"A parasite's existence is usually an elaborate compromise between extracting sufficient nourishment to maintain and propagate itself, and not impairing too much the vitality or reducing the numbers of its host, which is providing it with a home and a free ride. In consequence of this compromise, a parasite usually destroys only small portions of its host at a time, portions of which can often be replaced fairly quickly by regeneration of the tissues attacked. Or it may exploit the energies of its host in more subtle ways, as when it subsists on the food which the host has collected with great expenditure of time and energy".
In this definition and concept of parasitism an ecologist considers the situation as it exists under "normal conditions"—or under conditions where epidemiology and ecology are synonymous. From this state of "Happy Worms in Happy Hosts" to that of parasitic disease are many gradations between epidemiology and ecology. Moreover, the economic requirements of the host may modify the conditions. A worm burden which retards development and fattening of a young animal may be of negligible pathogenic or economic significance in adult breeding stock. The ecological concept properly does not take cognizance of disease which depends on numbers and gross damage—i.e., the outbreaks of parasitic disease.
However, the ecological concept does lay stress on a very significant aspect of parasitic damage, i.e., "a parasite usually destroys only small portions of its host at a time, portions of which can often be replaced fairly quickly by regeneration of the tissues attacked"—and this is what happens when the attack is not overwhelming and when the genera] health and well-being of the animal are near normal. However, the margin of safety is narrow and many things may lead to increases in worm burden and decline in general "resistance".
The severe manifestations of helminth diseases are generally well recognised and the symptoms are fairly clear. While outbreaks may be disastrous for individual owners and for a number of owners in a region at times, in the aggregate it is probable that much greater economic loss accrues from the continuous ill-effects of the so-called "subclinical" infestations. These effects are not measured easily and their magnitude undoubtedly varies greatly from year to year depending on seasonal conditions and the fluctuations in the size and nature of worm burdens.
There is a great variety of helminths having a great variety of habits and habitats. Almost every possible niche in the host animal has been occupied by a helminth. Their alimentary canals swarm with worms, there are helminths in the liver, the lungs, the kidneys, the pancreas, the brain, connective tissue, blood stream, urinary bladder, the skin, peritoneal cavity—the hydatid cyst even invades bones and the spleen.
Worms wander in their hosts, leaving damaged tissues behind them which sometimes stimulate the growth of other micro-organisms.
Worms feed in a great variety of ways—there are bloodsuckers, tissue feeders, absorbers of the gut contents; and there are still many whose mode of nutrition is not known. Their nutritional needs are probably very specialised, for their greatest product is eggs which contain highly complex organic compounds such as the nucleic acids. In 1934, Sir Charles Martin and Dr. Clunies Ross made some observations that indicated that 2,000 female Haemonchus contortus in a sheep required about 30 ml. blood daily to supply the amount of phosphorus in the eggs. From their figures it may be estimated that a heavy infestation with H. contortus may require 342 mg. phosphorus per month.
It is not surprising that the effects of helminth infestation are very various and that the symptoms of helminthiasis resemble those of many other conditions.
Before going on to discuss in more detail some of the ways in which helminths harm their hosts, there are some matters of terminology which merit discussion. First of all, "Parasitism" is not a disease—it is simply a special kind of association of two species of animal. "Parasitosis" may be applied to parasitic disease. In U.S.A. J.H. Whitlock has drawn some finer distinctions between "helminthiasis"—infestation by helminths— and "helminthosis"—the disease produced by helminths. He goes further still in discussing the trichostrongylidoses of sheep, i.e., the diseases of sheep associated with infestation by worms of the family Trichostrongylidae. He speaks of primary and secondary trichostrongylidoses and feels that haemonchosis is perhaps the only certain primary trichostrongylidosis and that infestation by Trichostrongylus spp., Ostertagia spp., Cooperia spp. and Nematodirus spp. are secondary trichostrongylidoses. This agrees in general with the experience of most of us—the occurrence of haemonchosis even in fat, thriving sheep, and the usual association of the other infestations with malnutrition. While these distinctions made by Whitlock may appear to be drawn too finely–and he does recognise that there are all sorts of gradations between them—they merit serious consideration because they are conditioning factors in diagnosis, epidemiology and control.
From a diagnostic point of view one must assess the relative significance of all the factors. Helminthologically one must do some kind of mathematical calculation which includes size of infestation (worm burden is a useful term) and duration of infestation. Experimentally, sheep have succumbed to haemonchosis when dosed with 50-100 larvae daily for over a year; or within a fortnight when given a single dose of 30,000-40,000 larvae. At post-mortem examination one may find a number of worms that experience suggests is not enough to be responsible for the symptoms shown by the animal. One must then ask, "How long have these worms been present, how long has the host been exposed to damage?" A precise answer may not be available, but epidemiological and climatological data may yield a possible answer. Then, pathologically one must assess the damage to the host, bearing in mind that the damage may not be macroscopic, nor even microscopic, but may take the form of a departure from physiological or production normal. Loss of appetite, impaired digestibility of food and more rapid passage of food through the bowel all contribute to malnutrition.
