Which type of infectious agent are pinworms hookworms trichinella and filaria

Transmission and Life Cycle

Blackfly vectors bite humans and transmit larvae into the skin. Nodules form in a few months to years, and the developed adults release microfilariae into the dermis. Adult worms can live for a decade or two.

Presenting Signs and Symptoms

Onchocerciasis results from inflammatory reactions to the microfilaria that can affect skin, eyes, and lymph nodes. An intensely pruritic papular rash is common. Atrophy and pigmentation changes can occur in long-term infection. Subcutaneous nodules, or onchocercomas, contain adult worms and are common over bony prominences. Conjunctivitis, uveitis, chorioretinitis, and optic atrophy result from ongoing optic inflammation; neovascularization and scarring of the cornea lead to corneal opacity and eventual blindness. Lymphadenopathy is also common.

Diagnosis and Medical Decision Making

The removal of an adult worm from onchocercomas or of microfilariae from skin snips leads to the definitive diagnosis. The Mazzotti test, involving a small dose of diethylcarbamazine (50 mg/kg) and subsequent observation for worsening rash or pruritus, can aid in diagnosis. Topical diethylcarbamazine (10% in lotion) can be applied to the skin as a localized Mazotti test; it is considered safer than an oral test. If there areOnchocerca microfilariae present in the ocular chamber, diethylcarbamazine treatment can lead to ocular damage.

Onchocerca species infestation

Onchocerca species can parasitize sheep and goats, although there are relatively few reports of the condition. A Finland study reported in 2008 found no evidence of sheep infected with Onchocerca species.120 Adult Onchocerca species can live in the connective tissues of sheep and goats, where they induce nodules. Adults produce microfilariae that migrate into the dermis of the ventral abdomen and thorax. Alopecia, erythema, and thickening of the skin develop because of the host’s response to dying larvae.

Other nematodes diagnosed in cases of focal dermatitis include Pelodera strongyloides, Strongyloides papillosus, and Parelaphostrongylus tenuis. These nematodes have been associated with dermatitis, but their clinical significance is minimal. Strongyloidiasis is seen on dependent regions of the body; the localized dermatitis is caused by an immune reaction to migrating larvae. P. tenuis infestation of the central nervous system may cause focal regions of hyperesthesia. This may lead to self-trauma that the keeper or clinician notes as excoriations or nonhealing ulcers.

Infection With Animal Filariae

The most commonly recognized zoonotic filarial infections are caused by members of the genusDirofilaria. The worms are introduced into humans by the bites of mosquitoes containing third-stage larvae. The most common filarial zoonosis in the United States isDirofilaria tenuis, a parasite of raccoons. In Europe, Africa, and Southeast Asia, infections are usually caused by the dog parasiteDirofilaria repens. Thedog heartworm,Dirofilaria immitis, is the second most frequently encountered filarial zoonosis worldwide. Other genera, includingDipetalonema-like worms,Onchocerca, andBrugia, are rare causes of zoonotic filarial infections.

Animal filariae do not undergo normal development in the human host. The clinical manifestations and pathologic findings correspond to the anatomic site of infection and can be categorized into 4 major groups: subcutaneous, lung, eye, and lymphatic. Pathologic examination of affected tissue reveals a localized foreign body reaction around a dead or dying parasite. The lesion consists of granulomas with eosinophils, neutrophils, and tissue necrosis.D. tenuis does not leave the subcutaneous tissues, whereasBrugia beaveri eventually localizes to superficial lymph nodes. Infections may be present for up to several months.D. immitis larvae migrate for several months in subcutaneous tissues and most frequently result in a well-circumscribed, coinlike lesion in a single lobe of the lung. The chest radiograph typically reveals a solitary pulmonary nodule 1-3 cm in diameter. Definitivediagnosis and cure depend on surgical excision and identification of the nematode within the surrounding granulomatous response.D. tenuis andB. beaveri infections present as painful, rubbery, 1-5 cm nodules in the skin of the trunk, of the extremities, and around the orbit. Patients often report having been engaged in activities predisposing to exposure to infected mosquitoes, such as working or hunting in swampy areas. Management is bysurgical excision.

Onchocerca

The number of described Onchocerca species that might result in zoonotic infections in humans is too great to list here, but the genus is cosmopolitan, and normal animal hosts include a wide range of ungulates, including cattle, horses, camels, various antelope, deer, and sheep. Onchocerca species have a predilection for residing in or near connective tissues in their natural hosts, and this has been the case in the majority of zoonotic infections as well. Two cases involving the eye have been reported,23,26 and there is at least one additional unpublished case of Onchocerca being recovered from the eye.

In sections (Figs. 101-20 through 101-24), Onchocerca have several prominent features including, in longitudinal section, a cuticle that bears external ridges and internal striae, and in transverse section, a thick cuticle that is often unevenly thickened; prominent hypodermal tissue not restricted to the lateral chords; and few muscle cells per quadrant that are distinctive in appearance, being atrophied and wispy. Because of the extreme length of female worms and their characteristic coiling, it is not unusual to see multiple sections of worm in a single tissue section.

