As of 2009, loiasis is endemic to 11 countries, all in western or central Africa, and an estimated 12–13 million people have the disease. The highest incidence is seen in Cameroon, Republic of the Congo, Democratic Republic of Congo, Central African Republic, Nigeria, Gabon, and Equatorial Guinea. The rates of "Loa loa" infection are lower but it is still present in and Angola, Benin, Chad and Uganda. The disease was once endemic to the western African countries of Ghana, Guinea, Guinea Bissau, Ivory Coast and Mali but has since disappeared.

Throughout "Loa loa"-endemic regions, infection rates vary from 9 to 70 percent of the population. Areas at high risk of severe adverse reactions to mass treatment (with Ivermectin) are at present determined by the prevalence in a population of >20% microfilaremia, which has been recently shown in eastern Cameroon (2007 study), for example, among other locales in the region.

Endemicity is closely linked to the habitats of the two known human loiasis vectors, "Chrysops dimidiata" and "C. silicea".

Cases have been reported on occasion in the United States but are restricted to travelers who have returned from endemic regions.

In the 1990s, the only method of determining "Loa loa" intensity was with microscopic examination of standardized blood smears, which is not practical in endemic regions. Because mass diagnostic methods were not available, complications started to surface once mass ivermectin treatment programs started being carried out for onchocerciasis, another filariasis. Ivermectin, a microfilaricidal drug, may be contraindicated in patients who are co-infected with loiasis and have associated high microfilarial loads. The theory is that the killing of massive numbers of microfilaria, some of which may be near the ocular and brain region, can lead to encephalopathy. Indeed, cases of this have been documented so frequently over the last decade that a term has been given for this set of complication: neurologic serious adverse events (SAEs).

Advanced diagnostic methods have been developed since the appearance the SAEs, but more specific diagnostic tests that have been or are currently being development (see: Diagnostics) must to be supported and distributed if adequate loiasis surveillance is to be achieved.

There is much overlap between the endemicity of the two distinct filariases, which complicates mass treatment programs for onchocerciasis and necessitates the development of greater diagnostics for loiasis.

In Central and West Africa, initiatives to control onchocerciasis involve mass treatment with Ivermectin. However, these regions typically have high rates of co-infection with both "L. loa" and "O. volvulus", and mass treatment with Ivermectin can have severe adverse effects (SAE). These include hemorrhage of the conjunctiva and retina, heamaturia, and other encephalopathies that are all attributed to the initial L. loa microfilarial load in the patient prior to treatment. Studies have sought to delineate the sequence of events following Ivermectin treatment that lead to neurologic SAE and sometimes death, while also trying to understand the mechanisms of adverse reactions to develop more appropriate treatments.

In a study looking at mass Ivermectin treatment in Cameroon, one of the greatest endemic regions for both onchocerciasis and loiasis, a sequence of events in the clinical manifestation of adverse effects was outlined.

It was noted that the patients used in this study had a "L. loa" microfilarial load of greater than 3,000 per ml of blood.

Within 12–24 hours post-Ivermectin treatment (D1), individuals complained of fatigue, anorexia, and headache, joint and lumbar pain—a bent forward walk was characteristic during this initial stage accompanied by fever. Stomach pain and diarrhea were also reported in several individuals.

By day 2 (D2), many patients experienced confusion, agitation, dysarthria, mutism and incontinence. Some cases of coma were reported as early as D2. The severity of adverse effects increased with higher microfilarial loads. Hemorrhaging of the eye, particularly the retinal and conjunctiva regions, is another common sign associated with SAE of Ivermectin treatment in patients with "L. loa" infections and is observed between D2 and D5 post-treatment. This can be visible for up to 5 weeks following treatment and has increased severity with higher microfilarial loads.

Haematuria and proteinuria have also been observed following Ivermectin treatment, but this is common when using Ivermectin to treat onchocerciasis. The effect is exacerbated when there are high "L. loa" microfilarial loads however, and microfilariae can be observed in the urine occasionally. Generally, patients recovered from SAE within 6–7 months post-Ivermectin treatment; however, when their complications were unmanaged and patients were left bed-ridden, death resulted due to gastrointestinal bleeding, septic shock, and large abscesses.

