2. Cyclically transmitted heteroxenous parasitoses
|Ecosystems are networks of interrelationships based on predominantly trophic dependencies in the broadest sense. With the onset of their formation numerous partners are always involved, even though in graduated intensity. The three-way association - parasite, intermediate and definitive host - did not necessarily develop from a two-way one. It appears more likely that in a web of multiple interrelationships, only those, which offered selective advantages for each of the partners, ultimately became established. The heteroxenic, cyclically transmitted parasitoses were formed polyphyletically. In an ecosystem not all the participants are actively engaged in directly competing with one another, but interact in an economic way. Rather, each organism preferentially develops only such qualities further, which contribute to the best chances of survival and requiring the lowest expenditures of energy.
No organism is able to optimize all its functions. It sets priorities according to the costs of energy and the effectivity of any given adaptation. Missing adaptations may firstly be due to a missed selection pressure, e.g. when the loss of individuals is neglegible in terms of the population as a whole. Invertebrate vectors are mostly affected by eucaryotic parasites only at low frequency. Invertebrate defence mechanisms have developed against procaryotic microorganisms, which affect them in geometrically increasing proportions. Secondly, eucaryotic parasites control their propagation by its own: they form a premunition which corresponds to the territorial defence of freeliving animals. By doing so, this prevents the overcrowding of the host organism.
In the life cycle of plasmodia, the protozoic pathogens of malaria, the youngest age group in the human population shows the highest prevalence, sometimes up to 90%. In the mosquito populations which contribute to the transmission of the pathogen, the prevalence is, however, only about 1% maximally. Therefore different priorities between the interactions of host and parasite exist in the vertebrate compared with the invertebrate host.
The infection of the mosquito by a plasmodium considerably shortens the insect’s life expectancy and thereby, the number of its descendants. In contrast, the lasting effect on the actual mosquito population hardly makes any difference. On the other hand, the survival of the infected mosquito is crucial to the plasmodium. Accordingly, the sporogonia is limited to 12 divisions (paragraph 126.96.36.199, page 17 and fig. 2.0, page 24). Just a small reduction in the chance of being transmitted, reduces the infection rate (incidence) of the warm-blooded host considerably. This is crucial to the plasmodium, because it is not necessary to reduce the infection rate to zero in order to extinct an endemia.
In the human host, and indeed in vertebrate hosts generally, the plasmodia achieve high percentages of infected persons (prevalences). The reproduction rate of the vertebrate host is smaller, however, the life expectancy is much longer. The plasmodium has to keep up with the turnover rate of the red blood cells (RBC). At the same time, it affects haematopoesis in the bone marrow and the spleen due to increased erythrocatalysis. The plasmodium is directly exposed to the humoral immune reaction, using it, however, for the regulation of the merogonia (fig. 2.2, page 15) and thereby stabilizing the parasitaemia. In addition, the plasmodium only goes through a limited number of propagation cycles, which may be repeated with each new infection: The infection heals spontaneously but, without leaving a protecting immunity. The plasmodium does survive within its human host not in spite of, but rather by means of the immune reaction. The same individual may serve as a host several times over. All these facts relating to a plasmodium infection cannot be compared with a microbial infection; its entomological, parasitological and clinical parameters are in harmony with each other. The balance of the cycle can be calculated quantitatively (fig. 2.10, page 27).
Depending on the nature of the host, vertebrate or invertebrate, intra- or interspecific feed back mechanisms have developed in parasites selectively for the self-control of its propagation. They are instantly recognisable as soon as we postulate that the parasite’s net reproductive rate has to be exactly one, calculated over many generations. Only in this way is the long-lasting existence of malaria and every heteroxenic parasitosis guaranteed, and the observation of an endemia possible.
