Exam 2 Study Guide (Chad)

Introduction to species interactions

Species interactions affect individuals, populations, communities, and evolution; they can be trophic (feeding: carnivory, herbivory, parasitism) or non-trophic (competition, facilitation) and can be +, −, or 0 for each species.

What is a trophic interaction

An interaction that involves feeding (e.g., carnivory, herbivory, parasitism).

What is a non-trophic interaction

An interaction that does not involve feeding (e.g., competition, facilitation/positive interactions).

Define symbiosis

Close physical/physiological association between species that can be positive or negative.

Define predation (broadly)

A trophic interaction where a predator kills and/or consumes all or part of a prey individual.

Define carnivory vs herbivory

Carnivory: predator and prey are animals; Herbivory: animal consumer and plant/algal prey.

Define parasitism

A predator (parasite) lives in/on a host, consumes certain tissues, typically harms but doesn’t immediately kill the host; pathogens are disease-causing parasites.

Define competition

Non-trophic interaction where species share limiting resources, reducing growth, reproduction, and/or survival of each competitor.

Define interspecific competition

Competition between different species (vs. intraspecific within a species).

Define positive interactions (facilitation)

Interactions in which at least one species benefits and none are harmed; includes mutualism and commensalism.

Define mutualism and commensalism

Mutualism: both benefit; Commensalism: one benefits, the other unaffected.

Define amensalism

One species is harmed while the other is unaffected (non-trophic).

Give examples of each interaction type

Carnivory (lion–gazelle), Herbivory (giraffe–acacia), Parasitism (ticks–dogs), Competition (weeds–flowers), Mutualism (coral–zooxanthellae), Commensalism (barnacles–whales), Amensalism (algae bloom shading understory).

Predator dietary strategies—generalist vs specialist

Many carnivores are generalists (broad diet/select most abundant prey); many herbivores are specialists (narrow diet, specific plant/parts).

Why do many carnivores have broad diets

Prey animals have high nutritional content and mobility; predators often take abundant prey.

Why do many herbivores have narrow diets

Plant tissues are abundant but lower in nutrients and defended; specialization overcomes defenses.

What is prey switching

Predators increase use of a prey type when it is relatively common, decreasing when it is rare.

Mechanisms predators use to capture prey

Speed/stealth, toxins, traps, sensory adaptations, handling strategies.

Prey defenses against carnivores

Physical (armor, spines, toxins), behavioral (vigilance, group defense, reduced foraging), and escape abilities (size, agility).

Trade-offs in prey defenses

Investment in defense (e.g., armor, vigilance) can reduce foraging, growth, or reproduction.

Plant strategies to avoid/tolerate herbivory—masting

Synchronously producing huge seed crops in some years and almost none in others to satiate herbivores.

Other plant defenses (structural vs chemical)

Structural: tough leaves, thorns, spines; Chemical: secondary metabolites/toxins and volatiles that attract predators of herbivores.

Inducible vs constitutive plant defenses

Inducible defenses are triggered by attack; constitutive defenses are always present.

Herbivore counter-defenses

Specialized digestive enzymes, sequestration/tolerance of toxins, and behavioral strategies; typically require costly specialization.

Example analogous strategies: cicada emergences

Mass, synchronous adult emergence reduces per-capita predation risk (akin to plant masting).

Predator–prey cycles: classic example

Snowshoe hare and Canadian lynx exhibit cyclic fluctuations; up to ~95% of hare deaths due to predation during certain phases.

Hypotheses for hare cycles and evidence

Food limits at high density but doesn’t halt cycles; predation strongly implicated; birth rates drop during declines; slow rebounds can occur even after predators drop.

Lotka–Volterra prey equation

dN/dt = rN − aNP (exponential prey growth reduced by predation term aNP).

Interpret prey parameters r, a, N, P

r: intrinsic growth rate; a: capture efficiency; N: prey abundance; P: predator abundance.

Lotka–Volterra predator equation

dP/dt = baNP − mP (predator births from prey consumption minus mortality).

Interpret predator parameters b and m

b: reproductive efficiency per prey eaten; m: predator mortality rate.

Prey zero-growth isocline (phase plane)

P = r/a (prey population stable when predator density equals r/a).

