Paragonimiasis Workup

  • Author: Seth D Rosenbaum, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Mar 13, 2012
 

Laboratory Studies

  • A CBC count with differential usually reveals eosinophilia in 10-30% of patients with paragonimiasis. The degree of eosinophilia is significantly higher in patients who have pleurisy. Leukocytosis with eosinophilia occurs early in the course of disease but then resolves over time.[2] Despite remarkable eosinophilia, total WBC count remains in the normal range or slightly elevated.
  • Obtain clinical samples for ova and parasites.
    • Definitive diagnosis of paragonimiasis requires detection of eggs in sputum, feces, pleural fluid, cerebrospinal fluid (CSF), or pus.[8, 9] However, eggs may not be present in feces and sputum for 2-3 months.[1]
    • Worms or eggs may be found in biopsies of pulmonary, cerebral, subcutaneous, or intra-abdominal nodules or cystic lesions. The specific species causing paragonimiasis can be identified from adult or immature flukes found in surgical specimens (rarely in the sputum).
    • Egg detection rates for paragonimiasis average 25-35% for a single sputum specimen but may reach 50% with multiple examinations. (As many as 7 examinations have been recommended.) The yield for specimens obtained via bronchoscopy is 53-67%.
    • Stool examinations are very useful to diagnose paragonimiasis in children because children tend to swallow sputum.
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Imaging Studies

  • Chest radiography reveals abnormalities in approximately 80-90% of patients; however, chest films are normal in 13-20% of confirmed cases.[2] Radiographic abnormalities may include ring shadows, which represent cavitating lesions, fibrosis, nodules or linear infiltrates with calcified foci, loculated pleural effusions, and pleural thickening.
  • Three radiographic stages of pulmonary infection have been described.[8]
    • Migration of larvae can result in pneumothorax with consolidation or exudative pleural effusions.
    • During fluke maturation nodular or cystic lesions predominantly develop in the periphery of the middle and lower lobes. Bronchiectasis can also occur.
    • Following treatment lesions gradually disappear over 3-26 months.
  • CT scanning or MRI of the head may reveal cerebral calcification, cystic lesions, or hydrocephalus. Chronic cerebral paragonimiasis may be suspected by the presence of a "soap bubble lesion," with scattered calcifications.
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Other Tests

  • Serology for paragonimiasis is useful because of the relatively low percentage of egg detection. Serologic tests aid in diagnosing extrapulmonary disease where eggs are not shed in the sputum or stool.
    • The complement fixation test is sensitive and is most useful following therapy because antibody levels fall 6-12 months after effective treatment.
    • The technical difficulties inherent in the complement fixation test make enzyme-linked immunosorbent assay (ELISA) the serological test of choice. ELISA has 92% sensitivity and is specific; however, antibody levels often take longer (ie, < 24 mo) to return to the reference range after successful treatment. Low-level positive results may occur with other trematode infections.
    • A rapid immunoblot test developed by the Centers for Disease Control and Prevention is 96% sensitive and 99% specific but cannot be used to differentiate active from past infection.
  • Skin testing
    • Intradermal skin testing with an extract of adult Paragonimus is reasonably sensitive, although rare false-negative results could occur. Results may remain positive for as long as 20 years after cure.
    • Skin testing is useful as an epidemiologic tool to detect prevalence of infection and is the most commonly used test for screening. Because this test can cross react with Clonorchis sinensis and Schistosoma japonicum, it should only be used for purposes of screening.[1]
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Procedures

  • Lumbar puncture: Examination of infected CSF reveals bloody or turbid fluid containing numerous eosinophils.
  • Thoracentesis: Infected pleural fluid is usually serosanguineous and has more than 1000 red cells with accompanying eosinophilia. The fluid is usually an exudate with a low glucose level. Parasitic eggs are rarely detected in the sediment of pleural effusions.
  • Biopsy: Lung biopsy specimens usually reveal adult worms or eggs.
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Histologic Findings

  • Pathological findings in the lung vary and depend on the worm burden and disease chronicity.
  • Adult flukes are typically encapsulated in cysts, which tend to occur in the right lung. Patients usually have fewer than 20 cysts, each of which contains 2-4 flukes. The cyst wall is thick, sclerotic, and sometimes calcified.
  • Microscopically, the cyst wall contains granulation tissue with fibroblasts, mononuclear cells, plasma cells, lymphoid cells, and eosinophils.
  • Numerous Charcot-Leyden crystals and eggs are formed in the cavity, and egg-containing granuloma frequently develop near the cyst.
  • Bronchial arteries may show hypertrophy or may rupture from damage.
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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, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

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.

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

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

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.

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.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

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, and Southern Medical Association

Disclosure: Nothing to disclose.

References
  1. Liu Q, Wei F, Liu W, Yang S, Zhang X. Paragonimiasis: an important food-borne zoonosis in China. Trends Parasitol. Jul 2008;24(7):318-23. [Medline].

  2. Boe DM, Schwarz MI. A 31-year-old man with chronic cough and hemoptysis. Chest. Aug 2007;132(2):721-6. [Medline].

  3. Vidamaly S, Choumlivong K, Keolouangkhot V, Vannavong N, Kanpittaya J, Strobel M. Paragonimiasis: a common cause of persistent pleural effusion in Lao PDR. Trans R Soc Trop Med Hyg. Jan 29 2009;[Medline].

  4. Rosen MJ. Chronic cough due to tuberculosis and other infections: ACCP evidence-based clinical practice guidelines. Chest. Jan 2006;129(1 Suppl):197S-201S. [Medline].

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  6. Cho AR, Lee HR, Lee KS, Lee SE, Lee SY. A case of pulmonary paragonimiasis with involvement of the abdominal muscle in a 9-year-old girl. Korean J Parasitol. Dec 2011;49(4):409-12. [Medline]. [Full Text].

  7. Diaz JH. Boil before eating: paragonimiasis after eating raw crayfish in the Mississippi River Basin. J La State Med Soc. Sep-Oct 2011;163(5):261-6. [Medline].

  8. Tsang KW, File TM Jr. Respiratory infections unique to Asia. Respirology. Nov 2008;13(7):937-49. [Medline].

  9. 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. Dec 2011;60(4):534-7. [Medline].

  10. 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. Mar 2011;49(1):73-7. [Medline]. [Full Text].

  11. 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. Sep-Oct 1998;92(5):566-9. [Medline].

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

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

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

  15. Dainichi T, Nakahara T, Moroi Y, et al. A case of cutaneous paragonimiasis with pleural effusion. Int J Dermatol. Sep 2003;42(9):699-702. [Medline].

  16. Hawn TR, Jong EC. Update on Hepatobiliary and Pulmonary Flukes. Curr Infect Dis Rep. Dec 1999;1(5):427-433. [Medline].

  17. Kagawa FT. Pulmonary paragonimiasis. Semin Respir Infect. Jun 1997;12(2):149-58. [Medline].

  18. Maguire JH. Trematodes (Schistosomes and other Flukes). In: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. Vol 2. 6th ed. Philadelphia, PA: Churchill Livingstone; 2004:3283-4.

  19. Nakamura-Uchiyama F, Mukae H, Nawa Y. Paragonimiasis: a Japanese perspective. Clin Chest Med. Jun 2002;23(2):409-20. [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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