Textbook of Medical Parasitology CK Jayaram Paniker
INDEX
×
Chapter Notes

Save Clear


General IntroductionCHAPTER 1

The earliest agents of human infection to have been observed were helminthic parasites. The common roundworm, often passed live and wriggling in stools, or emerging from the nostril of an infected child, would surely have caught the attention of ancient humans and could have been associated with illness. However, in some cultures the worms were considered as even useful, helping in the digestion of food. According to an old Chinese belief, a person had to have at least three worms to be in good health!
Intestinal worms and their empirical remedies were apparently known from early antiquity in different parts of the world. The well-preserved body of a young man who died on the snow-clad Alps mountain some 5300 years ago was discovered in 1991. Whipworm eggs were identified in the colonic contents. A pouch tied to the body contained plant materials with anthelmintic properties. This finding takes the history of human helminthic infection back to over five millennia.
In more recent times, parasites have figured in various milestones along the story of infectious disease. The first description of a human pathogenic microbe was given by the pioneer microscopist Leeuwenhoek in 1681, when he observed Giardia in his own stools and communicated to the Royal Society of London, unmistakably accurate diagrams of the protozoan parasite. In the 19th century, when the silkworm disease Pebrine caused devastating epidemics in Southern Europe, Louis Pasteur was requested to investigate it. Pasteur's results published in 1870 served to control the disease, which was caused by a microsporidian parasite. This was the first instance of a scientific study on a protozoal disease, leading to its control and prevention. This also was Pasteur's first introduction to applied microbiology.
With the coming of colonialism, interest in parasitic diseases suddenly soared as many of the tropical countries could be penetrated only after controlling parasitic infections like malaria, kala-azar, amoebiasis, trypanosomiasis and schistosomiasis. Their aetiological agents were identified and control measures introduced. A seminal discovery was made in 1878 by Patrick Manson about the role of mosquitoes in filariasis. This was the first evidence of vector transmission. Soon afterwards, Laveran in Algeria discovered the malarial parasite (1880) and Ronald Ross in Secunderabad, 2India showed its transmission by mosquitoes (1897). A large number of vector borne diseases have since been identified. This provided a new approach to disease control, by targeting the vectors.
Many parasitic infections are associated with overcrowding, poor sanitation, contaminated food and water, undernutrition and other poverty-related factors. They were considered the concern of the developing countries only. While this is generally true, the rich nations are not exempt, and infact there are some parasites like the pinworm which are more prevalent in the West.
A major drawback in the fight against parasitic diseases is the inability to prevent them by immunisation. No effective vaccine is currently available against any parasitic disease. However, host immunity is decisive in determining the course of many parasitic infections. Increased susceptibility to many parasitic infections is a consequence of immunodeficiency, as in the HIV infected. Many new parasitic infections have been identified in AIDS patients in the developed countries.
Control and eradication programmes had been carried out against some important parasitic diseases, such as malaria and filariasis, with varying degrees of success. But in many cases the benefits gained could not be maintained and the situation has reverted to the original level or worse. This has been due to slackening of control measures or due to drug resistance in the parasite or its vector.
By mid-twentieth century, with dramatic advances in antibiotics and chemotherapy, insecticides and antiparasitic drugs, and increased affluence and improved lifestyles, all infectious diseases seemed amenable to control. Great dreams of eradicating infectious diseases were entertained and when global eradication of the great scourge smallpox became a reality, euphoria prevailed. Then came nemesis, with microbes rebounding. Antibiotics and antipesticides lost their efficacy, faced with microbial and vector resistance. New emerging diseases became a serious threat. The HIV pandemic provided a fertile field for old and new pathogens to spread. This applies equally to parasitic infections as to bacterial, viral or mycotic infections. In this context a new enhanced interest attaches to the study of human parasites.
 
