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Epidemiology and Pathology

The commonest parasites to penetrate the bowel wall and cause helminthoma are the nematodes. The most important are the strongyli, Oesophagostomum apiostomum and Oesphagostomum stephanostomum (var. thomasi). Helminthoma can also be caused by Ancylostoma duodenale (the hookworm) or the rare Oesophagostomum brumpti and Oesophagostomum bifurium. Anisakis may occasionally cause ileal or cecal nodules (see Chap. 11 ). Although other worms, particularly Ascaris, have been known to escape from a bowel which has been infected and damaged by amebic or other dysentery, they do not provoke the same marked granulomatous reaction with surrounding fibrosis in the wall of the gut as occurs in a helminthoma.

Oesophagostoma are common parasites of the colons of sheep, goats, pigs, cattle, apes, monkeys and other wildlife, in which they may cause serious illness, characterized by emaciation, dysentery and peritonitis. These worms occur in West and East Africa, Brazil, Indonesia, the Philippines, China and less commonly, in central and southern Africa. Because the eggs may be indistinguishable from those of the hookworms (which are widely distributed and can also rarely cause helminthomas), the species causing human helminthomas may not be accurately identified. The exact incidence is difficult to assess; there is the often quoted figure of an infection rate for O. apiostomum of 4% in convicts in northern Nigeria, but this is a 1960 reference and probably no longer accurate. Elmes and McAdam (1954) described 28 patients with helminthoma in Uganda and thought this represented a small fraction of the total. There is no racial preference; Africans, Caucasians, Hispanics, Asiatics and anyone else living in the tropics may be affected at any age.

In the life cycle of Oesophagostomum, eggs are passed in the feces of the animal host; then the larvae hatch in the soil and develop to their infective stage and are ingested by a new host feeding on contaminated grass (man is always an accidental host for this parasite). Within their new host, larvae leave their sheaths and penetrate into the wall of the intestine, usually in the lower small bowel, and molt to their third stage. In 5 days they return to the intestinal lumen and move to the cecum and colon, where they undergo another molt and become adults. They may then penetrate the intestinal mucosa again, and the worms provoke an inflammatory reaction in the muscular layer of the bowel (Fig. 18.1). This can develop into an abscess, which may enlarge and extend into the mesocolon; it does not obstruct the bowel lumen. Adjacent small bowel and omentum may adhere to the enlarging abscess, forming a palpable, tender mass. After the acute phase has subsided, the abscess may:

1. Undergo resolution with absorption or calcification of the worm, which rarely may be visible on a plain film of the abdomen (Fig. 18.1D). Sometimes the calcified, dead worm may be recognized coincidentally on an abdominal radiograph or histologically without any clinical history of disease.

2. Perforate into the bowel lumen, causing diarrhea, or into the peritoneal cavity causing peritonitis.

3. Adhere to the abdominal wall.

4. Enter a chronic stage and become a further diagnostic problem!

Microscopically, in the very early stage, a granuloma may be recognized which is scarcely more than a nodule or small intramural tumor. There may be more than one. Secondary infection of the granuloma is likely to occur and cause the clinical swelling and tenderness. Usually there is edema with inflammation and fibrosis involving the submucosa, muscularis and pericolonic adipose tissue. Finding the worm may be difficult because it is dwarfed by the extent of the severe inflammatory reaction. Thus the diagnosis may be missed and an erroneous diagnosis of diverticulitis or other abscess may be made. The pathognomonic lesion of helminthoma is 2 to 4 cm in diameter and has a central zone of eosinophilic necrotic tissue, often with a zone of degenerating nuclei. There may be palisaded epithelioid cells surrounding the worm. Beyond the central necrosis are a mixture of eosinophils, lymphocytes and plasma cells. Granulation and scar tissue form the outer perimeter.

In the majority of patients, the worm will have degenerated and is no longer identifiable. O. apiostomum is approximately 1 cm long and 0.3 mm thick. O. stephanostomum is about twice this size. When the worm dies, it curls up and is eventually mineralized (calcified) and becomes visible radiographically. In the tropics, the tissues of many patients contain mineralized worms and eggs, and Oesphagostomum cannot be distinguished from any other mineralized parasites.

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Fig. 18.1 (A) Helminthoma of the transverse colon (C) of an Ugandan native. The large white granulomatous mass in the mesocolon contains an abscess cavity into which a small Oesophagostomum worm projects (arrow). Specific identification of these worms is difficult because intact specimens are rarely obtained. AFIP 76-2110. (Courtesy of Prof. M.S.R. Hutt, Kampala) (B) The surgical specimen of a helminthoma in the colon: it is impossible to make the correct diagnosis either clinically or by imaging, and it can be very difficult at surgery or from the surgical specimen. (C) Helminthoma: cross-sections of Oesophagostomum species larvae within a large abscess in the intestinal wall. Note that the worm has a relatively large intestine and meromyarian and plantmyarian somatic muscles. x11; MIS 74-13235. (From Marty and Andersen 1995) (D) The calcified remnant of a worm in a helminthoma. This is somewhat larger than the actual parasite.

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