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Des sources du savoir aux médicaments du futur

 | 
Jacques Fleurentin
, 
Jean-Marie Pelt
, 
Guy Mazars

1. Origine des pharmacopées traditionnelles

Natural barriers to the spreading of diseases in wild animals

Jean Blancou

Résumé

Abstract
The concept of natural barriers to the spread of animal diseases is a very ancient one. It incorporates not only the phenomenon of genetic resistance to pathogens, but also the influence of various other factors affecting the capacity of the pathogens to infect or to live as a parasite on certain animal species.
After having recalled historical data on the subject, the author described the three main parts composing these natural barriers: difficulties associated with wild animals coming into contact with the pathogen, the innate resistance of the host animal to penetration by the pathogen and, finally, the acquired resistance of the animal, based on cellular or humoral immune resistance mechanisms.
The author then examined possible weaknesses of these three components, which are linked to a variety of factors: modification of living conditions, biological rhythm or diet, penetration of skin or mucous barriers, adverse environmental conditions, etc.
He concluded that natural barriers were relatively fragile and highlighted the risk that spontaneous mutations of pathogens represent for these barriers.

Texte intégral

1The concept of natural barrier to the extension of diseases ("species barrier") has come into fashion with the emergence of bovine spongiform encephalopathy and the problem of its possible transmission to other animal species and to man.

  • 1 The "species barrier" concept will be taken in the wide sense of the term in this presentation as (...)

2This concept is, in fact, very old, covering, not only the phenomenon of natural genetic resistance to pathogenic agents, but also the influence of various other factors opposing the action of agents trying to infect or become parasites in specific certain animal species. The purpose of this presentation will thus be to evaluate the importance of the various components of the species barrier1 which these animals raise against the major infectious or parasitic diseases, though this evaluation will be restricted to the case of the wild vertebrate species.

3This study will be based on historical data as much as modern knowledge in epidemiology and genetics. The results will provide valuable information applicable to the diseases appearing currently in both man and animal.

Historical Data

4The authors of Antiquity had already been impressed by the fact that epidemics ignored species barriers, affecting indiscriminately man and animal. It is therefore not surprising that they focussed on this kind of epidemic, sometimes mixing up various episodes and not hesitating to worsen the epidemiologic picture to make an even stronger impression on readers. For instance, it seems that no barrier could ever stop the frightening panzoonosis described by Ovid in Metamorphoses, a kind of "pestilence" to which next to all inhabitants of the island of Egira and innumerable animals, both domestic and wild succumbed in 129 B.C.

  • 2 "Being first in the crowd of dogs, winged animals, birds and oxen, the evil power then overwhelms (...)

Strage canum primo volucrumque, aviumque, boumque
Inque feris subite deprehensa potentia morbis est2

5Numerous other authors of the same period reported about similar episodes during which mammals, birds, fish and reptiles were indiscriminately affected by various pestilencia.

6It is only later that the first veterinary surgeons reported about their observations on the resistance - natural or experimental - of certain animal species to infectious or parasitic diseases: cattle plague, bovine contagious peripneumonia, clavelée, glanders, etc. But these observations were generally based on the inoculation of virulent matter whose real content in pathogenic agents was unknown. It is only after Louis Pasteur had discovered microbes that it became possible to quantify with accuracy the virulence of various bacterial or viral stems. Pasteur was the first scientist to show that all the animal species are not receptive to the inoculation of a microbe to the same extent and this receptivity could be modified by serial passages of this microbe; other researchers applied the same method to the majority of infectious diseases, as new agents were discovered. In the mean time, the existence of species barriers, in particular those that man does not have with respect to the main pathogenic agents, has become a well known phenomenon.

7After establishing its bases and mechanisms, man has immediately sought to develop the concept of species barrier. Thus, when this barrier is missing, or is very low, man has used pathogenic agents as weapons in bacteriological warfare (for instance: the bacillus of carbocunlar fever) and, when the barrier existed and seemed to resist firmly, man used them in his biological struggle against certain wild species (for instance: the virus of the viral hemorrhagic rabbit fever).

The various components of the natural barriers

8In general, a pathogenic agent can come across three successive lines of defence when trying to cause infection or infestation of a potential host (table 1):

  • first, it may encounter difficulties to come across the organism of the host;
  • then, if it has managed to penetrate into this organism, it will have to overcome natural, constitutional, innate and nonspecific resistance mechanisms;
  • it might also come across a specific, adaptive, acquired resistance.

