HELMINTHS

STRUCTURE, CLASSIFICATION, GROWTH, DEVELOPMENT, PATHOGENESIS, AND DEFENSES

General Concepts

The helminths are worm-like parasites. The clinically relevant groups are separated according to their general external shape and the host organ they inhabit. There are both hermaphroditic and bisexual species. The definitive classification is based on the external and internal morphology of egg, larval, and adult stages.

Flukes (Trematodes)

Adult flukes are leaf-shaped flatworms. Prominent oral and ventral suckers help maintain position in situ. Flukes are hermaphroditic except for blood flukes, which are bisexual. The life-cycle includes a snail intermediate host.

Tapeworms (Cestodes)

Adult tapeworms are elongated, segmented, hermaphroditic flatworms that inhabit the intestinal lumen. Larval forms, which are cystic or solid, inhabit extraintestinal tissues.

Roundworms (Nematodes)

Adult and larval roundworms are bisexual, cylindrical worms. They inhabit intestinal and extraintestinal sites.

Classification

Helminth is a general term for a parasitic worm. The helminths include the Platyhelminthes or flatworms (flukes and tapeworms) and the Nematoda or roundworms.

Characteristics

All helminths are relatively large (> 1 mm long); some are very large (> 1 m long). All have well-developed organ systems, and most are active feeders. The body is flattened and covered with the plasma membrane (flatworms) or cylindrical and covered with cuticle (roundworms). Some helminths are hermaphrodites; others have separate sexes.

Epidemiology

Helminths are worldwide in distribution; infection is most common and most serious in developing countries. The distribution of these diseases is determined by climate, hygiene, diet, and exposure to vectors.

Infection

The mode of transmission varies with the type of worm; it may involve ingestion of eggs or larvae, penetration by larvae, the bite of vectors, or ingestion of stages in intermediate hosts’ meat. Worms are often long-lived.

Pathogenesis

Many infections are asymptomatic; pathologic manifestations depend on the worms’ size, activity, and metabolism. Immune and inflammatory responses also cause pathology.

Host Defenses

Nonspecific defense mechanisms limit susceptibility. Antibody- and cell-mediated responses are important, as is inflammation. Parasites survive defenses through many evasion strategies.

Introduction

Helminth is a general term meaning worm. The helminths are invertebrates characterized by elongated, flat, or round bodies. In medically oriented schemes, the flatworms or platyhelminths (platy from the Greek root meaning “flat”) include flukes and tapeworms. Roundworms are nematodes (nematode from the Greek root meaning “thread”). These groups are subdivided for convenience according to the host organ in which they reside, e.g., lung flukes, extraintestinal tapeworms, and intestinal roundworms. This chapter deals with the structure and development of the three major groups of helminths.

Helminths develop through egg, larval (juvenile), and adult stages. Knowledge of the different stages in relation to their growth and development is the basis for understanding the epidemiology and pathogenesis of helminth diseases and the diagnosis and treatment of patients harboring these parasites.

Platyhelminths and nematodes that infect humans have similar anatomic features that reflect common physiologic requirements and functions. The outer covering of helminths is the cuticle or tegument. Prominent external structures of flukes and cestodes are acetabula (suckers) or bothria (false suckers). Male nematodes of several species possess accessory sex organs that are external modifications of the cuticle. Internally, the alimentary, excretory, and reproductive systems can be identified by an experienced observer. Tapeworms are unique in lacking an alimentary canal. This lack means that nutrients must be absorbed through the tegument. The blood flukes and nematodes are bisexual. All other flukes and tapeworm species that infect humans are hermaphroditic.

With few exceptions, adult flukes, cestodes, and nematodes produce eggs passed in excretions or secretions of the host. The various stages and their unique characteristics will be reviewed in more detail as each major group of helminths is considered.

Helminths – worms – are some of the world’s commonest parasites (see Ch. 86). They belong to two major groups of animals, the flatworms or Platyhelminthes (flukes and tapeworms) and the roundworms or Nematoda. All are relatively large, and some are very large, exceeding one meter in length.