Prevention and Control

Individual protection against LF infection involves avoidance of infected mosquitoes through personal protective measures and long-lasting insecticide-treated bednets (LLINs); LLINs have been shown to be a valuable tool for the control and elimination of LF (Reimer et al., 2013). Elimination of microfilariae within communities can interrupt transmission because patent microfilaremia is necessary for mosquitoes to transmit the infection from person to person. However, because chemotherapy does not kill all of the adult worms, it is necessary to continue intermittent administration of antiparasitic drugs for many years, until the adult worms die of senescence. This strategy can be effective forW. bancrofti elimination (Molyneux, 2009) but is more challenging inBrugia-endemic areas because animals also serve as reservoirs of infection for the latter. MDA campaigns (involving distribution of single annual doses of albendazole plus either DEC or ivermectin, which have a sustained microfilaricidal effect to most of the population) are the mainstay of control programs in Africa (albendazole/ ivermectin) and elsewhere (albendazole/DEC). These campaigns have been successful in control and elimination of LF with many areas nearing elimination and are the primary reason for the decrease in global LF prevalence described previously. These programs have also prevented 19 million hydrocele cases globally since 2000, decreasing by half the number of hydroceles because of LF over that time period (Ramaiah and Ottesen, 2014). Encouragingly, recent small studies suggest that triple antiparasitic therapy (DEC + albendazole + ivermectin) reduces microfilaremia more profoundly and for a more prolonged time than dual antiparasitic therapy, with no additional serious adverse effects (Thomsen et al., 2016). If confirmed at a larger scale, this may herald a major advance for MDA programs in areas where all three drugs can be used together.

Onchocerciasis, also known asriver blindness, is a filarial infection usually caused byOnchocerciasis volvulus. The infection is transmitted bySimulium black flies; 99% of onchocerciasis cases are found in Africa, with limited foci in Latin America (within Brazil and Venezuela) and the Arabian Peninsula (Yemen). About 17 million people are infected globally (WHO, 2017), which represents a 55% decrease in prevalence compared with 2000, largely because of successful MDA programs. As with LF, transmission is inefficient and highly focal. Adult worms live for up to 15 years in subcutaneous nodules (mean natural life span, 9 to 10 years) and release microfilariae that travel through the skin (and eye).O. volvulus adults also harborWolbachia endosymbionts. Infection classically causes dermatitis/pruritis, keratitis, and chorioretinitis, with blindness as an end result after many years, from corneal scarring. Diagnosis is confirmed by microscopically examining skin snips for microfilariae, finding adult worms in subcutaneous nodules, or seeing microfilariae in the anterior chamber of the eye via slit lamp. Antibody and antigen detection tests are less well developed than for LF.

Terminology

Etiology/Pathogenesis

Clinical Issues

Microscopic Pathology

Differential Diagnosis

Diagnostic Checklist

Immune Characteristics

Laboratory studies have suggested that the parasite induces a complex immune response, perhaps partly autoimmune. Immunoglobulin E (IgE) production is a prominent feature of Onchocerca infestation, and circulating immune complexes that presumably contain parasite antigen can be detected.23 Cell-mediated responsivity is reduced,24 a phenomenon also noted in other helminth infections. Indeed, it appears that in addition to a predominantly B-cell (i.e., antibody) response, the immune system tries to minimize bystander tissue damage after the death of microfilariae by producing blocking antibodies and downregulating cytokines.25 Chan et al.26 examined the ocular fluid and serum from patients with onchocerciasis for the presence of antiretinal autoantibodies and found that these patients had antibodies directed toward the inner retina (nerve fiber, ganglion cell, and Müller cell) that could not be absorbed with the use of either S-antigen (S-Ag) or the interphotoreceptor-binding protein. These observations suggested that autoimmune mechanisms may play a role in the retinal degeneration and optic nerve disease seen so frequently in these patients. Van der Lelij et al.27 found high titers of anti-Onchocerca antibodies in the aqueous of patients with onchocerciasis and ocular disease and believed that retinal autoimmunity was an improbable factor in the pathogenesis of onchocercal chorioretinopathy.

However, immunologic cross-reactivity between an antigen of O. volvulus and that found in the retinal pigment epithelium (RPE) has been identified. Antisera from patients with onchocerciasis identified a 22-kDa antigen from Onchocerca, whereas a 44-kDa antigen from cultured human RPE was immunoprecipitated with the same antiserum.28 Klager et al.29 used Western blotting to show that antibody reactions to this antigen were seen in all patients with onchocerciasis and posterior pole disease but were not seen in controls. These interesting results suggest that molecular mimicry plays a role in the development of at least certain aspects of the ocular complications noted in this disorder. It also strengthens the notion that, as with ocular toxoplasmosis, inflammatory systems can no longer be restricted to only one mechanism and that in some ways, contradictory routes may be stimulated. Autoantibody responses are not restricted to the eye. Such cross-reactivity has been reported against five major autoantigens, anticalreticulin activity, and the 65-kDa arthritis-associated mycobacterial heat shock protein.30

