Many individuals do not experience symptoms. If symptoms do appear, they usually take from four to six weeks from the time of infection. The first symptom of the disease may be a general feeling of illness. Within twelve hours of infection, an individual may complain of a tingling sensation or light rash, commonly referred to as "swimmer's itch", due to irritation at the point of entrance. The rash that may develop can mimic scabies and other types of rashes. Other symptoms can occur two to ten weeks later and can include fever, aching, a cough, diarrhea, chills or gland enlargement. These symptoms can also be related to avian schistosomiasis, which does not cause any further symptoms in humans.

The manifestations of schistosomal infection vary over time as the cercariae, and later adult worms and their eggs migrate through the body. If eggs migrate to the brain or spinal cord, seizures, paralysis, or spinal cord inflammation are possible.

Dracunculiasis is diagnosed by seeing the worms emerging from the lesions on the legs of infected individuals and by microscopic examinations of the larvae.

As the worm moves downwards, usually to the lower leg, through the subcutaneous tissues, it leads to intense pain localized to its path of travel. The burning sensation experienced by infected people has led to the disease being called "the fiery serpent". Other symptoms include fever, nausea, and vomiting. Female worms cause allergic reactions during blister formation as they migrate to the skin, causing an intense burning pain. Such allergic reactions produce rashes, nausea, diarrhea, dizziness, and localized edema. When the blister bursts, allergic reactions subside, but skin ulcers form, through which the worm can protrude. Only when the worm is removed is healing complete. Death of adult worms in joints can lead to arthritis and paralysis in the spinal cord.

The first potential reaction is an itchy, papular rash that results from cercariae penetrating the skin, often in a person's first infection. The round bumps are usually one to three centimeters across. Because people living in affected areas have often been repeatedly exposed, acute reactions are more common in tourists and migrants. The rash can occur between the first few hours and a week after exposure and lasts for several days. A similar, more severe reaction called "swimmer's itch" reaction can also be caused by cercariae from animal trematodes that often infect birds.

Most conditions of STH have a light worm burden and usually have no discernible symptoms. Heavy infections however cause a range of health problems, including abdominal pain, diarrhoea, blood and protein loss, rectal prolapse, and physical and mental retardation.

Severe ascariasis is typically a pneumonia, as the larvae invades lungs, producing fever, cough and dyspnoea during early stage of infection.

Hookworm infections insinuate a skin reaction (dermatitis), increased white blood cells (eosinophils), a pulmonary reaction (pneumonitis), and skin rash (urticarial).

Iron deficiency anaemia due to blood loss is a common symptom.

Symptoms becomes evident only when the intensity of infection is relatively high. Thus the degree of negative outcomes is directly related to worm burden; more worms means greater severity of disease.

The symptoms of leishmaniasis are skin sores which erupt weeks to months after the person is bitten by infected sand flies.

Leishmaniasis may be divided into the following types:

- Cutaneous leishmaniasis is the most common form, which causes an open sore at the bite sites, which heals in a few months to a year and half, leaving an unpleasant-looking scar. Diffuse cutaneous leishmaniasis produces widespread skin lesions which resemble leprosy, and may not heal on its own.

- Mucocutaneous leishmaniasis causes both skin and mucosal ulcers with damage primarily of the nose and mouth.

- Visceral leishmaniasis or "kala-azar" ('black fever') is the most serious form, and is potentially fatal if untreated. Other consequences, which can occur a few months to years after infection, include fever, damage to the spleen and liver, and anemia.

Leishmaniasis is considered one of the classic causes of a markedly enlarged (and therefore palpable) spleen; the organ, which is not normally felt during examination of the abdomen, may even become larger than the liver in severe cases.

There are no specific symptoms or signs of hookworm infection, but they give rise to a combination of intestinal inflammation and progressive iron-deficiency anemia and protein deficiency. Coughing, chest pain, wheezing, and fever will sometimes result from severe infection. Epigastric pains, indigestion, nausea, vomiting, constipation, and diarrhea can occur early or in later stages as well, although gastrointestinal symptoms tend to improve with time. Signs of advanced severe infection are those of anemia and protein deficiency, including emaciation, cardiac failure and abdominal distension with ascites.

