Name: helminth drugs and how they work
Uploaded: 2026-03-12T13:35:47.000Z
Duration: 1 min 15 s
Channel: JoVE

구피제는 기생충을 제거하는 약물로, 주로 성충을 표적으로 하지만, 일부는 유충이나 알 단계에도 영향을 미칩니다.예를 들어, 프라지콴텔과 같은 피라지노이소퀴놀린 약물은 기생충의 보호 피세포를 표적으로 합니다.프라지콴텔이 이 세포에 들어가 이온 채널을 통해 칼슘 이온의 빠른 유입을 유도합니다.갑작스러운 칼슘 유입은 지속적인 근육 수축을 초래합니다. 결국 기생충은 수축 상태에서 마비됩니다.이 교란으로 인해 외피는 다공성이 되어 내부 표면과 내부 항원이 숙주 면역계에 노출됩니다.이러한 형태학적 변화는 기생충의 방어력을 약화시켜 면역 공격에 더 취약하게 만듭니다.그 결과, 항체와 같은 면역 조절제가 노출된 기생충 항원에 작용하여 숙주 면역 인식을 향상시킬 수 있습니다.이 면역 반응은 프라지콴텔과 시너지 작용하여 기생충 제거를 가속화합니다.

anthelminthic agents

Anthelminthic Agents

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Anthelmintic drugs differ significantly from antiparasitic therapies targeting protozoa, primarily due to differences in parasite biology. Whereas most ...

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Education

교육

JoVE Core

Microbiology

미생물학

Unit

단위

Antimicrobial Agents

항균제

KEY TERMS AND CONCEPTS

주요 용어 및 개념

선충성 작용제

helminth drugs and how they work

Helminth drugs work by attacking the weak points of parasitic worms. These anthelmintic medicines are different from drugs used against protozoa, because they are usually aimed at mature helminths rather than fast-dividing cells. They target the worm’s movement, glucose use, and microtubule structure to stop survival, reproduction, and location inside the host.

Benzimidazoles are broad-spectrum anthelmintics that block tubulin polymerization, which means they interfere with microtubules, the cell structures that help maintain shape and movement. Drugs in this group include albendazole, mebendazole, thiabendazole, and triclabendazole. By disrupting microtubule function, they reduce motility, energy metabolism, and reproduction in intestinal nematodes such as Ascaris and Trichuris, in cestodes such as Taenia and Echinococcus, and in some flukes such as Fasciola.

Albendazole also has activity against Giardia and is used in mass drug administration programs for filariasis. Other anthelmintics act on the worm’s nervous system and muscles. Pyrantel pamoate, a tetrahydropyrimidine, activates cholinergic receptors in nematode muscle cells and causes depolarization, which leads to paralysis and expulsion.

Diethylcarbamazine, or DEC, is a piperazine derivative that immobilizes microfilariae, the early blood stages of filarial worms. Its exact action is not fully defined, but it may involve altered arachidonic acid metabolism and better clearance by the host immune system. DEC is important in filariasis treatment and is increasingly given in single-dose regimens.

Ivermectin and praziquantel work through different mechanisms. Ivermectin, an avermectin, acts on chloride channels and causes hyperpolarization and paralysis, especially in intestinal nematodes and filariae, and it helps lower microfilarial loads in onchocerciasis. Praziquantel, a pyrazinoisoquinoline, acts as a calcium agonist in trematodes and cestodes, causing muscle contraction and damage to the tegument, the worm’s outer covering, which exposes antigens to host immune responses.

Niclosamide works in another way by uncoupling oxidative phosphorylation in cestodes, which drains ATP and immobilizes the parasite. Other selective agents, including oxamniquine, metrifonate, and suramin, are used for specific trematode and filarial infections. Together, these drug classes show how different helminths require tailored treatment strategies based on their biology.

Helminth Drugs and How They Work

inhibitors of gram-positive cell wall synthesis

inhibitors-of-gram-positive-cell-wall-synthesis

How Antibiotics Block Bacterial Cell Walls

Bacterial cell walls are rigid structures built mainly from peptidoglycan. This mesh-like polymer gives bacteria strength and helps maintain cell shape. Because peptidoglycan synthesis is essential for growth, it is a major target for antibiotics. Beta-lactam antibiotics, such as penicillin, stop peptidoglycan synthesis in actively growing cells. They have a four-membered beta-lactam ring that mimics the D-alanyl-D-alanine dipeptide, which is the natural substrate for transpeptidase, also...

inhibitors of bacterial protein synthesis

inhibitors-of-bacterial-protein-synthesis

Aminoglycosides: How They Stop Bacteria

Aminoglycosides are bactericidal antibiotics that stop bacteria by targeting the ribosome and disrupting protein synthesis. They are highly potent drugs made of amino-modified sugars linked by glycosidic bonds to an aminocyclitol core, such as 2-deoxystreptamine or streptamine. Their strong positive charge helps them bind tightly to the negatively charged phosphate backbone of ribosomal RNA, especially the 16S rRNA of the 30S subunit in the bacterial 70S ribosome. These antibiotics act at the...

inhibitors of bacterial dna synthesis

Fluoroquinolone Antibiotics and Bacterial DNA

Fluoroquinolone antibiotics target bacterial DNA replication by blocking two key type II topoisomerases: DNA gyrase and topoisomerase IV. These enzymes help bacteria manage DNA supercoiling and separate chromosomes during replication. When they are disrupted, bacterial pathogens cannot copy DNA efficiently and infection can spread less effectively. Fluoroquinolones are synthetic versions of quinolones. They work by stabilizing the short-lived DNA-enzyme cleavage complex, which stops strand...

