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.)

Visceral leishmaniasis (VL), also known as kala-azar, black fever, and Dumdum fever, is the most severe form of leishmaniasis and, without proper diagnosis and treatment, is associated with high fatality. Leishmaniasis is a disease caused by protozoan parasites of the "Leishmania" genus.

The parasite migrates to the internal organs such as the liver, spleen (hence "visceral"), and bone marrow, and, if left untreated, will almost always result in the death of the host. Signs and symptoms include fever, weight loss, fatigue, anemia, and substantial swelling of the liver and spleen. Of particular concern, according to the World Health Organization (WHO), is the emerging problem of HIV/VL co-infection.

This disease is the second-largest parasitic killer in the world (after malaria), responsible for an estimated 200,000 to 400,000 infections each year worldwide.

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.

Cutaneous

- Alopecia

- Skin lesions

- Ulcerative or exfoliative dermatitis

Visceral

- Epistaxis (nose bleeds)

- Kidney failure > increased urination and drinking

- Ocular signs

- Progressive loss of weight with decreased appetite

- Swollen lymphnodes

Post-kala-azar dermal leishmaniasis (PKDL) is a recurrence of kala-azar that may appear on the skin of affected individuals months and up to 20 years after being partially treated, untreated or even in those considered adequately treated. In Sudan, they can be demonstrated in up to 60% of treated cases. They manifest as hypopigmented skin lesions (such as macules, papules, nodules), or facial redness. Though any organism causing kala-azar can lead to PKDL, it is commonly associated with "Leishmania donovani" which gives different disease patterns in India and Sudan. In the Indian variant, nodules enlarge with time and form plaques but rarely ulcerate, but nodules from the African variety often ulcerate as they progress. Nerve involvement is common in African variety but rare in Indian subcontinent. Histology demonstrates a mixture of chronic inflammatory cells; there can be macrophage or epitheloid granuloma. Parasite concentration is not consistent among studies, perhaps reflecting low sensitivity of diagnostic methods used in earlier entries.

Current approach to diagnosis involves 1. demonstration of parasite by microscopy, "in vitro" culture or animal inoculation; 2. immunodiagnosis of parasite antigen; 3. detection of parasite DNA in tissue. Newer PCR based tools have higher sensitivity and specificity. Emergence of PKDL has been reported in HIV affected individuals and may become a problem in future.

Sodium stibogluconate alone or in combination with rifampicin is used for the treatment of PKDL for a long course of up to 4 months. Compliance can be an issue for such a long course.

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.

Mucocutaneous leishmaniasis is an especially disturbing form of cutaneous leishmaniasis, because it produces destructive and disfiguring lesions of the face. It is most often caused by "Leishmania braziliensis", but cases caused by "L. aethiopica" have also been described.

Mucocutaneous leishmaniasis is very difficult to treat. Treatment involves the use of pentavalent antimonial compounds, which are highly toxic (common side effects include thrombophlebitis, pancreatitis, cardiotoxicity and hepatotoxicity) and not very effective. For example, in one study, despite treatment with high doses of sodium stibogluconate for 28 days, only 30% of patients remained disease-free at 12 months follow-up. Even in those patients who achieve an apparent cure, as many as 19% will relapse. Several drug combinations with immunomodulators have been tested, for example, a combination of pentoxifylline (inhibitor of TNF-α) and a pentavalent antimonial at a high dose for 30 days in a small-scale (23 patients) randomised placebo-controlled study from Brazil achieved cure rates of 90% and reduced time to cure, a result that should be interpreted cautiously in light of inherent limitations of small-scale studies. In an earlier small-scale (12 patients) study, addition of imiquimod showed promising results which need yet to be confirmed in larger trials.

Canine leishmaniasis (LEESH-ma-NIGH-ah-sis) is a zoonotic disease (see human leishmaniasis) caused by "Leishmania" parasites transmitted by the bite of an infected phlebotomine sandfly. Canine leishmaniasis was first identified in Europe in 1903, and in 1940, 40% of all dogs in Rome were determined to be positive for leishmaniasis. Traditionally thought of as a disease only found near the Mediterranean basin, 2008 research claims new findings are evidence that canine leishmaniasis is currently expanding in continental climate areas of northwestern Italy, far from the recognized disease-endemic areas along the Mediterranean coasts. Cases of leishmaniasis began appearing in North America in 2000, and, as of 2008, "Leishmania"-positive foxhounds have been reported in 22 U.S. states and two Canadian provinces.

A canine vector-borne disease (CVBD) is one of "a group of globally distributed and rapidly spreading illnesses that are caused by a range of pathogens transmitted by arthropods including ticks, fleas, mosquitoes and phlebotomine sandflies." CVBDs are important in the fields of veterinary medicine, animal welfare, and public health. Some CVBDs are of zoonotic concern.