Larval invasion of the skin (mostly in the Americas) can produce a skin disease called cutaneous larva migrans also known as "creeping eruption". The hosts of these worms are not human and the larvae can only penetrate the upper five layers of the skin, where they give rise to intense, local itching, usually on the foot or lower leg, known as "ground itch". This infection is due to larvae from the "A. Braziliense" hookworm. The larvae migrate in tortuous tunnels between the "stratum basale" and "stratum corneum" of the skin, causing serpiginous vesicular lesions. With advancing movement of the larvae, the rear portions of the lesions become dry and crusty. The lesions are typically intensely itchy.

The term "hookworm" is sometimes used to refer to hookworm infection. A hookworm is a type of parasitic worm (helminth).

The most spectacular symptom of lymphatic filariasis is elephantiasis, a stage 3 lymphedema with thickening of the skin and underlying tissues. This was the first mosquito-borne disease to be discovered. Elephantiasis results when the parasites lodge in the lymphatic system and cause blockages to the flow of lymph. Infections usually begin in childhood.

The skin condition the disease causes is called "elephantiasis tropica" (also known as "elephantiasis arabum").

Elephantiasis mainly affects the lower extremities; the ears, mucous membranes, and amputation stumps are affected less frequently. However, various species of filarial worms tend to affect different parts of the body: "Wuchereria bancrofti" can affect the arms, breasts, legs, scrotum, and vulva (causing hydrocele formation), while "Brugia timori" rarely affects the genitals. Those who develop the chronic stages of elephantiasis are usually amicrofilaraemic and often have adverse immunological reactions to the microfilariae as well as the adult worms.

The subcutaneous worms present with skin rashes, urticarial papules, and arthritis, as well as hyper- and hypopigmentation macules. "Onchocerca volvulus" manifests itself in the eyes, causing "river blindness" (onchocerciasis), one of the leading causes of blindness in the world.

Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in addition to abdominal pain, because these worms are also deep-tissue dwellers.

Elephantiasis leads to marked swelling of the lower half of the body.

African trypanosomiasis symptoms occur in two stages. The first stage, known as the hemolymphatic phase, is characterized by fever, headaches, joint pains, and itching. Fever is intermittent, with attacks lasting from a day to a week, separated by intervals of a few days to a month or longer. Invasion of the circulatory and lymphatic systems by the parasites is associated with severe swelling of lymph nodes, often to tremendous sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. Occasionally, a chancre (red sore) will develop at the location of the tsetse fly bite. If left untreated, the disease overcomes the host's defenses and can cause more extensive damage, broadening symptoms to include anemia, endocrine, cardiac, and kidney dysfunctions.

The second phase of the disease, the neurological phase, begins when the parasite invades the central nervous system by passing through the blood–brain barrier. Disruption of the sleep cycle is a leading symptom of this stage and is the one that gave the disease the name 'sleeping sickness.' Infected individuals experience a disorganized and fragmented 24-hour rhythm of the sleep-wake cycle, resulting in daytime sleep episodes and nighttime periods of wakefulness.

Other neurological symptoms include confusion, tremor, general muscle weakness, hemiparesis and paralysis of a limb. Parkinson-like movements might arise due to non-specific movement disorders and speech disorders. Individuals may also exhibit psychiatric symptoms such as irritability, psychotic reactions, aggressive behaviour, or apathy which can sometimes dominate the clinical diagnosis. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma, systemic organ failure, and death. An untreated infection with "T. b. rhodesiense" will cause death within months whereas an untreated infection with "T. b. gambiense" will cause death after several years. Damage caused in the neurological phase is irreversible.

Tropical diseases are diseases that are prevalent in or unique to tropical and subtropical regions. The diseases are less prevalent in temperate climates, due in part to the occurrence of a cold season, which controls the insect population by forcing hibernation. However, many were present in northern Europe and northern America in the 17th and 18th centuries before modern understanding of disease causation. The initial impetus for tropical medicine was to protect the health of colonialists, notably in India under the British Raj. Insects such as mosquitoes and flies are by far the most common disease carrier, or vector. These insects may carry a parasite, bacterium or virus that is infectious to humans and animals. Most often disease is transmitted by an insect "bite", which causes transmission of the infectious agent through subcutaneous blood exchange. Vaccines are not available for most of the diseases listed here, and many do not have cures.

Human exploration of tropical rainforests, deforestation, rising immigration and increased international air travel and other tourism to tropical regions has led to an increased incidence of such diseases.