The corneal lesions of onchocerciasis have been studied using animal models. There is infiltration of granulocytes and eosinophils into the clear structures. Kaifi et al.31 found that vascular adhesion molecules are important in this process. These authors demonstrated a regulatory role for platelet endothelial cell adhesion molecule 1 and intercell adhesion molecule in that they recruit neutrophils and eosinophils to the cornea, as does P-selectin.32 Because there are antibodies that are directed against these molecules, it raises the possibility of their use in immune therapy for the cornea. Other studies by the same group33,34 demonstrated the importance of CD4+ T cells in the development of corneal opacification, but not in the early stages of the disease. Saint Andre et al.35 proposed that the predominant inflammatory response seen in the cornea of Onchocerca-infected animals is, in fact, directed against the endosymbiont of Onchocerca and Wolbachia. Indeed, it may be the essential player in the pathogenesis of river blindness.36 This endosymbiont is so essential to the nematode that embryogenesis of Onchocerca is completely dependent on the presence of Wolbachia. The O. volvulus–Wolbachia combination initiates activation of many immune indicators37 (Table 18.2). Indeed, this may open a new avenue for therapy (see below).

With studies of the specialized mechanisms of the parasite, an interesting concept has emerged.38 Lipid-binding proteins in the nematode, with no known counterpart in mammalian systems, exist. One of these, Ov-FAR-1, has a high affinity for retinal and fatty acids and is present in all life stages of the parasite.39 Retinol is believed to be important for the growth and differentiation of the organism and for its embryogenesis and glycoprotein synthesis.40 The concentration of retinol is eight times higher in the Onchocerca nodule than in the surrounding tissue.41 It is possible that Ov-FAR-1 causes a relatively local or systemic depletion of vitamin A in patients with onchocerciasis and may also be a trigger for the production of collagen, which is found in large quantities in Onchocerca nodules. These could explain why ivermectin therapy may not be effective for the retinal disease in this disorder because microfilaria already present in the retina would continue to produce this lipid-binding protein (see later discussion on ivermectin).

The regulation of interleukin (IL)-5 production in onchocerciasis has been evaluated. It has been suggested that in some helminthic infections, the production of IL-5 may be associated with an immune or a resistant state. It appears that in patients who are “immune” to the effects of Onchocerca, both IL-2 and IL-5 are produced in significantly higher levels than in those with acute infection. IL-2 production is required to induce IL-5.42 Toll-like receptor 2 (TLR2) appears to regulate chemokine production and neutrophil recruitment to the cornea in experimentally induced Onchocerca/Wolbachia keratitis.43 Interferon (IFN)-γ responses from TLR2 knockout mice are also deficient.44

Tropics and Subtropics

Because many people are infected with more than one species of helminth, there are more different species of helminths infecting people than there are people in the world. The numbers infected with hookworms, Ascaris, Trichuris, pinworm, schistosomes, Onchocerca, and filariae are each in the many millions, although they have often been “neglected” in tropical disease control priorities.1 A common trinity of intestinal helminthiasis, termed the soil-transmitted helminths, includes ascariasis, hookworm infection, and trichuriasis.2

The magnitude of disease caused by helminths is related to the intensity of infection. Individuals with light infections typically have few or no abnormal findings, whereas those with heavy and prolonged infections often have clinical symptoms and signs and can develop complications. This is well documented in schistosomiasis, hookworm disease, onchocerciasis, and filariasis.

Section 5.5 Nematoda

Life is hard. Then you die. Then they throw dirt in your face. Then the worms eat you. Be grateful it happens in that order.

David Gerrold

Eukaryota

 Bikonta (2-flagella)

 Excavata

   Metamonada

   Discoba

  Euglenozoa

  Percolozoa

 Archaeplastida

 Chromalveolata

   Alveolata

  Apicomplexa

  Ciliophora (ciliates)

   Heterokonta

 Unikonta (1-flagellum)

 Amoebozoa

 Opisthokonta

   Choanozoa

   Animalia

  Eumetazoa

    Bilateria

   Deuterostomia

     Chordata

    Craniata

   Protostomia

     Ecdysozoa

    Nematoda, roundworms

      Secernentea

     Ascaridida

       Anisakidae

      Anisakis (genus)

      Pseudoterranova (genus)

      Contracaecum (genus)

       Ascarididae

       Ascaris (genus)

       Baylisascaris (genus)

       Toxocaridae

       Toxocara (genus)

       Dioctophymatidae

       Dioctophyme (genus)

     Spirurida

       Spirurina

      Filarioidea

        Onchocercidae

       Brugia (genus)

       Loa (genus)

       Onchocerca (genus)

       Mansonella (genus)

       Wuchereria (genus)

       Camallanida

      Dracunculoidea

        Dracunculidae

       Dracunculus (genus)

     Oxyurida

      Oxyuridae

        Enterobius (genus)

     Rhabditida

       Strongyloididae

      Strongyloides (genus)

