Ivermectin and Single-Celled Parasites (Protozoa)

Table of Contents

1. Worms Versus Single-Celled Parasites
2. Leishmania
3. Trypanosomes
4. Malaria Parasites
5. Toxoplasma
6. Acanthamoeba
7. Giardia, Cryptosporidium, Babesia and Others
8. Amoebae and Trichomonads of the Mouth
9. Key Research Papers
10. Connections
11. Featured Videos

Worms Versus Single-Celled Parasites

Worms (helminths) and arthropods such as mites, lice, ticks and insects are animals with many cells, nerves and muscles. Protozoa are single cells, each with a nucleus, larger and more complex than a bacterium, with no nerves or muscles. Many switch between an active, feeding form, the trophozoite, and a tough resting form such as a cyst.

Ivermectin’s most common target is the glutamate-gated chloride channel [5], a gate in the nerve and muscle cells of worms and insects. When ivermectin holds it open, chloride floods in, the cell falls silent and the parasite is paralysed. The main Ivermectin page explains this, and why people are protected.

Protozoa are a different question. A 2022 computer analysis found that the classic structures of these channels are absent in the kinetoplastids, the group of protozoa that includes trypanosomes and Leishmania [5]. Any effect of ivermectin on them has to come about another way.

Other targets proposed by laboratory studies

• Importins, carrier proteins that move other proteins into the cell’s nucleus. Ivermectin bound directly to importin alpha of the malaria parasite Plasmodium falciparum and of Toxoplasma gondii, stopping it from binding the “address tags” (nuclear localization signals) that mark proteins for the nucleus, and it limits the malaria parasite’s growth in culture [6]. The same 2022 study found possible importin genes in the genomes of trypanosomes and related parasites and proposed them as a target [5].
• Mitochondria, the cell’s energy producers: preliminary work suggested that ivermectin targets those of Leishmania infantum [7].
• Oxidative damage: in Giardia lamblia, ivermectin raised reactive oxygen species (unstable, damaging forms of oxygen), fragmented the parasite’s DNA (its genetic material), halted its cell cycle and caused changes consistent with apoptosis, a form of programmed cell death [8].
• Energy and growth genes: in Trypanosoma evansi, ivermectin lowered the activity of eight of 13 genes studied as drug targets, among them genes for sugar breakdown (glycolysis), a calcium pump and enzymes involved in multiplication [9].

The concentration question

Laboratory studies usually report the IC50 (half-maximal inhibitory concentration): the concentration of a drug that halves the parasite’s growth; the lower it is, the stronger the drug. The concentration that harms half of the host’s own cells, divided by the IC50, gives the selectivity index; the higher it is, the more the drug spares host cells. Concentrations are given in micromolar (µM) or nanomolar (nM, a thousandth of a micromolar); for ivermectin, 1 µM is about 875 nanograms per millilitre. Whether a laboratory concentration can be reached in the body is a separate question:

• In hamsters given two standard doses (200 and 400 micrograms per kilogram), blood levels of ivermectin were in the nanograms-per-millilitre range. These levels killed blood-feeding sand flies for up to 10 days, while the Leishmania major parasites the flies carried appeared to tolerate them [1].
• A 2019 study that found activity against the malaria parasite at nanomolar concentrations wrote that these activities “might be difficult to reach with current regimens” [10].
• Against Trypanosoma evansi, the IC50 (13.82 µM) was close to the concentrations that harmed half of the horse white blood cells and monkey kidney cells used for comparison (17.48 and 22.05 µM) [9].

Leishmania

Leishmania parasites are spread by sand-fly bites. Depending on the species, they cause skin sores (cutaneous leishmaniasis) or visceral leishmaniasis, a disease of the spleen, liver and bone marrow. In the sand fly the parasite is a whip-tailed form, the promastigote; in the body it lives inside immune cells called macrophages as a small rounded form, the amastigote. Treatment of visceral leishmaniasis is held back by toxic or costly drugs and by parasite resistance [7].

