How Do Microbes Cause Disease Flashcards

1
Q

what is the standard pattern for stages of disease?

A

*Incubation period
-Asymptomatic period
-Toxins produced

*Prodromal stage
-Vague feelings of discomfort
-Nonspecific complaints

*Period of illness (invasion)
-Symptomatic and more specific signs and symptoms
-Effect of toxins

*Convalescence
-Persons immune system responds to infection (or medical intervention)

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2
Q

describe the complement system + its function. how do pathogens resist + subvert these host immune responses and persist in any host

A

complement system= its made up of plasma proteins (i.e. blood soluble proteins), the plasma proteins react with one another to opsonise pathogens + induce a series of inflammatory responses to fight infection [part of first response of Innate Immune system]

3 main functions of complement:
1- opsonisation (C3b) and pathogen clearance by phagocytes
2- MAC : membrane attack complex (C5b) and direct lysis of pathogens
3- enhancing inflammation (C5a): activation and recruitment of phagocytic cells by anaphylatoxins (C5a, C3a) released by digestion of complements components

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3
Q

explain how bacterial toxins induce damage to the host + contribute to disease

A
  • bacteria can prevent phagocytosis by macrophages by inhibitting chemoattractants, inhibiting chemotaxis e.g. Streptococcus pyogenes degrades C5a-specific serine protease
  • bacteria can prevent being ingested by phagocytosis by killing phagocytes, having capsules that protect them from opsonisation,
  • bacteria can escape from endosome-phagosome and grow in cytoplasm
  • bacteria can destroy antibodies e.g. IgA proteases {enzymes that break down antibodies are produced by following bacteria):
    *H. influenzae
    *N. meningitidis
    *S. pneumoniae
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4
Q

What are the 2 major factors of bacterial adherence to a host cell

A

1) PILI + FIMBRIAE
pili (singular: a pilus) is a hair-like microfiber appendage found on the surface of many bacteria and archaea.Pili only occur on gram -ve bacteria. Pilli are long and thick. Pili aid in bacterial conjugation

fimbriae= tiny, bristle-like fibers arising from bacteria. Fimbriae occur in both gram +ve and gram -ve bacteria. Fimbriae are short and thin. Fimbriae attach the bacterium to the substrate

SO BOTH THESE SURFACE STRUCTURES ARE A WAY IN WHICH THE BACTERIA ATTACK THE HOST CELL (these are a major factor of bacterial adhesion)

2)AFIMBRIAL ADHESIN
*membrane or mebrane bound glycoproteins or glycans that interact with host cell receptors via a bridging molecule{bring the bacteria in close contact to our cells} and help bacteria to adhere + attack them

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5
Q

what are biofilms? why are they clinically relevant?

A

Structured community of bacteria that produce a sugar polymer, known as extrapolymeric substance (EPS), that allows the biofilm to attach to a surface

clinical relevance
* biofilms have extreme resistance to antibiotics + other anti-microbial agents
* high resistance to host immune defences

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6
Q

some bacterial pathogen produce degradative enzymes (spreading factors) that participate in formation of lesions at the site of colonisation and facilitate growth and spread of the pathogen - They do not kill host cells.
What are the following spreading factors?
*hyaluronidase
*collagenase

A

hyaluronidase (spreading factor):
– breaks down hyaluronic acid (intracellular cement of connective tissue)
– e.g., Streptococcus spp, Staphylococcus aureus,
certain Clostridium spp

collagenase breaks down collagen network supporting tissues + promotes spread of infection e.g. some Clostridium perfringens {causes gas gangrene}

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7
Q

explain the 2 main mechanism of bacterial invasion into host cells: Trigger + Zipper

A

triggered invasion
e.g. used by salmonella bacteria
-bacteria inject virulence factors directly into host cell cytoplasm to activate their own uptake by the cell
-these virulence factors modify host cells to engulf them (i.e. ‘triggering’ cytoskeletal rearrangement in host cell)

zippered invasion
e.g. used by Listeria or Yersinia bacteria
-cell wall of bacteria has these high affinity receptors on it that recognise + BIND TO host cell receptors
-so now they are bound together + the bacteria activates signalling pathways inside host cell that encourage the host cell to take the bacteria in (zips its way in)

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8
Q

define opsonization of pathogens

A

Opsonization is an immune process which uses opsonins to tag foreign pathogens for elimination by phagocytes. Without an opsonin, such as an antibody, the negatively-charged cell walls of the pathogen and phagocyte repel each other

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9
Q

what is a zymogen

A

a zymogen is an inactive substance which is converted into an enzyme when activated by another enzyme

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10
Q

how does h.pylori invade the gastric mucosa

A

Helicobacter pylori is a gram-negative, flagellated, microaerophilic bacterium that selectively colonizes the gastric mucosa.

