Microbiology on specimen for example throat swab, sputum sample, urine sample (uti) or blood culture (if it is systemic) = gram stain
• Detection of antigens or nucleic acid (PCR)
• Blood culture

For viruses
• Antigen detection, viral nucleic acid detection (PCR)

82
Q

Supportive investigations - examples

A
  • Blood tests for example, full blood count (FBC),
    • C reactive protein (CRP),
    • liver and kidney function tests
    • Imaging (X-ray, ultrasound, CT scan, MRI scan
    • Blood test look for different components of the blood that are indicators of infection
83
Q

2 types of treatment

A
  • Specific treatment = right medication to get rid of infection (antivirals, antibiotics)
    • Supportive treatment = treatment that helps patient, hydration, pain relief etc
84
Q

Specific treatment - examples

A
  • Antimicrobials
    • Antivirals
    • Antibiotics
    • Surgery – in extreme cases e.g. infected replacement
    • Drainage of boils
    • Debridement – clean of pus and live bacteria
85
Q

Supportive treatment - excemples

A
  • Symptom relief = pain relief , alleviate negative effects

* Physiological restoration = hydrate them , rehabilitation for patients with paralysis or amputation

86
Q

Outcome -4 paths

A
  • Infection is cured due to right treatment given
    • Person is cured of their infection but due to impact of infection they are left with = disability
    • Acute infection becomes chronic = not all infection can be removed (e.g. bone infection)
    • death
87
Q

Immune system definition

A

Cells and organs that contribute to immune defences against infectious and non-infectious conditions (self vs non-self)
• T cells be cells, macrophages, neutrophils

88
Q

Infectious disease definition

A

• When the pathogen succeeds in evading and/or overwhelming the host’s immune defences

89
Q

Immunity definition

A

interafce of infectious diseases and immune system

90
Q

4 roles of the immune system

A
  • Pathogen recognition (macrophages) = Cell surface and soluble receptors
  • Containing/eliminating the infection (neutrophils) = Killing and clearance mechanisms
  • Regulating itself = Minimum damage to host(resolution)
  • Remembering pathogens (adaptive) = Preventing the disease from recurring

= Immuniological memory protection

91
Q

Properties of innate immune system

A 
---> contain and understand intital infection 
Fast
• Fast (within seconds) 
• Lack of specificity 
• Lack of memory 
• No change in intensity
92
Q

Properties of adaptive immune system

A 
--> tailors itself to organism
Very effective
Immunological memory 
• Slow (days) 
• Specificity 
• Immunologic memory 
• Changes in intensity
93
Q

Innate and adaptive immune system process

A
  • Innate and adaptive immune system happen at the same time
    • They can’t operate individually to be effective they work together

Innate system – ids pathogen treis to contain it
• Tells adaptive immune system cells what it is to create antibodies
Adaptive immune system produces and releases antibodies - directs innate immune system

94
Q

First line defences

A

Things present on or within body to limit entry and grow of pathogens

95
Q

4 parts of innate immunity - first line defences

A
  • Physical barriers
    • Physiological barriers
    • Chemical barriers
    • Biological barriers
96
Q

Innate immunity - physical barriers

A

• Skin
Anything breaking skin barrier = potential cause of infection

* Mucous membranes – capture and expel pathogens from these orifices below 
* Mouth 
* Respiratory tract – ciliated cells 
* GI tract 
* Urinary tract
97
Q

Innate immunity - physiological barriers

A

→ tries to eliminate infection by getting rid of whatever it is infecting

Diarrhoea
• Foodpoisoning

Vomiting
• Foodpoisoning - remove bacteria expel asap
• Hepatitis
• Meningitis

Coughing
• Pneumonia

Sneezing
• Sinusitis

98
Q

Innate immunity - chemical barriers

A

Low pH → activates enzymes but also damages pathogens that can’t survive in acidic conditions
- • Stomach(1-3) • Vagina(4.4)

Antimicrobial molecules
• IgA immunoglobulin that can capture and eliminate mircoorganisms from getting in the eye (Tears, saliva,mucous membrane )
• Lysozyme (sebum, perspiration, • urine)
• Mucus
• Beta-defensins(epithelium)
• Gastric acid + pepsin = within gut

99
Q

Innate immunity - biological barriers

A
  • Normal flora = commensals that take up space where an invading pathogen could exist good protection as they compete with pathogens
    • Non pathogenic microbes
    • Strategic locations
    • Nasopharynx • Mouth/Throat • Skin • GI tract • Vagina (lactobacillus spp)
    • Absent in internal organs/tissues
100
Q

Normal flora examples

A

• Staphylococcus aureus
- upper respiratory tract t skin , can become opportunistic causing skin and respiratory infections

• Candida albicans  Opportunistic pathogenic yeast in gut flora →

• streeptoccus pneumoniae
- in nasopharynx can lead to pneumonia

101
Q

Clinical problems → innate immunity

Normal flora

A

• occur when Normal flora is displaced from its normal location due to:

  • breaches in skin integrity
  • fecal oral route
  • fecal perineal urethral route
  • poor dental hygiene , denial work
102
Q

Clinical problems → innate immunity

High risk patients - examples

A
  • Serious infections in high-riskpatients
  • Asplenic (and hyposplenic)patients = patients who have had their spleen removed don’t clear infections and filter blood in the same way
  • Patients with damaged or prosthetic valves (heart, hip, dental)– natural pooling of blood which leads to bacteria build up
  • Patients with previous infective endocarditis - disrupted heart contractions
103
Q

Clinical problems → innate immunity

Immuno-compromised patients

A

Immuno-compromised patients

* At particular risk of infection 
* Even overgrowth of normal flora – this can become pathogenic if it enters body and isn't cleared easily
104
Q

Clinical problems → innate immunity

Antibiotic therapy

A

Antibitoics
• Can deplete normal flora – give rise for infections to take over place where flora would have been seen
• Intestine -> severe colitis (Clostridiumdifficile)
• Vagina -> thrush (Candida albicans)

105
Q

3 innate immunity - second line defences

A
  • Phagocytes
    • Chemicals
    • Inflammation

—> factors that will contain and clear infection

106
Q

Microbes - definition

A

Microroganism , especially bacterium causing disease or fermentation

107
Q

2 types of microbes

A

Exogenous – from outside environment breach a barrier and enter a system below the barrier

Endogenous → skin hora

108
Q

Innate factors

A
  • Activate phagocytes

Eg. Complement activates phagocytes

109
Q

Role of phagocytes

A

• Recognition process
• Killing process of infectious microbes
1. Phagocyte is trying to understand organism – first phagocyte = macrophage (tissue resident cells in tissue)
Macrophages eat pathogen to find out what it is and the signal neutrophils to eliminate t kill

110
Q

3 main phagocytes

A

Macrophages
Neutrophils
Monocytes

111
Q

Macrophages

A

▪Present in all organs
▪ Ingest and destroy microbes (Phagocytosis)
▪Present microbial antigens to T cells (adaptive immunity)
▪ Produce cytokines/chemokines = to recruit other cells

112
Q

Monocytes

A
  • Precurosor to macrophages
    • ▪ Present in the blood (5-7%)
    • ▪ Recruited at infection site and differentiate into macrophages at tissues
113
Q

Neutrophils

A

• Travel all around body
▪Present in the blood (60% of blood leukocytes)
▪Increased during infection
▪Recruited by chemokines to the site of infection
▪Ingest and destroy pyogenic bacteria: Staph. aureus and Strep. pyogenes

114
Q

4 other key cells → innate immunity

A

Basophils lmast cells
Eoisonophils
Natural killer cells
Dendritic cells

115
Q

Basophils/mast cell - function

A

▪ Early actors of inflammation(vasomodulation)
▪ Important in allergic responses
Recruit and change conditons of membrane around tissue

116
Q

Eoisonophils - function

A

▪ Defence against multi-cellular parasites (worms)

117
Q

Natural killer cells- function

A

▪Kill all abnormal host cells (virus infected or malignant)

Sit between innate and adaptive immune system

118
Q

Dendritic cells - function

A
  • Present microbial antigens to T cells – like phagocytes

* Acquired immunity

119
Q

Pathogen recognition

Microbial structures and phagocyes

A

Microbial structures: - things on pathogen that help us identify it
• Pathogen-associated molecular patterns (PAMPs): Carbohydrates, Lipids, Proteins, Nucleic acids

PAMPS bind to receptors on phagocytes

Phagocytes: - recognise things on pathogens
• Pathogen Recognition Receptors (PRRs): Toll Like Receptors (TLR) = help identify and internalize invading pathogen

120
Q

Examples of pamps and prr inveraction

A

Lps (lipopolysaccharide) interacts with tlr4 prp

- lps is found on surface of all gram negative bacteria

121
Q

Pathogen recognition

Opsonisation

A

—> once pathogen is recognise = oppsonisation of microber = tag maicrobes so other cells can chew them up

• Coating proteins called opsonins that bind to the microbial surfaces land coat them leading to enhanced attachment of phagocytes and clearance of microbes
122
Q

Examples of opsonins

A

Complement proteins
• C3 - mature adults
• C4

Antibodies
• IgG - mature adults
• IgM

Acute phase proteins – markers
• C-reactive protein (CRP) = elevated CRP in blood test = inflammation = infection
• Mannose-binding lectin (MBL)

123
Q

Clearance of opsonised pathogens

A
  1. neutropjil and invading organsims covered on complements and antibodies
    1. Antibody and complement bind to FC receptors on neutrophil
    2. Organism is internalsied and neutrophil destroys pathogen

• Phagocytes such as macrophages and neutrophils have Fc receptors on their surface which bind to the Fc region of an antibody which has formed a complex with an antigen.
– This leads to internalisation of the pathogen which has been coated in antibody
– The macrophage produces reactive oxygen species to destroy thepathogen.