Dracunculiasis, also called Guinea-worm disease (GWD), is an infection by the Guinea worm. A person becomes infected when they drink water that contains water fleas infected with guinea worm larvae. Initially there are no symptoms. About one year later, the person develops a painful burning feeling as the female worm forms a blister in the skin, usually on a lower limb. The worm then emerges from the skin over the course of a few weeks. During this time, it may be difficult to walk or work. It is very uncommon for the disease to cause death.

In humans, the only known cause is "Dracunculus medinensis". The worm is about one to two millimeters wide, and an adult female is 60 to 100 centimeters long (males are much shorter at ). Outside of humans, the young form can survive up to three weeks, during which they must be eaten by water fleas to continue to develop. The larva inside water fleas may survive up to four months. Thus, in order for the disease to remain in an area, it must occur each year in humans. A diagnosis of the disease can usually be made based on the signs and symptoms.

Prevention is by early diagnosis of the disease followed by keeping the person from putting the wound in drinking water to decrease spread of the parasite. Other efforts include improving access to clean water and otherwise filtering water if it is not clean. Filtering through a cloth is often enough. Contaminated drinking water may be treated with a chemical called temefos to kill the larva. There is no medication or vaccine against the disease. The worm may be slowly removed over a few weeks by rolling it over a stick. The ulcers formed by the emerging worm may get infected by bacteria. Pain may continue for months after the worm has been removed.

In 2015 there were 22 reported cases of the disease while in 2016 there were 25. This is down from an estimated 3.5 million cases in 1986. In 2016 the disease occurred in three countries, all in Africa, down from 20 countries in the 1980s. It will likely be the first parasitic disease to be globally eradicated. Guinea worm disease has been known since ancient times. The method of removing the worm is described in the Egyptian medical Ebers Papyrus, dating from 1550 BC. The name dracunculiasis is derived from the Latin "affliction with little dragons", while the name "guinea worm" appeared after Europeans saw the disease on the Guinea coast of West Africa in the 17th century. Other "Dracunculus" species are known to infect various mammals, but do not appear to infect humans. Dracunculiasis is classified as a neglected tropical disease. Because dogs may also become infected, the eradication program is monitoring and treating dogs as well.

Adult worms remain in subcutaneous nodules, limiting access to the host's immune system. Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. "Wolbachia" species have been found to be endosymbionts of "O. volvulus" adults and microfilariae, and are thought to be the driving force behind most of "O. volvulus" morbidity. Dying microfilariae have been recently discovered to release "Wolbachia" surface protein that activates TLR2 and TLR4, triggering innate immune responses and producing the inflammation and its associated morbidity. The severity of illness is directly proportional to the number of infected microfilariae and the power of the resultant inflammatory response.

Skin involvement typically consists of intense itching, swelling, and inflammation. A grading system has been developed to categorize the degree of skin involvement:

- Acute papular onchodermatitis – scattered pruritic papules

- Chronic papular onchodermatitis – larger papules, resulting in hyperpigmentation

- Lichenified onchodermatitis – hyperpigmented papules and plaques, with edema, lymphadenopathy, pruritus and common secondary bacterial infections

- Skin atrophy – loss of elasticity, the skin resembles tissue paper, 'lizard skin' appearance

- Depigmentation – 'leopard skin' appearance, usually on anterior lower leg

- Glaucoma effect – eyes malfunction, begin to see shadows or nothing

Ocular involvement provides the common name associated with onchocerciasis, river blindness, and may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve. The microfilariae migrate to the surface of the cornea. Punctate keratitis occurs in the infected area. This clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time, the entire cornea may become opaque, thus leading to blindness. Some evidence suggests the effect on the cornea is caused by an immune response to bacteria present in the worms.

The skin is itchy, with severe rashes permanently damaging patches of skin.

Neglected tropical diseases (NTDs) are a diverse group of tropical infections which are especially common in low-income populations in developing regions of Africa, Asia, and the Americas. They are caused by a variety of pathogens such as viruses, bacteria, protozoa and helminths. These diseases are contrasted with the big three diseases (HIV/AIDS, tuberculosis, and malaria), which generally receive greater treatment and research funding. In sub-Saharan Africa, the effect of these diseases as a group is comparable to malaria and tuberculosis. NTD co-infection can also make HIV/AIDS and tuberculosis more deadly.

