INTRODUCTION — The nematodes (roundworms) reviewed here include dirofilariasis, capillariasis, trichostrongyliasis, anisakiasis, Angiostrongylus costaricensis, dracunculiasis, and thelaziasis (table 1). Other tissue nematode infections are discussed separately, including gnathostomiasis, baylisascariasis, and Angiostrongylus cantonensis. (See "Eosinophilic meningitis".)
ANGIOSTRONGYLUS COSTARICENSIS
Epidemiology — A. costaricensis is a filariform nematode that causes eosinophilic enterocolitis, a granulomatous inflammatory reaction within the intestinal wall. The appendix, distal small bowel, or right colon may be involved. (See "Eosinophilic gastrointestinal diseases".)
The life cycle of A. costaricensis begins with eggs laid by adult worms in the mesenteric arterioles of rats, the definitive hosts (figure 1). The first-stage larvae are passed in the stool and ingested by a snail or slug (intermediate host). The life cycle is completed with mollusk ingestion by the rat, and the third-stage larvae (infective larvae) migrate to the ileocecal area.
Humans can acquire the infection by eating raw or undercooked snails or slugs infected with the parasite; infection may also be transmitted by raw produce contaminated with larva-containing slug secretions. Alternatively, infection can be transmitted by ingestion of infected paratenic animals, such as crab or freshwater shrimp. In humans, worms migrate to mesenteric arteries, especially ileocecal vessels, and release eggs into the intestinal tissues. Intense endothelial damage with subsequent arteritis and thrombosis can ensue, with necrosis of adjacent enteric tissue. Colonic mass lesions due to intravascular A. costaricensis infection may develop [1]. Humans are dead-end hosts and the parasite usually dies in the gastrointestinal tract; eggs are not shed in the stool.
A. costaricensis has been reported most frequently from Central and South America and the Caribbean, especially from Costa Rica (where it was first discovered) [2]. Cases have also occurred in the United States and elsewhere [3]. It most commonly affects school-aged children and young adults [3].
Clinical manifestations — Many infections are asymptomatic. For symptomatic patients, clinical manifestations are variable. Depending on the severity of the inflammatory reaction within the bowel wall, manifestations may include fever, abdominal pain, anorexia, vomiting, constipation, bowel obstruction, mesenteric ischemia, or perforation [3-5]. Patients often have clinical signs similar to those of acute appendicitis, corresponding to an eosinophilic infiltrate in the ileocecal region. However, the presentation can be indolent, with relapsing episodes of abdominal pain recurring over several months. Presentation with recurrent gastrointestinal bleeding or intestinal perforation have been described [5,6]. A tumor-like mass is frequently palpable in the right lower quadrant on abdominal examination.
Rarely, eggs and larvae can be carried to extraintestinal sites [2,7,8]. When this occurs, mesenteric lymph node enlargement, testicular involvement with pain and erythema, or hepatic lesions causing tender hepatomegaly can result.
The incubation period is uncertain; it is estimated to range from three weeks to several months [3].
Diagnosis — Definitive diagnosis may be established by identifying the organism on histopathologic examination of biopsies or surgical resections (picture 1). Eggs or larvae may be observed within the tissues, or adult worms may be found in the mesenteric arterial lumen or its branches [3]. Characteristic histopathologic findings include eosinophilic infiltration of the intestinal wall, granulomatous reaction, and eosinophilic vasculitis [3].
Adult parasites measure 2 to 3.5 cm. Stool examination is not helpful since neither eggs nor larvae appear in the stool, although stool examination may be useful to exclude other potential parasitic causes, particularly Enterobius vermicularis. Enzyme-linked immunosorbent assays, immunochromatographic testing, and polymerase chain reaction assays have been developed but are not widely available [9-13].
A high-grade peripheral eosinophilia (up to 20 to 50 percent) is often present and may help to differentiate this infection from acute appendicitis.
Differential diagnosis — Other causes of eosinophilic enteritis include anisakiasis, enterobiasis, strongyloidiasis, hookworm infection and Ancylostoma caninum. (See related UpToDate topics.)
Treatment — Most patients have a self-limited course and usually can be observed with supportive care in the absence of specific medical or surgical therapy. In some cases, surgery is pursued to exclude appendicitis or other causes of pathology or to manage any complicating peritonitis.