       Ancylostomatidae

      Ancylostoma (genus)

      Necator (genus)

       Metastrongylidae

       Angiostrongylus (genus)

       Trichostrongylidae

        Trichostrongylus (genus)

      Enoplea

      Dorylaimida

       Trichocephalida

      Trichinellidae

        Trichinella (genus)

        Capillaria (genus)

      Trichuridae

        Trichuris (genus)

    Arthropoda

      Chelicerata

      Hexapoda

      Crustacea

     Platyzoa

    Platyhelminthes

    Acanthocephala

   Fungi

Three large subclasses of animals comprise Class Protostomia: Class Platyzoa, Class Ecdysozoa, and Class Lophotrochozoa. Only the first two classes contain organisms that infect humans. Class Platyzoa contains Class Platyhelminthes and Class Acanthocephala. Class Ecdysozoa accounts for Class Arthropoda, and Class Nematoda.

Nematodes, also known as roundworms, lack a circulatory system, and a respiratory system. They are all pseudocoelomates, meaning that their body cavities are not fully lined by mesoderm. Compare this with the flatworms (Class Platyhelminthes) that are acoelomate (i.e., without body cavities). The Nematodes have a tube-shaped digestive tract, open at both ends (mouth and anus). The presence of a complete digestive tract is another property that distinguishes the roundworms from the flatworms; the digestive tract of flatworm has a single opening for the ingestion of food and the excretion of waste.

Nematodes are covered by a cuticle composed largely of extracellular collagen and other proteins (e.g., cuticulins) excreted by epidermal cells. The cuticle is shed repeatedly at various life stages of the nematode.

Two major subclasses of Class Nematoda contain the organisms that infect humans: Secernentea and Enoplea. These two classes have various anatomic features that distinguish one from the other. Their most relevant distinction, for health-care workers, is that members of Class Secernentea are terrestrial dwellers, while members of Class Enoplea are marine inhabitants.

Many pathogenic members of Class Secernentea are best described within their subclasses

Nematoda

 Secernentea

 Ascaridida

   Anisakidae

  Anisakis (genus)

  Contracaecum (genus)

  Pseudoterranova (genus)

Anisakiasis is the disease produced by members of Class Anisakidae, which includes the following genera: Anisakis, Contracaecum, and Pseudoterranova. Humans are infected by eating undercooked shellfish and fish infected with larvae. Most cases occur in countries where raw fish is regularly consumed. Only a handful of cases are reported in the United States, annually. Humans are a dead-end host for the worms. After ingestion, the larvae travel to the small intestine, and live for a time, eventually dying without reproducing. In rare cases, they may cause abdominal obstruction, but their most clinically significant effect is through an acute allergic reaction. An acute enteritis often occurs, and, in some cases, a generalized anaphylactic reaction. Some fishermen are so highly sensitized that they develop hyper-immune reactions simply from handling fish or crustaceans that are infected with the larvae.

Nematoda

 Secernentea

 Ascaridida

   Ascarididae

  Ascaris (genus)

  Baylisascaris (genus)

Ascaris lumbricoides, the cause of ascariasis, infects about 1.5 billion people worldwide, making it the most common helminth (worm) infection of humans [10]. Most cases occur in tropical regions, particularly in Africa and Asia. Humans are the exclusive primary host for the organism.

Infection occurs when humans ingest embryonated eggs contaminating water or food.

The ingested embryonated eggs produce larvae in the small intestine. The larvae invade through the intestinal wall and into the portal system, where they are transported to the alveoli of lungs. While in the lungs, they can produce a pneumonitis. From the lungs, they move upwards, through the bronchial system, to the pharynx, and drop back into the intestinal system via the esophagus. Among the largest of the nematodes, A. lumbricoides reach adulthood in the intestine, where they can grow to nearly 40 cm in length and have a lifespan of up to 2 years. Ascaris lumbricoides is not the only helminth that migrates through the lungs. In Class Rhabditida, Ancylostoma duodenale, Necator americanus, and Strongyloides stercoralis invade the pulmonary system.

Eggs produced by the adult worms leave the intestine via the feces and contaminate soil and water where sanitation is deficient. Adult worms may produce a wide range of symptoms due to obstruction of the intestines and ducts that connect with the intestine. Like members of Class Anisakidae, Ascaris lumbricoides may provoke an allergic reaction. An allergy to Ascaris lumbricoides may precipitate allergic reactions to shrimp and dust mites, as these unrelated species have some antigens in common (Fig. 5.15).

Readers should be careful not to confuse ascariasis with the similar-sounding anisakiasis (vida supra).

Baylisascaris procyonis causes baylisascariasis in humans. Raccoons are the primary host. The adult nematode lives in the raccoon intestine and eggs are dropped with raccoon feces. The eggs of Baylisascaris procyonis can survive for years, and they are extremely resistant to disinfectants and heat. In rare circumstances, humans may become infected, as the secondary host, by ingesting eggs. Eggs develop into larvae in the human intestine, and the larvae migrate out of the intestines and through various organs, where they eventually encyst. Involvement of the central nervous system by encysted larvae is an extremely serious condition.