From an epidemiological point of view a helminthiasis is a menace and given the appropriate conditions it may become a helminthosis, either because the worm burden increases or the host "resistance" decreases.
The approach to the control of parasitic diseases lies in knowledge of the factors which permit or facilitate the change from helminthiasis, which is present in most herds and flocks most of the time, to helminthosis. At best, prediction of these factors enables strategic control, and at second best enables tactical con!rol, and at worst enables an attempt at "economic salvage".
The difficulties of diagnosis—even the need for a diagnosis in the commonly accepted sense—should disappear with improved epidemiological information.
Control is not synonymous with eradication. It is a compromise between the needs of economic animal husbandry and the demands of preventive medicine—between what is best for the host and its general well-being and what is worst for the parasite. We may have to tolerate helminthiasis but we must not allow it to become helminthosis.
There are no very clear relationships between the harmfulness of helminth species and their habitats. All of the worms inhabiting the alimentary tract may cause ill-effects. Worms in connective tissue, e.g., Onchocerca spp., appear generally not-to cause ill-effects, even the nodules which form the habitat of 0. gibsoni do not inconvenience the host. There are some workers who feel that 0. cervicalis in the ligamentum nuchae of the horse may predispose to poll-evil and fistulous withers, possibly when there is a bacterial invasion of a necrotic area in the neighbourhood of a worm.
Worms in the blood stream may cause ill-effects indirectly, e.g., the Schistosomes deposit their eggs in the small veins in the mucosa of the alimentary tract or bladder and the damage occurs when the masses of eggs break through the mucosa. Dirofilaria immitus, the heartworm of dogs, may interfere with heart action if masses of worms prevent closure of the heart valves.
Worms in the air passages cause obstruction and collapse of portions of the lung, sometimes followed by a secondary pneumonia.
The cystic stages of some tapeworms, e.g., Echinococcus, cause damage to the tissue of the invaded organ by pressure.
When the helminths produce lesions which form their habitat within the host, the nature of the lesion may cause serious inconvenience and even severe damage to the host. The tumours in the stomach wall of the horse caused by Draschia megastoma may be very large and there may be several in the same stomach. The nodules caused by the larvae of Oesophagostomum columbianum, if present in sufficient numbers, cause serious interference with bowel motility and damage to the bowel wall. The verminous aneurysm caused by larvae and young adults of Strongylus vulgaris may interfere with the blood supply to the alimentary tract of the horse.
The feeding habits of helminths often provide information on how the host is harmed. There are bloodsuckers, tissue feeders, feeders on the contents of the alimentary canal and there are many whose feeding habits are not properly known, e.g., Trichostrongylus spp.
Among the bloodsuckers are H. contortis, Hookworms and Fasciola hepatica. The amount of blood removed may be considerable, e.g., 2,000 H. contortis may need about 30 ml. blood daily simply to provide the amount of phosphorus required to produce the 20,000,000 eggs which are laid, quite apart from other needs for food and the waste from bleeding at the sites of attack on the abomasal mucosa. It has been estimated by Andrews in U.S.A. that the quantities of blood lost during 10 days in two fatal cases of haemonchosis were 1492 and 2380 ml. or 1.57 and 2.5 tunes the original quantity of blood in the lambs concerned.
The dog hookworm, Ancylostoma caninum, may remove 0.8 ml. blood per worm each day, and in a heavily infested dog as much as one-third of the haemoglobin in the body may be lost daily. In addition, hookworms damage the mucosa by means of their large buccal capsule. H. contortis, which has a small mouth, does not damage the mucosa, though removing large amounts of blood. Fasciola hepatica feeds on blood and in chronic fluke disease the host becomes grossly anaemic. Anaemic ewes suffering haemonchosis and anaemic cows suffering chronic fluke disease produce less milk and the growth rate of the young is reduced.
Among the tissue feeding worms are Chabertia ovina, the large strongyles of horses (Strongyles spp.) and, not so well known, the fourth stage larvae of Oxyuris equi, the pin-worm of the horse. These tissue feeders have large buccal capsules and feed by drawing a piece of the mucosa into the mouth, digesting it, and moving on to repeat the process of attachment and digestion. Even a single worm can cause a great deal of damage and a close examination of the lesions produced by C. ovina provides a striking example.
