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In this article we will discuss about:- 1. General Features of Parasitic Infection 2. Factors Affecting the Shift from Parasitic Infection and Diseases 3. Examples.
Features of Parasitic Infection:
Some parasites (ectoparasites) live on the surface of the host and others (endoparasites) live inside the host. Some ectoparasites are important as disease agents in their own right (e.g. scabies mites) or as vectors of infection (e.g. fleas transmitting the plague bacillus, Yersinia pestis).
However, in general, endoparasites are potentially much more important as causes of disease, due to the much greater degree of intimate contact between parasite and host. (An extreme example is the malaria parasite which for part of its cycle lives inside the erythrocytes of humans.)
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Where and in which group of people parasitic infection is more likely to occur is determined to a large extent by environmental conditions (housing, water supply and sanitation) and climate (particularly rainfall and temperature). Even where infection is common, individuals differ in the degree to which they are exposed to infection, such factors as personal protection or personal hygiene being particularly important.
Although parasitic infections are most common in the ‘developing’ communities of the tropics and subtropics, they can occur wherever conditions are suitable. Furthermore, individuals may be infected with more than one parasite at any one time and this is particularly likely where a number of parasites are transmitted by a common route (e.g. the faecal-oral route).
Factors Affecting the Shift from Parasitic Infection and Diseases:
In the individual, the balance between parasitic infection and disease can be affected by a number of factors acting either independently or in concert. The inner-relationships between host and parasites are complex and are grouped under three broad headings: host-related; parasite-related; and immunological.
i. Host-Related Factors:
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a. Age:
Children upto to about 6 months old are rarely susceptible to parasitic infection because of the protection afforded by maternal antibodies and also because of a significantly lower risk of exposure to infection.
After about 6 months, a child is exposed to a wide variety of infectious agents and the prevalence and severity of infections rise dramatically, reaching a peak in the age group 6 months to 5 years. While older people may continue to be at risk of infection, the degree of exposure, the intensity of infection and the occurrence of disease are often lower.
b. Nutrition:
Malnourishment is important in shifting the balance from infection towards disease, a malnourished person being much less able to withstand the adverse effects of disease. This is a particular problem in the ‘developing’ world where malnutrition is common.
ii. Parasite-Related Factors:
Parasite-related factors include the physical size and/or number of parasites, their site of occurrence, their rate of multiplication, their metabolism, and differences in pathogenicity shown by different parasite strains.
a. Size:
Parasites which grow to a large physical size or multiply rapidly have a much greater potential for causing disease than those which are small or multiply slowly. Many protozoan parasites, such as Plasmodium spp. (malarial parasites), and those which live in the intestine, are capable of very rapid asexual multiplication so that they make up in numbers what they may lack in individual size. Thus, it is perhaps more meaningful to consider biomass rather than physical size as the important factor.
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b. Multiplication Rates:
Inherent differences in the rate of multiplication between closely related parasites are also important. P. falciparum has a considerably faster rate of multiplication than the other three species of malarial parasite affecting humans and this contributes substantially to the greater severity of the disease it causes.
c. Dose Size:
Another factor related to the rate of multiplication is the size of the infective dose necessary to establish an infection. The minimum infective dose for Giardia lamblia may be as low as 10 cysts whereas that for Entamoeba histolytica may be in the region of several thousand cysts.
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d. Site of Occurrence:
Site of occurrence is particularly important in determining whether infection shifts towards disease. For example, parasites in the intestine of an otherwise healthy individual generally cause little or no disease unless they become invasive (such as some strains of Entamoeba histolytica), multiply rapidly (such as Giardia lamblia) or migrate to inappropriate sites (such as adult Ascaris lumbricoides in the bile or pancreatic duct).
Parasites which have stages in the tissues or which become tissue invaders are generally more pathogenic than those which live in the intestine. This is because parasites in the tissues have more intimate contact with the body than those in the intestine, where parasites and their products (including metabolic products and eggs) are carried away in the gut contents and faeces.
While most parasites have a ‘normal’ site of occurrence in the body where they may or may not cause disease, some parasites may occasionally be found in appropriate sites where their effects can be much more serious. For instance, during its development, the human lung fluke, Paragonimus westermanii, migrates from the intestine through the diaphragm to the lungs where it produces eggs.