Mechanisms for SAE have been proposed. Though microfilarial load is a major risk factor to post-Ivermectin SAE, three main hypotheses have been proposed for the mechanisms.

The first mechanism suggests that Ivermectin causes immobility in microfilariae, which then obstructs microcirculation in cerebral regions. This is supported by the retinal hemorrhaging seen in some patients, and is possibly responsible for the neurologic SAE reported.

The second hypothesis suggests that microfilariae may try to escape drug treatment by migrating to brain capillaries and further into brain tissue; this is supported by pathology reports demonstrating a microfilarial presence in brain tissue post-Ivermectin treatment.

Lastly, the third hypothesis attributes hypersensitivity and inflammation at the cerebral level to post-Ivermectin treatment complications, and perhaps the release of bacteria from L. loa after treatment to SAE. This has been observed with the bacteria "Wolbachia" that live with "O. volvulus".

More research into the mechanisms of post-Ivermectin treatment SAE is needed to develop drugs that are appropriate for individuals suffering from multiple parasitic infections.

One drug that has been proposed for the treatment of onchocerciasis is doxycycline. This drug has been shown to be effective in killing both the adult worm of "O. volvulus" and "Wolbachia", the bacteria believed to play a major role in the onset of onchocerciasis, while having no effect on the microfilariae of "L. loa". In a study done at 5 different co-endemic regions for onchocerciasis and loiasis, doxycycline was shown to be effective in treating over 12,000 individuals infected with both parasites with minimal complications. Drawbacks to using Doxycycline include bacterial resistance and patient compliance because of a longer treatment regimen and emergence of doxycycline-resistant "Wolbachia". However, in the study over 97% of the patients complied with treatment, so it does pose as a promising treatment for onchocerciasis, while avoiding complications associated with L. loa co-infections.

Human loiasis geographical distribution is restricted to the rain forest and swamp forest areas of West Africa, being especially common in Cameroon and on the Ogooué River. Humans are the only known natural reservoir. It is estimated that over 10 million humans are infected with "Loa loa" larvae.

An area of tremendous concern regarding loiasis is its co-endemicity with onchocerciasis in certain areas of west and central Africa, as mass ivermectin treatment of onchocerciasis can lead to serious adverse events (SAEs) in patients who have high "Loa loa" microfilarial densities, or loads. This fact necessitates the development of more specific diagnostics tests for "Loa loa" so that areas and individuals at a higher risk for neurologic consequences can be identified prior to microfilaricidal treatment. Additionally, the treatment of choice for loiasis, diethylcarbamazine, can lead to serious complications in and of itself when administered in standard doses to patients with high "Loa loa" microfilarial loads.

Diethylcarbamazine has been shown as an effective prophylaxis for "Loa loa" infection.

A study of Peace Corps volunteers in the highly Loa—endemic Gabon, for example, had the following results: 6 of 20 individuals in a placebo group contracted the disease, compared to 0 of 16 in the DEC-treated group. Seropositivity for antifilarial IgG antibody was also much higher in the placebo group. The recommended prophylactic dose is 300 mg DEC given orally once weekly. The only associated symptom in the Peace Corps study was nausea.

Researchers believe that geo-mapping of appropriate habitat and human settlement patterns may, with the use of predictor variables such as forest, land cover, rainfall, temperature, and soil type, allow for estimation of Loa loa transmission in the absence of point-of-care diagnostic tests. In addition to geo-mapping and chemoprophylaxis, the same preventative strategies used for malaria should be undertaken to avoid contraction of loiasis. Specifically, DEET-containing insect repellent, permethrin-soaked clothing, and thick, long-sleeved and long-legged clothing ought to be worn to decrease susceptibility to the bite of the mango or deer fly vector. Because the vector is day-biting, mosquito (bed) nets do not increase protection against loiasis.

Vector elimination strategies are an interesting consideration. It has been shown that the "Chrysops" vector has a limited flying range, but vector elimination efforts are not common, likely because the insects bite outdoors and have a diverse, if not long, range, living in the forest and biting in the open, as mentioned in the vector section.