Many CVBD infect humans as well as companion animals. Some CVBD are fatal; most can only be controlled, not cured. Therefore, infection should be avoided by preventing arthropod vectors from feeding on the blood of their preferred hosts. While it is well known that arthropods transmit bacteria and protozoa during blood feeds, viruses are also becoming recognized as another group of transmitted pathogens of both animals and humans.

Some "canine vector-borne pathogens of major zoonotic concern" are distributed worldwide, while others are localized by continent. Listed by vector, some such pathogens and their associated diseases are the following:

- Phlebotomine sandflies (Psychodidae): "Leishmania amazonensis", "L. colombiensis", and "L. infantum" cause visceral leishmaniasis (see also canine leishmaniasis). "L. braziliensis" causes mucocutaneous leishmaniasis. "L. tropica" causes cutaneous leishmaniasis. "L. peruviana" and "L. major" cause localized cutaneous leishmaniasis.

- Triatomine bugs (Reduviidae): "Trypanosoma cruzi" causes trypanosomiasis (Chagas disease).

- Ticks (Ixodidae): "Babesia canis" subspecies ("Babesia canis canis", "B. canis vogeli", "B. canis rossi", and "B. canis gibsoni" cause babesiosis. "Ehrlichia canis" and "E. chaffeensis" cause monocytic ehrlichiosis. "Anaplasma phagocytophilum" causes granulocytic anaplasmosis. "Borrelia burgdorferi" causes Lyme disease. "Rickettsia rickettsii" causes Rocky Mountain spotted fever. "Rickettsia conorii" causes Mediterranean spotted fever.

- Mosquitoes (Culicidae): "Dirofilaria immitis" and "D. repens" cause dirofilariasis.

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.

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).

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.

A persistent or recurrent cough that gets aggravated at night, weakness, weight loss and a low fever raises the possible diagnosis of this disease. Some children with this disease may also have enlarged lymph nodes in the neck and elsewhere. Others may cough up a little blood and may also have a wheeze.

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%.

Porocephaliasis is a condition associated with species in the closely related genera "Porocephalus" and "Armillifer". (The term "pentastomiasis" encompasses all diseases of Pentastomida, which includes Porocephaliasis and Linguatulosis.)

Porocephaliasis is associated with contact with snakes. (This is in contrast with Linguatulosis, which is associated with contact with dogs or wolves.)

It has been reported from Africa, Malaysia and the Middle East. Its occurrence has been rare in Europe and North America where it has been found in immigrants and travelers.

Ancylostomiasis (also anchylostomiasis or ankylostomiasis) is a hookworm disease caused by infection with Ancylostoma hookworms. The name is derived from Greek ancylos αγκύλος "crooked, bent" and stoma στόμα "mouth".

Ancylostomiasis is also known as miner's anaemia, tunnel disease, brickmaker's anaemia and Egyptian chlorosis. Helminthiasis may also refer to ancylostomiasis, but this term also refers to all other parasitic worm diseases as well. In the United Kingdom, if acquired in the context of working in a mine, the condition is eligible for Industrial Injuries Disability Benefit. It is a prescribed disease (B4) under the relevant legislation.§

Ancylostomiasis is caused when hookworms, present in large numbers, produce an iron deficiency anemia by sucking blood from the host's intestinal walls.

Tropical (pulmonary) eosinophilia, or TPE, is characterized by coughing, asthmatic attacks, and an enlarged spleen, and is caused by "Wuchereria bancrofti", a filarial infection. It occurs most frequently in India and Southeast Asia. Tropical eosinophilia is considered a manifestation of a species of microfilaria. This disease can be confused with tuberculosis, asthma, or coughs related to roundworms.

Tropical pulmonary eosinophilia is a rare, but well recognised, syndrome characterised by pulmonary interstitial infiltrates and marked peripheral eosinophilia. This condition is more widely recognised and promptly diagnosed in filariasis-endemic regions, such as the Indian subcontinent, Africa, Asia and South America. In nonendemic countries, patients are commonly thought to have bronchial asthma. Chronic symptoms may delay the diagnosis by up to five years. Early recognition and treatment with the antifilarial drug, diethylcarbamazine, is important, as delay before treatment may lead to progressive interstitial fibrosis and irreversible impairment.

The condition of marked eosinophilia with pulmonary involvement was first termed tropical pulmonary eosinophilia in 1950. The syndrome is caused by a distinct hypersensitive immunological reaction to microfilariae of" W. bancrofti" and "Brugia malayi". However, only a small percentage (< 0.5%) of the 130 million people globally who are infected with filariasis apparently develop this reaction. The clearance of rapidly opsonised microfilariae from the bloodstream results in a hypersensitive immunological process and abnormal recruitment of eosinophils, as reflected by extremely high IgE levels of over 1000 kU/L. The typical patient is a young adult man from the Indian subcontinent.