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Normally, these eggs pass harmlessly out of the body in sputum, causing no ill effects to the host. However, occasionally some immature worms migrate to other body sites where they lay eggs. These eggs are unable to escape and a granuloma develops round them. If this occurs in the central nervous system, the consequences for the patient are quite different from the more typical lung infection.
e. Parasite Metabolism:
By definition, the parasite depends on the host for its nutrition and therefore the host is deprived (to a greater or lesser extent) of material which it could otherwise use for its own metabolic purposes.
Severe infection with some intestinal parasites (such as hookworm) can exacerbate an already poor nutritional state, even to the point where it becomes life-threatening. A second aspect is the effect that some parasite metabolites have on the host. The intra-erythrocytic stages of the malarial parasite metabolize haemoglobin in the infected red cell.
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When the red cell bursts, the products of this metabolism are released into the general circulation and provoke the characteristic malaria fever. The fever is itself an important part of the chain of events leading to severe illness or death in the untreated patient.
f. Strain Differences:
It is well known that some strains of parasite are potentially more pathogenic than others. Infection with Entamoeba histolytica acquired in the tropics is much more likely to cause disease than infections acquired elsewhere.
iii. Immunological Factors:
Although parasitic infections may stimulate the production of antibodies, in most cases these antibodies are not protective although they may be useful as indicator of existing, or of relatively recent, infection. Most anti-parasite antibodies persist for some time after successful treatment and, in general, antibody tests are of little value as tests of cure.
A marked feature of the immune reaction to helminthic infections is the high level of immunoglobulin E (IgE) antibody produced. Various roles are attributed to IgE in protective responses to parasitic infections including release of mast cells secretory products.
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The effectiveness of an individual’s immune response to a parasitic infection may be affected by a number of factors, including those outlined below:
i. Other infections (such as measles, which is particularly common in ‘developing’ countries) can lower the host’s resistance to, or tolerance of, parasitic infection and permit opportunist infections to develop.
ii. Pregnancy lowers the mother’s general resistance to infection and a parasitic infection which has been in a state of equilibrium may become life-threatening during pregnancy.
iii. Inherited or acquired immunodeficiency may substantially lower an individual’s immunity to a parasitic infection. This is well illustrated in the case of HIV infection and AIDS where affected individuals are more prone to a range of infections including those caused by parasites.
iv. Immunosuppressant drugs may have a similarly dramatic effect on an existing (and perhaps unsuspected) parasitic infection.
There are two other aspects of immunological relationship between the parasite and the host that are important. These are the host’s response to antigens of the parasite and the parasite’s response to host immunity.
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Much of the pathology caused by heavy infection with schistosome parasites results from the host’s reaction to metabolites produced by the small proportion of eggs laid by the female worms which become trapped in the tissue (around 95 percent of eggs pass out in the urine or faeces).
The host response is initially in the form of a giant cell reaction followed by progressive fibrosis, the formation of a granuloma round each egg (the final lesion being several times the volume of the egg that provoked it) and the replacement of normal tissue by these granulomas. The fibrous reaction associated with heavy infection of Schistosoma mansoni can cause constriction of the hepatic portal circulation leading to enlargement of the liver and spleen (hepato-splenomegaly).
Some species of parasite are able to avoid or to counteract the effects of host immunity. Some parasites are able to survive within macrophages and so are sheltered from any immune response. To do this they must block the normal microbiocidal mechanisms of the macrophage. Toxoplasma gondii, for example, inhibits phagosome-lysosome fusion, whereas Leishmania spp. are surrounded by a dense coat which can protect them from the oxidative burst.
During the early stages of their migration through the host, schistosome parasites incorporate host material into their outermost layers, effectively camouflaging their identity and preventing the host immune system from recognizing and destroying them.
On the other hand, trypanosomes causing African sleeping sickness provoke an immunological response by the host which is potentially fatal to the parasites. However, these organisms are able to evade this immune response by producing broods of antigenically different parasites in quick succession. The host’s immune response never quite catches up with these frequent changes in antigenicity and the parasites are able to survive.
Examples of Parasitic Infection:
The following examples are intended to illustrate some of the general principles of parasitic infection discussed above:
i. Amoebiasis:
Entamoeba histolytica infections occur throughout the world and account for the third most common cause of death from parasitic disease. Infection is particularly common in warm, moist environments and where sanitation is poor.
Transmission is faecal-oral and the parasites are normally found in the lumen of the large intestine feeding on food particles. The parasites become invasive in less than 20 percent of infections, lesions usually starting in the large intestine as small discrete, button like ulcers.