Antiparasitic agents have not proven efficacious in any clinical trial [2]. It may be best to avoid anthelminthic therapy if the diagnosis is certain, as treatment may lead to erratic migration followed by worsening of the disease [7].
There is no clear evidence of efficacy for anti-inflammatory agents [3].
ANISAKIASIS
Epidemiology — Anisakiasis is a zoonotic roundworm infection caused by Anisakis simplex, Anisakis physeteris, Anisakis pegreffii, or Pseudoterranova species. Marine mammals (eg, whales, sea lions, seals, dolphins, porpoises, and walruses) are the natural hosts; humans are incidental hosts. The human "equivalent" of anisakiasis is ascariasis.
Anisakiasis has been described in many regions but is most common in Japan, likely because of the frequent ingestion of raw fish [14-17]. It is also known as "sushi worm," "herring worm" (Anisakis species), or "cod worm" (Pseudoterranova species). The global prevalence of anisakiasis may be underestimated, given diagnostic limitations in diagnostic tools and protean clinical manifestations [16]; reports from the Americas and from Europe are increasing, especially from Italy and Spain [18-21]. Moreover, imported fish products may cause infection, even in landlocked countries [22].
The life cycle of anisakiasis begins with passage of unembryonated eggs in the stool of marine mammals (figure 2). In the water, first- and second-stage larvae are formed; subsequently, these are ingested by crustaceans and migrate to muscle tissues. The larvae are transferred to fish and squid via predation, which maintain third-stage larvae that are infective to humans and marine mammals. Upon ingestion by marine mammals, the larvae develop into adult worms, which become embedded in the stomach mucosa and produce eggs shed in the stool.
Humans become infected by eating undercooked, raw, or pickled infected marine or infrequently fresh water derived foods [21] Worms may be present in flesh meat, gonads, liver and peritoneal cavities of multiple fish species, and less commonly in cephalopods (eg, octopus, squid), shrimp, and clams.
In the United States, products implicated include ceviche (fish and spices marinated in lime juice); lomi lomi (salmon marinated in lemon juice, onion, and tomato); poisson cru (fish marinated in citrus juice, onion, tomato, and coconut milk); herring roe; sashimi (slices of raw fish); sushi (pieces of raw fish with rice and other ingredients); green herring (lightly brined herring); drunken crabs (crabs marinated in wine and pepper); cold-smoked fish; undercooked grilled fish [23]. Sources of infections in other countries including Columbia [24], Chile [24], and globally [14-16] have been recorded [21].
In general salmon, herring, cod, mackerel, and squid transmit Anisakis species; halibut, cod, and red snapper transmit Pseudoterranova species. The larvae are grossly visible in the fish; properly trained sushi chefs can detect them. After ingestion, the larva (usually one or two) penetrates the human gastric or intestinal mucosa. Maturation begins, but the parasite dies because it is not in its natural host. The dying organism induces an inflammatory reaction, and a tissue abscess develops with a predominance of eosinophils. In some cases, the larvae perforate the wall of the intestine and form an abscess within the peritoneal cavity.
Thorough cooking to 70°C or adequate freezing to -20°C for a minimum of 72 hours are the best preventive measures [23,25].
Clinical manifestations — Sequelae of tissue invasion by larvae include gastric and intestinal involvement. In addition, allergic disease may occur in sensitized individuals in response to anasakine allergens [16,21].
●Gastric anisakiasis – Gastric anisakiasis usually develops one to eight hours after ingestion of raw fish and is characterized by acute epigastric pain, nausea, and vomiting [26]. In a study of including 165 patients with gastric anisakiasis from Japan, 22 percent were asymptomatic [27].
●Intestinal anisakiasis – Intestinal anisakiasis usually develops five to seven days following ingestion of raw fish and may be associated with severe abdominal pain, abdominal distension, and a palpable inflammatory mass that causes intestinal obstruction [26,28]. Diarrhea with blood or mucus may also develop [29]. In a study from Spain including 71 patients, abdominal pain with nausea, vomiting, and occasional fever was reported [30]. intestinal anisakiasis was initially suspected in only two cases; intestinal obstruction was suspected in 30 percent and 10 appendicitis was suspected in 21 percent. Intestinal anisakiasis may be asymptomatic; in a study of 20 patients in Korea with intestinal anisakiasis, 40 percent were asymptomatic and were found harbor colonic larvae only by screening endoscopy [31].
