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Health And Society > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Innate immune response

A
  • tissue resident white blood cells (leukocytes) at site of infection
    • recognise invading pathogen
    • release chemical messenger proteins (chemokines recruit more WBC; cytokines activate more WBC
  • phagocytic cells engulf invading pathogens and destroy them in large numbers
    • Tissue resident macrophages – first responders
    • Recruited neutrophils – professional killers
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2
Q

Phagocytes and pattern recognition

A

Phagocytes recognise microbes through pattern recognition
- Shared structures unique to subsets of microbes =
Pathogen Associated Molecular Patterns (PAMPs) eg:
• LPS of Gram-negative bacteria
• flagellin of bacteria
• Viral RNA or viral DNA
- Toll-like receptors (TLRs) are Pattern Recognition Receptors (PRRs)
- Recognition sends danger signal
- Stimulates production and secretion of cytokines

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3
Q

Inflammation

A

• Cytokines induce inflammation
• Series of events in reaction to tissue damage – injury and/or infection
• Site becomes swollen, red, hot and painful – part of normal healing process
• Underlying mechanisms explain the symptoms
- Vasodilation – increase in blood vessel diameter and permeability
- Brings more WBCs to site of infection

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4
Q

Fever

A

• Cytokines, interleukin-1 (IL-1) induces fever
• Phagocytic cells more efficient at elevated body temperature
• Some pathogens unable to reproduce at higher temperatures, e.g. influenza virus
• If fever gets too high – dangerous and life threatening

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5
Q

Interferons

A

Cytokines that interfere with viral replication and spread
• IFNs made by infected cell in response to viral replication
• Act on neighbour to induce an antiviral state
• Cell in antiviral state do not allow viral replication
• Contribute to flu-like symptoms of aches, headache, chill

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6
Q

Antigen presenting cells (APCs)

A

• Macrophages and dendritic cells are antigen presenting cells (APCs)
• At sites of infection, APCs use TLRs to recognise a pathogen and then send signals for immune activation
• They ingest and digest pathogens
• Initiate adaptive immune response

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7
Q

Dendritic cells

A

• DCs that have picked up antigen at the site of infection migrate to nearby (local, draining) lymph nodes
• Activate adaptive immune cells responsible for microbial clearance – T and B cells
• Strategically located where they concentrate
components for adaptive immune responses
- Lymphatic system = network of vessels returning fluid that has leaked out of blood back to circulation
- Lymph = fluid
• Blood is filtered through the spleen
• Like a lymph node for blood-borne pathogens
• Other specialised lymphatic structures exists in areas of high pathogen exposure e.g. gut and respiratory tract

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8
Q

Lymphocytes

A

• WBCs of adaptive immune response
• T cells and B cells
• Initially formed in bone marrow
• Circulate through blood
• Can leave blood and enter lymph nodes looking for antigen presented by DCs
• If they find DCs presenting foreign antigen that they are specific for, they will become activated
• If they don’t, they keep moving
• Activated lymphocytes undergo rapid proliferation and lymph nodes swell

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9
Q

T cells

A

• T cells migrate from bone marrow to the thymus
• Complete development and maturation in thymus
• MATURE (but NAÏVE) T cells that have not seen foreign antigen before leave the thymus and begin to circulate
• Upon activation by DC + antigen, they become EFFECTOR T cells:
• Helper CD4+ T cells (Th) coordinate entire adaptive response – activate CTLs and B cells
• Cytotoxic/killer CD8+ T cells (Tc cells or CTLs) are professional killing cells – viruses and tumours
• During activation, some Th cells and Tc cells develop into relatively inactive = long-lived MEMORY T cells

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10
Q

T cell receptors

A

• **TCRs* recognise foreign antigen presented MHCs by APCs
• Each naïve CD4+ T cell has lots of identical TCRs (same specificity)
- Different CD4+ T cells have different TCRs and antigen specificities
• APC (DCS) release cytokines that attract and activate **naïve CD4+ T **
antigen presented on
• Naïve CD4+ T cells specific for presented activated and begins to divide antigen (C in this case) is activated and begins to divide
• Results in activated effector CD4+ T helper (Th) cells, all bearing TCRs specific for the activating antigen
• Process takes several days to complete = clonal expansion (lymph node swelling)

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11
Q

Microbial clearance

A

•DCS present antigen to CD4+ and CD8+ T cells activating them > effector Th cells and Tc cells
• Th cell specific for the same antigen secrete cytokines that further stimulate/help Tc cells
• Tc cells can then go looking for host cells infected with virus, displaying viral antigen on MHC
• Tc cells proliferate and leave lymph node in search of infected host cells
• Tc cells recognises infected cell displaying same foreign antigen bound to MHC on surface that was used to activate them from naive cells
• Releases toxic chemicals to cause infected cell to die = targeted cell killing; uninfected cells not displaying antigen are not affected

