Name the species Flashcards
M protein/ fimbriae
Group A Streptococci
Polysaccharide capsule
S. Pneumoniae
Surface slime / biofilm
Pseudomonas aeruginosa
O polysaccharide
LPS of E. Coli
K antigen / Vi antigen
E. Coli and Salmonella typhi
Cell-bound or soluble Protein A
Staph. Aureus
Protein A mechanism
Attaches to Fc region of IgG, blocks cytophilic domain, can’t bind cell, IgG no longer capable of opsonization
Part of cell wall released to inhibit cell fusion
Mycobacterium Tuberculosis
Phagolysosome formation inhibited in phagocyte
Chlamydiae - L. pneumophila - Salmonella typhimurium
Survival inside phagolysosome - Waxy, hydrophobic cell wall - MYCOLIC ACIDS
Mycobacteria
Survival inside phagolysosome - LPS of cell wall
B. abortus
Survival inside phagolysosome - catalase & superoxide dismutase
B. Abortus, S. Aureus
Survival inside phagolysosome - poly-D-glutamate capsule
Bacillus anthracis
Escape phagolysosome - phospholipase A degradation of membrane
Rickettsiae
Survival inside phagolysosome - Listeriolysin O (pore-forming) & two phospholipase C types, polymerization of actin cytoskeleton for movement through cell
Listeria monocytogenes
Survival inside phagolysosome - lyse phagosomal vacuole, induce actin cytoskeleton polymerization for movement & spread
Shigella
Killing phagocyte before ingestion - secrete pore formers (hemolysis/ leukocydins)
Gram positive pathogens
Killing phagocyte before ingestion - produce streptolysin –> lysosomes explode into cell cytoplasm
Streptococci
Killing phagocyte before ingestion - produces leukocidins –> discharge of lysosomal granules
Staphylococci
Killing phagocyte before ingestion - exotoxin A. (Who secretes it? What does it do?)
Pseudomonas aeruginosa - disrupts cell equilibrium and consumes ATP reserves needed for engulfment if things
How does Neisseria gonorrhoeae maintain antigenic diversity
Change fimbriae antigen confirmation during infection. “Pili switching” (phase variation) rapid turning on/off genes controlling pili
How does Borrelia recurrentis maintain antigenic variation?
Relapsing fever by multiplying bacteria in tissues, bacteria then “disappear” (hide), fever falls until mutant arises again
Factor H binding proteins - complement evasion (how? Which species use this?)
Bind Factor H so it can’t bind C3b so no complement.
- B. Burgdorferi (Erp proteins) and Leptospira interrogans (LfhA)
Ringworm
Dermatophytes! Microsporum, Trichosporum spp.
Feline ringworm
Microsporum Canis. (Yes, canis! And they are the main reservoir)
Favus or White Comb
Avian ringworm: Microsporum Gallinae
Red growth in dermatophyte test medium (DTM)
Indicates growth of dermatophyte
Ringworm in cow
T. Verrucosum
Ringworm in pigs
T. Nanum
Dermatomycoses
Malassezia spp., (pachydermatis & nana) , Trichosporon (not trichophyton the dermatoPHYTE). Geotrichum candidum.
Subcutaneous mycoses
Sporotrichosis (sporothrix schenkii) - Pythiosis - chromoblastomyxisis & Phaeohyphomycosis - mycetomas
African Horse Farcy
Histoplasma capsulatum var farciminosum. Granulomatous skin lesions
Pythiosis
Oomycoses - stramenophiles (not fungi!). - EDx: Pythium insidiosum