These rhabditiform larvae may now follow three alternative life cycles:

1. Autoinfection and endoautoinfection occur when the rhabditiform larvae are converted to infective filariform larvae within the lumen of the intestine. In endoautoinfection the filariform larvae reenter the host by penetrating through the mucosa of the distal small bowel or colon to enter mesenteric venules, migrate throughout the body, and repeat their life cycle. In autoinfection the filariform larvae reenter the body of the host by penetrating the anal and perianal skin, renewing the life cycle, as it were, bottom up! It is this phenomenon of autoinfection that perpetuates the existence of the infection in the host for up to 10 years or indefinitely--even after his or her environment has been changed and there is no opportunity for filariform larvae to obtain access to the feet.

2. The direct homogenic cycle is followed when the rhabditiform larvae in the feces develop into filariform larvae and reenter the skin of the host from the soil.

3. The indirect heterogenic cycle is followed when the rhabditiform larvae in the feces develop in the soil through four molts into free-living adults that copulate and produce eggs which become rhabditiform larvae and perpetuate the cycle. This "free-living" cycle continues until the environment becomes unfavorable (exactly what is involved in this change is not known), at which time some larvae become infective filariform larvae capable of penetrating human skin and beginning a parasitic life within the host's lungs and intestines.

The effect of this cycle on the lungs, intestines, and other organs is dependent on the parasitic load. When heavy, pulmonary hemorrhage and pneumonia may occur and the bowel mucosa may be honeycombed by both the adult worms and the hatching larvae, causing sloughing and hemorrhage. The tissue changes and reactions may be summarized as follows:

a. In the skin, larval invasion produces erythema, edema, and foreign body reaction. Scratching may cause superficial ulceration.

b. In the blood, eosinophilia is produced. In the late stages, Escherichia coli septicemia may be seen.

c. In the lungs, eosinophilic nodules may he formed with foreign body reaction due to larval penetration or, less commonly, adult worm penetration. Inflammatory changes can occur with development of pneumonitis or bronchopneumonia. Petechial hemorrhagic areas may be present.

d. In the intestines, based upon his observations on 10 fatal cases, DePaola has classified the different forms of enteritis seen in strongyloidiasis into three types:

1. Catarrhal enteritis is characterized by mucosal congestion and excessive mucus secretion. Hemorrhages and tiny mucosal ulcerations can sometimes be seen. The parasites are found only in the intestinal crypts.

2. Edematous enteritis is characterized by thickening of the intestinal wall by submucosal edema, swelling of the folds, and elongation of the villi, followed later by flattening and atrophy of the overlying mucosa, resembling the pattern seen in tropical sprue. Minimal inflammation is present. Parasites may be present in all layers of the intestinal wall.

3. Ulcerative enteritis is characterized by thickening of the intestinal wall by edema and fibrosis resulting in a rigid, tube-like appearance of the intestine. Longstanding disease can produce irreversible mural fibrosis and a pipestem or "ribbon bowel" configuration (although isolated case reports indicate that in some patients these changes are reversible with thiabendazole therapy). Mucosal atrophy, loss of villi, and ulcers will be seen at this stage (Fig. 13.3). Mucosal and submucosal inflammation with granuloma formation and eosinophil infiltration are present (Fig. 13.4). The inflammatory changes extend throughout the wall of the gut and into the serosa and mesenteric lymph nodes. Ulcers measuring up to 7 mm in diameter may also be present in the large bowel from autoinfection (Fig. 13.5). Worms may be seen throughout the wall of the bowel, and there is a marked inflammatory response because of secondary bacterial invasion. E. coli may be carried into the circulation by the larvae, thus accounting for the gram-negative septicemia which may be a complication in hyperinfected patients.

Any of these three forms of enteritis may be seen in fatal cases. Marked variation in the pathological response of the intestinal mucosa and wall to infection with S. stercoralis larvae accounts for the variety of gastrointestinal symptoms as well as the wide spectrum of radiological findings seen on small bowel series (discussed later). Both the radiological features and pathological changes in catarrhal and edematous enteritis are reversible with treatment. The changes seen in the ulcerative type are usually not reversible because of fibrosis.

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Fig. 13.3 (A and B) Intestinal strongyloidiasis in two fatal cases from Puerto Rico with hyperinfection. Note the numerous mucosal hemorrhages and ulcerations in each autopsy specimen. In (B) numerous filariform larvae and granulomas were present in the thickened wall of the colon. AFIP 63-2039 and 69-6753-1. (B Courtesy of Dr. Raul A. Marcial-Rojas, San Juan).

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Fig. 13.4 Strongyloides stercoralis --fatal infection in an institutionalized child. (A) Low magnification showing adult worm in lumen of bowel. (B and C) Portions of an adult worm in the mucosa. Note the intense inflammation. (D) Larval forms invading the submucosa with marked inflammatory response in the same patient. (A-D courtesy of Dr. Herman Zaiman).

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Fig. 13.5 Strongyloidiasis of the colon. (A) Transverse section of the splenic flexure obtained at autopsy. The patient was a woman from the Democratic Republic of the Congo with lepromatous leprosy who had been treated with corticosteroids for a reaction, with subsequent development of fatal hyperinfection strongyloidiasis. The colonic stenosis was evident in an antemortem barium enema. AFIP 72-863. (B) There are multiple ragged ulcers in the mucosal surface of the same colon. AFIP 72-884.