PARASITISM
Medical parasitology deals with the parasites which cause human infections and the diseases they produce. Parasites are organisms that infect other living beings. They live in or on the body of another living being, the host and obtain shelter and nourishment from it. They multiply or undergo development in the host. Parasitism arose early in the course of biological evolution. Some organisms, instead of remaining as free-living forms deriving nourishment from raw materials in the environment, learned to use the bodies of other organisms as readymade food. One manner of achieving this is by predation, where larger animals prey on smaller ones which they kill and eat. Another is saprophytism (from Sapros, Greek for decayed), in which organisms feed on the dead and decaying bodies of animals, plants and other organic matter and help to decompose them. Parasitism is a more durable and intimate association in which the parasite establishes itself in or on the living body of the 3host, being physically and physiologically dependent on it for at least part of its life cycle. This may or may not lead to disease in the host. Parasites which live in complete harmony with the host, without causing any damage to it are called commensals, while those which cause disease are called pathogens. This distinction is however not absolute, as many commensals can act as facultative or opportunist pathogens when the host resistance is lowered. Rarely, even free-living organisms may become pathogenic under special circumstances.
The discipline of parasitology, by tradition deals only with parasites belonging to the animal kingdom. Though bacteria, fungi and viruses are also parasitic, they are excluded from the purview of ‘parasitology.’ Human parasites may be either unicellular microbes (protozoa), or larger organisms (metazoa), some of which may be many metres in size.
Parasites may be classified as ectoparasites or endoparasites. Ectoparasites inhabit the body surface only, without penetrating into the tissues. Lice, ticks, mites and other haematophagous arthropods are examples of ectoparasites. They are important as vectors transmitting pathogenic microbes. The term infestation is often employed for parasitisation with ectoparasites in place of the term infection used with reference to endoparasites. Endoparasites live within the body of the host. All protozoan and helminthic parasites of humans are endoparasites.
Parasites may pass their life cycles in more than one host. The host in which the adult stage lives or the sexual mode of reproduction takes place is called the definitive host. The species in which the larval stage of the parasite lives or the asexual multiplication takes place is called the intermediate host. Man is the definitive host for most human parasitic infections (e.g. filaria, roundworm, hookworm), but is the intermediate host in some instances (e.g. malaria, hydatid disease). A vertebrate host in which a parasite merely remains viable without development or multiplication is called a paratenic host. Such a host may serve to pass on the infection to another and so is sometimes called a transport host.
Parasites infecting humans may be proliferous or nonproliferous. Proliferous parasites are those that proliferate in the human body so that the parasite originally introduced multiplies many fold to cause high intensity of infection. Protozoan parasites are proliferous. On the other hand, most adult helminths do not multiply in the human body. They are nonproliferous. High intensity of infection results from repeated infection as in roundworm, or from high multiplicity of initial infection as in trichinosis. A few helminths, such as Strongyloides stercoralis and Hymenolepis nana multiply in the human host.
Parasitic infections which humans acquire from animals are known as zoonotic infections or zoonoses. In most of these, the parasite lives normally in cycles involving domestic or wild animals, domestic zoonoses and feral or sylvatic zoonoses respectively without affecting humans. Human infections are only accidental events and may not profit the parasite because the chain of transmission is usually broken with human infection. The vertebrate species in which the parasite passes its life cycle and which may act as the source of human infection is called the reservoir host. Intermediate hosts in which metazoan parasites undergo multiplication are called amplifier hosts.4
The term anthroponoses has been applied for infections with parasitic species that are maintained in humans alone. Malaria and filariasis are exampIes. The term zooanthroponoses refers to infections in which human is not merely an incidental host, but an essential link in the life cycle of the parasite. Beef and pork tapeworms are examples of zooanthroponoses.
 
Sources of Infection
Parasitic infections originate from various sources and are transmitted by various routes. The major sources of infection are listed below:
 
Soil
  1. Embryonated eggs which are present in soil may be ingested, e.g. roundworm, whipworm.
  2. Infective larvae present in soil may enter by penetrating exposed skin, e.g. hookworm, strongyloides.
 
Water
  1. Infective forms present in water may be swallowed, e.g. cysts of amoeba and giardia.
  2. Water containing the intermediate host may be swallowed, e.g. infection with guinea worm occurs when the water that is drunk contains its intermediate host cyclops.
  3. Infective larvae in water may enter by penetrating exposed skin, e.g. cercariae of schistosomes.
  4. Free-living parasites in water may enter through vulnerable sites, e.g. Naegleria may enter through nasopharynx and cause meningoencephalitis.
 
Food
  1. Contamination with human or animal feces, e.g. amoebic cysts. pinworm eggs, echinococcus eggs. toxoplasma oocysts.
  2. Meat containing infective larvae, e.g. measly pork. Trichinella spiralis.
 
Insect Vectors
  1. Biological vectors
    1. Mosquito—malaria, filariasis
    2. Sandflies—kala-azar
    3. Tsetseflies—sleeping sickness
    4. Reduviid bugs—Chagas’ disease
    5. Ticks—Babesiosis.
  2. Mechanical vectors
    1. Housefly—amoebiasis.
5
 
Animals
  1. Domestic
    1. Cow, e.g. beef tapeworm, sarcocystis.
    2. Pig, e.g. pork tapeworm, Trichinella spiralis
    3. Dog, e.g. hydatid disease, leishmaniasis
    4. Cat, e.g. toxoplasmosis, opisthorchis.
  2. Wild
    1. Wild game animals, e.g. trypanosomiasis.
    2. Wild felines, e.g. Paragonimus westermani
  3. Fish, e.g. fish tapeworm
  4. Molluscs, e.g. liver flukes
  5. Copepods, e.g. guinea worm.
 
Other Persons
Carriers and patients, e.g. all anthroponotic infections, vertical transmission of congenital infections.
 