No vaccine has been developed for loiasis and there is little report on this possibility.

About 37 million people are infected with this parasite; about 300,000 of those had been permanently blinded. As of 2008, about 99% of onchocerciasis cases occurred in Africa. Onchocerciasis is currently endemic in 30 African countries, Yemen, and isolated regions of South America. Over 85 million people live in endemic areas, and half of these reside in Nigeria. Another 120 million people are at risk for contracting the disease. Due to the vector’s breeding habitat, the disease is more severe along the major rivers in the northern and central areas of the continent, and severity declines in villages farther from rivers. Onchocerciasis was eliminated in the northern focus in Chiapas, Mexico, and the focus in Oaxaca, Mexico, where "Onchocerca volvulus" existed, was determined, after several years of treatment with ivermectin, as free of the transmission of the parasite.

According to a 2002 WHO report, onchocerciasis has not caused a single death, but its global burden is 987,000 disability adjusted life years (DALYs). The severe pruritus alone accounts for 60% of the DALYs. Infection reduces the host’s immunity and resistance to other diseases, which results in an estimated reduction in life expectancy of 13 years.

The World Health Organization recommends mass deworming—treating entire groups of people who are at risk with a single annual dose of two medicines, namely albendazole in combination with either ivermectin or diethylcarbamazine citrate. With consistent treatment, since the disease needs a human host, the reduction of microfilariae means the disease will not be transmitted, the adult worms will die out, and the cycle will be broken. In sub-Saharan Africa, albendazole (donated by GlaxoSmithKline) is being used with ivermectin (donated by Merck & Co.) to treat the disease, whereas elsewhere in the world, albendazole is used with diethylcarbamazine. Transmission of the infection can be broken when a single dose of these combined oral medicines is consistently maintained annually for a duration of four to six years. Using a combination of treatments better reduces the number of microfilariae in blood. Avoiding mosquito bites, such as by using insecticide-treated mosquito bed nets, also reduces the transmission of lymphatic filariasis.

The Carter Center's International Task Force for Disease Eradication declared lymphatic filariasis one of six potentially eradicable diseases. According to medical experts, the worldwide effort to eliminate lymphatic filariasis is on track to potentially succeed by 2020.

For similar-looking but causally unrelated podoconiosis, international awareness of the disease will have to increase before elimination is possible. In 2011, podoconiosis was added to the World Health Organization's Neglected Tropical Diseases list, which was an important milestone in raising global awareness of the condition.

The efforts of the Global Programme to Eliminate LF are estimated to have prevented 6.6 million new filariasis cases from developing in children between 2000 and 2007, and to have stopped the progression of the disease in another 9.5 million people who had already contracted it. Dr. Mwele Malecela, who chairs the programme, said: "We are on track to accomplish our goal of elimination by 2020." In 2010, the WHO published a detailed progress report on the elimination campaign in which they assert that of the 81 countries with endemic LF, 53 have implemented mass drug administration, and 37 have completed five or more rounds in some areas, though urban areas remain problematic.

Secondary bacterial infection is common among patients with filariasis. Compromised immune function due to lymphatic damage in addition to lymph node ulcerations and abscesses exposure and impaired circulation due to elephantiasis can cause secondary bacterial or fungal infection. Elephantiasis, in addition to the physical burden of a swollen limb, can be a severely dehabilitating condition given bacterial infection. Part of the WHO's "Strategy to Eliminate Lymphatic Filariasis" targets hygiene promotion programs in order to alleviate the suffering of affected individuals (see Prevention Strategies).

However, clinical manifestations of infection are variable and depend on several factors, including host immune system, infectious dose, and parasite strain differences. Most infections appear asymptomatic, yet vary from individual to individual. Individuals living in endemic areas with microfilaremia may never present with overt symptoms, whereas in other cases, only a few worms can exacerbate a severe inflammatory response.

The development of the disease in humans, however, is not well understood. Adults typically develop worse symptoms, given the long exposure time required for infection. Infection may occur during childhood, but the disease appears to take many years to manifest. The incubation period for infection ranges from 1 month to 2 years and typically microfilariae appear before overt symptoms. Lymphedema can develop within six months and development of elephantiasis has been reported within a year of infection among refugees, who are more immunologically naive. Men tend to develop worse symptoms than women.