Their bodies have well-developed organ systems, especially reproductive organs, and most helminths are active feeders. Flatworms’ bodies are flattened and covered by a plasma membrane, whereas roundworms are cylindrical and covered by a tough cuticle. Flatworms are usually hermaphroditic, whereas roundworms have separate sexes; both have an immense reproductive capacity.

The most serious helminth infections are acquired in poor tropical and subtropical areas, but some also occur in the developed world; other, less serious infections are worldwide in distribution. Exposure to infection is influenced by climate, hygiene, food preferences, and contact with vectors. Host defenses eliminate many potential infections; others become established and persist for prolonged periods, even years. Although infections are often asymptomatic, severe pathology can occur. Because worms are large and often migrate through the body, they can damage the host’s tissues directly by their activity or metabolism. Damage also occurs indirectly as a result of host defense mechanisms. Almost all organ systems can be affected.

Host defense can act through nonspecific mechanisms of resistance and specific immune responses. Antibody-mediated, cellular, and inflammatory mechanisms all contribute to resistance. However, many worms successfully avoid host defenses in various ways and can survive in the face of otherwise effective host responses.

Flukes (Trematodes)

A dorsoventrally flattened body, bilateral symmetry, and a definite anterior end are platyhelminths features in general and of trematodes specifically. Flukes are leaf-shaped, ranging in length from a few millimeters to 7 to 8 cm. The tegument is morphologically and physiologically complex. Flukes possess an oral sucker around the mouth and a ventral sucker or acetabulum that can be used to adhere to host tissues. A body cavity is lacking. Organs are embedded in specialized connective tissue or parenchyma. Layers of somatic muscle permeate the parenchyma and attach to the tegument.
Flukes have a well-developed alimentary canal with a muscular pharynx and esophagus. The intestine is usually a branched tube (secondary and tertiary branches may be present) consisting of a single layer of epithelial cells. The main branches may end blindly or open into an excretory vesicle. The excretory vesicle also accepts the two main lateral collecting ducts of the excretory system, a protonephridia type with flame cells. A flame cell is a hollow, terminal excretory cell that contains a beating (flamelike) group of cilia. These cells, anchored in the parenchyma, direct tissue filtrate through canals into the two main collecting ducts.

Except for the blood flukes, trematodes are hermaphroditic, having both male and female reproductive organs in the same individual. The male organ usually consists of two testes with accessory glands and ducts leading to a cirrus, or penis equivalent, extending into the common genital atrium. The female gonad consists of a single ovary with a seminal receptacle and vitellaria, or yolk glands, connecting with the oviduct as it expands into an ootype. The tubular uterus extends from the ootype and opens into the genital atrium. Both self- and cross-fertilization occur. The components of the egg are assembled in the ootype. Eggs pass through the uterus into the genital atrium and exit ventrally through the genital pore. Fluke eggs, except for those of schistosomes, are operculated (have a lid).

The blood flukes or schistosomes are the only bisexual flukes that infect humans. Although the sexes are separate, the general body structure is the same as that of hermaphroditic flukes. Within the definitive host, the male and female worms inhabit the lumen of blood vessels and are found in close physical association. The female lies within a tegumental fold, the gynecophoral canal, on the male’s ventral surface. The medically important flukes belong to the taxonomic category Digenea. This fluke group has a developmental cycle requiring at least two hosts, one being a snail intermediate host. Other intermediate hosts may be involved in perpetuating the larval form that infects the definitive human host depending on the species.

Flukes go through several larval stages, each with a specific name, before reaching adulthood. Taking into account variations among species, a generalized life cycle of digenetic flukes runs the following course. Eggs are passed in the feces, urine, or sputum of humans and reach an aquatic environment. The eggs hatch, releasing ciliated larvae, or miracidia, which either penetrate or are eaten by a snail intermediate host. In rare instances, land snails may serve as intermediate hosts. A saclike sporocyst or redia stage develops from a miracidium within the tissues of the snail.