Laboratory findings

• Against Leishmania infantum (2021), ivermectin’s IC50 was 3.64 µM, against 427.50 µM for macrophages: a selectivity index of 117.45. Amphotericin B, a standard leishmaniasis drug, acted at a far lower concentration (0.12 µM) but was much less selective (8.90). Ivermectin reduced the share of infected macrophages and the parasites inside them, and parasites exposed to it beforehand infected fewer macrophages [7].
• In macrophages infected with Leishmania donovani or Leishmania amazonensis (2023), ivermectin reduced the infection and the parasite load [11].
• Ivermectin also slowed the multiplication of Leishmania mexicana (2022) [5].

Animal findings

• Visceral leishmaniasis in mice (2021). In mice infected with Leishmania infantum, ivermectin, ivermectin carried in polymeric micelles (microscopic carrier particles), and the standard drug miltefosine each significantly reduced the parasite load in the spleen, liver, bone marrow and nearby lymph nodes, with a type 1 immune response against the parasite. The micelle form gave better results than the other treatments, and the authors proposed it for future study as a treatment for visceral leishmaniasis [7].
• Skin leishmaniasis in mice (2023). In mice infected with Leishmania amazonensis (16 per group), ivermectin, free or in micelles, shrank the skin lesions and cut the parasite load in the infected skin, spleen, liver and lymph nodes, with low toxicity to the organs. The effect held 30 days after treatment, while untreated mice developed a type 2 immune response and high parasite loads [11].
• Skin leishmaniasis in mice (2025). In mice infected with Leishmania major (10 per group), two weeks of daily ivermectin significantly reduced the size of the sores compared with untreated mice, about as much as meglumine antimoniate, a standard antimony drug for leishmaniasis; the two together reduced them most [12].
• Sand flies on treated hamsters (2011). Infected sand flies that fed on hamsters 4 hours, 1 day or 2 days after the higher dose of ivermectin lived 1.6, 2.1 and 2.7 days on average, against 11.5 days on untreated hamsters. Yet the Leishmania major parasites taken from surviving flies moved and survived normally, and 21.7% of the treated hamsters developed skin sores after bites from infected flies [1].

Human findings

No study of ivermectin in people with leishmaniasis was found for this page.

Trypanosomes

Trypanosomes are whip-tailed parasites of the blood and tissues. Trypanosoma brucei, spread by tsetse flies, causes African sleeping sickness; Trypanosoma cruzi, spread by blood-sucking triatomine (“kissing”) bugs, causes Chagas disease, a long-lasting infection that can damage the heart; and Trypanosoma evansi causes surra in animals such as camels, horses and cattle. The two drugs for Chagas disease, benznidazole and nifurtimox, show limited efficacy and many side effects [5].

Laboratory findings

• Trypanosoma cruzi (2022). Ivermectin slowed, in step with the dose, the multiplication of the form that lives in the insect (the epimastigote) and reduced the survival of the forms that live inside the host’s cells (amastigotes) and in the blood (trypomastigotes). On the insect form it stopped growth at 50 µM and killed the parasites at 100 µM. Against the form inside cells, its selectivity index compared with monkey kidney cells was 12. With benznidazole or nifurtimox, the effects mostly added together [5].
• Trypanosoma evansi (2022). Ivermectin significantly inhibited the surra parasite’s growth, with an IC50 of 13.82 µM that the authors described as potent, but it also harmed horse white blood cells and monkey kidney cells at nearby concentrations (17.48 and 22.05 µM). The authors pointed to nano-sized formulations, or ivermectin relatives that are less toxic to cells and better absorbed, as directions for treating surra in animals [9].