Nematoda

 Secernentea

 Ascaridida

   Toxocaridae

  Toxocara (genus)

Humans are dead-end, accidental hosts for Toxocara canis (the dog toxocara) and Toxocara cati (the cat toxocara). Infected animals pass eggs in their feces. Larval development occurs within the eggs, and if matured eggs are ingested by humans, the larvae can hatch in the small intestine. The larvae migrate through various tissues: eyes, lung, liver, and brain being common destinations.

The disease caused by toxocara organisms is toxocariasis. During the migratory stage, the disease is often referred to as visceral larva migrans. Eye involvement is referred to as ocular larval migrans. Readers should not be lulled into a false sense of terminologic security. When toxocara migrate through the skin, the condition is NOT called cutaneous larva migrans: this term is reserved for cutaneous manifestations of Ancylostoma braziliense. An immune response to the migrating toxocara larvae may produce eosinophilia (i.e., an increase in eosinophils in the peripheral blood), and the term eosinophilic pseudoleukemia has been used to describe this condition.

After a period of migration, the worms, which cannot mature further in the human body, encyst to produce small, localized, permanent nodules in tissues.

Readers should not confuse “toxocara” with the similar-sounding “toxoplasma” (Class Apicomplexa), a problem aggravated when insouciant clinicians use the abbreviated and ambiguous form “toxo,” which can refer to either organism.

Nematoda

 Secernentea

 Ascaridida

   Dioctophymatidae

  Dioctophyme (genus)

Dioctophyme renale, also known as the giant kidney worm, is a rare cause of human disease. Humans, one of many animals serving as the primary host, are infected by ingesting an undercooked second intermediate host (usually fish or frogs) that had, in turn, ingested the first intermediate host (a freshwater earthworm). Ingested larvae penetrate the human intestines and migrate to the liver. From the liver, they migrate to a kidney (unilateral, usually the right kidney), where they become adults. Eggs laid by the adult worm are excreted in the urine. The infestation of large adult worms typically leads to the destruction of the kidney, if left untreated. Human disease is rare, and can occur anywhere in the world.

Nematoda

 Secernentea

 Spirurida

   Spirurina

  Filarioidea

    Onchocercidae

   Brugia (genus)

   Loa (genus)

   Onchocerca (genus)

   Mansonella (genus)

   Wuchereria (genus)

Filarial nematodes are string-like worms that are sufficiently small to fit into lymphatic vessels. About 150 million people are infected by the filarial nematodes (genera Brugia, Loa, Onchocerca, Mansonella, and Wuchereria) [11]. Wuchereria bancrofti and Brugia malayi, together, infect about 120 million individuals [11]. Most cases occur in Africa and Asia.

The life cycle for these organisms involves a human primary host, in which the adult filarial worms produce juveniles (microfilaria) that migrate through lymphatics and blood vessels, where the microfilaria are sucked out by a secondary host (i.e., a blood-feeding mosquito or fly). In the secondary host, they develop into larvae. The secondary host serves double duty as a vector by injecting larvae into the primary host when the insect has a blood meal. The larvae grow into adult threadworms within the primary host, a process that takes place over a year or more, and the cycle continues. The symptoms and severity of the disease are largely determined by the anatomic destinations of the migrating worms, and on the total load of worms, as multiple infections in the same person lead to a continuously increasing filarial burden.

Wuchereria bancrofti, Brugia malayi, and Brugia timori tend to cause lymph system obstruction, which can lead to elephantiasis. Elephantiasis is a condition wherein one or more extremities, usually the legs, are chronically swollen.

Other filarial worms preferentially inhabit the fatty tissue within the subcutis of skin: loa loa (the African eye worm), Mansonella streptocerca, and Onchocerca volvulus. The subcutaneous tissue is also the cause of infection by a nematode in Class Camallanida: Dracunculus medinensis (vida infra). Mansonella perstans and Mansonella ozzardi live in the abdominal peritoneum.

Onchocerca volvulus is the cause of river blindness, the second leading cause of infection-produced blindness (behind trachoma, caused by Chalmydia trachomatis, Class Chlamydiae). The ocular pathogenicity of Onchocerca volvulus is caused by an endosymbiont, Wolbachia pipientis (See discussion in Class Alpha Proteobacteria).

In addition to the filarial infections for which humans are the natural, primary host, there are reported cases of the so-called zoonotic filariasis, in which humans are a dead-end host. The zoonotic infections, as in the filarial infections for which humans are the natural hosts, are all transmitted by blood-feeding insects. The filaria live for a time in human tissues, where they eventually die, producing a localized inflammatory reaction. Though various species of filaria are found in a wide assortment of animal hosts, including birds and reptiles, only mammalian hosts have been associated with zoonotic filariasis in humans [12].