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12
Q

Antibody functions

A

a) Coat surface of viral particles preventing them from
attaching to host cell receptors = neutralisation
b) Each antibody has two antigen binding sites - large agglutinated clumps of antigen and antibody may form. Complexes are readily available to phagocytic cells = agglutination
c) Enhances phagocytosis by acting as opsonin for phagocytic cells which have receptors for antibody tail = opsonisation

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13
Q

Vaccines

A

Vaccines induce immune memory without causing disease
• Ability to mount ever stronger immune response with each antigen exposure is basis of vaccination
• Primary immune response stimulated by exposure to dead / inactivated, weakened / attenuated, or component of pathogen
• Subsequent exposure to live pathogen immediately triggers secondary adaptive response

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14
Q

Nosocomial infection

A

Defined as a hospital acquired infection
- “hot beds” for infection
• sick people - damaged barriers, weakened immunity
• Medical staff movement
- Preventable with basic control measures
• Hand washing
• Instrument sterilisation
- Antimicrobial resistance (AMR)
• Once curable infection no longer respond

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15
Q

Physical control: Manipulation of environment

A
  • Microbes have optimal growth temperature (range)
  • Direct and inexpensive
  • Heat is effective means of killing = ”cidal”
    • can penetrate an object and kill organisms throughout
    • denatures proteins (not suitable for all substances)
  • Cold generally doesn’t kill, it inhibits growth = ”static”
    • inhibits microbial replication
  • Heat to sterilise = complete elimination of all organisms
    • Dry heat (flame or hot oven) - requires considerable time and higher temps
    • Moist heat (for autoclaves add pressure) - penetrates more quickly at lower temps
  • Pasteurisation = temporary heating of liquids/ foods sensitive to prolonged heat (lose flavour)
  • Liquids that can’t tolerate high temps may be filtered through membrane with pores of size to exclude microbes
  • Radiation can be used to kill microorganisms in some situations
  • UV rarely sterilises, but can significantly reduce numbers on surfaces
    • Inhibits microbial DNA replication
  • Gamma radiation used for some food products
  • Drying is an “age-old” way of preserving fish and meat products
    • Coupled with water removal by salt/sugar
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16
Q

Chemical control on living and non-living materials

A
  • For non-living materials = disinfectants
    • Bleach (chlorine) – forms an acid when added to water
    • Alcohol – kills by denaturing proteins and disrupting microbial cell membranes
  • For living tissue = antiseptics
    • Iodine – binds enzymes to inhibit activity, also affects microbial cell membranes
    • Alcohol – good for skin, but not open wounds

• Soaps, detergents disrupt microbial adherence, can kill through disruption of microbial cell membrane

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17
Q

Antibiotics

A

Antibiotics are anti-bacterial agents
- Either Bactericidal or Bacteriostatic
- Initially produced by microorganisms
- Ideally inhibits microorganism without harming host = selective toxicity
- Selection of most appropriate antibiotic depends on:
• Known drug allergies
• Identification of infecting organism and antibiotic sensitivity
• Site of infection
• Cost
• Speed of infection progression and/or antibiotic effectiveness
- Some combat a wide variety of microorganisms = broad spectrum
• Used prophylactically – for immunocompromised patients – or if pathogen is not known
• Most likely to have off-target effects – disrupt normal microbiota
- Narrow spectrum = highly targeted to specific types of infection/bacterial pathogens

18
Q

Bactericidal Antibiotics

A
  • Bactericidal antibiotics KILL – e.g. Penicillin prevents bacterial cell wall synthesis causing rupture
    • More direct effect; essential in immunocompromised patients
19
Q

Bacteriostatic Antibiotics

A
  • Bacteriostatic antibiotics INHIBIT REPLICATION - hold numbers in check allowing the immune response a greater chance of clearance
    • Effect relies on continual presence of the drug until infection is cleared
20
Q

Why is selective toxicity harder to achieve against eukaryotic pathogens?