Animal findings

• Mice (2012). In mice infected with Trypanosoma brucei brucei, a subspecies that infects livestock and is widely used in research, the most effective single dose of ivermectin extended average survival from 5 to 12 days, whether given as treatment or beforehand as prevention, and eased the infection’s anaemia. The authors wrote that further studies would be required, including of more doses or combinations with other drugs [13].
• Dogs with Chagas disease (2005). Dogs kept for long-term Chagas disease research were treated with ivermectin for ticks. The drug was highly effective in eliminating the ticks but showed no apparent effect on the dogs’ Trypanosoma cruzi infection. Kissing bugs that fed on the dogs soon after treatment died in large numbers, an effect that quickly faded [14].

Human findings

No study of ivermectin in people with sleeping sickness or Chagas disease was found for this page.

Malaria Parasites

Malaria is caused by Plasmodium parasites, spread by Anopheles mosquitoes. After a bite, the parasites (sporozoites) multiply silently in the liver, then invade red blood cells; this blood stage causes the illness. Some become sexual forms (gametocytes) that mosquitoes take up; in the mosquito they form oocysts on the gut wall, which release new sporozoites. Plasmodium falciparum causes the most dangerous malaria; Plasmodium vivax can also rest in the liver as dormant hypnozoites; Plasmodium berghei of rodents and Plasmodium cynomolgi of monkeys are laboratory models. The malaria field turned to ivermectin mainly because it kills blood-sucking mosquitoes; its activity against the parasite itself has been only partly investigated [10].

Liver stage

• Mice (2017). Several avermectins, ivermectin’s compound family, inhibited the liver stage of Plasmodium in laboratory cultures. In infected animals, ivermectin strongly inhibited liver infection by impairing the parasite’s development inside liver cells, which lowered the later blood infection, reduced disease severity and improved survival [15]. A 2020 paper describes this rodent work as liver-stage inhibition of Plasmodium berghei in mice dosed by mouth with 1 to 10 milligrams per kilogram [16].
• Monkeys (2020). In macaque liver cells, ivermectin inhibited the growing liver forms of Plasmodium cynomolgi (IC50 10.42 µM) and its hypnozoites (IC50 29.24 µM) when given as a high dose for prevention, but not when given to clear an established liver infection. In rhesus macaques given 0.3, 0.6 or 1.2 milligrams per kilogram by mouth for 7 days, with or without chloroquine, no dose prevented or delayed the blood infection; ivermectin with chloroquine was well tolerated [16].
• Human liver cells (2024). In liver cells from human donors, ivermectin and two of its breakdown products inhibited the liver stage of Plasmodium falciparum when added on days 3 to 5 after infection (the “curative” mode), with only marginal activity on days 0 to 3 (the “prophylactic” mode); ivermectin’s IC50 ranged from 1.391 to 14.44 µM. It worked better with ketoconazole, which blocks cytochrome P450 3A4, a liver enzyme that breaks ivermectin down [17].
• People (2020). In a controlled human malaria infection trial, 8 volunteers took one dose of ivermectin (0.4 milligrams per kilogram) and 4 a placebo, 2 hours before 3,200 Plasmodium falciparum sporozoites were injected into a vein. All but one volunteer had parasites in the blood on day 11 or 12, with no significant effect of ivermectin; the authors concluded that at this dose it “has no clinically relevant activity against the pre-erythrocytic stages”, the stages before the blood [3].

A 2024 study summed up the liver-stage record: inhibition in a rodent malaria model, but none in a primate model or in a human malaria challenge trial [17].

