Kellermier, Harry C. MD; DiPersio, Joseph R. PhD
SUMMA Health System, Akron, OH.
Address correspondence and reprint requests to Harry C. Kellermier, MD, SUMMA Health System, Department of Pathology, 525 East Market Street, Akron, OH, 44304.
CLINICAL PATHOLOGICAL CONFERENCE
The patient is a 26-year-old woman with a medical history of Down syndrome, hypercholesterolemia, and hypothyroidism, who was brought into the emergency department accompanied by her parents. She complained of a 3-day history of fever, chills, nausea, vomiting, abdominal pain, and a temperature of up to 103.2°F (according to the parents). The abdominal pain was exacerbated by nothing. She was unable to keep solids or liquids down. Her medications consisted of L-thyroxine (Synthroid) and pravastatin (Pravachol). The review of systems was positive for headache, sore throat, cramping, and loss of appetite.
Vital signs were as follows: heart rate, 98 beats per minute; blood pressure 102/46 mm Hg; respiratory rate, 24 breaths per minute; temperature, 100.6°F, and oxygen saturation, 94% on room air. The patient looked minimally dehydrated. The abdominal examination initially showed pain and tenderness with guarding, predominantly located in the right upper quadrant; however, subsequent examinations showed it to be more localized in the right lower quadrant.
Levels obtained in chemistry studies and of liver enzymes were within reference range. Human chorionic gonadotropin was negative. A complete blood count showed hemoglobin of 13.7 g/dL; hematocrit of 0.406; 206,000 platelets/μL; and 20,300 white blood cells/μL. The differential showed 91.4% granulocytes, 2.2% lymphocytes, and 6.4% monocytes. Chest radiographs showed prominence of the superior mediastinum and possibility of enlarged nodes or other mass. The remainder of the lung fields was clear, and the heart was of normal size. An abdominal computed tomography scan showed fatty infiltration of the liver and no other significant abnormality. The appendix was not mentioned.
General surgery was consulted, and an exploratory laparotomy was performed with a preoperative diagnosis of appendicitis. An appendectomy was performed.
The specimen consisted of an appendix measuring 5.2 cm in length by 0.6 cm in diameter. The serosal and cut surfaces were grossly unremarkable. Histological examination revealed areas of mucosal inflammation and the structures shown in Figures 1, 2, and 3.
Enterobius vermicularis (pinworm)
Enterobius vermicularis, also known as pinworm, is a small nematode with females measuring approximately 8 to 13 mm by 0.3 to 0.5 mm and males measuring 2 to 5 mm by 0.1 to 0.2 mm.1 It is one of the most common human intestinal helminthes, with 5% to 15% of the US population infected.2 Worldwide, the prevalence has been reported as high as 88% in some populations.3 Humans are the only natural host. Unlike other parasitic infections, pinworms do not have a predilection for any particular socioeconomic class, affecting upper and lower classes equally. Children, aged 5 to 14 years, are most commonly affected. Most individuals are infected via the fecal-oral route; however, the eggs may survive in dust, resulting in an "airborne" route of infection. Autoinfection is also possible because of an apparent lack of protective immunity in humans, even after exposure.
Eggs hatch in approximately 6 hours after ingestion in the stomach or duodenum. Young worms mature in as little as 2 weeks and live for approximately 11 days to 2 months. Normally, mature adult worms reside in the proximal colon, terminal ileum, and appendix. Females migrate to the anus and deposit up to 11,000 eggs, most often at night, often resulting in symptoms of pruritis ani/vulvar pruritis.2,4 Other than these uncomfortable symptoms, pinworms are generally regarded as harmless.
E. vermicularis has been described in several extragastrointestinal organs including the lung, liver, breast, spleen, and fallopian tube.2,4-6 E. vermicularis was first described in the appendix in 1634 by Febricius Hildanus. Since the initial report of Still7 in 1899, associating appendiceal infestation with 19% of cases of pediatric appendicitis, the exact relationship of E. vermicularis and appendicitis has been a subject of some dispute.4 The reported worldwide incidence of E. vermicularis in the appendix of patients with signs and symptoms of appendicitis has ranged from 0.2% to 41.8%.4 Some studies show a strong correlation between the presence of pinworms in the appendix and acute or chronic appendiceal inflammation, whereas others show only a weak correlation or no correlation at all. Still others have shown that inflammation is more common in pinworm-infested appendectomies for symptomatic patients than incidental appendectomies in which pinworms were found. The sex of the infecting pinworm has not been found to impact the degree of inflammation.5
Some studies suggest the use of the term "appendiceal colic" to describe patients who presented with signs/symptoms of appendicitis without histological evidence of inflammation.3,4,8 Most sources agree that the presence of Enterobius eggs in the appendiceal lumen, an indication of obstruction, is more commonly associated with inflammation.
Histologically, E. vermicularis is characterized by a prominent esophageal bulb and spines along the outside of the worm called lateral alae (Figs. 1-3). Because fecal samples generally fail to show the presence of pinworm ova, the preferred diagnostic method is the "scotch tape test," in which cellophane tape is applied to the perianal area of the affected individual and examined for eggs which measure 50 to 60 μm by 20 to 32 μm9 and resemble a football which has been flattened on one side.1 Asymptomatic individuals are rarely treated. When necessary, symptomatic patients are treated with an oral dose of mebendazole, 100 mg PO, or pyrantel, 11 mg/kg, not to exceed 1 g. A second dosage is recommended in 1 to 2 weeks to ensure helminthic eradication and prevent reinfection.1,2 Albendazole, 400 mg, given orally once and then repeated in 2 weeks, may also be used.
1. Garcia L, Bruckner D. Diagnostic Medical Parasitology. 2nd ed. Washington, DC: American Society for Microbiology; 1993:191-194.
3. Wiebe BM. Appendicitis and Enterobius vermicularis. Scand J Gastroenterol. 1991;26:336-338.
4. Arca M, Gates R, Groner J. Clinical manifestations of appendiceal pinworms in children: an institutional experience and a review of the literature. Pediatr Surg Int. 2004;20:372-375.
5. Williams DJ, Dixon MF. Sex, Enterobius vermicularis and the appendix. Br J Surg. 1988;75:1225-1226.
6. Sterba J, Vlcek M. Appendiceal enterobiasis-its incidence and relationships to appendicitis. Folia Parasitol (Praha). 1984;31:311-318.
7. Still GF. Oxyuriasis vermicularis in children. Br Med J. 1899;1:898-900.
8. Nordstrand I, Lakshman J. Enterobius vermicularis and clinical appendicitis: worms in the vermiform appendix. ANZ Journal of Surgery 2004;74:1024.
9. Ash L, Orihel T. Atlas of Human Parasitology. 4th ed. Chicago, Ill: American Society of Clinical Pathologists; 1997:32-33, 184-187.
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