In some cases, the treatments are relatively inexpensive. For example, the treatment for schistosomiasis is US$0.20 per child per year. Nevertheless, in 2010 it was estimated that control of neglected diseases would require funding of between US$2 billion and US$3 billion over the subsequent five to seven years. Some pharmaceutical companies have committed to donating all the drug therapies required, and mass drug administration (for example mass deworming) has been successfully accomplished in several countries. However, preventive measures are often more accessible in the developed world, but not universally available in poorer areas.

Within developed countries, neglected tropical diseases affect the very poorest in society. In the United States, there are up to 1.46 million families including 2.8 million children living on less than two dollars a day. In countries such as these, the burdens of neglected tropical diseases are often overshadowed by other public health issues. However, many of the same issues put populations at risk in developed as developing nations. For example, from poverty stem problems such as lack of adequate housing, thus exposing individuals to the vectors of these diseases.

Twenty neglected tropical diseases are prioritized by the World Health Organization (WHO), though other organizations define NTDs differently. Chromoblastomycosis and other deep mycoses, scabies and other ectoparasites and snakebite envenoming were added to the list in 2017. These diseases are common in 149 countries, affecting more than 1.4 billion people (including more than 500 million children) and costing developing economies billions of dollars every year. They resulted in 142,000 deaths in 2013—down from 204,000 deaths in 1990. Of these 20, two were targeted for eradication (dracunculiasis (guinea-worm disease) by 2015 and yaws by 2020), and four for elimination (blinding trachoma, human African trypanosomiasis, leprosy and lymphatic filariasis by 2020).

The signs and symptoms of helminthiasis depend on a number of factors including: the site of the infestation within the body; the type of worm involved; the number of worms and their volume; the type of damage the infesting worms cause; and, the immunological response of the body. Where the burden of parasites in the body is light, there may be no symptoms.

Certain worms may cause particular constellations of symptoms. For instance, taeniasis can lead to seizures due to neurocysticercosis.

Leishmaniasis is a disease caused by parasites of the "Leishmania" type. It is spread by the bite of certain types of sandflies. The disease can present in three main ways: cutaneous, mucocutaneous, or visceral leishmaniasis. The cutaneous form presents with skin ulcers, while the mucocutaneous form presents with ulcers of the skin, mouth, and nose, and the visceral form starts with skin ulcers and then later presents with fever, low red blood cells, and enlarged spleen and liver.

Infections in humans are caused by more than 20 species of "Leishmania". Risk factors include poverty, malnutrition, deforestation, and urbanization. All three types can be diagnosed by seeing the parasites under the microscope. Additionally, visceral disease can be diagnosed by blood tests.

Leishmaniasis can be partly prevented by sleeping under nets treated with insecticide. Other measures include spraying insecticides to kill sandflies and treating people with the disease early to prevent further spread. The treatment needed is determined by where the disease is acquired, the species of "Leishmania", and the type of infection. Some possible medications used for visceral disease include liposomal amphotericin B, a combination of pentavalent antimonials and paromomycin, and miltefosine. For cutaneous disease, paromomycin, fluconazole, or pentamidine may be effective.

About 4 to 12 million people are currently infected in some 98 countries. About 2 million new cases and between 20 and 50 thousand deaths occur each year. About 200 million people in Asia, Africa, South and Central America, and southern Europe live in areas where the disease is common. The World Health Organization has obtained discounts on some medications to treat the disease. It is classified as a neglected tropical disease. The disease may occur in a number of other animals, including dogs and rodents.

This is an unusual form of epidemic epilepsy associated with onchocerciasis. This syndrome was first described in Tanzania by Louise Jilek-Aall, a Norwegian psychiatric doctor in Tanzanian practice, during the 1960s. It occurs most commonly in Uganda and South Sudan. It manifests itself in previously healthy 5–15-year-old children, is often triggered by eating or low temperatures and is accompanied by cognitive impairment. Seizures occur frequently and may be difficult to control. The electroencephalogram is abnormal but cerebrospinal fluid (CSF) and magnetic resonance imaging (MRI) are normal or show non-specific changes. If there are abnormalities on the MRI they are usually present in the hippocampus. Polymerase chain reaction testing of the CSF does not show the presence of the parasite.

