Parasitism is an association or a situation in which two organisms of different taxonomic positions live together where one enjoys all sorts of benefits (like derivation of nourishment, reproduction etc. which are basic requirements for existence) at the expense of the other. The benefited organism is called the parasite and the organism harbouring the parasite is called the host.
Hosts are not hospitable to parasites. Instead they consider parasites as foreign bodies and want to exterminate or overpower them by operating various devices like: producing antibodies, increased peristalsis, diarrhoea, mucus secretion, encystation by host tissues etc. Parasites to avoid host’s reaction for existence develop many specialities like increased fecundity, polyembryony, safe-habitat, production of special enzymes, a good deal of transmission etc.
Definition:
Due to close contact/intimate association, the responsive reactions and resistance displayed by a host to its parasite and the protective devices adopted by a parasite in response to its host’s reactions in order to establish them in their respective environments are called host-parasite-interactions. Parasitism is a very broad term and different types of parasites are recognised on different basis.
In the course of their life cycle, parasite may become associated with more than one host. In many cases the life cycle is characterised by numerous very rigid requirements. Whenever a parasite is able to live and reproduce within a host—the result is an elaborate host- parasite interactions.
Host Specificity of Parasites:
In mature condition a given parasite is quite often found in limited number of hosts. In extreme condition, distribution of a parasite may be restricted to a single host—mono-specific parasite. Even when poly-specific the different hosts are phylogenetically related. This host specificity is a function of physiological specialization and evolutionary age.
It is broadly divided into two parts:
(a) Ecological specificity:
The parasites are capable of making room in a foreign host but normally never reach another host due to ecological barriers. Such parasites are able to develop in more host-species under laboratory conditions than in nature.
(b) Physiological specificity:
The parasites are physiologically incapable of surviving and reproducing in a foreign host, e.g., Taenia solium in dog survives but never achieves reproductive ability. If the parasites find the conditions suitable for their development—then it is said to be compatible with that of the host. If not, it is said to be incompatible.
Host and Parasite: A Mutual Relation:
In the course of time a mutual adjustment or relation or tolerance frequently develops between the two which permits them to live together as a sort of compound organization without very serious effect or damage to either.
The virulant types, however, try to eradicate the hosts. But it is essential to keep the host alive and not to kill it by causing a high degree of pathogenecity. By killing the host it will ultimately lead to death of itself also. Accordingly Natural Selection leads to the elimination of most virulent species and maintains the less virulant ones.
Effects of Parasites on Hosts:
The effects of parasitism on the hosts are intimately associated to the effect of host on the parasites. These effects depend on several factors, such as—age, diet, genetic factors, susceptibility of the hosts, the size, number and virulence of the parasites, their mortality, migration, and method of feeding.
A. Destruction of Host’s Tissues:
Time and degree of damage vary greatly:
1. Time of injury:
i. Some parasites injure the host’s tissue during the process of entry, e.g. hookworms like Ancylostoma duodenale, whose infective larvae inflict extensive damage to cells and underlying connective tissue while penetrating the host’s skin.
ii. Some inflict tissue damage after they have entered, e.g., larvae of Ascaris lumbricoides while passing through lungs of human host cause physical damage to lung-tissue, leading to pneumonia.
iii. Others induce to histopathology changes by eliciting cellular immunologic response to their presence, e.g. Entamoeba histolytica actively lyses the epithelial cells lining the host’s large intestine and liver causing large ulcerations by the action of secreted enzymes.
2. Types of cell damage:
Three major types:
i. Parenchymatous or albuminous degenerative cells become swollen and packed with albuminous or fatty granules and pale cytoplasm. This type of damage is characteristic of liver, cardiac muscle and kidney cells.
ii. Fatty degeneration cells are filled with an abnormal amount of fat deposits, e.g. liver cells.
iii. Necrosis means any type of persistent cell degeneration which finally die, e.g. as the result of encystment of Trichinella spiralis in mammalian skeletal muscles; necrosis of surrounding tissue is followed by calcification.
3. Tissue changes:
Four main types:
(a) Hyperplasia:
i. Refers to an increased rate of cell division resulting from an increased level of cell metabolism.
ii. Leads to a greater total number of cells but not in their sizes.
iii. This commonly follows an inflammation and is the consequence of an excessive level of tissue repair.
iv. For example—thickening of bile duct in presence of Fasciola sp. is the result of hyperplasia.