Anisakiasis may be associated with eosinophilic esophagitis, gastroenteritis, or enterocolitis. A syndrome mimicking appendicitis may be observed if the ileocecal region is involved [32,33]. Symptoms are vague and the illness can be misdiagnosed as appendicitis, acute abdomen, stomach ulcer, or ileitis. Anisakis larvae occasionally penetrate into the peritoneal cavity or other visceral organs (extraintestinal anisakiasis) and cause eosinophilic granuloma, which may be confused with neoplasm [28].
●Allergic disease – An IgE-mediated allergic response to proteins found in anisakis species (some which may be resistant to heat inactivation) may occur [16,34]. Immediately after ingestion of infected raw fish, sensitized individuals may develop manifestations of IgE-mediated anaphylaxis, including pruritus and tingling of the posterior oropharynx. Allergic reactions ranging from mild urticaria to bronchoconstriction, angioedema, and anaphylactic shock can occur [19,35]. Severe laryngeal edema has been described, which can be fatal [36]. Associated fever and peripheral eosinophilia are common. Symptoms usually arise acutely; a chronic relapsing course can also occur. Allergic manifestations including urticaria and anaphylaxis may develop concomitantly in those with gastric or intestinal anisakiasis [37,38]. Allergic symptoms may mimic seafood allergy. Patients with severe allergic reactions should be warned against further consumption of marine fish or squid given the potential for infection with Anisakis [39]. (See "Seafood allergies: Fish and shellfish".)
Diagnosis — Anisakiasis should be considered in patients with gastrointestinal symptoms who have ingested raw or undercooked seafood.
The diagnosis of anisakiasis can be made via visualization of the worm recovered from emesis or by endoscopy (approximately 2 to 2.5 cm by 1 to 2 mm) (picture 2) [40-42]. Larvae may be grossly visible to the naked eye of the endoscopist, or endoscopic examination may demonstrate an ulcerated bleeding lesion in the stomach or duodenum with a worm at the center.
Barium studies may demonstrate narrowing of the intestinal lumen in areas with mucosal inflammation (image 1). A thread-like filling defect suggesting a worm is visualized in some cases [43].
Computed tomography (CT) or ultrasonography may demonstrate edematous wall thickening of the gastric or intestinal mucosa, dilated loops of small bowel, hyperperistalsis, perigastric stranding, and ascites [44-48]. In gastric anisakiasis CT shows wall stratification, thickened fat stranding and ascites; in intestinal anisakiasis CT demonstrates wall thickening, often in the long segment of the ileum, as well as fat stranding and ascites [30,49].
Total and Anisakis-specific immunoglobulin E levels are often elevated, particularly in patients who develop an allergic reaction following infection [50-52]. Commercial assays are available, although they detect IgE only to some putative allergenic anisakiasis peptides [34].
Differential diagnosis — The differential diagnosis of small bowel obstruction due to anisakiasis includes tumor, Crohn disease, primary eosinophilic gastroenteritis, other parasitic infections (Strongyloides, Ascaris, Toxocara, Ancylostoma, Gnathostoma), bacterial infections (Yersinia, tuberculosis), intussusception, and ischemia.
Treatment — For the gastrointestinal infection, physical removal of the parasite (by regurgitation, endoscopy, or surgery) is curative. Symptomatic therapy is usually adequate if the worm is in the distal bowel and cannot be retrieved by endoscopy, since Anisakis larvae can only survive for a few days in the human intestinal tract. Surgery may be necessary for worms that have penetrated the intestine, omentum, liver, or pancreas [53].
Successful treatment with albendazole (400 mg orally twice daily for 3 to 21 days) has been described, sometimes with the addition of prednisolone (20 mg/day up to 1 mg/kg/day) [54-56]; data are limited.
CAPILLARIASIS — There are two major clinical syndromes of capillariasis: intestinal disease (caused by Capillaria philippinensis) and hepatic disease (caused by Capillaria hepatica). Intestinal capillariasis occurs most frequently in Thailand and the Philippines, but it has also been observed in other countries [57]. Rare cases of human infections with C. hepatica have been reported worldwide [58].
