Parasitic infections can usually be treated with antiparasitic drugs.

Albendazole and mebendazole have been the treatments administered to entire populations to control hookworm infection. However, it is a costly option and both children and adults become reinfected within a few months after deparasitation occurs raising concerns because the treatment has to repeatedly be administered and drug resistance may occur.

Another medication administered to kill worm infections has been pyrantel pamoate. For some parasitic diseases, there is no treatment and, in the case of serious symptoms, medication intended to kill the parasite is administered, whereas, in other cases, symptom relief options are used. Recent papers have also proposed the use of viruses to treat infections caused by protozoa.

The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin. Ivermectin does not kill the "Strongyloides" larvae, only the adult worms, therefore repeat dosing may be necessary to properly eradicate the infection. There is an auto-infective cycle of roughly two weeks in which Ivermectin should be re-administered however additional dosing may still be necessary as it will not kill "Strongyloides" in the blood or larvae deep within the bowels or diverticula. Other drugs that are effective are albendazole and thiabendazole (25 mg/kg twice daily for 5 days—400 mg maximum (generally)). All patients who are at risk of disseminated strongyloidiasis should be treated. The optimal duration of treatment for patients with disseminated infections is not clear.

Treatment of strongyloidiasis can be difficult and "Strongyloides" has been known to live in individuals for decades; even after treatment. Continued treatment is thus necessary even if symptoms resolve.

Because of the high cost of Stromectol, the veterinary formula Ivomec can be used. Government programs are needed to help citizens finance lifelong medication.

Clothes and sheets must be washed with enzyme washing powder and dried on hot daily.

Broad-spectrum benzimidazoles (such as albendazole and mebendazole) are the first line treatment of intestinal roundworm and tapeworm infections. Macrocyclic lactones (such as ivermectin) are effective against adult and migrating larval stages of nematodes. Praziquantel is the drug of choice for schistosomiasis, taeniasis, and most types of food-borne trematodiases. Oxamniquine is also widely used in mass deworming programmes. Pyrantel is commonly used for veterinary nematodiasis. Artemisinins and derivatives are proving to be candidates as drugs of choice for trematodiasis.

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.

Toxocariasis will often resolve itself, because the "Toxocara" larvae cannot mature within human hosts. Corticosteroids are prescribed in severe cases of VLM or if the patient is diagnosed with OLM. Either albendazole (preferred) or mebendazole (“second line therapy”) may be prescribed. Granulomas can be surgically removed, or laser photocoagulation and cryoretinopexy can be used to destroy ocular granulomas.

Visceral toxocariasis in humans can be treated with antiparasitic drugs such as albendazole or mebendazole, tiabendazole or diethylcarbamazine usually in combination with anti-inflammatory medications. Steroids have been utilized with some positive results. Anti-helminthic therapy is reserved for severe infections (lungs, brain) because therapy may induce, due to massive larval killing, a strong inflammatory response. Treatment of ocular toxocariasis is more difficult and usually consists of measures to prevent progressive damage to the eye.

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.

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).

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.

After infection, steroids, such as prednisone may be used to relieve muscle pain associated with larval migration.

Early administration of anthelmintics, such as mebendazole or albendazole, decreases the likelihood of larval encystation, particularly if given within three days of infection. However, most cases are diagnosed after this time.

In humans, Mebendazole (200–400 mg three times a day for three days) or albendazole (400 mg twice a day for 8–14 days) are given to treat trichinosis. These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age.

The severe symptoms caused by the parasite can be avoided by cleansing the skin, surgery, or the use of anthelmintic drugs, such as diethylcarbamazine (DEC), ivermectin, or albendazole. The drug of choice is DEC, which can eliminate the microfilariae from the blood and also kill the adult worms with a dosage of 6 mg/kg semiannually or annually. A polytherapy treatment that includes ivermectin with DEC or albendazole is more effective than each drug alone. Protection is similar to that of other mosquito-spread illnesses; one can use barriers both physical (a mosquito net), chemical (insect repellent), or mass chemotherapy as a method to control the spread of the disease.

Mass chemotherapy should cover the entire endemic area at the same time. This will significantly decrease the overall microfilarial titer in blood in mass, hence decreasing the transmission through mosquitoes during their subsequent bites.

Antibiotic active against the Wolbachia symbionts of the worm have been experimented with as treatment. Wolbachia-free worms first become sterile, and later die prematurely.

If complications of helminthiasis, such as intestinal obstruction occur, emergency surgery may be required. Patients who require non-emergency surgery, for instance for removal of worms from the biliary tree, can be pre-treated with the anthelmintic drug albendazole.

The standard of care is administration of antifilarial drugs, most commonly Ivermectin or diethyl-carbamazine (DEC). The most efficacious dose in all nematode and parasitic infections is 200 µg/kg of ivermectin. There has also been other various anthelminthic drugs used, such as mebendazole, levamisole, albendazole and thiabendazole. In worst-case scenarios, surgery may be necessary to remove nematodes from the abdomen or chest. However, mild cases usually do not require treatment.

Parasitic worms and nematodes regulate many immune pathways of their host in order to increase their chances of survival. For example, molecules secreted by "Acanthocheilonema vitae" actually limit host effective immune mechanisms. These molecules are called excretory-secretory products. An effective excretory-secretory product released from "Acanthochelionema vitae" is called ES-62, which can affect multiple immune system cell types. ES-62 has anti-inflammatory effects when subjected to mice. The anti-inflammatory effect occurs because of a phosphorylcholine (PC)-containing moiety and signal transduction. More research needs to be completed; however there is some evidence that "Acanthocheilonema vitae" may have anti-inflammatory effects, and should be researched further.

