Mortality Mechanisms

For the overview of death and decomposition — including what happens to dead biomass after organisms die — see Death and Decomposition.

Why Death Is Not a Background Detail

Death is the primary mechanism that controls population size. It is not a passive cleanup process that removes old organisms — it is an active, multi-dimensional force that responds to temperature, oxygen, pH, salinity, ammonia, starvation, crowding, and predation all at once. An organism that is mildly stressed by warm temperatures, slightly low on food, and living in moderately crowded conditions can die faster than one facing a single extreme stressor, because the penalties stack. This additive stacking of mortality sources is what creates realistic population dynamics: species do not simply crash from one catastrophic event but erode under the cumulative weight of compounding stresses.

Mortality also drives nutrient recycling. Every organism that dies becomes detritus, which feeds decomposers, which release nutrients back into the water for the next generation of producers. The rate and timing of death shapes the nutrient pulse that follows — a sudden crash floods the system with organic matter and can trigger an oxygen crisis, while steady background mortality keeps nutrients flowing without overwhelming decomposition capacity.

How Mortality Works in the Model

Every species in the simulator faces multiple simultaneous threats to its survival. These threats are calculated independently and then added together — an organism dealing with both heat stress and low oxygen suffers the combined penalty at the same time. The total mortality rate is applied as a fraction of the organism's current biomass each hour, so a 10% per hour mortality rate on a population of 100 units would remove 10 units that hour.

To prevent numerical problems, every species has a maximum total mortality cap (typically 40-60% per hour). No matter how many stressors pile up, the combined mortality rate cannot exceed this cap.

The rest of this document describes each mortality mechanism in detail, moving from the ever-present background losses through environmental and chemical stressors to the biotic interactions that create density-dependent population control.

Background mortality

Base Mortality

Every species has a constant background death rate that is always active, regardless of environmental conditions. This represents the unavoidable baseline losses from aging, disease, genetic defects, and other natural causes. The rate is small — typically 1-5% of the population per day, depending on the species. For example, Daphnia lose about 2% per day, copepods about 1.5% per day, and heterotrophic bacteria about 3% per day.

Base mortality is adjusted by temperature using the Q10 system (described below under temperature mortality). At warmer temperatures, organisms live faster and die a bit sooner; at colder temperatures, even these background processes slow down.

Environmental stressors

The physical environment imposes hard limits on where organisms can survive. Temperature, salinity, and oxygen each define a window of tolerance — and when conditions push past the edge of that window, mortality ramps up fast. These stressors often arrive together (warm water holds less oxygen, for instance), which is why additive stacking matters so much.

Temperature Mortality

Every species has a comfortable temperature range bounded by four thresholds:

Stress low: below this, the organism starts to struggle
Stress high: above this, the organism starts to struggle
Lethal low: at or below this, mortality hits its maximum
Lethal high: at or above this, mortality hits its maximum

Between the two stress thresholds is the safe zone — no temperature-related mortality at all. Between a stress threshold and the corresponding lethal threshold, mortality ramps up linearly. For example, if a species has a high stress threshold of 28 degrees C and a high lethal threshold of 32 degrees C, then at 30 degrees C it is halfway between stress and lethal, so it experiences 50% of the maximum temperature mortality rate.

Beyond either lethal threshold, the organism suffers the full maximum temperature mortality rate.

Different species have very different temperature tolerances. Daphnia are comfortable from 4-25 degrees C with lethal limits at 0 and 30 degrees C. Copepods are hardier, comfortable from 2-28 degrees C with lethal limits at 0 and 33 degrees C. Heterotrophic bacteria are the toughest, comfortable from 5-35 degrees C with lethal limits at 0 and 45 degrees C.

An additional subtlety: the maximum temperature mortality rate itself is adjusted by a Q10 factor. At cold temperatures, even the process of dying from temperature stress is slowed down.

Salinity Mortality

Salinity mortality works exactly the same way as temperature mortality — four thresholds (stress low, stress high, lethal low, lethal high) with a linear ramp between stress and lethal. The safe zone sits between the two stress thresholds, and beyond the lethal thresholds mortality hits its maximum.