Intestinal capillariasis — Intestinal capillariasis is caused by C. philippinensis, a parasite of fish-eating birds (which seem to be the natural definitive host) [59]. Adult worms of C. philippinensis reside in the bird and human intestinal tracts (figure 3). Unembryonated eggs are passed in the stool and become embryonated in fresh water, where they are ingested by fish. Subsequently, larvae hatch, penetrate the fish intestine, and migrate to muscle tissues. Ingestion of raw or undercooked fish results in bird and/or human infections.
Unembryonated eggs can also become embryonated in the human intestine; released larvae can cause autoinfection, leading to hyperinfection (yielding a massive number of adult worms) [60]. Consequently, exposure to even a small parasite load can result in massive infection.
Clinical manifestations — Clinical symptoms associated with intestinal capillariasis include chronic watery diarrhea, abdominal pain, weight loss, malabsorption, and wasting [57]. Fever, abdominal pain, and peripheral eosinophilia may also be present. As the parasite burden increases, malabsorption can become very severe, resulting in edema and muscle wasting. Electrolyte abnormalities and protein loss result, leading to marked cachexia and cardiomyopathy. Untreated infection can lead to death within a few months [61].
Diagnosis and treatment — The diagnosis of intestinal capillariasis can be made by detecting characteristic eggs in stool specimens (picture 3). The eggs measure 45 by 20 microns with plugs at each end. Eggs may be shed intermittently, reducing the sensitivity of stool specimens. Larvae may also be found in stool specimens. In some cases, small intestine histopathology is needed to confirm the diagnosis and should be considered in cases of otherwise unexplained severe malabsorption. Enzyme-linked immunosorbent assay (ELISA), western blot, immunochromatographic lateral flow and stool polymerase chain reaction (PCR) tests have been developed but are not widely available [62-64].
Treatment for intestinal capillariasis consists of albendazole (400 mg on empty stomach either once or 200 mg twice daily, often given for 30 days [minimum 10 days]) or mebendazole (200 mg twice daily for 20 to 30 days) [65,66]; there are no randomized controlled trials evaluating the approach to therapy or optimal duration. Repeating the stool examination within a day of anthelminthic drug treatment may increase the sensitivity of a stool specimen to confirm the diagnosis [57].
Supportive therapy with fluids and nutritional supplements may be required. Relapse is common, particularly if patients do not complete the full course of therapy; in such cases, retreatment may be necessary [60]. The optimal management of relapse is uncertain; based on case reports, retreatment with albendazole or mebendazole (perhaps for a longer course if not administered for 30 days initially) is reasonable [67-69].
Hepatic capillariasis — Hepatic capillariasis is caused by C. hepatica, a parasite of rodents, dogs, pigs, and other mammals; humans are incidental hosts. Hepatic capillariasis has been described worldwide. Human infection is rare; infection is most common among children <3 years of age and is acquired by ingesting eggs in contaminated food, water, or soil [70,71].
The life cycle begins with ingestion of embryonated eggs by a suitable mammalian host (figure 4). Larvae are released in the intestine and migrate via the portal vein to the liver, where they mature into adults after about four weeks and lay eggs in the parenchyma. The adult worms in the liver are destroyed by host inflammation, but the eggs remain viable in the hepatic parenchyma. Occasionally, larvae migrate to the lungs, kidneys, or other organs.
Eggs are not passed in the stool of the host; they remain in the liver until the animal dies or is eaten by a predator. Eggs ingested by scavengers or predators are passed in the stool of these animals and embryonate in the environment after about 30 days.
Clinical manifestations — The triad of clinical manifestations includes fever, hepatomegaly, and eosinophilia [72]; symptoms also include acute or subacute hepatitis [73]. In a study of 16 patients in China with hepatic capillariasis, sustained fever was present in 56 percent, abdominal pain in 38 percent, diarrhea in 25 percent, leukocytosis in 94 percent and eosinophilia in 100 percent [73]. Large areas of parenchyma may be replaced by mass of eggs, leading to inflammation, granuloma formation, and fibrosis of the liver [74]. The clinical picture may resemble visceral larva migrans [75]. (See "Toxocariasis: Visceral and ocular larva migrans".)