The filarial worm Onchocerca volvulus, the pathogen of river blindness, is a metazoan parasite. The microfilariae, the stages which are being transmitted, stay alive in the lymph tissue of the skin. The vectors are also nematocera (blackflies of the genus Simulium) however, they breed in running water, are active during day and orientate themselves visually in finding their sexual partner and partly their blood hosts. In addition, the vector can also transmit the parasite Onchocerca spp.from wild animals, which may by chance reach humans (fig. 2.18, page 45). These interactions can be evaluated quantitavely (tab. 2.1, page 48). A synopsis of the parasite’s survival strategy is similar to that of plasmodium. Independent of either the occurrence of a high density of the vector as well as a low density of the definitive host , or vice versa, the transmission potential, i.e. the presence of the parasite, varies within small limits and therefore also its net reproduction rate (fig. 2.19, page 46).
In the case of filariae, the turnover rate of microfilariae within the blood stream is stabilized by two linked feed-back mechanisms, and is therefore independent of the worm load (fig.2.25-27, pages 58-59, box 2.2, page 62). The infective larvae distribute themselves within the vectors in a negatively binomial manner (fig. 2.20, page 47, 2.28, page 63 and 8.6, page 303). This leads to numerous repeated infections with a low dosage; high dosages remain the exception. In borderline cases, a single pair of infective larvae is sufficient to create a patent parasitosis of normal duration. The phases of a metazoic parasitosis, prepatency, patency and postpatency, are in close relationship with the immune reaction, in terms of conditioning, balance and experience.
In Wuchereria bancrofti, Brugia malayi, Loa loa and other filarial parasites, corresponding feed-back mechanisms may be assumed mutatis mutandis, that is to say all that was changed had to be changed as a function of adaptation and selection to their particular hosts.
The trypanosomiases and leishmaniases do not spontaneously heal (except for a few cutaneous leishmanioses). The course of the disease is typically chronic, apart from the East African sleeping sickness, a zoonosis. In the vectors the pathogens occur only in the flagellate form and are transmitted contaminatively only via by the biting apparatus, or by regurgitation after development in the gut, or via the faeces (stercoraria) or after migration through the haemolymph via the saliva (salivaria).
Trypanosoma cruzi, the pathogen of the chagas disease, propagates itself in the humans as a cellular parasite in the tissues of internal organs or muscles (heart). In the vectors, the robbery bugs (reduviidae), it propagates itself while passing through the intestine, varying in the different reduviid genera. The trypanosomes agglomerate temporarily in the no-digesting anterior intestine (stomoach) (fig. 2.32, page 70; exchange of genes?).
The pathogens which cause sleeping sickness, Trypanosoma brucei gambiense and T.b. rhodesiense, are purely liquid parasites and undergo a change of form by altering the position of the kinetoplast and thereby the origin of the flagellum. In addition they change the antigenic specifity of their surface, partially autonomically or partially reactively triggered. They do not go through any cellular parasitic stage, not even in the vectors, the glossinid flies, where they migrate through the haemolymph. An intraspecific exchange of genes is shown using an isoenzyme test and probably occurs in the vectors. The biting apparatus of glossinids is unique; the mechanism for piercing the vertebrate host’s skin is due to the flexibility of the chitinous skeleton (fig. 2.43-44, pages 87-88). The gonotrophic cycle, which occurs in the four ovarioles of the dipterous host (fig. 2.42, page 86) enables an exact determination of its age; however, in the nematocera, like mosquitoes, which have numerous ovarioles, their development is known to be directly connected with the digestion of the blood meal (fig. 6.7, page 250).
The leishmaniae parasites are always cellular in man. The pathogens, regarded as species, are characterised according to the symptoms they produce and the geographic region of the diseases they cause, i.e. by nosodemes. In contrast to the latter, the picture obtained by molecular-genetic methods does not correspond to this scenario; rather it is even more multifold. The immunologic balance in cutaneous leishmaniasis is achieved by the ‘cooperation’ of antigen presenting macrophages (fig. 2.52, page 100). In the vectors, the phlebotomines (sand flies), the parasites propagate exclusively in the midgut and are transmitted by regurgitation.
