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Baron S, editor. Medical Microbiology. Fourth edition. Galveston (TX): university of Texas clinical Branch in ~ Galveston; 1996.
Helminth is a basic term because that a parasitic worm. The helminths include thePlatyhelminthes or flatworms (flukes and also tapeworms) and also the Nematoda orroundworms.
All helminths are relatively huge (> 1 mm long); part are really large(> 1 m long). All have actually well-developed organ systems and most room activefeeders. The human body is one of two people flattened and covered through plasma membrane(flatworms) or cylindrical and covered through cuticle (roundworms). Part helminthsare hermaphrodites; others have actually separate sexes.
Helminths are global in distribution; infection is most common and mostserious in poor countries. The circulation of these conditions is figured out byclimate, hygiene, diet, and exposure come vectors.
The setting of transmission varies v the type of worm; it might involve ingestionof eggs or larvae, penetration by larvae, bite the vectors, or sloop down ofstages in the meat of intermediate hosts. Worms are often long-lived.
Many infections space asymptomatic; pathologic manifestations rely on the size,activity, and metabolism the the worms. Immune and inflammatory responses alsocause pathology.
Nonspecific defense mechanisms limit susceptibility. Antibody- and cell-mediatedresponses space important, together is inflammation. Parasites make it through defenses throughmany evasion strategies.
Helminths - worms - are few of the world"s commonest helminth (see Ch. 86). They belong to two major groupsof animals, the flatworms or Platyhelminthes (flukes and tapeworms) and also theroundworms or Nematoda. All space relatively huge and some are very large, exceedingone meter in length.
Their bodies have well-developed organ systems, especially reproductive organs, andmost helminths are active feeders. The body of flatworms room flattened and coveredby a plasma membrane, conversely, roundworms are cylindrical and covered through a toughcuticle. Flatworms room usually hermaphroditic conversely, roundworms have actually separatesexes; both have an tremendous reproductive capacity.
The most serious helminth epidemic are acquired in negative tropical and also subtropicalareas, but some also occur in the emerged world; other, much less serious, infectionsare an international in distribution. Exposure to epidemic is influenced by climate,hygiene, food preferences, and contact v vectors. Numerous potential epidemic areeliminated by hold defenses; others end up being established and also may persist because that prolongedperiods, even years. Although epidemic are frequently asymptomatic, major pathologycan occur. Due to the fact that worms are big and regularly migrate through the body, they candamage the host"s tissues directly by their activity or metabolism. Damages alsooccurs indirectly as a an outcome of organize defense mechanisms. Almost all body organ systemscan be affected.
Host defense can act v nonspecific instrument of resistance and throughspecific immune responses. Antibody-mediated, cellular, and also inflammatory mechanismsall contribute to resistance. However, plenty of worms effectively avoid host defensesin a variety of ways, and can endure in the confront of otherwise reliable hostresponses.
Transmission the Infection
Helminths room transmitted to humans in many different ways (Fig. 87-1). The easiest is by inadvertently ingestion ofinfective eggs (Ascaris, Echinococcus, Enterobius, Trichuris)or larvae (some hookworms). Other worms have actually larvae that actively penetrate theskin (hookworms, schistosomes, Strongyloides). In severalcases, infection requires an intermediate organize vector. In some cases theintermediate vector transmits infective stages when it bites the hold to take it ablood meal (the arthropod vectors that filarial worms); in various other cases, the larvaeare consisted of in the tissues of the intermediate host and also are bring away in once ahuman eats that host (Clonorchis in fish, tapeworms in meat andfish, Trichinella in meat). The levels of infection in humanstherefore rely on standards of restroom (as eggs and also larvae are regularly passed inurine or feces), ~ above the climate (which may favor survive of infective stages),on the methods in i beg your pardon food is prepared, and on the level of exposure to insectvectors.