124
Q

Roles of phagocytes

A

Recognition - pamps, opsonins
Englufment
Degredation of infectious microbes

125
Q

Basic phagocytosis

A
  1. Internalized into phagosome
    1. Phagosome fuse with lysosome
    2. Ros and enzymes in lysosomes destroys bacteria
    3. Neutrophil removes digest materials
126
Q

2 phagocyte intracellular kiling mechanisms

A

Oxygen-dependent pathway (respiratory burst)

Oxygen-independent pathways

127
Q

-Oxygen-dependent pathway (respiratory burst)

A
  • Toxic O2 products for the pathogens:

* Hydrogen peroxide, Hydroxyl radical, Nitric oxide, Singlet oxygen, Hypohalite

128
Q

Oxygen-independent pathways

A 
▪ Lysozyme
	▪ Lactoferrin or transferrin 
	▪ Cationic proteins(cathepsin) 
	▪ Proteolytic and hydrolytic enzymes 
	▪ NETs (Neutrophil Extracellular Traps)
129
Q

Netosis

A

—> The process by which neutrophils externally trap pathogens
– Release of decondensed chromatin and granule contents into the extracellular space (neutrophil genetic material) acts as a net for pathgoen
. • Can be used as a mechanism of neutrophil cell death.
• Commonly used to deal with pathogenic insult

130
Q

Second line of defence - 2 chemicals

A

Complement

Cytokines , chemokines

131
Q

Complement system

A
  • Activate cells and recruit cells

* Produce membrane attack complex – complement proteins from pore and punch hole through detsroy organism

132
Q

Complement proteins + roles

A
  • C3a and C5a: Recruitment of phagocytes
    • C3b-C4b: Opsonisation of pathogens
    • C5-C9: Killing of pathogens Membrane Attack complex
133
Q

Complement system -3 activating pathways

A

Classical pathway

Alternative Pathway

Mannose Binding Lectin pathway

134
Q

Complement system - classical pathways

A

nitiated by antibody-antigen

– reaction (membrane attack complex)

135
Q

Complement system - alternative pathway

A

Initiated by cell surface microbial – constituents (endotoxins on E. Coli) C3 and C5

136
Q

Complement system -Mannose Binding Lectin pathway

A

– Initiated when MBL binds to mannose containing residues of proteins found on many microbes (Salmonella spp. – Candida albicans)

137
Q

Actions of cytokines

A
  • Systemic actions
  • kickstart liver to produce (opsonins) • CRP • MBL (-> complement activation)
  • Bone marrow
    • Neutrophil mobilization
  • Hypothalamus
    • Increased body temperature = fever
  • Local inflammatory actions = cytokine storm initiated by macrophages
    • Blood vessels
    • Vasodilation
    • Vascular permeability
    • Expression of adhesion molecules -> attraction of neutrophils
138
Q

3 examples of cytokines

A

Tnf alpha

Il-1

Il-6

139
Q

Summary of innate response

A
  1. Innate barrier breached: entrance and colonization of the pathogens.
    1. Complement, mast cells and macrophages activation (PRR) Phagocytosis (opsonins)Cytokine/chemokine production
    2. Vascular changes Vasodilation/Vascular permeability Chemoattraction Neutrophils Monocytes (TNF, IL-8)
    3. Hypothalamus Fever Liver Acute phase response
    4. Redness, heat, swelling andpain: local inflammatio
140
Q

3 clinical problems when phagocytosis is reduced

A
  • Decrease spleen function
    • Asplenic patients (No spleen)
    • Hyposplenic patients (reduced spleen function)
  • Decrease neutrophil number (<1.8x109/l) too low can’t mount the repsonse = major effector phagocyte for clearance of infection
    • Cancer chemotherapy
    • Certain drugs(phenytoin)
    • Leukaemia andl ymphoma

• Decrease neutrophil function
• Chronic granulomatous disease (No respiratory burst)
• Chediak-Higashi syndrome (no phagolysosomes formation)
As you get older = neurtophil casues more collateral damage and don’t work as well
IL8 = chemoattractant for neutrophils

141
Q

How do soap and hand alcohol gel work

A

Soap - traps fragments of organisms in tiny bubbles that wash away

Alcohol hand gel - actually kills pathogen via denaturation breaking down proteins

142
Q

Gram negative bacteria on skin

A

Enterobacteria

E-coli

143
Q

Gram positive bacteria on skin

A
  • Staphylococcus
  • microccus
    Corynebacterium
144
Q

Examples of cytokines and when they are released

A

Vasodilatation – Histamine, Serotonin, Prostaglandins, Nitric Oxide

Increased vascular permeability – Histamine, Bradykinins, Leukotrienes, C3a & C5a

Chemotaxis – C5a, LTB4, TNF-alpha, IL-1, Bacterial Peptides

Fever – Prostaglandins, IL-1, TNF-a, IL-6

Pain – Bradykinin, Substance P, Prostaglandins

All TP1 and Some TP2 (11 decks)

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