Week 7 Bioscience Flashcards

1
Q

Two cell types make up all living organisms

A

Eukaryotic cells - True cells
* Membrane-bound nucleus and organelles
* e.g. animals, plants, fungi, protozoa, algae

Prokaryotic cells - Simple cells
* No membrane–bound organelles
* e.g. bacteria

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2
Q

Naming microbes

A
  • Binomial system of nomenclature
  • 2 names: a genus and a species name
  • underlined or italicised
    e.g. Staphylococcus aureus, where Staphylococcus is the genus name and aureus is the species name
  • Microbes may also have common names e.g. “golden staph”
  • Binomial nomenclature applies to all microbes except viruses
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3
Q

Bacteria

A
  • Bacteria (sing. bacterium) are very small, e.g. 1 - 5µm
  • Usually single celled
  • Three basic shapes:
    • rod - bacillus (plural bacilli)
    • spherical - coccus (plural cocci)
    • spiral – spirilla (plural spirillus) (also spirochete, or vibrio)
  • Feed on organic material
  • derived from either dead organisms or a living host
  • release enzymes → digest organic material extracellularly → internalising it in solution
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4
Q

Viruses

A
  • Very small (e.g. 20 nm - 100 nm)
  • Acellular (or non-cellular)
  • Package of genetic material (DNA or RNA)
  • No organelles
  • Obligate parasite = can only reproduce inside a host cell
  • Naked virus = genetic material surrounded by a protein coat (capsid)
  • Enveloped virus = naked virus plus an outer membrane or envelope - derived from the plasma membrane of the previous host cell
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5
Q

Typical viral infection = Lytic

A
  1. Attachment to target cell
  2. Penetration of target cell
    * naked viruses engulfed (endocytosis)
    * enveloped viruses fuse with host cell membrane
  3. Replication
  4. Maturation and release
    * naked viruses trigger lysis of the host cell → viral exit kills the cell
    * enveloped viruses bud from the host cell, taking part of the cell membrane as an envelope → usually kills the host cell
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6
Q

Fungi

A
  • Eukaryotic cells with a cell wall containing chitin
  • Feed on organic matter (like bacteria) and recycle organic matter in nature

Yeasts
* 5-10 µm ovoid cells
* Single-celled
* Reproduce by budding

Molds
* Small, multicellular
* Filamentous cells → mesh = mycelium

Mushrooms
* large, multicellular

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7
Q

Humans and Microbes

A

3 classes of microbes humans interact with:
1. Normal flora (resident flora / microbiota / microbiome)
2. Transient microbes
3. Pathogens

3 types of relationship possible between microbes and humans:
1. Commensalism – one partner benefits, the other is unaffected
2. Mutualism – both partners benefit
3. Parasitism – one partner benefits at the expense of the other

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8
Q

Normal flora

A
  • At birth humans are colonised by a variety of microbes (mainly bacteria, some fungi/yeasts)
  • Colonisation = establishment and growth on a body surface
  • Microbes colonise our body surfaces that contact the external environment
  • Derived from:
    • Vagina (during birth)
    • Diet
    • Environment
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9
Q

Transient microbes

A
  • Temporary residents – remain on the body for a short time (hours-days-months)
    • Usually acquired by contact
    • Unable to colonise body surfaces:
      • Cannot complete with normal flora for living space and nutrients
      • Eliminated by the bodies defences
      • Dislodged by human activity, i.e. hand washing
  • Can be found in the same locations as the normal flora
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10
Q

Pathogens

A
  • Microbes that can cause an infectious disease
    • Infection = invasion of the body by a pathogenic microbe (penetrates body surface to grow in deeper tissues)
    • Infectious disease = disorder of a structure or a function due to damage caused by a microbe
    • Infectious disease is not necessarily transmissible!
  • Includes viruses, bacteria, fungi and protozoa, worms and arthropods (insects)
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11
Q

Relationships - commensalism

A

Commensalism – one partner benefits, the other is unaffected
* Normal flora is in ecological balance with the host – benefits:
* Living space
* Nutrition
* Host – not affected/harmed