On the basis of the laboratory evidence and case reports, amphotericin B has been the traditional mainstay of PAM treatment since the first reported survivor in the United States in 1982.

Treatment has often also used combination therapy with multiple other antimicrobials in addition to amphotericin, such as fluconazole, miconazole, rifampicin and azithromycin. They have shown limited success only when administered early in the course of an infection. Fluconazole is commonly used as it has been shown to have synergistic effects against naegleria when used with amphotericin in-vitro.

While the use of rifampicin has been common, including in all four North American cases of survival, its continued use has been questioned. It only has variable activity in-vitro and it has strong effects on the therapeutic levels of other antimicrobials used by inducing cytochrome p450 pathways.

In 2013, the two most recent successfully treated cases in the United States utilized drug combinations that included the medication miltefosine as well as targeted temperature management to manage brain swelling that is secondary to the infection. As of 2015 there were no data on how well miltefosine is able to reach the central nervous system. As of 2015 the U.S. CDC offered miltefosine to doctors for the treatment of free-living ameobas including naegleria.

There are two drugs available, praziquantel and oxamniquine, for the treatment of schistosomiasis. They are considered equivalent in relation to efficacy against "S. mansoni" and safety. Because of praziquantel's lower cost per treatment, and oxaminiquine's lack of efficacy against the urogenital form of the disease caused by "S. haematobium", in general praziquantel is considered the first option for treatment. The treatment objective is to cure the disease and to prevent the evolution of the acute to the chronic form of the disease. All cases of suspected schistosomiasis should be treated regardless of presentation because the adult parasite can live in the host for years.

Schistosomiasis is treatable by taking by mouth a single dose of the drug praziquantel annually.

The WHO has developed guidelines for community treatment based on the impact the disease has on children in villages in which it is common:

- When a village reports more than 50 percent of children have blood in their urine, everyone in the village receives treatment.

- When 20 to 50 percent of children have bloody urine, only school-age children are treated.

- When fewer than 20 percent of children have symptoms, mass treatment is not implemented.

Other possible treatments include a combination of praziquantel with metrifonate, artesunate, or mefloquine. A Cochrane review found tentative evidence that when used alone, metrifonate was as effective as praziquantel.

Another agent, mefloquine, which has previously been used to treat and prevent malaria, was recognised in 2008–2009 to be effective against "Schistosoma".

For the treatment of individuals, doxycycline is used to kill the "Wolbachia" bacteria that live in adult worms. This adjunct therapy has been shown to significantly lower microfilarial loads in the host, and may kill the adult worms, due to the symbiotic relationship between "Wolbachia" and the worm. In four separate trials over 10 years with various dosing regimens of doxycycline for individualized treatment, doxycycline was found to be effective in sterilizing the female worms and reducing their numbers over a period of four to six weeks. Research on other antibiotics, such as rifampicin, has shown it to be effective in animal models at reducing "Wolbachia" both as an alternative and as an adjunct to doxycycline. However, doxycycline treatment requires daily dosing for at least four to six weeks, making it more difficult to administer in the affected areas.

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

In mass drug administration (MDA) programmes, the treatment for onchocerciasis is ivermectin (trade name: Mectizan); infected people can be treated with two doses of ivermectin, six months apart, repeated every three years. The drug paralyses and kills the microfilariae causing fever, itching, and possibly oedema, arthritis and lymphadenopathy. Intense skin itching is eventually relieved, and the progression towards blindness is halted. In addition, while the drug does not kill the adult worms, it does prevent them for a limited time from producing additional offspring. The drug therefore prevents both morbidity and transmission for up to several months.

Ivermectin treatment is particularly effective because it only needs to be taken once or twice a year, needs no refrigeration, and has a wide margin of safety, with the result that it has been widely given by minimally trained community health workers.

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.

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 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.

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

Some treatments for infection with "Toxocara cati" include drugs designed to cause the adult worms to become partially anaesthetized and detach from the intestinal lining, allowing them to be excreted live in the feces. Such medications include piperazine and pyrantel. These are frequently combined with the drug praziquantel which appears to cause the worm to lose its resistance to being digested by the host animal. Other effective treatments include ivermectin, milbemycin, and selamectin. Dichlorvos has also been proven to be effective as a poison, though moves to ban it over concerns about its toxicity have made it unavailable in some areas.

Treatment for wild felids, however, is difficult for this parasite, as detection is the best way to find which individuals have the parasite. This can be difficult as infected species are hard to detect. Once detected, the infected individuals would have to be removed from the population, in order to lower the risk of continual exposure to the parasites.

A primary method that has been used to lower the amount of infection is removal through hunting. Removal can also occur through landowners, as Dare and Watkins (2012) discovered through their research on cougars. Both hunters and landowners can provide samples that can be used to detect the presence of feline roundworm in the area, as well as help remove it from the population. This method is more practical than administering medications to wild populations, as wild animals, as mentioned before, are harder to find in order to administer medicinal care.

Medicinal care, however, is also another method used in round worm studies; such as the experiment on managing raccoon roundworm done by Smyser et al. (2013) in which they implemented medical baiting. However, medicine is often expensive and the success of the baiting depends on if the infected individuals consume the bait. Additionally, it can be costly (in time and resources) to check on baited areas. Removal by hunting allows agencies to reduce costs and gives agencies a more improved chance of removing infected individuals.

Anecdotal data gathered from helminth self-treaters and their physicians and presented in socio-medical studies suggest that a much larger number of diseases may be amenable to helminthic therapy than are currently being investigated by formal clinical trials.