Areas with the highest prevalence of helminthiasis are tropical and subtropical areas including sub-Saharan Africa, central and east Asia, and the Americas.

Until recently humans and water fleas ("Cyclops") were regarded as the only animals this parasite infects. It has been shown that baboons, cats, dogs, frogs and catfish ("Synodontis") can also be infected naturally. Ferrets have been infected experimentally.

Some types of helminthiases are classified as neglected tropical diseases. They include:

- Soil-transmitted helminthiases

- Roundworm infections such as lymphatic filariasis, dracunculiasis, and onchocerciasis

- Trematode infections, such as schistosomiasis, and food-borne trematodiases, including fascioliasis, clonorchiasis, opisthorchiasis, and paragonimiasis

- Tapeworm infections such as cysticercosis, taeniasis, and echinococcosis

Secondary bacterial infection is often observed with lymphatic filariasis. Rigorous hygiene practices, including washing with soap and water daily and disinfecting wounds can help heal infected surfaces, and slow and potentially reverse existing tissue damage. Promoting hygiene is essential for lymphatic filariasis patients given the compromised immune and damaged lymphatic systems and can help prevent suffering and disability.

"A. cantonensis" and its vectors are endemic to Southeast Asia and the Pacific Basin. The infection is becoming increasingly important as globalization allows it to spread to more and more locations, and as more travelers encounter the parasites. The parasites probably travel effectively through rats traveling as stowaways on ships, and through the introduction of snail vectors outside endemic areas.

Although mostly found in Asia and the Pacific where asymptomatic infection can be as high as 88%, human cases have been reported in the Caribbean, where as much as 25% of the population may be infected. In the United States, cases have been reported in Hawaii, which is in the endemic area [5]. The infection is now endemic in wildlife and a few human cases have also been reported in areas where the parasite was not originally endemic, such as New Orleans and Egypt.

The disease has also arrived in Brazil, where there were 34 confirmed cases from 2006 to 2014, including one death. The giant African land snail, which can be a vector of the parasite, has been introduced to Brazil as an invasive species and is spreading the disease. There may be more undiagnosed cases, as Brazilian physicians are not familiar with the eosinophilic meningitis associated to angiostrongyliasis and misdiagnose it as bacterial or viral.

Prevention focuses on protecting against mosquito bites in endemic regions. Insect repellents and mosquito nets are useful to protect against mosquito bites. Public education efforts must also be made within the endemic areas of the world to successfully lower the prevalence of "W. bancrofti" infections.

Deworming treatments in infected children may have some nutritional benefit, as worms are often partially responsible for malnutrition. However, in areas where these infections are common, there is strong evidence that mass deworming campaigns do not have a positive effect on children's average nutritional status, levels of blood haemoglobin, cognitive abilities, performance at school or survival. To achieve health gains in the longer term, improvements in sanitation and hygiene behaviours are also required, together with deworming treatments.

There are many public health strategies that can drastically limit the transmission of "A. cantonensis" by limiting contact with infected vectors. Vector control may be possible, but has not been very successful in the past. Education to prevent the introduction of rats or snail vectors outside endemic areas is important to limit the spread of the disease. There are no vaccines in development for angiostrongyliasis.

Control of this parasite should be directed against reducing the level of

environmental contamination. Treatment of heavily infected individuals is one

way to reduce the source of contamination (one study has estimated that 60% of

the total worm burden resides in less than 10% of the population). Other

obvious methods are to improve access to sanitation, e.g. toilets, but also

convincing people to maintaining them in a clean, functional state, thereby making

them conducive to use.

Elephantiasis caused by lymphatic filariasis is one of the most common causes of disability in the world. A 2012 report noted that lymphatic filariasis affected 120 million people and one billion people at risk for infection. About 40 million people were disfigured or incapacitated by the disease in 2015. It is considered endemic in tropical and subtropical regions of Africa, Asia, Central and South America, and Pacific Island nations.