The advancing ulcer becomes flask-shaped, eventually extending through all layers of the gut wall. Amoebae may be carried in the blood to other parts of the body where an abscess may develop. The liver (particularly the right lobe) is most frequently affected. The liver abscess is usually single but may be multiple, does not have a well-defined wall and is usually bacteriologically sterile.
Liver abscess is about 10 times more frequent in adults than in children and about five times more common in males than in females, but the degree to which differences in exposure are responsible for these variations is not clear.
Malnourishment may increase the severity of infection and immunodeficiency may elicit or worsen the clinical effects of infection. Asymptomatic female carriers may develop severe amoebiasis during pregnancy and the puerperium.
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ii. Malaria:
The four species of malaria parasites which infect humans are P. falciparum, P. vivax, P. ovale and P. malariae. The infective stage (sporozoites) are inoculated by an infected female mosquito during a blood meal and subsequently invade and develop inside hepatocytes. Each parasites multiplies asexually as a liver schizont, producing (according to species) between 10-40000 merozoites.
When the mature liver schizont bursts, the merozoites are released. They invade the erythrocytes, mature to trophozoites (ring forms) and then begin another cycle of asexual multiplication as erythrocytic schizonts. Each erythrocytic schizont contains, at maturity, between about eight and 24 merozoites. When mature, the erythrocytic schizont bursts, releasing the merozoites which invade other the cycle repeating itself every 36-72 hours according to the species.
The four species differ in their degreee of pathogenicity. P. falciparum is the most pathogenic because it produces more merozoites in both liver and erythrocytic schizont stages, invades red cells of all ages, and has the shortest schizogancy cycle in the blood. Numbers of P. falciparum organisms in the blood can rapidly reach life-threatening levels. Although the other three species can cause severe disease, their parasitamias are rarely life-threatening.
The disease process in malaria is complex. The liver stages have no effect on the individual but illness results directly or indirectly from the destruction of erythrocytes, the number destroyed increasing progressively with each schizogany cycle.
The regular destruction of red cells results in increasing anaemia, while the release of parasite metabolites causes fever which can itself have serious consequences if severe (when the erythrocytic schizogany cycle is well synchronized, the fever pattern may become sufficiently regular to be characteristic of the species).
Blockage of the capillaries by the erythrocytic schizonts (especially those of P. falciparum) leads to tissue anoxia and cell death. The kidneys, digestive and respiratory systems can all be affected, with accompanying renal failure, vomitting and diarrhoea. When capillary blockage occurs in the brain, cerebral malaria, coma and death result, unless treatment is initiated as an emergency.
iii. Hydatid disease:
The adult tapeworms, Echinococcus granulosus, live in the intestine of dogs and other carnivores. Eggs are passed in the faeces of the dog and the larval stages from so-called ‘hydatid cysts’ (cysts of varying sizes composed of developing larvae) in infected sheep and other herbivores. Dogs become infected when they eat carcasses or offal containing the hydatid cysts.
Human infection occurs in areas where there is a close association between sheep, sheep dogs and humans and results from the accidental ingestion of Echinococcus eggs. The eggs hatch in the intestine and the larvae bore their way into the gut wall and are carried around the body in the bloodstream before developing into the hydatid cyst. The usual site is the live but they can lodge in other parts of the body such as the bone marrow or brain.
As the hydatid cyst can grow to 100 mm or more in diameter its physical size can have serious effect on the organ in which it occurs. The fluid in the centre of the cyst is also highly allergenic and if the cyst burts (or is ruptured during surgical removal) the patient may well suffer a severe and possibly fata anaphylactic reaction.
iv. Ascariasis:
Although all age groups are susceptible to infection by Ascaris lumbricoides, children between the ages of about 1 and 5 years have the highest prevalence and intensity of infection (children living in poor environmental conditions may harbour more than 100 worms).
Adult worms are large (females measure up to about 35 cm in length and males up to about 20 cm), physically strong and normally live in the lumen of the small intestine. Provided the worms remain in the lumen of the intestine, light infections in a well-nourished person cause little or no problem. About 85 percent of infections are asymptomatic.
Obstruction of the intestine occurs more frequently in heavy infections and can be surgical emergency—in some part of the world more than 50 percent of children admitted to hospital with acute abdominal conditions suffer from ascariasis. Single worms occasionally migrate into and obstruct the bile or pancreatic duct, and the passage of relatively large numbers of larvae through the lungs at any one time causes a pneumonitis (lung inflammation) lasting a few days.
