Case Report: Disseminated Strongloides stercoralis Presenting as an Ulcerated Gastric Mass in an HIV-1-Infected Patient

ABSTRACT.

Disseminated Strongloides stercoralis is a common phenomenon among patients with immunosuppression. In this report, we present a case of disseminated Strongloides stercoralis presenting as a gastric mass in a 42-year-old male patient with a known history of HIV-1 infection and type 2 diabetes mellitus (T2DM). The patient presented with symptoms and signs suggestive of acute on chronic erosive gastritis, which included persistent vomiting. Endoscopic examination revealed a gastric mass with no signs of malignancy or dysplasia. There was noted to be chronic inflammation along with morphologic features consistent with the larvae and eggs of Strongloides nematodes in a biopsied gastric mass tissue and duodenum. The disease subsequently resulted in death despite the administration of ivermectin.

INTRODUCTION

Strongyloidiasis is caused by parasitic infection due to nematode of the genus Strongyloides, mainly Strongyloides stercoralis. The infection affects between 30 and 100 million people around the world—particularly in people residing in Africa, South America, and Southeast Asia.^1,2 Strongyloidiasis usually presents subclinically or with mild abdominal symptoms.³ Nonetheless, some patients with certain risk factors may develop Strongloides stercoralis hyperinfection or dissemination. In Strongloides stercoralis hyperinfection syndrome, the parasite results in a severe form of infection that mainly involves the organs under the larvae’s life cycle that is typically represented by the involvement of the lungs. However, in disseminated form of the disease, organs (such as the liver, spleen, etc.) other than those that are part of the parasite’s life cycle are involved. The most common risk factors associated with disseminated strongloidiasis include corticosteroid therapy, HTLV-1 infection, HIV-1 infection, organ transplantation, malnutrition, and chronic alcoholism.^4,5 Although a recent case series showed that type 2 diabetes mellitus (T2DM) was not a common risk factor for Strongloides dissemination or hyperinfection status,⁶ cases of disseminated strongloidiasis among patients with T2DM have been reported.^7,8

Involvement of the gastric mucosa during disseminated strongloidiasis is a rare phenomenon.⁹ Here, we present a case of a known HIV-1-infected patient with a recent history of uncontrolled T2DM, admitted to the intensive care unit (ICU) due to moderate anemia and signs of gastric outlet obstruction from gastric mass and duedenitis, complicated by disseminated strongloidiasis. The disease subsequently resulted in septic shock, multiorgan failure, and death despite the administration of ivermectin.

CASE REPORT

A 42-year-old male patient with a known history of T2DM of 4 years duration and HIV-1 infection of 6 months duration presented at Amin General Hospital with a history of epigastric pain and persistent vomiting of 1-week duration. The vomitus consisted of ingested, bilious matter. Vomiting was aggravated by ingestion of any kind of meal, and there was no known relieving factor. In addition, the patient noted low-grade, intermittent fever, dry cough, and fatigue, and he also claimed that he had lost 20 kg over 1 month before presentation to the hospital. He was on antiretroviral therapy for only 1 month before admission to the hospital. He was not taking any antidiabetic medications.

Physical examination revealed pale conjunctivae and buccal mucosa. Examination of the lungs and cardiovascular system was normal except for abdominal tenderness in the epigastric area. The patient’s leukocyte count was 9.9 × 10⁹/L, hemoglobin of 8.8 gm/dL, platelet count of 148 × 10⁹/L, eosinophil count of 0.50 × 10⁹/L, CD4⁺ count was 111 cells/µL, fasting blood glucose of 232 mg/dL, and HgA1c of 10%. Serology for hepatitis B and C viruses as well as RT-PCR for SARS-CoV-2 were all negative. Examination of the stool also revealed Strongloides parasites. Sputum and urine examinations were normal. Abdominal computed tomography scan revealed gastric wall thickening, and hepatomegaly with multiple small ring enhancing hypodense lesions in both liver lobes along with mild splenomegaly.

