Exam 2 Flashcards
- Entry through break in skin
- Mucous membrane contact
- Ingestion of fecal matter
Direct, horizontal transmission
- Congenital transfer
- From mother to fetus/newborn
Direct, vertical transmission
- Inhalation of respiratory droplets from an infected person
- Large, travel less than 1 meter before dropping out of the air
Direct, droplet transmission
- Inhalation of small droplets
- travel more than 1 meter, hang in the hair for long periods of time
Indirect, airborne/aerosol transmission
- Inanimate surface/reservoir contaminated
- Pathogen enters through break in skin, mucosal membranes, or ingestion
Indirect, contaminates fomite transmission
- vertebrate animal
- indirect or direct
- vector-borne
- vehicle transmission from contaminated food/water to humans
zoonoses
- ingestion of contaminated food or water
Vehicle transmission
- arthropod carries pathogen, but pathogen does not replicate in vector
vector-borne, mechanical transmission
- arthropod is essential for the pathogen to complete their life cycle
vector-borne, biological transmission
- proteins or carbohydrates on bacterial surfaces that help with adherence
- Ag43/AIDA
- LPS
Afimbrial adhesins
- P fimbriae
- Curli
- Type I pili
- Type 4 pili
Fimbrial adhesins
- Flagella
- Capsule
Atypical adhesins
- common in Gram-negative bacteria
- form bundles at bacterial poles
- adhere tp sugar residues on host cells
- responsible for twitching motility/can “walk” across moist surfaces without flagella
Type IV Pili
- produces shield to inhibit opsonization and phagocytosis
- usually polysaccharide/sometimes protein
capsule
- more sugar residues
- produces shield to inhibit MAC formation
- Long O-antigen
Long LPS
- shield that inhibits opsonization and phagocytosis
- related to binding antibodies
- Protein G
Surface protein with affinity for Fc of antibodies
- possessing hyaluronic acid or sialic acid (common host molecule)
- not immunogenic
how capsule or LPS prevents opsonization
- when original antibody mediated response is no longer effective because they cannot find their target
- variation when some proteins are changes
- switch when completely changes
- on/off when no longer produces
Antigenic switching
- cirvumvention of natural barriers
- Avoids agglutination by antibodies
- e.g., enters through M cells, allowing breach of mucosal barrier without prior injury
disarming the enemy
- production of IgA protease
Avoids agglutination by antibody
- Receptor binding
- Invasin proteins
- effector proteins
mechanisms of intracellular pathogens to induce endocytosis/phagocytosis “hide”
- replicate in phagosome, need to prevent phagosome/lysosome fusion
- replicate in cytoplasm, must escape from the phagosome
how intracellular pathogens enter host cells
- siderophores that compete for iron
- removal or iron from hemoglobin, transferrin, or lactoferrin
- production of proteases
- production of hemolysins
how iron/nutrients are acquired from the host
- actin from host aids in motility to infect neighboring cells
- cell-wide membrane damage results in necrotic cytolysis
dissemination
- break down DNA in pus (dead neutrophils)
DNases, dissemination
- degrade proteins in connective tissue
Collagenases, elastases, and proteases, dissemination
- degrade hyaluronic acid in host connective tissue
Hyaluronidases
- LPS (Endotoxin-Lipid A)
- LTA
Non-protein toxins
- binds TLRs on phagocytes
- strong cytokine response, stimulates vasodilation and capillary leakage
- active coagulation cascade (disseminated intravascular coagulation/hemorrhage)
- can cause septic shock and heath
LPS and LTA/ effect of non-protein toxins
- an inflammatory response triggered throughout the body
- due to bacteria or bacterial products in blood
- hypoglycemia and hypotension observed along with DIC thrombosis
septic shock
- bind to target cell surface and exert effect extracellularly
- do not enter host cell
- cause indirect damage due to overstimulation of immune system
- crosslink MHC on T cells
T-cell superantigens, actively released, protein exotoxin, indirect damage
- act on eukakaryotic cell membranes
membrane disrupting toxins, direct damage
- active only after entry into host cell
A-B dimeric/bicomponent toxins, direct damage
- bacteria usually not in blood
- cytokines produced by T cells
vs. - live bacteria may be in blood
- cytokines produced mainly by phagocytes
superantigen/toxic shock vs. endotoxin/septic shock
- digestion of phospholipids
- formation of pores in membranes
two mechanisms of membrane-disrupting toxins
- binds host receptor
- allows for endocytosis into endosome
vs. - enzymatically active inside the cell
- alters protein production
subunit B vs. subunit A in A-B toxins
How is the A subunit of the A-B toxin activated
Host cell cleaves sulfide bond, active when released
which secretion systems have an injectosomes that can deliver effector proteins into the cytosol of host cells
type III and IV