Diagnosis and treatment — The diagnosis of capillariasis in humans is usually made by finding adults and eggs in liver biopsy or autopsy specimens (picture 4). Adult worms are 2.3 to 4.3 mm long with a diameter of ≥50 micrometers [74]. Larva vary in size according to stage. Eggs are 40 to 67 micrometers by 27 to 35 micrometers. Eggs are not passed in the stool of the host; identification of C. hepatica eggs in stool reflects spurious passage of ingested eggs and is not diagnostic of clinical infection.
Imaging with ultrasound, computed tomography, or magnetic resonance imaging examinations show hepatomegaly and nodular hypoechoic or mixed hypo-/hyperechoic liver lesions, often with irregular peripheral enhancement [73]. Serologic tests (indirect fluorescent antibody and ELISA) and PCR have been developed but are not widely available [76].
The optimal treatment is uncertain. Albendazole (400 mg twice daily for at least two weeks) and thiabendazole have been used successfully in some cases [77,78], often in combination with corticosteroids. Albendazole acts on adult worms but is not effective against the eggs, so adding corticosteroids may reduce the associated inflammatory response [72].
DIROFILARIASIS — Dirofilariasis is caused by a zoonotic filarial nematode. The life cycle of dirofilariasis begins when an infected mosquito (Aedes, Culex, Anopheles, Mansonia) takes a blood meal, introducing third-stage (L3) filarial larvae (figure 5). Usually, a domestic dog or coyote is infected, although a wide variety of other animals can be infected including cats, weasels, aquatic mammals, beaver, horses, and humans. The L3 larvae molt into L4 larvae and then adults, which reside in the subcutaneous tissues (Dirofilaria repens) or the heart of the definitive host (Dirofilaria immitis). Humans are incidental hosts; in humans, D. immitis filaria lodge in pulmonary arteries and usually cannot fully mature into gravid worms. D. repens often lodge in subcutaneous or ocular tissue.
In definitive hosts, adult worms can live for 5 to 10 years. The female worms are capable of producing microfilariae that circulate in the peripheral blood and are ingested by a mosquito during a blood meal. In the mosquito's abdomen, the microfilariae develop into L1 and subsequently into L3 larvae, which can infect another host when the mosquito takes a blood meal.
Dirofilariasis is particularly common in the Mediterranean region but has been described in many regions, including the United States, eastern Europe, and central Asia [79]. In the Americas, D. immitis is the main species; in Europe, D. repens is often the causative agent [80-82]. D. immitis has a worldwide distribution; D. repens is found in Europe, Asia, and Africa [83]. Climate change and increases in the movement of reservoirs (mostly infected dogs) have broadened the geographical range of these parasites and the risk for human infection [84].
Clinical manifestations — There are two major clinical syndromes: pulmonary dirofilariasis (caused by D. immitis) and subcutaneous or ocular dirofilariasis (caused by a few different dirofilarial species, particularly D. repens). In addition to these syndromes, there have been reports of human dirofilariasis in other sites, such as the peritoneal cavity, male genital tract, liver, buccal mucosa, or central nervous system [85-89].
A peripheral eosinophilia of approximately 10 percent may be observed but is not uniformly present [90].
Pulmonary dirofilariasis — Pulmonary dirofilariasis is caused by D. immitis (also known as the dog heartworm since it is a common cause of congestive heart failure in dogs) (figure 5). In definitive hosts, adult worms of D. immitis live in the heart. In humans, larvae lodge in small caliber pulmonary arteries and never mature into fully gravid worms. The organisms can cause pulmonary infarcts or pneumonitis with granuloma formation, which may result in the appearance of nodules or cavities on chest radiography [91,92]. The radiographic appearance is often described as a "coin lesion" that is usually 1 to 3 cm in diameter and can be confused with a lung tumor.
Most human infections are asymptomatic; often, infection is discovered incidentally when chest imaging is performed for some other reason. Some patients develop chest pain, cough, hemoptysis, fever, and malaise [93,94].
Subcutaneous dirofilariasis — Subcutaneous dirofilariasis is caused by a few different dirofilarial species, including D. repens, D. tenuis, and others (figure 6). These species are parasites of dogs and cats (D. repens), raccoons (D. tenuis), or other mammals. Adult worms can develop in humans, but sexual maturity and production of microfilariae do not occur since humans are an incidental host.