Light infestations (<100 worms) frequently have no symptoms. Heavier infestations, especially in small children, can present gastrointestinal problems including abdominal pain and distension, bloody or mucus-filled diarrhea, and tenesmus (feeling of incomplete defecation, generally accompanied by involuntary straining). Mechanical damage to the intestinal mucosa may occur, as well as toxic or inflammatory damage to the intestines of the host. While appendicitis may be brought on by damage and edema of the adjacent tissue, if there are large numbers of worms or larvae present, it has been suggested that the embedding of the worms into the ileocecal region may also make the host susceptible to bacterial infection. A severe infection with high numbers of embedded worms in the rectum leads to edema, which can cause rectal prolapse, although this is typically only seen in small children. The prolapsed, inflamed and edematous rectal tissue may even show visible worms.

Growth retardation, weight loss, nutritional deficiencies, and anemia (due to long-standing blood loss) are also characteristic of infection, and these symptoms are more prevalent and severe in children. It does not commonly cause eosinophilia.

Coinfection of "T. trichiura" with other parasites is common and with larger worm burdens can cause both exacerbation of dangerous trichuriasis symptoms such as massive gastrointestinal bleeding (shown to be especially dramatic with coinfection with "Salmonella typhi") and exacerbation of symptoms and pathogenesis of the other parasitic infection (as is typical with coinfection with "Schistosoma mansoni", in which higher worm burden and liver egg burden is common). Parasitic coinfection with HIV/AIDS, tuberculosis, and malaria is also common, especially in Sub-saharan Africa, and helminth coinfection adversely affects the natural history and progression of HIV/AIDS, tuberculosis, and malaria and can increase clinical malaria severity. In a study performed in Senegal, infections of soil-transmitted helminths like "T. trichiura" (as well as schistosome infections independently) showed enhanced risk and increased the incidence of malaria.

Heavy infestations may have bloody diarrhea. Long-standing blood loss may lead to iron-deficiency anemia. Vitamin A deficiency may also result due to infection.

In extreme cases of intestinal infestation, the mass and volume of the worms may cause the outer layers of the intestinal wall, such as the muscular layer, to tear. This may lead to peritonitis, volvulus, and gangrene of the intestine.

Lymphadenitis, the swelling of the lymph nodes, is a commonly recognized symptom of many diseases. An early manifestation of filariasis, lymphadenitis more frequently occurs in the inguinal area during "B. malayi" infection and can occur before the worms mature.

When adult worms attach to the villi of the small intestine, they suck on the host's blood, which may cause abdominal pain, diarrhea, cramps, and weight loss that can lead to anorexia. Heavy infections can lead to the development of iron deficiency and hypochromic microcytic anemia. This form of anemia in children can give rise to physical and mental retardation. Infection caused by cutaneous larvae migrans, a skin disease in humans, is characterized by skin ruptures and severe itching.

Response to infection by "Leishmania donovani" varies a great deal, not only by the strength but also by the type of the patient's immune reaction. People with a history of infection by strains of leishmania that cause visceral leishmaniasis show a continuum of immune responses from protective to non-protective. Those who acquired protective immunity (skin test positive) without ever having visceral leishmaniasis have a strong type 1 CD4+ response to leishmania antigens. Antigen specific interferon-gamma and proliferation, as well as the ability to kill intracellular leishmania, are hallmarks of protective immunity. Because visceral leishmaniasis patients lack these responses to leishmania and other antigens, they usually die of secondary infections if left untreated. In addition, increased interleukin-10 secretion is characteristic of the disease. Addition of interleukin-12, anti-interleukin-10, or anti-interleukin-4 to peripheral blood mononuclear cells from acute patients sometimes increases interferon-gamma secretion and proliferation. Acute patient peripheral blood mononuclear cells include CD8+ T regulatory cells that decrease interferon-gamma secretion and proliferation responses to leishmania and other antigens and increase interleukin-10 secretion when added to autologous peripheral blood mononuclear cells harvested after successful treatment. Thus, the CD8+ T regulatory cells reproduce the immune response characteristic of visceral leishmaniasis. CD8+ T regulatory cells are also associated with post kala azar dermal leishmaniasis. Addition of interleukin-12 or interferon-gamma does not prevent CD8+ T regulatory activity. The dominance of type 1 CD4+ T cells in skin test positive adults maybe explained by their secretion of factors that inhibit and kill CD8+ T regulatory cells. Successfully treated patients rarely develop visceral leishmaniasis a second time. Their peripheral blood mononuclear cells show a mixed T1/T2 CD4+ and CD8+ T suppressor response but do have the ability to kill intracellular leishmania.