Self (autoinfection)
  1. Finger to mouth transmission, e.g. pinworm.
  2. Internal reinfection, e.g. strongyloides.
 
Modes of Infection
The major modes of transmission are the following:
 
Oral Transmission
The most common method of transmission is oral, through contaminated food, water, soiled fingers or fomites. Many intestinal parasites enter the body in this manner, the infective stages being cysts, embryonated eggs or larval forms. Infection with Entamoeba histolytica and other intestinal protozoa occurs when the infective cysts are swallowed. In most intestinal nematodes, such as the roundworm. whipworm or pinworm, the embryonated egg which is the infective form is swallowed. In trichinellosis and in beef, pork and fish tapeworm, infection occurs by ingestion of flesh containing the mature larval stages. Infection with the tissue nematode guinea worm follows consumption of water containing its arthropod host cyclops carrying infective larvae.
 
Skin Transmission
Entry through skin is another important mode of transmission. Hookworm infection is acquired when the larvae enter the skin of persons walking barefooted on contaminated soil. Schistosomiasis is acquired when the cercarial larvae in water penetrate 6the skin. Many parasitic diseases, including malaria and filariasis are transmitted by blood sucking arthropods. Arthropods which transmit infection are called vectors.
 
Vector Transmission
Parasites undergo development or multiplication in the body of true vectors, which are called biological vectors. Some arthropods may transmit infective parasites mechanically or passively without the parasites multiplying or undergoing development in them. For example, the housefly may passively carry amoebic cysts from faeces to food. Such vectors which act only as passive transmitters are called mechanical vectors. In the case of a mechanical vector there need be no delay between picking up a parasite and transferring it to a host. A housefly picking up amoebic cysts from feces can within seconds transfer the cysts by landing on food being eaten by a person, who may thereby get infected. But in the case of biological vectors. A certain period has to elapse after the parasite enters the vector before it becomes infective. This is necessary because the vector can transmit the infection only after the parasite multiplies to a certain level or undergoes a developmental process in its body. This interval between the entry of the parasite into the vector arthropod and the time it becomes capable of transmitting the infection is called the extrinsic incubation period. For example, an Anopheles mosquito picking up Plasmodium vivax gametocytes from a person in its blood meal becomes capable of transmitting the infective stage of the malaria parasite only some ten days later, i.e. the extrinsic incubation period is ten days.
 
Direct Transmission
Parasitic infection may be transmitted by person-to-person contact in some cases; by kissing in the case of gingival amoebae and by sexual intercourse in trichomoniasis. Inhalation of air-borne eggs may be one of the methods of transmission of pinworm infection. Congenital infection (vertical transmission) may take place in malaria and toxoplasmosis. Iatrogenic infection may occur as in transfusion malaria and toxoplasmosis after organ transplantation.
 
Course of Infection
Following its establishment in the host, the parasite has to multiply or undergo development before the infection is manifested either biologically or clinically. The interval of time between the initial infection and the earliest appearance of the parasite or its products in the blood or secretions is called the biological incubation period or prepatent period. The prepatent period in malaria is about a week; in filariasis it is a year or more. When the parasite becomes demonstrable and the host is potentially infectious to others, the infection is said to be patent. Clinical incubation period, which is the interval between the initial infection and the onset of the first evidence of clinical disease is usually longer than the biological incubation period.
7
 
PATHOGENESIS
Parasitic infections may remain inapparent or give rise to clinical disease. A few, such as Entamoeba histolytica may live as surface commensals, multiplying in the 1umen of the gut for long periods without invading the tissues. Some parasites may lead to completely asymptomatic infection even though they live inside tissues. Many persons with filarial infection may not develop any clinical illness though microfilariae are demonstrable in their blood. Clinical infection produced by parasites may take many forms—acute, subacute, chronic, latent or recurrent. Some of the pathogenic mechanisms in parasitic infections are as follows:
Intracellular protozoa can damage and destroy the cells in which they multiply. Malarial parasites rupture the infected erythrocytes causing anaemia as a long-term effect and fever as the immediate response.
Enzymes produced by some parasites can induce lytic necrosis. E. histolytica lyses intestinal cells, enabling it to penetrate the gut wall and produce abscesses and ulcers.
Damage may be due to physical obstruction. Masses of roundworms cause intestinal obstruction. Even a single worm can cause damage when it blocks the appendix or bile duct. Hydatid cysts cause illness due to pressure on surrounding tissues. Parasites in vulnerable sites such as brain and eyes may produce serious damage by pressure. Physical obstruction may sometimes cause severe secondary effects. Falciparum malaria may produce blockage of brain capillaries leading to fatal cerebral malaria.
Clinical disease may sometimes be due to trauma inflicted by parasites. Hookworms feeding on jejunal mucosa leave numerous bleeding points which ultimately lead to anaemia. Migration of helminth larvae through the lungs may rupture many pulmonary capillaries and cause considerable extravasation of blood. Schistosome eggs with their hooks tear vesical blood vessels and produce haematuria. Roundworms may perforate the intestine and cause peritonitis.
Clinical illness may be caused by host response to parasitic infection. This may be due to inflammatory changes and consequent fibrosis, as in the case of filariasis in which it leads ultimately to lymphatic obstruction and oedema. Host response may also be hypersensitive or allergic. Fatal anaphylactic shock may occasionally be caused by escape of hydatid fluid from the cyst.
A few parasitic infections have been shown to lead to malignancy. The liver flukes Clonorchis and Opisthorchis may induce bile duct carcinoma and Schistosoma haematobium may pave the way for bladder cancer.
Migrating parasites may seed bacteria and viruses in ectopic foci, leading to disease. Strongyloidiasis, particularly in the immunodeficient person may result in gram-negative bacillary septicaemia as the migrating helminth transports intestinal bacteria to the circulation.
 