Most species in the simulator are freshwater organisms and are very sensitive to salt. Daphnia are the most sensitive, with stress beginning above 4 PSU and lethal conditions above 10 PSU. Copepods are slightly more tolerant, with stress above 6 PSU and lethal above 15 PSU.

Chemical stressors

Where environmental stressors come from the physical world, chemical stressors come from what is dissolved in the water. pH and ammonia toxicity are particularly insidious because they interact with each other — high pH makes ammonia more toxic, and the processes that raise pH (photosynthesis consuming CO₂) tend to coincide with the conditions that produce ammonia (dense populations excreting waste).

pH Mortality

pH mortality follows the same linear-ramp pattern as temperature and salinity. There are four thresholds defining the safe zone and the lethal boundaries. Water that is too acidic or too alkaline causes increasing mortality.

Typical safe ranges vary by species. Daphnia are comfortable from pH 6.0 to 9.0, with lethal limits at 5.0 and 10.0. Copepods are a bit more tolerant, comfortable from pH 5.5 to 9.5, with lethal limits at 4.5 and 10.5.

Ammonia Toxicity

Ammonia exists in water in two forms: ammonium (NH4+) and un-ionized ammonia (NH3). The un-ionized form (NH3) is the toxic one — it can pass through cell membranes and cause damage. The fraction of total ammonia that is in the toxic NH3 form depends on two things:

pH: higher pH means more of the ammonia is in the toxic NH3 form. At pH 7.0 and 25 degrees C, only about 0.6% is NH3. At pH 8.0, it jumps to about 5.4%. At pH 9.0, roughly 36% is in the toxic form.
Temperature: warmer water also shifts more ammonia into the toxic form.

The simulator calculates the toxic NH3 fraction using the Emerson et al. (1975) equation, which accounts for both pH and temperature effects on the equilibrium between NH4+ and NH3.

Once the NH3 concentration is known, mortality follows the same linear ramp pattern: zero mortality below a stress threshold, ramping up to maximum at a lethal threshold. Daphnia are more sensitive (stress at about 0.05 mg/L NH3-N, lethal at about 1.0 mg/L), while Copepods are somewhat less sensitive (stress at about 0.07 mg/L, lethal at about 1.4 mg/L).

This mechanism is modeled for all consumer species (animals and microzooplankton including HNF and ciliates), not for algae or bacteria.

Hypoxia Mortality

Dissolved oxygen levels that are too low cause stress and death in aerobic organisms. This follows the same linear-ramp pattern, but inverted — mortality increases as oxygen decreases below a stress threshold, reaching maximum at a lethal threshold.

Daphnia begin to suffer below about 2.2 mg/L O2 and face maximum hypoxia mortality below about 0.6 mg/L. Copepods are somewhat more tolerant, with stress beginning below about 1.8 mg/L and lethal conditions below about 0.5 mg/L. Heterotrophic bacteria, being partially tolerant of low-oxygen conditions, have stress below about 1 mg/L and lethal below about 0.15 mg/L. Nitrifying bacteria, which depend on oxygen for their energy metabolism, are also subject to hypoxia mortality.

Biotic and density-dependent mortality

The stressors above come from the environment acting on organisms. The mechanisms below come from organisms acting on each other — or on themselves. Starvation, crowding, cannibalism, and viral lysis all intensify as populations grow, creating the density-dependent negative feedback loops that prevent any one species from dominating indefinitely.

Starvation Mortality (Consumers Only)

Animals that cannot find enough food to eat will starve. The simulator calculates starvation mortality by comparing food intake against metabolic needs.

The process works like this:

The organism's gross food intake (assimilated carbon) is reduced by the cost of digestion (called "specific dynamic action" or SDA, typically 18-20% of assimilated food). This gives the net energy available.
The organism's maintenance requirement is calculated from its metabolic rate and body size.
If net energy falls short of maintenance, the organism is in energy deficit. The severity of starvation is measured as the ratio of the deficit to the maintenance requirement (0 = fully fed, 1 = getting no food at all).
Mortality increases proportionally with starvation severity, up to a species-specific maximum rate.