It is prevalent in parts of Africa and Asia where eating snake meat is common. In Africa it has also been associated with groups who use the snake as a totem. Unlike linguatuliasis, humans are only ever an accidental intermediate host for "Armillifer", i.e. the larvae establish themselves in the visceral organs causing human visceral pentastomiasis, but adults do not occur in the human respiratory system. After a while the larvae die within the host and sometimes calcify, leaving characteristic crescent-shaped structures seen in X-ray. In extreme cases a heavy parasite burden can have serious medical consequences and can even be fatal.

African trypanosomiasis, also known as sleeping sickness, is an insect-borne parasitic disease of humans and other animals. It is caused by protozoa of the species "Trypanosoma brucei". There are two types that infect humans, "Trypanosoma brucei gambiense" (TbG) and "Trypanosoma brucei rhodesiense" (TbR). TbG causes over 98% of reported cases. Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.

Initially, in the first stage of the disease, there are fevers, headaches, itchiness, and joint pains. This begins one to three weeks after the bite. Weeks to months later the second stage begins with confusion, poor coordination, numbness and trouble sleeping. Diagnosis is via finding the parasite in a blood smear or in the fluid of a lymph node. A lumbar puncture is often needed to tell the difference between first and second stage disease.

Prevention of severe disease involves screening the population at risk with blood tests for TbG. Treatment is easier when the disease is detected early and before neurological symptoms occur. Treatment of the first stage is with the medications pentamidine or suramin. Treatment of the second stage involves eflornithine or a combination of nifurtimox and eflornithine for TbG. While melarsoprol works for both stages, it is typically only used for TbR, due to serious side effects. Without treatment it typically results in death.

The disease occurs regularly in some regions of sub-Saharan Africa with the population at risk being about 70 million in 36 countries. An estimated 11,000 people are currently infected with 2,800 new infections in 2015. In 2015 it caused around 3,500 deaths, down from 34,000 in 1990. More than 80% of these cases are in the Democratic Republic of the Congo. Three major outbreaks have occurred in recent history: one from 1896 to 1906 primarily in Uganda and the Congo Basin and two in 1920 and 1970 in several African countries. It is classified as a neglected tropical disease. Other animals, such as cows, may carry the disease and become infected in which case it is known as animal trypanosomiasis.

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.

There is some debate among the WHO, CDC, and infectious disease experts over which diseases are classified as neglected tropical diseases. Feasey, a researcher in neglected tropical diseases, notes 13 neglected tropical diseases: ascariasis, Buruli ulcer, Chagas disease, dracunculiasis, hookworm infection, human African trypanosomiasis, Leishmaniasis, leprosy, lymphatic filariasis, onchocerciasis, schistosomiasis, trachoma, and trichuriasis. Fenwick recognizes 12 "core" neglected tropical diseases: ascariasis, Buruli ulcer, Chagas disease, dracunculiasis, human African trypanosomiasis, Leishmaniasis, leprosy, lymphatic filariasis, onchocerciasis, schistosomiasis, trachoma, and trichuriasis.

These diseases result from four different classes of causative pathogens: (i) protozoa (for Chagas disease, human African trypanosomiasis, leishmaniases); (ii) bacteria (for Buruli ulcer, leprosy, trachoma, yaws), (iii) helminths or metazoan worms (for cysticercosis/taeniasis, dracunculiasis, echinococcosis, foodborne trematodiases, lymphatic filariasis, onchocerciasis, schistosomiasis, soil-transmitted helminthiasis); and (iv) viruses (dengue and chikungunya, rabies).

The World Health Organization recognizes the seventeen diseases below as neglected tropical diseases.

An anthroponotic disease, or anthroponosis, is an infectious disease in which a disease causing agent carried by humans is transferred to other animals. It may cause the same disease or a different disease in other animals. Since humans do not generally inflict bite wounds on other animals, the method of transmissions is always a "soft" contact such as skin to skin transmission. An example is chytridiomycosis which can be spread by humans with the fungus on their skin handling frogs with bare hands.

The reverse situation, a disease transmitted from animals to humans, is known as zoonotic.

It can also be defined as a human-to-human infection with no animal vector.

It is usually asymptomatic unless the complication and infection is severe. But in some recorded cases, symptoms include nasopharyngitis accompanied by pain, itching of throat and ears. Coughing, hemoptysis and vomiting are verifiable indications as well as sneezing, bleeding, dyspnea, and inflammation.

Viscerotropic leishmaniasis is a systemic infection reported in soldiers fighting in Operation Desert Storm in Saudi Arabia.

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.