The sporocyst gives rise either to rediae or to a daughter’s sporocyst stage. In turn, from the media or daughter sporocyst, cercariae develop asexually and migrate out of the snail tissues to the external environment, which is usually aquatic.

The cercariae, which may possess a tail for swimming, develop further in one of three ways. They either penetrate the definitive host and transform directly into adults or penetrate a second intermediate host and develop as encysted metacercariae. They encyst on a substrate, such as vegetation, and develop there as metacercariae. When a metacercarial cyst is ingested, digestion of the cyst liberates an immature fluke that migrates to a specific organ site and develops into an adult worm.

Tapeworms (Cestodes)

As members of the platyhelminths, the cestodes, or tapeworms, possess many basic structural characteristics of flukes and show striking differences.

Whereas flukes are flattened and generally leaf-shaped, adult tapeworms are flattened, elongated, and consist of segments called proglottids. Tapeworms vary in length from 2 to 3 mm to 10 m and may have three to several thousand segments.

Anatomically, cestodes are divided into a scolex, or head, which bears the organs of attachment, a neck that is the region of segment proliferation, and a chain of proglottids called the strobila. The strobila elongates as new proglottids form in the neck region. The segments nearest the neck are immature (sex organs not fully developed), and those more posterior are mature. The terminal segments are gravid, with the egg-filled uterus as the most prominent feature.

The scolex contains the cephalic ganglion, or “brain,” of the tapeworm nervous system. Externally, the scolex is characterized by holdfast organs. Depending on the species, these organs consist of a rostellum, bothria, or acetabula. A rostellum is a retractable, conelike structure located on the anterior end of the scolex, and in some species, it is armed with hooks. Bothria are long, narrow, weakly muscular grooves that are characteristic of the pseudophyllidean tapeworms. Acetabula (suckers like those of digenetic trematodes) are characteristic of cyclophyllidean tapeworms.

A characteristic feature of adult tapeworm is the absence of an alimentary canal, which is intriguing since all of these adult worms inhabit the small intestine. The lack of an alimentary tract means that substances enter the tapeworm across the tegument. This structure is well adapted for transport functions since it is covered with numerous microvilli resembling those lining the lumen of the mammalian intestine. The excretory system is of the flame cell type.

Cestodes are hermaphroditic, each proglottid possessing male and female reproductive systems similar to those of digenetic flukes. However, tapeworms differ from flukes in the mechanism of egg deposition. Eggs of pseudophyllidean tapeworms exit through a uterine pore in the center of the ventral surface rather than through a genital atrium, as in flukes. In cyclophyllidean tapeworms, the female system includes a uterus without a uterine pore. Thus, the cyclophyllidean eggs are released only when the tapeworms shed gravid proglottids into the intestine. Some proglottids disintegrate, releasing eggs voided in the feces, whereas other proglottids are passed intact.

The eggs of pseudophyllidean tapeworms are operculated, but those of cyclophyllidean species are not. Eggs of all tapeworms, however, contain at some stage of development an embryo or oncosphere. The oncosphere of pseudophyllidean tapeworms is ciliated externally and is called a coracidium. The coracidium develops into a procercoid stage in its micro-crustacean first immediate host and then into a plerocercoid larva in its next intermediate host, a vertebrate. The plerocercoid larva develops into an adult worm in the definitive (final) host. The oncosphere of cyclophyllidean tapeworms, depending on the species, develops into a cysticercus larva, cysticercoid larva, coenurus larva, or hydatid larva (cyst) in specific intermediate hosts. These larvae, in turn, become adults in the definitive host.

Roundworms (Nematodes)

In contrast to platyhelminths, nematodes are cylindrical rather than flattened; hence the common name roundworm. The body wall comprises an outer cuticle with a noncellular, chemically complex structure, a thin hypodermis, and musculature. The cuticle in some species has longitudinal ridges called alae. The bursa, a flaplike extension of the cuticle on the posterior end of some male nematodes species, is used to grasp the female during copulation.