inhibitors of viral protein synthesis

Interferons Block Viral Replication

Interferons block viral replication by shutting down protein synthesis and activating the cell’s antiviral defenses. Viruses need the host cell’s translational machinery to make proteins, because they do not have the machinery to do this on their own. When a virus is detected, infected cells release interferons, which are cytokines, or signaling proteins, that warn nearby uninfected cells. Interferons bind to receptors on nearby cells and activate the JAK-STAT signaling pathway. This turns on...

inhibitors of virion release

Neuraminidase Inhibitors and Flu Spread

Influenza viruses spread when new virions leave an infected cell and reach nearby cells. Influenza A and B are negative-sense, single-stranded RNA viruses with segmented genomes. They depend on two surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), to infect cells, make new viral particles, and release them. HA starts infection by binding to sialic acid on the surface of host epithelial cells. This binding helps the virus enter the cell by receptor-mediated endocytosis. After...

antiviral nucleoside inhibitors

How Antiviral Drugs Stop Viral Replication

Antiviral nucleoside inhibitors stop viruses by blocking DNA or RNA synthesis. These drugs are structural analogs, which means they look like natural nucleosides, the building blocks cells use to make genetic material. Because they resemble host nucleosides, they can interfere with viral polymerases and disrupt viral genome replication. Acyclovir is a guanosine analog with a three-carbon acyclic side chain. It mainly targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2...

antifungal agents

Amphotericin B and Fungal Membranes

Amphotericin B targets fungal cell membranes by binding to ergosterol, a sterol found mainly in fungal plasma membranes. Its amphipathic structure helps this selective binding. It has a hydrophobic polyene-lactone ring and a hydrophilic region with mycosamine and carboxylic acid groups. Weak binding to cholesterol can also affect human cells and helps explain the drug’s toxicity. One way amphotericin B kills fungi is through pore formation. In this model, amphotericin B-ergosterol complexes...

mechanism of antibiotic resistance in mrsa

mechanism-of-antibiotic-resistance-in-mrsa

How Bacteria Outsmart Antibiotics

Antibiotic resistance in bacteria happens when microbes evolve the ability to survive drugs that once killed them or slowed their growth. Genetic change and antibiotic exposure drive this process. Over time, useful treatments can stop working. Bacteria can resist antibiotics in several ways. Some make drug-inactivating enzymes, such as beta-lactamases. Others use efflux pumps to push antibiotics out of the cell. Resistance can also come from mutations that change the drug target, from lower...

Helminth drugs work by attacking the weak points of parasitic worms. These anthelmintic medicines are different from drugs used against protozoa, because they are usually aimed at mature helminths rather than fast-dividing cells. They target the worm’s movement, glucose use, and microtubule structure to stop survival, reproduction, and location inside the host. Benzimidazoles are broad-spectrum anthelmintics that block tubulin polymerization, which means they interfere with microtubules, the...

clinical significance of antibiotic resistance

clinical-significance-of-antibiotic-resistance

MRSA: Host Adaptation and Transmission

MRSA, or methicillin-resistant Staphylococcus aureus, is a major public health threat. It resists beta-lactam antibiotics because it carries the mecA gene inside the staphylococcal cassette chromosome mec, or SCCmec. The mecA gene makes penicillin-binding protein 2a, which reduces how well methicillin and related beta-lactam drugs can bind. MRSA has spread into separate clonal lineages that affect both humans and animals. These lineages fit the One Health idea, which links human, animal, and...

inhibitors of virion maturation and assembly

inhibitors-of-virion-maturation-and-assembly

HIV Protease Inhibitors and Maturation

HIV protease inhibitors block a key step in virus maturation. In human immunodeficiency virus (HIV), infected cells make two long precursor proteins called polyproteins. These are Gag and Gag-Pol. Gag provides the virus structure. Gag-Pol carries important viral enzymes, including reverse transcriptase, integrase, and protease. After these polyproteins are made, they move to the host cell membrane. There, they help build an immature viral particle that buds from the cell surface. Budding...

antiprotozoal agents

Leishmaniasis and Trypanothione Reductase

Leishmaniasis is a parasitic disease caused by several Leishmania species. It affects millions of people each year and remains a major public health problem in endemic regions. Treatment often relies on pentavalent antimonials, including meglumine antimoniate and sodium stibogluconate. The way these drugs work has not been fully clear. One important target is trypanothione reductase, or TR, an enzyme that helps keep Leishmania in redox balance. TR is not found in mammalian hosts, so it is a...

key terms and concepts

Learn how anthelmintic drugs treat helminths by targeting microtubules, muscle control, ion channels, calcium signals, and parasite energy use.

Helminth Drugs and How They Work | JoVE K12

JoVE Core Microbiology provides an engaging introduction to the microbial world and its influence on health, industry, and the environment. This comprehensive collection covers key concepts such as microbial structure, metabolism, genetics, and ecology. It introduces essential laboratory techniques and microscopy methods through visually engaging animations. Corresponding scientist-in-action videos bridge classroom concepts with real-world research and applications.

microbiology

Helminth Drugs and How They Work

Description

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