(b) Hypertrophy:
i. Refers to an increase in cell size.
ii. Commonly associated with intracellular parasites.
iii. For example in Erythrocytic phase of Plasmodium vivax, the parasitized RBC’s are commonly enlarged. Spermatogonial cells of Polymnia nebulosum (an Annelid) when parasitized with Caryotropha mesnili (a Protozoan), are enlarged.
(c) Metaplasia:
i. Refers to the changing of one type of tissue into another without the intervention of embryonic tissue.
ii. The encapsulating epithelial cells and fibroblasts of the fluke, Paragonimus westermani in human lungs are transformation of certain other type of cells in the lungs.
(d) Neoplasia:
i. This is the growth of cells in a tissue to form a new structure, e.g., a tumour.
ii. Neoplastic tumour is not inflammatory.
iii. This is not required for the repair of organs.
iv. It does not conform to a normal growth pattern.
v. It may be benign or malignant.
Example:
Eimeria sp. causes tumor in rabbit liver, Schistoma mansoni in human intestine and liver, Echinococcus granulosus in human lungs etc.
B. Competition for host’s nutrients:
i. Endoparasites with a great density causes nutritional deficiency in host by absorbing sugars, vitamins, amino-acids etc.
ii. Mal-nourished hosts are more proned to disease and infection.
Example:
Diphyllobothrium latum (a fish tapeworm) in human causes anaemia by absorbing profuse Vitamin B12 (as much as 10 to 50 times more than do other tape-worms). Vitamin B12 plays an important role in blood formation, thus its uptake by D. latum results in anaemia.
C. Utilisation of host’s non-nutritional materials:
Parasites in some cases also feed on host- substances, other than stored or recently acquired nutrients. Ectoparasites and endoparasites feed on host’s blood, 500 human hookworms can cause a loss of about 250 ml blood/day, leading to anaemia.
Mechanical interferences:
Mechanical interferences by parasite cause injuries to hosts, e.g. elephantiasis or filariasis in humans is caused by Wuchereria bancrofti. Increased number of those adult worms in lymph vessels coupled with aggregation of connective tissue may result in complete blockage of lymph flow.
Excess fluid behind the blockage seeps through the walls of lymph ducts into the surrounding tissues, causing edema and ultimately with scar tissues—the elephantiasis of limbs, breasts, scrotum etc.
Effects of toxins, poisons and secretions:
Specific poisons or toxins egested, secreted or excreted by parasites cause irritation and damage to hosts, e.g.
i. Antienzymes produced by intestinal parasites counteract host’s digestion.
ii. Allergin, a toxin as the body fluid of nematodes—Parascaris equorum and other ascarids, irritates the host’s cornea and nasopharyngeal mucous membrane.
iii. Toxin of pathogenic Entamoeba histolytica produces toxic symptoms in parasitized mammalian hosts and creates ulcerations within the large gut of man.
iv. Schistosome cercarial dermatitis is the result of an allergin reaction against an irritating parasitic secretion from the fluke.
v. Haemozoin pigment produced by trophozoites of P. vivax exert toxic effect in infected persons and the patients suffer from periodic effect of high fever with chilliness and shivering.
Other parasite-induced alterations:
(a) Sex reversals:
Gonads of parasitized hosts may change, leading to sex reversals; e.g. crab when parasitized by Sacculina (a crustacean) display sex reversals. Parasitized male crab acquired secondary female characteristics like broad abdomen, appendages modified to grasp eggs, chelae become smaller, testes with testicular cells at various stages of degeneration.
Parasite-removed male develops into hermaphrodite by regeneration of rest testicular cells. Parasitized female crab shows ovarian degeneration but does not show hermaphroditism on removal of parasite, as ovarian tissue cannot regenerate.
(b) Parasitic castration:
i. It refers to destruction of host’s gonadal tissues by a parasite.
ii. Reduces egg and/sperm production in host’s body or becomes sterile.
iii. The mudflat snail—Ilyanassa obsoleta are directly castrated by the trematode— Zoogonus lasius. Sporocysts of Z. lasius secrete a molecule that causes the destruction of host reproductive cells as well as inhibits same to genesis.
