Invasion

INVASION (from Latin invasio-attack), infection of an organism by animal parasites. Therefore, so-called invasive diseases are those whose causative agents are animal parasites. The concept of I. also applies to pseudoparasites, i.e., free-living animals that enter the organism and exist in it in the position of a parasite. Agents of I. are parasites, for the most part, at a certain stage of their life cycle. The invasive form of the dysentery ameba is not its motile form, but the immotile one (cysts); under natural conditions, humans are invaded only by sporozoites of the malarial plasmodium. Eggs of ascaris and whipworm invade humans only after an embryo has developed in them to the stage of a tiny worm; the larva of the dog hookworm, before invading the host, passes through two phases of development. In the armed tapeworm, both the egg and the mature finca are infectious to humans, but with completely different consequences for the host. Objects of I. are the hosts of the corresponding parasites, including humans. An object of I. can be subjected to I. either at any age or predominantly at a certain specific period of life. For example, a person can be infected with malaria throughout life, starting from the intrauterine period and ending in old age. Similarly broad is the range of times of human infection with dysentery ameba, pinworms, armed tapeworm, unarmed tapeworm, and other parasites. In other cases, I. is confined either exclusively or predominantly to one or another age. Larvae of ticks Ixodes ricinus, Boophilus, and other transmitters of piroplasmosis, originating from females that have drunk the blood of sick animals, become infected with the parasite only in the egg stage, while still in the mother's ovary. Old cows are much less frequently and weakly infected with larvae of the warble fly (Hypoderma). The time of I. in terms of calendar dates varies greatly depending on the peculiarities of the life cycle of a given parasite. Helminthic I., associated in their distribution with soil, have little chance of development in temperate climates in winter. Similarly, difficult or entirely impossible is winter I. through water by encysted cercariae of Fasciola hepatica. In contrast to this, infection with the armed tapeworm (from raw finca pork) can occur at any time of the year. Infection with cutaneous leishmaniasis ('penile ulcer') as a rule is confined in Central Asia to the second half of summer or to autumn. Infection with parasites spread through the agency of specific vectors occurs only in those months when these vectors are alive. These circumstances determine the seasonality of many I.; such are for example primary malaria, piroplasmosis, penile ulcer. The time of infection of the host during the day may also depend on the lifestyle of the vector. Species of Anopheles, which attack humans as a rule at twilight and at night, can only at this time drink blood from a malarial patient with gametocytes of the plasmodium or infect a person with malaria, if sporozoites are already in their saliva. Microfilariae, having periodicity, appear in the peripheral blood of humans during the day (Microfilaria diurna) or at night (Microfilaria nocturna), which determines the time when mosquito vectors can themselves become infected with these parasites and transmit them to humans. The source of I. is (in a broad sense) that environment in which the invasive forms of one or another parasite are found, or, to speak the language of zoogeography, the biotopes of the corresponding developmental stages of the parasite. The environment itself can be either only a transitional stage in the life of the parasite or the parasite lives and multiplies in it. Thus, bed bugs inhabit and breed in human dwellings or in poultry houses. Certain bodies of water are the laying places for mosquitoes and blood-sucking midges (Simulium). Water is a brief but essential link in the life cycle of the broad tapeworm: the embryo, having emerged from the egg, freely swims in water for some time until it is swallowed by the first host, the cyclops, or until it perishes. Along with this, the environment can also be a non-specific location for invasive parasites. Through water one can obtain cysts of dysentery amebas, eggs of pinworms, whipworms, ascarids, and other parasites; but soil can play the same role in infection with the named parasites. The source of I. by parasites can directly be a host infected with parasites, and I. can occur by various routes. Examples: a) with scabies, a person can become infected through direct contact with the body of a scabies patient or with a scabies-infested horse; similar relations are also observed in I. by lice; b) when eating trichinous pork (with live trichina larvae), a person becomes infected with these parasites and contracts trichinosis; c) balantidiasis can be contracted by inflating with the mouth raw pig intestines, insufficiently washed of cysts of Balantidium coli, which apparently happens to workers in intestinal and sausage production. Finally, the source of subsequent I. for the host itself can be the host itself, and I. proceeds in two ways: 1) a host infected once serves as a place for multiplication of parasites that have entered it, which intensify its I.: for example, a rabbit swallowed a batch of oocysts of coccidia Eimeria stiedae; the merozoites emerging from them multiply by division, and every new generation of them attacks new and healthy liver cells; thus the I. of the rabbit is intensified without it becoming reinfected with coccidia from the outside; a similar example is the multiplication of the dwarf tapeworm (Hymenolepis nana) in the human intestine; 2) in the host's body the parasite does not multiply, but I. is still intensified due to repeated infections from itself (so-called autoinvasion); an example is infection with pinworms due to the transfer by dirty hands of parasite eggs from the anal area, where they are deposited by females, to the mouth and their swallowing. Important sources of I. can be 'carriers of parasites' and animal reservoirs of the parasitic virus. Persons who have had amebic dysentery can for a long time, in the absence of signs of disease, disseminate cysts of the dysentery ameba and infect others (analogy with bacillus carriers). Antelopes in tropical Africa, infected with Trypanosoma gambiense, are a reservoir of the virus of sleeping sickness for tsetse flies (see Glossina), which transmit it further to humans. The ways of penetration of I. into the organism can be active or passive. 1. Parasites can actively penetrate their host, and the activity is manifested either by the parasite itself or by the female (who may actually lead a non-parasitic life), attaching her offspring to the host. Thus, for example, females of the sheep botfly (or Wohlfahrt's fly) give birth to larvae in flight and throw them into the nostrils of sheep and the eyes of humans. Along with this, larvae that have emerged from eggs of the human botfly (Dermatobia cyaniventris) or from eggs of the stomach botfly (Gastrophilus) themselves actively bore into the thickness of the human skin cover. Mature larvae of hookworms and cercariae of schistosomes behave similarly, penetrating the organism - the former from moist soil, the latter from water. 