Flashcards in Exam #1: Host Parasite Relationships Deck (36):
Symbiotic relationship where microorganism benefits but the host is unaffected
Symbiotic relationship where both host & microorganism benefit.
Symbiotic relationship where microorganism benefits but host is harmed.
What are normal microbiota & how are they beneficial to the host?
Normal microbiota= commensal or mutual symbionts adapted to specific niches.
- Beneficial to host because=
1) Out-compete pathogenic microorganisms for niche
2) Produce "bacteriocins" that are toxins that harm other pathogenic bacteria
Where is the most dense grouping of the normal microbiota?
Describe the distribution of bacteria along the GI tract. Where is the highest density of normal flora in the body?
- Esophagus & stomach= v. low density of bacteria
- Small Intestine= low density
- Large Intestine= high density
How are neonates colonized with bacteria? Is the fetus sterile?
Fetus is generally sterile & then with delivery the neonate is colonized with bacteria.
- Vaginal delivery= skin colonized during birth
- C-section= colonized shortly after birth
What areas of an infant are normally colonized with bacteria?
What areas of an infant are normally sterile?
How does the normal micobiota & its interaction with the immune system change throughout life?
- Childhood= developing immunity as exposed to new microbes, shifting normal microbiota
- Healthy adult= developed immunity & stable microbiota
- Elderly= immune senescence & increased susceptibility to infection
What is the difference between resident & transient microbiota?
Resident= long-term members of microbiota
Transient= organisms that attempt to colonize the body but are unable to remain because of:
1) Competition from resident
2) Elimination by immune system
3) Physical & chemical changes within the body
E.g. proton-pump inhibitors
Give an example of resident microbiota. Where is it found? List the characteristics of the bacteria. When is it associated with infection?
Staphyloccous epidermis is a resident bacterium of the skin, nose, & ears that is:
- Cocci in clusters
Infection associated w/ prosthetic device & intravenous catheters--also it is a common contaminant of blood cultures
Given an example of transient microbiota.
Group A Strep (GAS) or Streptococcus pyogens
- Gram +
- Cocci in chains
Transiently colonizes the oropharynx of children & young adults in the absence of clinical disease & causative agent of strep throat
What is a pathogen, & what is the difference between a strict pathogen & an opportunistic pathogen?
Pathogens= microorganisms that have the capability to cause disease i.e. almost anything
Strict= NOT associated w/ microbiota & always associated w/ disease
- E.g. mycobacterium tuberculosis (causitive agent of TB)
Opportunistic= part of the normal microbiota & take advantage of pre-existing conditions
Which type of pathogen more commonly causes disease?
What is the difference between pathogeniticty, virulence, & virulence factor?
Pathogenicity= ability of organism to cause disease
Virulence= measure of pathogenicity
Virulence factors= factors produced by organisms that enable it to infect, cause disease, and/or kill host
What is a carrier?
Carrier= harbor pathogens as part of their microbiota without showing signs of disease BUT they can transmit disease to others
- Can be transient of semi permanent e.g. "Typhoid Mary" & Salmonella Typhi
What are the general steps of infection?
General steps of infection:
1) Entry into host
2) Adhesion, colonization, & pathogenic action of bacteria
3) Mechanisms for escaping defense
How is entry gained into the host?
- Transplacental (mother to fetus)
- Secretions (aerosol, mucosal)
- Stool (fecal-->oral)
- Skin (cuts, incisions, abrasions, burns)
- Blood (STIs, IV drug use)
- Zoonotic (animal to human)
- Arthropod (insect to human)
What are the barriers to protect from pathogen entry?
- Mechanical (skin & cilia)
- Enzymatic (lysozome)
- Chemical (acidic pH)
- Immunity (complement & antibody)
- Physical (sheer forces & peristalsis)
How do bacteria adhere to a host?
Binding of bacterial "adhesin" to host receptors
- Note that "adhesins" or attachment proteins are often associated with pili
- Specific adhesin & receptor combinations often define tropism
i.e. where you have adhesin receptors defines where bacteria can adhere & infect
What is a biofilm?
Biofilm= bacteria encased in exopolymeric substance , found throughout nature on surfaces that are commonly moist/wet e.g. shower, teeth...etc.
- Most bacteria don't live "planktonically," or freely moving in solution
- Most are stationary
How are bacteria in a biofilm different from planktonic cells?
- Altered & generally slowed metabolism-->more difficult to treat
- Increased resistance to abx
- Increased genetic exchange
- Resistant to disinfection b/c of decreased diffusion & increased organic matter
How are biofilms related to disease?
Most chronic infections have a biofilm component
What happens after adhesion?
- Invasion into cell, often by hijacking host cell machinery to facilitate uptake
How do bacteria destroy tissue?
- Toxic byproducts of growth
- Bacterial secretion of degradation enzymes
E.g. Clostidium perfingens (gas gangrene)
What is endotoxin? What is the difference between endotoxin & exotoxins?
Endotoxin= lipid A portion of LPS which is very different from "exotoxin"
Exotoxin= bacterial products that directly harm tissue or lead to destruction
- Can be cytolytic or receptor binding
What are AB toxins?
A class of exotoxins/ receptor binding proteins that contains A & B subunits with different functions (and initiate toxic reactions)
- A= active
- B= binding
What are Non-AB toxins? Give examples of non-AB toxins.
Toxins that function without AB subunits. E.g:
- Tetani that blocks the release of inhibitory neurotransmitter leading to excitation paralysis
- Botulinism that blocks release of excitatory neurotransmitter leading to flaccid paralysis
What is superantigen?
An exotoxin that binds both TCR & MHC Class II w/out requiring antigen
- Can cause life-threatening autoimmune-like responses
What mechanisms do bacteria have for escaping host defenses?
1) Encapsulation= capsule masks more antigenic epitopes on surface to prevent binding of ab or complement
2) Antigenic Mimicry= bacteria produces compounds that host sees as self
- HA (hyaluronic acid)
3) Antigenic Variation/ Shift= bacteria quickly change antigenic make-up of proteins on cell surface
4) Inactivation of ab= secretion of proteases that degrade specific antibody isotypes
5) Resistance to complement mediated killing=
- Limiting access to the membrane e.g. Long LPS O-antigen
- Degradation of complement proteins
6) Escaping phagocytic clearance
What mechanisms do bacteria have for escaping host defenses?
1) Inhibit opsonization
2) Inhibit chemotaxis
3) Kill phagocyte
4) Inhibit lysosomal fusion
5) Escape from lysosome
6) Resist antibacterial lysosomal action
How do bacteria regulate virulence factors?
- Bacteria often do NOT constitutively express virulence factors; they sense their environment
What is Quorum Sensing?
Quorum sensing= way for bacteria to sense the size of their population
- When the bacteria sense high population/ "critical mass" then they turn on virulence factor expression
Where is normal human microbiota found?
Upper respiratory tract (superior to trachea)
*Females, vagina as well