Host determinants Influencing Susceptibility
Human actions is a significant factor influencing susceptibility to infection. If theinfective step of helminths are present in the environment, then details waysof behaving, particularly with regard to hygiene and also food, will an outcome ingreater exposure. Since helminths, with few exceptions (Strongyloides,Trichinella, part tapeworm larvae), execute not rise their numbersby replication in ~ the exact same host, the level of infection is directly relatedto the variety of infective step encountered. Obviously, not every exposureresults in the advancement of a maturation infection. Numerous infective biology arekilled by the host"s nonspecific defense mechanisms. That those that perform becomeestablished, many are destroyed or removed by specific defenses. The numberof worms current at any type of one time thus represents a dynamic balance betweenthe price of infection and the performance of defense. This balance (whichreflects the host"s all at once susceptibility) is transformed by changes in the host"sbehavior and capacity to express creates of defense. Kids are an ext susceptibleto countless helminths than space adults, and also frequently space the most greatly infectedmembers that a community. The waning the immune competence with period may likewise resultin boosted levels the infection. Individuals differ gene in theirability to resist infection, and also it is famed that in infected populations,some individuals are predisposed to more heavier infections 보다 others. Changes indiet may influence susceptibility, as do the hormonal-immune alters accompanyingpregnancy and lactation. An important cause of raised susceptibility is theimmune suppression the accompanies concurrent infections v some otherpathogens and also the breakthrough of specific tumors. Similarly, immunosuppressivetherapies (irradiation, immunosuppressant drugs) may improve susceptibility tohelminth infection. A certain hazard in immunocompromised patients is thedevelopment of disseminated strongyloidiasis, in which big numbers the larvaedevelop in the body by autoinfection from relatively small number of adultStrongyloides stercoralis. The is exciting that the humanimmunodeficiency virus walk not result in an in its entirety increase in susceptibilityto helminth infection.
Parasite determinants Influencing Susceptibility
The capacity of hosts to regulate infection is balance out by the capacity of parasites toavoid the host"s defenses and increase their survival. In addition to their abilityto evade certain immune defenses (see below), numerous worms are unaffected through thehost"s do the efforts to border their activities or to ruin them simply because they arelarge and also mobile. Plenty of important varieties measure numerous centimeters in size ordiameter (Ascaris, hookworms, hydatid cysts,Trichuris) and others might exceed one meter in length(tapeworms). Size alone renders countless defense mechanisms inoperative, as does thetough cuticle the adult roundworms. The capacity of worms to move actively throughtissues permits them come escape inflammatory foci.
Many the the pathogenic after-effects of worm infections are concerned the size,movement and longevity of the parasites, together the hold is exposed to irreversible damageand immune stimulation, as well as to the thin physical aftermath of beinginhabited by big foreign bodies.
Direct damage from Worm Activity
The most obvious forms of direct damages are those result from the blockage ofinternal organs or indigenous the results of push exerted by farming parasites(Fig. 87-2). LargeAscaris or tapeworms deserve to physically block the intestine,and this may happen after some develops of chemotherapy; migratingAscaris may likewise block the bile duct. Granulomas that formaround schistosome eggs might block the flow of blood v the liver, and thismay result in pathological alters in the organ and also elsewhere. Blockage the lymphflow, resulting in elephantiasis, is linked with the existence of adultWuchereria in lymphatics. Pressure atrophy ischaracteristic of larval tapeworm infections (hydatid cyst, the larva ofEchinococcus granulosus) wherein the parasite grows together alarge fluid-filled cyst in the liver, brain, lungs, or human body cavity. Themultilocular hydatid cysts led to by Echinococcusmultilocularis have a various growth form, metastasizing withinorgans and also causing necrosis. The larvae of Taenia solium, thepork tapeworm, frequently construct in the main nervous system (CNS) and also eyes.Some that the neurological symptom of the resulting condition, calledcysticercosis, are brought about by the press exerted through thecysts.
Intestinal worms cause a range of pathologic changes in the mucosa, somereflecting physical and chemical damage to the tissues, others resulting fromimmunopathologic responses. Hookworms (Ancylostoma andNecator) actively suck blood from mucosal capillaries. Theanticoagulants secreted by the worms cause the wounds come bleed for prolongedperiods, resulting in significant blood loss. Hefty infections in malnourishedhosts are connected with anemia and protein loss. Protein-losing enteropathiesmay also an outcome 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 also absorption might well aggravateundernutrition. The tapeworm Diphyllobothrium latum can causevitamin B12 deficiency through straight absorption that this factor.
