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FunMed Microbiology > How do microbes cause disease > Flashcards

How do microbes cause disease Flashcards

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Biology 101 flashcards
1
Q

describe how normal flora cause disease

A
  • Bacteria that do not cause disease in their environment, if the bacteria invade the new sites then they can cause diseases the innate immune system prevents this from happening
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2
Q

How does Nora flora compete with pathogens

A
  • It competes with pathogens at colonization sites and produces antibiotic substances that suppress other bacteria
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3
Q

how does normal flora inhibit pathogen action

A
  • Genital tract; lactobacilli produce lactic acid which lowers the pH and prevents colonization
  • Anaerobic bacteria- metabolic produces and FFAs that inhibit other organisms
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4
Q

what do infectious disease infect

A
  1. Entry of pathogen – portoal of entry/transmission
  2. Colonization – this happens usually at the site of entry
  3. Incubation period – asymptomatic period and toxins are produced
  4. Prodromal stage – vague feelings of discomfort, non specific complaints
  5. Period of illness (invasion) – symptomatic and more specific signs and symptoms, effect of toxins
  6. Convalesces – persons immune system responds to the infection
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5
Q

how do you get infected by infectious diseases

A
  • Direct contact
  • Airborne (inhalation of particles, respiratory droplets)
  • Vectors
  • Food-borne – such as salmonella and typhoid fever, this is an example for food-borne transmission
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6
Q

where do microbes enter the body

A

• Skin – open wound or punctures such as stepping on a nail, ulcers, infection from birth
• Respiratory system – inhalation such as influenza
– Ear nose and throat
• Oral – gastrointestinal - ingestion such as gastroenteritis
• Genitourinary system – sexual contact such as syphilis, chlamydia
• Placental
• Blood – needlestick injury such as hepatitis B, blood transfusions, vertile mother to baby

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7
Q

what disease can be caused by breach of skin

A
  • C.trachomatis (trachoma blindness)
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8
Q

what disease can be caused by the genito-urinary tract

A

syphilis, gonorrhoea, chlamydia

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9
Q

what diseases can be caused by transmission by infected blood

A
  • Blood transfusion – hepatis virus, malaria
  • Needlestick injuries – hepatitis A, B, C, HIV
  • Organ transplantation – organs with chronic viral infection
  • Vertical – mother to baby – viruses, syphilis
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10
Q

what are the stages in microbial infection

A
  1. Attachment to and/or entry into body
  2. Local or general spread
  3. Evasion of host defences
  4. Multiply and reproduce
  5. Damage the host
  6. Shedding (exit) from the body
  7. Host response
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11
Q

what are the adherences that bacteria use in order to get attachment and entry into the body

A
  • Fimbriae; interact with surface recetpors
  • Pili; transfer of DNA between bactiera; drug resistance
  • Biofilm – slimy plaque; well isolated colony
  • Haemagglutinin – glycoprotein in e.coli interacts with mannose
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12
Q

what is specific adherence

A
  • Haemagluttnin on infeuneza A and sialic acid receptor

- Haemagluttnin of E.coli and mannose receptor

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13
Q

whats the difference between pili and fimbriae

A
  • Hair like proteins
  • Fimbriae: interact with surface receptors similarly to antibody antigen interaction, present in multiple numbers
  • Pili not really an adherence mechanism, however, important to distinguish it from the fimbrae.
  • Pili: longer than fimbriae, present single or in pair; attach bacteria to each other to pass info, passage of drug resistance
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14
Q

what is the function of biofilm

A

– slimy plaque, well isolated colony

  • Make a community and grow as a community
  • Exchange DNA with each other
  • Become a mature biofilm – this is difficult to remove
  • The usm of all these adherence factors is a dense multi-cellular layer – biofilm
  • This protects the bacteria from host attack and being removed by peristalsis/tears and antibiotics
  • Hides the bacteria away from external stimuli and the immune system
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15
Q