Nematoda

 Secernentea

 Spirurida

   Camallanida

  Dracunculoidea

    Dracunculidae

   Dracunculus (genus)

Dracunculus medinensis is the single pathogenic species in Class Dracunculidae. Dracunculiasis, also known as guinea worm, has a dramatic clinical presentation and treatment. The adult female worm bursts forth from the skin, usually just above or below the knee. The astute physician coaxes the living worm, onto a stick, which he or she then winds slowly, thus delivering the intact worm and relieving the patient of his parasitic burden. The Rod of Asclepius, historically symbolizing the practice of medicine, is inspired by the ancient ritual whereby the Dracunculus worm is extracted (Fig. 5.16).

Human become infected when they drink water that has been contaminated with copepods (tiny organisms in Class Crustacea) containing a juvenile form of the organism. Readers will remember that copepods are a favored secondary host for cestodes (Class Platyhelminthes). After ingestion by humans, the copepods die, and larvae are released to penetrate the stomach wall. The male worms die, but the females migrate to subcutaneous tissue and continue to grow into adulthood (about 1 year later). The infectious cycle is perpetuated when the matured female adult (approaching a meter in length) pokes through the skin and releases its larvae, predestined for ingestion by secondary hosts (i.e., copepods).

As with several of the previously described nematodes (i.e., Ascaris lumbricoides, Enterobius vermicularis, and the common filarial species) humans are the exclusive primary host of Dracunculus medinensis. Public health measures have drastically reduced the occurrences of dracunculiasis in Africa and Pakistan.

Nematoda

 Secernentea

 Oxyurida

   Oxyuridae

  Enterobius (genus)

Enterobius vermicularis, known as the pinworm in the United States, causes enterobiasis, sometimes called oxyuriasis.

Humans are the primary and exclusive host of the pinworm. Eggs are ingested, and the larvae emerge in the duodenum. The larvae migrate in the direction of peristalsis, as they mature into adults. The adults mate in the ileum and settle in the distal ileum, the proximal colon, or the appendix, where the females become bloated with eggs. Afterwards, the adult females (now about 1 cm in length) migrate to the anal skin where they lay their eggs. The eggs infect other humans or re-infect the original host, through fecal-oral contamination or through dispersal in the air (e.g., when bed linens are shaken).

The most common symptom of pinworm is anal itching. Cases have been reported of appendicitis caused by gravid pinworms obstructing the lumen of the appendix.

Nematoda

 Secernentea

 Rhabditida

   Strongyloididae

  Strongyloides (genus)

   Ancylostomatidae

  Ancylostoma (genus)

  Necator (genus)

   Metastrongylidae

  Angiostrongylus (genus)

  Trichostrongylidae

    Trichostrongylus (genus)

Class Rhabditida is characterized by juvenile forms that are adept at free-living (usually in soil) and capable of a range of behavior usually associated with adult forms; particularly the ability to penetrate skin, to migrate through tissues, and to survive for extended periods.

Strongyloides stercoralis is a nematode that primarily infects humans; naturally occurring infection by Strongyloides stercoralis in animals other than humans is not known at this time. Humans become infected when larvae, passed from human feces, and free-living in contaminated soil, penetrate exposed skin and enter the circulation system. No secondary host is involved in the life cycle of Strongyloides stercoralis. Once in the bloodstream, Strongyloides stercoralis larvae move to the lungs, where they invade the bronchial tree, advance to the pharynx, and drop into the esophagus. When they reach the small intestine, they are adults, and female worms begin to lay eggs, thus renewing the infectious life cycle. Infections in humans are uncommon and occur in countries with poor sanitation.

Strongyloides has one important biological trick that contributes to its clinical presentation. Larvae that develop from eggs laid in the small intestine are capable of autoinfecting the host, by invading though the intestinal mucosa, or by invading through the anal skin (when they emerge from the large intestine). The larvae pass to the lung, renewing the infection cycle within their original human host. This step short-circuits the step wherein larvae dwell as free-living organisms in soil.

The consequences of autoinfection are several: infection can continue for a long time, sometimes extending throughout the lifespan of the host; the infectious load (i.e., Number of organisms in the body) can be immense.

The term applied to a high infectious load of Strongyloides stercoralis is “hyperinfection syndrome” [13]. Immune-compromised patients are at highest risk for hyperinfection syndrome. When hyperinfection occurs, the disease can be fatal.

In addition to Strongyloides stercoralis, other species that have been reported to infect humans are: Strongyloides fuelleborni and Strongyloides kellyi.

Class Anyclostomadea contains the two species responsible for nearly all cases of hookworm disease in humans: Ancylostoma duodenale and Necator americanus. The two species have similar clinical presentations, but different geographic distributions. Ancylostoma duodenale is common in the Middle East, North Africa, and India. Necator Americanus is common in North and South America, as well as parts of Africa and Asia. Hookworms infect about 1 billion people.