The freshwater snail, Lymnaea stagnalis is indirectly castrated by larvae (Sporocysts) of Trichobilharzia ocellata (a trematode). These larvae do not possess mouth and thus destroy the gonadal tissue by chemical means.
(c) Enhanced growth of host:
An interesting aspect of parasite induced change in hosts is responsible for enhanced growth; e.g.
i. Workers of the ant, Pheidole commutula become much larger when parasitized by the nematode, Mermis sp.
ii. Fresh water snail, Lymnaea ariculata infected with trematode larvae is larger than uninfected ones.
iii. Mice infected with larvae of Spirometra mansonoides (a tapeworm) grows faster than non-parasitized one.
iv. Rats when parasitized by Trypanosoma lewise increase their weight more rapidly than non-parasitized one.
The enhanced growth of the host is due to stimulation of growth-promoting molecules secreted by the parasites.
Host reaction:
In immuno-parasitology, the animal is the host and the parasite is either self (by molecular memory) or non-self (foreign).
When a host recognizes the parasite as non-self, it generally reacts against the invader in two ways:
1. Cellular (or cell mediated) reactions:
Where specialised cells become mobilised to arrest and eventually destroy the parasite as usual.
2. Humoral reactions:
Where specialised molecules in circulatory system (antibodies/ immunoglobulin’s in case of vertebrates) interact with the parasite, usually resulting in its immobilization and destruction.
Internal defense mechanisms:
The internal defense mechanisms of animals, both invertebrates and vertebrates, are of two types:
I. Innate (or natural) and
II. Acquired.
Theoretically each of them again can be of two types—cellular and humoral.
Invertebrate immunity:
I. Innate internal defense mechanism:
Cellular factors:
These includes the following chief categories:
(a) Phagocytosis:
When a foreign parasite (small enough to be phagocytosed) invades into an invertebrate host, it is usually phagocytosed by the host’s leucocytes, primarily the granulocytes.
Phagocytosis consists of three phases:
i. Attraction of phagocytes to the non-self material, commonly by chaemo-taxis.
ii. Attachment of foreign material to the surface of the phagocyte, usually involving a specific chemical binding site.
iii. Internalization of the foreign substance i.e. engulfment by the phagocyte.
Fate of phagocytosed parasites:
i. May be degraded intracellularly.
ii. May be transported by phagocytes across epithelial borders to the exterior.
iii. May remain undamaged within the phagocytes and some may even multiply within host cells.
(b) Encapsulation:
1. Parasites, that are too large to be phagocytosed, are encapsulated as invading non-self mass enveloped by cells and/or fibres of host origin, as found in insect and molluscan hosts.
2. Encapsulation consists of:
(i) First leucocytosis (increase in number of leucocytes);
(ii) Migration—many of these cells migrate by the process of chaemo-tactic movement towards the parasite and form a capsule of discrete cells around it, as found in insects and in other cases (i.e., in molluscs).
Host cells synthesize fibrous material which becomes deposited inter-cellularly and concentrically in layers around the parasite.
3. Encapsulation of Tetragonocephalum (a tapeworm) in the American oyster, Crassostrea virginica.
Fate of encapsulated parasite:
Destroyed and disintegrated parasite’s tissues are phagocytosed by host’s granulocytes.
(c) Nacrezation (i.e. pearl formation):
1. Nacrezation is another type of cellular defense mechanism, known in molluscs.
2. As certain helminth parasites, e.g., Meiogymnophallus minutus (a trematode) occurs between the inner surface of the shell (nacreous layer) and the mantle of marine bivalves. Now the mantle is stimulated to secrete nacre that becomes deposited around the parasite. In so doing, a pearl is formed and the enclosed parasite is killed.
(d) Melanization:
1. The process involves deposition of the black-brown pigment, melanin around the invading parasite.
2. Melanization is chemically the result of enzymatic oxidation of polyphenol by tyrosinase.
3. This is detrimental to the parasite and may lead to its death by interfering with such vital activities like hatching, moulting or feeding.