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12
Q

Relationships - mutualism

A

Mutualism – both partners benefit
* Normal flora is in ecological balance with the host – benefits:
* Living space
* Nutrition
* Host benefits:
* Colonisation and infection by pathogens is prevented as normal flora
* Take up living space and nutrition
* Maintain an unsuitable environment, e.g. Lactobacillus maintains an acidic environment in the vagina which suppresses the overgrowth of other microbes, e.g. Candida

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13
Q

Relationships - parasitism

A
  • Parasitism – one partner benefits at the expense of the other
  • Parasites
    • Use the host as a resource for growth
    • Cause tissue damage
    • Activate host defences (innate and adaptive defences)
  • Parasites are microbes capable of causing infectious diseases, i.e. pathogens
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14
Q

Pathogenicity

A
  • Whether or not infection and disease occurs depends on virulence = the capacity of a pathogen to cause disease
  • A more virulent microbe:
    • Causes a more severe disease e.g. common cold vs. rabies virus
    • Requires smaller number of pathogens to initiate infection
      • Infectious dose = minimum number of pathogens which will cause disease
      • Greater the virulence = fewer pathogens required for infection = lower infectious dose
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15
Q

Conducive environments

A
  • Environmental conditions affect:
    • The health status of individuals, e.g. nutrition, vaccination
    • Reservoir of infection – source of pathogens, , e.g. human host, insects or animals, non-living source (contaminated water)
    • Ease of pathogen transmission between hosts, e.g. sanitation, crowding, food and water sources, vectors
  • Conducive environments
    • Poverty, famine, natural disasters, conflict
    • Increase the likelihood of infectious disease occurring in a severe form and spreading easily
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16
Q

Pathogens and infection

A
  • Infectious disease is usually the result of infection by conventional pathogens
    • A microbe which causes disease in previously healthy people with normal defences e.g. measles virus, gonorrhea, influenza
  • Infections may be caused by opportunistic pathogens
    • Microbes that don’t normally cause infectious disease but can do so under certain circumstances
      • Normal flora
      • Environmental microbes
        → Opportunistic infections
17
Q

Opportunistic infections with normal flora

A

Microbes of the normal flora can cause opportunistic infection and disease when:
1. The ecological balance of the normal flora is upset
2. Microbes of the normal flora are relocated into parts of the body they are normally excluded from
3. Host innate and/or adaptive defences are compromised

18
Q

Upset ecological balance

A

e.g. Candida albicans (fungus - yeast)
* Occurs in the mouth, parts of the digestive tract, vagina
* Normally low numbers in the vagina due to:
* competition with bacteria * acidic environment (pH 4-4.5) maintained by the bacteria Lactobacillus
* Not affected by treatment with antibiotics kills pathogenic and normal flora bacteria
* Antibiotic treatment reduces competition for living space and nutrients → Candida “population explosion” → painful inflammatory condition, candidiasis (thrush)

19
Q

Relocation of the normal flora

A

Microbes of the normal flora are relocated into parts of the body they are normally excluded from
* E. coli of the large intestine → urethra (UTI) or vagina
* Perforation of the intestines → normal flora moves into abdominal cavity (normally sterile) → peritonitis
* Staphylococcus bacteria on the skin → enter deeper tissues via a cut (defensive barriers breached) → necrotising fasciitis

20
Q

Compromised host defences

A
  • Compromised host defences (immunocompromised) à inability to mount an effective defence
  • May involve:
    • Innate defences
      e.g. impaired mucociliary escalator allows normal flora of the mouth and throat to penetrate deeper lung tissues → pneumonia
  • Adaptive immunity e.g. AIDS patients have low numbers of TH cells → limited adaptive immunity
21
Q

Opportunistic infections with environmental microbes

A
  • Environmental (transient) microbes
    • Low pathogenicity
    • Do not usually interact with humans
    • Do not usually cause infection in healthy people
  • May cause opportunistic infectious disease in people with reduced defences (i.e. immunocompromised individuals) e.g. various fungi, such as Aspergillus can cause serious lung infection cancer and death
22
Q