What is the function of haemagglutinin

A
  • glycoprotein found on the surface of influenza viruses and E.coli. It is responsible for binding the virus to cells with sialic acid on the epithelial cells
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16
Q

what are the mechanisms of spread in the body

A

confinement to the skin
local spread
invasion of host cells

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17
Q

describe confident to the skin and give an example

A
  • easy to manage; doest move into other tissues
  • tinea corporis- ringworm fungal infection, HPV - warts- affect the basal keratinocytes and cause them to proliferate more
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18
Q

describe local spread and given an example

A
  • more serious, pathogens spread out, pass through mucosa and disrupt cell to cell interactions
  • Make enzymes that disrupt host cell to cell interactions making it easier for bacteria to spread
  • e.g. hyaluronidase, streptokinase and protease are enzymes that allows it to go into the blood stream as they break down the blood vessels and allow it to spread
  • Streptococcus pyogenes, Staphylococcus aureus
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19
Q

describe invasion of host cells

A
  • Spread directly through cells or via tight junctions
  • Some bacteria promote their entry/invasion into non-phagocytic cells; hide from host defences access to rich source of nutrients
  • Very serious as it can get access to circulation
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20
Q

what are the two mechanisms for bacteria to invade host cells

A

Trigger and Zipper

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21
Q

describe the zipper mechanism for invading host cells

A
  • Early mediated by high affinity binding of a pathogen surface protein with a transmembrane receptor on the host cell
  • Tight envelopment of the pathogen by the host cell membrane and uptake of the bacteria
  • Used by listeria monocytogenes Yersinia enterocolittica
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22
Q

describe the trigger mechanisms for bacteria invading host cells

A
  • Bacteria inject virulence factors directly into host cell cytoplasm to activate their own uptake by the cell
  • Bacteria only weakly adhere to the cell
  • Bacteria force the cell to extend local protrusions that engulf the bacterium
  • Type 3 secretion system-dependent
  • Used by salmonella spp, shigella Flexneri
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23
Q

what bacteria uses the zipper mechanism

A
  • Used by listeria monocytogenes Yersinia enterocolittica
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24
Q

what bacteria use the trigger mechanism

A
  • Used by salmonella spp, shigella Flexneri
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25
Q

describe the example of the trigger mechanism using salmonella

A
  • Employs a molecular syringe – type III secretion
  • Injects toxins into host cell which mediate invasion
  • Disrupt intracellular signalling pathways
  • Activate cytoskeleton by actin polymerisation
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26
Q

how do microbes spread throughout the whole body

A
  • if they gain access to the lymphatics or bloodstream they can spread throughout the whole body
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27
Q

what is scepiceameia

A

pathogen in blood with evidence of host damage

28
Q

what is bacterieamia and viremia

A

bacteria / virus in blood

29
Q

once the bacteria is in the blood what is is exposed to

A
  • Complement
  • Phagocytes
  • Antibodies
30
Q

what is complement part of

A

part of the innate immune system

31
Q

how does complement work

A
  • inactive form in circulation and activated by pathogen detection
  • proteolytic system with more than 30 proteins
  • chain reaction, activated proteins activate, activated by cleavage
32
Q

what are the 3 main functions of complement

A
  1. opsonisation (C3b)– and pathogen clearance by phagocytes
  2. MAC (C5b) - membrane attack complex and direct lysis of pathogens
  3. Enhancing inflammation (C5a)– activation and recruitment of phagocytic cell by anaphylatoxisn released by digestion of complements components (mast cells degranulation)
33
Q

what are the outcomes of complement activation

A
  • Cytolysis
  • Opsonization
  • Inflammation
34
Q

how do phagocytes kill microsomes

A
  • Binding microbe signals activation of killing mechanisms – phagolysosome
  • Antimicrobials lysosomal enzymes: cationic peptides - -defensins
  • Reactive oxygen species (ROS): superoxide, hydrogen peroxide
  • Nitric oxide (NO)
35
Q