Blood stage

• Laboratory (2019). Ivermectin acted against the blood stages of Plasmodium falciparum at nanomolar concentrations (IC50 about 100 nM) and against late-stage gametocytes (500 nM), apparently halting the cycle at the trophozoite stage. The authors wrote that these activities “might be difficult to reach with current regimens” but would matter more with high-dose regimens under investigation [10].
• Laboratory (2023). In artemisinin-sensitive and artemisinin-resistant Plasmodium falciparum, the IC50 was 0.81 µM, and ivermectin’s breakdown products were 2 to 4 times less active. It neither strengthened nor weakened the artemisinins (the main malaria drugs), their partner drugs or atovaquone. The authors concluded that ivermectin “does not have clinically relevant activity against the asexual blood stages” [18].
• Laboratory (2018). Plasma from healthy volunteers who had taken a single dose of ivermectin (200 micrograms per kilogram) affected the development of blood-stage Plasmodium vivax [19].
• People (2023). In a pilot trial in Gabon, 34 adults carrying Plasmodium falciparum without symptoms were randomly assigned to ivermectin (300 micrograms per kilogram daily for 3 days) or placebo. The parasite count fell by 90% in a median of 24.1 hours with ivermectin and 32.0 hours with placebo (hazard ratio 1.38, 95% confidence interval 0.64 to 2.97, a range that includes no difference); the authors concluded that the parasites were “reduced similarly” with both. No severe or serious adverse events occurred, and the authors called for studies of higher doses in larger groups [4].

In the mosquito

Ivermectin taken by people can cut malaria transmission, mainly by killing the mosquitoes that bite them; the parasites a dead mosquito carries die with it. That is a mosquito effect, not a direct effect on the parasite.

• People and mosquitoes (2015). In a double-blind trial in Burkina Faso, 120 people carrying Plasmodium falciparum without symptoms received the malaria treatment artemether-lumefantrine with a placebo or with one or two doses of ivermectin (200 micrograms per kilogram). Mosquitoes that fed on their blood a day after ivermectin died 4 to 7 times more often. There was no evidence that ivermectin reduced Plasmodium infection in the surviving mosquitoes; the 27% and 35% falls in estimated transmission in the first week came from the mosquito-killing effect [20].
• Laboratory mosquitoes (2018). In South American Anopheles mosquitoes fed on blood carrying Plasmodium vivax, ivermectin added to the blood (10 to 40 nanograms per millilitre), or plasma from volunteers hours to days after a dose, reduced the share of mosquitoes that developed oocysts, and more mosquitoes died. The study’s title calls this a sporontocidal effect, one on the parasite’s development inside the mosquito [19].

The two differ: the trial found no evidence of an effect on infection in surviving mosquitoes, while the laboratory study, with another parasite species and other mosquitoes, found fewer infected mosquitoes.

Toxoplasma

Toxoplasma gondii causes toxoplasmosis. Cats are its main host, and people catch it from undercooked meat, soil or cat faeces. In most people it stays silent as resting cysts in the brain and muscles, but it can harm unborn babies and people with weakened immune systems. Its fast-multiplying form is called the tachyzoite.

Laboratory findings

In a 2013 study of Toxoplasma gondii grown in human cells (a laryngeal cancer cell line), ivermectin significantly inhibited the multiplication of tachyzoites. After 48 hours its IC50 was 0.2 micrograms per millilitre, against 7.3 for sulfadiazine, a standard toxoplasmosis drug, and none of the concentrations tested harmed the human cells after 72 hours [21]. Another laboratory study found that ivermectin binds directly to the importin alpha of Toxoplasma gondii [6].

Animal findings

In a 2023 study, mice with a chronic brain infection, whose immune systems had been suppressed with the steroid dexamethasone, were treated with ivermectin. It reduced the size and number of Toxoplasma cysts in the brain, with a reduction rate of 68.85%, and improved the brain tissue seen under the microscope. It also raised GABA (gamma-aminobutyric acid), a calming nerve messenger that the infection had depleted: its expression in brain tissue measured 22.1 in healthy mice, 3.78 in untreated infected mice and 19.8 in infected mice given ivermectin. In infected mice given spiramycin, a drug used against Toxoplasma, it stayed significantly below normal [22].

Human findings

No study of ivermectin in people with toxoplasmosis was found for this page.

Acanthamoeba

Acanthamoeba is a free-living amoeba of water and soil. It can cause Acanthamoeba keratitis, a painful, sight-threatening infection of the cornea seen mostly in contact-lens wearers, and, rarely, an infection of the brain.