Attachment

A
  • In order to establish an infection, pathogens must attach themselves to host tissues at their portal of entry
  • Many pathogens have adhesins on their surface à bind surface receptors on host target cells e.g. E. coli adhere to epithelial cells in the urethra à UTI
  • Some bacteria secrete a sticky substance, a glycocalyx, that cements them to a body surface, e.g. bacteria, involved in tooth decay
  • Many viruses adhere to specific surface molecules on their target cells. e.g. human immunodeficiency virus (HIV) attaches to a protein present on TH cells and macrophages
    e.g. influenza has an envelope protein, haemagglutinin, that attaches to many cell surface glycoproteins
23
Q

Portals of entry

A
  • The site at which a pathogen enters the human body to reach deeper tissues
    • Most pathogens have a preferred portal of entry
      • Portal of entry can be a pre-requisite for disease
      • Example: Streptococcus bacteria cause pneumonia if inhaled but not if swallowed
  • Some pathogens can use multiple portals
    • Example: Bacillus anthracis (anthrax) can cause disease via multiple portals (broken skin, respiratory and digestive tracts)

Skin
* Hair follicles, sweat glands
* Some pathogens can live in, or bore through, the skin e.g. various bacteria, fungi, papilloma virus, hook worms
* Compromised barriers i.e. penetrated/injured, i.e. puncture, injection, bite, wound, surgery e.g. tetanus, rabies, HIV, hepatitis viruses

Mucous membranes
* Respiratory tract (most common portal) via droplets or particulates, e.g. influenza virus, measles, COVID19
* Gastrointestinal tract via food, water, contaminated hands etc., e.g. Hepatitis A, Salmonella
* Urinary tract, e.g. E. coli
* Reproductive tract (sexually transmitted), e.g. genital warts, chlamydia, HIV, hepatitis viruses
* Conjunctiva of the eyes, e.g. bacteria (conjunctivitis), HIV, hepatitis

24
Q

Multiplication and spread

A
  • The development of infectious disease requires that the pathogens multiply to a critical population size
  • The incubation period of an infectious disease = the time during which the pathogen is overcoming early host defences and utilising host resources to multiply to a critical population size
    • Extracellular pathogens - the majority of bacteria and fungi obtain their nutrients from the ECF
    • Intracellular pathogens - all viruses, and some bacteria and fungi, obtain nutrients from within host cells
  • Spread – involves overcoming host defences
25
Q

Overcoming host defences

A
  • In order to establish an infection, pathogens must penetrate, avoid or inactivate host defences
  • The better pathogens are at overcoming host defences the more virulent they are
  • Strategies (= virulence factors) include:
    1. Overcoming innate defences:
  • Overcoming surface barriers
  • Resisting phagocytes
    2. Overcoming adaptive defences
  • Degrading antibodies
  • Antigenic variation
26
Q
  1. Overcoming surface barriers
A
  • Some pathogens release enzymes that break down epithelial/connective tissue barriers to invade deeper tissues e.g. Streptococcus, Clostridium
  • Bordetella pertussis (whooping cough) secretes a toxin that inactivates the mucociliary escalator
27
Q
  1. Resisting phagocytes
A
  • Some bacteria have slippery capsules (i.e. glycocalyx) that prevent phagocytes adhering and engulfing them e.g. Streptococcus pneumoniae
  • Some bacteria release toxins that kill phagocytes or release enzymes that inactive their digestive enzymes
    e.g. Staphylococcus produces
    1. leukocidin → kills neutrophils
    2. catalase → destroys lysosomal enzymes
28
Q
  1. Degrading antibodies
A
  • Some pathogens can produce enzymes that can destroy antibodies
    • IgA proteases → destroy IgA antibodies in mucus at mucosal surfaces → prevents neutralisation by antibodies
  • Examples:
    Neiserria gonorrhoea → gonorrhea
    Neiserria meningitdis → meningitis
29
Q
  1. Antigenic variation
A
  • Some pathogens can alter their surface molecules – i.e. antigens that host memory lymphocytes would normally respond to – thus preventing a protective secondary response
    e.g. Neiserria gonorrhoea → gonorrhea
    Influenza virus
    Plasmodium → malaria
30
Q

Damage to the host

A
  • Damage to the host may arise:
    1. Directly from the activities of the pathogen
    • Damage caused by enzymes or toxins
    • Cytopathic effects
    • Use of host as a food source
      2. Indirectly from the host’s innate and/or adaptive defences
    • Inflammation – swelling, phagocytic enzymes, complement, scarring
    • Antibodies and cytotoxic cells
31
Q

