Filariasis such as loiasis most often consists of asymptomatic microfilaremia. Some patients can develop lymphatic dysfunction causing lymphedema. Episodic angioedema (Calabar swellings) in the arms and legs, caused by immune reactions are common. Calabar swellings are 3–10 cm in surface non erythematous and not pitting. When chronic, they can form cyst-like enlargements of the connective tissue around the sheaths of muscle tendons, becoming very painful when moved. The swellings may last for 1–3 days, and may be accompanied by localized urticaria (skin eruptions) and pruritus (itching). They reappear at referent locations at irregular time intervals. Subconjunctival migration of an adult worm to the eyes can also occur frequently, and this is the reason Loa loa is also called the "African eye worm." The passage over the eyeball can be sensed, but it usually takes less than 15 min. Gender incidence of eyeworms have approximately the same frequency, but it tends to increase with age. Eosinophilia is often prominent in filarial infections. Dead worms may cause chronic abscesses, which may lead to the formation of granulomatous reactions and fibrosis.

In the human host, "Loa loa" larvae migrate to the subcutaneous tissue where they mature to adult worms in approximately one year, but sometimes up to four years. Adult worms migrate in the subcutaneous tissues at a speed less than 1 cm/min, mating and producing more microfilariae. The adult worms can live up to 17 years in the human host.

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.

"Loa loa" filariasis is a skin and eye disease caused by the nematode worm "Loa loa". Humans contract this disease through the bite of a deer fly or mango fly ("Chrysops" spp), the vectors for "Loa loa". The adult "Loa loa" filarial worm migrates throughout the subcutaneous tissues of humans, occasionally crossing into subconjunctival tissues of the eye where it can be easily observed. "Loa loa" does not normally affect one's vision but can be painful when moving about the eyeball or across the bridge of the nose. The disease can cause red itchy swellings below the skin called "Calabar swellings". The disease is treated with the drug diethylcarbamazine (DEC), and when appropriate, surgical methods may be employed to remove adult worms from the conjunctiva.

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.

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.

"B. malayi" is one of the causative agents of lymphatic filariasis, a condition marked by infection and swelling of the lymphatic system. The disease is primarily caused by the presence of worms in the lymphatic vessels and the resulting host response. Signs of infection are typically consistent with those seen in bancroftian filariasis—fever, lymphadenitis, lymphangitis, lymphedema, and secondary bacterial infection—with a few exceptions.

Clinical presentation of sparganosis most often occurs after the larvae have migrated to a subcutaneous location. The destination of the larvae is often a tissue or muscle in the chest, abdominal wall, extremities, or scrotum, although other sites include the eyes, brain, urinary tract, pleura, pericardium, and spinal canal. The early stages of disease in humans are often asymptomatic, but the spargana typically cause a painful inflammatory reaction in the tissues surrounding the subcutaneous site as they grow. Discrete subcutaneous nodules develop that may appear and disappear over a period of time. The nodules usually itch, swell, turn red, and migrate, and are often accompanied by painful edema. Seizures, hemiparesis, and headaches are also common symptoms of sparganosis, especially cerebral sparganosis, and eosinophilia is a common sign. Clinical symptoms also vary according to the location of the sparganum; possible symptoms include elephantiasis from location in the lymph channels, peritonitis from location in the intestinal perforation, and brain abscesses from location in the brain. In genital sparganosis, subcutaneous nodules are present in the groin, labia, or scrotum and may appear tumor-like.

Ocular sparganosis a particularly well-described type of sparganosis. Early signs of the ocular form include eye pain, epiphora (excessive watering of the eye), and/or ptosis (drooping of the upper eyelid). Other signs include periorbital edema and/or edematous swelling that resembles Romana’s sign in Chagas disease, lacrimation, orbital cellulitis, exophthalmos (protrusion of the eyeball), and/or an exposed cornea ulcer. The most common sign at presentation is a mass lesion in the eye. If untreated, ocular sparganosis can lead to blindness.

In one case of brain infestation by "Spirometra erinaceieuropaei", a man sought treatment on suffering headaches, seizures, memory flashbacks and strange smells. Magnetic resonance imaging (MRI) scans showed a cluster of rings, initially in the right medial temporal lobe, but moving over time to the other side of the brain. The cause was not determined for four years; ultimately a biopsy was performed and a 1 cm-long tapeworm was found and removed. The patient continued to suffer symptoms.

Infections by "Mansonella perstans", while often asymptomatic, can be associated with angioedema, pruritus, fever, headaches, arthralgias, and neurologic manifestations. "Mansonella streptocerca" can manifest on the skin via pruritus, papular eruptions and pigmentation changes. "Mansonella ozzardi" can cause symptoms that include arthralgias, headaches, fever, pulmonary symptoms, adenopathy, hepatomegaly, and pruritus. Eosinophilia is often prominent in all cases of Mansonelliasis. "M. perstans" can also present with Calabar-like swellings, hives, and a condition known as Kampala, or Ugandan eye worm. This occurs when adult M. perstans invades the conjunctiva or periorbital connective tissues in the eye. "M. perstans" can also present with hydrocele in South America. However, it is often hard to distinguish between the symptoms of Mansonelliasis and other nematode infections endemic to the same areas.