The cellular hypodermis bulges into the body cavity or pseudocoelom to form four longitudinal cords—a dorsal, a ventral, and two lateral cords—which may be seen on the surface as lateral lines. Nuclei of the hypodermis are located in the region of the cords. The somatic musculature lying beneath the hypodermis is a single layer of smooth muscle cells. When viewed in cross-section, this layer can be separated into four zones by the hypodermal cords. The musculature is innervated by extensions of muscle cells to nerve trunks running anteriorly and posteriorly from ganglion cells that ring the esophagus’ midportion.

The space between the muscle layer and viscera is the pseudocoelom, which lacks a mesothelium lining. This cavity contains fluid and two to six fixed cells (celomocytes), usually associated with longitudinal cords. The function of these cells is unknown.

The alimentary canal of roundworms is complete, with both mouth and anus. The mouth is surrounded by lips bearing sensory papillae (bristles). The esophagus, a conspicuous feature of nematodes, is a muscular structure that pumps food into the intestine; it differs in shape in different species.

The intestine is a tubular structure composed of a single layer of columnar cells possessing prominent microvilli on their luminal surface.

Some nematodes’ excretory system consists of an excretory gland and a pore located ventrally in the mid-esophageal region. In other nematodes, this structure is drawn into extensions that give rise to the more complex tubular excretory system, usually H-shaped, with two anterior limbs and two posterior limbs located in the lateral cords. The gland cells and tubes are thought to serve as absorptive bodies, collecting wastes from the pseudocoelom and function in osmoregulation.

Nematodes are usually bisexual. Males are usually smaller than females, have a curved posterior end, and possess (in some species) copulatory structures, such as spicules (usually two), a bursa, or both. In a few cases, the males have one or (in a few cases) two testes, which lie at the free end of a convoluted or recurved tube leading into a seminal vesicle and eventually into the cloaca.

The female system is tubular also and usually is made up of reflexed ovaries. Each ovary is continuous, with an oviduct and tubular uterus. The uteri join to form the vagina, which in turn opens to the exterior through the vulva.

Copulation between a female and a male nematode is necessary for fertilization except in the genus h3yloides. Parthenogenetic development occurs (i.e., the development of an unfertilized egg into a new individual). Some evidence indicates that sex attractants (pheromones) play a role in heterosexual mating. During copulation, sperm is transferred into the vulva of the female. The sperm enters the ovum, and the zygote secretes a fertilization membrane. This membrane gradually thickens to form the chitinous shell. A second membrane, below the shell, makes the egg impervious to essentially all substances except carbon dioxide and oxygen. A third proteinaceous membrane is secreted in some species as the egg passes down the uterus by the uterine wall and is deposited outside the shell. Most nematodes that are parasitic in humans lay eggs that, when voided, contain either an uncleaved zygote, a group of blastomeres, or a completely formed larva. Some nematodes, such as the filariae and Trichinella spiralis, produce larvae deposited in host tissues.

The developmental process in nematodes involves egg, larval, and adult stages. Each of the four larval stages is followed by a molt in which the cuticle is shed. The larvae are called second-stage larvae after the first molt, and so on.

Infection

Transmission of Infection
Helminths are transmitted to humans in many different ways. The simplest is accidental ingestion of infective eggs (Ascaris, Echinococcus, Enterobius, Trichuris) or larvae (some hookworms). Other worms have larvae that actively penetrate the skin (hookworms, schistosomes, h3yloides). In several cases, infection requires an intermediate host vector. In some cases, the intermediate vector transmits infective stages when it bites the host to take a blood meal (the arthropod vectors of filarial worms); in other cases, the larvae are contained in the tissues of the intermediate host and are taken in when a human eats that host (Clonorchis in fish, tapeworms in meat and fish, Trichinella in meat). The levels of infection in humans, therefore, depend on standards of hygiene (as eggs and larvae are often passed in urine or feces), on the climate (which may favor the survival of infective stages), on how food is prepared, and on the degree of exposure to insect vectors.