2. More common is the passive method of I., when the parasite enters the host without any effort or action on its part. Rat trypanosomes penetrate a rat when the latter eats infected fleas with developmental stages of them. Larvae of the nematode Gongylonema develop in a cockroach when it itself swallows eggs of this parasite, etc. The routes of penetration of I. into the organism are twofold: parasites enter the host through its skin cover or through the natural openings of cavity organs, first of all through the mouth, as well as through the anal opening (e.g., larvae of Wohlfahrt's fly), urogenital organs (infection of horses with Trypanosoma equiperdum during mating, pinworms crawling into the genital cleft), nostrils, auditory opening, etc. Some parasites penetrate through intact skin, while others make use of accidentally existing wounds or ulcers (e.g., certain flies). The duration of I. by parasites that do not multiply in the host's body or give rise to only one generation in it is determined primarily by the duration of life of the parasite itself or its offspring. There are indications that the broad tapeworm can live up to 14 years. I. with trichina ends when the larvae in encapsulated capsules die and lime is deposited in them. Various influences from the host organism on the parasite can interrupt I. much earlier than its natural end. The duration of I. by parasites that multiply repeatedly in the organism depends on the intensity of multiplication, properties of the parasite, and resistance of the host. There are examples of rapid death in tropical malaria; but much more often after several generations of plasmodia cease to multiply, and the invasion becomes latent. Such a latent I., under the influence of various insults, again passes into an overt one (relapses of malaria). Natural liberation of the organism from I. is the result of 1) the parasite leaving the host and 2) the death of the parasite from natural causes or from the influence of the host organism. The leaving of the host by the parasite is usually observed in those forms that accomplish only part of their life cycle in the host.

Mature larvae of the skin botfly fall out of the skin fistulas on their own; similarly, the pre-puparial larvae of the stomach botfly exit from the horse's intestine. Along with this, the parasite can leave its host under abnormal circumstances; for example, the expulsion of human roundworms during febrile diseases is noted. Old tapeworm scolexes die and the cysts open in the muscles. Larvae of certain parasitic wasps, parasitizing in the body cavity of caterpillars, sometimes perish when attacked by the caterpillars' blood cells, S37 and such caterpillars survive. The organism's reaction to additional or repeated invasions (super- and reinvasion) is very diverse, depending on the species of parasite and the development of immunity in the host's body. Re-infection of humans with pinworms occurs very easily, whereas in dogs, not only re- but also superinvasion with the nematode Strongyloides is impossible. Having had cutaneous leishmaniasis causes immunity to re-infection, proven experimentally (Marcinowski). Similarly, immunity to infection with Dermatobia is also observed. The doctrine of insusceptibility to agents of I. is still in its infancy (see Immunity to metazoan parasites). Intrauterine I.-infection of the organism by parasites during its development in the mother's body or even in the egg stage, enclosed in the mother's ovary. Intrauterine I. can be assumed when a newborn or infant already has parasites, which the child could not have contracted on its own under the conditions of its free life outside the mother's body. The main path of I. of the fetus is the mother's blood. With the blood, through a damaged placenta, malarial parasites can enter the fetus and cause the appearance of 'congenital' malaria in the child. Theoretically, another route of infection of the child with malaria is also possible, namely through injury to the child's skin during childbirth and the flow of the mother's blood into the wound (V. Blacklock, R. Gordon). There are reports of cases of intrauterine infection with kala-azar (Low), trypanosomes of sleeping sickness (Kellersberger), trypanosomes causing Chagas' disease (Trypanosoma Cruzi), etc. However, not every case of finding trypanosomes in newborn animals can be explained by intrauterine infection of the fetus, since some authors have proven the possibility of infection of sucklings through the milk of a trypanosome-infected mother (observation of Bassett-Smith on guinea pigs). More numerous data exist on intrauterine infection with various parasitic worms, and first of all with those that undergo a specific migration in the host's body. It is known that certain larvae (especially of dog roundworms--Belascaris marginata) enter the systemic circulation and from there into various organs, including the uterus of a pregnant animal. Experiments by several authors have shown that in this case, the embryos developing in the uterus can also become infected. Apparently, the age of the mother is a factor influencing the degree of infection with roundworms in both herself and her offspring (D. Augustine). Calf roundworm (Ascaris vitulorum) also gives cases of intrauterine invasion. Hookworms have been found in a two-week-old child as well as in young piglets, which can also be explained only by assuming infection with migrating larvae. The finding of eggs of the dioecious fluke (Schistosoma japonicum) in newborns is the result of their intrauterine infection (Narabayashi). If the case of finding a hydatid in the liver of a twelve-day-old child can be explained by the penetration of the parasite's embryo hematogenously from the mother's intestine into the fetus's body, then the rare cases of tapeworms parasitizing in the intestines of infants depend on the swallowing of the scolexes of the worm during embryonic life, localized in the mother's amniotic sac. The earliest known cases of intrauterine invasion are in ticks of the Ixodoidea superfamily. When an adult tick is infected with piroplasms, the parasites pass into the body cavity and at a certain stage of development penetrate into the eggs of the ovary. When the larva hatches from the laid egg, it is already infected with parasites, which in turn infect healthy cows or other animals when they suck their blood (Ixodes, etc.). Similar phenomena also occur in the body of the tick Ornithodorus, various species of which are vectors of relapsing fever spirochetes. Thanks to this, febris recurrens is transmitted not only by the feeding female herself but also by her offspring.