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Flashcards in Microbial Pathogens Deck (30):

What are the two classes of virulence factors?

Those that facilitate:

1. microbial invasion
2. host damage

ex. adhesins, capsules, biofilms, intracellular survival, superantigens, antigenic variation, latency, spores, cysts, exotoxins, endotoxin, antigenic variation, proteolysis of antibodies (extracellular proteases)


What are the 4 factors of invasion by microbial agents?

1. portal of entry
2. surface colonization
3. surviving host defenses
4. portal of exit and transmission to a new host


What are the primary portals of entry?

1. skin
2. mucosal membrane
3. organ transplants/blood transfusion


What two means of adhesion do pathogens use to colonize the surface of a portal of entry?

1. adhesins
2. bind to host receptors (hijack)


What are 4 ways pathogens survive in the cell?

1. inhibit lysosome fusion with phagosome
2. escape into cytoplasm
3. resist lysosomal enzymes
4. inhibit phagocytes' oxidative pathway (prevent oxidative burst)


Give an example of a pathogen that survives host defenses via immunosuppression:


depletes CD4+ T cells


Give an example of a pathogen that survives host defenses by diverting lymphocyte function through stimulation of immune system in nonproductive ways:

Streptococcus pyogenes and superantigens: stimulate nonspecific T cell response


What is an example of a protein that prevents opsonization of a pathogen?

What is an example organism that produces this protein?

Protein A- binds IgG on 'wrong end' of Fc

ex. Staphylococcus spp.


List the portals of exit:

-Mucosal membrane: resp tract, GI tract, Genital tract, Conjuntiva, Urinary tract
-Organ transplants/blood transfusion


What are the modes of transmission?

-Contact (direct, indirect, fecal-oral)
-Droplet (2 metres)
-Common vehicle (same needle)


What are two main strategies of transmission used by pathogens (to enhance being passed from host to host)? Give examples of each and organisms that use these.

1. Exaggerate host response:
-cough, sneeze: mycobacterium tuberculosis, influenza viruses
-rhinorrhea: common cold viruses
-diarrhea: norovirus, salmonella spp., shigella spp. , campylobacter spp.

2. Increase environmental survival:
-spores: clostridium difficile
-cysts: protozoa


What are the 4 main ways microbial agents harm us/cause damage?

1. damage due to host immune response

2. toxins: exotoxin (secreted into host), endotoxin (lipopolysaccharide in membrane, gram-)

3. apoptosis

4. mechanical causes


Are exotoxins usually necessary for bacterial growth?

No. They are dispensable (as with the plasmid they are carried on)


What are the 5 main mechanisms of action of exotoxins?

1. help bacteria spread in tissues:
-streptokinase (streptococcus pyogenes)
-DNase (staphylococcus aureus)
-hyaluronidase (S. aureus, S. pyogenes)

2. lyse cells:
-leukocidins (S. aureus)
-hemolysins (S aureus, S pyogenes)
-lecithinase (clostriudium perfringens)

3. block protein synthesis

4. elevate/suppress normal cell function:
-clostridium tetani (tetanus toxin), clostridium botulinum (botulism toxin)

5. block nerve functions


How does tatanus toxin work?

Retrograde transport to spinal cord (CNS)--> inhibits GABA--> rigid muscle contraction (resp muscles)--> death


How does botulinum toxin work?

Blocks release of ACh at NMJ (peripheral nerve endings)--> irreversible relaxation of muscles--> paralysis and resp arrest


How do we prevent and treat the effects of exotoxins?

-immune protection: vaccination with toxoids ex. tetanus, diptheria

-treatment with antitoxins ex. tetanus, diptheria, botulism


How to the endotoxins on GN bacteria work to cause host damage?

lipopolysaccharide on outer membrane of GN bacteria-->

Low levels: interacts with phagocytes--> cytokine release--> fever, vasodilation

High levels: alarming cytokine response--> septic shock and intravascular coagulation (lethal)


What is an example of a organism that blocks apoptosis of host cells (immortalize cells)

Human papillomavirus


What are 2 examples of organisms that cause premature apoptosis in host cells?




What kind of organisms can cause host damage via mechanical mechanisms (think BIG!)

helminths that cause obstruction:

heavy infestation with large roundworm 'Ascaris' (15-35 cm long, 0.5 cm thick)--> occludes intestinal lumen


What are the 2 major groupings of pathogens (disease causing microorganisms)?

1. opportunistic pathogens

2. true pathogens


What is the difference b/w opportunists and true pathogens?

Opportunists have no/few virulence factors (wouldn't infect if not for opportunity ie break in host defense)

True pathogens have many virulence factors

(*this is a spectrum)


Where is normal flora found (mostly bacteria)?

-skin (esp moist areas)
-respiratory tract: nose, oropharynx
-GI tract: mouth, large intestine
-GU tract: peri-urethra area, vagina


List 3 skin commensals/normal flora:

-staphylococcus spp. (GPCA= gram pos cocci aerobe)

-corynebacterium spp. (GPBA)

-bacillus spp. (GPBA)


List 4 examples of normal oropharynx flora:

-viridans group streptococci (GPCA)

-neisseria spp. (GNCA)

-haemophilus spp. (GNCBA)

-candida spp.


List 5 examples of normal large intestine flora:

-enterococcus spp. (GPCA)

-enteric bacilli/enterobacteriaceae: E coli, Klebsiella spp. (GNBAn)

-bacteroides spp. (GNBAn)

-clostridium spp. (GPBA)

-candida spp.


List 4 normal vaginal flora:

-viridans group streptococci (GPCA)

-peptostreptococcus spp.

-lactobacillus spp.

-candida spp.


What are the benefits of the normal flora in our bodies?

-immune stimulation (cross-reaction bw Ab to normal flora and virulent organisms)

-infection prevention (competition, produce inhibitory substances)

-human nutrition (GI bact flora: e coli, bacteroides spp.)--> synthesize vitamin K



List 10 main organisms that make up the normal microbial flora (our friends...unless opportunity presents to be our enemies):

-Staphyloccocus spp.
-Streptococcus spp.
-Enterococcus spp.
-Corynebacterium spp.
-Bacillus spp.
-Escherichia coli
-Haemophilus spp.
-Neisseria spp.
-Clostridium spp.
-Bacteroides spp.