  • H. pylori expresses Lewis X antigen (LPS=lipopolysaccharide), a normal component of gastric epithelium. Allows unrecognised colonization of gastric antrum.

n.b. the LPS mediates the binding of the bacterium to laminin, and interferes with gastric cell receptor-laminin interaction, thereby potentially contributing to the loss of mucosal integrity

  • Antrum: the lower portion (near the small intestine), where the food mixes with gastric juice. Pylorus: the last part of the stomach, which acts as a valve to control the emptying of the stomach contents into the small intestine
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11
Q

what is the difference between an endotoxin and an exotoxin

A

endotoxins are part of the outer portion of the cell wall of gram -ve bacteria. They are released when bacteria die + cell wall breaks apart
endotoxins include: cell wall components; lipopolysaccharide(LPS), peptidoglycan, teichoic acids

exotoxins are released from live bacteria + are mostly produce by gram +ve bacteria

3 main types of exotoxins:
*Cytolysins with cell membrane targets (stimulate production of cytokines and can drive body into toxic shock)
*Bipartite A-B toxins: intracellular targets
*Toxins acting on host defences (superantigens)

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12
Q

what is cholera caused by and explain the mechanism of the cholera toxin?

A

Vibrio cholerae bacteria produces Cholera toxin: speeds-up normal excretory process in gut epithelium leading to massive fluids loss with diarrhoea and severe dehydration

how does cholera toxin induce diarrhoea?
* Cholera toxin is an A-B toxin
*ADP-ribosylates large G proteins that regulates cyclic AMP (cAMP)
* Increase of cAMP (up to X100)
*Stimulates chloride ions secretion via cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel
*Water and other electrolytes osmotically follow which cause diarrhea

*Severe cases: up to 12 liters of liquid lost per day
*Untreated cases: mortality about 50%
*Treatment: fluids and electrolytes

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13
Q

what is a superantigen?

A

Normal situation: antigen is presented by class II MHC and recognized by only a specific sets of T cells with right T cell receptor.
T cells produce and release cytokines locally and activate only B cells specific from antigen.
0.01 to 0.001 % of T-cells activated

super antigen= induces non-specific class II MHC – T-cell receptor binding.
Cause widespread non-specific stimulation of T-cells.
Excessive cytokine release, systemic. Leads to fever, vomiting, diarrhea and circulation/organs failure and death
20 to 30% of T-cells activated

n.b. Toxic Shock Syndromes are mediated by exotoxins which activate the immune system to release inflammatory cytokines. These exotoxins act as superantigens, causing T cell activation and the resulting “cytokine storm” (TNF-alpha, interleukin [IL]-1, and IL-6)

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14
Q

Some viruses incorporate their nucleic acid into the host genome which can cause the development of cancers; what are some examples of viruses that can do this

A
  • Hep B – hepatocellular carcinoma
    • Epstein Barr – Burkitts lymphoma
    • HIV – lymphoma
  • HPV – cervical carcinoma
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15
Q

what are some examples of disease caused by A-B EXOTOXINS

A

Examples of disease caused by A-B EXOTOXINS

  • Diphtheria – caused by Corynebacterium diphtheriae
    – Toxin inhibits protein synthesis in heart muscle & other cells
    Symptoms=
  • Tetanus – caused by Clostridium tetani
    – Toxin affects neuromuscular junctions → blocks release of inhibitory neurotransmitters (GABA- Glycine) in CNS→ leads to irreversible contraction of muscle and spastic paralysis
    Symptoms=
  • Botulism – caused by Clostridium botulinum
    – Toxin affects neuro
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16
Q

what is LIPOPOLYSACCHARIDE (LPS)

A

Lipopolysaccharide (LPS) is a type of endotoxin (LPS is a component of the outer membrane of Gram-negative bacteria. LPS is localized in the outer layer of the membrane and is, in noncapsulated strains, exposed on the cell surface.)

  • lipid A is the toxic portion, activates complement and stimulates production of cytokines

=results in septic shock:(Septicaemia): fever and diffuse haemorrhage

LPS net effect is induction of fever inflammation, intravascular coagulation, which can lead to haemorrhage and endotoxic shock