Micro Chapter 15

Primary pathogen

causes disease in healthy host

opportunistic pathogen

Microorganism that doesn't normally cause disease, but can become pathogenic under some circumstances

Pathogenicity

ability to cause disease

Virulence

-Degree of pathogenicity
-More virulent= more likely to cause a successful infection

Virulence Factors

-Traits of a pathogen that help it escape immune responses and cause infection
-Structures, enzymes and other proteins, and genetic changes

Portals of entry

Mucous membranes, skin, and parenteral route

Mucous membranes

Pathogens penetrate mucous membranes (resp. tract, GI tract, Gu tract, etc)

Skin

-Intact skin can't be penetrated by pathogens easily
-Few pathogens can use this portal (ex: fungi)

Parenteral route

-microbes are directly deposited into tissues because of a broken barrier (broken skin or damaged mucous membrane)
-Ex: cuts, burns, wounds, insect bites

preferred portal of entry

-Most pathogens have a preferred route to enter host
-Many pathogens only cause disease if they enter via their preferred portal

ID50

-Infectious dose needed to cause infection in 50% of a sample pop
-Not a fixed number
-Measures virulence

Lower ID50 = ?

higher virulence

LD50

-Lethal dose that causes death in 50% of a sample pop.
-Measures potency of a toxin

Lower LD50 = ?

Higher potency

Establishing infection while escaping host immune system

1.) adhesion
2.) Avoid or penetrate host defenses
3.) Damage host

Adherence

Essential first step in establishment of infection

Adhesins

-Ligands on the pathogen that bind to receptors on host cells
-Ex: glycocalyx (capsule or slime layer), fimbriae, and pili

Capsules

-Impair phagocytosis(avoid attachment step of phagocytosis)
-Used for attachment of pathogens to host cells
-Ex: Strep. pneumoniae, Haemophilus influenzae, bacillus anthracis, and Yesinia pestis

M Protein

-Mediates attachment of bacterium to host and resists phagocytosis
-Ex: Strep. pyogenes

Opa Protein

-In cell wall, allows attachment to host cells
-Ex: Neisseria gonorrhoeae

Waxy lipid (mycolic acid)

-Resists digestion by phagocytic cells (bacteria can even multiply inside phagocytes)
-Ex: Mycobacterium tuberculosis

Coagulases

-Coagulate fibrinogen into a blood clot
-Blood clot protects and isolates bacteria from phagocytosis and other host defenses
-Ex: Some staphylococcus species

Kinases

-Digest fibrin clots so pathogen can spread
-Ex: Strep. pyogenes

Hyaluronidase

-Digests hyaluronic acid that holds cells together
-Helps pathogen spread from initial site of infection

Collagenase

breaks down collagen to help pathogen spread

IgA protease

-Destroys IgA antibodies
-Escape antimicrobial effect of antibodies

Antigenic variation

-Process of a pathogen altering their surface antigen
-Immune responses are ineffective when pathogen changes the epitope
-Ex: Neisseria gonorrhoeae and Influenza

Invasins

-Surface proteins made by bacteria
-Rearrange actin to cause membrane ruffling of host cell so pathogen can enter
-Ex: salmonella

Using actin to move

-Bacteria using host actin to propel themselves from host cell to host cell
-Invisible spread of pathogens
-Ex: listeria and Shigella

survival inside phagocytes

1.) bacteria survive in phagolysosome (ex: Coxiella burnetii)
2.) Bacteria escape phagosome before it fuses w/lysosome (ex: listeria and shigella)
3. Bacteria prevents fusion of lysosome and phagosome (ex: mycobacterium tuberculosis)

Exotoxins

-Secreted by mostly gram + bacteria
-Proteins
-Released during growth of bacteria
-Unstable in heat
-High toxicity
-Doesn't cause fever
-Can be neutralized by antitoxin
-Small lethal dose
-Ex: gangrene, tetanus, etc.

Endotoxins

-Released by gram - bacteria
-Lipids (lipid A part of LPS)
-Released when cell dies
-Heat stable
-Low toxicity
-Can cause fever
-Not neutralized by antitoxin
-Large lethal dose
-ex: typhoid fever, UTI, and meningococcal meningitis

Antitoxins

antibodies against specific exotoxins

Toxoids

Vaccines that protect against bacterial toxins