Hookworm eggs and larvae live in soil. Like the previously described member of Class Rhabditida, Strongyloides stercoralis, larvae of Ancylostoma duodenale and Necator Americanus penetrate the skin of human hosts. Ancylostoma duodenale may also infected by oral ingestion. The larvae invade tissues and travel to the lung, where they travel up the bronchial tree, eventually dropping into the esophagus, passing down the alimentary tract to the small intestine, where they mature into adults. Eggs laid by the female adult worms pass into the environment, with feces. Humans are the only natural host for the hookworms. There is no secondary host (Fig. 5.17).

The distinctive biological feature of the hookworms, distinguishing them from other nematodes, is hemophagia (i.e., blood eating). The hookworms suck blood from the host, producing anemia and malnutrition. Children are particularly vulnerable to the effects of hookworm infection, which may causes delays in mental and physical development.

Ancylostoma braziliense is a hookworm of dogs and cats. It occasionally penetrates the skin of humans, a dead-end host, and causes localized inflammation of the skin or limited subcutaneous migration (cutaneous larva migrans or creeping eruption).

Class Metastrongylidae contains two genera that contain infectious organisms: Angiostrongylus and Trichostrongylus.

Angiostrongylus cantonensis is a parasitic nematode (roundworm) that causes angiostrongyliasis, the most common cause of eosinophilic meningitis in Southeast Asia. Angiostrongylus cantonensis lives in the pulmonary arteries of rats; hence its common name, rat lungworm. Snails are the most common intermediate hosts, where larvae develop until they are infective. Humans are incidental hosts of this roundworm, and may become infected through ingestion of raw or undercooked snails or from water or vegetables contaminated by snails or slugs or deposited larvae. Ingested larvae travel through the blood to the brain, where the larvae may die or may progress to juvenile adults before eventually dying. The dead and dying organisms produce an allergic inflammatory reaction in the brain, with an increase in eosinophils in cerebral spinal fluid. Other species of Genus Angiostrongylus that may infect humans include Angiostrongylus costaricensis and Angiostrongylus mackerrasae.

Genus Trichostrongylus contains a variety of species that infect a wide range of animals; 10 species are known to infect humans. Humans are infected when larvae are ingested by ingesting contaminated water or vegetables. The larvae mature in the gut, and adult organisms live in the small intestine. Infections are often asymptomatic. Symptoms, when they occur, are typically those of enteritis. Eosinophilia (increased eosinophils in the blood) often occurs, and severe symptoms arise in some individuals.

Nematoda

 Enoplea

 Dorylaimida

   Trichocephalida

  Trichinellidae

    Trichinella (genus)

    Capillaria (genus)

  Trichuridae

    Trichuris (genus)

The nematodes that cause infection in humans belong to the Class Secernentea or Class Enoplea. The human pathogens in Class Secernentea have been described (via supra). Class Enoplea has three genera containing species that are infectious to humans: Trichinella, Capillaria, and Trichuris.

Trichinella spiralis is the cause of trichinosis, also known as trichinellosis. Humans are simultaneously the primary and the secondary host for this organism as the adult worms live in the intestines, producing eggs that hatch into larvae within the body of the female adult. The female adult worms live for about 6 weeks. The larvae leave the adult and penetrate the intestinal mucosa and migrate to muscles, where they encyst, waiting to be eaten by another potential host. Encysted larvae live within individual muscle cells. A full developed larva is about 80 μm in length, so the larva curls tightly within the muscle cell, allowing it to fit in a tight space (Fig. 5.18).

Humans typically become infected after eating the undercooked infected meat. More than 150 different animals have been reported as sylvatic hosts. Most infections in the United States come from eating pork. In the early decades of the 20th century, hogs were fed on pig meat, thus magnifying the infectious burden in the hog population. Methods for cooking pork were lax, and trichinosis in humans was common. With improved, regulated diets for hogs, and with proper methods of cooking pork, the incidence of trichinosis in the United States has dropped. Clinically, trichinosis produces enteric symptoms when the adult worms are reproducing in the intestines; muscle aches when the larvae are invading muscle cells.

Hepatic capillariasis, caused by Capillaria hepatica, is a rare human infection, with only a few dozen cases reported, most them occurring in children. Eggs in soil are ingested, hatched larvae penetrate the intestinal mucosa, and the larvae are carried through the portal system to the capillaries of the liver, where they mature to adults. The adults lay their eggs in the liver. This leads to liver fibrosis. If the parasite burden is high, cirrhosis may eventually develop. The parasite infects a wide range of animals, but rats are the most likely source of human infections. When an infected rat dies, its body decomposes, and eggs within the liver are released into the soil, where the life cycle resumes.

Trichuris trichiura is called the human whipworm, named for its tightly wound, thick segment, from which a straight, thinner segment extends (i.e., handle and whip). The disease caused by Trichuris trichiura is trichuriasis. Humans are the natural primary host for the organism. No secondary host is involved. Ingested eggs hatch in the small intestine, and larvae mature in the large intestine. The matured worms, which can live up to 5 years, anchor in the colonic mucosa and release eggs that pass out of the colon with feces. Eggs in the soil contaminate food, and the life cycle resumes.

