Exam 1 Flashcards
what is allometric scaling?
body size influences physiological patterns, most commonly rates of interactions
as size increases, metabolic rate decreases
as size decreases, metabolic rate increases
volume:surface area
1cm– 1cc: 6cm^2
10cm– 1000cc:600cm^2
what is phenotypic plasticity?
single genotype generates more than one phenotype depending on environmental conditions
example: armored daphnia v. not
can be reversible or irreversible
reversible: acclimation (lab conditions, steroids), acclimatization (natural, breathing at sea level v. bozeman)
irreversible: polyphenism–developmental plasticity
what is fitness?
is not about observable traits..is about how many of an individual’s alleles make it into future generations
who REPRODUCES? “sneaky fuckers” aka the scottish deer
survival + reproduction
acclimation v. acclimatization
acclimation–under lab conditions,,steroids
acclimatization–natural, , breathing at sea level v. Everest
what are model organisms?
“for such a large number of problems there will be some animal of choice or a few such animals on which it can be most conveniently studied”
what is homeostasis?
strategies for coping with changing environmental conditions
conformers: allow internal conditions to change to match external conditions
regulators: maintain relatively constant internal conditions regardless of external conditions
osmoregulators: match salt concentrations of body to salt concentrations of sea water (sharks)
feedback loops and reflex control pathways
negative feedback loops: shut off at desired conditions (air conditioning)
positive feedback loop: rare, vomiting and other emergency defense mechanisms
what are the unifying themes of animal physiology?
communication between cells, tissues and systems, homeostasis, movement, senses, organ systems
disease
an interaction in which a disease organism lives on or within a host plant or animal to the benefit of the disease agent and to the detriment of the host
microparasite
single cell organisms
bacteria (prokaryotes)
protozoa (eukaryotes)–prions, viruses
viral infection
virus has harpoon that matches a docking protein of the host cell, viral RNA is injected into the cell and the host makes more virus
macroparasites
large, sometimes visible to naked eye
multicellular: worms, ticks, leeches, mosquitos
parasite categories
endoparasites: internal
ectoparasites: external
virulence
violence of the interaction between host and the parasite
can be variable within same species host and parasite
sub-lethal effects
decrease reproduction,, decrease fitness
increased vulnerability to predation
epidemic
the number of infections in human population increases
epizootic
the number of infected animals increases
currently: CWD chronic wasting disease
zoonosis, zoonotic disease
disease jumps from nonhuman animals to humans
examples: measles, seasonal flu
horizontal transmission
disease transfer from individual to individual
direct transmission
vertical transmission
disease transfer from parent to offspring,, gestation or birth
indirect transmission
disease transfer through intermediary(vector), usually insects
examples: lyme disease, rocky mountain spotted fever
definitive host
where the parasite has sex,, sexual reproduction of pathogen
SIR model
b births–> N susceptible –beta*cN–>infected–gamma–> recovered–v (Nu)–>susceptible
beta: how contagious is the disease
c: contact rate
N: number of susceptibles in starting population
alpha: death due to disease
v (Nu): lost immunity, back to susceptible pool
gamma: recovery, how long you’re sick, how much you transmit
d: background death
b: births
Ro
average number of infected people due to one infected person
Ro<1, disease is decreasing
Ro=1, not epidemic and not increasing
Ro>1, epidemic, number of infections is increasing
Ro equation
Ro=betacN/gamma
the infection rate(beta) x number of contacts (cN) divided by the recovery rate (gamma)
vaccine= decreasing susceptibility, decrease N
Ro should decrease as epidemic progresses because N decreases due to immunity
sero positive
have antibodies for antigen/pathogen or have pathogen on board
sero prevalent
proportion of individuals in a population that are sero positive
reservoir
population of hosts that carry pathogen
what is an evolutionary arms race?
