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.

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).

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 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.

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

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.

Oral anti-parasitic drugs such as praziquantel are the treatment of choice. Treatment with praziquantel has been approved by the U.S. Food and Drug Administration and is quite effective against these parasites. Usual treatments are with praziquantel (5–10 mg/kg, single-administration) or niclosamide (adults and children over 6 years: 2 g, single-administration after a light breakfast, followed after 2 hours by a laxative; children aged 2–6 years: 1 g; children under 2 years: 500 mg). Albendazole is also highly effective. Atrabine is quite effective but has adverse effects in humans.

Tapeworms are treated with medications taken by mouth, usually in a single dose. The drug of choice for tapeworm infections is praziquantel. Niclosamide can also be used.

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.

Several drugs are effective for fascioliasis, both in humans and in domestic animals. The drug of choice in the treatment of fasciolosis is triclabendazole, a member of the benzimidazole family of anthelmintics. The drug works by preventing the polymerization of the molecule tubulin into the cytoskeletal structures, microtubules. Resistance of "F. hepatica" to triclabendazole has been recorded in Australia in 1995 and Ireland in 1998.

Praziquantel treatment is ineffective.

There are case reports of nitazoxanide being successfully used in human fasciolosis treatment in Mexico. There are also reports of bithionol being used successfully.

More recently, Mirazid, an Egyptian drug made from myrrh, has been investigated as an oral treatment of trematode-caused ailments including fascioliasis.

Nitazoxanide has been found effective in trials, but is currently not recommended. The life cycle includes freshwater snails as an intermediate host of the parasite.

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.

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As the disease is self-limiting, at least when exposure to the parasite is limited, management is mostly confined to treatment. Due to the secondary infection that can cause serious medical issues, the recommended course of action upon diagnosis is a surgical extraction of the fleas followed by the application of a topical antibiotic. Care should be taken to avoid tearing the flea during the extraction procedures as severe inflammation will result. The same will occur if part of the flea is left behind. Sterile equipment should always be used, as contaminated instruments could act as mechanical vectors for pathogens to enter the body.

There is no drug that has proven to be effective against embedded fleas. Oral niridazole was once considered a therapeutic drug, but well-designed studies are lacking and, given the severe adverse effects, this is one drug that is likely to cause more harm than good. However, it has some anecdotal evidence of lysing the fleas altogether. Oral ivermectin is considered by some in endemic areas to be a panacea against the fleas but studies using high doses have failed to validate this hypothesis. Other drugs such as topical ivermectin and metrifonate have been somewhat successful, but not enough to be significant. [2,5] For superinfections, trimethoprim, sulfamethoxazole, metronidazole, amoxicillin, (with/without clavulanate) have been used successfully, though these treat only secondary infections.

Successful topical treatments also include cryotherapy and electrodesiccation of the lesion. If formaldehyde, chloroform, or DDT are used topically, care should be taken when dealing with the resulting morbidity. The "T. penetrans" flea can also be suffocated using occlusive petrolatum, while Vaseline will kill the organism as well, most likely due to suffocation as the stigmatas would be covered. The gum of the mammee apple ("Mammea americana"), a fruit that also goes by the name Saint Domingo apricot, has also been used to kill the chigoe flea, though this has not been reported in the main "T. penetrans" literature.

Even without treatment, the burrowed fleas will die within five weeks and are naturally sloughed off as the skin sheds.

The fundamental prevention strategy is hygiene and sanitation. Secondary measures include stricter meat-inspection standards, livestock confinement, health education, safe meat preparation, mass drug therapy, and identifying and treating human and pig carriers. Moreover, a high level of sanitation and prevention of human faecal contamination of pig feeds also plays a major role in prevention. Infection can be prevented with proper disposal of human faeces around pigs, cooking meat thoroughly and/or freezing the meat at −10 °C for 5 days. For human cysticercosis, dirty hands are attributed to be the primary cause, and especially common among food handlers.

Proper cooking of meat is an effective prevention. For example, cooking (56 °C for 5 minutes) of beef viscera destroys cysticerci. Refrigeration, freezing (−10 °C for 9 days) or long periods of salting is also lethal to cysticerci. Inspection of beef and proper disposal of human excreta are also important measures.

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.

Lymphatic filariasis is also known as elephantiasis. There are approximately 120 million individuals infected and 40 million with deformities. Approximately two-thirds of cases are in Southwest Asia and one-third in Africa. Lymphatic filariasis is rarely fatal. Lymphatic filariasis has lifelong implications, such as lymphoedema of the limbs, genital disease, and painful recurrent attacks. Most people are asymptomatic, but have lymphatic damage. Up to 40 percent of infected individuals have kidney damage. It is a vector-borne disease, caused by nematode worms that are transmitted by mosquitoes.