The degree of morbidity is determined by the number of parasitic worms. Heavy infections can produce bloody diarrhea, anemia, and even rectal prolapse (from the aggregate weight of worms the rectum). Trichuriasis often accompanies other parasitic infections in the same individual.

Infectious Genera

Anisakis

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Ascaridomorpha: Ascaridoidea: Anisakidae: Anisakis

Infection. Anisakis simplex complex (anisakiasis)

Baylisascaris

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Ascaridomorpha: Ascaridoidea: Ascarididae: Baylisascaris

Infection. Baylisascaris procyonis (baylisascariasis, larva migrans with brain involvement)

Pseudoterranova

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Ascaridomorpha: Ascaridoidea: Anisakidae: Pseudoterranova

Infection. Pseudoterranova decipiens (anisakiasis)

Ascaris

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Ascaridomorpha: Ascaridoidea: Ascarididae: Ascaris

Infection. Ascaris lumbricoides (ascariasis, ascaris pneumonitis)

Toxocara

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Ascaridomorpha: Ascaridoidea: Toxocaridae: Toxocara

Infection. Toxocara canis, the dog roundworm (toxocariasis, visceral larva migrans, ocularis larva migrans)

Infection. Toxocara cati, or Tococara mystax, or the feline roundworm (toxocariasis, visceral larva migrans, ocularis larva migrans)

Enterobius

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Oxyuridomorpha: Oxyuroidea: Oxyuridae: Enterobius

Infection. Enterobius vermicularis, also called pinworm in the United States and as threadworm in the United Kingdom, or sometimes as seatworm (enterobiasis or oxyuriasis)

Strongyloides

Lineage. Nematoda: Chromadorea: Rhabditida: Tylenchina: Panagrolaimomorpha: Strongyloidoidea: Strongyloididae: Strongyloides

Infection. Strongyloides stercoralis, known as threadworm in US and pinworm in United Kingdom (strongyloidiasis)

Ancylostoma

Lineage. Nematoda: Chromadorea: Rhabditida: Rhabditina: Rhabditomorpha: Strongyloidea: Ancylostomatidae: Ancylostomatinae: Ancylostoma

Infection. Ancylostoma duodenale (hookworm, along with Necator americanus)

Necator

Lineage. Nematoda: Chromadorea: Rhabditida: Rhabditina: Rhabditomorpha: Strongyloidea: Ancylostomatidae: Bunostominae: Necator

Infection. Necator americanus (hookworm, along with Ancylostoma duodenale)

Angiostrongylus

Lineage. Nematoda: Chromadorea: Strongylida: Metastrongyloidea: Angiostrongylidae: Angiostrongylus

Infection. Angiostrongylus cantonensis (angiostrongyliasis)

Infection. Angiostrongylus costaricensis (abdominal angiostrongyliasis, intestinal angiostrongyliasis)

Infection. Angiostrongylus mackerrasae (eosinophilic meningitis)

Trichostrongylus

Lineage. Nematoda: Chromadorea: Rhabditida: Rhabditina: Rhabditomorpha: Strongyloidea: Trichostrongylidae: Trichostrongylus

Infection. Trichostrongylus orientalis (trichostrongyliasis, trichostrongylosis)

Dracunculus

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Dracunculoidea: Dracunculidae: Dracunculus

Infection. Dracunculus medinensis (dracunculiasis, guinea worm disease)

Brugia

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Spiruromorpha: Filarioidea: Onchocercidae: Brugia

Infection. Brugia malayi (lymphatic filariasis, elephantiasis)

Infection. Brugia pahangi (animal filariasis, rarely infecting humans) [14]

Infection. Brugia timori (lymphatic filariasis)

Loa

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Spiruromorpha: Filarioidea: Onchocercidae: Loa

Infection. Loa loa (loa loa filariasis, loiasis, loaiasis, Calabar swellings, Fugitive swelling, Tropical swelling, African eye worm)

Mansonella

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Spiruromorpha: Filarioidea: Onchocercidae: Mansonella

Infection. Mansonella ozzardi (serous cavity filariasis, seldom causes clinical disease, but generalized symptoms including fever, lymphadenopathy, joint pain, headache and pruritis are occasionally encountered)

Infection. Mansonella perstans, formerly Dipetalonema perstans (serous cavity filariasis, bung-eye disease)

Infection. Mansonella streptocerca, formerly Dipetalonema streptocerca (streptocerciasis)

Onchocerca

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Spiruromorpha: Filarioidea: Onchocercidae: Onchocerca

Infection. Onchocerca volvulus (onchocerciasis, river blindness)

Wuchereria

Lineage. Nematoda: Chromadorea: Rhabditida: Spirurina: Spiruromorpha: Filarioidea: Onchocercidae: Wuchereria

Infection. Wuchereria bancrofti (filariasis)

Trichinella

Lineage. Nematoda: Enoplea: Dorylaimia: Dioctophymatida: Dioctophymatoidea: Dioctophymatidae: Dioctophyme

Which type of infectious agent consists solely of proteins?

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What helminth is referred to as a pinworm?