The one direct study found is a 1996 laboratory test of Acanthamoeba castellanii against three drugs: chloroquine, ivermectin and the antifungal amphotericin B. The amoeba was sensitive to ivermectin and amphotericin B but not to chloroquine, and the authors wrote that ivermectin and amphotericin B “show promise as therapeutic agents against this parasite” [23]. Its abstract gives no concentrations.

No animal or human study of ivermectin against Acanthamoeba was found. Ivermectin for Acanthamoeba sets this single study in context, including later laboratory findings on the amoeba’s resilience to amphotericin B.

Giardia, Cryptosporidium, Babesia and Others

Giardia

Giardia lamblia is a flagellate that causes giardiasis, a common gut infection with diarrhoea, abdominal cramps and nausea. Its treatments have remained unchanged for 40 years, and resistant strains have emerged [8].

• Laboratory (2024). Ivermectin was toxic to Giardia trophozoites in step with the dose. It raised reactive oxygen species, fragmented their DNA, stopped them in the S phase of the cell cycle (when DNA is copied) and caused changes consistent with apoptosis [8].
• Animal (2015). In colonies of laboratory rats naturally infected with Giardia, the pinworm Syphacia and the dwarf tapeworm Hymenolepis nana, ivermectin in the drinking water for 72 hours was reported to be a safe and highly effective treatment for Giardia and the dwarf tapeworm [24].
• Human. No study of ivermectin in people with giardiasis was found for this page.

Cryptosporidium

Cryptosporidium causes watery diarrhoea, most dangerous for people with weakened immune systems and for malnourished children. Infected people and animals pass its hardy, egg-like oocysts in their stool, and studies measure treatment by counting them. Nitazoxanide is the drug approved for it in the United States.

• Animal (2021). In diabetic mice infected with Cryptosporidium, ivermectin alone cut the oocysts in the stool by 82%, nitazoxanide alone by 63% and the two together by 92%; adding selenium raised ivermectin’s figure to 84%. Every treatment except nitazoxanide alone significantly improved the damage to the gut lining [25].
• Human (2023). An observational study of 210 people seen after COVID-19 (coronavirus disease 2019) at Cairo University’s Faculty of Medicine, 49 of whom carried Cryptosporidium, found that having been given azithromycin, hydroxychloroquine and ivermectin was significantly related to a higher risk of Cryptosporidium infection [26]. A link found in an observational study does not show that the medicines caused the infection.

Babesia and Theileria

Babesia parasites live inside red blood cells and are spread by ticks; they infect cattle, horses and dogs, and some species infect people. Theileria are related blood parasites of horses and cattle.

• Laboratory (2019). Ivermectin inhibited Babesia bovis, Babesia bigemina, Babesia divergens, Babesia caballi and Theileria equi, with IC50 values from 30.1 to 98.6 µM; it harmed the three cell lines used for comparison at 138.9 to 287.5 µM [2].
• Animal (2019). In mice infected with Babesia microti, a species that also infects people, ivermectin (4 milligrams per kilogram injected into the abdomen) inhibited the parasite’s growth by 63%. At half doses, ivermectin combined with the drugs diminazene aceturate, atovaquone or clofazimine cut the peak level of parasites in the blood by 83.7%, 76.5% and 74.4%, and no Babesia microti DNA was found 49 days after infection in the mice given ivermectin with diminazene aceturate or with atovaquone [2].

Amoebae and Trichomonads of the Mouth

Two single-celled parasites live in the human mouth: the gum amoeba, Entamoeba gingivalis, and Trichomonas tenax, a flagellate that swims with whip-like tails. Both live in the pockets between gums and teeth; their links with gum disease are set out on Entamoeba gingivalis: The Gum Amoeba and Trichomonas tenax.

