pathogenicity Flashcards
mention some portals of entry
mucous membranes: respiratory tract, genitourinary, digestive and conjuctivae
skin
parenteral route
vertically transmitted infections- transplacental
what is the infectious dose?
titre of microorganism that initiates detectable symptoms, antibody or other response in 50% of a sample population.
ID50 and also expressed as virulence
what is LD50
Potency of the toxins. titre of organism that kills 50% of a sample population. Lethal dose
bacterial adherance to cells
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
Used for penetration into the host cell
Capsule-antiphagocytic
Cell wall structures
-mycolic acid
- M protein
- opacity Proteins
Enzymes
-coagulases
- kinases
-IgA proteases
- hyaluronidases
-collagenase
Explain the role of mycolic acid in penetration into the host
resists digestion by phagocytes, can multiply in phagocytes
M proteins in penetration into the host
- 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
Opacity proteins in penetration into the host
Membrane protein that mediate firm attachment/binding to epithelial and phagocytic cells.
Coagulases in penetration into host and bacterial species example
convert fibinogen to fibrin
isolate bacteria eg bacterial abscess, and protect from phagocytosis via fibrin layer around them
staphylococcus aureus
Bacteria species with M proteins in cell wall
Streptococcus pyogenes
Bacterial species with Opa proteins
Neisseria gonorrhoeae
kinases in penetration into host and bacterial species examples
breakdown fibrin formed by the body to isolate infection
streptokinase: streptococcus pyogenes
staphylokinase: staphylococcus aureus
hyaluronidases in penetration into host cell
hydrolyze hyaluronic acid in matrix holding together connective tissue thereby helping bacteria to spread
collagenase in penetration of host cell and example of species
break down collagen in connective tissue and organs. example Clostridium species
IgA proteases in penetration into host and examples of bacteria species
IgA protease helps prevent reaction where IgA produced by host traps bacteria in mucus
Neisseria gonorrhoeae and Neisseria menengitidis
what are antigenic and phase variation and their function
process by which some infectious agents change their surface antigens
help in evading adaptive immunity and may contriute to dissemination (spread)
specific definition of phase variation and antigenic variation
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
how pathogens damage host cells
using their nutrients
direct damage in immediate vicinity of invasion
produce toxins
induce hypersensitivity reactions
what are siderophores
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.
how bacterial cells cause direct damage to host cells
produce toxins, enzymes, their metabolism and multiplication in host cells, inducing host cells to engluf them and use them as transport, spreading throughout host
types of exotoxins
super antigens, AB toxins and Membrane disturbing toxins
AB toxins
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.
Superantigens- how they work
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.
how membrane disrupting toxins work and examples.
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
2 types of membrane disrupting toxins produced and example of who they’re produced by and name of toxin
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
examples of bacteria that release AB toxins
Clostridium tetani, staphylococcus aureus
examples of bacteria that release superantigens and diseases they cause
staphyloccus aureus - toxic shock syndrome, food poisining
production of endotoxins
lipid A portion of LPS in outer membrane is the endotoxin. released when bacterial cells die and lyse and during multiplication.
symptoms of endotoxins
produce same signs and symptoms no matter the species. chills, fever, weakness, generalized aches, shock and death.
how endotoxins work
- 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