Estimates of the amounts of mucous membrane removed by the large Strongyles in the horse have been made by Rogers who determined the amount of zinc in the worms and mucosa. He estimated that S. edentatus required 3.9-21.2 g. mucous membrane to provide the amount of zinc in the worm, while for S. vulgaris the figures were 0.7-3.4 g. It is probable that C. ovina may remove similar quantities of mucous membrane from the colon of sheep.
It is accepted generally that tapeworms absorb material from the contents of the alimentary canal of the host, but there is some evidence that by lying close to the mucosa these worms may absorb material, if not from the mucosa itself, at least from the layers of ingesta about to be absorbed by it. In U.S.A. Chandler has found that some tapeworms may have very special nutrient needs from the host.
The significance of tapeworm infestations in sheep is still under investigation in U.S.A. and the latest conclusion is that very little ill-effect occurs. In experimental infestations in lambs large masses of Moniezia spp. were present but there had been no interference with health and productivity. It may be that tapeworms harm their hosts only when there are serious special dietary deficiencies.
The feeding habits of many helminths are not well known and many worms, e.g., Ascarids, which usually are supposed to feed on ingesta may take material, in fact, from the mucosa by feeding close to it and ingesting material about to be absorbed. Trichostrongylus spp. may feed in the same way. It has been found that Ascarids (e.g., Ascaridia galli in fowls) can absorb phenothiazine through their cuticle, and it may be that food materials may enter the worm in the same way. Studies at the McMaster Laboratory with radio-active phosphorus and its absorption by worms and tissues suggested that Trichostrongylus spp. are tissue feeders but also absorb phosphorus through the cuticle. H. contortis appeared to be a tissue feeder but absorbed little phosphorus through the cuticle. Oe. columbianum was a tissue feeder.
The larvae of some helminths, Strongyloides spp., hookworms (including the species in sheep and cattle), Stephanurus dentatus, and the cercariae of the Schistosomes, can infect the host by skin penetration. Skin lesions may be produced especially when repeated infestations occur. In many cases the reaction is severe, and probably has value immunologically because the larvae are trapped and destroyed in the skin.
Many helminths have a migratory phase in their life-cycle and may wander extensively in the body of the host animal. In their wanderings they may cause extensive damage, and especially if they spend some time—days, weeks or months—in damaged viscera.
There is increasing recognition of the significance of infestations with immature worms even when there is no migratory phase in their life-cycle. Fatal infestations have been produced in sheep with immature H. contortus, Trichostrongylus spp. and Oe. columbianum at the McMaster Laboratory. The serious ill-effects caused by immature worms in cattle have been stressed by Mayhew in U.S.A. The serious ill-effects caused by immature amphistomes in cattle are well known.
Infestations by immature worms provide difficulties in diagnosis and treatment. Ante-mortem diagnosis is practically impossible and most immature worms appear to be more difficult to kill with anthelmintics.
From a pathological point of view, and again in control, the damage done by immature worms is very important. Often it is not only very severe, but the worms may not be accessible to treatment during that phase of development, e.g., young Oe. columbianum in nodules, young S. vulgaris in the verminous aneurysm. The immature F. hepatica which cause acute fluke disease can be destroyed by increasing the dose of carbon tetrachloride, but immature Oe. columbianum in nodules and immature S. vulgaris in verminous aneurysms cannot be destroyed by any of the anthelmintics now in use.
The damage occasioned by immature worms directs attention to a special aspect of control. It is not simply a matter of preventing heavy worm burdens becoming established, but of preventing as far as possible the initial invasion of the body. Once the larvae have been swallowed little can be done to deal with them until they have completed their migrations—and by then they may have caused tremendous damage, or even death.
An attack on the contamination phase of the life-cycle is the great need and may be achieved by strategic use of highly efficient anthelmintics, and by the use of repeated doses of anthelmintics, e.g., phenothiazine, which depress egg laying—and kill the free-living stages in faeces. This line of attack has been successful against horse parasites—daily doses of 1 g. phenothiazine for 20 days each month appears practically to have eliminated contamination of pastures and has protected young horses against strongylosis, especially damage which results in the verminous aneurysm.
The migrations of ascarid larvae through the lungs of pigs and foals cause severe and often fatal damage.
It has been found in England that the immature Dictyocaulus viviparus in cattle are capable of causing severe ill-effects with symptoms-like those of classical "husk". The worms may be still microscopic and would not be seen at post-mortem examination unless scrapings of the lining of the air passages and press preparations from the lungs are examined microscopically. A very interesting feature is that immature worms have been found in the lungs as long as 10 weeks after artificial infection. They usually mature in about 6 weeks. This delayed development appears to be part of an immunity reaction, and some of the ill-effects may be in the nature of anaphylactic or allergic manifestations.