Endoscopic examination revealed edematous gastric mucosa that appeared like an infiltrating mass lesion and loss of gastric rugae, extending from the body to the antral part, along with multiple superficial erosions, fibrin coated multiple ulcerations, and hypoactive stomach. In addition, there was evidence of severe submucosal petechial hemorrhages and intense inflammation also involving the superior parts of duodenum (Figure 1A–C). Multiple biopsies from the gastric mass and the duodenum were obtained for pathological examination. Microscopic examination revealed regular mucosal glands accompanied by chronic inflammation. There were also morphologic features present confirming the presence of Strongloides eggs and larvae (Figure 1D–F). There were no features of malignancy observed within the limit of the biopsied area. Nonetheless, we did not perform biopsy of the liver and the spleen because the patient was critically ill.

Figure 1.

Strongloides stercoralis hyperinfection syndrome in an HIV-1-infected patients with type 2 diabetes mellitus. Endoscopy showing (A) multiple superficial erosions and fibrin coated multiple ulcerations, (B) subepithelial petechial hemorrhages and intense inflammation, (C) multiple edematous gastric mucosa that appeared like an infiltrating mass lesion, and (D–F) Strongloides stercoralis rhabditiform larvae (blue arrows) seen in the gastric antral glands. This figure appears in color at www.ajtmh.org.

The patient was admitted to the ICU and treated with daily doses of ivermectin (200 µg/kg body weight), and broad-spectrum antibiotics (vancomycin 1 g IV twice/day, and meropenem 1 g IV 3×/day) administered for 2 weeks. His course was complicated by respiratory failure and intractable shock, requiring intubation, supported with noradrenaline and dopamine drips in addition to the fluid administration. Despite treatment, his condition deteriorated, and the patient eventually died of multiorgan failure after a 2-week period in the ICU.

DISCUSSION

Recent systematic review and meta-analysis conducted in Ethiopia reported an overall pooled prevalence of 5.1% Strongloides stercoralis infection among HIV‐1-infected patients.⁴ Whereas the use of microscopy to diagnose the infection yielded a pooled prevalence of 3.6%, the utility of culture and serological-based methods increased the detection rate to 10.8% and 12.4%, respectively.⁴ This finding indicates that the method of diagnosis is highly relevant in identifying cases of Strongloides stercoralis infection correctly.

Infection with the parasite Strongyloides stercoralis is extremely common in Ethiopia with a prevalence of 56% in some settings.⁹ Moreover, the prevalence of Strongloides stercoralis infection among HIV-1-infected patients in Ethiopia is estimated to be approximately 5.6%.⁹ Notably, the risk is increased by 4.6-fold when the CD4⁺ T-cell count is < 200 cells/µL,⁹ resulting in complications including hyperinfection syndrome or dissemination. Although T2DM appears to be insignificant risk factor, it might be associated with Strongloides stercoralis hyperinfection syndrome or dissemination.^6–8 Our patient suffered from chronic immunosuppression demonstrated by his low CD4⁺ T-cell count, which was related to poorly controlled HIV-1 infection. In addition, the patient had uncontrolled newly diagnosed T2DM that may have contributed significantly to the profound immunosuppression and disseminated Strongloides stercoralis infection, involving the gastric, duodenum, and most probably the liver and the spleen. The involvement of the liver and spleen is not typical finding for patients with strongloidiasis.^4,9 However, the involvement of the liver and spleen by Strongloides or other common opportunistic infections, such as Toxoplasma, was not ascertained in our cases because we did not perform biopsy and histopathology exams. As is the case presented in this report, patients with advanced HIV and Strongloides stercoralis fail to respond to the standard course of thiabendazole or ivermectin treatment and may die because of disseminated infection and other complications.¹⁰ Overall, the mortality of patients with disseminated Strongloides stercoralis infection can reach as high as 70% to 90% despite aggressive therapy.¹¹

To date, few cases of disseminated Strongloides stercoralis infection leading to gastric mass and severe erosive duodenitis in patients coinfected with HIV-1 have been documented.^12–17 Disseminated Strongloides stercoralis infection with gastric involvement has been reported in patients with T2DM.⁷ To the best of our knowledge, our patient represents the first case of Strongloides stercoralis infection presenting with a gastric mass and duodenitis in a patient with HIV-1 infection. A high index of suspicion is necessary to diagnose and treat such patients presenting with a gastric mass at the earliest and to prevent morbidity and mortality. Disseminated strongloidiasis should be considered in high-risk patients with inflammatory gastric mass and anemia.