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Pathogenicity
ability of an MO to overcome hosts defences and cause a disease
Virulence
measure of pathogenicity of an MO, higher virulence = greater ability to cause a disease
Portals of entry
pathway that MO take to enter the body and cause disease, MOs can cause disease through only one portal or many
Portals of entry - mucous membranes
respiratory, MOs breathed in (influenzavirus, Bordetella pertussis - whooping cough, Streptococcus pneumoniae, Mycobacterium tuberculosis), gastrointestinal (shigella, salmonella, s. typhi), genitourinary tract (STIs)
Portals of entry - skin
usually impermeable to MOs, conjuctiva of eyes is more susceptible, hair follicles, sweat glands, some MOs can penetrate such as dermatophytic fungi and hookworms
Portals of entry - parenteral route
MO bypasses the skin, typically though an open wound
Measuring virulence
ID50 value, infectious dose is sufficient to infect half of the tested population, evaluated experimentally, can change
Measuring toxicity
measured as an LD50 value, lethal dose is sufficient to kill half of the tested population, tested on mice
Toxins tested in mice - lowest to highest dose
botulinum toxin, shiga toxin, staphyloccol enterotoxin
Bacterial damage - use of host cell nutrients
MOs uses metabolites before host cell can, analogous to a tapeworm, iron siderophores
Bacterial damage - direct damage
MOs grow so large in number that the host cells burst or rupture, intracellular MOs such as viruses and some bacteria (Chlamydia, Rickettsia), or protozoans (Plasmodium), produces enzymes that degrade plasma membrane - entry
Bacterial damage - toxins
poisonous substances produced by bacteria (or other MOs) that affect the host, toxigenicity
Exotoxins
mostly gram positive, synthesized during bacterial metabolism, secreted during growth or upon cell lysis, highly toxic, associated diseases often due to toxin, not the bacteria
Exotoxin examples
Botulism - Clostridium botulinum
Staphylococal food poisoning - Staphylococcus
Endotoxins
part of outer membrane of gram negative cells, lipid A of lipopolysaccharide, released when bacteria die, cell wall components break down, toxin is released, can be triggered by antibiotics - more bacteria die, more toxins