Host Factors Influencing Susceptibility
Human behavior is a major factor influencing susceptibility to infection. If the infective stages of helminths are present in the environment, then certain ways of behaving, particularly with regard to hygiene and food, will result in greater exposure. Because helminths, with few exceptions (h3yloides, Trichinella, some tapeworm larvae), do not increase their numbers by replicating within the same host, the infection level is directly related to the number of infective stages encountered. Obviously, not every exposure results in the development of a mature infection. The host’s nonspecific defense mechanisms kill many infective organisms. Of those that do become established, many are destroyed or eliminated by specific defenses. Therefore, the number of worms present at any one time represents a dynamic balance between the rate of infection and the efficiency of defense. This balance (which reflects the host’s overall susceptibility) is altered by changes in the host’s behavior and ability to express forms of defense. Children are more susceptible to many helminths than adults and frequently are the most heavily infected community members. The waning of immune competence with age may also result in increased levels of infection. Individuals differ genetically in their ability to resist infection, and it is well known that some individuals are predisposed to heavier infections in infected populations than others. Changes in diet may affect susceptibility, as do the hormonal-immune changes accompanying pregnancy and lactation. An important cause of increased susceptibility is the immune suppression that accompanies concurrent infections with some other pathogens and certain tumors’ development. Similarly, immunosuppressive therapies (irradiation, immunosuppressant drugs) may enhance susceptibility to helminth infection. A particular hazard in immunocompromised patients is the development of disseminated h3yloidiasis, in which large numbers of larvae develop in the body by autoinfection from relatively small numbers of adult h3yloides stercoralis. It is interesting that the human immunodeficiency virus does not result in an overall increase in susceptibility to helminth infection.

Parasite Factors Influencing Susceptibility
The ability of hosts to control infection is offset by the ability of parasites to avoid the host’s defenses and increase their survival. In addition to their ability to evade specific immune defenses (see below), many worms are unaffected by the host’s attempts to limit their activities or destroy them simply because they are large and mobile. Many important species measure several centimeters in length or diameter (Ascaris, hookworms, hydatid cysts, Trichuris), and others may exceed one meter in length (tapeworms). Size alone renders many defense mechanisms inoperative, as does the tough cuticle of adult roundworms. The ability of worms to move actively through tissues enables them to escape inflammatory foci.

Many of the pathogenic consequences of worm infections are related to the size, movement, and longevity of the parasites, as the host is exposed to long-term damage and immune stimulation and the sheer physical consequences of being inhabited by large foreign bodies.

Pathogenesis

Direct Damage from Worm Activity
The most obvious forms of direct damage resulting from the blockage of internal organs or the effects of pressure exerted by growing parasites. Large Ascaris or tapeworms can physically block the intestine, and this may occur after some forms of chemotherapy; migrating Ascaris may also block the bile duct. Granulomas that form around schistosome eggs may block blood flow through the liver, which may lead to pathological changes in that organ and elsewhere. Blockage of lymph flow, leading to elephantiasis, is associated with adult Wuchereria in lymphatics. Pressure atrophy is characteristic of larval tapeworm infections (hydatid cyst, the larva of Echinococcus granulosus). The parasite grows as a large fluid-filled cyst in the liver, brain, lungs, or body cavity. The multilocular hydatid cysts caused by Echinococcus multilocularis have a different growth form, metastasizing within organs and causing necrosis. The larvae of Taenia solium, the pork tapeworm, frequently develop in the central nervous system (CNS) and eyes. Some of the neurological symptoms of the resulting condition, called cysticercosis, are caused by the cysts’ pressure.