The piroplasms of cattle are transmitted by hard ticks. The babesiae attack all internal organs of the ticks except muscles. They are transmitted by its saliva and transovarially (fig. 2.52, page 100). In mammals they attack only the RBCs. The theileriae propagate synchronously in the ticks. They are transmitted transstadially to one of the three types of acini of the salivary gland only, specifically in the cells adjacent to the exit duct (fig. 2.57, page 112). In mammals they stimulate lymphoblastoid cells in the regional lymphnodes to divide and are also distributed in this way. They eventually enter RBCs. Piroplams seem to occupy the niche of plasmodia in ungulates. The epidemiology of the piroplasmoses is determined by the biology of hard ticks. As vectors, ticks, in contrast to insects, induce an immunologically-based resistance which limits their feeding and results in a considerable variation of the number of individual ticks attacking a particular vertebrate host. Together with a premunition against the pathogen, a balance arises, termed enzootic stability.
The Sarcosporidiae, to which Toxoplasma gondii also belongs, are exclusively cellular parasites. The pathogen changes between two vertebrate hosts, linked by a predator prey association. The carnivorous definitive hosts are family specific, whilst the herbivorous intermediate hosts, are however, much less specific. Both have the same immune apparatus; sporozoites and cystozoites, respectively, which invade the epithelial cells of the intestine, undergo completely different development programmes in each host. A synopsis of the genetic, physiological and ecological functions in the two categories of hosts reveals the balancing effects of such parasites in an ecosystem (Box 2.4, page 120). Sarcosporidiae demonstrate the importance of parasites for evolutionary processes. Without sarcosporidiiae, the great whales for example probably would and could not exist (Fig. 2.67, page 127). The diaplacental infection of the human foetus corresponds to that of the sheep, the lamb of which was attacked in former times by the lynx, now nearly extinct in Europe (Fig. 2.60, page 124). Sarcosporidiae exhibit the particular structures of apicomplexa and the endodyogenia as a unique kind of cell division.
The prevalence of human Schistosomiosis depends primarily on the behaviour of man as the definitive host. He contaminates the biotope of the intermediate host snails with the eggs of the trematode and there makes contact with the cercariae. The symptoms of the parasitosis, all caused by damming ups, appear only at an overload of flukes. Therefore no selective pressure occurs against the drift of the eggs towards the liver. The synchronisation of the propagation of parasite and host can be observed in cattle as well as in humans, in spite of the fact that in cattle the parasite requires for one generation about the same time in months for its development, as it needs in years when man is the host (fig. 2.71, page 145). The fecundity of the flukes already begins to reduce at a worm load of a few pairs. Such a sensitive self-control mechanism as shown by the parasite’s propagation is indicative of specific signalling agents. Comparison of the body mass of the flukes with that of the human host suggests that the highly specific agents in question most probably originate in the immune reaction. The miracidia find their intermediate host by orientating to the pheromones, which the intermediate snail host discharges into the biotope in order to facilitate the snails’ dispersion. The potentially unlimited propagation of the trematode stages in the snail is significantly curtailed as soon as the snail’s metabolism slows down due to exhaustion by the trematode stages. A synopsis of the survival strategy of Schistosoma mansoni shows the basic outline associated with heteroxenous parasites (Box 2.7, page 148).
The flukes of liver, intestine and lungs develop in snails as their first intermediate hosts, followed by fishes, arthropods and even plants as facultative secondary intermediate hosts. Such a broad spectrum of hosts illustrates the polyphyletic origin of the parasites’ life cycles, even if they belong to systematically closely related groups, as mentioned above.
The cestodes propagate simultaneously in the definitive host sexually as well as asexually i.e. parthenogenetically. The spectrum of their intermediate hosts extends from arthropods to mammals. The transmission pathways are correspondingly manifold, and relate to the construction of their eggs, in turn reflecting the manner of their delivery (fig. 2.76 and 2.77, pages 160, 161). Due to the structure of their scoleces (fig. 2.73, 2.74, pages 156), they not only anchor themselves to the intestinal wall of the host but also make tissue contact, the importance of which is explained in the case of intestinal nematodes (chapt. 3.1, page 176 ff.). When warm blooded animals act as intermediate hosts, some cestodes develop second larval stages, which propagate asexually. These lead to multiple infestations of the definitive host, whereas the body mass and the potential life expectancy of the adult cestodes is meanwhile reduced.