Predator zero-growth isocline (phase plane)

N = m/(ba) (predator population stable when prey density equals m/(ba)).

Equilibrium in LV predation model

Intersection of prey and predator isoclines; perturbations produce closed orbits (cycles) with predator lagging prey by ~¼ cycle.

Effect of adding prey density dependence

Logistic limits can dampen/alter cycles; position of isoclines still determines dynamics.

In LV, what happens to prey with no predators

Prey increase exponentially (density-independent assumption of the basic model).

Huffaker’s predator–prey experiments show what

Spatial complexity/dispersal refuges can enable long-lasting predator–prey oscillations.

Krebs’ hare–lynx field experiment takeaway

Both predation and food interact to shape hare dynamics; excluding predators and adding food had strongest effects.

Parasite definition and ecological role

Organisms living in/on hosts, feeding on tissues/fluids; strongly shape host population dynamics and communities.

Macroparasites vs microparasites

Macroparasites are large (e.g., worms, arthropods); microparasites are microscopic (e.g., viruses, bacteria, fungi).

Ectoparasites vs endoparasites (with pros/cons)

Ectoparasites live on host surface (easier transmission, higher environmental exposure); endoparasites live within hosts (safer from environment, higher immune exposure).

Horizontal vs vertical transmission

Horizontal: among non-parent–offspring; Vertical: parent to offspring.

Host defenses against parasites—physical

Barriers like skin/exoskeleton.

Host defenses—immune system

Innate/Adaptive immunity; vertebrate memory cells reduce reinfection risk.

Host defenses—biochemical and symbionts

Nutrient sequestration (e.g., iron-binding proteins), defensive symbionts (microbiome) that suppress pathogens.

Host–parasite coevolution key idea

Reciprocal adaptation (“arms race”) often favors intermediate parasite virulence and costly host resistance.

Red grouse de-worming experiment result

Reducing parasite loads reduced population fluctuations, implicating parasites in host cycles.

SIR model compartments and flows

S (susceptible) → I (infected) → R (resistant via recovery/immunity); infections at rate S·I·β, removal at rate I·m.

Define β and m in SIR

β: transmission coefficient (infection rate parameter); m: recovery or death rate of infected.

SIR reproductive ratio (R₀) formula

R₀ = (S·I·β)/(I·m) = S·β/m; if R₀>1 infection spreads, if R₀<1 infection declines.

Threshold susceptible density (S_T) formula

ST = m/β; disease persists/spreads when S > ST.

How do S, β, m affect R₀

Increasing S or β increases R₀; increasing m decreases R₀; I cancels in R₀ expression (no direct effect).

Prairie dog vaccination and R₀

Reducing susceptibles (via vaccination) lowers R₀, making epidemics less likely (example: R₀ from 18 to 4 when S drops from 90 to 20 with β=2, m=10).

Primary plague transmission to prairie dogs/ferrets

Vector-borne via fleas for prairie dogs; ferrets mainly via consuming infected prey tissue.

Competition—definition recap and consequences

Shared limiting resources reduce survival/growth/reproduction; can narrow fundamental → realized niches.

Limiting resources examples

Food, water, nutrients, light, space/territory, nesting sites.

Exploitation vs interference competition

Exploitation: indirect via resource depletion; Interference: direct prevention of resource use (e.g., fighting, overgrowing).

General properties of competition

Stronger when resources are scarcer; often asymmetrical; can cause competitive exclusion or allow coexistence.

Tansley’s bedstraw experiment—lesson

Outcome of competition depends on environment (soil type), showing context-dependent dominance.

Tillman’s diatoms (Synedra vs Asterionella)—lesson

Species that can draw a limiting resource (silica) to the lowest level can exclude competitors.

Rocky intertidal barnacles—lesson

Balanus excludes Chthamalus from lower intertidal via interference (overgrowth/smothering).

Rodents vs ants—seed competition study

Removing one competitor increased that group; removing both boosted seeds massively—evidence for exploitative competition for seeds.

Competitive exclusion principle (Gause)

Two species using the same limiting resource in the same way cannot coexist indefinitely.

Resource (niche) partitioning

Species reduce competition by using different portions/components of a limiting resource, enabling coexistence.

Character displacement

Evolutionary divergence in traits reduces niche overlap where competitors co-occur.