how do bacteria persistence in the body

A
  • evasion of phagocytosis
  • detoxification of harmful substances from itself and the host
  • stealth
  • destroy antibodies
36
Q

explain how the Bacteria persist in the body by evading phagocytes

A
  • Inhibition of adherence (S.pyogenes), kill phagocytes (S.aureus), survive in phagolysosome (Coxiella burnetti)
    • S. pneumoniae cell surface proteins disrupt complement binding
    • M proteins in S. pyogenes inhibit phagocytes
    • Production of antiphagocytic enzymes
    – Leucocidin (S. aureus)
    – Streptolysin (S. pyogenes
37
Q

explain how the Bacteria persist in the body by detoxification of harmful substances from itself and the host

A
  • Stress causes upregulation of the genes producing these enzymes
  • Allows the bacteria to survive even if phagocytotic cells are active by neutralising toxic substances,
  • superoxide dismutase neutralises free radicals
  • Staph. Aureus, Enterobacter, H.Pylori produces urea which neutralizes gastric acid
38
Q

explain how the Bacteria persist in the body by stealth

A
  • S. aureus proteins A and G bind host antibody in the wrong orientation
  • B. pertussis binds heparin, host glycoproteins and glycolipids on its cell surface
  • H. pylori expresses Lewis X antigen, a normal component of gastric epithelium. Allows unrecognized habitation of gastric antrum.
39
Q

explain how the Bacteria persist in the body by destroying antibodies

A
  • H.influenzae and N.meningitis – produce proteases that destroys IgA
40
Q

How do bacteria obtain nutrients

A
  • Sugar and fatty acids are in the host
  • They need iron, there is very little in the host – it is stored in ferritin or bound to transferrin,
  • Bacteria possess efficient mechanisms to obtain host Fe
  • Bacteria have Fe chelating agents that have a high affinity for Fe – release these siderophores – enterobactin and aerobactin
  • Regulation of these factors is controlled by the degree of free Fe
41
Q

What are the mechanisms that viruses persist in the body

A
  • latency
  • evasion of phagocytes
  • hiding in human sites
  • antigenic varation
42
Q

explain how the virus persists in the body by latency

A

remains dormant following the infection and reactivates when immune-compromised (Herpes virus)

43
Q

explain how the virus persists in the body by evasion of phagocytes

A

prevent phagosome-lysosome fusion (HIV)

44
Q

explain how the virus persists in the body by hiding in human sites

A

sites protected from immune system (Herpes virus, Ebola, Rubella)

45
Q

explain how the virus persists in the body by antigenic variation

A

viral replication isn’t precise and mixing of different strains occurs (Influenza virus)

46
Q

what are the microbial toxins

A
  • exotoxins

- endotoxic

47
Q

what are exotoxins

A

proteins made by gram positive and gram negative

48
Q

what are endotoxic

A

the lipopolysaccharide component of gram negative bacteria cell wall

49
Q

what are the 3 classification of exotoxins

A
  • enzymatic - help bacteria spread in tissue: hyaluronidase, collagenase, epidermolysin (cleaves desmosomes)
  • damage membranes - lyse cells (cytolysins): phospholipases e.g. lecithinase of
    C. perfringens, haemolysins; pore forming proteins e.g. alpha toxin of S. aureus
  • activate immune response - super antigens
50
Q

what do all exotoxins do

A
  • They are all break down cell to cell interactions
  • Lyse cells, form pores leading to death of the host cell
  • Affect intracellular processe (protein synthesis)
51
Q

what are the two exotoxin subunits

A

A - enzymatic activity (active domain)

B - binding domain (membrane receptor on host cells allows translation of A subunit into the cytoplasm)