4. Melanization of the nematode, Heterotylenchus autumnalis in haemocoel of larval house-fly—Musca domestica.
Humoral factors:
These fall into two categories:
(a) Innate humoral factors:
These are two types:
i. Those are directly parasitocidal, e.g. several marine molluscan species contain a constituent in their tissue extract that is lethal to Cercariae of the trematode, Himasthla quissetensis.
ii. Those that enhance cellular reactions, e.g., naturally occurring agglutinins or lectins. These glycoprotein molecules enhance phagocytosis of the non-self-material.
(b) Acquired humoral factors:
These are also of two types:
i. Lysosomal enzyme:
When challenged with non-self-parasites, some invertebrate’s granulocytes (haemocytes) hypersynthe size certain lysosomal enzymes and subsequently release them into some parasites. When they come in contact with elevated enzymes are killed either directly or indirectly whereas the parasite’s body surface by action of lysosomal enzyme undergoes chemical alteration and thus is recognized as non-self-material and consequently get attacked by host’s haemocytes.
ii. Antimicrobial molecules:
When challenged with micro-organisms, some insects synthesize antimicrobial molecules which are quite different from vertebrate antibody but kill the microorganisms, e.g.; the synthesis of two small basic proteins (PgA and PgB) by the moth, Hyalophora cearopia when challenged with E. coli and these proteins kill the bacterium.
Vertebrate Immunity:
Immunity refers to resistance against disease caused by a foreign agent. This is based on antigen-antibody interaction. In vertebrates this reaction is very specific. Antigen is the only foreign substance (Proteins, glycoproteins, nucleoproteins etc.) which on introduction induces the synthesis of antibody under some appropriate conditions. All zoo-parasites theoretically contain multiple antigens.
These are chiefly of two types:
i. Somatic antigens molecules comprising some of parasites.
ii. Metabolic antigen molecules are associated with secretion and excretion, e.g., moulting fluid of nematode is highly antigenic.
Antibody—Refers to proteins synthesized by host tissue in response to the administration of an antigen and which specifically react with that antigen to immobilize and destroy it.
Mechanism of antigen-antibody interactions:
i. Antigens on introduction are able to bind with specific cell surface receptor of lymphocytes (both B and T-lymphocytes).
ii. Host lymphocytes are now stimulated to proliferate and differentiate.
iii. As a consequence, clones of progeny lymphocytes are formed.
iv. In the process of proliferation, some progeny differentiate into effector cells (the functional end products of the immune response). Plasma cells are B-lymphocyte effector cells that secrete antibodies. Killer T-cells are such T-lymphocyte effector cells that eliminate foreign cells simply by contact.
v. As soon as immunoglobulin’s are produced, immunogens are coated with such antibodies and are rapidly destructed and / or phagocytosed.
The parasites try to establish itself within the host while the latter tries to destroy it which results in dynamic state of equilibrium. The reaction of the host in the presence of a parasite is termed as resistance. If resistance is sufficiently high to prevent parasite reproduction, it is known as absolute resistance and if parasite is able to overcome it and still reproducing it is called partial resistance.
(a) In case of larger parasites there is considerable damage to host tissues where histamin is released, macrophages are attracted and a primary stage of inflammation is set up.
(b) In the second stage, the cells of the lymphoid macrophage system elaborate antibodies. The immunoglobulin’s appears in various molecular forms differing in properties and actions. The macroglobulin’s (IgM) is the first to appear in an infected animal. This is followed by the appearance of gamma-globulin and alpha-globulin (IgA). The properties and number of antibodies vary from individual to individual parasitic infections.
(c) Interferons also play an important role in the immunity reaction of the host. These are known to operate in malaria and other viral reactions by rendering the host cells unfit for habitation by intercellular parasites.
Categories of antigen-antibody interactions:
These are of three types:
1. Primary interaction:
Refers to the basic event during which the antigen is bound to and/or more available sites on the antibody molecule.