Different species handle starvation differently. Rotifers are the most vulnerable, with a maximum starvation mortality of about 10% per day — they have no lipid reserves and crash rapidly without food. Daphnia have a maximum starvation mortality of about 7% per day. Copepods are hardier, with a maximum of about 4% per day — they can survive longer without food thanks to lipid reserves and the ability to enter a kind of dormancy.

Crowding Mortality (Daphnia, Rotifers, Ostracods)

At very high population densities, Daphnia, rotifers, and ostracods experience additional mortality from crowding. This represents the combined effects of:

Increased competition for food particles
Elevated ammonia and other metabolic waste products
Reduced filtering efficiency from physical interference between individuals
Increased disease and parasite transmission

The crowding mortality rate follows Michaelis-Menten kinetics (a saturation curve). At low population densities, there is essentially no crowding effect. As density increases, mortality rises but gradually levels off. For Daphnia, the maximum is about 5% per day with a half-saturation density of about 4 mg N/L. For rotifers, the maximum is about 6% per day.

For ostracods, crowding is calculated differently: instead of using volumetric density (mol N per liter), it uses areal density (mol N per cm² of crawlable benthic substrate). This reflects the reality that benthic animals compete for floor and wall space rather than for water volume. Surfaces with benthic_fraction > 0 (ceramic, sand, gravel — but not glass walls or filamentous algae) contribute to the available area. For ostracods the maximum crowding mortality is about 10% per day.

Density-Dependent Feeding Interference (Cherry Shrimp and Bladder Snails)

The crawling benthic grazers — cherry shrimp and bladder snails — do not self-limit through extra mortality. Instead, crowding suppresses their per-capita feeding rate: as density rises, individuals interfere with one another and each one eats less. This follows the experimental evidence for pulmonate snails (Brown, Carman & Inchausty 1994), where per-capita grazing rate falls steeply above ~4 snails per 25 cm² through behavioural interference, with food-depletion and chemical-cue explanations explicitly ruled out — crowded animals retain more ingested carbon and respire more rather than dying.

Mechanically, ingestion is multiplied by a factor K^n / (K^n + σ^n) where σ is the areal density (mol N per cm²) and K the half-feeding density. Because reduced feeding means reduced growth and reproduction, the population plateaus at the density where intake just covers maintenance — a stable, logistic-like equilibrium that is mass-conserving (uneaten food simply stays in the pool). This produces the boom-then-level-off that real snail populations show, and lets shrimp and snails coexist rather than one crowding the other to death. Crucially, the density is computed over the whole wetted surface (glass, hardscape, plant leaves), because shrimp and snails crawl everywhere — not just the benthic floor. (The earlier model counted only the floor and applied crowding as mortality, which drove cherry shrimp to spurious extinction at perfectly normal stocking densities.)

Bladder snails additionally facilitate the shrimp: by shredding and microbially conditioning coarse settled detritus into fine particles (a parallel settled → suspended detritus flux, like the amphipod shredder), they generate food that collector-grazers re-graze — the shredder→collector facilitation and cross-species coprophagy documented in stream-detritus ecology.

Cannibalism (Copepods Only)

Cyclopoid copepods are well-documented cannibals. Adult copepods will eat their own young (nauplii and early copepodites). In the confined space of a small container, encounter rates between adults and juveniles are high, making cannibalism a significant source of mortality.

Like crowding mortality, cannibalism follows Michaelis-Menten kinetics scaled by population density. At low densities, cannibalism is negligible. At high densities, the rate approaches a maximum of about 8% per day. The half-saturation density is about 5 mg N/L of Copepods biomass.

This creates a natural negative feedback loop: as the Copepods population grows, cannibalism intensifies, which limits further population growth.

Viral Lysis

Viruses are everywhere in natural water — typically outnumbering their microbial hosts by an order of magnitude — and they are a major population control mechanism across the microbial world. In the simulator, viral lysis provides density-dependent mortality for heterotrophic bacteria, nitrifiers, HNF and ciliates, and planktonic phytoplankton (cyanobacteria, green algae, and diatoms).

The mechanism follows Michaelis-Menten kinetics: as host density rises, the encounter rate between viruses and host cells climbs with it, driving more infections and more lysis. At low densities, lysis is negligible; at bloom densities it becomes one of the dominant mortality terms.