9In all cases, these three defence lines of defence are in part genetically determined and we can also consider that they correspond to what any prey would defend itself with against the predator: the gazelle which did not sense the lurking lion will have to outdistance it by relying on its natural velocity or escape its claws by learning how to zigzag away for its life...

10We will now examine in more detail these three main components of the species barrier, in the broad sense of the term. It will however be impossible for us to provide an exhaustive review of this topic which has been the subject of innumerable scientific works and we will be content with providing some significant examples following the general structure of figure 1.

Figure 1. Successive barriers to protect a potential host from being infected by a pathogenic intracellular agent.

Table 1. Species Barrier to some infectious diseases

Table 1. Species Barrier to some infectious diseases

+: resistance to the natural disease
-: no resistance to the natural disease
(*): exceptional cases

The first defense: the difficulty of meeting of the vertebrate host with the pathogenic agent

11The encounter between the pathogenic agent and its potential vertebrate host can be made difficult in various circumstances, which raises a first specific barrier to its contamination [reviewed in Pastoret, 1990].

12For instance, the way of life of wild animals living in the water or in the air reduces their chance to come across a pathogenic agent whose usual host is a terrestrial species, and vice versa, even if this is not in all cases an insuperable obstacle, as we will see in the second part of this presentation.

13The biological rate of activity of a given species (diurnal, night...) can also be an obstacle to an encounter with a pathogenic agent. The best known example of this influence is that of chronobiologic adaptation where the rates of activity of a parasite and that of its potential host are matched. This matching is conducive to "promoting" the introduction of a parasite into a given species [Combes, 1995] and, a contrario, runs counter the contamination of other species, which can be regarded as a specific barrier. The best documented case of this type of barrier is the case relating to the infestation of man (or wild rodents) by Schistosoma mansoni (figure 2).

14The diet of an animal species can prohibit (or make very improbable) an encounter with the pathogenic agent. The most traditional examples are surely those of parasitic cycles which can endure only if a specific wild animal ingests a specific prey which is itself an intermediate host for the parasite. The same barrier can exist with respect to the infectious diseases of dietary origin, depending on the medium (ground, water...) or the organism of a specific mammal, bird, fish, invertebrate, etc. in which the pathogenic agent may multiply.

15The behaviors of the various animal species can, therefore, represent a more or less effective species barrier to being contaminated. The natural aversion or mistrust displayed by a species towards the other species (preys and predators, domestic and wild species, lynxes and foxes, etc.) will reduce the chance of an encounter and an exchange of common pathogenic agents whereas overpopulation or gregariousness will on the contrary favour this exchange; for that matter, refer to the second part. Certain wild animals instinctively eliminate ectoparasites attacking them: the African antelopes bite their ticks off, the primates do the same with their fleas, the birds with their lice, etc.

Figure 2. Chronobiologic adaptation to parasitic transmission. In the transmission sites where the man is the major host for Schistosoma mansoni the aquatic larvae (cercaires) of this parasite stem from the molluscs carrying them in the middle of the daytime; in such sites where the rodents are the major hosts, larvae emerge at the end of the afternoon. The "exit time" feature is genetically determined (in Combes, 1995).

The second defence line: the host's innate resistance

16If an encounter with the pathogenic agent could not be avoided, new mechanisms of genetic resistance - called non-specific, constitutional, natural or innate - will appear and become active. The best qualifier is probably the last mentioned as these mechanisms exist before any contact with the pathogenic agent. They are generally dependent on several different genes, but they have the same result: preventing the pathogenic agent from penetrating, then invading the organism. Innate resistance is itself made up of several components; the main one is a resistance to being penetrated by the pathogenic agent.

Resistance to penetration by the pathogenic agent

17The penetration of the pathogenic agent into the organism of a vertebrate can be prevented, or delayed, by various mechanisms, in particular the following ones:

18The resistance of the skin or the mucous membranes to a penetration of pathogenic agent: the nature, structure or thickness of their skin make it possible for many species (in particular pachyderms, batrachians and reptiles) to raise a first effective barrier to the attack by ectoparasites, the larvae of endoparasites, and even by some microbes.

19The existence of various anti-microbial substances (lysozyme, antibiotics, etc.) on the surface of the skin or mucous membranes of certain species, or its acid pH, raise a second effective barrier to the penetration of bacteria (staphilococcus, colon bacillus) or viruses (Sendai virus). A contrario, the absence of certain factors which are essential to the development of a microbe for specific species will protect it against infection. For instance, guinea-pigs cannot develop genital infection caused by Brucella abortus because of a lack of erythritol in the cells of foetal sacs, whereas this sugar exists in ruminants [Rumyantsev, 1992].