Filariasis is a parasitic disease caused by an infection with roundworms of the Filarioidea type. These are spread by blood-feeding black flies and mosquitoes. This disease belongs to the group of diseases called helminthiases.

Eight known filarial nematodes use humans as their definitive hosts. These are divided into three groups according to the niche they occupy in the body:

- Lymphatic filariasis is caused by the worms "Wuchereria bancrofti", "Brugia malayi", and "Brugia timori". These worms occupy the lymphatic system, including the lymph nodes; in chronic cases, these worms lead to the syndrome of "elephantiasis".

- Subcutaneous filariasis is caused by "Loa loa" (the eye worm), "Mansonella streptocerca", and "Onchocerca volvulus". These worms occupy the subcutaneous layer of the skin, in the fat layer. "L. loa" causes "Loa loa" filariasis, while "O. volvulus" causes river blindness.

- Serous cavity filariasis is caused by the worms "Mansonella perstans" and "Mansonella ozzardi", which occupy the serous cavity of the abdomen. "Dirofilaria immitis", or the dog heartworm rarely infects humans.

The adult worms, which usually stay in one tissue, release early larval forms known as microfilariae into the host's bloodstream. These circulating microfilariae can be taken up with a blood meal by the arthropod vector; in the vector, they develop into infective larvae that can be transmitted to a new host.

Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic", depending on whether microfilariae can be found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilariae in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood.

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.

In intestinal schistosomiasis, eggs become lodged in the intestinal wall and cause an immune system reaction called a granulomatous reaction. This immune response can lead to obstruction of the colon and blood loss. The infected individual may have what appears to be a potbelly. Eggs can also become lodged in the liver, leading to high blood pressure through the liver, enlarged spleen, the buildup of fluid in the abdomen, and potentially life-threatening dilations or swollen areas in the esophagus or gastrointestinal tract that can tear and bleed profusely (esophageal varices). In rare instances, the central nervous system is affected. Individuals with chronic active schistosomiasis may not complain of typical symptoms.

Physiological reactions to "Toxocara" infection depend on the host’s immune response and the parasitic load. Most cases of "Toxocara" infection are asymptomatic, especially in adults. When symptoms do occur, they are the result of migration of second stage "Toxocara" larvae through the body.

Covert toxocariasis is the least serious of the three syndromes and is believed to be due to chronic exposure. Signs and symptoms of covert toxocariasis are coughing, fever, abdominal pain, headaches, and changes in behavior and ability to sleep. Upon medical examination, wheezing, hepatomegaly, and lymphadenitis are often noted.

High parasitic loads or repeated infection can lead to visceral larva migrans (VLM). VLM is primarily diagnosed in young children, because they are more prone to exposure and ingestion of infective eggs. "Toxocara" infection commonly resolves itself within weeks, but chronic eosinophilia may result. In VLM, larvae migration incites inflammation of internal organs and sometimes the central nervous system. Symptoms depend on the organ(s) affected. Patients can present with pallor, fatigue, weight loss, anorexia, fever, headache, rash, cough, asthma, chest tightness, increased irritability, abdominal pain, nausea, and vomiting. Sometimes the subcutaneous migration tracks of the larvae can be seen. Patients are commonly diagnosed with pneumonia, bronchospasms, chronic pulmonary inflammation, hypereosinophilia, hepatomegaly, hypergammaglobulinaemia (IgM, IgG, and IgE classes), leucocytosis, and elevated anti-A and –B isohaemagglutinins. Severe cases have occurred in people who are hypersensitive to allergens; in rare cases, epilepsy, inflammation of the heart, pleural effusion, respiratory failure, and death have resulted from VLM.

Ocular larva migrans (OLM) is rare compared with VLM. A light "Toxocara" burden is thought to induce a low immune response, allowing a larva to enter the host’s eye. Although there have been cases of concurrent OLM and VLM, these are extremely exceptional. OLM often occurs in just one eye and from a single larva migrating into and encysting within the orbit. Loss of vision occurs over days or weeks. Other signs and symptoms are red eye, white pupil, fixed pupil, retinal fibrosis, retinal detachment, inflammation of the eye tissues, retinal granulomas, and strabismus. Ocular granulomas resulting from OLM are frequently misdiagnosed as retinoblastomas. "Toxocara" damage in the eye is permanent and can result in blindness.

A case study published in 2008 supported the hypothesis that eosinophilic cellulitis may also be caused by infection with "Toxocara". In this study, the adult patient presented with eosinophilic cellulitis, hepatosplenomegaly, anemia, and a positive ELISA for "T. cani"s.

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.

Infection first presents with severe abdominal pain, nausea, vomiting, and weakness, which gradually lessens and progresses to fever, and then to CNS symptoms and severe headache and stiffness of the neck.

