There are two approaches to treating Chagas disease: antiparasitic treatment, to kill the parasite; and symptomatic treatment, to manage the symptoms and signs of the infection. Management uniquely involves addressing selective incremental failure of the parasympathetic nervous system. Autonomic disease imparted by Chagas may eventually result in megaesophagus, megacolon and accelerated dilated cardiomyopathy. The mechanisms that explain why Chagas targets the parasympathetic autonomic nervous system and spares the sympathetic autonomic nervous system remain poorly understood.

Antiparasitic treatment is most effective early in the course of infection, but is not limited to cases in the acute phase. Drugs of choice include azole or nitro derivatives, such as benznidazole or nifurtimox. Both agents are limited in their capacity to completely eliminate "T. cruzi" from the body (parasitologic cure), especially in chronically infected patients, and resistance to these drugs has been reported.

Studies suggest antiparasitic treatment leads to parasitological cure in more than 90% of infants but only about 60–85% of adults treated in the first year of acute phase Chagas disease. Children aged six to 12 years with chronic disease have a cure rate of about 60% with benznidazole. While the rate of cure declines the longer an adult has been infected with Chagas, treatment with benznidazole has been shown to slow the onset of heart disease in adults with chronic Chagas infections.

Treatment of chronic infection in women prior to or during pregnancy does not appear to reduce the probability the disease will be passed on to the infant. Likewise, it is unclear whether prophylactic treatment of chronic infection is beneficial in persons who will undergo immunosuppression (for example, organ transplant recipients) or in persons who are already immunosuppressed (for example, those with HIV infection).

Stage I of the condition is usually treated with pentamidine or suramin through intramuscular injection or intravenous infusion if sufficient observation is possible. Stage II of the disease is typically treated with melarsoprol or eflornithine preferably introduced to the body intravenously. Both pentamidine and suramin have limited side effects. Melarsoprol is extremely effective but has many serious side effects which can cause neurological damage to a patient, however, the drug is often a patient's last hope in many late stage cases. Eflornithine is extremely expensive but has side effects that may be treated with ease. In regions of the world where the disease is common eflornithine is provided for free by the World Health Organization.

For "T. b. gambiense" the combination of nifurtimox and eflornithine (NECT) or eflornithine alone appear to be more effective and result in fewer side effects. These treatments may replace melarsoprol when available with the combination being first line. NECT has the benefit of requiring less injections of eflornithine.

Intravenous melarsoprol was previously the standard treatment for second-stage (neurological phase) disease and is effective for both types. Melarsoprol is the only treatment for second stage "T. b. rhodesiense"; however, it causes death in 5% of people who take it. Resistance to melarsoprol can occur.

The current treatment for first-stage disease is intravenous or intramuscular pentamidine for "T. b. gambiense" or intravenous suramin for "T. b. rhodesiense".

The use of trypanotolerant breeds for livestock farming should be considered if the disease is widespread.

Fly control is another option but is difficult to implement.

The main approaches to controlling African trypanosomiasis are to reduce the reservoirs of infection and the presence of the tsetse fly. Screening of people at risk helps identify patients at an early stage. Diagnosis should be made as early as possible and before the advanced stage to avoid complicated, difficult and risky treatment procedures.

As with many diseases in developing nations, (including trypanosomiasis and malaria) effective and affordable chemotherapy is sorely lacking and parasites or insect vectors are becoming increasingly resistant to existing anti-parasite drugs. Possibly due to the lack of financial return, new drugs are slow to emerge and much of the basic research into potential drug targets takes place in universities, funded by charitable organizations. Product Development Partnerships (PDPs) like Drugs for Neglected Diseases "initiatives" also work on the development of new treatments (combination treatments and new chemical entities) for visceral leishmaniasis.

The traditional treatment is with pentavalent antimonials such as sodium stibogluconate and meglumine antimoniate. Resistance is now common in India, and rates of resistance have been shown to be as high as 60% in parts of Bihar, India.

The treatment of choice for visceral leishmaniasis acquired in India is now Amphotericin B in its various liposomal preparations. In East Africa, the WHO recommended treatment is SSG&PM (sodium stibogluconate and paromomycin) developed by Drugs for Neglected Diseases "initiative" (DNDi)in 2010.