It can be treated with cost-effective antihelminthic treatments, and washing skin can slow or even reverse damage. It is diagnosed with a finger-prick blood test.

Evidence in support of the idea that helminthic infections reduce the severity of autoimmune diseases is primarily derived from animal models. Studies conducted on mice and rat models of colitis, muscular sclerosis, type 1 diabetes, and asthma have shown helminth-infected subjects to display protection from the disease. While helminths are often considered a homogenous group, considerable differences exist between species and the utilization of species in clinical research varies between human and animal trials. As such, caution must be exercised when interpreting the results from animal models.

Helminthic therapy is currently being studied as a treatment for several (non-viral) autoimmune diseases in humans including celiac disease, Crohn's disease, multiple sclerosis, ulcerative colitis, and atherosclerosis. It is currently unknown which clinical dose or species of helminth is the most effective method of treatment. Hookworms have been linked to reduced risk of developing asthma, while "Ascaris lumbricoides" (roundworm infection) was associated with an "increased" risk of asthma. Similarly, "Hymenolepis nana", "Trichoris trichiura", "Ascaris lumbricoides", "Strongyloides stercolaris", "Enterobius vermicularis", and "Trichuris suis" ova have all been found to lower the number of symptom exacerbations, reduce the number of symptom relapses, and decrease the number of new or enlarging brain lesions in patients with multiple sclerosis at doses ranging from 1,180 to 9,340 eggs per gram. However, "Ascaris lumbricoides", "Strongyloides stercolaris" and "Enterobius vermicularis" are not considered suitable for therapeutic use in humans because they do not meet the criteria for a therapeutic helminth.

"Trichuris suis" ova has been used in most cases to treat autoimmune disorders because it is thought to be non-pathogenic in humans and therefore has been rendered as safe.

The use of "Trichuris suis" ova has been granted by the USA Food and Drug Administration as an investigational medicinal product (IMP). While in the UK, the hookworm "Necator americanus" has been granted an IMP license by the Medicines and Healthcare Regulatory Authority. This hookworm is likely to be relatively safe, although it can cause temporary gastrointestinal side effects, especially following the initial inoculation and with larger doses.

The general ideal characteristics for a therapeutic helminth are as follows:

- Little or no pathogenic potential

- Does not multiply in the host

- Cannot be directly spread to close contacts

- Produces a self-limited colonization in humans

- Produces an asymptomatic colonization in humans

- Does not alter behaviour in patients with depressed immunity

- Is not affected by most commonly used medications

- Can be eradicated with an anti-helminthic drug

- Can be isolated free of other potential pathogens

- Can be isolated or produced in large numbers

- Can be made stable for transport and storage

- Easy to administer

Currently, there is no vaccine against human granulocytic anaplasmosis, so antibiotics are the only form of treatment. The best way to prevent HGA is to prevent getting tick bites.

Cattle infested with bovine pediculosis are generally treated chemically, by drugs like ivermectin and cypermethrin.

Helminths are extremely successful parasites capable of establishing long-lasting infections within a host. During this time, helminths compete with the host organism's cells for nutrient resources and thus possess the potential to cause harm. However, the number of organisms hosted by individuals undergoing helminthic therapy is very small and any side effects are typically only encountered in the first three months of infection. In the long term, the vast majority of clinically infected individuals are asymptomatic, with no significant nutrient loss. In fact, nutrient uptake can be enhanced in some subjects who are hosting a small number of helminths. If the side effects from helminthic therapy were to become unmanageable, they can be alleviated by the use of anthelminthic medications.[1][7][8] The most common clinical symptoms which may be encountered while undergoing helminthic therapy can include:

- Fatigue

- Gastrointestinal discomfort

- Anemia

- Fever

- Abdominal pain

- Weight loss

- Anorexia

- Diarrhea

- General malaise

Doxycycline is the treatment of choice. If anaplasmosis is suspected, treatment should not be delayed while waiting for a definitive laboratory confirmation, as prompt doxycycline therapy has been shown to improve outcomes. Presentation during early pregnancy can complicate treatment. Doxycycline compromises dental enamel during development. Although rifampin is indicated for post-delivery pediatric and some doxycycline-allergic patients, it is teratogenic. Rifampin is contraindicated during conception and pregnancy.

If the disease is not treated quickly, sometimes before the diagnosis, the person has a high chance of mortality. Most people make a complete recovery, though some people are intensively cared for after treatment. A reason for a person needing intensive care is if the person goes too long without seeing a doctor or being diagnosed. The majority of people, though, make a complete recovery with no residual damage.

In the 15th century, topical mercury treatment was used to treat pediculosis.

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.

Doxycycline and minocycline are the medications of choice. For people allergic to antibiotics of the tetracycline class, rifampin is an alternative. Early clinical experience suggested that chloramphenicol may also be effective, however, in vitro susceptibility testing revealed resistance.