20Finally, the body temperature of the animals belonging to a given species may represent an obstacle to the multiplication of thermosensitive microbes. For instance, reptiles and batrachians (homeothermal) are less sensitive than mammals or birds to tetanic and bobulinic toxins that act only at relatively high temperatures [Rumyantsev, 1992], Certain reptiles (Dipsosaurus dorsalis can even use this mechanism for the purpose of eliminating microbes [Kluger et al. 1975].

Resistance by an absence of cellular receptors

21The intracellular pathogenic agents that have succeeded in crossing the first defence line of the organism and breaking into it are not really victorious yet as they still have to find their way to the heart of the cells of this organism.

22That is possible only if there is mutual recognition between these cells and the pathogenic agent: this recognition - representing an essential stage for the multiplication of intracellular pathogenic agents - depends on the existence of complementary molecules adapted to the host. Consequently, the adherence of microbes to the cells of their potential hosts is related to the existence of highly specific microbial adhesines. The latter should correspond to a given receptor for the cells of the host so that the microbe can penetrate into the cell and multiply there.

23There are many other examples of genetic resistance of the animals related to the absence of suitable cellular receivers: resistance of the rodents to the action of diphteric toxin, or several species with the cytolysis by the salmonellas [Rumyantsev, 1992]. In animal virology, the most known examples are those of the resistance of certain lines aviaires to viruses A or B of leucosis aviaire, or that of the Bovidae to the virus of bovine leucosis, both related to the absence of receiver for these viruses [Young et al., 1993].

Resistance related to a non-specific cellular reaction

24There is a third form of innate resistance to pathogenic agents - be they intracellular or not - based on the reaction of certain non-specialized cells.

  • 3 Natural resistance association macrophage protein 1.

25Without having ever been in contact with a pathogenic agent, an organism can indeed defend itself through a reaction of several types of polynuclear cells (macrophages) whose activity varies according to the animal species considered. It was shown in particular that the resistance offered by mice to intracellular parasitism by certain mycobacteria, salmonellae and the leishmaniae depends on the NRamp gene3 [Blackwell, 1996; Skamene et al., 1982], For instance, the resistance offered by certain lines of bovines to infection by Brucella abortus depends on the activity - which is genetically controlled - of macrophages [Adams & Templeton, 1995].

  • 4 Calmette & Guérin biliary bacillus

26It is interesting to note that the innate resistance which chronologically precedes acquired resistance, can be combined to it: in the case of mice infected by the BCG4 bacillus, Nramp gene controls the infection, and then the genes of group H2 takes over [Nadeau et al., 1995]

The third defence line: the acquired resistance of the host

27Acquired resistance - which can develop only after there has been a first contact with the pathogenic agent - presupposes that there is molecular recognition of the antigenic determinants of this agent. This recognition will enable it to develop an appropriate form of resistance based on experience: this is a Nurture vs. Nature, acquired vs. innate process. We have two types of acquired resistance:

Resistance to cellular mediation

28In this mode of resistance, the pathogenic agent is destroyed by the direct action of the immune cells (generally the T-lymphocytes) that have come in contact with them. For the pathogenic agent to be vulnerable, its antigens should first "be introduced" to the T-lymphocytes by other intermediate cells, in particular the macrophages and B-lymphocytes. This introduction presupposes that the organism being attacked has the molecules necessary for this introduction process. The existence of these molecules depends itself on the presence of genes, most of them being located in a part of the genome of the cell holding the antigen called CMH II, or that of coding genes for the receptors of the T-lymphocytes (T-cell receptors).

29Intensive research carried out on mice have shown that the differences in resistance by the various lines of these rodents to certain nematodes, in particular Trichinella spiralis, was determined genetically at the level of CMH [Wassom et al., 1984]. Other research work has then shown that there were also genes of the CMH (class I or II) or neighbouring genes that accounted for the acquired resistance against parasitic attacks by the nematodes of other animal species [Stear & Murray, 1994].

Resistance to humoral mediation

30This mode of resistance is generally related to the existence of specific immunoglobulines (antibodies) produced by the B-lymphocytes following a first contact with the pathogenic agent. The specificity and quantity of antibodies thus produced are in turn dependent on one or several genes, as was shown for the first time in the case of the resistance of some suidae to infection by Brucella am. [Cameron et al., 1943]. Experimental work also showed that the quantity of antibodies produced by certain lines of mice ("High or low responder") was genetically controlled [Biozzi et al., 1984], The absence (or inactivity) of B-lymphocytes in charge of producing these antibodies - possibly as a consequence of a mutation - causes the elimination of any species barrier. This failure, be it spontaneous or induced, makes the animals sensitive to various infections: cf. second part of this presentation.