Miltefosine is the first oral treatment for this disease. The cure rate of miltefosine in Phase III clinical trials is 95%; Studies in Ethiopia show that is also effective in Africa. In HIV immunosuppressed people which are coinfected with leishmaniasis it has shown that even in resistant cases 2/3 of the people responded to this new treatment.

Miltefosine has received approval by the Indian regulatory authorities in 2002, in Germany in 2004 and in U.S.A. in 2014. It is now registered in many countries.

The drug is generally better tolerated than other drugs. Main side effects are gastrointestinal disturbance in the first or second day of treatment (a course of treatment is 28 days) which does not affect the efficacy. Because it is available as an oral formulation, the expense and inconvenience of hospitalization is avoided, and outpatient distribution of the drug becomes an option, making Miltefosine a drug of choice.

Incomplete treatment has been cited as a major reason of death from visceral leishmaniasis.

The nonprofit Institute for OneWorld Health has adopted the broad spectrum antibiotic paromomycin for use in treating VL; its antileishmanial properties were first identified in the 1980s. A treatment with paromomycin costs about $15 USD. The drug had originally been identified in the 1960s. The Indian government approved paromomycin for sale and use in August 2006.

If the outbreak is detected early, the organism can be destroyed by quarantines, movement controls, and maybe even put infected animals under euthanasia medication. Tsetse fly populations can be reduced or eliminated by traps, insecticides, and by treating infected animals with antiparasitic drugs. The Tse Tse habitat can be destroyed by alteration of vegetation so they can no longer live there.There are some drugs available that can prevent trypanosomiasis called prophylactic drugs.These drugs are very effective to protect animals during the times they are exposed to challenged diseases. Since they have been around for so long, some were not properly used which caused resistance to these drugs in some places.

There are no vaccines or preventive drugs for visceral leishmaniasis. The most effective method to prevent infection is to protect from sand fly bites. To decrease the risk of being bitten, these precautionary measures are suggested:

- Outdoors:

1. Avoid outdoor activities, especially from dusk to dawn, when sand flies generally are the most active.

2. When outdoors (or in unprotected quarters), minimize the amount of exposed (uncovered) skin to the extent that is tolerable in the climate. Wear long-sleeved shirts, long pants, and socks; and tuck your shirt into your pants.

3. Apply insect repellent to exposed skin and under the ends of sleeves and pant legs. Follow the instructions on the label of the repellent. The most effective repellents generally are those that contain the chemical DEET (N,N-diethylmetatoluamide).

- Indoors:

1. Stay in well-screened or air-conditioned areas.

2. Keep in mind that sand flies are much smaller than mosquitoes and therefore can get through smaller holes.

3. Spray living/sleeping areas with an insecticide to kill insects.

4. If you are not sleeping in a well-screened or air-conditioned area, use a bed net and tuck it under your mattress. If possible, use a bed net that has been soaked in or sprayed with a pyrethroid-containing insecticide. The same treatment can be applied to screens, curtains, sheets, and clothing (clothing should be retreated after five washings)."

On February 2012, the nonprofit Infectious Disease Research Institute launched a clinical trial of the visceral leishmaniasis vaccine. The vaccine is a recombinant form of two fused Leishmania parasite proteins with an adjuvant. Two phase 1 clinical trials with healthy volunteers are to be conducted. The first one takes place in Washington (state) and is followed by a trial in India.

Some of the strategies for controlling tropical diseases include:

- Draining wetlands to reduce populations of insects and other vectors, or introducing natural predators of the vectors.

- The application of insecticides and/or insect repellents) to strategic surfaces such as clothing, skin, buildings, insect habitats, and bed nets.

- The use of a mosquito net over a bed (also known as a "bed net") to reduce nighttime transmission, since certain species of tropical mosquitoes feed mainly at night.

- Use of water wells, and/or water filtration, water filters, or water treatment with water tablets to produce drinking water free of parasites.

- Sanitation to prevent transmission through human waste.

- In situations where vectors (such as mosquitoes) have become more numerous as a result of human activity, a careful investigation can provide clues: for example, open dumps can contain stagnant water that encourage disease vectors to breed. Eliminating these dumps can address the problem. An education campaign can yield significant benefits at low cost.

