• A Case of Duodenal Ulcers from Strongyloides

A Case of Duodenal Ulcers from Strongyloides


Researchers describe a nearly missed case of Strongyloides infection in the April issue of Gastroenterology, had it not been for analysis of duodenal biopsies.

Douglas Grunwald et al describe the case of a 74-year-old Jamaican-born woman with a 3-month history of dyspepsia, nausea, bloating, early satiety, and weight loss of 40 lbs. In the past, she had been infected with Helicobacter pylori and Strongyloidesboth of which were treated; she also had a history of acid reflux, diabetes, and hypertension. Her medications included metformin, simvastatin, and losartan.

An abdominal computed tomography (CT) scan showed signs of endometrial cancer. She subsequently had an uncomplicated abdominal hysterectomy. However, she continued to have nausea, anorexia, and failure to thrive.

Gastro_parasite

On readmission to the hospital 15 days after surgery, a CT scan showed small bowel hyperenhancement, edema, and anasarca. Tests of stool for  Strongyloides ova, parasite, and antibodies all gave negative results. The physicians performed an esophagogastroduodenoscopy and found large, geographic duodenal ulcers with brownish discoloration of the mucosa (arrows in figure A). She had not used nonsteroidal anti-inflammatory drugs and tested negative for H pylori.

Duodenal biopsies revealed parasitic forms consistent with Strongyloides species (figure B).

Strongyloides is a soil-transmitted helminth—its primary mode of infection is through contact with soil that is contaminated with free-living larvae. When the larvae come in contact with skin, they penetrate it and migrate through the body, eventually finding their way to the small intestine, where they burrow and lay their eggs. Unlike other soil-transmitted helminths like hookworm or whipworm, whose eggs do not hatch until they are in the environment, the eggs of Strongyloides hatch into larvae in the intestine. Most of these larvae are excreted in the stool, but some of the larvae molt and immediately re-infect the host either by burrowing into the intestinal wall or by penetrating the perianal skin.

Gastrointestinal manifestations of Strongyloides infection include nausea, vomiting, anorexia, abdominal pain, and protein-losing enteropathy. Patients are usually treated with anti-helminth drugs (eg, ivermectin, albendazole).

The researchers say that they did not have positive results from stool studies or ELISAs for Strongyloidesserum antibodies because the sensitivity of repeated stool evaluation is around 50%, and sensitivity of the ELISA test is 65%–90%. Furthermore, the antibodies are often not detected in immune-compromised patients.

Grunwald et al  state that the best way to detect this infection is by histopathology analysis of duodenal biopsies. The endoscopic features of duodenal Strongyloides infection are broad and include edema, brown discoloration of the mucosa, erythema, subepithelial hemorrhages, and megaduodenum. These features are nonspecific and are also seen in patients with ischemic ulcers, users of nonsteroidal anti-inflammatory drugs, or patients with cancer or H pylori infection.

Due to the patient’s history of previous Strongyloides infection, the authors began treating her with ivermectin before pathologic confirmation of the parasite.

Grunwald et al say that the severity of the patient’s illness was likely precipitated by her recent malignancy and a new diagnosis of human T-lymphotropic virus (HTLV-1) infection, which is endemic to the Caribbean and commonly observedin combination with Strongyloides.

The authors propose that HTLV-1 disrupts the ability of T cells to detect and eliminate Strongyloides. 

The patient was treated successfully with an extended regimen of ivermectin and nutritional support. Four months after treatment, her weight was stable, her albumin level increased, and a repeat esophagogastroduodenoscopy showed normal duodenal mucosa.

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