In areas endemic for podoconiosis, prevalence can be 5% or higher. In communities where lymphatic filariasis is endemic, as many as 10% of women can be afflicted with swollen limbs, and 50% of men can suffer from mutilating genital symptoms.

Filariasis is considered endemic in 73 countries; 37 of these are in Africa.

- In the Americas, it is present in Brazil, Costa Rica, the Dominican Republic, Guyana, Haiti, Suriname, and Trinidad and Tobago.

- In Asia, it is present in Bangladesh, Cambodia, India, Indonesia, Laos, Malaysia, Maldives, the Philippines, Sri Lanka, Thailand, Timor-Leste, and Vietnam.

- In the Middle East, it is present only in Yemen.

- In the Pacific region, it is endemic in American Samoa, the Cook Islands, Fiji, French Polynesia, Micronesia, Niue, Papua New Guinea, Samoa, Tonga, Tuvalu, and Vanuatu.

In many of these countries, considerable progress has been made towards elimination of filariasis. In July 2017, the World Health Organization (WHO) announced that the disease had been eliminated in Tonga. Elimination of the disease has also occurred in Cambodia, China, the Cook Islands, Niue, the Marshall Islands, South Korea, and Vanuatu, according to the WHO.

Filariasis can also affect domesticated animals, such as cattle, sheep, and dogs.

Dracunculiasis is caused by drinking water contaminated by water fleas that host the "D. medinensis" larvae. Dracunculiasis has a history of being very common in some of the world's poorest areas, particularly those with limited or no access to clean water. In these areas, stagnant water sources may still host copepods, which can carry the larvae of the guinea worm.

After ingestion, the copepods die and are digested, thus releasing the stage 3 larvae, which then penetrate the host's stomach or intestinal wall, and then enter into the abdominal cavity and retroperitoneal space. After maturation, which takes approximately three months, mating takes place; the male worm dies after mating and is absorbed by the host's body.

Approximately one year after mating, the fertilized females migrate in the subcutaneous tissues adjacent to long bones or joints of the extremities. They then move towards the surface, resulting in blisters on the skin, generally on the distal lower extremity (foot). Within 72 hours, the blister ruptures, exposing one end of the emergent worm. The blister causes a very painful burning sensation as the worm emerges, and the sufferer will often immerse the affected limb in water to relieve the burning sensation. When a blister or open sore is submerged in water, the adult female releases hundreds of thousands of stage 1 guinea worm larvae, thereby contaminating the water.

During the next few days, the female worm can release more larvae whenever it comes in contact with water, as it extends its posterior end through the hole in the host's skin. These larvae are eaten by copepods, and after two weeks (and two molts), the stage 3 larvae become infectious and, if not filtered from drinking water, will cause the cycle to repeat. Infected copepods can live in the water for up to four months.

The male guinea worm is typically much smaller () than the female, which, as an adult, can grow to long and be as thick as a spaghetti noodle.

Infection does not create immunity, so people can repeatedly experience Dracunculiasis throughout their lives. Several worms may emerge simultaneously; the average is 1.8. Up to 14 worms have been reported in one individual.

In drier areas just south of the Sahara desert, cases of the disease often emerge during the rainy season, which for many agricultural communities is also the planting or harvesting season. Elsewhere, the emerging worms are more prevalent during the dry season, when ponds and lakes are smaller and copepods are thus more concentrated in them. Guinea worm disease outbreaks can cause serious disruption to local food supplies and school attendance.

The infection can be acquired by eating a fish paratenic host, but this is rare. No reservoir hosts are known; that is, each generation of worms must pass through a human – or possibly a dog.

Snakebite was added to the list in 2017, after years of criticism of the WHO by activists for not making it a priority. The greatest burden of snakebite morbidity is in India and Southeast Asia. Globally, there are an estimated 421,000 envenomings each year (about 1 in 4 snakebites) and 20,000 deaths, but snakebites often go unreported.

