8.1 Ecological balance

The long-time survival of any organism in a certain region requires that its permanent reproduction has to avoid either lasting increase or decrease. The net reproduction rate and the net case reproduction rate of any pathogen and parasite, respectively, both designed by R0 , finally had to be exactly one. Any lasting aberrations above or below this level lead to the extinction of both. Another question that arises is at what population density does the stasis oscillate. In all cases, R0 =1 can be achieved only by regulation, mostly involving feedback mechanisms. Two opposite groups of pathogens have been found based on the long-term strategies with which they coexist with their host populations.

Alternative strategists (fig. 8.1, page 282, left side).

A microbial pathogen might infect a mammalian host individual. After the incubation period, two pathways can be taken following the crisis: either the host survives, acquires a specific protective immunity and can later propagate, or the host perishes together with the pathogen. In the latter case, the pathogen has to reach another host individual before the first one expires, whereas the offspring of the immunized host can be reached by the pathogen later on and thus passes to the next host generation.

At high host density, the intraspecific competition between the hosts is strong, their physical non-specific resistance is stressed and more hosts will succumb to the infection. The population density is thus lowered, the competition also becomes lower and more hosts will survive. In short, non-specific but density-dependent factors of the physiology of the host decide the outcome of the encounter. However, for this kind of population-density regulation, it is crucial that protective immunity is memorized, but not inheritable. The mechanisms that the strategy is based on are simply reduced to a race between the reproduction potential of the pathogen and the defensive reaction potential of the immune apparatus. The regulation of the host population density is achieved during its various generations by periodic epidemics or a permanent endemia. The transmission of the pathogen depends on the contact rate between infected and susceptible hosts. The more immunized hosts that are present, the less that susceptible ones are contacted by the pathogen. The very last susceptible individuals escape any infection, because they are passively protected by the many immunized hosts, and thereby the genetic conservation of susceptibility is guaranteed. The transmission of the pathogen takes place without special stages and such pathogens are not sexually differentiated.

The potential case reproduction rate of the disease is the possible number of secondary infections that a single case may create during its patency (tranferent phase of the infection) without measures being taken against it. For German measles, a single case in Europe may induce 6 secondary cases, whereas in Gambia, there will be 15 cases; for measles in Africa, 18 secondary cases have been calculated. Such rates induce rapidly increasing epidemics and, once they pass a maximum, they accordingly disappear quickly. The virulence of the pathogen and the lethality of the disease determine the effect on the long-range population density. Regulation prevents either the complete eradication of the host population or of the pathogen. Thereby, the coexistence of host and pathogen is guaranteed. The best examples are the above-mentioned microbial pathogens causing acute infections.

Balance strategists (fig. 8.1, page 282, right side).

A eukaryotic, proto- or metazoan parasite might infect or infest (see below) a mammalian host individual. After the prepatent period, the parasite’s propagation stages will be directly transferred by the faeces or by an intermediate host or they appear in the circulating blood ready for transmission by a vector. Transmission stages are produced as long as the adult parasites live or the infection persists. Acquired immune reactions are induced – a delayed type hypersensitivity (DTH) – but they are not protective. Superinfections lead to accumulated parasite loads; in endemic regions multiple reinfections are the rule, particularly in short-term spontaneously curing infections. Chronically infected hosts are stressed and became victims of their enemies or succumb to their competitors. Nevertheless, they may propagate simultaneously with their parasites, which will be passed on to the host’s offspring during infancy, often by generative (prenatal, lactogen transovarial) transmission.

The physiological balance of power between parasite and host is based on the regulation potential of the parasite, e.g. by self-control of its propagation, the feedback mechanisms between the two partners and the reversible modulations of the immune reactions induced by the parasite. The regulation of the host population density is achieved indirectly by the reduction of the host’s fitness. Parasite and host propagate simultaneously. Transmission is carried out by specifically differentiated parasite stages, mostly linked with sexual differentiation. For example, in malaria, only the sexual differentiated circulating stages, the gamonts (gametocytes), develop in the vector mosquito.

The potential case reproduction rate is extremely high for parasitoses that are cyclically transmitted by invertebrate vectors: A case of malaria caused by Plasmodium falciparum induces more than 100 secondary cases during 7 months of tranferency, whereas a case of onchocerciasis causes several hundreds of cases during 10 years of patency.

Regulation of host population density

Alternative strategists regulate the density of their host population over generations. A sequence of epidemics with endemic intervals is accompanied by periodically changing population densities. Balance strategists, however, regulate the host population density during the individual life time of their hosts. The increase of parasite load caused by superinfestations reduces the host’s fecundity. Parasite stages that invade hosts that are already infected or infested are often repulsed by premunition, which is analogous to the territorial defence of free-living animals. The combination of an arthropod and a mammal provides a selective advantage for the parasite: The high density of arthropod individuals sustains the parasite’s dispersion but its extreme seasonal variation is bridged by the homeostatic mammal whose body mass makes a base for nutrition and energy. The more complex the life cycle of a parasite, the more possibilities arise for feedback mechanisms (see Box 2.1 Malaria and Culicids and 2.9 Schistosomiasis and snails on this website).

The outcome of interventions for the control of infections can be estimated by mathematical models. For microbial pathogens, their virulence, immunogenicity and the lethality of the disease are constant, whereas the contact rates with their hosts are the main changing parameters. The latter can be influenced by interventions. In eukaryotic parasites, the various main developmental stages are assigned to compartments and the transitions between them are expressed as probabilities. The resulting stochastic model can be provided with values for the limits of the different parameters. Computerized programmes are used to calculate the influence of quantitative modifications, the results of which can be represented as graphs in two or three dimensions (see fig. 2.12, page 32).

Deterministic models are constructed by use of values established beforehand in the field. The relationships between them are expressed as mathematical formulae. The calculated outcomes reflect a real situation, explaining the reasons of a certain epidemiological situation and the interventions necessary in order to change it (see chapt., page 144ff).
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