Skin lesions consist of a coiled, degenerating worm in subcutaneous tissues, typically around the eye or on the genitalia or limbs (picture 5) [95-97]. Frequently, the worm is encased in dense fibrous tissue. The nodule can be erythematous and tender and may be associated with an abscess. Concomitant allergic symptoms including urticaria and fever may also develop.
D. repens infection has also been reported as a cause of cutaneous larva migrans syndrome, with creeping eruption and elevated sinuous track under the skin [98,99].
Ocular dirofilariasis — Ocular dirofilariasis is usually caused by D. repens [81]. The conjunctiva is the most common site of nodules; involvement of the orbit (palpable mass) and eyelid have also been described [100]. The vitreous tissues may also be affected. Presentation with orbital cellulitis has been described. The vitreous tissues may also be affected causing floaters [101]. Patients often complain of discomfort, ocular pain, grittiness, and redness of the eye.
Concurrent subcutaneous and ocular D. repens infection has been described [102].
Diagnosis — Definitive diagnosis of dirofilariasis requires biopsy of the involved tissue for histopathologic identification. Dirofilaria are often 10 to 30 cm in length and 300 to 400 microns in diameter and characterized by a thick multilayered cuticle [97]. The cuticle of D. repens worms is spiked, whereas that of D immitis worms is smooth [81]. In one series of 60 patients with solitary pulmonary nodules presumed to be caused by D. immitis, 90 percent contained a single worm; occasionally, two or three worms were present in the same nodule [103]. Circulating microfilariae occasionally have been found [82,104,105].
Serology using either enzyme-linked immunosorbent assay or indirect hemagglutination is not well standardized or widely used [93,106]. Polymerase chain reaction has also been used for diagnosis and species identification but is not widely available.
Subcutaneous lesions may be examined with ultrasonography for visualization of motile worms [107,108].
Treatment — Treatment consists of simple extraction or complete surgical excision of the worm [109]. In general, no specific medical therapy for dirofilariasis is required routinely. However, treatment with ivermectin may be given, particularly in cases where microfilaremia is present. Alternatively, for D. repens infection, doxycycline may be given to target the bacterial endosymbiont Wolbachia [105,110,111]. Often, the lesions calcify without treatment [103].
DRACUNCULIASIS — Dracunculiasis (also known as guinea worm) is caused by Dracunculus medinensis. Infection is mainly transmitted by consumption of unfiltered water containing copepods (small crustaceans) infected with larvae of D. medinensis (figure 7). It may also be transmitted by eating fish or other aquatic animals [112]; these routes may be particularly important in acquisition of infection by dogs. Following ingestion, the copepods die and release larvae that penetrate the host's stomach and intestinal wall; thereafter, they enter the abdominal cavity and retroperitoneal space.
After maturation into adult worms, the males die and the females (70 to 120 cm in length) migrate in the subcutaneous tissues. Approximately one year after infection, the fertilized female worm migrates to the surface of the skin and induces a painful papule (usually on the distal lower extremity but may occur on the genitalia, buttocks, or trunk). One or more worms emerge, and the patient experiences a burning sensation. When the patient soaks the leg in fresh water to relieve the discomfort, the worm releases larvae into the water. The larvae are ingested by a copepod and become infective after two weeks (and two molts). Human ingestion of the copepods completes the cycle.
Clinical manifestations and diagnosis — Just prior to the formation of the skin papule, systemic symptoms can develop including fever, urticaria, pruritus, dizziness, nausea, vomiting, and diarrhea. The papule measures 2 to 7 cm, and pain is severe as the worm emerges (picture 6). This clinical manifestation is the basis for diagnosis. A peripheral eosinophilia may be present.
Rarely, the worm can migrate to ectopic sites, such as the lung, eye, pericardium, or spinal cord and can produce abscesses at these locations. Secondary infections can lead to systemic sepsis. Chronic arthritis and contractures can develop, particularly if the worm migrates through a joint.
In some cases, the worms die before they can emerge through the skin. In such cases, the worms eventually calcify and may be detected incidentally on radiographs or may be palpable beneath the skin [113].
Treatment — Treatment consists of slow extraction of the worm combined with wound care and pain management. The worm should be wound around a stick, extracting a few centimeters each day. It may take many weeks or months for the entire worm to be removed. If the worm is broken or not fully extracted, an intense, painful inflammatory reaction with swelling along the worm tract can develop.