52
Q

name an example of exotoxin

A
  • most toxins active as enzymes are AB toxins
53
Q

what to AB toxins activate

A

enterotoxins (intestine) cytotoxins and neurotoxins

54
Q

what are the diseases caused by AB exotoxins

A

 Diphtheria – caused by Corynebacterium diphtheriae
– Toxin inhibits protein synthesis in heart muscle & other cells
- Stops action of elongation factor needed for translation
 Tetanus – caused by Clostridium tetani
– Toxin affects neuromuscular junctions → blocks release of inhibitory neurotransmitters (GABA)→ irreversible contraction of muscle and spastic paralysis
 Botulism – caused by Clostridium botulinum
– Toxin affects neuromuscular junctions → prevents release of excitatory neurotransmitter (acetyl choline) → lack of stimulus to muscle and flaccid paralysis

55
Q

what is the action of the cholera toxin

A
  • Activates secondary messenger pathways cAMP which affects downstream intracellular mechanisms leading to increase secretion of chlorine and consequently sodium and water leading to secretory diarrhoea
  • Enter the cells and deregulate their metabolism
  • Binds to receptors in the gut and then the toxin is transported into the cells of the gut
56
Q

what is the action of the diphtheria toxin

A

• In normal protein synthesis EF-Tu is required to transfer transfer tRNA to growing polypeptide

57
Q

name an example of an enterotoxin

A

staphylococcal

58
Q

describe staphylococccal enterotoxin and how it works

A
  • Staphylococcal enterotoxins act as superantigens
  • Does not need antigen for interaction
  • Causes huge cytokine release
59
Q

what is an enterotoxin

A

Enterotoxin is a toxin produced in or affecting the intesitnes such as those causing food poisoning or cholera

60
Q

how do endotoxins lipopolysaccharides work

A
  1. Macrophage ingest Gram-negative bacteria
  2. Bacteria is degraded in vacuole and so it releases the endotoxins which cause macrophage to produce cytokines
  3. These cytokines travel in bloodstream to the brain (hypothalamus)
  4. Cytokines induce hypothalamus to produce prostaglandins which reset body’s thermostat to a higher temperature, producing fever.
61
Q

what produces the endotoxin

A

gram negative

62
Q

what does the endotoxin do

A
  • Release of large quantities which cause overreaction of the immune response and host damage
  • Gram positive organisms also cause septic shock, probably from peptidoglycan fragments and teichoic acids
63
Q

what are the symptoms of an endotoxic shock

A
  • Fever or hypothermia (low body temperature)
  • Hyperventilation (rapid breathing)
  • Chills
  • Shaking
  • Warm skin
  • Skin rash
  • Rapid heart beat
  • Confusion or delirium
  • Decreased urine output
64
Q

what damage do microbes cause to the host

A

• Viruses often induce histological changes in certain cell lines
– giant cells
• Other viruses cause cells to enter apoptosis
– e.g HIV
• Some bacteria thrive and grow intracellularly causing granulomas
– M. tuberculosis
• Physical presence
– obstruction of lymphatics/gut/bile ducts by worms
• Direct cell destruction
– RBC’s with malaria

65
Q

what are the hypersensitivity reactions

A

• Type II hypersensitivity
– M. pneumonia
– Antibodies against the patients own RBC’s are produced and cells are lysed by complement
• Type III hypersensitivity
– S. pyogenes glomerulonephritis
– Polyarteritis nodosa in Hepatitis B infection
– Get rashes
• Type IV hypersensitivity
– Granuloma formation M. tuberculosis and M. leprae

66
Q

what microbes cause the development of cancers

A
  • Hep B – hepatocellular carcinoma
  • Epstein Barr – Burkitts lymphoma
  • HIV – lymphoma
  • HPV – cervical carcinoma
67
Q

What are the portals of exit

A
  • Ear ear wax
  • Broken skin – blood
  • Skin – flakes
  • Anus – faeces
  • Seminal vesicles seme and lubricating secretions
  • Eyes – tears
  • Nose – secretes
  • Mouth.- saliva and septum
  • Urethra – urine
  • In females – mammary glands, milk secretions
  • Vagina – secretions and blood

FunMed Microbiology (7 decks)

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