- Development and use of vaccines to promote disease immunity.

- Pharmacologic pre-exposure prophylaxis (to prevent disease before exposure to the environment and/or vector).

- Pharmacologic post-exposure prophylaxis (to prevent disease after exposure to the environment and/or vector).

- Pharmacologic treatment (to treat disease after infection or infestation).

- Assisting with economic development in endemic regions. For example, by providing microloans to enable investments in more efficient and productive agriculture. This in turn can help subsistence farming to become more profitable, and these profits can be used by local populations for disease prevention and treatment, with the added benefit of reducing the poverty rate.

- Hospital for Tropical Diseases

- Tropical medicine

- Infectious disease

- Neglected diseases

- List of epidemics

- Waterborne diseases

- Globalization and disease

Inclusion of NTDs into initiatives for malaria, HIV/AIDS, and tuberculosis, as well as integration of NTD treatment programs, may have advantages given the strong link between these diseases and NTDs. Some neglected tropical diseases share common vectors (sandflies, black flies, and mosquitos). Both medicinal and vector control efforts may be combined.

A four-drug rapid-impact package has been proposed for widespread proliferation. Administration may be made more efficient by targeting multiple diseases at once, rather than separating treatment and adding work to community workers. This package is estimated to cost US$0.40 per patient. When compared to stand-alone treatment, the savings are estimated to be 26–47%. While more research must be done in order to understand how NTDs and other diseases interact in both the vector and the human stages, safety assessments have so far produced positive results.

Many neglected tropical diseases and other prevalent diseases share common vectors, creating another opportunity for treatment and control integration. One such example of this is malaria and lymphatic filariasis. Both diseases are transmitted by the same or related mosquito vectors. Vector control, through the distribution of insecticide treated nets, reduces the human contact with a wide variety of disease vectors. Integrated vector control may also alleviate pressure on mass drug administration, especially with respect to rapidly evolving drug resistance. Combining vector control and mass drug administration deemphasizes both, making each less susceptible to resistance evolution.

Biotechnology companies in the developing world have targeted neglected tropical diseases due to need to improve global health.

Mass drug administration is considered a possible method for eradication, especially for lymphatic filariasis, onchocerciasis, and trachoma, although drug resistance is a potential problem. According to Fenwick, Pfizer donated 70 million doses of drugs in 2011 to eliminate trachoma through the International Trachoma Initiative. Merck has helped The African Programme for the Control of Onchocerciasis (APOC) and Oncho Elimination Programme for the Americas to greatly diminished the effect of Onchocerciasis by donating ivermectin. Merck KGaA pledged to give 200 million tablets of praziquantel over 10 years, the only cure for schistosomiasis. GlaxoSmithKline has donated two billion tablets of medicine for lymphatic filariasis and pledged 400 million deworming tablets per year for five years in 2010. Johnson & Johnson has pledged 200 million deworming tablets per year. Novartis has pledged leprosy treatment, EISAI pledged two billion tablets to help treat lymphatic filariasis.

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.

Animal trypanosomiasis, also known as nagana and nagana pest, or sleeping sickness, is a disease of vertebrates. The disease is caused by trypanosomes of several species in the genus "Trypanosoma" such as "Trypanosoma brucei". "Trypanosoma vivax" causes nagana mainly in West Africa, although it has spread to South America. The trypanosomes infect the blood of the vertebrate host, causing fever, weakness, and lethargy, which lead to weight loss and anemia; in some animals the disease is fatal unless treated. The trypanosomes are transmitted by tsetse flies.

An interesting feature is the remarkable tolerance to nagana pathology shown by some breeds of cattle, notably the N'Dama – a West African "Bos taurus" breed. This contrasts with the susceptibility shown by East African "Bos indicus" cattle such as the zebu.

The term Winterbottom's sign derives from descriptions of the posterior cervical lymphadenopathy associated with African trypanosomiasis made by a slave trader using the sign to weed out the ill.

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.