Pathogen-induced damage: cytopathic effects

A
  • Cytopathic effect → microbe activity damage → kills host cells
  • Viruses → lytic infections → host cell death
  • Bacteria can kill host cells to gain nutrients, e.g. liver cells to gain essential iron
  • Microbial toxins → kill host cells (many damage cell membranes), e.g. cytotoxins
32
Q

Pathogen-induced damage: enzymes & toxins

A
  • Enzymes → tissue damage
    • Collagenase - breaks down the collagen fibres connective tissue , e.g. Streptococcus causes necrotising fasciitis
  • Toxins → fever, cardiovascular and nervous system disturbances, shock, diarrhoea → death
    • Toxins that kill phagocytes, e.g. leukocidin
    • Tetanus toxin acts in the CNS → sustained muscle contractions (tetany)
    • Botulinium toxin (“botox”) blocks the release of ACh at the NMJ → flaccid paralysis
33
Q

Host defences cause tissue damage

A
  • Damage to the host may arise from the activities of the host’s own defences (see previous week’s content):
    • Innate defences, e.g. phagocyte and complement activation, inflammation, natural killer (NK) cell activity
      • Inflammation
        • Universal feature of infectious disease – triggered by tissue damage
        • Process enhanced by immune complexes and complement
        • Can damage healthy tissue (next slide)
  • Adaptive defences
    • Antibodies (immune complexes) and cytokines – promote phagocyte activity and inflammation
    • Cytotoxic T cells – perforins and granzymes may kill both infected (target) cells and bystander cells
34
Q

Portals of exit

A
  • Pathogens leave the body via portals of exit to spread to a new host
  • The most common: the respiratory and digestive tracts
  • Damage to body tissues may assist in exit, e.g. coughing
  • The more pathogens that are shed, the greater the chance of reaching a new host
  • Body fluids/wastes provide excellent vehicles for exit
35
Q

Host defences cause tissue damage

A
  • Damage to the host may arise from the activities of the host’s own defences (see previous week’s content):
    • Innate defences, e.g. phagocyte and complement activation, inflammation, natural killer (NK) cell activity
      • Inflammation
        • Universal feature of infectious disease – triggered by tissue damage
        • Process enhanced by immune complexes and complement
        • Can damage healthy tissue (next slide)
  • Adaptive defences
    • Antibodies (immune complexes) and cytokines – promote phagocyte activity and inflammation
    • Cytotoxic T cells – perforins and granzymes may kill both infected (target) cells and bystander cells
36
Q

The course of infectious disease

A

The course of the infection depends on how effectively the host defences deal with the pathogen as it multiplies:
* If the pathogen is eliminated quickly
* the disease follows an acute course
* recovery is generally rapid
* If the pathogen is eliminated slowly, or not at all
* The infection may be
* Chronic (persistent) – very slow or no recovery
* Latent – apparent recovery interrupted by recurrent illness

37
Q

Chronic infection

A
  • An initial acute, symptomatic disease (red line) period is followed by apparent recovery (appears to be acute infection), but …
  • The pathogen is not completely eliminated and continues to multiply slowly and cause increasing amounts of damage (green line)
  • Depending on the pathogen, it is eliminated/cleared very slowly (long term infection) or never eliminated (lifelong infection) and subsequent acute episodes may occur
  • The host acts as a carrier, transmitting the pathogen even while appearing healthy (as the pathogen is multiplying it can be transmitted)
  • Example: Hepatitis B
38
Q

Latent Infection

A
  • The initial acute, symptomatic disease (red line) period is followed by apparent recovery without complete elimination of the pathogen
  • The pathogen does not multiply but becomes “dormant” as it “hides” inside cells from body defences – it cannot be transmitted as it is not multiplying (and thus host is asymptomatic)
  • This latent period may last for many years
  • The pathogen may be “reactivated”, grow and cause acute disease (blue line) – however, the symptoms may be quite different from the symptoms of the initial disease
  • Example: Herpes viruses, i.e. chickenpox/shingles or cold sores
39
Q
A