Chapter 25: Host-Pathogen Interactions Flashcards
opportunistic pathogens
many elements of normal flora act as opportunistic pathogens in susceptible hosts (heart disease, immunosuppression, radiation therapy, chemotherapy, MRSA)
obligate pathogens
never part of normal flora, always cause disease, usually require host for multiplication (HIV, hansen’s disease/leprosy)
mucous membrane barrier
first line of defense against pathogens
secrets glycoproteins (retain water)
lysozymes
antibodies
averts infection by flushing: sneezing, swallowing, erosion etc.
virulence
relative ability to cause disease
virulence factors
structures or molecules of an organism that increase its pathogenicity
examples of virulence factors
flagella- motility, attachment
frimbriae- attachment
capsule- concealment, attachment
adhesions- receptors of pathogen surface, glycoproteins, lipoproteins
exotoxins
endotoxins
endotoxin
structural part of outer membrane
secreted as part of normal physiological activity during membrane vesicle trafficking while also excreting other virulence factors and proteins
set free passively when cells die or disintegrated
lipopolysaccharide (lps) layer
replaces most of phospholipids in outer half of outer membrane
lipid a- host receptor recognition, differing chemistry among species
lps/lipid a structure determines immunogenicity
can cause inflammatory reactions
disregulation of: immune system, clotting cascade, blood pressure regulation
results in: fever, wbc count, hemorrhaging/clotting/ lowered bp, shock, death
exotoxins
inhibits host cell function or kills host cells
proteins release from pathogen cells as it grows
categories of exotoxins
cytolytic toxins, ab-toxins, superantigen toxins
cytolytic toxins
work by degrading cytoplasmic membrane integrity causing cell lysis and death
examples of cytolytic toxins
hemolysin: lyses RBCs
leukocidin: lyces WBCs
phospholipases: hydrolyze phospholipids into fatty acids
diptheria ab-exotoxin
blockage of protein synthesis
causes thick covering in back of throat
leads to difficulty breathing, heart failure, paralysis, death
neurological exotoxins
botulinum and tetanus
clostridium tetani and botulinum
produce potent AB-exotoxins that affect nervous tissue
botulinum toxins most potent biological toxins known
tetanus
opposite effect of botulinum
muscular rigidity/arrest in tension
rigid paralysis
enterotoxin
ab-exotoxins whose activity affects small intestine
cause massive secretion of fluid into lumen, vomiting and diarrhea
cholera toxin in vibrio cholerae
superantigens
cause overstimulation of immune sytstem
shock and death
due to localized infecion with systemic effects
can cause bacteremia or septicemia
causes non specific activation of t-cells resulting in polyclonal t-cell activation and massive cytokine release
fever, kidney disruption, liver etc.
exo-enzymes as virulence factors
invasiveness requires a pathogen break down host tissues, often done with enzymes that attack host cells
examples of exo-enzymes as virulence factors
enzymes that
break down tissue
manipulate clotting of fibrin
measuring virulence
not how many factors, bu how aggressively an infection and disease is established
estimated from experimental studies of LD50
highly virulent pathogens
show little difference in number of cells required to kill 100% of population
compromised host
one or more resistance mechanisms are inactive:
genetic predisposition
permanent primary infection
temporary condition
medical procedures
predispose individuals to develop disease
attenuation
decrease or loss of virulence
attenuated strains are valuable to clinical medicine, used as vaccines