2. Secondary interactions:
Include agglutination, precipitation, complement-dependent reaction, neutralisation, immobilisation etc.
i. Agglutination reaction:
Antibodies (agglutinins) clump microbes representing antigens and visible conglomerates are formed. This is referred to as agglutination reaction.
ii. Lysin and lysis reaction:
Lysin (antibodies) dissolves or lyses antigens. The reaction occurs in the presence of complement, a substance in normal serum representing a system of enzymes. Complement is sensitive to heat, chemical substances, ultraviolet rays, long-term storage etc.
iii. Complement-dependent reaction:
In the first phase of this reaction mutual adsorption of antigen-antibody takes place and precipitation occurs. In the second phase of reaction the fixation of complement by antigen-antibody occurs which is used for detecting many of the parasitological infections.
iv. Precipitin reaction:
Precipitin is the antibody that brings about the formation of a minute deposit (precipitation) when interacted with specific antigen (precipitinogen). While in agglutination the entire microbial bodies act as antigen, in precipitin the antigen will be the results of breakdown of microbial bodies or their products. This precipitin reaction is used for detecting infections like plague, anthrax, tularaemia etc.
v. Phagocytosis:
Refers to the engulfment of non-self-material by host cell like macrophages. In vertebrates, this is introduced through the action of antigen, antibody and complement.
This occurs in two ways:
(1) Accumulation of leucocytes through complement sequence and
(2) Certain antibodies called opsonins become coated on to the foreign materials and they enhance phagocytosis.
Opsonins are antibodies occurring in normal as well as in immune sera which inhibit microbes making them more amenable to phagocytosis.
3. Tertiary interaction:
Refers to in vivo expressions of antigen-antibody reactions. At times these may be of survival value to the host, but at other times they may lead’ to a disease through immunologic injury.
Immunity to parasites:
Vertebrate hosts always develop some degree of acquired immunity in the presence of parasites.
This is usually of two types:
i. Concomitant immunity:
Where immunity, either complete or partial, may be maintained only while the parasites are present.
ii. Sterile immunity:
Where immunity persists long after the complete disappearance of the parasites.
Protozoan blood parasites:
i. Cattle infected with certain species of Babesia shows premonition.
ii. While cattle, long after Theileria parva has disappeared, shows sterile immunity.
iii. For malaria-causing parasites—Premonition usually occurs in case of avian- infecting species of Plasmodium while sterile immunity can be produced with the rodent malaria causing agents P. berghei and P. vinckei (Fig. 16.3).
iv. Certain breeds of cattle develop partial immunity against Trypanosoma.
Protozoan tissue parasites:
(a) Antibodies are produced by host cells when they come in contact with antigens of parasites. Thus,
i. When Entamoeba histolytica resides in host’s intestinal lumina, no detectable antibody occurs, but when the Amoeba invades the mucosa and other tissues, antibodies are evident.
ii. For Leishmania tropica, if the sores produced by this parasite are allowed to heal spontaneously, the host becomes totally immuned to reinfection.
iii. Immunity to Toxoplasma gondii is evident in adult humans who show the antibodies, while congenital infection with T. gondii leads usually to death and those who survive, show a hydrocephalus condition. Immunity can control the intracellular stages only if the macrophage becomes successfully activated, which requires production of cytokines by T-cells.
iv. The trophozoites of gregarines (Gregarina sp) exhibit an eerie gliding movement. Various theories have been put forward. Similar movement has been noticed for the trophozoites of Plasmodium and Eimeria. There is little evidence of an effective immunity against merozoites of Eimeria sp and Gregarina sp.
Experimental studies have shown that immunity can directly affect intracellular developmental stages in both initial and subsequent infections. This immunity relies on the production of cytokine interferon, presumably activating an intracellular defence mechanism that is capable of preventing sporozoite and merozoite development.
(b) Special manifestations are shown by Trypanosoma. Parasites may change their surface antigens during their life cycle in vertebrate hosts. Continuous variation in major surface antigens is also shown by African trypanosomes. In such case, infected individual show waves of blood parasites. Each wave comprises of parasites expressing a surface antigen that is different from the previous wave.
Thus, by the time the host produces antibodies against the parasites, an antigenically new organism has grown out. Such continuous antigenic variations make it difficult to effectively vaccinate the infected individuals (Fig. 16.2).
Blood helminths:
i. Include adult Schistosomes and certain microfilariae. Concomitant immunity is shown by rodents on Rhesus monkeys against infection of Schistosoma.
ii. Microfilariae of Wuchereria, Brugia etc. can survive long period in human blood, indicating in their normal hosts they invoke very little immune response.
Tissue helminths:
Example: Trichinella spiralis, Echinococcus granulosus etc. produce antibodies against tissue nematode.