Winterbottom's sign is seen in the early phase of African trypanosomiasis, a disease caused by the parasites "Trypanosoma brucei rhodesiense" and "Trypanosoma brucei gambiense" which is more commonly known as African sleeping sickness. Dr. Anthony Martinelli describes Winterbottom's sign as the swelling of lymph nodes (lymphadenopathy) along the back of the neck, in the posterior cervical chain of lymph nodes, as trypanosomes travel in the lymphatic fluid and cause inflammation.

It may be suggestive of cerebral infection.

There is no cure for EEE. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation, and antipyretics. About four percent of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage.

There is currently no effective marburgvirus-specific therapy for MVD. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections. Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of MARV has been used successfully in nonhuman primate models as post-exposure prophylaxis. Novel, very promising, experimental therapeutic regimens rely on antisense technology: phosphorodiamidate morpholino oligomers (PMOs) targeting the MARV genome could prevent disease in nonhuman primates. Leading medications from Sarepta and Tekmira both have been successfully used in European humans as well as primates.

The disease can be prevented in horses with the use of vaccinations. These vaccinations are usually given together with vaccinations for other diseases, most commonly WEE, VEE, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans there is no vaccine for EEE so prevention involves reducing the risk of exposure. Using repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention

Intestinal parasites are extremely prevalent in tropical areas. These include hookworms, roundworms, and other amoebas. They can aggravate malnutrition by depleting essential nutrients through intestinal blood loss and chronic diarrhea. Chronic worm infections can further burden the immune system. At the same time, chronic worm infections can cause immune activation that increases susceptibility of HIV infection and vulnerability to HIV replication once infected.

Schistosomiasis (bilharzia) is a parasitic disease caused by the parasitic flatworm trematodes. Moreover, more than 80 percent of the 200 million people worldwide who have schistosomiasis live in sub-Saharan Africa. Infections often occur in contaminated water where freshwater snails release larval forms of the parasite. After penetrating the skin and eventually traveling to the intestines or the urinary tract, the parasite lays eggs and infects those organs. It damages the intestines, bladder, and other organs and can lead to anemia and protein-energy deficiency. Along with malaria, schistosomiasis is one of the most important parasitic co-factors aiding in HIV transmission. Epidemiological data shows schistosome-endemic areas coincide with areas of high HIV prevalence, suggesting that parasitic infections such as schistosomiasis increase risk of HIV transmission.

The primary method for controlling the incidence of gaffkaemia is improved hygiene. Other measures include limiting damage to the exoskeleton (preventing the bacterium's entry), reducing the water temperature, and reducing the stocking density. Antibiotics may be effective against the bacterium, but only tetracycline is currently approved by the U.S Food and Drug Administration for use in American lobsters.

Antibiotics, in non-resistant strains of the pathogen, can prevent the vegetative state of the bacterium forming. Drug treatment to prevent the American foulbrood spores from successfully germinating and proliferating is possible using oxytetracycline hydrochloride (Terramycin).

Another drug treatment, tylosin tartrate, was approved by the US Food and Drug Administration (FDA) in 2005.

Chemical treatment is sometimes used prophylactically, but this is a source of considerable controversy because certain strains of the bacterium seem to be rapidly developing resistance. In addition, hives that are contaminated with millions of American foulbrood spores have to be prophylactically treated indefinitely. Once the treatment is suspended the American foulbrood spores germinate successfully again leading to a disease outbreak.

Because of the persistence of the spores (which can survive up to 40 years), many State Apiary Inspectors require an AFB diseased hive to be burned completely. A less radical method of containing the spread of disease is burning the frames and comb and thoroughly flame scorching the interior of the hive body, bottom board and covers. Dipping the hive parts in hot paraffin wax or a 3% sodium hypochlorite solution (bleach) also renders the AFB spores innocuous. It is also possible to sterilize an infected hive without damaging either the structure of the hive or the stores of honey and pollen it contains by sufficiently lengthy exposure to an atmosphere of ethylene oxide gas, as in a closed chamber, as hospitals do to sterilize equipment that cannot withstand steam sterilization.

Brigham Young University is currently studying the use of phage therapy to treat American foulbrood.

Since marburgviruses are not spreading via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids, or possibly contaminated materials and utensils. Patients ought to be isolated but still have the right to be visited by family members. Medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, ought to be discouraged or modified, ideally with the help of local traditional healers.