CNS symptoms begin with mild cognitive impairment and slowed reactions, and in a very severe form often progress to unconsciousness. Patients may present with neuropathic pain early in the infection. Eventually severe infection will lead to ascending weakness, quadriparesis, areflexia, respiratory failure, and muscle atrophy, and will lead to death if not treated. Occasionally patients present with cranial nerve palsies, usually in nerves 7 and 8, and rarely larvae will enter ocular structures. Even with treatment, damage to the CNS may be permanent and result in a variety of negative outcomes depending on the location of the infection, and the patient may suffer chronic pain as a result of infection.

The tsetse fly bite erupts into a red chancre sore and within a few weeks, the person can experience fever, swollen lymph glands, blood in urine, aching muscles and joints, headaches and irritability. In the first phase, the patient has only intermittent bouts of fever with lymphadenopathy together with other non-specific signs and symptoms. The second stage of the disease is marked by involvement of the central nervous system with extensive neurological effects like changes in personality, alteration of the biological clock (the circadian rhythm), confusion, slurred speech, seizures and difficulty in walking and talking. These problems can develop over many years and if not treated, the person dies. It is common to the African continent.

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.

Wuchereria bancrofti is a human parasitic roundworm that is the major cause of lymphatic filariasis. It is one of the three parasitic worms, together with "Brugia malayi" and "B. timori", that infect the lymphatic system to cause lymphatic filariasis. These filarial worms are spread by a variety of mosquito vector species. "W. bancrofti" is the most prevalent of the three and affects over 120 million people, primarily in Central Africa and the Nile delta, South and Central America, the tropical regions of Asia including southern China, and the Pacific islands. If left untreated, the infection can develop into a chronic disease called elephantiasis. In rare conditions it also causes tropical eosinophilia, an asthmatic disease. There is no commercially available vaccine however high rates of cure have been achieved with various anti-filarial regimens and lymphatic filariasis is the target of the WHO Global Program to Eliminate Lymphatic Filariasis with the aim to eradicate the disease as a public health problem by 2020.

In humans, this parasitic infection causes a variety of symptoms, depending on where the cyst occurs. The tapeworm larvae group together to form fluid filled cysts in various body tissues. These cysts start out small, but as the larvae grow, the cyst can reach the size of an egg. The cysts of "T. multiceps" are usually between 2 and 6 cm in diameter and are most commonly found in the CNS and can contain anywhere from a few to over a hundred worm larvae within them. "T serialis" and "T. glomerata" cysts present in the CNS, muscles, or subcutaneous tissue, and "T. brauni" cysts occupy these same areas but occur in the eye more frequently than the other three species.

When the cyst occurs in the brain, as it often does, the infected individual may experience headaches, seizures, vomiting, paralysis affecting one side of the body (hemiplegia), paralysis involving one limb (monoplegia), and loss of ability to coordinate muscles and muscle movements. Many of these symptoms are due to the buildup of inter-cranial pressure from the growing cyst or from the cyst pressing on other parts of brain.

When the cyst occurs in the spinal cord, it can cause severe pain and inflammation, and loss of feeling in some nerves.

When the cyst occurs in the eyes, it causes decreased vision and headaches.

In the muscular and subcutaneous tissues, the cyst causes disfiguring nodules that can protrude out of the body. These nodules can be painful, uncomfortable, and can cause loss of muscle function.

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.

A few days after ingestion epigastric pain, fever, vomiting, and loss of appetite resulting from migration of larvae through intestinal wall to the abdominal cavity will appear in the patient. Migration in the subcutaneous tissues (under the skin) causes intermittent, migratory, painful, pruritic swellings (cutaneous larva migrans). Patches of edema appear after the above symptoms clear and are usually found on the abdomen. These lesions vary in size and can be accompanied by pruritus, rash, and stabbing pain. Swellings may last for 1 to 4 weeks in a given area and then reappear in a different location. Migration to other tissues (visceral larva migrans), can result in cough, hematuria, ocular (eye) involvement, meningitis, encephalitis and eosinophilia. Eosinophilic myeloencephalitis may also result from invasion of the central nervous system by the larvae.

The incubation period for "Toxocara canis" and "cati" eggs depends on temperature and humidity. "T. canis" females, specifically, are capable of producing up to 200,000 eggs a day that require 2-6 weeks minimum up to a couple months before full development into the infectious stage. Under ideal summer conditions, eggs can mature to the infective stage after two weeks outside of a host. Provided sufficient oxygen and moisture availability, "Toxocara" eggs can remain infectious for years, as their resistant outer shell enables the protection from most environmental threats.However, as identified in a case study presented within the journal of helminthology, the second stage of larvae development poses strict vulnerabilities to certain environmental elements. High temperatures and low moisture levels will quickly degrade the larvae during this stage of growth.

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.

Because the larvae are in an abnormal host, they do not mature to adults but instead migrate

through the skin until killed by the host's inflammatory response. This migration causes

local intense itching and a red serpiginous lesion. Treatment with a single dose of oral ivermectin results in cure rates of 94–100%.