IMMUNITY IN PARASITIC INFECTIONS
Like other infectious agents, parasites also elicit immune responses in the host, both humoral as well as cellular. But immunological protection against parasitic infections 8is much less efficient than it is against bacterial and viral infections. Several factors may contribute to this.
Compared to bacteria and viruses, parasites are enormously larger and more complex structurally and antigenically so that the immune system may not be able to focus attack on the protective antigens. Many protozoan parasites are intracellular in location and this protects them from immunological attack. Several parasites, both protozoa and helminths live inside body cavities as in the intestines. This location limits the efficiency of immunological attack and also facilitates dispersal of the infective forms. Secretory IgA which is so effective against luminal virus infections does not appear to play an important role in defence against parasites. Some parasites live within cysts whose capsules are partly composed of host tissues. In this location they are safe from immunological attack.
Trypanosomes causing sleeping sickness exhibit antigenic variation within the host. When antibody response to one antigenic form reaches high levels, a genetic switch causes a new set of antigens to appear, which are unaffected by the antibodies present. This enables the prolonged persistence of the parasites in the host. A similar mechanism may be operative in the recrudescences in human malaria.
Some parasites adopt antigenic disguise. Their surface antigens are so closely similar to some host components that they are not recognised as foreign by the immune system. Many nematodes have a cuticle which is antigenically inert and evokes little immune response. Immunological tolerance is established in some parasitic infections. Some infections may produce immunodeficiency due to extensive damage to the reticuloendothelial system, as for example in visceral leishmaniasis.
Unlike in other microbial infections, complete elimination of the infecting agent followed by immunity to reinfection is seldom seen in parasitic infections. A possible exception is cutaneous leishmaniasis in which the initial infection heals, leaving behind good protection against reinfection. However, the general situation in parasitic infections is that immunity to reinfection lasts only so long as the original infection persists at least in a small degree. Once the parasitic infection is completely eliminated, by natural means or by therapy, the host becomes again susceptible to reinfection. This type of immunity to reinfection dependent on the continued presence of a residual parasite population is known as premunition. A similar phenomenon is seen in syphilis.
In most parasitic infections a balance is established, the parasite being kept in check by the host without being completely eliminated. This may be achieved by the immune response controlling the numbers of the parasite (numerical restraint) or by limiting the space it occupies (topical restraint). The fact that immunity normally plays an important role in the containment of parasitic infections is illustrated by the florid manifestations caused by opportunistic parasites such as Pneumocystis carinii and Toxoplasma gondii when the immune response is inadequate as in AIDS and other immunodeficiencies.
Immune response to parasitic infections has been employed for diagnostic purposes.
9
zoom view
FIGURE 1.1: Eosinophils surrounding schistosomulum (An example of immune attack in bloodstream)
Antibodies to the infecting parasites may be demonstrated by various serological techniques, but serodiagnosis in parasitic infections is vitiated by numerous cross reactions and so does not have the precision and specificity present in bacterial and viral infections. Antibodies belonging to the different immunoglobulin classes are produced in response to parasitic infections. Selective tests for IgM antibodies are helpful in differentiating current from old infections. However, IgA antibodies are not very prominent. Instead there occurs an excessive IgE response, particularly in intestinal helminthiases. Polyclonal activation of B lymphocytes with excessive production of irrelevant immunoglobulins is seen in some parasitic disease, as in kala-azar. Cell-mediated response to parasitic antigens also has been employed in diagnostic tests, but here again cross reactions are frequent. A characteristic cellular response in parasitic infection is eosinophilia, both local and systemic (Fig. 1.1).
Immunoprophylaxis and immunotherapy have not been significantly successful in parasitic infections. Though no vaccine is as yet available for any parasitic disease, great progress has been made in identifying protective antigens in malaria and some other infections, with a view to eventual development of prophylactic vaccines.