Cysts, tumours, aneurysms, nodules, sites of attachment of tissue feeding worms, fibrotic changes and gross anaemia are obvious lesions caused by helminths. There are some infestations which may be fatal and yet there are no macroscopic lesions and even examination of microscopic sections may not reveal gross changes. Trichostrongylosis of sheep and Cooperia spp. infestations in calves are in this category. It may be that closer examination of specially prepared sections will in fact reveal lesions of the mucosa, but it may be that the lesion is a biochemical rather than a histological one.
Most of the pathological effects of helminth infestations are not specific or diagnostic. Mixed infestations are usual and there may be additive effects if there is a concurrent infestation with species having similar ill-effects. Sheep may suffer fasciolosis and haemonchosis at the same time and both will cause anaemia. A combination of relatively mild infestations with H. contortus and F. hepatica in sheep may result in a fatal anaemia. In cattle a combination of H. contortus and Bunostomum phlebotomum (hookworm) and F. hepatica or other combinations of these worms may lead to severe anaemia. The effects of such combinations must be considered when assessing the significance of egg counts and worm burdens seen at post-mortem.
Dietary deficiencies of copper and cobalt may cause anaemia, and if an infestation with blood-sucking worms is added the combined effects may be fatal. The important point is that the number of worms found, or the egg count, may be less than one usually associates with anaemia due to helminths alone (e.g., 4000 H. contortus may be required to cause fatal anaemia in a grown sheep but if the sheep were already anaemic with red cell numbers down to 5 or 6 million, then 1000-1500 worms may be enough to kill it).
Whether succulent, watery pastures with low dry matter content, which usually cause scouring in sheep and cattle, may have additive effects to helminth infestations which also cause scouring (trichostrongylosis, ostertagiosis, etc.) remains to be examined experimentally—but it appears likely that any further speeding up of the passage of ingesta through the alimentary canal may reduce still further the time for digestion and absorption.
There is little doubt that malnutrition in general (too little food or food of very poor quality) and helminthoses which reduce appetite and depress digestibility (trichostrongylosis, oesophagostomosis) have additive effects. The value of improved nutrition in control of these diseases is well known and is a logical procedure when one considers the symptoms and progress of the conditions.
It is probable that there is a tremendous amount of unthriftiness and poor productivity due to prolonged, medium to light infestations with Trichostrongylus spp. and probably many other nematode infestations. These ill-effects are not obvious and although they can be measured very simply (body weight and wool growth) it is essential to have a control group in which worm burdens are kept as low as possible by means of repeated, regular treatments with phenothiazine.
The significance of sub-clinical infestations will vary from year to year depending on nutritional and climatic conditions. The intensity of treatments and their economics can be determined only by numerous field trials extending over a number of years. An accumulation of epidemiological information is essential if haphazard control measures are to be avoided.
Better nutrition and management are the basic requirements for control of helminthoses in general, and have particular application to control of the sub-clinical infestations.
Sheep which have suffered severe infestations often recover very slowly even when their worm burdens have been removed with anthelmintics. The reason for this is not known and is a problem requiring a full investigation.
In the field, recovery usually is hastened if the level of nutrition can be raised substantially. In pens we have measured the slow recovery from helminthosis and slow malnutrition.
Slow recovery often may be the reason behind apparent failures of anthelmintics.
In cattle, Roberts in Queensland has reported similar effects; and often calves remain unthrifty for many weeks after they have thrown off their worm burdens.
In U.S.A. the administration of yeast to calves and sheep hastened recovery from trichostrongylidoses, possibly by stimulation of rumenal organisms, possibly by restoration of appetite. There is a wide field for work along these lines in Australia.
It has been customary to attribute many of the ill-effects seen in helminthoses to toxic materials absorbed from the worms' excretory products. However, it is very doubtful whether any specific toxins exist. For most of the helminthoses there is adequate evidence to account for the ill-effects without postulating toxins.
There is, however, a fairly new field for investigation. Infested animals do absorb something from their helminths and their products, and may produce antibodies (D.F. Stewart). Some aspects of the immunological reactions in helminth infestations are undoubtedly allergic or anaphylactic manifestations. Whether these manifestations affect the host adversely, as well as the parasites, has yet to be determined. Whether continued diarrhoea associated with helminthoses may have a helminth-allergy basis is a problem for investigation.
Helminths harm their hosts in many ways, some of which are not yet understood. Helminthosis may be a complex disease and is commonly associated with and aggravated by general and special nutritional deficiencies. The importance of damage caused by immature worms, particularly those which wander in the tissues, is stressed because the commonly applied measures may not control this form of parasitic attack. Recovery from severe helminthosis may be very slow and in the field may cast doubts on the efficiency of anthelmintics. The necessity for control measures, particularly those based on improvements in nutrition, in addition to anthelmintics is clear.