The serious and often fatal results of trichiniasis are due to the offspring of the infecting worms and not to the adult worms in the intestine. The resistance of mice to Trichinella infection can be enhanced by injection of secretions and excretions of Trichinella larvae and adults. T. spiralis arctica is essentially incapable of infecting rats but readily infects mice, deer and certain carnivores.
i. Hosts can inhibit totally or partially the establishment of the parasitic development of Cooperia curticei in sheep.
ii. Parasites develop anatomic abnormalities along with oedema and necrosis, decreased albumin levels and significant reduction in weight gain and often death follows; e.g. Ostertagia sp. It fails to develop a vulvar flop in calves.
iii. Parasite does not grow as rapidly or reach its normal size, e.g., Trichinella spiralis in man.
iv. Parasite’s life-cycle is altered, e.g. Strongyloides sp., in naive pigs etc.
Antibodies, although, do not generally cause the death of adult worms but affected worms undergo retarded growth with destrobilisation.
Protective Immunity is absent in case of tissue trematodes like Fasciola sp., Paragonimus westermani etc.
Molecular mimicry:
Endoparasites, both protozoans and helminths can survive long durations in immunologically hostile environments. Such parasites are immunologically inert because they produce immunogens which are antigenic, similar to those of the hosts so that they are recognised as ‘self’.
This phenomena of antigen shearing between hosts and parasites is called molecular mimicry.
There are three possibilities regarding its origin:
(i) Mimicry by natural selection,
(ii) Mimicry by host induction, and
(iii) Mimicry resulting from incorporated host antigens (Fig. 16.4).
Effects of parasitism on parasites:
The parasites undergo elaborate adaptations in order to harmonize with the host.
This adaptation takes place by two ways as follows:
(a) Degeneration of organ system:
i. Sense organs are poorly developed.
ii. Less developed locomotory organs.
iii. Intestinal parasites have no well-developed digestive organs, e.g., in Taenia solium there is complete loss of digestive tract.
(b) Specialization: New attainment of organs or systems:
1. In External parasites:
i. Compressed bodies with backwardly projecting spines for attachment, e.g., Flea.
ii. Tactile hairs in mites.
iii. Barbed proboscis in ticks.
The ectoparasites also show degeneration in the following organs:
i. Loss of eyes and sometimes sense organs.
ii. Loss of wings e.g., Flea.
iii. Sometimes reduction of legs.
2. In Internal parasites:
The endoparasites possess peculiar admixture of both degenerated and specialised parts as follows:
i. They possess all sorts of hooks, barbs, suckers as organs for attachment, although they have lost sense organs or special organs for locomotion.
ii. Very simple nervous system and sometimes complete loss of digestive systems.
iii. The most remarkable specialization of the endoparasites brought forth in their reproductive systems which enabled them to a greater power of reproduction. For them every structure, every function, and every instant of their life are modified to a certain extent for the sole purpose of reproduction.
“A fluke does not eat to live”—it lives and thus eats only for reproduction. The highest specialization of reproductive system is achieved by the tapeworm. In the mature proglottids both male and female reproductive organs are present in tapeworm while others (proglottids) contain either male or female reproductive systems.
Host susceptibility and specificity:
For a parasite to live habitually in a host-body there must be:
i. Suitable conditions for the transmission of parasites from one host to another;
ii. Able to establish itself in a host when it reaches a new one;
iii. Satisfactory conditions for growth and reproduction after its establishment.
Hosts and Parasites: A mutual tolerance:
In course of time, a mutual adjustment or tolerance frequently develops between the two (2)— host and parasite, which results to lead their life as a sort of compound organisms, without any serious effect to either. It may not” be in the best interest of the parasites to destroy its host for it would do it—invariably it would destroy itself.
Thus, parasitism is a specialised mode of living within a broader ecological category— symbiosis. In parasitism—the host and the parasite have a very intimate association where all the benefits are derived by the parasites from its prey—the host and the two (2) systems constantly interacting with each other.
Thus the criticism of the story—”Host- Parasite Interaction” is one of the compromise—a key (parasite) to unlock the box (host) of an unrevelled mysterious entity—in which the parasites making elaborate efforts to overcome the match against the host while the host making attempts to keep the ball in the goal of parasites, thus trying to eradicate it.