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Surgical Rounds®

September 2007
Volume0
Issue 0

What is causing the small bowel filling defect?

Daniel Sutton, MD, LT, MC, USN

Radiology Resident

Naval Medical Center Portsmouth

Portsmouth, VA

Maria Flynn, MD

Suffolk Radiology Associates

Suffolk, VA

Jennifer Pierce, MD, LCDR, MC, USN

Staff Radiologist

Academic Chief of Musculoskeletal Imaging

Naval Medical Center Portsmouth

Portsmouth, VA

Each month, Dr. Maria Flynn issues a Radiology Challenge, presenting images from one of a variety of imaging modalities and a case report. Can you diagnose the condition? Follow the link to find out whether your answer was correct, what was really wrong with the patient, and how the patient was treated. Then, come back next month to test your radiographic reading skills on a new case!

Case report

A 52-year-old man with a history of traveling to remote locations presented to his primary care physician because of intermittent midabdominal discomfort that had started 2 to 3 weeks earlier. Physical examination and routine laboratory analysis were unremarkable. Contrast-enhanced computed tomography (CT) scans of the abdomen and pelvis showed a small bowel filling defect (Figures).

Challenge: What is causing the small bowel filling defect?

  1. Small bowel intussusception
  2. Ascariasis
  3. Foreign body
  4. Small bowel polyp

Answer: b. Ascariasis.

Ascaris lumbricoides

Helminthic infections are one the most prolific parasitic diseases to afflict humans. is the most common infectious organism within the helminthic species and affects more than 1.4 billion individuals worldwide; this is 25% of the world's population.1 Four million individuals are infected annually in the United States. These cases are associated primarily with immigrants to the country. Globally, 12 million new cases are reported annually, and there are between 10,000 and 20,000 deaths per year.2

A lumbricoides

Infection with is usually associated with poor sanitation and rudimentary agricultural practices, such as using human feces or "night soil" to enrich vegetable beds. Ascariasis is most commonly observed in children between 4 and 10 years of age and is considered a significant component of intellectual deterioration and malnutrition in areas where this disease is prevalent.3

Historically, intestinal parasitic infections have been viewed as diseases related to lower socioeconomic classes. With the increasing globalization of markets and economies, agricultural products once obtained from farms within our borders are imported from countries that do not adhere to the same stringent agricultural practices.4,5 Efficient and rapid transportation, in conjunction with a world market, have facilitated the access of infectious diseases to every economic hub. As a result, medical systems around the world must remain vigilant for outbreaks of infections that previously were relegated to isolated and impoverished regions.6,7

A lumbricoides

A lumbricoides

The life cycle of begins with the fertilization of an ovum within the human small intestine, normally the jejunum. The fertilized egg is excreted into the environment, and embryonation occurs approximately 3 to 6 weeks later. The eggs can remain viable in warm, moist soil for approximately 72 months. Because these eggs are resistant to the chemical and environmental degradation that is known to inactivate the majority of pathogens, many research laboratories use to test wastewater-treatment protocols.8 After the embryonated eggs are ingested, they hatch into larvae. These larvae invade the intestinal mucosa and proceed through the portal system and systemic circulation until they reach the lungs. The young larvae reside there and mature for a period of 1 to 2 weeks before penetrating the alveolar walls. After penetrating the bronchial airway, the larvae migrate into the posterior pharynx, where they are again ingested. The larvae develop into mature worms within the jejunum, where they can survive for approximately 1 to 2 years. A female worm can produce more than 200,000 eggs daily during its lifetime.9,10

Because of the massive number of eggs the gravid female produces, standard microscopic evaluation of stool smears is diagnostic. Prior to the production of ova, the presence of larvae in sputum samples or mature worms within feces or the oropharynx also is diagnostic.11,12

A lumbricoides

During the pulmonary stage, Ascariasis can produce mild fever, cough, and eosinophilia, with pulmonary infiltrates observable on plain chest radiographs (Loeffler's syndrome); the syndrome is usually mild and transient and produces no permanent lung damage.13 infection of the small bowel produces vague symptoms, which include nausea, vomiting, and colicky abdominal pain. Sometimes the adult worm can be visualized within the oropharynx or passing from the rectum. Moderate-to-large worm burdens can cause small bowel obstruction, volvulus, or intussusception. Additionally, migration of the worm into the biliary tract may lead to biliary colic, cholecystitis, cholangitis, intrahepatic abscess, and pancreatitis.14-16

A lumbricoides

A lumbricoides

Radiographically, ingest barium. Finding a central white line of barium within the worm's alimentary tract surrounded by a filling defect caused by the worm's body is diagnostic.17 Positive findings during longitudinal ultrasonography of the hepatobiliary tree demonstrate a hypoechoic, well-defined tube with echogenic walls and a central anechoic tube that corresponds to the worm's gastrointestinal tract. The worm may be seen as a "target sign" in the transverse plane. Additionally, a curling motion has been described on real-time ultrasonography.18 Ultrasonography of the fluid-filled small bowel demonstrates worms that resemble "winding highways" or "parallel lines."19 Contrast-enhanced CT scanning may show the actual worm within the small bowel lumen, and the oral contrast within the worm's alimentary canal demonstrates the "target sign" (Figures).