Lotka–Volterra competition model (species 1)

dN₁/dt = r₁N₁[(K₁ − N₁ − αN₂)/K₁]; species 2 imposes effect α on species 1.

Lotka–Volterra competition model (species 2)

dN₂/dt = r₂N₂[(K₂ − N₂ − βN₁)/K₂]; species 1 imposes effect β on species 2.

Isocline for species 1 (dN₁/dt=0)

N₁ = K₁ − αN₂ (line with intercepts K₁ on N₁ axis and K₁/α on N₂ axis).

Isocline for species 2 (dN₂/dt=0)

N₂ = K₂ − βN₁ (intercepts K₂ on N₂ axis and K₂/β on N₁ axis).

Four graphical outcomes in LV competition

(1) Species 1 wins (exclusion), (2) Species 2 wins, (3) Stable coexistence (intersection with stable equilibrium), (4) Unstable coexistence (priority effects).

How to diagnose coexistence graphically

Isoclines cross with each species’ K lying inside the other’s scaled intercept (K₁/α and K₂/β) so both can persist at the intersection.

Unstable coexistence signature

Each species’ isocline lies outside the other’s carrying capacity; the winner depends on initial densities (priority effects).

Link time-series to phase planes

Use single-species K values and competition outcomes to place isocline intercepts and the intersection point.

Only formulas to memorize (per guide)

LV predation (dN/dt = rN − aNP; dP/dt = baNP − mP), LV competition (two-species logistic with α, β), SIR (R₀ = Sβ/m; S_T = m/β).

How to change R₀ below 1 in SIR

Reduce S (e.g., vaccination), reduce β (transmission control), or increase m (faster recovery/treatment).

How does niche partitioning enable real-world coexistence

Species differ in resource use (e.g., diet, microhabitat, time), reducing direct overlap predicted to cause exclusion.

When do predators and prey cycle in LV

Near the intersection of isoclines, disturbances lead to neutrally stable cycles with predator ~¼ cycle behind prey.

What shifts predator–prey cycle amplitude

Initial densities and parameter values (r, a, b, m) set isocline positions and thus the trajectory magnitude.

Why do parasites often not kill hosts quickly

Selection favors transmission; overly lethal parasites reduce opportunities to spread.

What increases competition intensity

Greater scarcity of the limiting resource.

What makes competition asymmetrical

Species differ in resource acquisition/efficiency or interference ability, so one is harmed more than the other.

How can environment flip the competitive winner

Abiotic conditions (e.g., soil type) change the relative performance of competitors (Tansley bedstraws).

What determines who wins in resource competition

The species that can depress the limiting resource to the lowest equilibrium level can exclude others (R* concept illustrated by diatoms).

How does vaccination create herd protection in SIR

It lowers S below S_T (m/β), so R₀<1 and chains of transmission die out.

How to locate the prey isocline quickly

Draw a horizontal line at P = r/a on the N–P phase plane.

How to locate the predator isocline quickly

Draw a vertical line at N = m/(ba) on the N–P phase plane.

What does “predators > r/a” imply

Prey decline (dN/dt<0) because predator density exceeds prey’s zero-growth threshold.

What does “prey > m/(ba)” imply

Predator increase (dP/dt>0) because prey exceed predator’s zero-growth threshold.

How can spatial structure affect predator–prey persistence

Refuges and dispersal heterogeneity (Huffaker) can stabilize or extend oscillations.

Why are generalists common among carnivores but specialists among herbivores

Animal prey are nutrient-rich but variable; plant defenses and low nutrient content favor specialized counter-defenses.

How can inducible defenses be advantageous

They save costs when enemies are absent and deploy when attack risk rises.

How do defensive symbionts help hosts

Beneficial microbes can inhibit pathogens or prime host immunity, reducing infection success.

What are α and β in LV competition

Per-capita competitive effects: α converts N₂ into “equivalent” N₁ and β converts N₁ into “equivalent” N₂ in the logistic terms.

Graphical signature of stable coexistence in LV competition

Isoclines cross with each species limiting itself more than it limits the other (K₁/α > K₂ and K₂/β > K₁).

How to tell which species wins (exclusion) in LV competition

The species whose isocline lies “outside” (reaches the other’s K) excludes the other (relative positions of K, K/α, K/β determine winner).