Intestinal worms cause a variety of pathologic changes in the mucosa, some reflecting physical and chemical damage to the tissues, others resulting from immunopathologic responses. Hookworms (Ancylostoma and Necator) actively suck blood from mucosal capillaries. The anticoagulants secreted by the worms cause the wounds to bleed for prolonged periods, resulting in considerable blood loss. Heavy infections in malnourished hosts are associated with anemia and protein loss. Protein-losing enteropathies may also result from the inflammatory changes induced by other intestinal worms. Diversion of host nutrients by competition from worms is probably unimportant, but interference with normal digestion and absorption may well aggravate undernutrition. The tapeworm Diphyllobothrium latum can cause vitamin B12 deficiency through direct absorption of this factor.

Many helminths undertake extensive migrations through body tissues, which both damage tissues directly and initiate hypersensitivity reactions. The skin, lungs, liver, and intestines are the organs most affected. Petechial hemorrhages, pneumonitis, eosinophilia, urticaria and pruritus, organomegaly, and granulomatous lesions are among the signs and symptoms produced during these migratory phases.

Feeding by worms upon host tissues is an important cause of pathology, particularly when it induces hyperplastic and metaplastic changes in epithelia. For example, liver fluke infections lead to hyperplasia of the bile duct epithelium. Chronic inflammatory changes around parasites (for example, the granulomas around schistosome eggs in the bladder wall) have been linked with neoplasia, but the nature of the link is not known. The continuous release by living worms of excretory-secretory materials, many of which are known to have direct effects upon host cells and tissues, may also contribute to pathology.

Indirect Damage from Host Response
As with all infectious organisms, it is impossible to separate the pathogenic effects caused strictly by mechanical or chemical tissue damage from those caused by the immune response to the parasite. All helminths are “foreign bodies” not only in the sense of being large and invasive but also in the immunologic sense: they are antigenic and therefore stimulate immunity. An excellent illustration of this interrelation between direct and indirect damage is seen in the pathology associated with schistosome infections, especially with Schistosoma mansoni. Hypersensitivity-based, granulomatous responses to eggs trapped in the liver cause a physical obstruction to blood flow, leading to liver pathology. Hypersensitivity-based inflammatory changes probably also contribute to the lymphatic blockage associated with filarial infections (Brugia, Wuchereria).

Immune-mediated inflammatory changes occur in the skin, lungs, liver, intestine, CNS, and eyes as worms migrate through these structures. Systemic changes such as eosinophilia, edema, and joint pain reflect local allergic responses to parasites. The pathologic consequences of immune-mediated inflammation are seen clearly in intestinal infections (especially h3yloides and Trichinella infections). Structural changes, such as villous atrophy, develop. The permeability of the mucosa changes, fluid accumulates in the gut lumen and reduced intestinal transit time. Prolonged changes of this type may lead to protein-losing enteropathy. The inflammatory changes that accompany the passage of schistosome eggs through the intestinal wall also cause severe intestinal pathology. Heavy infections with the whipworm Trichuris in the large bowel can lead to inflammatory changes, resulting in blood loss and rectal prolapse.

The severity of these indirect changes is a result of the chronic nature of the infection. The fact that many worms are extremely long-lived means that many inflammatory changes become irreversible, producing functional changes in tissues. Three examples are the hyperplasia of bile ducts in long-term liver fluke infections, the extensive fibrosis associated with chronic schistosomiasis, and the skin atrophy associated with onchocerciasis. Severe pathology may also result when worms stray into abnormal body sites.

Defenses Against Infection

Nonspecific Resistance
Infective stages attempting to enter via the mouth or through the skin are opposed by the same non-specific defenses that protect humans from invasion of other pathogens. Following oral ingestion, parasites must survive passage through the acid stomach to reach the small bowel. The natural parasites of humans are adapted to do this, but opportunistic parasites may be killed. Similarly, natural parasites are adapted to the bowel’s environmental conditions (and in many cases require them as cues for development), but accidental parasites may find them inappropriate. Penetration into the intestinal wall may trigger inflammatory responses that immobilize and kill the worm. This may itself lead to serious pathology (as in Anisakis infection). Worms entering through the skin must survive the skin secretions, penetrate the epidermal layers, and avoid inflammatory trapping in the dermis. Invasion of humans by the larvae of dog and cat hookworms (Ancylostoma spp.) results in dermatitis and “creeping eruption” as the worms become the focus of inflammatory reactions that form trails in the skin.