It is estimated that a third of all pregnant women in developing countries are infected with hookworm, 56% of all pregnant women in developing countries suffer from anemia, 20% of all maternal deaths are either directly or indirectly related to anemia. Numbers like this have led to an increased interest in the topic of hookworm-related anemia during pregnancy. With the understanding that chronic hookworm infection can often lead to anemia, many people are now questioning if the treatment of hookworm could effect change in severe anemia rates and thus also on maternal and child health as well. Most evidence suggests that the contribution of hookworm to maternal anemia merits that all women of child-bearing age living in endemic areas be subject to periodic anthelmintic treatment. The World Health Organization even recommends that infected pregnant women be treated after their first trimester. Regardless of these suggestions, only Madagascar, Nepal and Sri Lanka have added deworming to their antenatal care programs.

This lack of deworming of pregnant women is explained by the fact that most individuals still fear that anthelmintic treatment will result in adverse birth outcomes. But a 2006 study by Gyorkos et al. found that when comparing a group of pregnant women treated with mebendazole with a control placebo group, both illustrated rather similar rates in adverse birth outcomes. The treated group demonstrated 5.6% adverse birth outcomes, while the control group had 6.25% adverse birth outcomes. Furthermore, Larocque et al. illustrated that treatment for hookworm infection actually led to positive health results in the infant. This study concluded that treatment with mebendazole plus iron supplements during antenatal care significantly reduced the proportion of very low birth weight infants when compared to a placebo control group. Studies so far have validated recommendations to treat infected pregnant women for hookworm infection during pregnancy.

A review of effects of antihelminthics (anti-worm drugs) given in pregnancy found that there was not enough evidence to support treating pregnant women in their second or third trimesters. The women who were treated in the second trimester and the women who had no treatment showed no difference in numbers of maternal anemia, low birth weight, preterm birth or deaths of babies.

The intensity of hookworm infection as well as the species of hookworm have yet to be studied as they relate to hookworm-related anemia during pregnancy. Additionally, more research must be done in different regions of the world to see if trends noted in completed studies persist.

Latest estimates indicate that the total annual death toll which is directly attributable is as high as 135,000. The death toll due to the malnutrition link is likely to be much higher.

Some species of cattle such as the African buffalo, N'dama, and Keteku appear trypanotolerant and do not develop symptoms. Calves are more resistant than adults.

The definitive hosts for these "Taenia" species are canids. The adult tapeworms live in the intestines of animals like dogs, foxes, and coyotes. Intermediate hosts such as rabbits, goats, sheep, horses, cattle and sometimes humans get the disease by inadvertently ingesting tapeworm eggs (gravid proglottids) that have been passed in the feces of an infected canid. This can happen from ingesting food, water or soil that has been contaminated by dog feces. The disease cannot be transmitted from one intermediate host to another, but it is still not a good idea to eat meat that presents with cystic nodules from coenurosis.

Ivermectin kills the parasite by interfering with the nervous system and muscle function, in particular, by enhancing inhibitory neurotransmission. The drug binds to and activates glutamate-gated chloride channels. These channels, present in neurons and myocytes, are not invertebrate-specific, but are protected in vertebrates from the action of ivermectin by the blood–brain barrier. Ivermectin is thought to irreversibly activate these channel receptors in the worm, eventually causing an inhibitory postsynaptic potential. The chance of a future action potential occurring in synapses between neurons decreases and the nematodes experience flaccid paralysis followed by death.

Ivermectin is directly effective against the larval stage microfilariae of "O. volvulus"; they are paralyzed and can be killed by eosinophils and macrophages. It does not kill adult females (macrofilariae), but does cause them to cease releasing microfilariae, perhaps by paralyzing the reproductive tract. Ivermectin is very effective in reducing microfilarial load and reducing number of punctate opacities in individuals with onchocerciasis.

Filarial diseases in humans offer prospects for elimination by means of vermicidal treatment. If the human link in the chain of infection can be broken, then notionally the disease could be wiped out in a season. In practice it is not quite so simple, and there are complications in that multiple species overlap in certain regions and double infections are common. This creates difficulties for routine mass treatment because people with onchocerciasis in particular react badly to treatment for lymphatic filariasis.

The WHO is coordinating an effort to eradicate filariasis. The mainstay of this programme is the mass use of antifilarial drugs on a regular basis for at least five years.

In April 2011, Sri Lanka was certified by the WHO as having eradicated this disease.