an increase in pathogen virulence in response to increased host defenses
innate immunity
a series of defenses that act immediately upon infection and are the same whether or not the pathogen has been encountered before, outside of the cell, interstitial space
all animals have it
rapid, recognizes broad range of pathogens, no memory
adaptive immunity/acquired immunity
a system that learns to recognize specific pathogens and remembers them for future battles
once cell is penetrated
slower, has memory for specific pathogens
differs from individual to individual, depending on what pathogens they have been previously exposed to
can be achieved by vaccination
invertebrate immune response
rely solely on innate immunity:
exoskeleton, additional physical barriers, low pH, the enzyme lysozyme, immune cells capable of phagocytosis (cellular ingestion and digestion of foreign substances)
innate response players
external barriers: skin, secretions, mucous membranes, hairs, cilia
internal barriers: phagocytic cells, natural killer cells, defensive proteins, inflammatory response, interferon
tissue damage triggers innate response
neutrophils (WBC) diffuse out of widened, leaky capillary into interstitial fluid
mast cells secrete histamines and cytokines (signaling molecules)
macrophages release cytokines
additional fluid and cells accumulate around injury causing swelling
both macrophages and neutrophils attack and eat invaders/bacteria
interferons
limit the use of them because they affect viral and normal DNA
viral nucleic acid–>interferon genes turn on–>interferon DNA transcribes to mRNA–>inerferon proteins are made–> host cell 1 dies making interferon
host cell 2 is stimulated by interferon proteins and turns on genes for antiviral proteins–> antiviral proteins block viral reproduction
natural killer t cells
recognize cancer cells or cells infected by virus through cell surface signaling mechanisms
bind to receptors on distressed cells, releases perforins, and enzymes that enter the cell cause apoptosis, kills both natural killer cell and infected cell
antigens
any molecule that elicits an adaptive immune response
non self molecules that protrude from pathogens or other particles such as viruses, bacteria, mold spores, pollen, house dust, or the cell surfaces of transplanted organs
antibodies
attached to antigens
proteins found in blood plasma that attach to one particular kind of antigen and help counter its effects
made by cells formed from lymphocytes
lymphocytes
white blood cells that spend most of their time in the blood and tissues and organs of the lymphatic system
responsible for adaptive immunity
provide specialized defenses that act on pathogens located in either body fluids or inside cells
made from bone marrow
B cells (mature in bone marrow) and T cells (mature in thymus)
active immunity
person’s own immune system actively produces antibodies
passive immunity
receiving pre-made antibodies, boosters
lymphatic system
as lymph circulates through lymphatic organs it collects microbes, parts of microbes, and microbial toxins
transports them to lymphatic organs where macrophages engulf the invaders and lymphocytes my mount an adaptive immune response
returns fluid(lymph) that leaks out in capillary beds
drains into veins in the neck
collects excess filtered fluid and returns it to circulatory system–> lymph nodes filter lymph to remove pathogens–> lymphatic veins and ducts contain valves to prevent backflow
edema–accumulation of interstitial fluid
humoral response
action against free floating antigens
players: B cells and T cells
cell mediated response
action against infected cells
player: T cells
antigen receptors
specific protein that differentiates B cells and T cells
capable of binding to one specific type of antigen, which are then incorporated into the plasma membrane
all antigen receptors in the surface of a single lymphocytes are identical and recognize a particular antigen
B cells
participate in the humoral response
defend primarily against bacteria and viruses present in bodily fluids
secrete antibodies into the blood and lymph
clonal selection: fight current infections and remember the pathogen for future infection
clonal selection
antigens bind to a B cell that has corresponding antigen receptors
B cells with different antigen receptors are unaffected by this antigen
–>the selected B cell gives rise to a clone of B cells with antigen receptors for the same antigen–>
some B cells become effector cells(plasma cells), which secrete antibodies into the blood and lymph
some B cells become memory cells
memory cells
help activate the immune system upon subsequent infection
lasts for decades
antibodies do not kill pathogens
an antibody has two functions in the humoral response
1. to recognize and bind to a certain antigen
2. to assist in eliminating that antigen
inactivates antigens by:
neutralization (blocks viral binding sites, coats bacteria)
agglutination of microbes (clumps viruses and cells together)
precipitation of dissolved antigens (clumps of soluble antigens come out of solution)
^^^enhances phagocytosis
activation of the complement system (activated complement protein form membrane complexes)
^ leads to cell lysis
t cells
participate in the cell-mediate immune response and humoral response
defend against infections inside body cells
attack cells infected with bacteria or viruses
promote phagocytosis by other white blood cells and by stimulating B cells to produce antibodies
activated helper T cells secrete signaling molecules that have three major effects
- they stimulate clonal selection of the helper T cell, producing memory cells and more effector helper T cells
- they help activate B cells, this stimulating the humoral response
- they stimulate the activity of cytotoxic t cells of the cell-mediated response
helper t cell pathway
antigen presenting cell has surface self-nonself complex–> activated helper t cell–> helper t cell releases chemical messengers that stimulate more helper t cell production, activate b cells, and activate cytotoxic t cells
cytotoxic t cells (killer t cells)
only t cells that kill infected cells
once activated, clonal selection ensues and effector cytotoxic t cells identify infected cells through a self-nonself complex
play a role in protecting the body against the spread of some cancers
-HPV
-hepatitis B
-epstein-barr (causes lymphomas)
cytotoxic t cell pathway
infected cell presents self-nonself complex–> cytotoxic t cell containing perforin binds to an infected cell (“paul revere”)–> perforin makes holes in the infected cell’s membrane and enzymes that promote apoptosis–> perforin moves down concentration gradient into infected host cell–> infected cell is destroyed
primary immune response
occurs upon first exposure to an antigen
is slower than the secondary immune response
secondary immune response
occurs upon the second exposure to an antigen
is faster and stronger than the primary response
helper T cells, memory cells, and antibodies are already on board