Bacteria. Bacteriophages reach a maximum lysis rate of about 4% per hour (~100%/day at saturating density), with a half-saturation around 3.4 mg N/L of bacterial biomass. Without this term, bacteria would bloom uncontrollably whenever DOM is available.

Phytoplankton. Cyanophages, chloroviruses, and diatom-infecting viruses are a primary mechanism of bloom termination — frequently more important than grazing or nutrient depletion. Maximum rates differ by group:

Group	Max rate	≈ %/day cap	Notes
Cyanobacteria	0.025/h	~60%/day	Cyanophages routinely drive Microcystis / Synechococcus crashes
Planktonic green algae	0.012/h	~29%/day	Chloroviruses (Brussaard 2004)
Planktonic diatoms	0.012/h	~29%/day	Frustule offers no protection from internal infection

Realised rates at typical aquarium bloom densities sit at 10–25%/day — consistent with the 5–40%/day range reported in the literature (Suttle 2007 Nature Reviews Microbiology 5:801–812; Brussaard 2004 J. Eukaryotic Microbiology 51:125–138).

Surface-attached (biofilm) phytoplankton are not subject to viral lysis in the model. Pelagic viruses don't follow biofilm cells into the EPS matrix at meaningful rates, and the diffusion boundary layer further suppresses encounter. This is the same shelter that protects embedded bacteria — see biofilm protection. Macrophytes are also exempt: structural tissues and slow turnover mean viral mortality on rooted, floating, and submerged plants is ecologically minor.

The viral shunt. When a phytoplankton or bacterial cell is lysed by a virus, its cytoplasm spills directly into the water as labile DOM — not as particulate detritus. Bacteria immediately begin consuming that DOM, releasing inorganic N and P back into the water column. This rapid recycling loop is the viral shunt (Wilhelm & Suttle 1999 BioScience 49:781–788). In simulator output you'll see it as a bacterial bloom following a phytoplankton crash, with detritus staying low because the lysed biomass never made it that far. Background mortality (senescence, environmental stress) still routes to detritus as before.

How Mortality Sources Stack

All applicable mortality sources are added together before being applied. This additive stacking is the single most important thing to understand about mortality in the model, because it means organisms rarely die from one overwhelming cause — they die from the accumulated weight of everything going wrong at once.

Consider a concrete example. A population of Daphnia in a small, warm jar on day 60 of a simulation. The temperature is 27°C — two degrees above Daphnia's stress threshold but well below its lethal limit, so the temperature penalty is modest, maybe 15% of the maximum rate. Algae are thin because the Daphnia have been grazing hard, so there is a mild starvation penalty — perhaps 20% of the maximum starvation rate. The population is dense at 3.5 mg N/L, triggering crowding mortality at about 30% of its maximum. Meanwhile, a nitrification surge has pushed pH to 8.5 while total ammonia sits at 1 mg N/L, putting the toxic NH₃ fraction at about 0.07 mg/L — just above the stress threshold, adding perhaps 5% of the maximum ammonia mortality. And base mortality ticks along at its usual 2% per day.

None of these stressors alone is lethal. The temperature stress is mild. The starvation is partial. The crowding is moderate. The ammonia is barely above threshold. But added together, this Daphnia population is losing biomass at a rate that outpaces its reproduction. The population starts to decline — slowly at first, then faster as the shrinking population changes the conditions around it. If the algae recover (less grazing pressure means more food), the starvation penalty eases. If the temperature drops at night, the heat stress lifts. The ecosystem is constantly renegotiating these overlapping pressures, and whether the Daphnia stabilize or crash depends on whether the relief arrives fast enough.

This is what makes additive stacking ecologically realistic. In nature, mass die-offs are almost never caused by a single factor — they happen when multiple moderate stresses converge. A fish kill in a warm pond does not happen because the water was too warm, or because oxygen was too low, or because ammonia was too high — it happens because all three hit at once, each made worse by the others (warm water holds less oxygen and makes ammonia more toxic). The model captures this compounding effect through simple addition, capped at each species' maximum total mortality rate (typically 40-60% per hour) to prevent numerical instability.