No study of ivermectin against either mouth parasite

No laboratory, animal or human study testing ivermectin against the gum amoeba or against Trichomonas tenax was found in the published record. The literature search for this page found no study of ivermectin against any Trichomonas species, and none of the studies on this page applied ivermectin to the gums or tested it in the mouth. Whether ivermectin affects either mouth parasite has not been shown in either direction.

What exists for other Entamoeba species

• Laboratory (2009). Ivermectin showed activity against trophozoites of Entamoeba histolytica, the amoeba of amoebic dysentery and amoebic liver abscess, grown in culture. The concentration needed to halve their growth was higher than for the other antiparasitic drugs tested, and the authors wrote that its activity in animal models remained to be demonstrated [27].
• Human (1993). In 129 people given a single dose of ivermectin (150 micrograms per kilogram) for river blindness, stool samples taken before and 3 days after treatment showed a significant fall in the cysts of Entamoeba coli, a gut amoeba generally regarded as harmless, with a cure rate of 46% for the cysts. Roundworm (Ascaris lumbricoides) eggs also fell, whipworm and blood-fluke (Schistosoma mansoni) eggs showed no significant short-term change, and hookworm egg output rose. The authors called for further studies to verify these changes [28].

A finding in one single-celled parasite cannot be assumed to hold for another, even a close relative: in the 2022 laboratory study above, ivermectin slowed Leishmania mexicana but not the related insect parasite Crithidia fasciculata [5]. The gum amoeba is a relative of Entamoeba histolytica and Entamoeba coli, but it has not itself been tested.

The chat-group accounts of ivermectin paste on the gums, case reports of ivermectin used against fly larvae, mites and worm larvae in the tissues of the mouth, and the 1914 episode in which gum disease was treated with an anti-amoeba drug are collected on Ivermectin for Gum Disease.