Epidemiology and prevention — Dracunculiasis occurs most commonly among adults in rural settings. In 1986, an estimated 3.5 million cases occurred each year in 20 countries in Africa and Asia. In 2021, 15 cases were reported; in 2022, 13 human cases were reported [112,114,115]. Infection continues to occur in five countries. Most infections are reported from Chad, but Angola, Ethiopia, Mali, and South Sudan also are reporting cases, and Cameroon continues to be affected by imported cases.
Previously, humans were thought to be the only known host of D. medinensis; emergence of infections in animals (predominantly domestic dogs) has complicated eradication efforts. Novel transmission pathways have been postulated; these include consumption of copepods from water by dogs, consumption of infective larvae in the entrails of aquatic animals, or consumption of raw or undercooked fish containing ingested copepods carrying infective larvae [116]. The target for eradication of Dracunculiasis has been pushed to 2030 [117].
Case containment to prevent water supply contamination can prevent infection [118]. Community surveillance and education regarding the mode of transmission is important for control. Other strategies include using of nylon filters for drinking water to remove copepods, use of insecticides in drinking water sources to kill copepods, covering papules with occlusive dressings, and covering drinking water sources so that infected individuals do not immerse infectious papules to propagate infection.
However, dogs may act as alternative hosts of the worm and may serve as reservoirs of D. medinensis, which (together with insecurity and civil unrest) may thwart the final steps toward eradication [112]. Control efforts are concentrating on containment of infection in dogs, particularly in Chad where most zoonotic infections occur [112].
THELAZIASIS — Thelaziasis, also referred to as the oriental eye worm, is an ocular infection caused by Thelazia species that is transmitted by drosophilid flies that feed on lacrimal secretions. Typically affected animals include dogs, cats, wild carnivores, horses, and cattle.
In humans, thelaziasis is an uncommon zoonotic infection that has been observed in Asia, Europe and North America [119]. Most human infections are due to Thelazia callipaeda. In the western United States, infection due to Thelazia californiensis and Thelazia gulosa has been described [120,121]. Children and older adults in resource-limited settings are most frequently affected [122].
Infection is transmitted by flies that feed on lacrimal secretions of infected animals. Within the flies, larvae develop into infective third-stage larvae that can be introduced from the fly into the conjunctival sac of host. Larvae develop further over one month into adult worms that live in the conjunctival sac or lacrimal apparatus. Adult worms are 1 to 2 cm in length and are cream colored.
Clinical manifestations — As one or more adult worms develop around the eye, infected patients may experience ocular pruritus, lacrimation, exudative conjunctivitis, a foreign body sensation in the eye, hypersensitivity to light, and keratitis [123]. Presentation with periorbital swelling has also been described [124]. In severe cases, corneal ulceration and scarring may lead to blindness [125].
Diagnosis — The diagnosis of thelaziasis is usually made by visualizing one or more worms in the conjunctival sac or lacrimal secretions. Polymerase chain reaction-based diagnosis has also been described [126].
Treatment — Adult worms and larvae can be removed by rinsing the conjunctival sac with sterile saline, and adults can be removed with forceps or cotton swabs. Repeated removal may be needed when several adults reside in the lacrimal secretions [120,125]. The utility and safety of anthelminthic treatments are not documented; physical removal of adult worms is sufficient.
TRICHOSTRONGYLOSIS — Trichostrongylosis is caused by several nematodes of the Trichostrongylus species, which infect sheep, cattle, and other herbivorous mammals worldwide; humans are incidental hosts. Human infections can occur globally in pastoral settings where humans have close contact with the ruminant animals [127].
Eggs are passed in the stool of the definitive host (usually a herbivorous mammal), and rhabditiform larvae hatch within several days; they become infective filariform (third-stage) larvae after 5 to 10 days (and two molts) (figure 8). Infection is transmitted to humans by ingestion of these larvae, which mature into adults in the small intestine. Trichostrongylosis is typically transmitted by ingestion of unwashed vegetables fertilized with contaminated manure [128,129].
Occasionally, infection can occur via larval penetration of the skin. Larvae mature to adults in the small intestine, where they embed in the mucosa and cause inflammation.
