pathogenicity Flashcards

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1
Q

mention some portals of entry

A

mucous membranes: respiratory tract, genitourinary, digestive and conjuctivae
skin
parenteral route
vertically transmitted infections- transplacental

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2
Q

what is the infectious dose?

A

titre of microorganism that initiates detectable symptoms, antibody or other response in 50% of a sample population.

ID50 and also expressed as virulence

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3
Q

what is LD50

A

Potency of the toxins. titre of organism that kills 50% of a sample population. Lethal dose

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4
Q

bacterial adherance to cells

A

Attach to specific receptors (usually carbs) using adhesins (located on pili, fimbrae or flagella) or ligands. These can be glycoproteins, lipoproteins.

Biofilms: Cells bound within a sticky web of polysaccharide. requires sufficient amount of bacteria (quorum). adhere to living and non living surfaces. found on teeth, indwelling catheters

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5
Q

Used for penetration into the host cell

A

Capsule-antiphagocytic
Cell wall structures
-mycolic acid
- M protein
- opacity Proteins
Enzymes
-coagulases
- kinases
-IgA proteases
- hyaluronidases
-collagenase

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6
Q

Explain the role of mycolic acid in penetration into the host

A

resists digestion by phagocytes, can multiply in phagocytes

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7
Q

M proteins in penetration into the host

A
  • M proteins: Major type proteins. anchored in cell membrane and portrude through the cell surface. interfere with phagocytosis by blocking he binding site for complement protien C3b
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8
Q

Opacity proteins in penetration into the host

A

Membrane protein that mediate firm attachment/binding to epithelial and phagocytic cells.

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9
Q

Coagulases in penetration into host and bacterial species example

A

convert fibinogen to fibrin
isolate bacteria eg bacterial abscess, and protect from phagocytosis via fibrin layer around them
staphylococcus aureus

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10
Q

Bacteria species with M proteins in cell wall

A

Streptococcus pyogenes

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11
Q

Bacterial species with Opa proteins

A

Neisseria gonorrhoeae

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12
Q

kinases in penetration into host and bacterial species examples

A

breakdown fibrin formed by the body to isolate infection
streptokinase: streptococcus pyogenes
staphylokinase: staphylococcus aureus

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13
Q

hyaluronidases in penetration into host cell

A

hydrolyze hyaluronic acid in matrix holding together connective tissue thereby helping bacteria to spread

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14
Q

collagenase in penetration of host cell and example of species

A

break down collagen in connective tissue and organs. example Clostridium species

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15
Q

IgA proteases in penetration into host and examples of bacteria species

A

IgA protease helps prevent reaction where IgA produced by host traps bacteria in mucus

Neisseria gonorrhoeae and Neisseria menengitidis

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16
Q

what are antigenic and phase variation and their function

A

process by which some infectious agents change their surface antigens
help in evading adaptive immunity and may contriute to dissemination (spread)

17
Q

specific definition of phase variation and antigenic variation

A

phase varitaion- switch on or off the expresssion of some components– allows expression of a given phenotype to be switched on or off

antigenic variation - alter the antigenic structure–expression of a number of alternative forms of an antigen on the cell surface, found in Neisseria gonorrhoeae

18
Q

how pathogens damage host cells

A

using their nutrients
direct damage in immediate vicinity of invasion
produce toxins
induce hypersensitivity reactions

19
Q

what are siderophores

A

small protein iron chelators, secreted to retrieve iron away from the iron transport proteins ( heme proteins and iron chelating proteins).
iron-siderophore complex is then taken up by siderophore receptors on the surface.
iron may be realesed from the complex or used to produce toxins that destroy host cells and release iron.

20
Q

how bacterial cells cause direct damage to host cells

A

produce toxins, enzymes, their metabolism and multiplication in host cells, inducing host cells to engluf them and use them as transport, spreading throughout host

21
Q

types of exotoxins

A

super antigens, AB toxins and Membrane disturbing toxins

22
Q

AB toxins

A

Dimeric, made of active and binding compenent. Made inside bacterial cell and then excreted. B part is used to bind to a specific cell surface receptor and A enters goes within the cell and inhibits protein synthesis and kills the host cell. Its main targets are the ribosomes, transport mechanisms and cell signaling. Tissues targeted by AB toxins are very defined and limited.

23
Q

Superantigens- how they work

A

modulate the activity between APC and helper T cells by interacting between the MHC, CD4 and TCR(T cell recepetor) interaction. It acts as a somewhat stimulatory mechanism to enhance this interaction and stimulate the ploriferation of T cells (increase in number) leading to a great release of cytokines.
These hormones regulate the immune response (inflammatory response) nad cell to cell communication—> increase leads to negative symptoms such as fever, nausea, diarrhoea, vomiting, shock and death.

24
Q

how membrane disrupting toxins work and examples.

A

these cause lysis of host cells by causing direct effects on their membrane. Some form protein channels/ pores eg Staphylococcus aureus and others affect the phospholipid bilayer eg Clostridium perfringens

25
Q

2 types of membrane disrupting toxins produced and example of who they’re produced by and name of toxin

A

Leucocidins- kill WBC eg staphylococci and streptococci
Haemolysins- kill RBC- produced by eg.streptococci. These procued by streptococci are called streptolysin O and streptolysin S

26
Q

examples of bacteria that release AB toxins

A

Clostridium tetani, staphylococcus aureus

27
Q

examples of bacteria that release superantigens and diseases they cause

A

staphyloccus aureus - toxic shock syndrome, food poisining

28
Q

production of endotoxins

A

lipid A portion of LPS in outer membrane is the endotoxin. released when bacterial cells die and lyse and during multiplication.

29
Q

symptoms of endotoxins

A

produce same signs and symptoms no matter the species. chills, fever, weakness, generalized aches, shock and death.

30
Q

how endotoxins work

A
  • binds to macrophage, activates release of cytokines. interleukins stimulate the hypothalamus to raise temp leading to fever. other cytokines increase capillary permeability and vasodilation leading to low blood pressure. sustained low BP leads to multi organ failure and then septic shock.
  • activate complement system–> histamine release, increase in inflammation and edema (leads to hypotension)
  • activates tissue factor III and others –> blood clot formation and decrease in clotting proteins–> Disseminated Intravascular Coagulation DIC