Key Research Papers

1. Hanafi HA, Szumlas DE, Fryauff DJ, El-Hossary SS, Singer GA, Osman SG, et al. Effects of ivermectin on blood-feeding Phlebotomus papatasi, and the promastigote stage of Leishmania major. Vector Borne Zoonotic Dis. 2011;11(1):43-52. PubMed PMID: 20518644
2. Batiha GE, Beshbishy AM, Tayebwa DS, Adeyemi OS, Yokoyama N, Igarashi I. Evaluation of the inhibitory effect of ivermectin on the growth of Babesia and Theileria parasites in vitro and in vivo. Trop Med Health. 2019;47:42. PubMed PMID: 31337949
3. Metzger WG, Theurer A, Pfleiderer A, Molnar Z, Maihöfer-Braatting D, Bissinger AL, et al. Ivermectin for causal malaria prophylaxis: a randomised controlled human infection trial. Trop Med Int Health. 2020;25(3):380-386. PubMed PMID: 31808594
4. Ekoka Mbassi D, Mombo-Ngoma G, Held J, Okwu DG, Ndzebe-Ndoumba W, Kalkman LC, et al. Efficacy and safety of ivermectin for the treatment of Plasmodium falciparum infections in asymptomatic male and female Gabonese adults - a pilot randomized, double-blind, placebo-controlled single-centre phase Ib/IIa clinical trial. EBioMedicine. 2023;97:104814. PubMed PMID: 37839134
5. Fraccaroli L, Ruiz MD, Perdomo VG, Clausi AN, Balcazar DE, Larocca L, et al. Broadening the spectrum of ivermectin: Its effect on Trypanosoma cruzi and related trypanosomatids. Front Cell Infect Microbiol. 2022;12:885268. PubMed PMID: 35967842
6. Walunj SB, Wang C, Wagstaff KM, Patankar S, Jans DA. Conservation of Importin α Function in Apicomplexans: Ivermectin and GW5074 Target Plasmodium falciparum Importin α and Inhibit Parasite Growth in Culture. Int J Mol Sci. 2022;23(22). PubMed PMID: 36430384
7. Reis TAR, Oliveira-da-Silva JA, Tavares GSV, Mendonça DVC, Freitas CS, Costa RR, et al. Ivermectin presents effective and selective antileishmanial activity in vitro and in vivo against Leishmania infantum and is therapeutic against visceral leishmaniasis. Exp Parasitol. 2021;221:108059. PubMed PMID: 33338468
8. Barzola FN, Laiolo J, Cotelo C, Joray MB, Volpini X, Rivero MR, et al. Cytotoxic effects of ivermectin on Giardia lamblia: induction of apoptosis and cell cycle arrest. Front Microbiol. 2024;15:1484805. PubMed PMID: 39545240
9. Gupta S, Vohra S, Sethi K, Gupta S, Bera BC, Kumar S, et al. In vitro anti-trypanosomal effect of ivermectin on Trypanosoma evansi by targeting multiple metabolic pathways. Trop Anim Health Prod. 2022;54(4):240. PubMed PMID: 35869164
10. de Carvalho LP, Sandri TL, José Tenório de Melo E, Fendel R, Kremsner PG, Mordmüller B, et al. Ivermectin Impairs the Development of Sexual and Asexual Stages of Plasmodium falciparum In Vitro. Antimicrob Agents Chemother. 2019;63(8). PubMed PMID: 31109978
11. Freitas CS, Lage DP, Machado AS, Vale DL, Martins VT, Cardoso JMO, et al. Exploring drug repositioning for leishmaniasis treatment: Ivermectin plus polymeric micelles induce immunological response and protection against tegumentary leishmaniasis. Cytokine. 2023;164:156143. PubMed PMID: 36774730
12. Rahmani A, Maspi N, Hasanpour H, Falahi S, Nayeri T, Naserifar R. The Impact of Ivermectin on Immune Response and Wound Healing in a Mouse Model Infected With Leishmania major. J Trop Med. 2025;2025:5579789. PubMed PMID: 40860959
13. Udensi UK, Fagbenro-Beyioku AF. Effect of ivermectin on Trypanosoma brucei brucei in experimentally infected mice. J Vector Borne Dis. 2012;49(3):143-50. PubMed PMID: 23135008
14. Dias JC, Schofield CJ, Machado EM, Fernandes AJ. Ticks, ivermectin, and experimental Chagas disease. Mem Inst Oswaldo Cruz. 2005;100(8):829-32. PubMed PMID: 16444412
15. Mendes AM, Albuquerque IS, Machado M, Pissarra J, Meireles P, Prudêncio M. Inhibition of Plasmodium Liver Infection by Ivermectin. Antimicrob Agents Chemother. 2017;61(2). PubMed PMID: 27895022
16. Vanachayangkul P, Im-Erbsin R, Tungtaeng A, Kodchakorn C, Roth A, Adams J, et al. Safety, Pharmacokinetics, and Activity of High-Dose Ivermectin and Chloroquine against the Liver Stage of Plasmodium cynomolgi Infection in Rhesus Macaques. Antimicrob Agents Chemother. 2020;64(9). PubMed PMID: 32660993