Once in the tissues, worms need the correct sequence of environmental signals to mature. Absent or incomplete signals constitute a form of nonspecific resistance that may partially or completely prevent further development. However, the parasite may not die; indeed, prolonged survival at a larval stage may result in pathology from the continuing inflammatory response (e.g., Toxocara infection).

Specific Acquired Immunity
There is no doubt that specific immunity is responsible for the most effective forms of host defense. However, the dividing line between nonspecific and specific mechanisms is difficult to draw with precision. All helminths stimulate h3 immune responses, which can easily be detected by measuring specific antibodies or cellular immunity. Although these responses are useful for diagnosing infection, they frequently appear not to be protective. The high prevalence of helminth infection in endemic areas (sometimes approaching 100 percent) and the fact that individuals may remain infected for many years and can easily be reinfected after they are cured by chemotherapy suggest that protective immunity against helminths is weak or absent in humans. However, some degree of immunity appears to operate because the intensity of infection often declines with age. Many individuals in endemic areas remain parasitologically negative and/or clinically normal. Evidence from laboratory studies provides some clues as to the mechanisms involved. Antibodies that bind to surface antigens may focus on complement- or cell-mediated effectors that can damage the worm. Macrophages and eosinophils are the prime cytotoxic effector cells, and IgM, IgG, and IgE are the important immunoglobulins. Antibodies may also block enzymes released by the worm, thus interfering with its ability to penetrate tissues or to feed. Inflammatory changes may concentrate effector cells around worms, and the release of cellular mediators may then disable and kill the worm. Encapsulation of trapped worms by inflammatory cells may also result in the death of the worm, although this is not always the case. Intestinal worms can be dislodged by the structural and physiologic changes that occur in the intestine during acute inflammation. It has long been suspected that IgE-mediated hypersensitivity reactions involving mast cells and basophils contribute to this process, but the evidence is still circumstantial. Despite the abundance of IgA in the intestinal lumen, there is no conclusive evidence that it is involved in protective immunity in humans. However, some field and laboratory data suggest it is.

Avoidance of Host Defenses
Despite their immunogenicity, many helminths survive for extended periods in the bodies of their hosts. Some of the reasons have already been mentioned (size, motility), but we now know that worms employ many sophisticated devices to render host defenses ineffective. Some worms (schistosomes) disguise their outer surface by acquiring host molecules which reduce their antigenicity; intrinsic membrane changes also make these worms resistant to immune attack. Filarial nematodes acquire serum albumin on their cuticle, which may act as a disguise. Many worms release substances that depress lymphocyte function, inactivate macrophages, or digest antibodies. Larval cestodes appear to prolong their survival by producing anti-complement factors which protect their outer layers from lytic attack. Antigenic variation in the strict sense is not known to occur. Still, many species show a stage-specific change of antigens as they develop, and this phenomenon may delay the development of effective immune mechanisms. All helminths release relatively large amounts of antigenic materials, and this voluminous production may divert immune responses or even locally exhaust immune potential. Irrelevant antibodies produced by the host may block the activity of potentially protective antibodies, as has been shown to be the case in schistosome infections.

It is striking that many helminth infections are associated with a degree of immune suppression, which may affect specific or general responsiveness. Many explanations have been proposed for this immune suppression, including antigen overload, antigenic competition, induction of suppressor cells, and production of lymphocyte-specific suppressor factors. Reduced immune responsiveness may not only prolong the survival of the original infecting worm species but increase the host’s susceptibility to other pathogens. Epidemiologic evidence also raises the possibility that infections acquired early in life—before or shortly after birth—may induce a form of immune tolerance, allowing heavy worm burdens to accumulate in the body.

The subtlety with which parasitic worms manipulate the host’s immune system increases their importance as pathogens and creates formidable problems for their control and eradication.

For more information, view the source: Medical Microbiology

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