A
  • Limited drug options against protozoa and fungi
    • Similar to human cells – far fewer unique drug targets
  • Side effects common
  • Quinine - plant extract effective against malaria parasites
  • Chloroquine, synthetic analogue, produced after
    global (WWII) shortage
    • Today, resistance is spreading…new drugs are needed!
21
Q

Antiviral Drugs

A

Antiviral drugs interfere with viral replication
- viral replication inside host cells
- viruses have some unique features - selective toxicity possible
- Newer, innovative anti-viral drugs on horizon

22
Q

Drug resistance

A
  • Antibiotic Misuse has led to drug resistance
    • when antibiotics used inappropriately to treat non-bacterial infections (no effect on viruses!!)
  • Antibiotic resistance is not new, but is now a major public health threat
  • Mechanisms of antibiotic resistance (R) are well understood
23
Q

Antibiotics and selection pressure

A
  • Resistance is genetically determined
  • Evolves through natural selection
  • After each dose, increasingly more resistant bacteria are left behind
  • If halted early, more resistant bacteria may reproduce
24
Q

Epidemiology

A
  • The study of disease in population and factors that influence a disease’s frequency and distribution
  • Aim to predict future problems and make recommendations that might prevent disease or limit spread
25
Q

Prevalence

A

Total number of individuals in a population who have a disease or health condition at a specific period of time = usually expressed as a percentage of the population

26
Q

Incidence

A

Number of individuals who develop (new cases) a specific disease or experience a specific health-related event during a particular time period (such as a month or year)

27
Q

Rates

A

Mortality rate– number/percentage of deaths in a given population

Morbidity rate – number/percentage of people who have complications/illness

28
Q

Outbreak

A

Occurrence of cases of disease in excess of that normally expected in a defined community, geographical area or season

29
Q

Epidemic

A

A sudden increase in the number of cases of a specific disease, beyond what is considered to be a normal number of cases; rapid spread

30
Q

Common source epidemic

A

A single contaminated site gives rise to a common source epidemic
•e.g. cholera contaminated water supply in London
• Rapid rise in cases with all affected individuals becoming ill in a short time
• Once source is eliminated, cases will continue to be reported for a time period approx. equal to one incubation
period (time between exposure to organisms and first sign of symptoms)
• Usually occur because of a breakdown in sanitation

31
Q

Host-to-Host epidemics

A

Host-to-host epidemics spread from infected to uninfected individuals
• No single source; multiple new sources are made
• e.g. flu epidemic
• Start slowly, picks up speed until number of cases reaches a peak, slowly wanes for as long as some susceptible individuals remain with chance of exposure
• Multiple factors that often interact e.g. weather and immune status of population

32
Q

Immunity

A
  • When immunity is sufficiently high, an epidemic becomes unlikely or impossible (to few susceptible people)
  • Host-to-host epidemics often occur in cycles associated with cyclic population immunity
33
Q

Herd immunity

A

Immunity is so high that possible routes of transmission are reduced
• Provides protection for susceptible people who can’t achieve their own protection e.g. immunocompromised

34
Q

Epidemic threshold

A

Minimum proportion of population that must be immune to specific pathogen to prevent an epidemic
(vaccination aims to achieve coverage above this threshold)

35
Q

Antigenic drift

A

A minor genetic change in antigenic make up of virus due to random mutations (errors)
- Immune memory against an original antigen may no longer confer protection

36
Q

Antigenic shift

A

A major change when gene segments form different strains of virus, infecting a cell at same time =, recombine to create a new strain
- facilitated by animal reservoirs
- population immunity to these new strains is generally very low or non-existent

37
Q

Case definition

A

Helps authorities determine if unusual cases are related
- is a list of common symptoms for a particular medical condition
- is a standard criteria for categorising an individual as a case, or probable case
- helps local doctors identify patients with similar symptoms
- time, place and personal characteristics of a new disease provides clues to disease’s identity

38
Q

Case-control studies

A
  • Once time, place and personal charecteristics are defined, next step is to develop a case-control study
  • used to determine what factor(s) link affected individuals and distinguish them from uninfected individuals - often provide the missing clues
  • Affected people = cases
  • Each matched to uninfected individual = control
    • Should be as similar as possible to each other (sex, age, place of residence, etc)
39
Q

Emerging and Re-emerging diseases

A

Emerging and Re-emerging diseases are new or changing diseases that are increasing in importance

• A new or changing disease that is increasing in importance = emerging
• A disease that was considered to be under control but is now causing
increasingly serious problems = re-emerging
• Changes in pathogen, environment, and human behaviour can all contribute to emergence and reemergence
- Increasing human population and urbanisation
- Increasing global travel and trade

40
Q

Categorisation of emerging diseases

A
  1. Invasion of a new host population by a known pathogen
    • Commonly zoonoses (animal reservoirs), e.g. Zika virus
  2. Appearance of a completely new, previously undescribed disease
    • e.g. AIDS and Ebola
  3. Association of a well known disease with a new pathogen
    • e.g. Helicobacter pylori as cause of gastric ulcers; HIV as cause of Kaposi’s sarcoma
  4. Increased virulence or a renewed problem with a well-known but previously less virulent or well-controlled pathogen = re-emerging
    • e.g. multi-drug resistant Staphylococcus aureus and Mycobacterium tuberculosis

Health And Society (7 decks)

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