Many helminths undertake extensive migrations through body tissues, which bothdamage organization directly and initiate hypersensitivity reactions. The skin,lungs, liver, and also intestines are the organs many affected. Petechialhemorrhages, pneumonitis, eosinophilia, urticaria and pruritus, organomegaly,and granulomatous lesions are amongst the signs and symptoms created during thesemigratory phases.
Feeding by worms upon host tissues is an important cause the pathology,particularly as soon as it induces hyperplastic and also metaplastic transforms in epithelia.For example, liver fluke infections cause hyperplasia of the bile ductepithelium. Chronic inflammation changes about parasites (for example, thegranulomas about schistosome egg in the bladder wall) have actually been attached withneoplasia, however the nature of the link is not known. The continuous release byliving worms of excretory-secretory materials, many of i beg your pardon are known to havedirect impacts upon organize cells and tissues, may additionally contribute topathology.
Indirect damage from organize Response
As with all infectious organisms, it is difficult to different the pathogeniceffects resulted in strictly by mechanical or chemistry tissue damages from thosecaused by the immune an answer to the parasite. Every helminths are“foreign bodies” not just in the sense of being big andinvasive but likewise in the immunologic sense: they room antigenic and thereforestimulate immunity. Fantastic illustration of this interrelation betweendirect and indirect damage is seen in the pathology connected with schistosomeinfections, especially with Schistosoma mansoni (Fig. 87-3). Hypersensitivity-based,granulomatous responses to egg trapped in the liver cause a physicalobstruction to blood flow, which leader to liver pathology.Hypersensitivity-based inflammatory transforms probably likewise contribute come thelymphatic blockage associated with filarial epidemic (Brugia,Wuchereria).
Pathogenesis: indirect damages caused through immunopathologicresponses (for example, in Schistosomiasis).
Immune-mediated inflammatory changes occur in the skin, lungs, liver, intestine,CNS, and also eyes together worms migrate through this structures. Systemic changes suchas eosinophilia, edema, and also joint ache reflect regional allergic responses toparasites. The pathologic consequences of immune-mediated inflammation are seenclearly in intestinal infections (especially Strongyloides andTrichinella infections). Structure changes, such asvillous atrophy, develop. The permeability of the mucosa changes, fluidaccumulates in the gut lumen, and also intestinal transit time is reduced. Prolongedchanges the this type may result in a protein-losing enteropathy. The inflammatorychanges the accompany the passage of schistosome eggs through the intestinalwall additionally cause severe intestinal pathology. Heavy infections v the whipwormTrichuris in the large bowel have the right to lead come inflammatorychanges, causing blood loss and also rectal prolapse.
The severity of this indirect transforms is a an outcome of the chronic nature that theinfection. The truth that numerous worms are exceptionally long-lived method that manyinflammatory changes end up being irreversible, producing functional changes intissues. Three examples are the hyperplasia of bile ducts in irreversible liverfluke infections, the considerable fibrosis associated with chronicschistosomiasis, and the skin atrophy associated with onchocerciasis. Severepathology might also an outcome when worms stray right into abnormal human body sites.
Infective step attempting to enter via the mouth or through the skin areopposed through the very same non-specific defenses that defend humans from invasion ofother pathogens. Following oral ingestion, parasites should survive passagethrough the mountain stomach to with the small bowel. The organic parasites ofhumans are adjusted to perform this, but opportunistic parasites may be killed.Similarly, organic parasites are adapted to the environmental problems of thebowel (and in many situations require them together cues because that development), however accidentalparasites may find them inappropriate. Penetration right into the intestinal wall surface maytrigger inflammatory responses the immobilize and also kill the worm. This mayitself cause serious pathology (as in Anisakis infection).Worms entering with the skin need to survive the skin secretions, pass through theepidermal layers, and avoid inflammatory trapping in the dermis. Intrusion ofhumans by the larvae that dog and cat hookworms (Ancylostomaspp.) outcomes in dermatitis and “creeping eruption” as theworms come to be the emphasis of inflammatory reaction that kind trails in theskin.
Once in the tissues, worms need the exactly sequence of eco-friendly signals tomature. Lacking or incomplete signal constitute a type of nonspecific resistancethat may partially or completely prevent additional development. The parasite maynot die, however; indeed, an extensive survival in ~ a larval phase may result inpathology native the proceeding inflammatory solution (e.g.Toxocara infection).