When people develop visceral leishmaniasis, the most typical symptoms are fever and the enlargement of the spleen, with enlargement of the liver sometimes being seen as well. The blackening of the skin that gave the disease its common name in India does not appear in most strains of the disease, and the other symptoms are very easy to mistake for those of malaria. Misdiagnosis is dangerous, as without proper treatment the mortality rate for kala-azar is close to 100%. "L. donovani" itself is not usually the direct cause of death in kala-azar sufferers, however. Pneumonia, tuberculosis, and dysentery are omnipresent in the depressed regions where leishmaniasis thrives, and, as with AIDS, it is these opportunistic infections that are more likely to kill, flaring up in a host whose immune system has been weakened by the "L. donovani" infection. Progress of the disease is extremely variable, taking anywhere from one to twenty weeks, but a typical duration for the Sudanese strain of the disease is narrower, between twelve and sixteen weeks.

Even with recovery, kala-azar does not always leave its hosts unmarked. Some time after successful treatment—generally a few months with African kala-azar, or as much as several years with the Indian strain—a secondary form of the disease may set in, called post kala-azar dermal leishmaniasis, or PKDL. This condition manifests first as small, measle-like skin lesions on the face, which gradually increase in size and spread over the body. Eventually the lesions may coalesce to form disfiguring, swollen structures resembling leprosy, and occasionally causing blindness if they spread to the eyes. (This disease is not the same as cutaneous leishmaniasis, a milder disease caused by another protozoan of the Leishmania genus which also causes skin lesions.)

Lymphangitis is the inflammation of the lymphatic vessels in response to infection. It occurs early in the course of infection in response to worm development, molting, death, or bacterial and fungal infection. The affected lymphatic vessel becomes distended and tender, and the overlying skin becomes erythemous and hot. Abscess formation and ulceration of the affected lymph node occasionally occurs during "B. malayi infection", more readily than in Bancroftian filariasis. Remnants of adult worms can sometimes be found in the ulcer drainage.

Lymphatic filariasis, also known as elephantiasis, is a human disease caused by parasitic worms known as filarial worms. Most cases of the disease have no symptoms. Some people, however, develop a syndrome called elephantiasis, which is marked by severe swelling in the arms, legs, breasts, or genitals. The skin may become thicker as well, and the condition may become painful. The changes to the body may harm the affected person's social and economic situation.

The worms are spread by the bites of infected mosquitoes. Three types of worms are known to cause the disease: "Wuchereria bancrofti", "Brugia malayi", and "Brugia timori", with "Wuchereria bancrofti" being the most common. These worms damage the lymphatic system. The disease is diagnosed by microscopic examination of blood collected during the night. The blood is typically examined as a smear after being stained with Giemsa stain. Testing the blood for antibodies against the disease may also permit diagnosis. Other roundworms from the same family are responsible for river blindness.

Prevention can be achieved by treating entire groups in which the disease exists, known as mass deworming. This is done every year for about six years, in an effort to rid a population of the disease entirely. Medications used include antiparasitics such as albendazole with ivermectin, or albendazole with diethylcarbamazine. The medications do not kill the adult worms but prevent further spread of the disease until the worms die on their own. Efforts to prevent mosquito bites are also recommended, including reducing the number of mosquitoes and promoting the use of bed nets.

In 2015 about 38.5 million people were infected. About 950 million people are at risk of the disease in 54 countries. It is most common in tropical Africa and Asia. Lymphatic filariasis is classified as a neglected tropical diseases and one of the four main worm infections. The disease results in economic losses of many billions of dollars a year.

Strongyloides infection occurs in five forms. On acquiring the infection, there may be respiratory symptoms (Löffler's syndrome). The infection may then become chronic with mainly digestive symptoms. On reinfection (when larvae migrate through the body), there may be respiratory, skin and digestive symptoms. Finally, the hyperinfection syndrome causes symptoms in many organ systems, including the central nervous system.