An unusual cause of overt gastrointestinal bleeding in a malnourished child

Introduction

Soil-transmitted helminths are the most common cause of parasitic infestation worldwide. ¹ Species that infect humans includes the whipworm Trichuris trichiura, the roundworm Ascaris lumbricoides, and the hookworm Ancylostoma duodenale. Trichuriasis is caused by various species, mostly in humans by Trichuris trichiura. Hookworm causing overt gastrointestinal bleeding (GI) has been reported. ² A severe form of trichuris infestation is known as Trichuris dysentery syndrome (TDS). It manifests as mucous diarrhoea, bleeding, malnutrition and stunting or even life-threatening anaemia. ³ We report a child who presented with TDS mimicking inflammatory bowel disease. She was successfully treated with oral albendazole. This report highlights TDS as one of the causes of overt GI bleeding in tropical countries.

Case report

A 7-year-old girl presented with loose bloody stools with mucus for 2 months. She had five to six bowel movements a day with generalised abdominal pain, which woke her frequently at night. Bleeding was initially 8–10 drops per stool but subsequently her condition worsened and she became lethargic just prior to admission. On enquiry, her mother had noticed these symptoms intermittently for 2 years, but had not consulted any doctor. Over this period, she had lost 7 kg weight. She denied perianal pain, itching, any rectal protrusion or passage of worms in the stool. She denied ingesting soil. She came from a family of low socioeconomic status.

Physical examination revealed a tachycardia (112/min) and a tachypnoea (24 breaths/min). She had marked pallor, pedal oedema and koilonychia. She was listless with sparse and hypopigmented hair. Weight and height were 16 kg and 100 cm, respectively (below 3rd centile). There were crepitations over both lung bases.

Laboratory results showed a microcytic anaemia (Hb, 3.8 g/dL; MCV, 60 fl; Hematocrit, 0.16). There was microcytic hypochromic anaemia, and eosinophilia (10%) on a peripheral smear. Erythrocyte sedimentation rate (ESR) was 40 mm/hr. The HIV status was negative. Stool microscopic examination showed numerous red blood cells. Colonoscopy showed numerous small, white, mobile worms in the entire colon (Figure 1a–c). The parasites were extracted with biopsy forceps; T. Trichiura larvae were reported and eggs confirmed (Figure 1d). A biopsy revealed non-specific colitis. In view of her symptomatic anaemia, she was transfused blood. Albendazole 400 mg orally was initiated for 3 days, after which she showed marked clinical improvement and was discharged. Oral iron supplements were recommended for 3 months. Family screening was advised. Follow-up stool examination after 2 weeks was negative for Trichuris eggs. OPEN IN VIEWER

Discussion

Trichuriasis infestation is found predominantly in tropical and subtropical regions of Asia, especially in China, India and Southeast Asia. Prevalence may attain 95% among children. ⁴ Humans acquire Trichuriasis infection after ingestion of embryonated eggs via contaminated food or water. The eggs hatch and mature in the distal small bowel. After maturation in about 2–3 months, adult worms are found in the caecum and ascending colon. T. trichiura begins to produce eggs 3 months after the infection and undergoes development in soil.

In view of normally light infestation, most patients with Trichuriasis are asymptomatic. However, with a heavy worm load, TDS may develop. ⁵ High infestation may be due to poor sanitary habits as well as pica. ⁶ The clinical syndrome comprises chronic diarrhoea, anaemia, abdominal pain, weight loss and malnutrition. Bloody stools may cause severe or even life-threatening anaemia, leading to clubbed fingers, poor growth, and developmental and cognitive deficits. Most case reports of patients with T. trichiura infestation describe chronic bloody stools or chronic diarrhoea.^7–9 Intestinal bleeding is thought to arise from adult worms using a spear-like projection at their anterior end to attach to the intestinal lining, which leads to intestinal mucosal ulceration responsible for a daily blood loss of 0.005 mL per worm per day. ¹⁰

The pathogenesis of TDS remains unclear. Increased numbers of tissue infiltrating monocytes and increased local production of tumour necrosis factor (TNF-α) have been found in the colonic mucosa. ¹¹ The profound growth retardation in TDS is a consequence of a chronic inflammatory response as well as a decrease in plasma insulin-like growth factor-1 (IGF-1) and increase in TNF-α. Despite the striking overlapping clinical features with inflammatory bowel disease, the colonic mucosa in TDS shows minimal inflammatory changes if at all. The treatment of choice is mebendazole (100 mg twice daily) or albendazole (400 mg daily) for 3 days. ⁸ Both regimes achieve a success rate in the range of 70–80%. A repeat course of therapy may be needed in subjects who fail to clear the infestation. Albendazole requires dose reduction to 200 mg in children aged 12–24 months. Under the age of 1 year, the dosage of these drugs is not specified. TDS is reversed by repeated treatment of the infestation, together with iron supplementation. ¹² Increasing positive psychological stimulation in the child's environment is necessary for significant developmental and cognitive deficits. ¹ Control measures focused particularly on personal hygiene, avoidance of pica, proper sanitation and faecal disposal, boiling water before drinking can also help prevent re-infection and interrupt transmission.