Drs. Sutton and Pierce are military service members. This work was prepared as part of their official duties. Title 17 U.S.C. 105 provides that 'Copyright protection under this title is not available for any work of the United States Government.' Title 17 U.S.C. 101 defines a United States Government work as a work prepared by a military service member or employee of the United States Government as part of that person's official duties.

The views expressed in this article are those of the author(s) and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

References

  1. Khuroo MS. Ascariasis. Gastroenterol Clin North Am. 1996;25(3):553-577.
  2. de Silva NR, Chan MS, Bundy DA. Morbidity and mortality due to ascariasis: re-estimation and sensitivity analysis of global numbers at risk. Trop Med Int Health. 1997;2(6):519-528.
  3. Hotez P, deSilva N, Booker S, et al. Soil transmitted helminth infection: the nature, causes and burden of the conditions. DCPP Working Paper No. 3. Available at: www.dcp2.org/file/19/wp3.pdf. Accessed September 18, 2007.
  4. Shewmake R, Dillon B. Food poisoning: causes, remedies, and prevention. Postgrad Med. 1998;103(6):125-136.
  5. Erdog O, Sener H. The contamination of various fruits and vegetable with Enterobius vermicularis, Ascaris eggs, Entamoeba histolyca cyst and Giardia cysts. Food Control. 2006;12(6):557-560.
  6. Dwosh H, Hong H, Austgarden D, et al. Identification and containment of an outbreak of SARS in a community hospital. CMAJ. 2003;168(11):1415—1420.
  7. Division of Occupational Safety and Health Policy and Procedures Manual. Interim tuberculosis control enforcement guidelines. Available at: www.dir.ca.gov/DOSHPol/P&PC-47.htm. Accessed September 18, 2007.
  8. Pecson B, Barrios J, Johnson D, et al. A real-time PCR method for quantifying viable Ascaris eggs using the first internally transcribed spacer region of ribosomal DNA. Appl Environ Microbiol. 2006;72(12):7864—7872.
  9. Centers for Disease Control and Prevention. Division of Parasitic Diseases. Parasitic disease information. Ascaris information. Available at: www.cdc.gov/ncidod/dpd/parasites/ascaris/moreinfo_ascaris.htm. Accessed September 18, 2007.
  10. Mandell G, Bennett J, Raphael D. Mandell, Bennett, & Dolin: Principles and Practice of Infectious Diseases. 6th ed. New York, NY: Churchill Livingstone; 2005:chap 285.
  11. Branda JA, Lin TY, Rosenberg ES, et al. A rational approach to the stool ova and parasite examination. Clin Infect Dis. 2006;42(7):972-978.
  12. Cartwright C. Utility of multiple-stool-specimen ova and parasite examinations in a high-prevalence setting. J Clin Microbiol. 1999;37(8):2408-2411.
  13. Chitkara RK, Krishna G. Parasitic pulmonary eosinophilia. Semin Respir Crit Care Med. 2006;27(2):171-184.
  14. Danaci M, Belet U, Polat V, et al. MR imaging features of biliary ascariasis. AJR Am J Roentgenol. 1999;173(2):503.
  15. Alper F, Kantarci M, Bozkurt M, et al. Acute biliary obstruction caused by biliary acariasis in pregnancy: MR cholangiography findings. Clin Radiol. 2003;58(11):896-898.
  16. Rodriguez E, Gama M, Ornstein S, Anderson W. Ascariasis causing small bowel volvulus. Radiographics. 2003;23(5):1291-1293.
  17. Reeder MM. The radiological and ultrasound evaluation of ascariasis of the gastrointestinal, biliary, and respiratory tracts. Semin Roentgenol. 1998;33(1):57-78.
  18. Schulman A, Loxton AJ, Heydenrych JJ, et al. Sonographic diagnosis of biliary ascariasis. AJR Am J Roentgenol. 1982;139(3):485-489.
  19. Mahmood T, Mansoor N, Quraishy S, et al. Ultrasonographic appearance of Ascaris lumbricoides in the small bowel. J Ultrasound Med. 2001;20(3):269-274.

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