17. Annamalai Subramani P, Tipthara P, Kolli SK, Nicholas J, Barnes SJ, Ogbondah MM, et al. Efficacy of ivermectin and its metabolites against Plasmodium falciparum liver stages in primary human hepatocytes. Antimicrob Agents Chemother. 2024;68(8):e0127223. PubMed PMID: 38904389
18. Yipsirimetee A, Tipthara P, Hanboonkunupakarn B, Tripura R, Lek D, Kümpornsin K, et al. Activity of Ivermectin and Its Metabolites against Asexual Blood Stage Plasmodium falciparum and Its Interactions with Antimalarial Drugs. Antimicrob Agents Chemother. 2023;67(7):e0173022. PubMed PMID: 37338381
19. Pinilla YT, C P Lopes S, S Sampaio V, Andrade FS, Melo GC, Orfanó AS, et al. Promising approach to reducing Malaria transmission by ivermectin: Sporontocidal effect against Plasmodium vivax in the South American vectors Anopheles aquasalis and Anopheles darlingi. PLoS Negl Trop Dis. 2018;12(2):e0006221. PubMed PMID: 29444080
20. Ouédraogo AL, Bastiaens GJ, Tiono AB, Guelbéogo WM, Kobylinski KC, Ouédraogo A, et al. Efficacy and safety of the mosquitocidal drug ivermectin to prevent malaria transmission after treatment: a double-blind, randomized, clinical trial. Clin Infect Dis. 2015;60(3):357-65. PubMed PMID: 25414262
21. Bilgin M, Yıldırım T, Hökelek M. In Vitro Effects of Ivermectin and Sulphadiazine on Toxoplasma gondii. Balkan Med J. 2013;30(1):19-22. PubMed PMID: 25207063
22. Fahmy MA, Shalaby MA, Issa R, Badawi M, Magdy M, Afife AA, et al. Ivermectin modulated cerebral γ-aminobutyric acid (GABA) and reduced the number of chronic Toxoplasma gondii cysts significantly in the brains of immunocompromised mice. J Parasit Dis. 2023;47(3):635-643. PubMed PMID: 37520203
23. Rain AN, Radzan T, Sajiri S, Mak JW. In vitro drug susceptibility of Acanthamoeba castellani to chloroquine, ivermectin and fungizon. Southeast Asian J Trop Med Public Health. 1996;27(2):319-24. PubMed PMID: 9279996
24. Foletto VR, Vanz F, Gazarini L, Stern CA, Tonussi CR. Efficacy and security of ivermectin given orally to rats naturally infected with Syphacia spp., Giardia spp. and Hymenolepis nana. Lab Anim. 2015;49(3):196-200. PubMed PMID: 25480657
25. Fahmy MA, Abdelaal AA, Hassan SI, Shalaby MA, Ismail MAM, Khairy RA, et al. Antiparasitic and immunomodulating effects of nitazoxanide, ivermectin and selenium on Cryptosporidium infection in diabetic mice. Rev Bras Parasitol Vet. 2021;30(4):e012121. PubMed PMID: 34852131
26. Enas AE, Hadel MA, Emad AA, Ibrahim BE, Morsy S, Noha MA. Post-COVID-19 cryptosporidiosis: A serious risk or mere association? Trop Biomed. 2023;40(2):199-207. PubMed PMID: 37650408
27. González-Salazar F, Mata-Cárdenas BD, Vargas-Villareal J. [Sensibility of Entamoeba histolytica trophozoites to ivermectin]. Medicina (B Aires). 2009;69(3):318-20. PubMed PMID: 19622479
28. Njoo FL, Belling GA, Oosting J, Vetter JC, Stilma JS, Kijlstra A. Concurrent parasitic infections in onchocerciasis and the occurrence of adverse reactions after ivermectin treatment. Am J Trop Med Hyg. 1993;48(5):652-7. PubMed PMID: 8517484

PubMed Topic Searches

1. PubMed: Ivermectin and protozoa
2. PubMed: Ivermectin and Leishmania
3. PubMed: Ivermectin and Plasmodium (malaria parasites)
4. PubMed: Ivermectin and Toxoplasma
5. PubMed: Ivermectin and Entamoeba
6. PubMed: Ivermectin and Trichomonas

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Connections

• Ivermectin
• All Drugs
• Cancer and Parasites
• Parasite Organisms
• Malaria
• Leishmania
• Trypanosoma
• Toxoplasma
• Acanthamoeba
• Ivermectin for Acanthamoeba
• Giardia
• Cryptosporidium
• Babesia
• Entamoeba histolytica
• Entamoeba gingivalis (Gum Amoeba)
• Trichomonas tenax
• Trichomonas vaginalis
• Ivermectin for Gum Disease
• Ivermectin Antibacterial Research
• How Ivermectin Works
• Ivermectin Treatment for Strongyloides

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