Possible cause of failure of natural barriers

31The various defence lines which species subspecies or a line of vertebrates can raise to a pathogenic agent may at all times fail to work; let us mention some examples of such cases.

Facilitating the encounter between host and pathogenic agent

32The encounter of the host with the pathogenic agent depends, as we have seen above, on several factors.

33The way of life of a given species, which can be an effective barrier to diseases affecting other species that do not have the same biotope, can be modified. As a consequence, unknown (or very rare) diseases in wild species living in isolation or in small groups, spread much more easily among these species as soon as they are living being fences, or among their congeners raised in intensive breeding systems. They can then be contaminated when in contact with these other species, including man.

34The displacement of wild animal species by man (for breeding, hunting, recreational purposes) has probably played a significant role in the course of history, and facilitated the contamination of animals that had been until then protected by their being sedentary. There are many examples illustrating this situation for several infectious and parasitic diseases [reviewed in Moutou, 1994].

35A modification of the rate/rhythm of activity can also facilitate the meeting with a pathogenic agent: the passage of a diurnal way of life to a night way of life of certain wild species, under the pressure of the human activities (drives out, tourism, etc.) can lead them to meet pathogenic agents for animals of night.

36Any modification of the diet of a given species may induce the weakening (or elimination) of the first defence line against a pathogenic agent. This change may be accidental when an animal ingests an unusual prey which happens to be the host of a parasite common for another species, even if the parasite is then often in a "dead end" where complete development is not possible [Euzeby, 1997], This can be apply when certain predators adopt deviant dietary preferences, because of famine or a lack of experience (young animals).

  • 5 In some cases, a behavioural change of the species carrying the pathogenic agent will cause the br (...)

37The behavioural changes in a species can facilitate contact with an infectious or parasitic agent that it was not supposed to encounter5. This behaviour can be related to environmental changes (climatic variations...), shifts in population distribution (migrations...), cases of accidental promiscuity, etc, that bring together species living usually in separate areas.

Superseding the innate resistance of the host

38As we saw above, the penetration of the pathogenic agent into the organism of a vertebrate may be facilitated when the defence mechanisms of the potential host have been destroyed or weakened.

39As a consequence, any breaking of the cutaneous or mucous barriers or any disappearance or neutralization of the antimicrobial substances protecting them can facilitate the contamination of a normally resistant species. This holds true if these barriers have been weakened by various accidents such as a burn, aggression by chemicals or radiation, allergy, inflamation, etc.

40In the same way, a modification of its body temperature can make a species sensitive to a pathogenic agent which it usually resists. It is Louis Pasteur who showed it the first while succeeding in contaminating, with the agent of the carbonaceous fever of the bovines, of the hens which it had in experiments cooled in their soaking the legs in frozen water. This cooling can be sometimes observed, accidentally, in nature.

41Likewise, it is possible to transfer to a species that is naturally resistant to a disease all the cellular receptors that are necessary for it tto become sensitive to the corresponding pathogenic agent. This genetic mainpulation, consisting in introducing the genes coding the expression of the specific cellular receptors into the genome of the host, made it possible to make mice sensitive to certain pathogenic agents such as transmissible forms of spongiform encephalopathy [Collinge et al., 1995]

42In nature, such a transfer seems to be highly improbable but, on the other hand, the genetic rearrangements or recombinations of the pathogenic agent can modify their cellular target in the host, thus making the latter sensitive to this "new" pathogenic agent, as is often the case with the flu virus.

43However, the non-specific cellular reactions protecting a species against a pathogenic agent can be neutralized, which causes a collapse of the first cellular defence line. The causes for this failure are practically the same ones as those for specific defence lines (cf. § 3 below) and can be assigned to the action of various factors:

  • physical factors: adverse conditions in the the medium (extreme temperatures, abnormal hygroscopy), excessive production of radiation (natural or accidental), etc.;
  • chemical factors: action by any product modifying the rate or quality of the cell production by the organism, in particular of immune cells (immunosuppressors);
  • biological factors: infection by pathogenic immunoreducing agents (e.g.: retroviruses), physiological stress (malnutrition, overpopulation) or psychological, autoimmune diseases, etc. [Morris & Potter, 1997].

Neutralising the acquired resistance of the host

44Resistance to cellular mediation can also be reduced under the influence of the factors previously described. The species barrier to specific intercellular parasites (protozoa, bacteria or virus) is then reduced or abolished. For instance, wild species that are normally resistant to trypanosomoses, coccidia, tuberculosis, etc, may be affected by these diseases when in contact with the stocks following a collapse of cellular immunity.

