Inpopulation ecology,density-dependent processes occur whenpopulation growth rates are regulated by the density of apopulation.[1] This article will focus on density dependence in the context ofmacroparasite life cycles.
Positive density-dependence, density-dependent facilitation, or theAllee effect describes a situation in whichpopulation growth is facilitated by increased population density.[citation needed]
Indioecious (separate sex) obligatory parasites, mated female worms are required to complete a transmission cycle. At low parasite densities, the probability of a female worm encountering a male worm and forming a mating pair can become so low that reproduction is restricted due to single sex infections. At higher parasite densities, the probability of mating pairs forming and successful reproduction increases. This has been observed in the population dynamics ofSchistosomes.[2]
Positive density-dependence processes occur inmacroparasite life cycles that rely onvectors with a cibarial armature, such asAnopheles orCulex mosquitoes. ForWuchereria bancrofti, a filarial nematode, well-developed cibarial armatures in vectors can damage ingestedmicrofilariae and impede the development of infective L3larvae. At low microfilariae densities, most microfilariae can be ruptured by teeth, preventing successful development of infective L3 larvae. As more larvae are ingested, the ones that become entangled in the teeth may protect the remaining larvae, which are then left undamaged during ingestion.[3]
Positive density-dependence processes may also occur in macroparasite infections that lead toimmunosuppression.Onchocerca volvulus infection promotes immunosuppressive processes within the human host that suppress immunity against incoming infective L3 larvae. This suppression of anti-parasite immunity causes parasite establishment rates to increase with higher parasite burden.[4]
Negative density-dependence, or density-dependent restriction, describes a situation in which population growth is curtailed by crowding, predators and competition.[citation needed]
Incell biology, it describes the reduction incell division. When a cellpopulation reaches a certain density, the amount of requiredgrowth factors andnutrients available to each cell becomes insufficient to allow continuedcell growth.[citation needed]
This is also true for other organisms because an increased density means an increase inintraspecific competition. Greater competition means an individual has a decreased contribution to the next generation i.e. offspring. Density-dependent mortality can be overcompensating, undercompensating or exactly compensating.[citation needed]
There also existsdensity-independent inhibition, where other factors such asweather or environmental conditions anddisturbances may affect a population'scarrying capacity.[citation needed]
An example of a density-dependent variable is crowding and competition.
Density-dependentfecundity exists, where the birth rate falls as competition increases. In the context of gastrointestinal nematodes, the weight of femaleAscaris lumbricoides and its rates of egg production decrease as host infection intensity increases. Thus, the per-capita contribution of each worm to transmission decreases as a function of infection intensity.[5]
Parasite-induced vector mortality is a form of negative density-dependence. TheOnchocerciasis life cycle involves transmission via ablack fly vector. In this life-cycle, the life expectancy of the black fly vector decreases as the worm load ingested by the vector increases. BecauseO. volvulusmicrofilariae require at least seven days to mature into infective L3 larvae in the black fly, the worm load is restricted to levels that allow the black fly to survive for long enough to pass infective L3 larvae onto humans.[6]
Inmacroparasite life cycles, density-dependent processes can influence parasite fecundity, survival, and establishment. Density-dependent processes can act across multiple points of the macroparasite life cycle. Forfilarial worms, density-dependent processes can act at the host/vector interface or within the host/vector life-cycle stages. At the host/vector interface, density-dependence may influence the input of L3 larvae into the host's skin and the ingestion of microfilariae by the vector. Within the life-cycle stages taking place in the vector, density-dependence may influence the development of L3 larvae in vectors and vector life expectancy. Within the life-cycle stages taking place in the host, density-dependence may influence the development of microfilariae and host life expectancy.[7]
In reality, combinations ofnegative (restriction) andpositive (facilitation) density-dependent processes occur in the life cycles of parasites. However, the extent to which one process predominates over the other vary widely according to the parasite, vector, and host involved. This is illustrated by theW. bancrofti life cycle. InCulex mosquitoes, which lack a well-developed cibarial armature,restriction processes predominate. Thus, the number of L3 larvae per mosquito declines as the number of ingested microfilariae increases. Conversely, inAedes andAnopheles mosquitoes, which have well-developed cibarial armatures,facilitation processes predominate. Consequently, the number of L3 larvae per mosquito increases as the number of ingestedmicrofilariae increases.[3]
Negative density-dependent (restriction) processes contribute to the resilience of macroparasite populations. At high parasite populations,restriction processes tend to restrict population growth rates and contribute to the stability of these populations. Interventions that lead to a reduction in parasite populations will cause a relaxation of density-dependentrestrictions, increasing per-capita rates of reproduction or survival, thereby contributing to population persistence and resilience.[7]
Contrariwise, positive density-dependent or facilitation processes make elimination of a parasite population more likely. Facilitation processes cause the reproductive success of the parasite to decrease with lower worm burden. Thus, control measures that reduce parasite burden will automatically reduce per-capita reproductive success and increase the likelihood of elimination when facilitation processes predominate.[8]
Theextinction threshold refers to minimum parasite density level for the parasite to persist in a population. Interventions that reduce parasite density to a level below this threshold will ultimately lead to the extinction of that parasite in that population.Facilitation processes increase the extinction threshold, making it easier to achieve using parasite control interventions. Conversely,restriction processes complicates control measures by decreasing the extinction threshold.[8]
Anderson and Gordon (1982) propose that the distribution of macroparasites in a host population is regulated by a combination of positive and negative density-dependent processes. In overdispersed distributions, a small proportion of hosts harbour most of the parasite population. Positive density-dependent processes contribute tooverdispersion of parasite populations, whereas negative density-dependent processes contribute tounderdispersion of parasite populations. As mean parasite burden increases, negative density-dependent processes become more prominent and the distribution of the parasite population tends to become less overdispersed.[9]
Consequently, interventions that lead to a reduction in parasite burden will tend to cause the parasite distribution to become overdispersed. For instance, time-series data forOnchocerciasis infection demonstrates that 10 years of vector control lead to reduced parasite burden with a more overdispersed distribution.[10]