Specific acquired Immunity
There is no doubt that specific immunity is responsible for the many effectiveforms of organize defense, back the separating line in between nonspecific andspecific mechanisms is difficult to attract with precision (Fig. 87-4). All helminths stimulate solid immuneresponses, i beg your pardon can conveniently be recognize by measuring certain antibody orcellular immunity. Although this responses are valuable for diagnosing infection,they frequently show up not to it is in protective. The high ubiquity of helminthinfection in endemic areas (sometimes draw close 100 per cent), and the factthat people may remain infected for numerous years and also can quickly be reinfectedafter they are cured by chemotherapy, imply that protective immunity againsthelminths is weak or absent in humans. However, some degree of immune doesappear come operate, due to the fact that the soot of epidemic often declines with age,and many individuals in endemic areas remain parasitologically an adverse and/orclinically normal. Evidence from activities studies offers some ideas as tothe mechanisms involved. Antibodies that bind to surface ar antigens may focuscomplement- or cell-mediated effectors the can damages the worm. Macrophages andeosinophils are the prime cytotoxic effector cells, and also IgM, IgG and also IgE are theimportant immunoglobulins. Antibodies may also block enzymes released by theworm, thus interfering v its capability to permeate tissues or come feed.Inflammatory changes may concentration effector cells about worms, and therelease of cellular mediators may then disable and also kill the worm. Encapsulationof trapped worms by inflammation cells may also result in the death of the worm,although this is not constantly the case. Intestinal worms have the right to be dislodged by thestructural and also physiologic alters that happen in the intestine throughout acuteinflammation. It has actually long to be suspected the IgE-mediated hypersensitivityreactions, including mast cells and basophils, contribute to this process, butthe evidence is quiet circumstantial. In spite of the diversity of IgA in theintestinal lumen, over there is no conclusive evidence that it is involved inprotective immunity in humans, although part field and laboratory data suggestit is.
Host defense and also parasite escape. A schematic diagram of the breakthrough and expression of acquiredimmunity come helminths and of the methods in which helminth escape theimmune response.
Avoidance of hold Defenses
Despite their immunogenicity, numerous helminths make it through for extended periods in thebodies of their hosts. Several of the reasons have currently been stated (size,motility), yet we now recognize that worms employ many sophisticated devices torender host defenses ineffective (Fig.87-4). Part worms (schistosomes) disguise their external surface byacquiring host molecules which minimize their antigenicity; intrinsic membranechanges likewise make these worms resistant come immune attack. Filarial nematodesacquire serum albumin on your cuticle, which might act as a disguise. Countless wormsrelease substances that depress lymphocyte function, inactivate macrophages, ordigest antibodies. Larval cestodes show up to extend their survival by producinganticomplement components which protect their external layers indigenous lytic attack.Antigenic sport in the strict sense is not recognized to occur, however many speciesshow a stage-specific readjust of antigens together they develop, and also this phenomenonmay hold-up the advancement of effective immune mechanisms. Every helminths releaserelatively big amounts the antigenic materials, and this voluminous productionmay draw away immune responses or even locally exhaust immune potential. Irrelevantantibodies developed by the hold may block the activity of potentially protectiveantibodies, as has actually been presented to be the instance in schistosome infections.
It is highlight that plenty of helminth infections are linked with a degree ofimmune suppression, which may affect particular or basic responsiveness. Manyexplanations have actually been proposed because that this immune suppression, including antigenoverload, antigenic competition, induction that suppressor cells, and productionof lymphocyte-specific suppressor factors. Diminished immune responsiveness may notonly extend the survive of the initial infecting worm varieties but increasethe host"s susceptibility to other pathogens. Epidemiologic evidence also raisesthe possibility that infections acquired at an early stage in life—before orshortly ~ birth—may induce a kind of immune tolerance, allowingheavy worm burdens come accumulate in the body.
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The subtlety v which parasitic worms manipulate the host"s immune device notonly increases their prominence as pathogens but likewise creates formidableproblems for their control and eradication.
Crewe W (ed): Blacklock and Southwell"s guide toHuman Parasitology. 11th Ed. Chapman and also Hall, London, 1990