  • 6 Severe combined immunodeficiency.

45Resistance to humoral mediation may be overcome exactly for the same reasons, and the resulting interruption of antibody production may eliminate the species barrier. This phenomenon may be investigated experimentally in many ways, by inducing immuno-sup- pression through physical, chemical or biological methods, or using natural mutants (athymic "nude" mice infected with SCID6), or inducing artificial changes, or removing resistance genes...

46These procedures are in common use in laboratories to obtain animals becoming receptive to diseases against which they offer natural resistance. This ranges from very simple processes, such as controlling certain vaccines (e.g. inoculating calcium chloride together with Clostridium chauvei to make the guinea-pig sensitive to symptomatic bovine anthrax) to more elaborate systems used to create an animal model for human diseases (e.g. introducing human genes into mice, or removing resistance genes from them: for example from the "knock-out" mice used for research on forms of spongiform encephalopathy).

47In nature, such events have very few chances to occur. However, they could help us understand why some individuals catch diseases whose stock is usually to be found in other species: for instance, the African lions have probably been contaminated by the virus of the young dog disease [Brown, 1997], the terrestrial wild mammals have probably caught bat rabies [Blancou, 1997], man has probably caught AIDS or small-pox by contact with the African monkeys, malaria by contact with birds, measles in contact with ruminants suffering cattle plague, schistosmosis in contact with rodents, etc. [Combes, 1995]. These viruses, in various successive stages, have probably adapted gradually to their new host whom they infected then without difficulty as the species barrier has been eliminated for good. [Blancou, 1986].

48This unexpected crossing-over of the species barrier can be accounted for on the basis of conditions contrary to the operation of the immune system, as a consequence in particular of a deterioration of living conditions: overpopulation involving malnutrition involving in turn nutritional deficiencies and hypogammaglobulinemy...

Conclusion

49The concept of species barrier as a natural obstacle to the extension of diseases seems to be of increasing significance in the eyes of biologists and doctors.

50In human medicine, the study of this notion has become essential before considering that a disease is a zoonosis (present or potential) and it calls for the implementation of special measures to monitor and combat it.

51In veterinary medicine, the positive aspect of resistance to diseases deserves particular attention. A branch of science has developed to identify the subjects that are naturally resistant to diseases (genetic markers), facilitate their reproduction (genetic selection) and transfer their resistance potential to other species (genetic engineering). The results provided by this research generally aim at finding a makeshift for the absence of vaccine or treatment, or reduce their use and the costs involved. But when you talk of species barrier, we should never lose sight of two significant factors:

  • the natural barrier existing in wild species is very rarely insuperable: it might appear as such at a given time under the influence of several natural factors, especially - and in an increasing number of conditions - under the influence (direct or indirect) of man;
  • the barrier raised by a wild species to a pathogenic agent is under permanent threat due to a mutation of this pathogenic agent: the struggle between the resisting host and the pathogenic agent, as the two aim at securing greater reproductive success (fitness) induces a kind of "arms race" [Dawkins & Krebs, 1979] that can undermine the resistance of either one. As this race is based on a capacity to have fast genetic changes (modifying the cellular targets), the pathogenic agent has better chances of winning, with due account for the smaller size of its genome [Combes, 1995]. There are very many examples of this unexpected destabilization of a potential host with respect to a pathogenic agent otherwise considered innocuous. The most recent example is the abolition of the resistance of man to the virus of fowl plague: this emergent disease has killed several people in Hong Kong in 1997 because a genetic réassortant of this chicken virus (H5N1 ) had suddenly managed to cross over man's species barrier.

52For all these considerations, biologists should never claim that a species barrier will never be crossed over. They should also avoid having full confidence in this species barrier when they rely on a pathogenic agent to fight against the multiplication of a wild vertebrate species which they consider noxious.

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Notes

1 The "species barrier" concept will be taken in the wide sense of the term in this presentation as we will consider, not only the bariers between species defined in the strict sense, but also those between sub-species or even lines of vertebrates.

2 "Being first in the crowd of dogs, winged animals, birds and oxen, the evil power then overwhelms the wild animals"

3 Natural resistance association macrophage protein 1.

4 Calmette & Guérin biliary bacillus

5 In some cases, a behavioural change of the species carrying the pathogenic agent will cause the break of the species barrier: rabid bats transmit the virus to other willd terrestrial mammals only because their instinct of preservation is eliminated by the rabies virus and they no longer stay at a distance from these mammals.

6 Severe combined immunodeficiency.

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