Clinical manifestations — Most infections with Trichostrongylus spp are asymptomatic. In the setting of heavy infection, abdominal pain, diarrhea, and anemia can develop. Malabsorption and wasting can ensue if mucosal damage is severe. A peripheral eosinophilia may be observed.
Diagnosis — The diagnosis of trichostrongylosis is generally established by identifying characteristic eggs in the stool (picture 7). Stool concentration techniques may be needed, particularly in the setting of light infections. The diagnosis can also by identification of characteristic Trichostrongylus larvae or adult worms on endoscopic evaluation of the duodenum. Polymerase chain reaction assays have been developed but are not widely available [130,131].
Treatment — Treatment of trichostrongylosis consists of mebendazole (100 mg twice daily for three days) or albendazole (400 mg orally once on empty stomach) [128]. Pyrantel pamoate (11 mg/kg orally once; maximum dose of 1 g) can also be used.
Prevention — Fresh vegetables and salads should be washed carefully. Only dried manure should be used as an organic fertilizer [132].
SUMMARY AND RECOMMENDATIONS
●Angiostrongyliasis – Angiostrongylus costaricensis causes eosinophilic enterocolitis. The primary life cycle consists of transmission between rodents and snails or slugs; humans are incidental hosts (figure 1). The diagnosis may be established by identifying the organism on histopathological examination of biopsies or surgical resections (picture 1). Most patients have a self-limited course and usually can be observed with supportive care in the absence of specific medical or surgical therapy. (See 'Angiostrongylus costaricensis' above.)
●Anisakiasis – Anisakiasis causes gastroenteritis or enterocolitis. Anisakiasis may also elicit allergic and anaphylactic reactions in sensitized individuals. The primary life cycle consists of transmission between marine mammals, crustaceans, fish, and squid; humans are incidental hosts (figure 2). The diagnosis may be established by visualization of the worm recovered from emesis or by endoscopy (picture 2). Physical removal of the parasite (by regurgitation, endoscopy, or surgery) is curative (See 'Anisakiasis' above.).
●Capillariasis – Capillaria philippinensis causes intestinal capillariasis. The primary life cycle consists of transmission between birds and fish; humans are incidental hosts (figure 3). The diagnosis may be established by detecting characteristic eggs in stool specimens (picture 3). We suggest treatment with albendazole or mebendazole (Grade 2C); dosing is outlined above. (See 'Capillariasis' above.)
●Dirofilariasis – Dirofilariasis consists of two major clinical syndromes: pulmonary dirofilariasis (caused by Dirofilaria immitis) and subcutaneous/ocular dirofilariasis (caused by a few different species, mainly Dirofilaria repens). The primary life cycle consists of transmission between dogs and mosquitoes; humans are incidental hosts (figure 5 and figure 6). The diagnosis may be established by biopsy of the involved tissue for histopathologic identification. No specific therapy for dirofilariasis is required. (See 'Dirofilariasis' above.)
●Dracunculiasis – Dracunculiasis causes guinea worm infection. Humans were thought to be the only host; however, the majority of cases are now reported in dogs. Infection is transmitted by consumption of unfiltered water containing copepods (small crustaceans) infected with larvae of Dracunculus medinensis (figure 7). Transmission may also occur via ingestion of raw fish or other aquatic animals; these routes may be particularly important in dogs. Following ingestion, larvae penetrate the gastrointestinal tract and adult worms migrate to the subcutaneous tissues, where they induce painful papules (picture 6). Treatment consists of slow extraction of the worm combined with wound care and pain management. (See 'Dracunculiasis' above.)
●Thelaziasis – Thelaziasis is an ocular infection caused by Thelazia species that is transmitted by flies that feed on lacrimal secretions. Affected animals include dogs, cats, horses, and cattle. The diagnosis is made by visualizing one or more worms in the conjunctival sac or lacrimal secretions. Treatment consists of physical removal of the adult worms. (See 'Thelaziasis' above.)
●Trichostrongylosis – Trichostrongylosis causes asymptomatic infection or gastrointestinal illness. The primary life cycle consists of transmission between herbivorous animals; humans are incidental hosts (figure 8). The diagnosis may be established by identifying characteristic eggs in the stool (picture 7). We suggest treatment with mebendazole or albendazole (Grade 2C); dosing is outlined above. (See 'Trichostrongylosis' above.)
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