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Paragonimiasis Medication

  • Author: Seth D Rosenbaum, MD; Chief Editor: Russell W Steele, MD  more...
 
Updated: Jun 17, 2016
 
 

Antiparasitic agents

Class Summary

Praziquantel and triclabendazole are the 2 agents that the World Health Organization (WHO) recommended to treat paragonimiasis. Praziquantel is the most commonly used and has a cure rate of 80-90%.[1, 13]

Triclabendazole is currently not approved for use in the United States but is available on a compassionate care protocol from the Centers for Disease Control and Prevention Drug Services at (404) 639-3670. In areas where triclabendazole is available, it is becoming first-line therapy for treatment of paragonimiasis. Triclabendazole is administered at a dose of 10 mg/kg/d for 3 days or 20 mg/kg/d divided in 2 doses for 1 day. Cure rates have been as high as 98.5%.[1]

A study done in Ecuador randomized 62 patients with confirmed pulmonary paragonimiasis to one of four groups (praziquantel or one of three groups with differing doses of triclabendazole).[14] This study found improved clinical response and quicker decreases in sputum production in patients treated with triclabendazole. Parasitological response was found to be more rapid in those individuals treated with triclabendazole. The study suggested that triclabendazole may have more rapid killing of adult flukes but the mechanism of action remains unknown.[14]

Older therapies (eg, bithionol [30-50 mg/kg qod for 10-15 doses] or niclofolan), despite their effectiveness (cure rates ≥ 90%), have unacceptable adverse effect profiles compared with praziquantel.

Praziquantel (Biltricide)

 

Increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. Produces vacuolization and disintegration of schistosome tegument, followed by attachment of phagocytes to parasite and death.

Tab should be swallowed whole with some liquid during meals. Keeping tab in mouth may reveal bitter taste, which can produce nausea or vomiting.

 
 
Contributor Information and Disclosures
Author

Seth D Rosenbaum, MD Attending Physician in Infectious Diseases, Medical Specialty Associates, PA

Seth D Rosenbaum, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Annette C Reboli, MD Professor of Medicine, University of Medicine and Dentistry of New Jersey; Head, Division of Infectious Diseases, Department of Medicine, Cooper University Hospital and University Medical Center

Annette C Reboli, MD is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Jennifer Patterson, DO Fellow, Department of Infectious Diseases, Cooper University Hospital, Robert Wood Johnson School of Medicine

Jennifer Patterson, DO is a member of the following medical societies: American Osteopathic Association

Disclosure: Nothing to disclose.

References
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  12. Xia Y, Chen J, Ju Y, You C. Characteristic CT and MR imaging findings of cerebral paragonimiasis. J Neuroradiol. 2016 Jun. 43 (3):200-6. [Medline].

  13. Doanh PN, Dung do T, Thach DT, Horii Y, Shinohara A, Nawa Y. Human paragonimiasis in Viet Nam: epidemiological survey and identification of the responsible species by DNA sequencing of eggs in patients' sputum. Parasitol Int. 2011 Dec. 60(4):534-7. [Medline].

  14. Kyung SY, Cho YK, Kim YJ, Park JW, Jeong SH, Lee JI, et al. A paragonimiasis patient with allergic reaction to praziquantel and resistance to triclabendazole: successful treatment after desensitization to praziquantel. Korean J Parasitol. 2011 Mar. 49(1):73-7. [Medline]. [Full Text].

  15. Anonymous. Drugs for parasitic infections. Med Lett Drugs Ther. 2004 Aug. 46(1189):1-12.

  16. Blair D, Xu ZB, Agatsuma T. Paragonimiasis and the genus Paragonimus. Adv Parasitol. 1999. 42:113-222. [Medline].

  17. Calvopina M, Guderian RH, Paredes W, Chico M, Cooper PJ. Treatment of human pulmonary paragonimiasis with triclabendazole: clinical tolerance and drug efficacy. Trans R Soc Trop Med Hyg. 1998 Sep-Oct. 92(5):566-9. [Medline].

  18. Christie JD, Garcia LS. Emerging parasitic infections. Clin Lab Med. 2004 Sep. 24(3):737-72. [Medline].

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This micrograph depicts an egg from the trematode parasite Paragonimus westermani. Eggs range in size from 68-118 µm x 39-67 µm. They are yellow-brown and ovoidal or elongated, with a thick shell. They are often asymmetrical, with one end slightly flattened. At the large end, the operculum (ie, lid or covering) is visible. Photo courtesy of The Centers for Disease Control and Prevention.
This is an illustration of the life cycle of Paragonimus westermani, one of the causal agents of paragonimiasis. Photo courtesy of The Centers for Disease Control and Prevention.
 
 
 
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